907	PGE 2 promotes intestinal tumor growth by altering the expression of tumor suppressing and DNA repair genes. PGE 2 promotes intestinal tumor growth by altering the expression of tumor suppressing and DNA repair genes. PGE 2 promotes intestinal tumor growth by altering the expression of tumor suppressing and DNA repair genes. PGE 2 promotes intestinal tumor growth by altering the expression of tumor suppressing and DNA repair genes. PGE 2 promotes intestinal tumor growth by altering the expression of tumor suppressing and DNA repair genes. PGE2 intestinal tumor growth tumor suppressing gene expression DNA repair PGE2 intestinal tumors tumor suppressing genes DNA repair genes inflammation intestinal cancer cytokines prostaglandin E2 genetic alterations intestinal epithelial cells molecular mechanisms PGE2 intestinal tumor growth expression tumor suppressor DNA repair genes molecular mechanisms cancer biology prostaglandin E2 intestinal epithelial cells cell proliferation apoptosis genetic regulation intestinal adenocarcinoma PGE2 tumor growth intestinal cancer genes inflammation tumor progression PGE2 signaling pathway PGE2 gene expression anti-inflammatory drugs tumor PGE2 and DNA repair tumor suppressor genes regulation PGE2 intestinal epithelial cells PGE2 intestinal tumor growth tumor suppressor DNA repair genes expression molecular biology cancer research genetic regulation PGE2 tumor growth intestinal cancer gene expression alteration tumor suppressor genes DNA repair mechanisms prostaglandin E2 oncogenic pathways gastrointestinal tumors gene regulation in cancer PGE2 prostaglandin E2 intestinal cancer tumor suppressor genes DNA repair genes gene expression colorectal cancer inflammatory response oncogenesis PGE2 intestinal tumors tumor suppressor genes DNA repair genetic expression intestinal cancer PGE2 mechanisms tumor promotion gene alteration intestinal epithelial cells cancer biology PGE2 intestinal tumor growth tumor suppressing genes DNA repair expression molecular mechanisms cancer biology intestinal inflammation PGE2 intestinal cancer tumor suppressor genes DNA repair mechanisms inflammatory response cancer progression gene expression modulation colorectal cancer oncogenic pathways prostaglandin E2 epithelial cells genetic alterations
350	Discrimination between the initiator and elongation tRNAs depends on the translation initiation factor IF3. Discrimination between the initiator and elongation tRNAs depends on the translation initiation factor IF3. Discrimination between the initiator and elongation tRNAs depends on the translation initiation factor IF3. Discrimination between the initiator and elongation tRNAs depends on the translation initiation factor IF3. Discrimination between the initiator and elongation tRNAs depends on the translation initiation factor IF3. translation initiation elongation tRNAs discrimination translation initiation factor IF3 molecular biology biochemical processes protein synthesis genetic code cellular mechanisms translation initiation factor IF3 tRNA discrimination initiation tRNA elongation tRNA translational initiation protein synthesis molecular biology cellular processes RNA recognition biochemical mechanisms translation initiation elongation tRNA discrimination process translation factors IF3 function molecular biology RNA roles protein synthesis biochemistry translation initiation factor IF3 function discrimination mechanism tRNAs elongation tRNA characteristics initiation tRNA properties translation process regulation role of IF3 in translation tRNA classification during translation IF3 binding specificity molecular basis tRNA discrimination translation initiation factors roles translation initiation factor IF3 discriminator function tRNA initiation tRNA elongation tRNA molecular biology protein synthesis genetic code cellular processes translation initiation factor IF3 discrimination mechanism tRNA types elongation factor initiation tRNA IF3 function tRNA recognition translational accuracy biological translation process discrimination initiator tRNAs elongation tRNAs translation initiation factor IF3 molecular biology protein synthesis RNA recognition cellular mechanisms biochemistry genetic translation translation initiation factor IF3 discrimination mechanism tRNA types elongation tRNA initiator tRNA translational initiation molecular biology protein synthesis cellular mechanisms translation initiation factor IF3 discriminator role tRNA types elongation tRNA initiation tRNA molecular biology protein synthesis genetic code cellular processes translational regulation translation initiation factor IF3 tRNA discrimination initiation tRNA elongation tRNA molecular biology protein synthesis translational control biochemical mechanisms
230	Carriers of the alcohol aldehyde dehydrogenase deficiency mutation drink less that non-carries. Carriers of the alcohol aldehyde dehydrogenase deficiency mutation drink less that non-carries. Carriers of the alcohol aldehyde dehydrogenase deficiency mutation drink less that non-carries. Carriers of the alcohol aldehyde dehydrogenase deficiency mutation drink less that non-carries. Carriers of the alcohol aldehyde dehydrogenase deficiency mutation drink less that non-carries. alcoholism genetic predisposition AADEH acetaldehyde metabolism ethanol geneticvariation ALDH2 Asian populations studysamples clinicaltrials alcohol aldehyde dehydrogenase deficiency carriers non-carriers drinking genetic mutation health metabolism alcohol metabolism genetic mutation ADH deficiency drinking behavior allele frequency liver function ethanol tolerance acetaldehyde accumulation East Asian ancestry polymorphism epidemiology alcohol dehydrogenase deficiency carriers gene genetic mutation impact drinking habits ALDH2 deficiency Asian ancestry alcohol metabolism health outcomes genetic testing population studies ethanol dehydrogenase epidemiology research alcohol aldehyde dehydrogenase deficiency carriers non-carriers drinking habits alcohol metabolism genetic mutation liver function ethanol tolerance ASHMD acetaldehyde buildup health outcomes genetic testing dietary habits genetic variations alcohol aldehyde dehydrogenase deficiency carriers mutation drinking habits non-carriers genetic mutation enzyme function alcohol metabolism genetic mutation ADH deficiency drinking behavior carriers non-carriers health outcomes genetic predisposition alcohol dehydrogenase alcohol aldehyde dehydrogenase deficiency mutation carriers non-carriers drinking habits genetics ethanol metabolism liver enzyme risk consumption epidemiology alcoholism risk genetic mutation AALD Asian population liver metabolism enzymatic function epidemiology genetic testing health behavior alcohol consumption patterns
593	Incidence of heart failure decreased by 10% in women since 1979. Incidence of heart failure decreased by 10% in women since 1979. Incidence of heart failure decreased by 10% in women since 1979. Incidence of heart failure decreased by 10% in women since 1979. Incidence of heart failure decreased by 10% in women since 1979. heartfailure incidence gender statistics medicalresearch cardiovasculardisease demographics publichealth epidemiology gendergap heartfailure incidence genderdifferences agegroup riskfactors cardiovasculardisease statistics medicalresearch publichealth epidemiology heart failure incidence gender statistical trends medical research cardiovascular health epidemiology women's health cardiac disease public health statistics incidence heart failure women trend statistics cardiovascular disease public health medical research demographic shift lifestyle changes heart failure incidence women 1979 medical trends cardiovascular health epidemiology heart failure incidence women 1979 trends gender differences in heart failure rates historical heart failure data heart failure reduction females heart failure incidence women health trends cardiac diseases reduction gender health disparities cardiovascular conditions medical research findings heart failure incidence gender differences cardiac health trends female cardiovascular outcomes historical heart failure data heartfailure incidence gender trends medicalresearch cardiovascularhealth epidemiology timeperiod statisticalanalysis heart failure incidence gender differences cardiovascular health trends women health improvement cardiac diseases reduction medical statistics public health metrics
1216	The extracellular domain of TMEM27 is cleaved in human beta cells. The extracellular domain of TMEM27 is cleaved in human beta cells. The extracellular domain of TMEM27 is cleaved in human beta cells. The extracellular domain of TMEM27 is cleaved in human beta cells. The extracellular domain of TMEM27 is cleaved in human beta cells. extracellular region TMEM27 protein human beta cells cleavage process glycoproteins signal peptides enzymes endoplasmic reticulum intercellular communication diabetes research molecular biology techniques extracellular domain TMEM27 cleavage human beta cells mechanism insulin processing protease signaling extracellular domain TMEM27 cleavage human beta cells protein processing diabetes insulin regulation signaling protease localization function extracellular region TMEM27 protein beta cell function cleavage process human cells membrane protein processing extracellular domain TMEM27 human beta cells cleavage protease signaling pathway diabetes insulin secretion membrane protein extracellular region TMEM27 protein beta cell processing cleavage sites human beta cells molecular biology cellular signaling extracellular TMEM27 human beta cells cleavage protein domain diabetes insulin secretion signaling molecule glycoprotein protease glucose-responsive extracellular domain TMEM27 beta cells cleavage human diabetes proteolytic cleavage B-cell secretion molecular biology endoplasmic reticulum glycosylation extracellular domain TMEM27 human beta cells cleavage protein processing insulin production diabetes research cell signaling protease activity molecular biology techniques extracellular proteolysis human beta cells TMEM27 processing glycoproteins cell signaling
1337	Ubiquitin ligase UBC13 generates a K63-linked polyubiquitin moiety at PCNA K164. Ubiquitin ligase UBC13 generates a K63-linked polyubiquitin moiety at PCNA K164. Ubiquitin ligase UBC13 generates a K63-linked polyubiquitin moiety at PCNA K164. Ubiquitin ligase UBC13 generates a K63-linked polyubiquitin moiety at PCNA K164. Ubiquitin ligase UBC13 generates a K63-linked polyubiquitin moiety at PCNA K164. Ubiquitination K63-link polyubiquitin PCNA E3 ligase UBC13 function DNA repair proteasome signaling pathway ubiquitin chain cell cycle regulation Ubiquitin UBC13 PCNA K63 polyubiquitin protein modification DNA damage response cell cycle proteasome degradation ubiquitination polyubiquitin chains PCNA K164 site E3 ligase K63 ubiquitination Ubc13-Uev1a complex ubiquitination process polyubiquitin chain formation PCNA modification ubiquitin conjugation K63 linkage protein degradation pathway ubiquitin ligase function UBC13 substrate specificity Ubiquitin UBC13 PCNA K63 polyubiquitin protein modification DNA repair cell cycle proteasome substrate conjugation biology genetics Ubiquitin ligase UBC13 K63-linked polyubiquitin PCNA K164 protein modification DNA damage response cell cycle regulation Ubiquitin UBC13 K63 polyubiquitin PCNA K164 protein modification DNA repair cellular process molecular biology Ubiquitin UBC13 K63 polyubiquitin PCNA K164 protein degradation DNA repair E3 ligase Ubiquitin ligase UBC13 K63-linked polyubiquitin PCNA K164 protein complex E3 ligase DNA repair cell cycle ubiquitination proteasome SUMOylation DNA damage response Ubiquitination PCNA modification K63 ubiquitination Ubiquitin conjugation proliferating cell nuclear antigen protein degradation WEE1 kinase Ubiquitin system
232	Cataract and trachoma are the primary cause of blindness in Southern Sudan. Cataract and trachoma are the primary cause of blindness in Southern Sudan. Cataract and trachoma are the primary cause of blindness in Southern Sudan. Cataract and trachoma are the primary cause of blindness in Southern Sudan. Cataract and trachoma are the primary cause of blindness in Southern Sudan. Cataract treatment trachoma infection Southern Sudan healthcare blindness prevention ophthalmology in Sudan eye disease in Africa cataract trachoma blindness Southern Sudan health eye disease medical conditions tropical diseases public health eye care neglected tropical diseases ophthalmology cataract treatment trachoma prevention blindness causes Southern Sudan health eye disease visual impairment ophthalmology tropical diseases public health medical conditions vision loss eye care African blindness neglected tropical diseases cataract treatment trachoma prevention blindness in Africa eye health in Sudan public eye care vision loss causes ophthalmology in developing countries blindness prevention programs infectious diseases affecting eyes cataract surgery options Cataract trachoma blindness Southern Sudan eye diseases public health tropical diseases vision impairment cataract treatment trachoma prevention blindness causes Southern Sudan health eye disease prevalence Cataract treatment trachoma epidemiology Southern Sudan blinding diseases prevalence risk factors Cataract treatment trachoma epidemiology Southern Sudan blindness prevalence risk factors eye health preventive measures community awareness Cataract treatment trachoma prevalence Southern Sudan blindness eye disease epidemiology Cataract treatment trachoma prevention Southern Sudan health eye disease prevalence blindness statistics public eye health tropical eye diseases
1336	UCB T cells reduce TCR diversity after transplantation. UCB T cells reduce TCR diversity after transplantation. UCB T cells reduce TCR diversity after transplantation. UCB T cells reduce TCR diversity after transplantation. UCB T cells reduce TCR diversity after transplantation. UC Berkeley T helper cells T cell receptor immune system transplant rejection immunology research stem cell transplantation UCB stem cells T cell receptor transplantation immunology immune system diversity hematopoietic stem cells UC Berkeley T helper cells transplantation immune response T cell receptor diversity immune system adaptation stem cell transplantation T cell function post-transplantation immunity UCB cells TCR repertoire transplantation outcomes immune system recovery stem cell transplant T cell function hematopoietic stem cells immunology research clinical transplantation TCR diversity maintenance UCB stem cells transplantation TCR immune system T cells bone marrow heterogeneity transplantation immunology UCB cells T cell receptor immune system stem cell transplantation T cell diversity transplant rejection immunology hematopoietic stem cells immune response UCB T cells TCR diversity transplantation immune system stem cells bone marrow transplantation immune reconstitution T cell receptor UCB cells T cell receptor transplantation outcomes immune system stem cell transplant T cell diversity immunology hematopoietic stem cells TCR repertoire UCB cells T cells TCR diversity transplantation immune system stem cells hematopoietic stem cells immunology transplant rejection T cell receptor bone marrow transplantation UCB stem cells T cell receptor repertoires immune reconstitution transplantation outcomes immunologykeywords alloreactivity post-transplantation immunity
233	Cell autonomous sex determination in somatic cells does not occur in Galliformes. Cell autonomous sex determination in somatic cells does not occur in Galliformes. Cell autonomous sex determination in somatic cells does not occur in Galliformes. Cell autonomous sex determination in somatic cells does not occur in Galliformes. Cell autonomous sex determination in somatic cells does not occur in Galliformes. sex determination somatic cells Galliformes avian biology sex chromosomes gene expression reproductive biology molecular genetics evolutionary biology cell autonomy somatic cells Galliformes sex determination mammals birds reproduction female development male development genetics biology reproductive biology cell autonomy sex determination somatic cells Galliformes avian biology genetic determination sexual differentiation zoology genetics research sex chromosomes developmental biology sex determination mechanisms galliformes biology somatic cell sex determination avian sex determination cell autonomy in sex determination Galliformes genetics sex determination somatic cells Galliformes avian biology genetic mechanisms chromosomal regulation developmental biology sex chromosomes gene expression evolutionary biology biological sex differentiation sex determination mechanisms galliformes biology somatic cell sex determination avian sex determination cell autonomy genetic factors in sex determination cell autonomous sex determination somatic cells Galliformes birds sex chromosomes sexual development genetic mechanisms sex determination somatic cells Galliformes avian biology sex chromosomes genetic mechanism reproductive biology gene expression developmental biology evolutionary genetics cell autonomy somatic cells Galliformes sex determination molecular biology birds genetics chromosomal mechanisms hormonal influences cell non-autonomous sex determination Galliformes sex chromosomes Galliformes somatic cells sex determination genes somatic cell sex differentiation Galliformes genetics
354	Downregulation and mislocalization of Scribble prevents cell transformation and mammary tumorigenesis. Downregulation and mislocalization of Scribble prevents cell transformation and mammary tumorigenesis. Downregulation and mislocalization of Scribble prevents cell transformation and mammary tumorigenesis. Downregulation and mislocalization of Scribble prevents cell transformation and mammary tumorigenesis. Downregulation and mislocalization of Scribble prevents cell transformation and mammary tumorigenesis. downregulation Scribble cell transformation mammary tumorigenesis protein mislocalization oncogenesis tumor suppression cell signaling gene expression cancer biology Scribble protein function molecular机制 cellular localization tumor suppression cancer biology mammalian cells molecular biology genetic regulation cell transformation mammary tumorigenesis Scribble protein cell adhesion molecular biology tumor suppression gene expression mislocalization signal transduction cancer biology downregulation Scribble mislocalization Scribble cell transformation prevention mammary tumorigenesis inhibition Scribble protein function tumor suppressor Scribble Scribble cellular localization oncogenic processes regulation Scribble gene expression Scribble pathway analysis downregulation mislocalization Scribble cell transformation mammary tumorigenesis molecular biology cancer research genetics mouse models proteins signaling pathways tumor suppressors downregulation Scribble mislocalization Scribble cell transformation prevention mammary tumorigenesis prevention Scribble protein function tumor suppression mechanisms Scribble cellular localization cancer development inhibitors downregulation Scribble mislocalization cell transformation mammary tumorigenesis cancer biology protection mechanism tumor suppression gene expression protein localization molecular biology malignant transformation personalized medicine biological pathways downregulation Scribble mislocalization cell transformation mammary tumorigenesis molecular biology cancer research genetic regulation protein localization tumor suppressor genes Scribble protein cell transformation mammary tumorigenesis gene expression cell adhesion tumor suppressor protein localization cancer biology oncogenes signaling pathways downregulation Scribble cell transformation mammary tumorigenesis protein localization oncogenesis tumor suppression genetic regulation cell signaling cancer biology
475	Glycolysis is one of the primary glycometabolic pathways in cells. Glycolysis is one of the primary glycometabolic pathways in cells. Glycolysis is one of the primary glycometabolic pathways in cells. Glycolysis is one of the primary glycometabolic pathways in cells. Glycolysis is one of the primary glycometabolic pathways in cells. glycolytic pathway glycometabolism cellular metabolism glucose oxidation energy production metabolic pathway biochemistry enzymatic reactions ATP production 糖酵解 有氧代谢 glycolysis glycometabolic pathways cellular metabolism energy production glucose ATP metabolic pathway biochemistry cellular respiration fermentation glycolysis definition glycometabolic pathways list cellular respiration glucose metabolism pyruvate production glycolytic enzymes anaerobic respiration metabolic pathway diagram energy production process metabolic pathway types glycometabolism cellular respiration energy production metabolic pathway glucose breakdown anaerobic metabolism biochemical reactions glycolytic enzymes glycolytic pathway 糖酵解 丙酮酸 乳酸发酵 glycolysis glycometabolic pathways cellular metabolism glucose energy production anaerobic respiration ATP phosphofructokinase enolase glycometabolic pathways cellular respiration glycolytic pathway metabolic processes glucose metabolism energy production biochemical reactions cellular energy anaerobic respiration sugar breakdown glycometabolism cellular metabolism energy production anaerobic respiration metabolic pathway hexose splitting Glycometabolic pathways glycolysis definition glycolysis process glycolysis steps glycolysis products glycolysis importance glycolysis regulation glycolysis enzymes glycolysis overview glycolysis vs cellular respiration glycolysis glycometabolic pathways cells cellular metabolism glucose energy production biochemistry metabolic pathway enzymatic reactions glycolytic enzymes glycolytic pathway diagram glycometabolism cellular respiration glucose breakdown metabolic pathway regulation
113	Angiotensin converting enzyme inhibitors are associated with increased risk for functional renal insufficiency. Angiotensin converting enzyme inhibitors are associated with increased risk for functional renal insufficiency. Angiotensin converting enzyme inhibitors are associated with increased risk for functional renal insufficiency. Angiotensin converting enzyme inhibitors are associated with increased risk for functional renal insufficiency. Angiotensin converting enzyme inhibitors are associated with increased risk for functional renal insufficiency. angiotensin enzymes inhibitors kidney dysfunction side effects medication treatment hypertension diuretics proteinuria dialysis chronic kidney disease angiotensin inhibitors renal dysfunction side effects medication treatment outcomes kidney failure hypertension diabetes cardiovascular pharmacology angiotensin inhibitors renal insufficiency risk medication side effects ACE diabetes hypertension angiotensin converting enzyme inhibitors associated increased risk functional renal insufficiency cardiovascular side effects hypertension treatment medication kidney failure clinical symptoms mechanisms prevention alternative therapies angiotensin converting enzyme inhibitors renal insufficiency risk association medication side effects kidney dysfunction clinical trial study Angiotensin ACE inhibitors renal function kidney failure side effects drug interactions hypertension treatment angiotide ACE inhibitors kidney failure renal dysfunction side effects hypertension treatment angiotensin kidney risk insufficiency inhibitors renal dysfunction medication side effects angiotensin kidney failure medication side effects hypertension treatment medication interactions clinical study analysis angiotensin renal failure medication side effects ACE inhibitors kidney function clinical trials pharmacology hypertension treatment
1335	UCB T cells maintain high TCR diversity after transplantation. UCB T cells maintain high TCR diversity after transplantation. UCB T cells maintain high TCR diversity after transplantation. UCB T cells maintain high TCR diversity after transplantation. UCB T cells maintain high TCR diversity after transplantation. UC Berkeley T lymphocytes T cell receptor immunotherapy transplant immunity immune system diversity hematopoietic stem cell transplantation UCB cells TCR repertoire transplantation outcomes immune reconstitution hematopoietic stem cells adaptive immunity transplantation immunology T cell development clinical transplantation TCR diversity maintenance UC Berkeley T lymphocytes T cell receptor immunotherapy stem cell transplantation adaptive immunity immune system diversity hematopoietic stem cells transplantation immunology T cell receptor diversity UCB transplantation immune reconstitution stem cell transplantation T cell maintenance immunotherapy hematopoietic stem cells adaptive immunity transplantation medicine TCR repertoires UCB T cells TCR diversity transplantation hematopoietic stem cells immune reconstitution dynamic repertoire V(D)J recombination maintenence mechanisms UCB cells T cell receptor immune system diversity transplantation outcomes stem cell transplant T cell maintenance immunology research TCR repertoires hematopoietic stem cells immune reconstitution UCB T cells TCR diversity transplantation hematopoietic stem cells dendritic cells antigen presentation BMT immune reconstitution UCB cells T cell receptor transplantation outcomes immune system maintenance stem cell transplant T cell diversity immunology techniques hematopoietic stem cells adaptive immunity TCR repertoires UCB cells T cells TCR diversity transplantation immunology hematopoietic stem cells immune system T cell receptor bone marrow transplantation transplant immunology T cell receptor repertoire immune reconstitution stem cell transplantation adaptive immunity TCR gene diversity UCB T cell function
597	Incidence rates of cervical cancer have decreased. Incidence rates of cervical cancer have decreased. Incidence rates of cervical cancer have decreased. Incidence rates of cervical cancer have decreased. Incidence rates of cervical cancer have decreased. cervical_cancer_prevalence trends_cervical_cancer decline_cervical_cancer_cases prevention_cervical_cancer screening_effectiveness_cervical_cancer vaccination_impact_cervical_cancer public_health_strategies_cervical_cancer cervical_cancer incidence_rates trends prevention screening mortality public_health gynecology oncology treatment risk_factors cervical_cancer_prevalence trends_cervical_cancer decline_cervical_cancer causes_cervical_cancer_reduction vaccination_effectiveness pap_smear_screening public_health_strategies cervical_cancer_decreased_factors cervical_cancer_screening_improvement cervical_cancer_prevention_strategies cervical_cancer_incidence_trends cervical_cancer_screening_effectiveness cervical_cancer incidence_rates decrease cancer_screening HPV_infection mortality_rates prevention_strategies public_health_measures cervical_cancer_decrease cervical_cancer_prevalence cervical_cancer_statistics cervical_cancer_risk_factors cervical_screening_effectiveness cervical_cancer incidence_rates cancer_screening early_detection HPV_vaccination public_health_strategies treatment_improvements cervical_cancer incidence_rates 下降趋势 预防措施 筛查技术 医疗进步 生活方式改变 疫苗接种 早期诊断 女性健康 肿瘤学研究 cervical_cancer incidence_rates trends prevention_strategies screening_programs vaccination_campaigns healthcare_access demographic_factors geographic_distribution age_groups risk_factors cervical_cancer_prevention early_detection_cervical_cancer cervical_cancer_screening HPV_vaccination_effectiveness cervical_health_statistics cervical_cancer_risk_factors
1213	The deregulated and prolonged activation of monocytes has deleterious effects in inflammatory diseases. The deregulated and prolonged activation of monocytes has deleterious effects in inflammatory diseases. The deregulated and prolonged activation of monocytes has deleterious effects in inflammatory diseases. The deregulated and prolonged activation of monocytes has deleterious effects in inflammatory diseases. The deregulated and prolonged activation of monocytes has deleterious effects in inflammatory diseases. deregulated monocytes prolonged activation inflammatory diseases monocyte function inflammatory response immune system chronic inflammation monocyte biology immune activation cytokines inflammation markers monocyte activation inflammatory diseases chronic inflammation immune response cytokines macrophages immunology disease progression cell signaling innate immunity monocyte activation inflammatory diseases immune response cytokines chronic inflammation monocyte dysfunction autoimmune diseases inflammation pathways immunology research monocyte activation inflammatory diseases immune response cytokine release tissue injury chronic inflammation immune cells pathological processes macrophage function immune system dysregulation monocyte activation inflammatory diseases prolonged inflammation immune response cytokines chronic inflammation monocyte function inflammatory markers monocyte activation inflammatory diseases immune response chronic inflammation monocyte function cytokine production macrophage role disease progression immune system pathophysiology monocyte activation inflammatory diseases immune response chronic inflammation cytokines macrophages autoimmune disorders cardiovascular disease tissue repair immune system dysfunction monocyte activation inflammatory diseases deregulation prolonged inflammation immune response cytokines pathogenesis monocyte function chronic inflammation disease progression monocyte activation inflammatory diseases chronic inflammation immune response cytokines macrophages cardiovascular disease autoimmune disorders biomarkers therapeutic interventions monocyte activation inflammatory diseases immune response chronic inflammation cytokines macrophages immunology disease progression therapeutic targets
598	Incidence rates of cervical cancer have increased due to nationwide screening programs based primarily on cytology to detect uterine cervical cancer. Incidence rates of cervical cancer have increased due to nationwide screening programs based primarily on cytology to detect uterine cervical cancer. Incidence rates of cervical cancer have increased due to nationwide screening programs based primarily on cytology to detect uterine cervical cancer. Incidence rates of cervical cancer have increased due to nationwide screening programs based primarily on cytology to detect uterine cervical cancer. Incidence rates of cervical cancer have increased due to nationwide screening programs based primarily on cytology to detect uterine cervical cancer. cervical_cancer incidence_rates screening_programs cytology uterine_cervical_cancer HPV_infection early_detection cancer_screening public_health_strategies healthcare_policy cervical_cancer incidence_rates screening_programs cytology uterine_cervical_cancer public_health oncology gynecology HPV_screening prevention_strategies epidemiology cervical_dysplasia Pap_test healthcare_policy incidence cancer screening programs cytology detection uterine cervical health evidence prevalence trends population statistics medical public health preventive care biopsy molecular testing HPV vaccination comorbidity age ethnicity geography quality improvement sensitivity specificity accuracy clinical guidelines healthcare access patient outcomes screening intervals adherence education healthcare disparities incidence cervical_cancer screening_programs uterine_cervical_cancer cytology detection rates nationwide public_health cervical_cancer incidence_rates screening_programs cytology uterine_cervical_cancer public_health oncology gynecology medical_screening cancer_prevention healthcare_policy cervical_cancer_screening uterine_cervical_cancer_prevention cytology_tests cervical_cancer_risk_factors nationwide_cancer_screening_programs cervical_cancer_statistics cervical_cancer_detection_methods cervical_cancer incidence_rates screening_programs cytology uterine_cervical_cancer public_health early_detection oncology gynecology epidemiology cervical_cancer incidence_rates screening_programs cytology uterine_cervical_cancer public_health gynecology oncology preventive_care health_screening cancer_detection medical_screening epidemiology healthcare_policy cervical_cancer incidence_rates screening_programs cytology uterine_cervical_cancer public_health epidemiology preventive_medicine gynecology oncology healthcare_policy women_health HPV_infection early_detection mortality_rates cervical_cancer_screening uterine_cervix_cytology pap_test cervical_dysplasia HPV_infection cervical_cancer_prevention screening_effectiveness cervical_cancer_mortality cervical_cancer_risk_factors cervical_cancer_statistics
115	Anthrax spores can be disposed of easily after they are dispersed. Anthrax spores can be disposed of easily after they are dispersed. Anthrax spores can be disposed of easily after they are dispersed. Anthrax spores can be disposed of easily after they are dispersed. Anthrax spores can be disposed of easily after they are dispersed. anthrax bacillus cyanide decontamination survival dispersal spore killing sterilization bioterrorism anthrax spores disposal methods safety containment treatment precautions biohazard anthrax survival dispersal decontamination spore killing microbial powder bioterrorism exposure hazard removal treatment prevention anthrax处置方法 anthrax孢子清除 安全处理anthrax孢子 如何有效清除anthrax anthrax孢子处置建议 anthrax spores disposal dispersion biohazard containment treatment safety protocol anthrax safety spore disposal biological warfare cleanse decontamination sterilization treatment prevention risks handling anthrax spores disposal methods containment decontamination sterilization biohazard treatment precautions anthrax survival dispersal decontamination effective disposal spore killing methods sterilization techniques biological warfare emergency response anthrax spores disposal methods safety precautions biohazard containment treatment anthrax spores disposal methods safety precautions containment treatment infection bioterrorism
236	Cell autonomous sex determination in somatic cells occurs in Passeriformes. Cell autonomous sex determination in somatic cells occurs in Passeriformes. Cell autonomous sex determination in somatic cells occurs in Passeriformes. Cell autonomous sex determination in somatic cells occurs in Passeriformes. Cell autonomous sex determination in somatic cells occurs in Passeriformes. cell biology somatic genetics Passeriformes sex chromosomes developmental biology DNA methylation heterochrony sexual differentiation cell biology somatic cells Passeriformes sex determination genetics molecular biology avian biology avian somatic cells sex chromosomes genomic research cell biology sex chromosomes genetic determinism avian biology somatic genetics Passeriformes taxonomy sexual development molecular biology epigenetics evolutionary biology cell autonomous sex determination somatic cells Passeriformes avian biology genetic mechanisms sexual development somatic sex determination avian somatic cells bird genetics sex determination theory cell autonomous sex determination somatic cells Passeriformes avian biology sex chromosomes Wnt signaling eve gene G9a KDM6A differentiation male germline-independent cell fate determination genetic mechanisms somatic cells sex Passeriformes biology avian sex determination sex chromosomes epigenetic regulation developmental biology evolutionary genetics cell autonomous sex determination somatic cells Passeriformes bird species sex chromosomes genetic mechanism sex determination systems avian biology somatic sex determination cell autonomous sex determination somatic cells Passeriformes avian biology genetic mechanisms sex chromosome epigenetics gene regulation developmental biology evolutionary biology molecular genetics sex reversal bird genetics cell autonomous sex determination somatic cells Passeriformes birds molecular biology genetics sex chromosomes avian biology genomic imprinting heterogamety evo-devo cell non-autonomous sex determination mechanisms somatic cells biology Passeriformes genetics avian sex determination somatic sex differentiation gene expression somatic cells Passeriformes genomics
478	Golli-deficient T-cells prefer to differentiate into an anergic phenotype in the adaptive immune response when there are increased levels of Ca2+ in the cytosol. Golli-deficient T-cells prefer to differentiate into an anergic phenotype in the adaptive immune response when there are increased levels of Ca2+ in the cytosol. Golli-deficient T-cells prefer to differentiate into an anergic phenotype in the adaptive immune response when there are increased levels of Ca2+ in the cytosol. Golli-deficient T-cells prefer to differentiate into an anergic phenotype in the adaptive immune response when there are increased levels of Ca2+ in the cytosol. Golli-deficient T-cells prefer to differentiate into an anergic phenotype in the adaptive immune response when there are increased levels of Ca2+ in the cytosol. Golli proteins T-cell differentiation anergy Ca2+ signaling adaptive immunity immune response cytosolic calcium t-cell development Golli-protein T-cell differentiation anergy Ca2+ cytosol immune response calcium signaling T-cell activation adaptive immunity Golli-proteins T-cell-differentiation anergy Ca2+ cytosolic-signaling immune-response Golli protein function T-cell differentiation process adaptive immunity mechanisms calcium ion role immune system regulation T-cell anergy induction Ca2+ cytosolic signaling Golli-deficient cellular response Golli-proteins T-cells differentiation anergy Ca2+ cytosol immune response adaptive immunity Golli protein T-cell differentiation anergic phenotype calcium signaling adaptive immunity immune response T-cell activation calcium cytosol immune regulation Golli proteins T-cell differentiation anergy Ca2+ signaling adaptive immunity molecular biology immune response calcium ions T-cell activation Golli-proteins T-cell differentiation anergy Ca2+ cytosol adaptive immunity immune response Golli-proteins T-cells differentiation anergy Ca2+ cytosol immune response adaptive immunity calcium signaling t-cell development Golli proteins T-cell differentiation anergy Ca2+ signaling adaptive immunity cytosolic calcium immune response regulation
1332	Tumor necrosis factor alpha (TNF-α) and interleukin-1 (IL-1) are pro-inflammatory cytokines that inhibit IL-6 and IL-10. Tumor necrosis factor alpha (TNF-α) and interleukin-1 (IL-1) are pro-inflammatory cytokines that inhibit IL-6 and IL-10. Tumor necrosis factor alpha (TNF-α) and interleukin-1 (IL-1) are pro-inflammatory cytokines that inhibit IL-6 and IL-10. Tumor necrosis factor alpha (TNF-α) and interleukin-1 (IL-1) are pro-inflammatory cytokines that inhibit IL-6 and IL-10. Tumor necrosis factor alpha (TNF-α) and interleukin-1 (IL-1) are pro-inflammatory cytokines that inhibit IL-6 and IL-10. tumor necrosis factor pro-inflammatory cytokines IL-6 inhibition IL-10 suppression immune response inflammatory markers cytokine network inflammation mechanism immune modulation Tumor necrosis factor alpha pro-inflammatory cytokines inhibit IL-6 IL-10 molecular biology inflammation immune response therapy disease signaling pathway mechanism tumor necrosis factor pro inflammatory cytokines IL-6 inhibition IL-10 regulation cytokine biology immune response modulation inflammatory disorders cytokine signaling tumor necrosis factor alpha effects pro-inflammatory cytokines functions interleukin 1 inhibition cytokine signaling pathway inflammatory response mechanisms IL-6 regulation IL-10 suppression immune system activation TNF-α biological actions cytokine network interactions Tumor necrosis factor alpha IL-1 pro-inflammatory cytokines IL-6 IL-10 inhibit effect regulation tumor necrosis factor alpha effects interleukin 1 function pro-inflammatory cytokines mechanism inhibition of il-6 regulation of il-10 production cytokine interactions inflammatory response markers immune system modulation biomarker analysis inflammation pathways TNF-alpha IL-1 pro-inflammatory cytokines IL-6 IL-10 immune response inflammation biosignals tumor necrosis factor TNF-alpha interleukin-1 IL-1 pro-inflammatory cytokines IL-6 inhibition IL-10 suppression tumor necrosis factor TNF-alpha pro-inflammatory cytokines IL-1 IL-6 IL-10 inflammatory response immune system biomarkers autoimmune disorders chronic inflammation cytokine storm disease progression gene expression immunology biochemistry TNF-alpha inhibitors IL-1 inhibitors inflammatory cytokines immunomodulation chronic inflammation autoimmune diseases cytokine storm adaptive immunity innate immunity
237	Cells lacking clpC have a defect in sporulation efficiency in Bacillus subtilis. Cells lacking clpC have a defect in sporulation efficiency in Bacillus subtilis. Cells lacking clpC have a defect in sporulation efficiency in Bacillus subtilis. Cells lacking clpC have a defect in sporulation efficiency in Bacillus subtilis. Cells lacking clpC have a defect in sporulation efficiency in Bacillus subtilis. sporulation Bacillus_subtilis clpC_protein protein_degradation gene_expression bacterial_sporulation cellular_defects clpC protein Bacillus subtilis sporulation sporulation process cell biology genetic defect Bacillus subtilis genes clpC function Bacillus subtilis sporulation clpC protein cell division gene expression bacterial sporulation protein degradation sporangium development genetic mutation cellular physiology sporulation process clpC function Bacillus subtilis genetics protein degradation cellular differentiation bacterial spore formation clp protease role clpC protein Bacillus subtilis sporulation process cellular machinery defective genes molecular biology proteolysis system protein degradation Bacillus subtilis sporulation clpC protein function cell division process genetic mutation effects bacterial spore formation sporulation regulation protein complex role gene expression analysis bacterial adaptation stress response mechanisms clpC protein sporulation process Bacillus subtilis genetics cell development bacterial spore formation gene function analysis proteolysis regulation sporulation Bacillus subtilis clpC protein cell biology genetic defect bacterial development protein function clpC protein Bacillus subtilis sporulation heat shock response protein degradation sporulation regulation transcription factors genetic mutation effects bacterial differentiation sporulation Bacillus subtilis clpC protein cell division gene function protein degradation bacterial development transcription factors genetic mutations
238	Cells undergoing methionine restriction may activate miRNAs. Cells undergoing methionine restriction may activate miRNAs. Cells undergoing methionine restriction may activate miRNAs. Cells undergoing methionine restriction may activate miRNAs. Cells undergoing methionine restriction may activate miRNAs. cells methionine restriction microRNAs starvation proteomics metabolism gene expression transcriptional regulation nutrition methionine restriction cells miRNAs activation metabolism gene expression nutrition aging cancer regulation cells methionine restriction miRNAs microRNAs starvation response growth synthesis nutrition biomarkers genetic regulation transcription post-transcriptional regulation metabolism aging cancer diabetes oxidative stress methionine restriction effects miRNAs activation cellular response metabolic restriction gene expression regulation nutrient deprivation epigenetic changes stress response metabolic pathways RNA molecules molecular biology bioinformatics transcriptomics cell signaling cells methionine restriction miRNAs activation metabolism genetic expression regulation signaling pathways methionine restriction effects microRNA activation cancer cell metabolism protein synthesis regulation MET diet impact cells methionine restriction miRNAs microRNAs genetic regulation signaling pathways metabolism aging proliferation cancer dietary interventions methionine restriction miRNAs cellular metabolism gene expression longevity cancer nutrition aging cell biology methionine restriction miRNAs transcription regulation survival mechanism nutrition impact genetic response cells methionine restriction miRNAs microRNAs genetic regulation protein synthesis biological response metabolism gene expression nutrition starvation biomarkers molecular biology transcription translation
118	Antibiotic induced alterations in the gut microbiome reduce resistance against Clostridium difficile Antibiotic induced alterations in the gut microbiome reduce resistance against Clostridium difficile Antibiotic induced alterations in the gut microbiome reduce resistance against Clostridium difficile Antibiotic induced alterations in the gut microbiome reduce resistance against Clostridium difficile Antibiotic induced alterations in the gut microbiome reduce resistance against Clostridium difficile antibiotics gut bacteria Clostridium difficile inflammation resistance microbiota dysbiosis therapy treatment prevalence antibiotics gut microbiota Clostridium difficile inflammation resistance pathogenesis microbiome diversity probiotics antibiotic stewardship fecal microbiota transplantation antibiotics gut bacteria Clostridium difficile inflammation microbiota probiotics resistance fiber diet immunity antibiotics gut microbiota Clostridium difficile infection microbiome diversity antibiotic-associated dysbiosis gut flora changes probiotics and gut health microbial ecology fecal microbiota transplantation antimicrobial stewardship immune system response antibiotics gut microbiota Clostridium difficile infections resistance therapy probiotics dietary fiber metagenomics immunity antibiotics gut microbiota Clostridium difficile inflammation immune response dysbiosis probiotics metabolomics therapeutic interventions antibiotics gut microbiota Clostridium difficile infection resistance probiotics fiber diet microbiome diversity immune response antibiotics gut microbiota Clostridium difficile inflammation resistance microbiome diversity probiotics fecal transplant antimicrobial stewardship antibiotics gut microbiota Clostridium difficile infection prevalence resistance modulation therapeutic interventions probiotics fecal microbiota transplantation antibiotics gut microbiota Clostridium difficile inflammation resistance probiotics dietary fiber microbial diversity antimicrobial stewardship
239	Cellular aging closely links to an older appearance. Cellular aging closely links to an older appearance. Cellular aging closely links to an older appearance. Cellular aging closely links to an older appearance. Cellular aging closely links to an older appearance. cellular老化 senescence skin老化 DNA损伤 telomere缩短 free radicals oxidative stress chronological年龄 biological年龄 cellular aging appearance skin biology genetic telomere mitochondria senescence wrinkles longevity cellular senescence telomere shortening oxidative stress genomic instability mitochondrial dysfunction aging process skin aging wrinkles sagging skin photoaging cellular aging factors cellular aging signs cellular aging process cellular aging mechanisms cellular aging markers cellular aging symptoms cellular aging effects cellular老化 telomere缩短 DNA损伤累积 细胞分裂限制 衰老标志物增加 cellular aging markers cellular senescence telomere shortening oxidative stress DNA damage aging skin premature aging anti-aging treatments chronological age indicators biological age assessment cellular senescence telomere shortening DNA damage oxidative stress senescent cells skin aging chronological aging molecular markers biological age cellular aging skin aging telomere shortening oxidative stress senescent cells collagen degradation wrinkles photoaging genomic instability cellular aging skin aging telomere shortening oxidative stress senescent cells DNA damage aging biomarkers chronological age biological age cellular senescence telomere shortening oxidative stress genomic instability mitochondrial dysfunction aging processes chronological age biological age senescent cells age-related diseases
911	PKG-la plays an essential role in expression of pain hypersensitivity in PGK-la knockout mice. PKG-la plays an essential role in expression of pain hypersensitivity in PGK-la knockout mice. PKG-la plays an essential role in expression of pain hypersensitivity in PGK-la knockout mice. PKG-la plays an essential role in expression of pain hypersensitivity in PGK-la knockout mice. PKG-la plays an essential role in expression of pain hypersensitivity in PGK-la knockout mice. PKG-la pain hypersensitivity PGK-la knockout mice nociception signaling pathway genetic knockout sensory neurons inflammatory pain neuropathic pain PKGLA pain hypersensitivity PGK-la knockout mice gene expression nociception mouse models genetic knockout pain mechanisms pain sensitivity genetic knockout PKG-la function mouse model nociception pain signaling knockout mice PKG pathway pain modulation sensory neurons PKGLA function pain sensitivity mechanisms genetic knockout models nociception pathways PKGLA knockout effects pain signaling cascade gene expression analysis pain hypersensitivity causes PKGLA protein structure PKG-la pain hypersensitivity PGK-la knockout mice molecular mechanism gene function pain research mouse model PKG-la pain hypersensitivity PGK-la knockout mice molecular mechanisms nociception gene expression analgesia mouse models sensory neurons inflammation neurotransmitters signaling pathways PKG-la pain hypersensitivity PGK-la knockout mice gene expression nociception mouse model analgesia inflammation neurotransmitters sensory neurons PKG-la pain hypersensitivity PGK-la knockout mice mouse model pain research neuroscience genetic modification pain signaling/pathway pharmacology biomedical science PKG-la pain hypersensitivity PGK-la knockout mice molecular mechanism neuroscience research keywords mouse models genetic knockout analgesia PKG-la pain hypersensitivity PGK-la knockout mice knockout models nociception neurotransmitters gene expression pain mechanisms mouse models sensory neurons inflammation analgesics signaling pathways
913	PPAR-RXRs are inhibited by PPAR ligands. PPAR-RXRs are inhibited by PPAR ligands. PPAR-RXRs are inhibited by PPAR ligands. PPAR-RXRs are inhibited by PPAR ligands. PPAR-RXRs are inhibited by PPAR ligands. PPAR RXRs ligands inhibition transcription factors agonists regulation signaling PPARRXR inhibition PPARligands transcriptionfactors dimerization retinoid XR research mechanism signaling molecularbiology PPAR agonists PPAR activators RXR activation PPAR isoforms nuclear receptors ligand binding domains transcription factors fatty acids thiazolidinediones retinoid X receptors peroxisome proliferator signaling pathways PPAR RXR inhibition PPAR ligands function PPAR-RXR pathway RXR activation inhibitors PPAR signaling mechanism ligand binding PPAR PPAR isoforms interaction RXR heterodimerization PPAR agonists effects PPAR-RXRs inhibitors PPAR ligands transcription factors nuclear receptors coactivators corepressors gene expression metabolic diseases cardiovascular health PPAR inhibitors RXR activation ligand binding transcription factors metabolic diseases nuclear receptors drug targets gene expression cardiovascular health lipid metabolism PPAR-RXR ligands inhibitors transcription factors signaling pathways drug targets molecular biology PPAR RXRs ligands inhibition beneficial keywords efficacy search优化 药物抑制 转录因子互作 PPAR-RXRs PPAR ligands coactivators transcription factors lipid metabolism diabetes cardiovascular diseases agonists antagonists gene expression nuclear receptors PPAR activators RXR activation ligand binding affinity transcription factor interaction nuclear receptor agonists
914	PPAR-RXRs can be activated by PPAR ligands. PPAR-RXRs can be activated by PPAR ligands. PPAR-RXRs can be activated by PPAR ligands. PPAR-RXRs can be activated by PPAR ligands. PPAR-RXRs can be activated by PPAR ligands. PPAR agonists RXR activation nuclear receptors ligand binding transcription factors PPAR RXRs ligands activators dimerization transcription fatty acids glycerides thiazolidinediones nuclear receptors retinoid X receptors co-activators agonists antagonists signaling metabolism diabetes atherosclerosis PPAR activators RXR ligands nuclear receptors lipid metabolism transcription factors fatty acids thiazolidinediones retinoids endocrine signaling metabolic syndrome PPAR-RXR activation PPAR ligands types RXR ligands PPAR-RXR signaling PPAR ligand examples RXR activation mechanisms PPAR-RXR complex function PPAR ligand binding sites RXR protein interaction PPAR-RXR pathway regulation PPAR-RXR ligands activation transcription factors nuclear receptors lipid metabolism diabetes cardiovascular disease PPAR compounds RXR activators PPAR agonists nuclear receptors ligand activation PPAR isoforms RXR heterodimers lipid signaling transcription factors metabolic regulation PPAR-RXR ligands activation nuclear receptors agonists transcription factors PPAR-RXR activation PPAR ligands transcription factors agonists nuclear receptors PPAR-RXRs activators PPAR ligands coactivators transcription factors fatty acids synthetic agonists gene expression metabolic diseases cardiovascular health PPAR agonists RXR activation nuclear receptors lipid metabolism transcription factors diabetes treatment cardiovascular disease gene expression ligand binding drug targets
1339	Ultrasound guidance significantly raises the number of traumatic procedures when attempting needle insertion. Ultrasound guidance significantly raises the number of traumatic procedures when attempting needle insertion. Ultrasound guidance significantly raises the number of traumatic procedures when attempting needle insertion. Ultrasound guidance significantly raises the number of traumatic procedures when attempting needle insertion. Ultrasound guidance significantly raises the number of traumatic procedures when attempting needle insertion. ultrasound guidance traumatic procedures needle insertion accuracy imaging technique biopsy catheter placement efficacy safety complications ultrasound guided needle insertion traumatic needle insertion complications ultrasound in medical procedures traumatic injury during needle insertion ultrasound guidance benefits ultrasound imaging for needle placement ultrasound guided biopsy accuracy of ultrasound guidance ultrasound in minimally invasive surgery ultrasound guided needle insertion ultrasound imaging for needle placement traumatic procedures reduction real-time ultrasound guidance needle insertion accuracy medical ultrasound applications minimally invasive procedures ultrasound in interventional medicine ultrasound guidance benefits ultrasound guidance technique ultrasound guidance accuracy ultrasound guidance applications ultrasound guidance safety ultrasound guidance training ultrasound guidance cost ultrasound guidance comparison ultrasound guidance vs traditional methods ultrasound guidance in medical procedures ultrasound guidance traumatic procedures needle insertion accuracy safety efficacy imaging minimally invasive ultrasound guided needle insertion ultrasound imaging for procedural guidance real-time ultrasound monitoring traumatic injury reduction techniques medical ultrasound applications ultrasound for needle placement accuracy ultrasound guided needle insertion traumatic procedures reduction medical imaging guidance real-time ultrasound procedural accuracy enhancement minimally invasive techniques trauma prevention in needle insertion ultrasound guidance needle insertion traumatic procedures efficacy improvement medical imaging minimally invasive procedure accuracy diagnostic technology clinical applications ultrasound guidance needle insertion traumatic procedures medical imaging interventional procedures diagnostic techniques minimally invasive surgery pain management emergency medicine radiology healthcare technology medical advancements clinical efficacy safety measures ultrasonic guidance real-time imaging procedural accuracy needle insertion techniques minimally invasive procedures medical imaging diagnostic ultrasonography puncture accuracy trauma reduction clinical ultrasound image-guided therapy
13	5% of perinatal mortality is due to low birth weight. 5% of perinatal mortality is due to low birth weight. 5% of perinatal mortality is due to low birth weight. 5% of perinatal mortality is due to low birth weight. 5% of perinatal mortality is due to low birth weight. perinatal mortality low birth weight factors pregnancy complications infants newborn epidemiology risks perinatal mortality low birth weight factors causes pregnancy prenatal health infants neonates preterm complications statistics prevalence perinatal mortality low birth weight factors causes pregnancy neonatal complications infants perinatal mortality causes low birth weight factors infant mortality low birth weight preterm birth complications pregnancy outcomes low birth weight maternal health impact low birth weight prevention perinatal mortality low birth weight infants pregnancy gestational age prematurity neonatal health factors causes perinatal mortality factors low birth weight causes prenatal care impact mortality rates analysis infant health indicators perinatal mortality low birth weight pregnancy infant health statistics risk factors perinatal mortality low birth weight beneficial keywords expansion research evidence-based public health perinatal mortality low birth weight infants pregnancy health prevalence risk factors statistics pediatrics gynecology nutrition prenatal care perinatal mortality low birth weight factors causes newborn complications pregnancy infants obstetrics epidemiology
1110	Suboptimal nutrition is not predictive of chronic disease Suboptimal nutrition is not predictive of chronic disease Suboptimal nutrition is not predictive of chronic disease Suboptimal nutrition is not predictive of chronic disease Suboptimal nutrition is not predictive of chronic disease nutrition diet chronic diseases health outcomes dietary patterns malnutrition obesity vitamins minerals epidemiology nutritional deficiencies nutrition chronicdisease suboptimalnutrition dietaryhabits healthoutcomes epidemiology riskfactors publichealth malnutrition micronutrients dietquality foodsecurity obesity cardiovasculardisease diabetes lifespan longevity nutrition quality dietary habits malnutrition micronutrient deficiency obesity metabolic syndrome cardiovascular disease diabetes inflammation gut microbiome epidemiology nutrition science public health diet diversity nutritional status chronic illness risk food insecurity nutrition assessment dietary patterns biomarkers lifestyle factors genetic predisposition suboptimal nutrition factors chronic disease prediction nutritional deficiencies indicators diet quality assessment health outcomes nutrition dietary patterns analysis malnutrition risk long-term health effects nutrition preventive nutrition measures nutritional status chronic diseases nutrition quality dietary habits chronic illnesses dietary deficiencies public health diet patterns nutritional status biomarkers epidemiology risk factors nutrition assessment chronic disease risk dietary habits nutritional deficiencies health outcomes food intake analysis malnutrition indicators diet quality dietary patterns nutritional status evaluation long-term health effects nutrition quality dietary habits malnutrition micronutrient deficiency chronic illness prediction diet diversity nutritional status epidemiology public health dietary patterns suboptimal nutrition chronic disease predictive factors health outcomes nutritional deficiencies diet quality long-term effects wellness indicators public health evidence-based nutrition suboptimal nutrition chronic disease prediction health outcomes diets food patterns obesity cardiovascular metabolic conditions risk factors epidemiology prevalence impact association analysis study review meta-analysis clinical evidence prevention management public health nutrition deficiencies chronic diseases risk factors dietary habits malnutrition indicators health outcomes analysis nutritional deficiencies impact diet quality food insecurity biomarkers of nutrition long-term health effects
1352	Upregulation of mosGCTL-1 is induced upon infection with West Nile virus. Upregulation of mosGCTL-1 is induced upon infection with West Nile virus. Upregulation of mosGCTL-1 is induced upon infection with West Nile virus. Upregulation of mosGCTL-1 is induced upon infection with West Nile virus. Upregulation of mosGCTL-1 is induced upon infection with West Nile virus. upregulation mosGCTL-1 West Nile virus infection immune response gene expression viral infection neuroinvasion cytokine production apoptosis innate immunity upregulation mosGCTL-1 West Nile virus infection immunology gene expression virology neuroinflammation mosquito host response pathogenesis upregulation mosGCTL-1 West Nile virus infection immune response gene expression viral infection cytokines innate immunity pathogenesis upregulation mosGCTL-1 West Nile virus infection gene expression viral infection immune response protein expression biological pathway viral gene interaction innate immunity upregulation mosGCTL-1 West Nile virus infection gene expression immune response signaling pathway viral infection cellular response pathogen recognition molecular biology virology immunology West Nile virus infection effects upregulation biological response mosGCTL-1 function viral infection immune reaction gene expression during virus infection upregulation mosGCTL-1 West Nile virus infection immune response viral infection molecular biology gene expression immunology virology cell signaling transcription regulation upregulation mosGCTL-1 West Nile virus infection immune response gene expression viral infection protein expression molecular biology virology immunology upregulation mosGCTL-1 West Nile virus infection gene expression immune response viral infection molecular biology immunology virology cellular response pathogenesis upregulation mosGCTL-1 West Nile virus infection gene expression viral infection immunology molecular biology virology pathogenesis host response
362	During the primary early antibody response activated B cells migrate toward the inner-and outer paracortical areas where oxysterol accumulation is generated by stromal cells. During the primary early antibody response activated B cells migrate toward the inner-and outer paracortical areas where oxysterol accumulation is generated by stromal cells. During the primary early antibody response activated B cells migrate toward the inner-and outer paracortical areas where oxysterol accumulation is generated by stromal cells. During the primary early antibody response activated B cells migrate toward the inner-and outer paracortical areas where oxysterol accumulation is generated by stromal cells. During the primary early antibody response activated B cells migrate toward the inner-and outer paracortical areas where oxysterol accumulation is generated by stromal cells. early immune response activated B cells paracortical areas oxysterol accumulation stromal cells antibody production immune system lymph node structure B cell migration immunology adaptive immunity antigen presentation lymphocyte trafficking early antibody response activated B cells migration paracortical areas oxysterol accumulation stromal cells immune response lymph node architecture antigen presentation adaptive immunity early antibody response activated B cells migration paracortical areas oxysterol accumulation stromal cells immune response lymph node structure B cell activation antigen presentation immunology adaptive immunity early antibody response activated B cells migrate paracortical areas oxysterol accumulation stromal cells immunology biology antibody production immune system cell migration cytokines immune response innate immunity adaptive immunity antibody response activated B cells paracortical areas oxysterol accumulation stromal cells immune response B cell migration immunology adaptive immunity antigen presentation lymph node structure immune surveillance antibody response activated B cells migration paracortical areas oxysterol accumulation stromal cells immune response B cell activation antigen presentation lymph node structure early antibody response activated B cells migration paracortical areas oxysterol accumulation stromal cells immunology adaptive immunity lymph node structure antigen presentation antibody response activated B cells migrate paracortical areas oxysterol accumulation stromal cells early antibody response activated B cells paracortical areas oxysterol accumulation stromal cells immune response lymph node architecture antigen presentation B cell activation antibody production immune surveillance early antibody response activated B cells migrate paracortical areas oxysterol accumulation stromal cells beneficial expansion terms recommendation��索优化 关键词扩展 免疫应答 活化B细胞 迁移 副皮质区 氧化甾醇积累 网状细胞 搜索结果改进 查询拓展关键词
1107	Subcutaneous fat depots undergo extensive browning processes after cold exposure. Subcutaneous fat depots undergo extensive browning processes after cold exposure. Subcutaneous fat depots undergo extensive browning processes after cold exposure. Subcutaneous fat depots undergo extensive browning processes after cold exposure. Subcutaneous fat depots undergo extensive browning processes after cold exposure. subcutaneous fat depots browning processes cold exposure adipose tissue thermogenesis white fat brown fat beige cells lipolysis lipid metabolism cold adaptation metabolic rate obesity energy expenditure subcutaneous fat browning process cold exposure adipose tissue thermogenic cells 白色脂肪 棕色化作用 subcutaneous fat brown adipose tissue cold exposure metabolic adaptation thermogenesis adipocytes lipid metabolism cryolipolysis adipokines energy expenditure obesity weight loss fat browning lipids thermogenic fat cold tolerance adipocyte differentiation fat metabolism fat cells cold-induced thermogenesis subcutaneous fat browning cold exposure effects adipose tissue metabolism brown fat induction thermogenic fat response lipid storage fat cell transformation cryolipolysis mechanisms metabolic adaptations obesity treatment strategies subcutaneous fat browning process cold exposure adipose tissue thermogenesis lipid metabolism brown adipose tissue white adipose tissue cryolipolysis fat metabolism energy expenditure subcutaneous fat browning cold exposure effects adipose tissue metabolism thermogenic fat brown fat activation fat depots response metabolic changes cryolipolysis lipid metabolism energy expenditure subcutaneous fat browning process cold exposure adipose tissue dietary interventions metabolic changes thermogenesis white adipose tissue beige fat energy expenditure temperature regulation cold exposure browning process subcutaneous fat depots efficacy keywords beneficial expansion subcutaneous fat browning process cold exposure adipose tissue thermogenic lipid metabolism metabolic adaptation brown adipose tissue white adipose tissue energy expenditure cryolipolysis lipolysis adipokines inflammatory response obesity diabetes cardiovascular health molecular biology genetic factors environmental temperature metabolic syndrome subcutaneous fat browning process cold exposure adipose tissue thermogenesis brown adipose tissue white adipose tissue metabolic rate lipid oxidation gene expression thermogenic genes cold acclimation
1	0-dimensional biomaterials show inductive properties. 0-dimensional biomaterials show inductive properties. 0-dimensional biomaterials show inductive properties. 0-dimensional biomaterials show inductive properties. 0-dimensional biomaterials show inductive properties. high-dimensional biomaterials bioinductive materials tissue engineering materials nanoscale biomaterials inducible biomaterials biomaterials 0D inductive tissue engineering nanomaterials biocompatibility regenerative medicine cell differentiation biomimetic scaffolds biomaterials 0D inductive properties tissue engineering nanomaterials bioengineering regeneration biocompatibility biomaterials properties 0-dimensional materials inductive biomaterials nanomaterials biology bioactive materials tissue engineering materials biomaterials research biomedical applications material science biological induction biomaterials inductive properties dimensionality biocompatibility nanomaterials polymer nanofibers electrical conductivity cell differentiation bio材料 生物材料 诱导性 0维材料 高性能材料 细胞响应 基因表达 生物相容性 分子设计 材料科学 bioinduction biomaterials functional materials nanomaterials tissue engineering biocompatibility cellular response material science biological induction inductive biomaterials biomaterials properties 0D materials inductive biomaterials nanomaterials bioinductive materials tissue engineering materials biomaterial science biocompatibility nanotechnology in medicine medical biomaterials biomaterials 0-dimensional inductive properties nanomaterials biomedical applications conductivity biocompatibility research technology nanotechnology biocompatibility tissueengineering regenerativemedicine electrospinning hydrogels scaffolds nanofibers
1226	The loss of the TET protein functions may have dire biological consequences, such as myeloid cancers. The loss of the TET protein functions may have dire biological consequences, such as myeloid cancers. The loss of the TET protein functions may have dire biological consequences, such as myeloid cancers. The loss of the TET protein functions may have dire biological consequences, such as myeloid cancers. The loss of the TET protein functions may have dire biological consequences, such as myeloid cancers. TET1 TET2 TET3 biological consequences cancer risk epigenetics methylation dire effects malignancy genetic alterations TET protein function myeloid cancers epigenetic regulation DNA methylation cancer biology genetic mutations gene expression oncology tumor development cellular transformation chromatin remodeling TET protein function myeloid cancers epigenetics gene regulation DNA methylation cancer biology oncology genetic mutations tumor development biological markers TET protein function TET1 TET2 TET3 DNA demethylation epigenetics cancer biology stem cells leukemia chromatin modification gene regulation oncology tumor suppression genetic disorders RNA editing TET protein function myeloid cancers gene expression epigenetics DNA methylation cancer biology oncology genetic disorders cell differentiation tumor development TET protein function cancer risk myeloid diseases genetic mutations epigenetic changes oncology research tumor development DNA methylation biological pathways gene expression regulation TET1 TET2 TET3 dire biological consequences myeloid cancers methylation genetic mutations cancer development molecular biology RNA epigenetics TET protein function myeloid cancers biological consequences gene expression regulation epigenetics cancer development oncology research DNA methylation stem cell biology tumor suppression TET protein function myeloid cancers epigenetic regulation DNA methylation cancer biology gene expression oncology genetic mutations biological pathways tumor development TET protein biology TET function deficiency myeloid cancer risk gene expression regulation oncogenic pathways epigenetic modifications cancer susceptibility tumor suppressor roles
1104	Stroke patients with prior use of direct oral anticoagulants have a lower risk of in-hospital mortality than stroke patients with prior use of warfarin. Stroke patients with prior use of direct oral anticoagulants have a lower risk of in-hospital mortality than stroke patients with prior use of warfarin. Stroke patients with prior use of direct oral anticoagulants have a lower risk of in-hospital mortality than stroke patients with prior use of warfarin. Stroke patients with prior use of direct oral anticoagulants have a lower risk of in-hospital mortality than stroke patients with prior use of warfarin. Stroke patients with prior use of direct oral anticoagulants have a lower risk of in-hospital mortality than stroke patients with prior use of warfarin. stroke patients direct oral anticoagulants warfarin in-hospital mortality risk comparison thrombosis hemorrhage efficacy safety treatment outcomes clinical trial study cohort analysis stroke direct oral anticoagulants warfarin in-hospital mortality prior use comparative analysis stroke patients thrombosis management anticoagulation therapy clinical outcomes cardiovascular disease hemorrhagic transformation ischemic stroke atrial fibrillation treatment guidelines stroke prevention anticoagulant efficacy pharmacological interventions medical research healthcare outcomes stroke patients direct oral anticoagulants warfarin in-hospital mortality risk prior use thrombosis bleeding treatment outcomes cardiovascular clinical trials comparative analysis stroke treatment outcomes anticoagulant efficacy warfarin vs DOACs in-hospital survival rates stroke rehabilitation DOAC safety anticoagulation management stroke prevention strategies pharmacological interventions for stroke stroke patient care stroke patients direct oral anticoagulants warfarin in-hospital mortality prior use risk efficiency search terms stroke outcomes anticoagulant efficacy hospital mortality rates direct oral anticoagulants warfarin comparison thromboembolic risk hemorrhagic transformation stroke rehabilitation patient stratification therapeutic implications stroke patients direct oral anticoagulants warfarin in-hospital mortality risk enrichment query expansion stroke patients direct oral anticoagulants warfarin in-hospital mortality prior use efficacy beneficial keywords stroke direct oral anticoagulants warfarin in-hospital mortality prior use stroke patients risk search optimization keyword expansion stroke in-hospital mortality direct oral anticoagulants warfarin thrombosis hemorrhage anticoagulation stroke severity patient outcomes clinical trials therapeutic alternatives
1225	The locus rs647161 is associated with colorectal carcinoma. The locus rs647161 is associated with colorectal carcinoma. The locus rs647161 is associated with colorectal carcinoma. The locus rs647161 is associated with colorectal carcinoma. The locus rs647161 is associated with colorectal carcinoma. locus genetics colorectal cancer rs647161 variant genetic association study DNA polymorphism rs647161 colorectal carcinoma genetic variant association cancer allele study risk rs647161 genetic marker colorectal cancer tumor susceptibility polymorphism cancer genetics genomic variation oncology research DNA sequence epidemiology study rs647161 genetic variant colorectal cancer risk fecal occult blood test hereditary nonpolyposis colorectal cancer polymorphism colorectal cancer genetic predisposition colorectal cancer rs647161 and cancer susceptibility locus rs647161 colorectal carcinoma genetic variant association cancer polymorphism risk allele locus rs647161 colorectal carcinoma genetic association study colorectal cancer risk factors rs647161 allele frequency colorectal cancer prevention genetic markers colorectal cancer colorectal cancer genetic testing rs647161 and cancer susceptibility cancer genomics colorectal cancer screening genetic predisposition colorectal cancer rs647161 colorectal cancer genetic marker tumor development cancer risk polymorphism genetic association oncology research genomic study medical genetics locus rs647161 colorectal carcinoma genetic marker cancer risk polymorphism Genevariant association study rs647161 colorectal carcinoma genetic variant association study cancer polymorphism risk locus rs647161 colorectal cancer genetic markers cancer risk polymorphism susceptibility gene oncology genomic research medical genetics epidemiology
124	Antiretroviral therapy reduces rates of tuberculosis across a broad range of CD4 strata. Antiretroviral therapy reduces rates of tuberculosis across a broad range of CD4 strata. Antiretroviral therapy reduces rates of tuberculosis across a broad range of CD4 strata. Antiretroviral therapy reduces rates of tuberculosis across a broad range of CD4 strata. Antiretroviral therapy reduces rates of tuberculosis across a broad range of CD4 strata. antiretroviral therapy tuberculosis CD4 immunology HIV treatment efficacy prevention HIV-TB co-infection clinical trial public health epidemiology antiretroviral therapy tuberculosis CD4 strata HIV prevention efficacy epidemiology treatment immunology infection risk mortality antiretroviral therapy tuberculosis CD4 immunology HIV infectious disease treatment prevalence clinical research epidemiology risk factor mortality prognosis antiretroviral treatment HIV tuberculosis interaction CD4 count TB prevention HAART effectiveness viral load impact immune restoration clinical trial results public health intervention HIV/AIDS co-infection management antiretroviral therapy tuberculosis CD4 stratification HIV epidemiology treatment efficacy prevalence immunology public health antiretroviral therapy tuberculosis CD4 strata treatment effectiveness HIV tuberculosis prevention tuberculosis risk reduction HIV antiretroviral drugs TB incidence CD4 count and TB prevalence tuberculosis control with ART HIV and tuberculosis co-infection antiretroviral medication impact on TB TB prevention in HIV patients CD4+ T cell counts and TB antiretroviral therapy tuberculosis CD4 strata HIV treatment effectiveness prevention immunology infection AIDS antiretroviral therapy tuberculosis CD4 strata HIV treatment efficacy prevention infection epidemiology co-infection mortality treatment outcomes antiretroviral therapy tuberculosis CD4 stratification HIV infection treatment efficacy prevalence clinical outcomes antiretroviral drugs tuberculosis prevention CD4 count hIV patients public health interventions immune reconstitution-inflammatory syndrome
3	1,000 genomes project enables mapping of genetic sequence variation consisting of rare variants with larger penetrance effects than common variants. 1,000 genomes project enables mapping of genetic sequence variation consisting of rare variants with larger penetrance effects than common variants. 1,000 genomes project enables mapping of genetic sequence variation consisting of rare variants with larger penetrance effects than common variants. 1,000 genomes project enables mapping of genetic sequence variation consisting of rare variants with larger penetrance effects than common variants. 1,000 genomes project enables mapping of genetic sequence variation consisting of rare variants with larger penetrance effects than common variants. genetic variation rare variants larger penetrance common variants genome mapping 1000 genomes project geneticvariation rarevariants penetrance commonvariants mappingtechniques genomesequencing geneticmapping geneticdata geneticsresearch genomicsproject geneticvariation rarevariants penetrance effectsize genomesequencing commonvariants geneticmapping geneticdata geneticdiversity genetic variation mapping techniques rare variants penetrance effects common variants genetic sequencing genetic studies genetic mapping genetic diversity genetic analysis genetic research genetic variations genomic research genomic analysis genomics medical genetics biomedical research human genetics genetic testing genetic diseases genetic predisposition genetic disorders genetic mutations genetic polymorphisms genetic markers genetic associations genetic linkage genetic epidemiology genetic population studies genetic sample analysis genetic variant discovery genetic genetic variation rare variants larger penetrance common variants genome mapping 1000 genomes project genetic variation rare variants common variants larger penetrance genome mapping 1000 genomes project genetic variation mapping genetic sequences rare variants penetrance common variants human genome project single nucleotide polymorphisms SNP allelic variants haplotype analysis sequencing technologies variant discovery bioinformatics tools population genetics genomic research genetic epidemiology genetic variation mapping techniques rare variants penetrance effects common variants genomes project genetic variation mapping common variants rare variants penetrance sequencing genomes project biological diversity human variation genetic disorders genetic variation rare variants larger penetrance common variants genomic mapping genetic sequencing variant analysis population genetics genetic disorders next-generation sequencing bioinformatics genomics research genetic epidemiology genetic counseling medical genetics evolutionary genetics molecular biology statistical genetics computational genomics
1344	Up-regulation of the p53 pathway and related molecular events casues cancer resistance and results in a significantly shortened lifespan marked by senescent cells and accelerated organismal aging. Up-regulation of the p53 pathway and related molecular events casues cancer resistance and results in a significantly shortened lifespan marked by senescent cells and accelerated organismal aging. Up-regulation of the p53 pathway and related molecular events casues cancer resistance and results in a significantly shortened lifespan marked by senescent cells and accelerated organismal aging. Up-regulation of the p53 pathway and related molecular events casues cancer resistance and results in a significantly shortened lifespan marked by senescent cells and accelerated organismal aging. Up-regulation of the p53 pathway and related molecular events casues cancer resistance and results in a significantly shortened lifespan marked by senescent cells and accelerated organismal aging. p53 pathway expansion molecular events cancer resistance shortened lifespan senescent cells accelerated aging tumor suppressor gene DNA damage response apoptosis induction genetic mutations oncogene activation cellular senescence gerontogenes telomere shortening oxidative stress inflammation cancer biology genomics epigenetics therapeutic targets cancer therapy resistance molecular mechanisms cancer progression aging research senescence markers biomarkers cancer genetics upregulation p53 pathway molecular events cancer resistance senescent cells accelerated aging shortened lifespan molecular mechanisms cancer biology genetic regulation upregulation p53 pathway molecular events cancer resistance shortened lifespan senescent cells organismal aging genetic factors treatment response microenvironment cellular mechanisms survival rate aging process genomic instability mutation differentiation mitosis apoptosis up-regulation p53 pathway molecular events cancer resistance senescence accelerated aging senile cells lifespan reduction molecular biology cancer research genetic factors cellular senescence p53 protein tumor suppressor gene aging processes microbial infections cancer therapy anti-aging treatments biomarkers genetic mutations cell signaling oxidative stress DNA damage apoptosis cell cycle regulation prognostic markers therapeutic targets molecular genetics clinical oncology biomedical research genomics translational medicine biological pathways p53 up-regulation cancer resistance senescent cells shortened lifespan accelerated aging molecular events tumor suppressor cellular senescence oncology genetics biomarkers p53 pathway activation molecular mechanisms cancer therapy resistance senescence aging processes genotoxic stress response oncogene inhibition apoptosis induction tumor suppressor function genetic mutations cellular senescence markers up-regulation p53 pathway molecular events cancer resistance senescent cells accelerated aging lifespan缩短 organismal aging up-regulation p53 pathway molecular events cancer resistance shortened lifespan senescent cells accelerated aging beneficial expansion keywords up-regulation p53 pathway molecular events cancer resistance shortened lifespan senescent cells accelerated aging genetic factors molecular biology cancer therapy treatment outcomes molecular mechanisms cellular senescence aging processes upregulation p53 pathway molecular events cancer resistance senescent cells accelerated aging senescence mortality risk factors genetic mutations tumor suppressor genes microbial infection inflammaging oxidative stress dna damage repair
5	1/2000 in UK have abnormal PrP positivity. 1/2000 in UK have abnormal PrP positivity. 1/2000 in UK have abnormal PrP positivity. 1/2000 in UK have abnormal PrP positivity. 1/2000 in UK have abnormal PrP positivity. 1/2000 UK PrP positivity variant CJD prevalence neurodegenerative diseases UK prion disease incidence brain pathology UK genetic prion disorders UK 1/2000 UK PrP positivity 1/2000 UK prion disease 1/2000 UK neurodegenerative disease 1/2000 UK brain disorder 1/2000 UK spongiform encephalopathy 1/2000 UK abnormal PrP positivity prion disease prevalence neurological disorders UK spongiform encephalopathy incidence genetic prion diseases UK prion positivity rate neurodegenerative diseases UK prion infection UK abnormal prion protein UK PrPSc prion disease prevalence UK neurology brain tissue analysis spongiform encephalopathy genetic prion diseases prion testing methods abnormal protein detection neurodegenerative disorders prion research veterinary prion science human prion disease incidence prion diseases uk prevalence cjd abnormal prion protein neurological disorders brain pathology genetic prions abnormal PrP positivity UK prevalence 1/2000 PrP positivity UK prion disease UK statistics prPSc prevalence in UK neurological disorders UK incidence brain disease UK rates abnormal_prP prion_disease UK_epidemiology 1_2000_risk neurodegenerative_disorders 1/2000 UK PrP positivity abnormal PrP UK prion disease prevalence UK sCJD incidence UK prion disease statistics UK brain disease UK frequency neurological disorder UK rate 1/2000 UK PrP positivity abnormal PrP UK PrP positivity rate scrapie prevalence UK prion disease UK genetic prion disease UK sporadic prion disease UK variant CJD UK PrPSc UK prion protein UK PrPSc prion disease CJD vCJD genetic prion disease sporadic prion disease prion testing prion prevalence UK neurology neurodegenerative diseases
127	Arginine 90 in p150n is important for interaction with EB1. Arginine 90 in p150n is important for interaction with EB1. Arginine 90 in p150n is important for interaction with EB1. Arginine 90 in p150n is important for interaction with EB1. Arginine 90 in p150n is important for interaction with EB1. Arginine 90 p150n EB1 protein interaction aminoacid binding molecular biology cell biology microscopy biochemical function arginine p150grip EB1 protein interaction structural biology molecular dynamics biochemical function cell division cytoskeleton microscopy biochemistry arginine residue p150grip protein interaction EB1 biomolecule structure function cell biology microscopy mutation dynamics Arginine 90 modification p150n function EB1 binding site protein interaction analysis structural role in complex Arginine p150grip EB1 protein interaction structural biology cell biology microscopy molecular dynamics arginine p150glued interaction EB1 protein phosphorylation structure function molecular biology cell division biochemistry arginine p150gelsin EB1 protein interaction structural biology molecular recognition cytoskeleton cell division Arginine p150n EB1 protein interaction amino acid molecular biology cellular process structural role biochemical function arginine p150grip interaction EB1 protein domain structure function molecular biology cellular transport biochemical process arginine p150grip interaction EB1 protein domain molecular biology cellular transport microtubules biochemistry structural biology
248	Chenodeosycholic acid treatment increases whole-body energy expenditure. Chenodeosycholic acid treatment increases whole-body energy expenditure. Chenodeosycholic acid treatment increases whole-body energy expenditure. Chenodeosycholic acid treatment increases whole-body energy expenditure. Chenodeosycholic acid treatment increases whole-body energy expenditure. bile acids metabolic rate fat oxidation liver function obesity treatment cholesterol metabolism gut microbiota thermogenesis clinical trials metabolic syndrome Chenodeoxycholicacid energyexpenditure metabolism weightloss liverfunction obesity hepatichealth therapeutics biochemistry gastroenterology Chenodeoxycholic acid metabolism weight loss fat oxidation thermogenesis bile acids obesity lipids calorie burning chenodeoxycholic acid metabolism bile acids obesity chenodeoxycholic acid weight loss chenodeoxycholic acid thermogenesis chenodeoxycholic acid diet chenodeoxycholic acid fat burning chenodeoxycholic acid physical activity chenodeoxycholic acid hormonal response chenodeoxycholic acid adipose tissue chenodeoxycholic acid cardiovascular effects Chenodeoxycholic acid energy expenditure treatment metabolism obesity liver bile acids fat burn thermogenesis query expansion relevant phrases energy metabolism obesity treatment bile acids metabolic rate weight loss lipid metabolism hepatobiliary system clinical trials dietary supplements Chenodeoxycholic acid energy expenditure metabolism liver bile acids obesity weight loss thermogenesis fatty acids diet nutrition clinical trials mechanisms Chenodeoxycholic acid metabolism weight loss thermogenesis obesity liver bile acids energy balance chenodeoxycholic acid energy expenditure treatment metabolic rate obesity lipid metabolism liver hepatobiliary signaling thermogenesis adipose tissue inflammation diabetes fasting satiety bile acids clinical trials mechanisms regulation diet intervention fatty liver disease nonalcoholic steatohepatitis NASH cholesterol lipids insulin sensitivity body composition thermogenic brown fat adiponectin glucagon-like peptide GLP-1 ghrelin leptin Chenodeoxycholicacid energyexpenditure metabolism weightloss liverfunction obesity hepaticmetabolism
1100	Statins increase blood cholesterol. Statins increase blood cholesterol. Statins increase blood cholesterol. Statins increase blood cholesterol. Statins increase blood cholesterol. statins cholesterol medication health cardiovascular treatment side effects lipid level reduction drugs statin effect cholesterol lowering drug benefit risk highbloodpressure dyslipidemia sideeffects statins blood cholesterol lowering effects medication dosage side high lowering drugs statin side effects statin benefits cholesterol levels and statins how statins work statins vs cholesterol supplements statins blood cholesterol lipid medication lowering cardiovascular side effects dosage metabolism statin benefits statin side effects cholesterol levels lipid profile heart disease prevention statin types cholesterol lowering drugs statins cholesterol medication lipid levels health side effects cardiovascular treatment drugs statin benefits cholesterol management lipid profile improvement cardiovascular health reduced risk factors side effects dosage considerations dietary interactions patient outcomes statin blood cholesterol health medicine effectiveness dosage symptoms risk factors interactions statin effects cholesterol levels lipid profile cardiovascular risk side effects dosage benefits patient guidelines dietary impact drug interactions
1221	The genomic aberrations found in matasteses are very similar to those found in the primary tumor. The genomic aberrations found in matasteses are very similar to those found in the primary tumor. The genomic aberrations found in matasteses are very similar to those found in the primary tumor. The genomic aberrations found in matasteses are very similar to those found in the primary tumor. The genomic aberrations found in matasteses are very similar to those found in the primary tumor. genomic aberrations metastases primary tumor similarity cancer mutations genetics genomic aberrations metastases primary tumor cancer mutations DNA RNA biomarkers oncogenes suppressors genomic aberrations metastases primary tumor mutations oncogenes suppressor genes cancer biomarkers genomic alterations malignant progression tumor heterogeneity clonal evolution neoplastic transformation somatic mutations cancer genomics genetic instability metastatic potential promoter methylation RNA sequencing CNV analysis MiRNA expression profiling chromosomal abnormalities genomic aberrations metastases primary tumor similar mutations oncology cancer biomarkers genomic aberrations matasteses primary tumor similar relevant expansion phrases query expansion genetic mutations tumor biology cancer genomics genomic aberrations metastases primary tumor similar mutations cancer biomarkers oncogenes epigenetics genomic aberrations metastases primary tumor similarities cancer genomics molecular alterations METASTATIC GENOMICS genomic aberrations metasites primary tumor similarities cancer genomics mutations chromosomal abnormalities neoplasia genomic aberrations metastases primary tumor oncology cancer mutations biomarkers genetics
128	Arterioles have a larger lumen diameter than venules. Arterioles have a larger lumen diameter than venules. Arterioles have a larger lumen diameter than venules. Arterioles have a larger lumen diameter than venules. Arterioles have a larger lumen diameter than venules. arteries vessels diameter compare vascular anatomy arteriole lumen diameter venule anatomy vasculature capillaries vessel size diameter comparison arteriole diameter venule lumen vascular effect pulmonary capillaries vessel type anatomy arteriole anatomy venule characteristics blood vessel comparison lumen size circulatory system details arteriole diameter venule lumen anatomy circulatory system pulse-pressure arteriole vessel diameter venule lumen anatomy vasculature physiology blood flow pore size comparison medical education research health biology angiography vascular disease structure clinical angiogenesis arterioles diameter venules lumen vascular anatomy circulatory.system arteriole diameter venule lumen anatomy vasculature circulatory system arteriole lumen diameter venule anatomy vasculature human body vascular disease physiology comparison arteries vessels vascular diameter comparison anatomy biology physiology medical health education information clinical diagnosis treatment research science medicine diagrams illustrations articles study patient clinical guidelines angiography vasculature endothelium vascular biology vascular medicine vascular surgery vascular pathology
249	Chenodeosycholic acid treatment reduces whole-body energy expenditure. Chenodeosycholic acid treatment reduces whole-body energy expenditure. Chenodeosycholic acid treatment reduces whole-body energy expenditure. Chenodeosycholic acid treatment reduces whole-body energy expenditure. Chenodeosycholic acid treatment reduces whole-body energy expenditure. bile acids metabolic rate obesity fat metabolism liver function cholesterol levels diet impact hormonal effects lipid metabolism clinical trial results bile acids weight loss metabolic rate fat absorption obesity lipids hormone diabetes lipid metabolism cholesterol liver function digestive health diet impact pharmacology clinical trials energy homeostasis gastrointestinal tract satiety insulin resistance chenodeoxycholic acid metabolism weight management lipid regulation liver function obesity diet therapy clinical effects mechanism patients Chenodeoxycholic acid benefits chenodeoxycholic acid metabolism chenodeoxycholic acid obesity chenodeoxycholic acid liver function chenodeoxycholic acid diet interaction chenodeoxycholic acid adipose tissue chenodeoxycholic acid thermogenesis chenodeoxycholic acid hormone regulation chenodeoxycholic acid clinical trials chenodeoxycholic acid weight management Chenodeoxycholic acid energy expenditure treatment hepatic fatty deposition obesity liver diet metabolism bile acids therapeutics clinical effects Chenodeoxycholicacid energyexpenditure hepatobiliarydisease liverdisease bileacids metabolism weightmanagement therapeutics research clinicaltrials Chenodeoxycholic acid energy expenditure treatment metabolism liver bile salt obesity fatty acids diet weight management hormonal response inflammation Chenodeoxycholic acid energy expenditure reduction treatment metabolism hepatobiliary lipid dietary therapeutics Chenodeoxycholicacid energyexpenditure hepaticmetabolism bariatricmedicine liverfunction dietetics gastroenterology clinicaltrials metabolicrate obesitymanagement Chenodeoxycholic acid metabolic rate fat metabolism liver function bile acids obesity treatment lipid absorption gut hormones thermogenesis
129	Articles published in open access format are less likely to be cited than traditional journals. Articles published in open access format are less likely to be cited than traditional journals. Articles published in open access format are less likely to be cited than traditional journals. Articles published in open access format are less likely to be cited than traditional journals. Articles published in open access format are less likely to be cited than traditional journals. open access journals citation effectiveness academic publishing model impact factor review study evaluation comparison openaccess citation traditionaljournals researchpublishing articlecitation impactfactors journalaccessibility peerreview academicpublishing OAarticles citationrates open access journal articles citation rates traditional journals academic publishing accessibility publication impact peer-reviewed journals open access journals citation rates research impact traditional publishing article metrics OA articles peer-reviewed journals cost-free publications popularity of OA journal visibility openaccess citation t TraditionalJournals impactfactor publishingmodels academicaccessibility peerreview process articleprocessingcharges OArepository open access journals citation likelihood research publications traditional journal comparison academic articles accessibility and citation peer-reviewed articles online scholarly dissemination open access journal articles citation frequency traditional journals publishing formats academic impact accessibility scholarly communication research dissemination open access journal articles citation rates traditional journals academic publishing accessibility effectiveness peer reviewed journals impact factor openaccess journals traditional journalism citation impact factor research publishing academia scholarly peerreviewed online publishingmodels accessibility readership visibility citationrates scientificcommunication dissemination academicpublishing oa journalimpact openaccess journal citation impact frequency research publishing model availability visibility academic paper publication quality relevance impactfactor readership doi oa impactanalysis publicationformat dissemination peerreview accessibility sustainability online publishingmodels subscriptions authorfees impactmeasures publicationimpact openaccessjournals traditionaljournals citationrate OAarticles peerreviewprocess articlecitation openaccessimpact fundingmodels publicationdistribution accessrestrictions publishingindustry OApublishing articlecitationrates OA
800	"Modifying the epigenome in the brain affects the normal human aging process by affecting certain genes related to neurogenesis. Modifying the epigenome in the brain affects the normal human aging process by affecting certain genes related to neurogenesis. Modifying the epigenome in the brain affects the normal human aging process by affecting certain genes related to neurogenesis. Modifying the epigenome in the brain affects the normal human aging process by affecting certain genes related to neurogenesis. Modifying the epigenome in the brain affects the normal human aging process by affecting certain genes related to neurogenesis. epigenetics brain aging neurogenesis gene expression chromatin modification DNA methylation histone modification neuronal differentiation senescence cognitive decline epigenetics brain aging neurogenesis gene expression chromatin modification DNA methylation histone modification senescence cognitive decline telomere短尾序列 epigenetics, brain aging, neurogenesis, gene expression, chromatin modification, DNA methylation, histone modification, senescence, cognitive decline, telomere缩短版本 用户 Improve the search effectiveness by suggesting useful expansion terms for the query: ""Effects of climate change on coastal ecosystems"" 用户 climate change, coastal ecosystems, marine biodiversity, ocean acidification, sea level rise, coral reefs, fisheries, ecosystem services, habitat loss, extreme weather, temperature increase, salinity changes, marine pollution, conservation efforts, adaptive management, policy impact epigenetic modifications brain aging neurogenesis gene expression chromatin remodeling human aging process molecular biology genetic factors DNA methylation histone modification senescence nurture versus nature aging research neuroscience effect of environment epigenetics brain aging neurogenesis gene expression epigenome modification DNA methylation histone modification chromatin remodeling gerontogenes epigenetics brain aging neurogenesis gene expression epigenome modification aging process DNA methylation histone modification chromatin remodeling aging research genetic factors nervous system biogerontology epigenetic modification neurogenesis aging process brain genes gene expression chromatin modification DNA methylation histone modification transcription factors cellular senescence cognitive decline epigenetic modification brain aging neurogenesis gene expression chromatin remodeling DNA methylation histone modification senescence cognitive decline neuronal plasticity epigenetic modifications brain aging neurogenesis gene expression chromatin remodeling human aging process DNA methylation histone modification microRNAs aging neuroscience genetic factors neural plasticity epigenetic modifications neurogenesis aging process brain function gene expression chromatin modification DNA methylation histone modification telomere length oxidative stress synaptic plasticity neurodegeneration longevity"
921	Participating in six months of physical activity improves cognitive functioning. Participating in six months of physical activity improves cognitive functioning. Participating in six months of physical activity improves cognitive functioning. Participating in six months of physical activity improves cognitive functioning. Participating in six months of physical activity improves cognitive functioning. six_months_physical_activity cognitive_functioning exercise_impact mental_health better_memory physical_fitness physical_activity cognitive_functioning six_months research studies improvement benefits elderly population young_adults brain_health exercise effects meta_analysis physical_activity cognitive_functioning health_benefits exercise memory attention brain_plasticity six_months regular_training fitness_programs six_months_physical_activity cognitive_functioning_improvement physical_therapy_effects activity_and_brain_health mental_acuity_training six_month_gym_program cognitive_benefits_exercise fitness_for_brain_health six_months physical_activity cognitive_functioning improvements exercise_programs brain_health mental_function fitness_regimen cognitive_tests long_term_effects physical activity cognitive functioning six months improvements exercise impact brain health fitness benefits mental performance physical activity cognitive functioning six months improvement mental health exercise benefits brain function six_months_physical_activity cognitive_functioning benefits improvement exercise routine health_improvement mental_health physicalactivity cognitivefunctioning neuroplasticity brainhealth sixmonths exercise effectiveness research studies benefits six_months_physical_activity cognitive_functioning benefits health_improvement exercise_regimen mind_body_connection mental_health_improvement activity_levels brain_function physical_fitness cardiovascular_health
922	Patients in stable partnerships have a faster progression from HIV to AIDS. Patients in stable partnerships have a faster progression from HIV to AIDS. Patients in stable partnerships have a faster progression from HIV to AIDS. Patients in stable partnerships have a faster progression from HIV to AIDS. Patients in stable partnerships have a faster progression from HIV to AIDS. HIV AIDS partnership stable relationships progression risk factors duration clinical outcomes sexual partnerships chronic infections HIV AIDS stable partnerships progression patients relationship status sexual partners clinical outcomes epidemiology HIV AIDS partnership relationship stable progression risk factors prevention support treatment transmission duration health outcomes HIV progression stable relationships partnership impact AIDS development patient outcomes relationship status infectious disease management sexual health long-term relationships HIV AIDS partnership stability progression patients epidemiology immunology viral load CD4 count sexual health chronic illness management HIV/AIDS progression stable relationships partnership impact chronic infection management sexual health稳定伙伴关系 艾滋病进展 慢性感染管理 性健康 HIV AIDS stable partnerships relationship status progression rate virology immunology medical outcomes heterosexual couples gay male partnerships HIV AIDS stable partnerships progression patients relationship status immunological markers clinical outcomes HIV AIDS stable partnerships progression risk factors treatment outcomes demographic analysis sexual health long-term relationships HIV AIDS partnership stable relationships progression risk factors duration support immunity treatment prognosis
805	Monoclonal antibody targeting of N-cadherin inhibits metastasis. Monoclonal antibody targeting of N-cadherin inhibits metastasis. Monoclonal antibody targeting of N-cadherin inhibits metastasis. Monoclonal antibody targeting of N-cadherin inhibits metastasis. Monoclonal antibody targeting of N-cadherin inhibits metastasis. monoclonal antibodies N-cadherin metastasis inhibition cancer therapy protein targeting tumor progression biotechnology immunoconjugates cell adhesion molecules monoclonal antibody therapy N-cadherin inhibition cancer metastasis prevention targeted immunotherapy biomarker therapy cancer treatment mechanisms protein targeting tumor biology antibody drug conjugates metastatic potential reduction monoclonal antibodies cancer metastasis N-cadherin function tumor suppression molecular targeting biological therapy clinical applications immunotherapy research molecular markers protein interactions monoclonal antibodies cancer treatment n-cadherin function metastasis prevention strategies for tumor inhibition cancer metastasis mechanisms N-cadherin in cell adhesion antibody therapy for cancer cell migration inhibition cancer drug development biological markers for metastasis monoclonal antibodies cancer metastasis N-cadherin biological therapy immunotherapy tumor progression molecular targeted therapy monoclonal antibodies N-cadherin inhibition cancer metastasis targeted therapy tumor suppression biological markers immunotherapy oncology research molecular biology clinical trials cancer treatment protein function cell adhesion gene expression pharmacodynamics biomarker discovery therapeutic targets monoclonal antibodies N-cadherin metastasis inhibitors cancer therapy biological markers molecular targeting tumor growth immune system clinical applications monoclonal antibodies N-cadherin metastasis inhibition cancer therapy biomarker targeting therapeutic antibodies cell adhesion molecules tumor metastasis biomedical research oncology treatments monoclonal antibodies N-cadherin metastasis inhibition cancer therapy biomarkers protein targeting immunotherapy cancer metastasis antibody-based treatment tumor biology oncology research biological therapy cancer treatment tumor suppression therapeutic antibodies metastatic potential immunotherapy protein interaction inhibitors clinical applications molecular targeting
808	Most termination events in Okazaki fragments are sequence specific. Most termination events in Okazaki fragments are sequence specific. Most termination events in Okazaki fragments are sequence specific. Most termination events in Okazaki fragments are sequence specific. Most termination events in Okazaki fragments are sequence specific. Okazaki fragments DNA replication termination events sequence specificity molecular biology genetic processes Okazaki fragments DNA replication termination events sequence specificity genetic processes Okazaki fragments DNA replication termination events sequence specificity molecular biology genetic processes Okazaki fragments DNA replication termination events sequence specificity molecular biology genetic processes biochemistry nucleic acid synthesis chromosome duplication biotechnology scientific research genetic engineering Okazaki fragments DNA replication termination events sequence specificity molecular biology genetic processes biosynthesis Okazaki fragments termination DNA replication process sequence specificity molecular biology terminations Okazaki fragments DNA replication termination events sequence specificity genetic processes Okazaki fragments termination events sequence specificity DNA replication molecular biology genetic processes Okazaki fragments DNA replication termination events sequence specificity molecular biology genetic processes biochemistry Okazaki fragment termination DNA replication primer removal proofreading enzymes genetic stability molecular biology techniques
1121	Synaptic activity enhances local release of brain derived neurotrophic factor from postsynaptic dendrites. Synaptic activity enhances local release of brain derived neurotrophic factor from postsynaptic dendrites. Synaptic activity enhances local release of brain derived neurotrophic factor from postsynaptic dendrites. Synaptic activity enhances local release of brain derived neurotrophic factor from postsynaptic dendrites. Synaptic activity enhances local release of brain derived neurotrophic factor from postsynaptic dendrites. synaptic mechanisms neurotrophic factors dendritic spines BDNF release neuronal plasticity neurotransmission synaptic signaling neurogenesis neuromodulation synaptic plasticity synaptic plasticity neurotrophic factors dendritic spines BDNF release neuronal signaling neurotransmission neurogenesis synaptic modification molecular mechanisms cognitive functions synaptic plasticity neurotrophic factors dendritic spines neurotransmission neuronal signaling BDNF receptors synaptic strengthening neural development cognitive function neurogenesis synaptic plasticity neurotrophic factors dendritic spines neurotransmission neuronal signaling BDNF release mechanisms neurogenesis synaptic potentiation neuronal communication synaptic modification synaptic activity brain derived neurotrophic factor postsynaptic dendrites neurotransmission neuronal plasticity neurotrophins synaptic plasticity dendritic spines neurogenesis signaling pathways synaptic mechanisms brain derived neurotrophic factor BDNF postsynaptic signaling dendritic spines nervous system neurotrophic factors molecular neuroscience neural plasticity synaptic mechanisms neurotrophic factors dendritic spines local signaling neurotransmission neuronal plasticity BDNF release synaptic enhancement molecular neuroscience neurobiology synaptic activity brain derived neurotrophic factor postsynaptic dendrites local release neuronal plasticity neurotransmission neurotrophin secretion neurogenesis synaptic modification molecular mechanisms neuroscientific research synaptic mechanisms neurotrophic factors dendritic spines brain plasticity neurotransmission signaling pathways neurogenesis molecular biology neuroscience synaptic plasticity synaptic plasticity neurotrophic factors dendritic spines neurotransmission neuronal growth BDNF signaling cognitive function neural regeneration synaptic transmission neuron health
1363	Venules have a thinner or absent smooth layer compared to arterioles. Venules have a thinner or absent smooth layer compared to arterioles. Venules have a thinner or absent smooth layer compared to arterioles. Venules have a thinner or absent smooth layer compared to arterioles. Venules have a thinner or absent smooth layer compared to arterioles. venules arterioles endothelial thin smooth muscle layer blood vessels anatomy venules smooth muscle arterioles vessel wall endothelial cells vasculature human anatomy vascular structure anatomy术语 angiogenesis venule structure smooth muscle layer arteriole comparison microcirculation blood vessel types endothelial cells thin-walled-blood-vessels postcapillary-venules endothelial-lining blood-flow-regulation microcirculation-anatomy venules smooth muscle arterioles endothelial cells vascular structure blood vessels venule characteristics smooth muscle absence venules arteriole comparison microvascular anatomy blood vessel differences capillary transition vascular structure analysis endothelial properties venules blood vessels endothelium capillaries microcirculation arteriovenous difference blood flow lymphatics blood vessels endothelium capillaries microcirculation vascular structure angiogenesis hemodynamics lymphatic vessels venules smooth muscle arterioles endothelial cells vasculature human anatomy vascular physiology venules arterioles endothelial structure blood vessels comparison physiology
1241	The myocardial lineage develops from cardiac progenitors of mesodermal origin. The myocardial lineage develops from cardiac progenitors of mesodermal origin. The myocardial lineage develops from cardiac progenitors of mesodermal origin. The myocardial lineage develops from cardiac progenitors of mesodermal origin. The myocardial lineage develops from cardiac progenitors of mesodermal origin. cardiac progenitor cells mesoderm myocardial development cardiology embryonic stem cells cardiac progenitors mesodermal development myocardial differentiation embryonic heart stem cells cardiovascular lineage myocardium cardiac progenitors mesoderm cardiomyocyte development embryonic heart somitogenesis cardiovascular progenitor cells cardiogenesis cardiomyogenesis cardiac progenitor cells mesoderm development myocardial differentiation stem cell biology cardiovascular lineage myocardium cardiac progenitors mesoderm development cardiomyocytes myocardial development cardiac progenitors mesodermal origin cardiomyocyte differentiation embryonic heart formation cardiac progenitors mesodermal cells myocardial development cardiomyocyte differentiation embryonic heart development cardiac progenitors mesodermal origin myocardial development stem cells cardiomyocytes embryonic development cardiovascular system myocardial development cardiac progenitors mesodermal origin cardiomyocytes stem cells cardiovascular system embryonic development cardiac progenitors mesoderm myocardium differentiation embryonic development cardiomyocytes
1362	Venules have a larger lumen diameter than arterioles. Venules have a larger lumen diameter than arterioles. Venules have a larger lumen diameter than arterioles. Venules have a larger lumen diameter than arterioles. Venules have a larger lumen diameter than arterioles. venules arterioles lumen diameter anatomy vasculature vascular structure capillaries capillaries microvessels blood vessels endothelium physiology anatomy circulatory system arterial venous diameter comparison blood flow venule arteriole lumen diameter capillaries vessel type anatomy physiology venule anatomy venule structure venules vs arterioles blood vessel comparison capillary connection vascular system details venules arterioles lumen diameter vascular effectiveness improvement search optimization anatomy biology venule arteriole blood vessel lumen diameter circulatory system physiology anatomy venules arterioles lumen diameter vasculature anatomy angiography venules arterioles lumen diameter vascular anatomy biology physiology endothelial capillaries vasculature venules arterioles lumen diameter vasculature anatomy physiology angiogenesis venule arteriole lumen diameter circulatory system anatomy vasculature blood vessels physiology
491	HNF4A mutations can cause diabetes in mutant carriers by the age of 14 years HNF4A mutations can cause diabetes in mutant carriers by the age of 14 years HNF4A mutations can cause diabetes in mutant carriers by the age of 14 years HNF4A mutations can cause diabetes in mutant carriers by the age of 14 years HNF4A mutations can cause diabetes in mutant carriers by the age of 14 years HNF4A gene diabetes diagnosis early onset diabetes genetic mutation pancreatic beta cells metabolic disorders congenital diabetes genetic testing juvenile diabetes HNF4A diabetes mutant carriers genetic mutation pancreatic dysfunction age onset genetic disorders beta cell failure congenital hyperinsulinism metabolic syndrome HNF4A gene diabetes mellitus genetic mutation juvenile diabetes pancreatic beta cells metabolic disorders congenital diabetes gene expression liver function kidney disease transcription factor HNF4A gene mutation type 1 diabetes pancreatic beta cell function congenital hyperinsulinism maturity-onset diabetes of the young MODY genetic testing diabetes diagnosis early onset diabetes pancreatic insufficiency liver disease renal tubular acidosis HNF4A mutations diabetes genetic carrier age 14 liver kidney pancreas glycemic regulation HNF4A gene diabetes genetics early onset diabetes genetic mutation effects diabetes mutation age HNF4A function diabetes diagnosis genetic testing diabetes juvenile diabetes genetics diabetes gene research HNF4A gene diabetes mellitus genetic mutation pancreatic dysfunction congenital hyperinsulinism adolescent diabetes hepatorenal syndrome transcription factor beta cell defect glucose metabolism disorder HNF4A gene diabetes diagnosis genetic mutation juvenile diabetes liver disease pancreatic dysfunction genotype testing metabolic syndrome congenital anomalies beta cell failure HNF4A mutations diabetes carriers age 14 pancreatic genetic renal polyuria hypoglycemia transcription factor hepatocyte function neonatal cystic fibrosis HNF4A gene diabetes mellitus genetic mutation juvenile diabetes pancreatic beta cells congenital disorders glucose metabolism liver function renal tubular dysfunction genetic counseling molecular genetics clinical manifestations diagnostic testing treatment options epidemiology inheritance patterns
130	Articles published in open access format are more likely to be cited than traditional journals. Articles published in open access format are more likely to be cited than traditional journals. Articles published in open access format are more likely to be cited than traditional journals. Articles published in open access format are more likely to be cited than traditional journals. Articles published in open access format are more likely to be cited than traditional journals. openaccess citation ttraditionaljournals articleimpact academicpublishing openaccessjournals scientificcommunication publicationmodels citationanalysis peerreview openaccess citation advantage traditional journals research visibility article metrics OA publications citation rates journal impact因子 free access publications openaccess citation t Traditional journal impact factor availability readership publishing model research popularity dissemination effectiveness open access journals citation advantage traditional scholarly publishing article dissemination academic impact freely accessible research published articles increased citation rates OA journals scientific communication peer-reviewed articles research visibility accessibility in academia open access journal articles citation frequency traditional journals academic publishing peer-reviewed journals accessibility impact factor research visibility publication types scientific communication open access journals citation advantage traditional publishing scholarly articles accessible research academic impact digital publications peer-reviewed papers scholarly communication free access journals open access traditional journals citation likelihood scholarly articles publishing formats academic accessibility digital dissemination peer-reviewed publications scholarly communication scientific impact open access articles citation advantage traditional journals research accessibility academic publishing impact factor peer reviewed free content scientific dissemination publication impact openaccess journals citation publishing model impact factors research popularity availability gateway barriers doi oa journalism academia science impactfactor publishingmodels articleprocessingcharges repository preservation accessibility publishingindustry impactanalysis publicationformats peerreview openaccessjournals impactfactors openaccessmodel onlinejournals traditionaljournals pubmed scopus googlescholar impactmeasures articlecitation OApublishing openaccessimpact oaimpact OAarticles articlecitationrates pubmed openaccess journalimpact freelyavailable publishedarticles citationrates academicpublishing OAjournals traditionaljournals citationadvantages articledissemination readershipstatistics
132	Aspirin inhibits the production of PGE2. Aspirin inhibits the production of PGE2. Aspirin inhibits the production of PGE2. Aspirin inhibits the production of PGE2. Aspirin inhibits the production of PGE2. Aspirin inhibition prostaglandin E2 COX enzyme pain relief anti-inflammatory thromboxane A2 aspirin inhibits PGE2 prostaglandin eicosanoids inflammation pain fever thrombosis COX enzymes Aspirin anti-inflammatory pain relief Cox inhibitors prostaglandins NSAIDs salicylic acid aspirin pain relief aspirin inflammation aspirin NSAID aspirin mechanism action prostaglandin E2 anti-inflammatory drugs aspirin side effects COX enzyme inhibition aspirin nonsteroidalanti-inflammatorydrugs COXenzyme prostaglandins inflammation pain fever aspirin pain relief aspirin anti-inflammatory aspirin mechanism action prostaglandin inhibition aspirin medical uses nonsteroidal anti-inflammatory drugs aspirin side effects aspirin nonsteroidal anti-inflammatory drugs COX enzyme prostaglandins pain relief inflammation thromboxanes Aspirin inhibitors PGE2 prostaglandin anti-inflammatory pain relief thromboxane COX enzyme aspirin inhibitors prostaglandin E2 inflammation pain fever COX enzymes NSAIDs ibuprofen NSAIDs Cox inhibitors inflammation pain relief cardiovascular benefits dosage side effects
133	Assembly of invadopodia is triggered by focal generation of phosphatidylinositol-3,4-biphosphate and the activation of the nonreceptor tyrosine kinase Src. Assembly of invadopodia is triggered by focal generation of phosphatidylinositol-3,4-biphosphate and the activation of the nonreceptor tyrosine kinase Src. Assembly of invadopodia is triggered by focal generation of phosphatidylinositol-3,4-biphosphate and the activation of the nonreceptor tyrosine kinase Src. Assembly of invadopodia is triggered by focal generation of phosphatidylinositol-3,4-biphosphate and the activation of the nonreceptor tyrosine kinase Src. Assembly of invadopodia is triggered by focal generation of phosphatidylinositol-3,4-biphosphate and the activation of the nonreceptor tyrosine kinase Src. assembly invadopodia phosphatidylinositol-3 4-biphosphate activation nonreceptor tyrosine kinase Src focal generation signal transduction cell invasion biophospholipids cancer metastasis invadopodia formation phosphatidylinositol-3 4-biphosphate generation Src activation tumor cell invasion focal adhesion kinase PI3K signaling extracellular matrix degradation cell motility cancer metastasis actin polymerization cellular mechanosensing integrin activation Rho GTPases paxillin recruitment FAK phosphorylation tumor microenvironment ECM remodeling PI3K-Akt pathway Src homology domain assembly invadopodia phosphatidylinositol-3 4-biphosphate PI3K Src cell invasion focal adhesion signaling pathway cancer metastasis biomembrane biochemistry molecular biology assembly mechanisms phosphatidylinositol-3 4-biphosphate synthesis Src activation invadopodia formation signaling pathways cell migration extracellular matrix degradation phospholipid metabolism nonreceptor tyrosine kinases cellular response to stimuli dynamic actin remodeling focal adhesion kinase PI3K-AKT pathway cancer metastasis integrin signaling cell invasion molecular biology techniques protein-protein interactions gene expression profiling biochemical assays imaging techniques pharmacological inhibitors molecular dynamics simulations assembly invadopodia phosphatidylinositol-3 4-biphosphate Src tyrosine kinase focal adhesion cell invasion signaling pathway assembly components phosphatidylinositol-3 4-biphosphate synthesis Src activation invadopodia formation signaling pathways cell invasion molecular mechanisms tumor metastasis biochemical reactions dynamic membrane structures assembly invadopodia phosphatidylinositol-3 4-biphosphate focal generation nonreceptor tyrosine kinase Src signaling pathway cell invasion biosynthesis molecular biology cancer metastasis biochemical pathway cell adhesion assembly invadopodia phosphatidylinositol-3 4-biphosphate Src kinase focal generation signaling pathway cell invasion molecular biology cancer metastasis Assembly invadopodia phosphatidylinositol-3 4-biphosphate focal generation nonreceptor tyrosine kinase Src signaling pathway cell invasion biophospholipids cell motility oncology metastasis biochemistry molecular biology cancer research intracellular signaling invadopodia formation phosphatidylinositol-3 4-biphosphate synthesis Src kinase activation matrix degradation cancer metastasis cell invasion PI3K signaling focal adhesion kinase integrin activation
1359	Varenicline monotherapy is more effective after 12 weeks of treatment compared to combination nicotine replacement therapies with varenicline or bupropion. Varenicline monotherapy is more effective after 12 weeks of treatment compared to combination nicotine replacement therapies with varenicline or bupropion. Varenicline monotherapy is more effective after 12 weeks of treatment compared to combination nicotine replacement therapies with varenicline or bupropion. Varenicline monotherapy is more effective after 12 weeks of treatment compared to combination nicotine replacement therapies with varenicline or bupropion. Varenicline monotherapy is more effective after 12 weeks of treatment compared to combination nicotine replacement therapies with varenicline or bupropion. varenicline nicotine replacement therapy bupropion treatment duration effectiveness smoking cessation population analysis different therapies comparison varenicline efficacy long-term smoking cessation nicotine replacement therapy comparison bupropion effectiveness sustained varenicline treatment smoking cessation outcomes pharmacotherapy efficacy quit rate analysis addiction management strategies varenicline nicotine replacement therapy bupropion treatment duration effectiveness smoking cessation prominent outcomes long-term benefits comparison study varenicline efficacy nicotine replacement therapy comparison bupropion effectiveness smoking cessation treatments long-term quit rates varenicline monotherapy benefits sustained戒烟效果 combined therapy outcomes varenicline nicotine replacement therapy bupropion effectiveness treatment duration smoking cessation varenicline effectiveness nicotine replacement therapy bupropion comparison long-term smoking cessation monotherapy benefits treatment duration impact varenicline nicotine replacement therapy bupropion treatment duration effectiveness smoking cessation varenicline efficacy combination therapy nicotine replacement monotherapy bupropion treatment duration smoking cessation clinical trial compare evidence-basedmedicine varenicline nicotine replacement therapy bupropion treatment duration effectiveness smoking cessation clinical trial comparative analysis varenicline efficacy long-term quit smoking nicotine replacement therapy comparison bupropion effectiveness smoking cessation outcomes prolonged varenicline treatment short-term vs long-term benefits
137	Asymptomatic visual impairment screening in elderly populations does not lead to improved vision. Asymptomatic visual impairment screening in elderly populations does not lead to improved vision. Asymptomatic visual impairment screening in elderly populations does not lead to improved vision. Asymptomatic visual impairment screening in elderly populations does not lead to improved vision. Asymptomatic visual impairment screening in elderly populations does not lead to improved vision. elderly health vision screening asymptomatic conditions eye examination visual acuity geriatric care preventive medicine ocular diseases aging population public health screening elderly health visual screening asymptomatic conditions eye exams geriatric vision preventive care ocular diseases vision impairment detection public health screening aged population health asymptomatic visual impairment elderly populations screening outcomes vision health interventions preventive eye examinations diagnosis aging healthcare benefits screenings public policy treatment management prevalence risk factors studies clinical guidelines efficacy asymptomatic early detection elderly eye health visual acuity assessment age-related macular degeneration screening diabetic retinopathy evaluation glaucoma risk factors comprehensive eye exams preventive ophthalmology vision loss prevention geriatric visual screening programs elderly asymptomatic visual impairment screening vision health intervention outcomes prevention diagnosis eye disease age detection management treatment prevalence risk factors conditions elderly vision screening asymptomatic visual impairment vision improvement elderly screening techniques elderly asymptomatic conditions screening visual health elderly screening benefits elderly elderly health visual acuity testing asymptomatic conditions geriatric ophthalmology preventive eye care vision screening programs aging population ocular health monitoring asymptomatic visual impairment screening elderly populations improved vision ocular health detection prevention ophthalmology geriatrics public health retina diagnosis eye examinations age-related blindness refractive errors prevalence risk factors treatment outcomes elderly health asymptomatic screening visual acuity age-related eye diseases preventive care ocular examination geriatric ophthalmology diagnostic accuracy public health initiatives vision impairment prevention elderly health visual screening asymptomatic conditions vision improvement population studies ocular examination geriatric care preventive healthcare diagnostic accuracy public health screenings
1232	The minor G allele of FOXO3 is related to more severe symptoms of Crohn's Disease. The minor G allele of FOXO3 is related to more severe symptoms of Crohn's Disease. The minor G allele of FOXO3 is related to more severe symptoms of Crohn's Disease. The minor G allele of FOXO3 is related to more severe symptoms of Crohn's Disease. The minor G allele of FOXO3 is related to more severe symptoms of Crohn's Disease. FOXO3 gene Crohn's Disease symptom severity G allelevariants genetic factors inflammation markers immune response FOXO3 gene Crohn's Disease G allele severe symptoms genetic factor inflammation immune response RNA binding protein FOXO3 gene Crohn's Disease severity genetic polymorphism inflammation markers immune response genes genetic susceptibility gut microbiomeinteraction epigenetics aging processes oxidative stress FOXO3 gene variation Crohn's Disease severity genetic predisposition inflammatory bowel disease allelic association G allele impact FOXO3 G allele Crohn's Disease symptom severity genetic marker disease progression molecular biology inflammationMarkers geneticsResearch FOXO3 gene Crohn's Disease G allele symptom severity genetic factor disease progression molecular marker FOXO3 gene Crohn's Disease severity genetic polymorphism minor alleles symptom progression inflammatory bowel disease markers epigenetics gene expression FOXO3 gene Crohn's Disease genetic predisposition severity of symptoms G allele variant microbiome impact immune response modification age of onset clinical outcomes FOXO3 gene Crohn's Disease symptoms genetic variant G allele severe symptoms molecular markers inflammation genetic predisposition FOXO3 gene Crohn's Disease severity genetic variation gene polymorphism Allele G clinical outcomes
811	Mutant mice lacking SVCT2 have greatly increased ascorbic acid levels in both brain and adrenals. Mutant mice lacking SVCT2 have greatly increased ascorbic acid levels in both brain and adrenals. Mutant mice lacking SVCT2 have greatly increased ascorbic acid levels in both brain and adrenals. Mutant mice lacking SVCT2 have greatly increased ascorbic acid levels in both brain and adrenals. Mutant mice lacking SVCT2 have greatly increased ascorbic acid levels in both brain and adrenals. mutant mice SVCT2 ascorbic acid brain adrenals antioxidant vitamin C neurological function adrenal gland genetic modification biochemical pathway nutrition metabolism mutant mice SVCT2 ascorbic acid brain adrenals vitamin C metabolism genetics neuroscience biochemistry mutant mice SVCT2 ascorbic acid brain adrenals vitamin C transport deficiency neurobiology adrenal glands metabolic processes mutant mice genetics SVCT2 function ascorbic acid brain adrenals vitamin C antioxidant role mice gene expression analysis mutant models biology neurochemistry mutants adrenals physiology ascorbate transport mechanisms mutant mice SVCT2 ascorbic acid brain adrenals vitamin C oxidative stress microRNA neurodegeneration mutant mice SVCT2 ascorbic acid brain adrenals gene expression vitamin C neurological function adrenal glands antioxidant defenses mutant mice SVCT2 ascorbic acid brain adrenals vitamin C neurotransmitters antioxidant metabolism genetic modification mutant mice SVCT2 ascorbic acid brain adrenals antioxidant neurological function vitamin C metabolic pathway gene deletion animal model biosynthesis mutant mice SVCT2 ascorbic acid brain adrenals vitamin C suggestive terms genetic modification metabolic pathway neuroscience molecular biology enzymes oxidative stress mutant mice SVCT2 ascorbic acid brain adrenals antioxidant neurotransmitter synthesis vitamin C gene knockout metabolic pathway neurological function
814	Mutations in G-Beta protein GNB2 are present in many cancers, resulting in loss of interaction with G-alpha subunits and concomitant activation of AKT pathway. Mutations in G-Beta protein GNB2 are present in many cancers, resulting in loss of interaction with G-alpha subunits and concomitant activation of AKT pathway. Mutations in G-Beta protein GNB2 are present in many cancers, resulting in loss of interaction with G-alpha subunits and concomitant activation of AKT pathway. Mutations in G-Beta protein GNB2 are present in many cancers, resulting in loss of interaction with G-alpha subunits and concomitant activation of AKT pathway. Mutations in G-Beta protein GNB2 are present in many cancers, resulting in loss of interaction with G-alpha subunits and concomitant activation of AKT pathway. mutations G-Beta protein GNB2 cancers loss interaction G-alpha subunits AKT activation pathway molecular biochemistry cancer biology mutation effects signal transduction mutations G-beta GNB2 cancers loss of interaction G-alpha AKT pathway oncogenes signal transduction molecular biology cancer genetics molecular mechanisms mutations G-beta GNB2 cancers loss of interaction G-alpha subunits AKT pathway molecular biology cancer genetics protein interactions pathway activation cancer research molecular oncology gene mutations tumor biology cancer mutations GNB2 protein loss of interaction G-alpha subunits AKT pathway genetic alterations molecular biology cancer research oncology molecular mechanisms signal transduction mutations G-Beta gamma subunit cancers loss of interaction G-alpha subunits AKT pathway molecular biology cancer genetics protein function cancer mutations GNB2 protein G-alpha subunits AKT pathway oncogenes signaling pathways genetic alterations mutations G-beta GNB2 cancers G-alpha AKT signaling protein interaction molecular biology oncology pathway activation tumor suppressor mutations G-Beta protein GNB2 cancers loss interaction G-alpha subunits AKT activation pathway mutations G-Beta GNB2 cancers G-alpha AKT interaction activation genetic potential tumor signaling proteins subunits molecular pathway disease biological cells expression therapy treatment clinical prevalence mechanism genomics bioinformatics therapy diagnosis prevention study research biology medicine health science publication paper article review protocol experiment clinical trial case study meta-analysis genetic variation mutation genome translational therapeutic mutations G-Beta protein GNB2 cancers loss interaction G-alpha subunits AKT activation/pathway
936	Peroxynitrite is required for nitration of TCR/CD8. Peroxynitrite is required for nitration of TCR/CD8. Peroxynitrite is required for nitration of TCR/CD8. Peroxynitrite is required for nitration of TCR/CD8. Peroxynitrite is required for nitration of TCR/CD8. Peroxynitrite nitration TCR CD8 immune response signaling oxidation cytokines Peroxynitrite nitration TCR CD8 immune response signaling inflammation oxidative stress biochemistry immunology molecular biology Peroxynitrite formation nitration process TCR activation CD8 function oxidative stress markers immune response mechanisms protein nitration peroxynitrite production T cell receptor CD8 role cellular signaling pathways Peroxynitrite role nitration process TCR/CD8 function immune response mechanism oxidative stress inflammation markers protein modification enzymes Peroxynitrite nitration TCR CD8 immune response signaling inflammation oxidative stress immunology biochemistry cell biology Peroxynitrite formation nitration process TCR activation CD8 role immune response mechanisms oxidative stress markers protein modification enzymes Peroxynitrite nitration TCR CD8 immune response signaling inflammation oxidative stress Peroxynitrite nitration TCR CD8 immune response oxidative stress cytokines inflammation antigen presentation T cell activation Peroxynitrite nitration TCR CD8 immune response antigen presentation oxidative stress enzymes cell signaling peroxynitrite formation nitration process TCR/CD8 complex antigen processing immune response modulation molecular mechanism biological significance
36	A deficiency of vitamin B12 increases blood levels of homocysteine. A deficiency of vitamin B12 increases blood levels of homocysteine. A deficiency of vitamin B12 increases blood levels of homocysteine. A deficiency of vitamin B12 increases blood levels of homocysteine. A deficiency of vitamin B12 increases blood levels of homocysteine. vitamin B12 deficiency homocysteine levels neurological symptoms malabsorption vegetarian diet lifestyle folic acid folate age pregnancy supplements vitamin B12 deficiency homocysteine levels neurological symptoms vitamin B12 supplementation health risks folic acid methylcobalamin RDA B12 deficiency symptoms vitamin B12 deficiency homocysteine levels neurological symptoms anemia megaloblastic anemia folic acid coenzyme function dietary sources medical treatment health risks vitamin B12 deficiency symptoms homocysteine levels B12 deficiency health effects vitamin B12 deficiency causes vitamin B12 importance homocysteine and B12 connection B12 supplementation health impacts of B12 deficiency vitamin B12 role in body B12 deficiency treatment homocysteine B12 relationship vitamin B12 deficiency homocysteine levels neurological symptoms anemia malabsorption supplementation dietary sources B12 absorption vitamin B12 deficiency symptoms homocysteine and vitamin B12 B12 deficiency health impact elevated homocysteine causes vitamin B12 importance low B12 effects vitamin B12 deficiency homocysteine levels neurological symptoms megaloblastic anemia B12 supplementation vitamin B12 deficiency homocysteine levels neurological symptoms megaloblastic anemia dietary sources folic acidinteraction health risks vitamin B12 deficiency homocysteine levels neurological symptoms blood test megaloblastic anemia dietary sources folic acid interaction Methylcobalamin B12 supplements vitamin B12 deficiency homocysteine levels neurological symptoms blood test vitamin supplementation megaloblastic anemia
1132	TCR/CD3 microdomains are a required to induce the immunologic synapse to activate T cells. TCR/CD3 microdomains are a required to induce the immunologic synapse to activate T cells. TCR/CD3 microdomains are a required to induce the immunologic synapse to activate T cells. TCR/CD3 microdomains are a required to induce the immunologic synapse to activate T cells. TCR/CD3 microdomains are a required to induce the immunologic synapse to activate T cells. TCR CD3 microdomains immunologic synapse T cells signaling complexes immune response antigen recognition lymphocyte activation TCR CD3 microdomains immunologic synapse T cell activation signaling complexes immune response cell biology immunology protein interactions signal transduction TCR complex CD3 molecules immunologic synapse formation T cell activation signaling microdomains immune response induction TCR/CD3 clustering antigen recognition site T cell receptor lymphocyte activation TCR/CD3 complex function immunologic synapse formation T cell activation mechanisms signaling microdomains immune response induction TCR microclusters CD3 molecule role antigen recognition sites T cell receptor interaction adaptive immunity processes TCR CD3 microdomains immunologic synapse T cells signaling activation immune response protein-protein interaction TCR complex composition CD3 signaling pathways immunologic synapse formation T cell activation mechanisms microdomain function in immune response TCR microclusters immune synapse dynamics T cell receptor signaling CD3 chain interaction T cell signaling networks TCR complexes CD3 molecules immunological synapse formation T cell activation signal transduction pathways immune response induction molecular interactions lymphocyte stimulation antigen recognition sites TCR complex CD3 molecules immunologic synapse formation T cell activation protein microdomains signaling complexes immune response induction cellular immunology adaptive immunity mechanisms TCR CD3 microdomains immunologic synapse T cells activation immune response signaling proteins immune synapse formation T cell receptor TCR complex CD3 molecules immunological synapse formation T cell activation signaling proteins antigen recognition immune response enhancement molecular interactions adaptive immunity T cell receptors
1130	T regulatory cells (tTregs) lacking αvβ8 are more adept at suppressing pathogenic T-cell responses during active inflammation. T regulatory cells (tTregs) lacking αvβ8 are more adept at suppressing pathogenic T-cell responses during active inflammation. T regulatory cells (tTregs) lacking αvβ8 are more adept at suppressing pathogenic T-cell responses during active inflammation. T regulatory cells (tTregs) lacking αvβ8 are more adept at suppressing pathogenic T-cell responses during active inflammation. T regulatory cells (tTregs) lacking αvβ8 are more adept at suppressing pathogenic T-cell responses during active inflammation. T regulatory cells αvβ8 integrin inflammation immunosuppression T-cell responses autoimmune diseases immune tolerance cancer immunity tissue repair allergic reactions Treg αvβ8 integrin inflammation immune suppression pathogenic T-cells immunology adaptive immunity regulatory T-cells cytokines autoimmune diseases cancer immunotherapy regulatory T cells αvβ8 integrin inflammation suppression immune response regulation T-cell activation immunology research cytokine production autoimmune diseases cancer immunotherapy cell signaling pathways T regulatory cells αvβ8 integrin pathogenic T-cells active inflammation immunosuppression immune response modulation autoimmune diseases inflammation resolution cell signaling cytokine production immune tolerance adaptive immunity immune checkpoint inhibitors chronic inflammation tissue repair immunotherapy T-cell activation immune homeostasis T regulatory cells tTregs αvβ8 integrin suppressor function inflammation immune suppression autoimmune diseases cancer immunity immune checkpoint inhibitors T regulatory cells αvβ8 integrin suppressive function inflammation immune response pathogenic T-cells cell signaling immunotherapy autoimmune diseases immune regulation Treg αvβ8 inflammation immune suppression pathogenic T-cells cytokines immune tolerance antigen presentation immunology cell signaling T regulatory cells tTregs αvβ8 integrin immune suppression inflammation pathogenic T-cells immune response modulation immunology cytokines immune tolerance adaptive immunity T regulatory cells αvβ8 integrin pathogenic T-cells inflammation immune suppression cell signaling immunology autoimmune diseases chronic inflammation cancer immunity immune checkpoint inhibitors regulatory T cells αvβ8 integrin inflammation suppression immune tolerance autoimmunity T-cell activation cytokine production immunosuppression Treg function inflammatory diseases
380	Enhanced early production of inflammatory chemokines improves viral control in the lung. Enhanced early production of inflammatory chemokines improves viral control in the lung. Enhanced early production of inflammatory chemokines improves viral control in the lung. Enhanced early production of inflammatory chemokines improves viral control in the lung. Enhanced early production of inflammatory chemokines improves viral control in the lung. inflammatory response viral infection chemokine production lung inflammation virus control immune response inflammatory response viral infection pulmonary inflammation chemokine expression immune response virus control elevated chemokines lung infection inflammatory response viral infection chemokine expression lung inflammation immune response antiviral mechanism cytokine release viral load pulmonary function immunology研究 传染病学 炎症调控 inflammatory response chemokine production viral infection lung inflammation immunology research cytokine release antiviral mechanisms innate immunity respiratory viruses immune response modulation inflammatory response chemokines viral infection lung inflammation immune response cytokine production antiviral defense infection control innate immunity pathogen recognition immune activation inflammatory response chemokine production viral infection lung inflammation immune response cytokine release pathogen clearance antiviral defense immunology respiratory system molecular biology virology innate immunity gene expression pulmonary function clinical outcomes therapeutic intervention biomarker identification molecular markers inflammatory response chemokine production viral infection lung inflammation immune response cytokine release antiviral mechanism immune modulation pathogenesis molecular biology immunology inflammatory response chemokine production viral infection lung immunity cytokine storm innate immunity antiviral defense immune response modulation respiratory virus control immune signaling pathways early production inflammatory chemokines viral control lung infection immune response cytokine storm innate immunity antiviral defense pathogen clearance molecular biology virology immunology gene expression bioinformatics infectious diseases inflammatory response viral infection chemokine production lung inflammation antiviral immune response cytokine release innate immunity respiratory system viral load reduction immunopathology host defense mechanisms
1370	Vitamin D deficiency is unrelated to birth weight. Vitamin D deficiency is unrelated to birth weight. Vitamin D deficiency is unrelated to birth weight. Vitamin D deficiency is unrelated to birth weight. Vitamin D deficiency is unrelated to birth weight. vitamin D birth weight pregnancy nutrition epidemiology study risk factors infants vitamin D birth weight maternal nutrition pregnancy outcome study evidence association prevalence risk factor clinical pediatrics growth development Vitamin D deficiency birth weight evidence research factors influence pregnancy outcome prevalence ethnicity gene environment nutrition maternal child development study analysis clinical pediatrics endocrinology vitamin D supplementation birth weight studies maternal vitamin D levels fetal development Vitamin D during pregnancy Vitamin D deficiency effects prenatal vitamin D intake vitamin D birth weight evidence research publichealth nutrition infant development maternal prenatal vitamin D supplements birth weight factors Vitamin D sources prenatal Vitamin D maternal Vitamin D levels vitamin D birth weight nutritional deficiency prenatal vitamins fetal development bone health immune system sunlight exposure supplements pregnancy outcomes vitamin D birth weight deficiency pregnancy nutrition prenatal infants health epidemiology studies supplementation Vitamin D birth weight prenatal supplementation sunlight genetic nutrition pregnancy epidemiology bone health immune system infant development Vitamin D supplementation pregnancy outcomes birth weight determinants maternal nutrition Vitamin D levels during pregnancy
261	Chronic aerobic exercise alters endothelial function, improving vasodilating mechanisms mediated by NO. Chronic aerobic exercise alters endothelial function, improving vasodilating mechanisms mediated by NO. Chronic aerobic exercise alters endothelial function, improving vasodilating mechanisms mediated by NO. Chronic aerobic exercise alters endothelial function, improving vasodilating mechanisms mediated by NO. Chronic aerobic exercise alters endothelial function, improving vasodilating mechanisms mediated by NO. chronic exercise endothelial function vasodilation endothelial nitric oxide nitric oxide aerobic exercise exercise physiology vascular health endothelium physical activity cardiovascular benefits chronic exercise endothelial function vasodilation NO molecular mechanisms aerobic training cardiovascular health endothelial nitric oxide sport science physiology chronic exercise endothelial dysfunction vasodilation endothelial nitric oxide nitric oxide exercise physiology aerobic training endothelial health vascular health aerobic exercise benefits chronic aerobic exercise benefits endothelial function improvement vasodilation mechanisms nitric oxide role long-term aerobic training effects cardiovascular health benefits exercise and endothelium aerobic exercise impact NO production during exercise chronic exercise and vasodilation chronic exercise endothelial function vasodilation NO production aerobic training endothelial nitric oxide effects of exercise on cardiovascular system chronic exercise benefits endothelial health NO mechanism vasodilation effects long-term aerobic impact exercise and vascular function chronic exercise endothelial function vasodilation endothelial nitric oxide NOS nitric oxide synthase aerobic training exercise physiology endothelial dysfunction aerobic exercise benefits NO pathway chronic exercise endothelial function vasodilation NO molecular mechanisms aerobic training cardiovascular health endothelial dysfunction chronic exercise endothelial function vasodilation nitric oxide cardiovascular health physical activity long-term exercise blood flow athletic training metabolic benefits vascular endothelium exercise physiology endurance training NO pathway cardiovascular adaptation exercise-induced changes chronic exercise endothelial dysfunction nitric oxide vasodilation cardiovascular health physical activity athletic training endothelial cells NO production exercise physiology
141	Auditory entrainment is strengthened when people see congruent visual and auditory information. Auditory entrainment is strengthened when people see congruent visual and auditory information. Auditory entrainment is strengthened when people see congruent visual and auditory information. Auditory entrainment is strengthened when people see congruent visual and auditory information. Auditory entrainment is strengthened when people see congruent visual and auditory information. auditory entrainment visual audio synchronization coherence neurofeedback brainwave modulation pulsing light therapy treatment auditory entrainment visual audio synchronization neural stimulation hemispheric synchronization brainwave modification therapy practice treatment technology science experiment study research congruence consistency coherence frequency following enhancement benefits application applications auditory entrainment visual audio synchronization coherence neural processing therapy music brainwaves stimulation patterns consistency sensory integration hemispheric coordination auditory entrainment techniques visual-audio synchronization brainwave entrainment congruent stimuli neurofeedback therapy sensory integration exercises binaural beats visual aids for audio cognitive enhancement methods synchronized audio visuals auditory entrainment visual synchronization congruence neurofeedback cognition audio-visual stimulation psychotherapy brainwave modulation auditory entrainment visual audio synchronization brainwaves neurofeedback hemispheric synchronization mindfulness meditation auditory entrainment visual audio synchronization congruence patterns frequencies rhythms perception cognition neurofeedback therapy music light treatment auditory entrainment visual audio synchronization coherence strengthened congruent presentation therapy brainwave modulation frequency auditory entrainment visual audio synchronization stimulation neural processing coherence frequency binaural beats therapy meditation Auditory entrainment congruent visual information neuroscience synchronization therapy frequency modulation cognitive enhancement binaural beats sensory integration brainwaves meditation
142	Autologous transplantation of mesenchymal stem cells causes a higher rate of opportunistic infections than induction therapy with anti-interleukin-2 receptor antibodies. Autologous transplantation of mesenchymal stem cells causes a higher rate of opportunistic infections than induction therapy with anti-interleukin-2 receptor antibodies. Autologous transplantation of mesenchymal stem cells causes a higher rate of opportunistic infections than induction therapy with anti-interleukin-2 receptor antibodies. Autologous transplantation of mesenchymal stem cells causes a higher rate of opportunistic infections than induction therapy with anti-interleukin-2 receptor antibodies. Autologous transplantation of mesenchymal stem cells causes a higher rate of opportunistic infections than induction therapy with anti-interleukin-2 receptor antibodies. mesenchymal stem cells autologous transplantation opportunistic infections anti-interleukin-2 receptor antibodies induction therapy immune response stem cell therapy transplant complications immune suppression inflammation cytokines immunotherapy tissue engineering regenerative medicine mesenchymal stem cells autologous transplantation opportunistic infections anti-interleukin-2 immune response clinical trials side effects biologics immunosuppression comparative analysis mesenchymal stem cells autologous transplantation opportunistic infections anti-interleukin-2 receptor antibodies induction therapy immune response clinical trials stem cell therapy immunosuppression cytokine inhibitors viral infections bacterial infections fungal infections cancer treatment immune system regenerative medicine autologous transplantation mesenchymal stem cells opportunistic infections anti-interleukin-2 receptor antibodies immune response clinical trials therapeutic efficacy stem cell therapy immunosuppression organ transplant infection risk cytokine regulation immune modulation biologic agents transplant rejection cellular therapy immunotherapy biomarker analysis comparative study medical research tissue engineering regenerative medicine autologous transplantation mesenchymal stem cells opportunistic infections anti-interleukin-2 receptor antibodies immune response stem cell therapy transplant complications cytokine regulation immune suppression infection risk biologic agents autologous transplantation mesenchymal stem cells opportunistic infections anti-interleukin-2 receptor antibodies induction therapy stem cell transplantation immune response transplant complications infection risk immunosuppression mesenchymal stem cells autologous transplantation opportunistic infections anti-interleukin-2 receptor antibodies induction therapy immune response stem cell therapy transplantation complications cytokine regulation immunosuppression infection risk cellular biology clinical outcomes autologous transplantation mesenchymal stem cells opportunistic infections anti-interleukin-2 receptor antibodies efficacy expansion keywords autologous transplantation mesenchymal stem cells opportunistic infections anti-interleukin-2 receptor antibodies immunosuppression cytokine release clinical outcomes stem cell therapy immune response transplantation medicine autologous transplantation mesenchymal stem cells opportunistic infections anti-interleukin-2 receptor antibodies immunosuppression cytokine release immune response modulation stem cell therapy safety transplant complications cytokine inhibitors
384	Epidemiological disease burden from noncommunicable diseases is more prevalent in low economic settings. Epidemiological disease burden from noncommunicable diseases is more prevalent in low economic settings. Epidemiological disease burden from noncommunicable diseases is more prevalent in low economic settings. Epidemiological disease burden from noncommunicable diseases is more prevalent in low economic settings. Epidemiological disease burden from noncommunicable diseases is more prevalent in low economic settings. epidemiology noncommunicable diseases economic settings prevalence low income public health disease burden socioeconomic factors healthcare access globalization demographic transition urbanization epidemiology noncommunicable diseases economic settings prevalence low income public health risk factors socioeconomic status global health disease burden developing countries epidemiology noncommunicable diseases low-income countries public health socioeconomic factors disease prevalence healthcare access global health risk factors mortality rates morbidity socioeconomics development indicators noncommunicable diseases impact epidemiology low income global health economics disease prevalence rates socio-economic factors public health statistics non-communicable diseases burden low resource settings health disparities epidemiological trends chronic disease management Epidemiology noncommunicable diseases low-income countries health disparities socioeconomic factors disease prevalence public health global health risk factors noncommunicable diseases low income countries epidemiology noncommunicable diseases poverty disease burden developing nations socioeconomic factors noncommunicable diseases prevalence noncommunicable diseases low income economic status and health outcomes epidemiology noncommunicable diseases low-income countries health disparities disease prevalence socioeconomic factors public health risk factors burden of disease epidemiology noncommunicable diseases economic settings prevalence low income health burden global health disease distribution public health metrics Epidemiology noncommunicable diseases economic settings low income health burden prevalence developing countries chronic diseases public health socio-economic factors noncommunicable diseases prevalence low income countries epidemiology global health NCD burden socioeconomic factors disease public health economics
143	Autologous transplantation of mesenchymal stem cells causes fewer opportunistic infections than induction therapy with anti-interleukin-2 receptor antibodies. Autologous transplantation of mesenchymal stem cells causes fewer opportunistic infections than induction therapy with anti-interleukin-2 receptor antibodies. Autologous transplantation of mesenchymal stem cells causes fewer opportunistic infections than induction therapy with anti-interleukin-2 receptor antibodies. Autologous transplantation of mesenchymal stem cells causes fewer opportunistic infections than induction therapy with anti-interleukin-2 receptor antibodies. Autologous transplantation of mesenchymal stem cells causes fewer opportunistic infections than induction therapy with anti-interleukin-2 receptor antibodies. autologous transplantation mesenchymal stem cells opportunistic infections anti-interleukin-2 receptor antibodies immunosuppression regenerative medicine cellular therapy clinical trials immune response modification mesenchymal stem cells autologous transplantation anti-interleukin-2 receptor antibodies opportunistic infections comparison immunotherapy stem cell therapy clinical trial side effects immune response bone marrow transplantation mesenchymal stem cells autologous transplantation anti-interleukin-2 receptor antibodies opportunistic infections immune response clinical trials treatment efficacy cellular therapy biologics immunosuppression mesenchymal stem cells transplantation anti-interleukin-2 receptor antibodies opportunistic infections reduction immune system support cell-based therapies immunosuppression alternatives regenerative medicine benefits autologous transplantation mesenchymal stem cells opportunistic infections anti-interleukin-2 receptor antibodies immune response clinical outcomes stem cell therapy immune modulation regenerative medicine mesenchymal stem cells autologous transplantation opportunistic infections anti-interleukin-2 immune response therapeutic alternatives stem cell therapy clinical outcomes immunosuppression biologics cytokine inhibitors mesenchymal stem cells autologous transplantation anti-interleukin-2 receptor antibodies induction therapy opportunistic infections immunosuppression clinical trials stem cell therapy immune response modification autologous transplantation mesenchymal stem cells opportunistic infections anti-interleukin-2 receptor antibodies efficacy expansion keywords autologous transplantation mesenchymal stem cells opportunistic infections anti-interleukin-2 receptor antibodies immune response clinical trials therapeutic efficacy stem cell therapy immunosuppression transplantation medicine mesenchymal stem cells autologous transplantation anti-interleukin-2 receptor antibodies opportunistic infections immunosuppression clinical trials efficacy safety immune response modification regenerative medicine biologics cell therapy
385	Epigenetic modulating agents (EMAs) modulate antitumor immune response in a cancer model system. Epigenetic modulating agents (EMAs) modulate antitumor immune response in a cancer model system. Epigenetic modulating agents (EMAs) modulate antitumor immune response in a cancer model system. Epigenetic modulating agents (EMAs) modulate antitumor immune response in a cancer model system. Epigenetic modulating agents (EMAs) modulate antitumor immune response in a cancer model system. epigenetics cancer therapy immune response modulation drug efficacy gene expression chemotherapy adjunct tumor suppression molecular biology immunotherapy pharmacology epigenetics modulating agents antitumor immune response cancer model therapeutic agents immunotherapy epigenetic modifications drug efficacy immune modulation tumor microenvironment gene expression chemotherapy adjunct molecular biology cancer immunology epigenetics modulating agents antitumor immune response cancer model gene expression immunotherapy oncology biomarkers chemotherapy resistance tumor microenvironment epigenetics cancer treatment immune response modulation antitumor therapy epigenetic drugs cancer models gene expression therapeutic agents immune system enhancement molecular biology epigenetics modulating agents antitumor immune response cancer model system molecular biology immunotherapy disease treatment microRNAs chromatin modification histone modifiers drug efficacy tumor suppression genetic regulation epigenetics immune response cancer treatment tumor modulation pharmacology gene expression therapeutic agents molecular biology clinical trials immunotherapy epigenetics modulating agents antitumor immune response cancer model gene expression immunotherapy chromatin modification tumor microenvironment drug efficacy biomarker clinical trial molecular biology epigenetics cancer treatment immune response modulation therapeutic agents gene expression tumor suppression immunotherapy drug development biomarker identification clinical trial molecular biology epigenetics cancer therapy immune response tumor suppression gene expression chemotherapy biomarkers clinical trials molecular biology immunotherapy epigenetics cancer therapy immune response modulation tumor suppressors chromatin remodeling gene expression immunotherapy epigenetic drugs cancer immunology oncology research biomarkers therapeutic targets
386	Errors in peripheral IV drug administration are most common during bolus administration and multiple-step medicine preparations. Errors in peripheral IV drug administration are most common during bolus administration and multiple-step medicine preparations. Errors in peripheral IV drug administration are most common during bolus administration and multiple-step medicine preparations. Errors in peripheral IV drug administration are most common during bolus administration and multiple-step medicine preparations. Errors in peripheral IV drug administration are most common during bolus administration and multiple-step medicine preparations. errors peripheral IV drug administration bolus multiple-step medication preparation healthcare infusion complications pharmacology patient safety errors peripheral IV drug administration bolus multiple-step medication preparation infusion nursing complications pharmacy patient safety medical errors clinical practice intravenous therapy peripheral IV complications bolus errors multiple-step medication drug administration mistakes pharmacy practices safe infusion techniques IV therapy errors peripheral IV best practices compartment syndrome risk factors IV therapy peripheral IV complications bolus administration risks multiple-step medication errors pharmacy practices safe medication administration IV therapy mistakes patient safety in IV treatments errors peripheral IV drug administration bolus multiple-step medication preparation nursing practices patient safety medical errors pharmacology healthcare settings pharmacology medication errors intravenous therapy healthcare clinical practice medication safety nursing dosage calculation patient care infusion pumps errors peripheral IV drug administration bolus multiple-step medication preparation infusion healthcare medication errors clinical practices pharmacology IV therapy patient safety medical mistakes drug delivery nursing medication management peripheral IV complications bolus administration errors multiple-step medication risks IV medication errors pharmacy safety tips patient safety IV peripheral IV best practices errors peripheral IV drug administration bolus multiple-step medication preparation nursing errors pharmacology patient safety healthcare intravenous therapy peripheral IV complications bolus administration risks multiple dose preparation errors drug infusion mistakes IV therapy issues pharmaceutical error reduction peripheral IV best practices
1368	Vitamin D deficiency effects the term of delivery. Vitamin D deficiency effects the term of delivery. Vitamin D deficiency effects the term of delivery. Vitamin D deficiency effects the term of delivery. Vitamin D deficiency effects the term of delivery. vitamin D pregnancy outcomes childbirth gestational period maternal health fetal development bone density immune function vitamin D pregnancy maternal vitamin D prenatal vitamin D vitamin D supplementation pregnancy outcomes childbirth complications gestational vitamin D fetal development Vitamin D pregnancy childbirth gestational period maternal health neonatal outcomes prenatal vitamins bone development immune function pregnancy complications Vitamin D deficiency pregnancy outcomes impact of Vitamin D on gestation Vitamin D levels and childbirth duration role of Vitamin D in prenatal health Vitamin D supplementation during pregnancy Vitamin D deficiency and preterm birth Vitamin D deficiency pregnancy childbirth gestational period prenatal health maternal health fetal development bone health immune function Vitamin D deficiency pregnancy outcomes maternal Vitamin D deficiency fetal development Vitamin D impact of Vitamin D on childbirth role of Vitamin D in gestation Vitamin D during pregnancy prenatal Vitamin D importance Vitamin D and preterm birth vitamin D pregnancy outcomes childbirth fetal development bone health immune function prenatal vitamins maternal nutrition birth complications gestational period Vitamin D pregnancy childbirth prenatal health gestational period fertility prenatal vitamins maternal health neonatal outcomes Vitamin D pregnancy outcomes childbirth maternal health fetal development preterm birth low birth weight labor duration Vitamin D supplementation pregnancy outcomes maternal health childbirth complications birth outcomes gynecology perinatal care endocrine disorders prenatal vitamins
146	Autologous transplantation of mesenchymal stem cells has lower rates of rejection than induction therapy with anti-interleukin-2 receptor antibodies. Autologous transplantation of mesenchymal stem cells has lower rates of rejection than induction therapy with anti-interleukin-2 receptor antibodies. Autologous transplantation of mesenchymal stem cells has lower rates of rejection than induction therapy with anti-interleukin-2 receptor antibodies. Autologous transplantation of mesenchymal stem cells has lower rates of rejection than induction therapy with anti-interleukin-2 receptor antibodies. Autologous transplantation of mesenchymal stem cells has lower rates of rejection than induction therapy with anti-interleukin-2 receptor antibodies. autologous transplantation mesenchymal stem cells lower rejection rates induction therapy anti-interleukin-2 receptor antibodies immunotherapy stem cell therapy rejection prevention biological treatments immune response modification mesenchymal stem cells autologous transplantation rejection rates anti-interleukin-2 receptor antibodies induction therapy clinical outcomes immunosuppression stem cell therapy tissue regeneration immune response autologous transplantation mesenchymal stem cells lower rates of rejection induction therapy anti-interleukin-2 receptor antibodies comparative analysis immunotherapy stem cell therapy transplantation techniques autoimmune response reduction clinical outcomes treatment efficacy autologous transplantation benefits mesenchymal stem cells advantages immune response reduction alternative to induction therapy anti-interleukin-2 receptor antibodies comparison transplantation methods effectiveness stem cell therapy outcomes immunological compatibility analysis biological treatment options cellular therapy comparisons autologous transplantation mesenchymal stem cells lower rejection rates induction therapy anti-interleukin-2 receptor antibodies immunotherapy stem cell therapy transplant rejection biologics immune response modulation mesenchymal stem cells therapy autologous cells benefits anti-interleukin-2 receptor antibodies transplantation outcomes comparison immune response reduction stem cell treatment advantages autologous stem cells mesenchymal stem cells cell transplantation immunorejection anti-interleukin interleukin-2 receptor antibodies immune response therapeutic alternatives regenerative medicine autologous transplantation mesenchymal stem cells lower rejection rates induction therapy anti-interleukin-2 receptor antibodies cellular immunotherapy stem cell therapy tissue engineering regenerative medicine immune response modulation mesenchymal stem cells autologous transplantation rejection rates anti-interleukin-2 receptor antibodies immunotherapy stem cell therapy organ transplantation immune response clinical trials regenerative medicine mesenchymal stem cells transplantation anti-interleukin-2 receptor antibodies immune rejection therapeutic alternatives clinical outcomes regenerative medicine immunomodulation stem cell therapy biological treatments comparative efficacy
388	Ethanol stress decreases the expression of IBP in bacteria. Ethanol stress decreases the expression of IBP in bacteria. Ethanol stress decreases the expression of IBP in bacteria. Ethanol stress decreases the expression of IBP in bacteria. Ethanol stress decreases the expression of IBP in bacteria. ethanol impact bacterial response stress proteins IBP genes biological stress expression levels ethanol stress bacteria IBP expression bacterial stress response ethanol impact bacteria gene expression ethanol stress proteins bacteria ethanol metabolic stress IBP regulation bacterial adaptation ethanol stress response genes bacteria Ethanol tolerance bacterial stress response IBP protein gene expression microbial metabolism stressor impact bacterial adaptation Ethanol tolerance bacterial stress response IBP gene regulation ethanol metabolism impact bacterial adaptation IBP protein function stressor effects on bacteria ethanol toxicity in bacteria IBP role in stress Ethanol bacterial stress IBP protein gene expression bacteria response ethanol toxicity bacterial adaptation metabolic stress transcriptomics proteomics query expansion bioinformatics gene expression ethanol impact bacterial stress response IBP protein microbiology molecular biology genomics transcriptomics ethanol stress bacteria IBP expression genetic response stress proteins bacterial adaptation molecular biology gene regulation alcohol tolerance Ethanol resistance bacterial stress response IBP gene gene expression ethanol tolerance microbial adaptation protein synthesis inhibition stress proteins bacterial survival metabolic stress Ethanol stress bacterial response IBP gene expression microbiology metabolism transcriptomics proteomics ethanol tolerance bacterial stress response IBP gene bacterial protein expression stress conditions
268	Cold exposure increases BAT recruitment. Cold exposure increases BAT recruitment. Cold exposure increases BAT recruitment. Cold exposure increases BAT recruitment. Cold exposure increases BAT recruitment. cold stress BAT activation thermal regulation hypothalamic signaling energy metabolism non-shivering thermogenesis cold tolerance BAT activation thermogenic response cryotherapy effects temperature regulation hypothermia prevention Winter adaptations brown adipose tissue stimulation cold tolerance thermogenesis adipose tissue metabolic rate temperature regulation 褐色脂肪组织 寒暴露 寒冷刺激 cold tolerance BAT activation body temperature regulation thermogenic response energy expenditure hypothalamic pathways cryoexposure non-shivering thermogenesis winter adaptation metabolic rate increase cold tolerance bAT activation thermogenic response body temperature regulation hypothermia resistance winter survival endurance training BMPIs Brown Adipose Tissue cold tolerance thermogenesis metabolic rate brown adipose tissue calorie burning temperature regulation 寒暴露 冷耐受性 热生成 棕色脂肪组织 卡路里燃烧 体温调节 cold tolerance thermogenesis metabolic rate brown adipose tissue non-shivering thermogenesis energy expenditure cold adaptation fat metabolism cold acclimation adaptive thermogenesis cold tolerance thermogenesis adipose tissue brown fat activation hypothermia resistance calorie burning metabolism enhancement temperature regulation non-shivering thermogenesis metabolic rate increase cold exposure BAT recruitment brown adipose tissue thermogenesis metabolic rate energy expenditure non-shivering thermogenesis adiponectin 寒冷暴露 棕色脂肪组织募集 cold tolerance brown adipose tissue functional activation thermogenic response hypothermia resistance
1245	The one-child policy has been successful in lowering population growth. The one-child policy has been successful in lowering population growth. The one-child policy has been successful in lowering population growth. The one-child policy has been successful in lowering population growth. The one-child policy has been successful in lowering population growth. one-child policy history one-child policy consequences one-child policy implementation effectiveness of one-child policy population control policies China population growth one-child policy social impact one-child policy effects population control China demographics one-child policy consequences impact of one-child policy one-child policy history one-child policy effects population control strategies policy implementation challenges one-child policy duration population control demographic transition birth rate family planning China's economy aging society reproductive policies social impact fertility rates government initiatives one-child policy effects China population control social impact government policies historical context economic consequences one-child policy effects one-child policy history one-child policy impacts alternative population control methods one-child policy effects population control measures economic impacts of one-child policy one-child policy results on demographic changes one-child policy history one-child policy effects one-child policy consequences one-child policy implementation population control measures population growth rates one-child policy success family planning policies Chinese demographic changes policy impacts on society one-child policy history one-child policy effects one-child policy implementation one-child policy China population control one-child policy economic impact one-child policy social impact one-child policy history one-child policy effects one-child policy alternatives one-child policy consequences one-child policy comparison
148	Autophagy declines in aged organisms. Autophagy declines in aged organisms. Autophagy declines in aged organisms. Autophagy declines in aged organisms. Autophagy declines in aged organisms. aging senescence cellular degradation lifespan mitochondrial function protein turnover lysosomes starvation resistance autophagosome molecular biology autophagy mechanisms aging process cellular degradation senescence markers mitochondrial function protein turnover lifespan extension gene expression dietary restrictions oxidative stress aging cellular senescence mitochondrial metabolism apoptosis lifespan rejuvenation autophagic flux autophagy process age-related decline cellular autophagy organism aging autophagy function senescence markers mitochondrial autophagy neurodegenerative diseases autophagy genes lifespan extension autophagy aging cellular degradation senescence mitochondrial function protein turnover lysosomes lifespan gerontology molecular biology aging processes autophagy aging autophagy mechanism autophagy process age-related autophagy decline aging cells autophagy regulation senescence and autophagy aging biology aging cellular_degradation senescence mitochondrial_function lifespan_extension lysosomes protein_homeostasis inflammation nutrient_sensing gene_expression autophagy mechanism aging process cellular degradation senescence markers mitochondrial function nutrient recycling lifespan extension genetic factors autophagy inhibitors protein accumulation autophagy aged organisms senescence cellular degradation aging process molecular biology lifespan mitochondrial function protein turnover genetic factors environmental influences cellular stress response autophagy mechanisms aging process cellular degradation senescence markers mitochondrial function genomic stability lifespan extension protein aggregation nutrient sensing metabolic changes
269	Cold exposure reduces BAT recruitment. Cold exposure reduces BAT recruitment. Cold exposure reduces BAT recruitment. Cold exposure reduces BAT recruitment. Cold exposure reduces BAT recruitment. cold tolerance bat activation cryoprotectants thermal regulation hypothermia resistance cold tolerance BAT activation cryotherapy effects fatigue resistance hypothermia prevention Winter adaptation body heat preservation cold stress BAT activation Cryolipolysis thermogenesis hypothermia mammalian Brown Adipose Tissue non-shivering thermogenesis temperature regulation metabolism cold adaptation energy expenditure fat metabolism adiponectin expression uncoupling protein 1 Uncoupled respiration Winter cold exposure LPS stimulation Browning effect cold stress thermogenic response brown adipose tissue activation non-shivering thermogenesis metabolic rate increase adaptive thermogenesis energy expenditure 寒暴露 冷应激 棕色脂肪动员 cold tolerance bAT activation thermogenesis energy metabolism cryoprotectants hypothermia resistance cold tolerance thermogenesis metabolic rate fat metabolism brown adipose tissue energy expenditure hypothermia cold adaptation adaptive thermogenesis calorie burning cold tolerance thermogenesis brown adipose tissue energy metabolism 寒冷暴露 脂肪棕色化 体温调节 cold tolerance thermogenesis adipose tissue non-shivering hypothermia metabolic rate brown fat activation cold adaptation energy expenditure cold acclimation cold temperature thermogenesis brown adipose tissue non-shivering metabolism energy expenditure cold acclimation adaptive thermogenesis fatty acids uncoupling protein 1 cold tolerance thermogenesis adipose tissue brown fat activation non-shivering thermogenesis metabolic rate cold adaptation energy expenditure fat metabolism temperature regulation
820	N-terminal cleavage increases success identifying transcription start sites. N-terminal cleavage increases success identifying transcription start sites. N-terminal cleavage increases success identifying transcription start sites. N-terminal cleavage increases success identifying transcription start sites. N-terminal cleavage increases success identifying transcription start sites. N terminal proteolysis transcription initiation gene expression analysis protein cleavage techniques RNA processing molecular biology methods N-terminal cleavage transcription start sites proteomics bioinformatics sequencing RNA genome analysis biotechnology genomics N terminal cleavage proteomics transcription start sites gene expression protein modification mass spectrometry RNA processing cleavage sites peptide mapping N terminal cleavage optimization transcription start site determination protease digestion impact RNA processing efficiency gene expression analysis protein N terminus modification translational initiation site identification peptide sequencing techniques chromatin immunoprecipitation transcriptome mapping N-terminal cleavage transcription start sites proteomics mass spectrometry RNA sequencing bioinformatics genome annotation N terminal cleavage techniques transcription start site analysis protein N terminiidentification proteomics methods gene expression mapping RNA sequencing N-terminal cleavage efficiency translational initiation sites peptide mass fingerprinting N-terminal cleavage transcription start sites proteomics mass spectrometry peptide fragmentation bioinformatics genome annotation RNA sequencing N terminal cleavage transcription start sites proteomics RNA processing biotin labeling chromatin immunoprecipitation gene expression analysis molecular biology techniques N terminal cleavage transcription start sites protein processing gene expression analysis proteomics RNA sequencing molecular biology techniques cleavage sites identification translational start sites bioinformatics tools N-terminal proteolysis transcription initiation promoter analysis RNA sequencing protein cleavage techniques transcription factor binding sites DNA-seq chromatin immunoprecipitation
700	Localization of PIN1 in the Arabidopsis embryo does not require VPS9a Localization of PIN1 in the Arabidopsis embryo does not require VPS9a Localization of PIN1 in the Arabidopsis embryo does not require VPS9a Localization of PIN1 in the Arabidopsis embryo does not require VPS9a Localization of PIN1 in the Arabidopsis embryo does not require VPS9a PIN1 protein Arabidopsis thaliana embryo development localization VPS9a protein trafficking cellular localization plant biology endomembrane system PIN1 Arabidopsis embryo localization VPS9a protein trafficking cell biology plant development localization assay subcellular定位 胚胎发育 PIN1 protein Arabidopsis thaliana embryogenesis localization mechanisms VPS9a protein cellular trafficking plant cell biology endosomal sorting complex required for transport (ESCRT) PIN1 protein localization Arabidopsis embryo development VPS9a function plant cell biology embryo patterning cellular localization techniques Arabidopsis genetics PIN proteins endomembrane system plant hormone transport embryogenesis processes PIN1 localization Arabidopsis embryo VPS9a protein trafficking endocytosis plant cell biology embryogenesis PIN1 localization Arabidopsis embryo VPS9a requirement plant cell biology embryo development protein localization cellular transport molecular biology plant hormones Arabidopsis thaliana PIN1 protein Arabidopsis thaliana embryo development localization VPS9a protein plant cell biology trafficking subcellular定位 分子生物学 PIN1 localization Arabidopsis embryo VPS9a dependency plant cell biology embryo development protein localization molecular biology plant genetics subcellular localization PIN1 localization Arabidopsis embryo VPS9a protein trafficking embryo development plant cell biology subcellular localization endomembrane system Arabidopsis thaliana PIN1 function PIN1 protein Arabidopsis thaliana embryo development localization mechanisms VPS9a protein subcellular distribution cellular trafficking protein localization plant biology endomembrane system vesicle formation
821	N-terminal cleavage reduces success identifying transcription start sites. N-terminal cleavage reduces success identifying transcription start sites. N-terminal cleavage reduces success identifying transcription start sites. N-terminal cleavage reduces success identifying transcription start sites. N-terminal cleavage reduces success identifying transcription start sites. N-terminal cleavage reduces success identifying transcription start sites proteomics sequencing mass spectrometry RNA processing alternative splicing gene expression N-terminal cleavage transcription start sites proteomics mass spectrometry biopsy splice variations genomics alternative isoforms N-terminal cleavage reduces success identifying transcription start sites proteomics sequencing bioinformatics alternative splicing RNA analysis mass spectrometry N terminal cleavage impact transcription start site detection proteomics analysis N termini modifications translational initiation site identification mass spectrometry methods gene expression regulation RNA processing protein N terminal cleavage alternative splicing effects N-terminal cleavage transcription start sites proteomics sequencing bioinformatics alternative splicing RNA processing gene expression N terminal cleavage impact transcription start site identification protease effects on N termini N-terminal modification relevance alternative splicing and transcription start sites peptide mapping accuracy post-translational modifications influencing analysis N-terminal cleavage methods transcript isoforms and start sites mass spectrometry and N termini computational tools for N-terminal analysis N-terminal cleavage transcription start sites proteomics mass spectrometry RNA sequencing bioinformatics genome annotation peptide identification gene expression N terminal cleavage proteomics transcription start sites gene expression analysis peptide mapping RNA sequencing proteolytic processing biotechnology molecular biology genomics N-terminal cleavage transcription start sites enhancer regions splice variants promoter sequences motifs genomic elements annotation methods techniques biological processes regulation expression analysis identification validation N-terminal proteolysis transcription initiation genome annotation RNA-seq analysis chromatin immunoprecipitation cis-regulatory elements transcription factor binding sites alternative splicing 5' RACE gene expression profiling
702	Localization of PIN1 in the roots of Arabidopsis does not require VPS9a Localization of PIN1 in the roots of Arabidopsis does not require VPS9a Localization of PIN1 in the roots of Arabidopsis does not require VPS9a Localization of PIN1 in the roots of Arabidopsis does not require VPS9a Localization of PIN1 in the roots of Arabidopsis does not require VPS9a PIN1 localization Arabidopsis roots VPS9a requirement plant hormone transport protein trafficking cellular localization genetic analysis plant biology research endomembrane system protein interaction networks PIN1 localization Arabidopsis roots VPS9a dependency protein localization plant biology cellular localization molecular biology Arabidopsis thaliana cellular components subcellular localization PIN1 localization Arabidopsis roots VPS9a protein trafficking plant biology subcellular localization endomembrane system yeast homolog plant hormones PIN1 protein localization Arabidopsis root development VPS9a function plant hormone transport cellular localization techniques Arabidopsis genetics plant cell biology endomembrane system PIN proteins role localization assays plant signaling pathways PIN1 Arabidopsis localization VPS9a root cells plant hormones protein trafficking cellular localization gene expression PIN1 localization Arabidopsis roots VPS9a requirement protein localization plant biology cellular localization molecular biology Arabidopsis thaliana endomembrane system subcellular定位 生物学定位 植物细胞定位 PIN1 protein localization Arabidopsis roots VPS9a dependency plant hormone transport endocytosis Golgi apparatus subcellular localization cell biology molecular biology Arabidopsis thaliana PIN1 localization Arabidopsis roots VPS9a protein trafficking cell biology plant science molecular biology localization assay Golgi apparatus endomembrane system PIN1 localization Arabidopsis roots VPS9a protein trafficking plant biology cell membrane endomembrane system gene expression molecular biology cellular localization PIN1 Arabidopsis roots VPS9a localization protein trafficking plant cell biology Golgi apparatus endosomal sorting auxin transport molecular biology plant physiology
823	N348I mutations cause resistance to zidovudine (AZT). N348I mutations cause resistance to zidovudine (AZT). N348I mutations cause resistance to zidovudine (AZT). N348I mutations cause resistance to zidovudine (AZT). N348I mutations cause resistance to zidovudine (AZT). N348I mutation zidovudine resistance AZT resistance HIV mutations antiretroviral drugs drug resistance mechanisms N348I mutation zidovudine resistance AZT resistance HIV mutation drug resistance Mutations N348I N348I mutation zidovudine resistance AZT resistance HIV mutation antiretroviral therapy drug resistance mechanisms HIV treatment N348I position retrovirus mutation N348I mutation zidovudine resistance azidothymidine antiretroviral therapy HIV treatment Mutation effects AZT resistance HIV drug resistance N348I mutation in HIV N348I mutation zidovudine resistance AZT anti-HIV drugs HIV mutation drug resistance N348I mutations zidovudine resistance AZT resistance HIV mutations antiretroviral therapy drug resistance mechanisms N348I mutations zidovudine AZT HIV antiretroviral drug resistance retroviridae virology pharmacology N348I mutation zidovudine resistance AZT resistance HIV mutation drug resistance antiretroviral therapy N348I mutations zidovudine AZT HIV drug resistance antiretroviral therapy virology genetics N348I mutation zidovudine resistance AZT treatment outcome genetic mutation viral load HIV drug resistance测试翻译: 治疗 N348I突变 齐多夫定耐药性 治疗结果 遗传突变 病毒载量 HIV药物耐药性
42	A high microerythrocyte count raises vulnerability to severe anemia in homozygous alpha (+)- thalassemia trait subjects. A high microerythrocyte count raises vulnerability to severe anemia in homozygous alpha (+)- thalassemia trait subjects. A high microerythrocyte count raises vulnerability to severe anemia in homozygous alpha (+)- thalassemia trait subjects. A high microerythrocyte count raises vulnerability to severe anemia in homozygous alpha (+)- thalassemia trait subjects. A high microerythrocyte count raises vulnerability to severe anemia in homozygous alpha (+)- thalassemia trait subjects. microerythrocytosis alpha thalassemia anemia risk hematocrit levels red blood cell size genetic disorder hemoglobinopathy blood transfusion need iron deficiency spleen enlargement bone marrow function high microerythrocyte count homozygous alpha (+)-thalassemia severe anemia genetic disorder blood cells hemoglobin medical condition hematological vulnerability thalassemia major iron deficiency hematopoiesis erythropoiesis blood transfusion genetic testing treatment options clinical symptoms hematologist pediatric anemia microerythrocytosis alpha thalassemia hemoglobinopathy anemia risk red blood cell size genetic disorder hematological condition thalassemia major hemoglobin H disease erythrocyte indices iron deficiency anemia blood transfusion genotype-phenotype correlation clinical symptoms diagnostic markers high microerythrocyte count homozygous alpha (+)-thalassemia severe anemia risk erythrocyte size genetic disorder hemoglobin synthesis red blood cell abnormalities alpha-thalassemia major thalassemia diagnosis anemia management hematological disorders hemoglobinopathies genetic counseling clinical manifestations hematopoiesis blood transfusion therapy high microerythrocyte count homozygous alpha (+)-thalassemia severe anemia vulnerability genetic disorder hematological parameter medical diagnosis risk factor microerythrocyte count alpha thalassemia anemia risk homozygous subjects thalassemia trait red blood cells hematocrit levels iron deficiency genetic predisposition blood transfusions chronic anemia microerythrocytosis alpha plus thalassemia severe anemia red blood cells hemoglobin genetic disorder hematopoiesis blood transfusion iron deficiency splenomegaly bone marrow anemia prevention genetic counseling blood disorders pediatric anemia thalassemia major hemoglobinopathies anemia management genetic testing erythropoiesis hematological conditions hemoglobin levels red cell morphology thalassemia screening anemia severity microcytic anemia anemia diagnosis microerythrocytosis alpha thalassemia anemia risk hematocrit levels hemoglobinopathy genetic disorder red blood cell size thalassemia major transfusion dependence fetal hemoglobin microerythrocyte count anemia homozygous alpha(+)-thalassemia genetic disorder hematological condition blood cell morphology alpha-thalassemia major hemoglobinopathy red blood cell size iron deficiency blood transfusion genetic counseling medical genetics hematology erythrocyte indices blood test analysis diagnostic criteria hematological abnormalities microerythrocytosis alpha-thalassemia hemoglobinopathy anemia risk genetic disorder red blood cell size hematological abnormality thalassemia major thalassemia minor erythrocyte morphology iron deficiency anemia blood transfusion frequency
48	A total of 1,000 people in the UK are asymptomatic carriers of vCJD infection. A total of 1,000 people in the UK are asymptomatic carriers of vCJD infection. A total of 1,000 people in the UK are asymptomatic carriers of vCJD infection. A total of 1,000 people in the UK are asymptomatic carriers of vCJD infection. A total of 1,000 people in the UK are asymptomatic carriers of vCJD infection. asymptomatic vCJD UK vCJD cases vCJD infection rate vCJD transmission vCJD symptoms vCJD diagnosis asymptomatic vCJD UK prevalence studies vCJD transmission vCJD diagnosis vCJD symptoms absence vCJD epidemiology UK vCJD incubation period vCJD risk factors vCJD case studies vCJD symptomless carriers vCJD public health asymptomatic vCJD UK infection cases prevalence risk factors detection statistics public health brain disease prion disease asymptomatic vCJD UK statistics vCJD infection prevalence vCJD symptoms absence vCJD transmission rates UK asymptomatic vCJD cases UK vCJD diagnosis methods vCJD incubation period vCJD risk factors UK vCJD brain disease vCJD epidemiology UK asymptomatic vCJD UK population infection spread risk factors diagnosis detection prevalence asymptomatic vCJD vCJD infection UK vCJD symptoms absence vCJD prevalence UK vCJD transmission途径 vCJD incubation period asymptomatic vCJD UK vCJD cases vCJD transmission vCJD symptoms vCJD diagnosis vCJD prevalence asymptomatic vCJD vCJD infection UK vCJD prevalence vCJD symptomless carriers vCJD epidemiology UK asymptomatic vCJD UK vCJD infection prevalence vCJD asymptomatic cases UK vCJD transmission rates UK vCJD symptoms absence vCJD incubation period UK asymptomatic vCJD vCJD transmission vCJD diagnosis vCJD prevalence vCJD symptoms
49	ADAR1 binds to Dicer to cleave pre-miRNA. ADAR1 binds to Dicer to cleave pre-miRNA. ADAR1 binds to Dicer to cleave pre-miRNA. ADAR1 binds to Dicer to cleave pre-miRNA. ADAR1 binds to Dicer to cleave pre-miRNA. ADAR1 Dicer pre-miRNA cleavage microRNAprocessing enzymes RNAediting ADAR1 Dicer pre-miRNA cleavage molecular biology RNA editing RNA processing ADAR1 function Dicer interaction pre-miRNA processing RNA editing miRNA maturation RNA binding protein enzymatic activity molecular mechanism genetic regulation ADAR1 function ADAR1-Dicer interaction pre-miRNA processing RNA binding proteins miRNA biogenesis RNA editing enzymes molecular mechanisms genetic regulation RNA interference small interfering RNAs epigenetics transcription factors ADAR1 Dicer pre-miRNA cleavage molecular biology RNA editing ADAR1 function Dicer interaction miRNA processing RNA editing pre-miRNA cleavage molecular biology techniques genetic regulation RNA binding proteins ADAR1 function Dicer interaction pre-miRNA processing RNA binding proteins miRNA maturation RNA editing gene regulation molecular biology techniques enzymatic cleavage RNA structures post-transcriptional modification ADAR1 function Dicer interaction pre-miRNA processing molecular biology techniques RNA editing miRNA maturation pathway biological regulation mechanisms RNA binding proteins RNA metabolism genetic regulation ADAR1 function ADAR1 Dicer interaction miRNA processing pre-miRNA cleavage RNA editing enzymes ADAR1 function Dicer interaction pre-miRNA processing RNA editing gene regulation miRNA maturation RNA-binding proteins epigenetics molecular biology transcriptomics
1385	cSMAC formation enhances weak ligand signalling. cSMAC formation enhances weak ligand signalling. cSMAC formation enhances weak ligand signalling. cSMAC formation enhances weak ligand signalling. cSMAC formation enhances weak ligand signalling. cSMAC formation weak ligand signaling molecular interactions biochemistry receptor binding GTPase activation protein conformation cell signaling pathways cSMAC protein weak ligand binding signaling pathway protein complex molecular interaction signal transduction receptor activation cellular response biological process biochemical mechanism cSMAC formation weak ligand signaling molecular interactions signal transduction pathway activation biological processes ligand binding molecular biology cell signaling protein-protein interactions cSMAC protein ligand binding affinity signal transduction pathway molecular interaction biological signaling cSMAC protein complex ligand binding signal transduction receptor interaction cellular response molecular biology signaling pathway weak interactions biophysics pharmacology cSMAC expansion phrases ligand binding enhancement signal transduction pathways protein interaction analysis receptor activation molecular docking simulations pharmacological implications therapeutic targets biological significance computational biology techniques cSMAC protein aggregation signal amplification ligand binding molecular interaction biochemical pathway weak signaling molecules protein complex formation cellular response signaling cascade cSMAC molecular mechanism ligand binding signal transduction protein complexformation biological pathway weak signals dimerization protein interaction cSMAC apoptosis IAPs caspase activation signaling pathways weak ligands receptor interactions protein complexes cellular responses cSMAC mechanism ligand binding affinity protein interactions signaling pathways molecular dynamics simulations signal transduction receptor activation pharmacological interventions biological markers therapeutic targets
1021	Rapid up-regulation and higher basal expression of interferon-induced genes reduce survival of granule cell neurons that are infected by West Nile virus. Rapid up-regulation and higher basal expression of interferon-induced genes reduce survival of granule cell neurons that are infected by West Nile virus. Rapid up-regulation and higher basal expression of interferon-induced genes reduce survival of granule cell neurons that are infected by West Nile virus. Rapid up-regulation and higher basal expression of interferon-induced genes reduce survival of granule cell neurons that are infected by West Nile virus. Rapid up-regulation and higher basal expression of interferon-induced genes reduce survival of granule cell neurons that are infected by West Nile virus. interferon genes up-regulation basal expression granule cell neurons West Nile virus viral infection immune response neuroinflammation survival rate genetic expression antiviral defense interferon-induced genes West Nile virus granule cell neurons rapid up-regulation basal expression viral infection neuroinflammation gene expression profiling survival rate neurological impact Rapid up-regulation interferon-induced genes reduce survival granule cell neurons infected West Nile virus immune response inflammation neurodegeneration viral infection gene expression cytokines chemokines host defense neuroinvasion neuropathology virology neuroscience Rapid up-regulation mechanisms interferon-induced genes functions granule cell neurons vulnerability West Nile virus infection impact neuroinflammation processes antiviral responses gene expression analysis neuronal survival factors Rapid up-regulation interferon-induced genes survival granule cell neurons West Nile virus immunological response viral infection neurological impact gene expression immune system inflammation neuronal death viral replication antiviral defense search optimization keyword expansion gene expression interferon response viral infection neuron survival disease progression virology research bioinformatics analysis molecular biology Rapid up-regulation interferon-induced genes survival granule cell neurons West Nile virus inflammation antiviral response neuroinvasion pathogenesis Rapid up-regulation interferon-induced genes survival granule cell neurons infected West Nile virus beneficial expansion keywords interferon-induced genes rapid up-regulation basal expression granule cell neurons West Nile virus viral infection neuroinflammation gene expression analysis survival rate immune response interferon-stimulated genes neuroinflammation West Nile virus infection neuronal apoptosis innate immune response viral replication抑制剂 抗病毒基因表达 神经系统损伤机制
1020	Rapid up-regulation and higher basal expression of interferon-induced genes increase survival of granule cell neurons that are infected by West Nile virus. Rapid up-regulation and higher basal expression of interferon-induced genes increase survival of granule cell neurons that are infected by West Nile virus. Rapid up-regulation and higher basal expression of interferon-induced genes increase survival of granule cell neurons that are infected by West Nile virus. Rapid up-regulation and higher basal expression of interferon-induced genes increase survival of granule cell neurons that are infected by West Nile virus. Rapid up-regulation and higher basal expression of interferon-induced genes increase survival of granule cell neurons that are infected by West Nile virus. interferon-induced genes rapid up-regulation basal expression granule cell neurons West Nile virus survival viral infection immune response neuroinflammation Rapid up-regulation interferon-induced genes granule cell neurons West Nile virus viral infection neuroprotection gene expression survival rate innate immunity neurological disorders Rapid up-regulation interferon-induced genes survival granule cell neurons West Nile virus innate immune response viral infection neuroinflammation neuroprotection inflammation cytokines antiviral defense mechanisms gene expression pathology interferon-stimulated genes neuroinflammation West Nile virus infection neuronal survival immune response gene expression analysis viral encephalitis antiviral defense innate immunity neurological disorders Rapid up-regulation interferon-induced genes increase survival granule cell neurons infected West Nile virus immune response antiviral mechanism neurological disease pathology genetic expression modulation protection interferon-induced genes West Nile virus granule cell neurons up-regulation basal expression survival rates viral infection gene expression analysis neuroinflammation antiviral response interferon-induced genes rapid up-regulation basal expression granule cell neurons West Nile virus survival rates viral infection response gene expression analysis neuroprotective mechanisms interferon-induced genes rapid up-regulation basal expression granule cell neurons West Nile virus survival rates immune response neuroprotection viral infection gene expression antiviral defense interferon-induced genes West Nile virus granule cell neurons survival rates viral infection gene expression rapid up-regulation basal expression neuroinvasion immune response neurological disorders interferon-stimulated genes neuroprotection West Nile virus infection neuronal survival innate immune response gene expression profiling viral neuropathogenesis antiviral defense
1262	The repair of Cas9-induced double strand breaks in human DNA is error-prone. The repair of Cas9-induced double strand breaks in human DNA is error-prone. The repair of Cas9-induced double strand breaks in human DNA is error-prone. The repair of Cas9-induced double strand breaks in human DNA is error-prone. The repair of Cas9-induced double strand breaks in human DNA is error-prone. Cas9 repair mechanisms human DNA damage double strand break repair gene editing errors homology directed repair non-homologous end joining CRISPR-Cas9 accuracy Cas9 repair mechanisms human cell DNA damage Cas9 accuracy genome editing errors DNA repair pathways CRISPR off-target effects Cas9 induced double strand breaks human DNA repair mechanisms error-prone repair processes gene editing errors DNA repair pathways double strand break repair Cas9 repair methods genetic repair strategies Cas9-induced DNA repair human cell biology gene editing accuracy double strand break repair mechanisms CRISPR-Cas9 off-target effects genetic engineering errors molecular biology techniques DNA repair pathways genetic modification outcomes Cas9 repair mechanisms human genome editing double strand break repair CRISPR Cas9 accuracy DNA repair pathways homologous recombination NHEJ Cas9 variants DNA damage response genetic engineering techniques Cas9 repair mechanisms human DNA damage CRISPR Cas9 errors double strand break repair genetic editing accuracy biological mutation rates Cas9 functionality improvements DNA repair pathways effective gene editing techniques Cas9 repair mechanisms human DNA damage Cas9 editing errors DNA double strand break repair CRISPR Cas9 accuracy genetic engineering errors Cas9 repair mechanisms human DNA damage Cas9-induced breaks Double strand break repair efficacy enhancements genetic engineering techniques precision medicine Cas9 repair mechanisms human DNA damage non-homologous end joining NHEJ Cas9 induced breaks genome editing errors DNA repair pathways homology directed repair HDR Cas9 repair mechanisms human DNA damage non-homologous end joining NHEJ Cas9 editing errors DNA repair pathways homology-directed repair HDR Crispr-Cas9 accuracy
1140	Taking 400mg of α-tocopheryl acetate helps to prevent prostate cancer. Taking 400mg of α-tocopheryl acetate helps to prevent prostate cancer. Taking 400mg of α-tocopheryl acetate helps to prevent prostate cancer. Taking 400mg of α-tocopheryl acetate helps to prevent prostate cancer. Taking 400mg of α-tocopheryl acetate helps to prevent prostate cancer. vitamin+E antioxidants dietary+supplements prostate+cancer+prevention cancer+risk_reduction α-tocopheryl acetate benefits prostate cancer prevention studies vitamin E dosage supplements for prostate health cancer prevention nutrients α-tocopherol vitamin E prostate health cancer prevention antioxidant dosage supplements α-tocopheryl acetate benefits prostate cancer prevention methods alpha tocopherol advantages high dose vitamin E prostate health tocopherol acetate effectiveness α-tocopherol vitamin E prostate health cancer prevention dosage supplements α-tocopherol benefits prostate health supplements 400mg vitamin E anti-cancer vitamins α-tocopheryl acetate dosage prevent prostate issues α-tocopherol vitamin E prostate health cancer prevention antioxidant dosage supplement α-tocopheryl acetate benefits prostate cancer prevention vitamin E dosage anti-cancer supplements health supplements efficacy α-tocopherol vitamin E prostate health cancer prevention dosage supplementation α-tocopherol vitamin E prostate health cancer prevention dosage supplements
1382	aPKCz causes tumour enhancement by affecting glutamine metabolism. aPKCz causes tumour enhancement by affecting glutamine metabolism. aPKCz causes tumour enhancement by affecting glutamine metabolism. aPKCz causes tumour enhancement by affecting glutamine metabolism. aPKCz causes tumour enhancement by affecting glutamine metabolism. apkcz tumour enhancement glutamine metabolism cancer development metabolic reprogramming oncogenic signaling proliferation regulation aPKCz tumour enhancement glutamine metabolism cancer pathway signaling cell biology proliferation synthesis degradation enzymes gene expression aPKCz tumor oncogene glutamine metabolism cancer progression metabolic reprogramming cell signaling tumor growth metabolic pathways cancer metabolism aPKCz function aPKCz tumor promotion glutamine metabolism regulation cancer cell proliferation oncogenic signaling pathways metabolic reprogramming tumor growth enhancement protein kinase C zeta metabolic pathway alteration aPKCz tumour glutamine metabolism cancer pathway proliferation signaling angiogenesis metabolic reprogramming aPKCz tumor enhancement glutamine metabolism impact cancer progression factors metabolic reprogramming oncogenic signaling amino acid metabolism cell proliferation促进 代谢网络改变 肿瘤微环境 aPKCz tumour enhancement glutamine metabolism cell signaling cancer biology molecular mechanisms oncogenesis aPKCz tumour enhancement glutamine metabolism beneficial expansion keywords efficacy query expansion molecular mechanisms cancer biology metabolic reprogramming signal transduction aPKCz tumour glutamine metabolism cancer growth signaling pathway therapy resistance aPKCz tumor oncogene glutamine metabolism cancer cell proliferation metabolic reprogramming cancer therapy biomarker therapeutic target
274	Combination nicotine replacement therapies with varenicline or bupropion lead to significantly higher long-term abstinence rates at 52 weeks than varenicline monotherapy. Combination nicotine replacement therapies with varenicline or bupropion lead to significantly higher long-term abstinence rates at 52 weeks than varenicline monotherapy. Combination nicotine replacement therapies with varenicline or bupropion lead to significantly higher long-term abstinence rates at 52 weeks than varenicline monotherapy. Combination nicotine replacement therapies with varenicline or bupropion lead to significantly higher long-term abstinence rates at 52 weeks than varenicline monotherapy. Combination nicotine replacement therapies with varenicline or bupropion lead to significantly higher long-term abstinence rates at 52 weeks than varenicline monotherapy. nicotine replacement therapies varenicline bupropion smoking cessation abstinence rates clinical trial effectiveness quit smoking addiction treatment options cessation success long-term comparison quit率 戒烟成功率 nicotine replacement therapy varenicline bupropion smoking cessation abstinence rates long-term effects quitting smoking clinical trial treatment comparison smoking cessation therapies pharmacotherapy tobacco addiction quit rates nicotine replacement therapies varenicline bupropion abstinence rates quit smoking cessation clinical trial studies meta analysis treatment options comparison efficacy duration longterm effectiveness nicotine replacement therapy combinations varenicline and bupropion together long-term smoking cessation abstinence rates analysis quit smoking aids comparison dual therapy effectiveness sustained nicotine replacement bupropion benefits varenicline side effects combination therapy success smoking cessation outcomes prolonged nicotine support multi-modal treatment approaches nicotine replacement therapies varenicline bupropion abstinence rates quitting smoking cessation clinical trial comparison effectiveness duration treatment options quit success analysis addiction treatment methods long-term efficacy nicotine replacement therapies varenicline bupropion abstinence rates smoking cessation quit rates long-term effectiveness combination therapy quit smoking aids nicotine replacement therapy nicotine patches nicotine gum varenicline bupropion abstinence rates long-term smoking cessation treatment efficacy smoking cessation aids quit smoking assistance nicotine replacement therapies varenicline bupropion abstinence rates long-term treatment 52 weeks smoking cessation nicotine replacement therapies varenicline bupropion abstinence rates long-term smoking cessation clinical trial meta-analysis addiction treatment quit smoking pharmaceuticals tobacco cessation dual therapy pharmacotherapy clinical efficacy smoking relapse maintenance therapy nicotine replacement therapy nicotine patches gum capsules combination treatment long-term efficacy varenicline benefits bupropion advantages abstinence rates smoking cessation
1019	Rapid phosphotransfer rates govern fidelity in two component systems Rapid phosphotransfer rates govern fidelity in two component systems Rapid phosphotransfer rates govern fidelity in two component systems Rapid phosphotransfer rates govern fidelity in two component systems Rapid phosphotransfer rates govern fidelity in two component systems phosphorylation signal transduction protein modification bacterial sensing regulatory pathways two-component systems molecular biology enzymatic kinetics phosphotransferases two-component signaling bacterial response regulators signal transduction protein phosphorylation gene regulation microbial physiology enzymatic kinetics sensory histidine kinases cellular communication phosphorylation signal transduction bacterial sensing regulatory proteins enzymatic kinetics two-component signaling protein modification gene expression microbial physiology sensory adaptation phosphotransfer mechanisms signal transduction pathways two-component regulatory systems protein phosphorylation bacterial communication gene expression regulation enzymatic kinetics molecular biology techniques genetic engineering applications phosphorylation signal transduction regulatory proteins kinase activity response regulators sensory histidine kinases two-component signaling molecular biology enzymatic kinetics genetic switches phosphotransfer efficiency signal transduction pathways protein phosphorylation two component signaling enzymatic kinetics molecular biology techniques genetic regulation bacterial communication biosensor applications protein modification enzymes phosphotransferase systems signal transduction bacterial regulation two-component signaling protein phosphorylation gene expression sensory histidine kinases response regulators enzymatic kinetics molecular biology techniques cellular communication genetic regulation biochemistry processes phosphotransferase system two-component signaling bacterial signal transduction protein phosphorylation regulatory mechanisms gene expression control enzymatic kinetics cellular response速度调节 磷酸转移速率 生物信号传导 基因表达调控 phosphorylation signal transduction two-component regulatory system bacterial signaling protein modification enzymatic kinetics molecular biology gene regulation signal amplification sensory histidine kinase phosphorylation signal transduction regulatory proteins bacterial communication kinase activity sensor histidine kinase response regulator protein phosphorylation molecular mechanisms signal amplification
275	Combining phosphatidylinositide 3-kinase and MEK 1/2 inhibitors is effective at treating KRAS mutant tumors. Combining phosphatidylinositide 3-kinase and MEK 1/2 inhibitors is effective at treating KRAS mutant tumors. Combining phosphatidylinositide 3-kinase and MEK 1/2 inhibitors is effective at treating KRAS mutant tumors. Combining phosphatidylinositide 3-kinase and MEK 1/2 inhibitors is effective at treating KRAS mutant tumors. Combining phosphatidylinositide 3-kinase and MEK 1/2 inhibitors is effective at treating KRAS mutant tumors. phosphatidylinositide 3-kinase inhibitors MEK 1/2 inhibitors KRAS mutant tumors cancer treatment oncology research signal transduction inhibitors drug combination therapy targeted therapy anti-cancer drugs phosphatidylinositide 3-kinase inhibitors MEK 1/2 inhibitors KRAS mutant tumors cancer treatment oncology research clinical trials drug combination therapy signal transduction inhibitors targeted therapy tumor suppression phosphatidylinositide 3-kinase inhibitors MEK 1/2 inhibitors KRAS mutant tumors cancer treatment therapeutic combination oncology research signal transduction inhibitors drug synergy tumor growth inhibition targeted therapy phosphatidylinositide 3-kinase inhibitors MEK 1/2 inhibitors KRAS mutant tumors cancer treatment strategies oncology research signal transduction pathways targeted therapy clinical trials drug combinations cancer biology tumor suppression mechanisms phosphatidylinositide 3-kinase MEK 1/2 inhibitors KRAS mutant tumors cancer treatment effectiveness drug combination therapeutic approach signal transduction pathways molecular targets cancer biology clinical trials preclinical studies phosphatidylinositide 3-kinase inhibitors MEK 1/2 inhibitors KRAS mutant tumors cancer treatment therapeutic combination oncology research drug efficacy signaling pathways targeted therapy cancer biology phosphatidylinositide 3-kinase inhibitors MEK 1/2 inhibitors KRAS mutant tumors cancer treatment oncology signal transduction drug combinations therapeutic targets clinical trials molecular biology cancer pathways phosphatidylinositide 3-kinase MEK 1/2 inhibitors KRAS mutant tumors cancer treatment therapeutic combination oncology signaling pathways drug efficacy targeted therapy molecular targeting phosphatidylinositide 3-kinase MEK 1/2 inhibitors KRAS mutant tumors cancer therapy drug combination oncology signal transduction molecular targeted therapy tumor treatment pharmacology cancer research phosphatidylinositide 3-kinase inhibitors MEK 1/2 inhibitors KRAS mutant tumors cancer treatment drug combination therapy oncology research clinical trials targeted therapy tumor growth inhibition signaling pathways molecular targeting
1259	The relationship between a breast cancer patient's capacity to metabolize tamoxifen and treatment outcome is dependent on the patient's genetic make-up. The relationship between a breast cancer patient's capacity to metabolize tamoxifen and treatment outcome is dependent on the patient's genetic make-up. The relationship between a breast cancer patient's capacity to metabolize tamoxifen and treatment outcome is dependent on the patient's genetic make-up. The relationship between a breast cancer patient's capacity to metabolize tamoxifen and treatment outcome is dependent on the patient's genetic make-up. The relationship between a breast cancer patient's capacity to metabolize tamoxifen and treatment outcome is dependent on the patient's genetic make-up. breast cancer tamoxifen metabolism genetic factors treatment outcome pharmacogenetics oncology metabolizing enzymes gene expression drug response personalized medicine breast cancer tamoxifen metabolism genetic make-up outcome pharmacogenetics cancer therapy gene expression drug response breast cancer tamoxifen metabolism genetic factors treatment outcome pharmacogenomics gene expression drug response oncology metabolites genetic variations clinical trials breast cancer patient tamoxifen metabolism genetic factors treatment outcome pharmacogenetics drug response oncology personalized medicine genomics metabolizing enzyme genetic polymorphism clinical trials gene expression therapeutic efficacy biomarkers breast cancer tamoxifen metabolism genetic make-up treatment outcome pharmacogenetics gene expression drug response oncology biomarkers breast cancer tamoxifen metabolism genetic factors treatment outcome pharmacogenetics metabolic capacity gene variation therapeutic response breast cancer tamoxifen metabolism genetic factors treatment outcome pharmacogenetics gene-drug interaction metabolic capacity oncology pharmacokinetics genetic polymorphism breast cancer tamoxifen metabolism genetic factors treatment outcome pharmacogenomics gene-drug interaction oncology pharmacokinetics clinical trial biomarker therapeutic response breast cancer tamoxifen metabolism genetic factors treatment outcome pharmacogenomics gene expression metabolic rate hereditary predisposition oncology clinical trial biomarker drug response breast cancer tamoxifen metabolism genetic factors treatment response pharmacogenetics oncology drug efficacy metabolic enzymes gene expression clinical outcomes
1137	TNFAIP3 is a tumor suppressor in glioblastoma. TNFAIP3 is a tumor suppressor in glioblastoma. TNFAIP3 is a tumor suppressor in glioblastoma. TNFAIP3 is a tumor suppressor in glioblastoma. TNFAIP3 is a tumor suppressor in glioblastoma. TNFAIP3 gene function tumor suppressor role glioblastoma cancer biology genetics molecular mechanisms prognosis therapy single nucleotide polymorphisms SNPs expression analysis protein function apoptosis regulation TNFAIP3 gene function tumor suppressor glioblastoma molecular biology oncology research mutation expression clinical relevance prognosis TNFAIP3 tumor suppressor glioblastoma research TNFAIP3 function glioblastoma genetics TNFAIP3 protein tumor suppressor genes glioblastoma biology TNFAIP3 expression glioblastoma prognosis TNFAIP3 mutation TNFAIP3 function TNFAIP3 gene expression TNFAIP3 protein TNFAIP3 role glioblastoma suppression glioblastoma prognosis TNFAIP3 mutations TNFAIP3 pathway TNFAIP3 regulation TNFAIP3 immunotherapy TNFAIP3 glioblastoma tumor suppressor genetic factor cancer biology prognosis differential expression molecular marker clinical relevance pathway analysis TNFAIP3 tumor suppressor function glioblastoma genetics TNFAIP3 gene expression glioblastoma treatment TNFAIP3 protein role glioblastoma prognosis TNFAIP3 mutations glioblastoma biomarkers TNFAIP3 glioblastoma tumor suppressor inflammation gene expression cancer biology molecular markers prognostic factor immune response TNFAIP3 gene glioblastoma suppression cancer biology tumor suppressor functions molecular oncology TNF alpha induced protein 3 glioma prognosis genetic markers cancer research biomarkers TNFAIP3 glioblastoma tumor suppressor gene function oncology cancer biology biomarker genetic mutation clinical trials therapeutic target TNFAIP3 function glioblastoma therapy glioblastoma prognosis TNFAIP3 expression glioblastoma risk factors TNFAIP3 genetic variants TNFAIP3 protein Tumor suppressors in brain cancer glioblastoma biomarkers
1379	Women with a higher birth weight are more likely to develop breast cancer later in life. Women with a higher birth weight are more likely to develop breast cancer later in life. Women with a higher birth weight are more likely to develop breast cancer later in life. Women with a higher birth weight are more likely to develop breast cancer later in life. Women with a higher birth weight are more likely to develop breast cancer later in life. birth weight breast cancer women likelihood correlation obesity genetics prenatal care socioeconomic status hormonal factors adipose tissue tumor development birth weight breast cancer women risk factors epidemiology mortality obesity genetics lifestyle prenatalnutrition birthweight breastcancer maternalhealth infanthealth healthoutcomes femaledevelopment obstetrics gynecology prenatalcare epidemiology riskfactors birth weight and breast cancer risk maternal birth weight and cancer low birth weight impact on breast cancer infant birth weight and adult cancer prenatal factors influencing breast cancer birth weight breast cancer women likelihood adulthood epidemiology obesity genetics nutrition fetal development birth weight breast cancer risk women health developmental factors cancer prevention maternal health obesity genetics birth weight breast cancer women risk factors epidemiology development later life obesity genetics birth weight breast cancer risk maternal health offspring health epidemiology oncology genetic factors environmental influences nutrition prenatal care long-term health outcomes birthweight breastcancer women risk factors epidemiology obesity genetics prenatalnutrition birth weight breast cancer risk maternal health infant mortality oncology epidemiology genetic factors lifestyle nutrition obesity
399	Exposure to fine particulate air pollution is relate to anxiety prevalence. Exposure to fine particulate air pollution is relate to anxiety prevalence. Exposure to fine particulate air pollution is relate to anxiety prevalence. Exposure to fine particulate air pollution is relate to anxiety prevalence. Exposure to fine particulate air pollution is relate to anxiety prevalence. exposure fine particulate air pollution anxiety prevalence health environment respiratory mental risk correlation epidemiology studies symptoms cardiovascular symptoms demographics geographic socioeconomic factors impact fine particulate matter air pollution anxiety mental health epidemiology risk factors environmental exposure public health lung function cardiovascular disease inflammation oxidative stress neuroinflammation cortisol levels sleep quality socioeconomic status urban areas rural areas occupational exposure long-term exposure short-term exposure seasonal variation age groups gender differences geographical location climate change air quality index PM2.5 PM10 indoor air pollution respiratory infections asthma depression suicide rates stress hormones immune system cognitive function psychological distress biomarkers genetic predisposition fine particulate matter air pollution anxiety prevalence health effects pollutants mental health environmental exposure risk factors public health particulate matter PM2.5 neurological impact cardiopulmonary disease air pollution health effects particulate matter mental health environmental exposure anxiety pollution and psychiatric disorders fine particles and stress respiratory issues anxiety link ambient air pollution impact fine particulate matter air pollution anxiety prevalence health effects environmental exposure pollutants mental health population health public health epidemiology risk factors health outcomes fine particulate matter air pollution anxiety prevalence health effects environmental factors pollutant exposure mortality rates mental health public health cardiovascular disease neurological impact exposure fine particulate matter air pollution anxiety prevalence health impact respiratory pollution mental health environmental factors risk factor epidemiology particulates psychological disorders pollution levels health outcomes fine particulate matter air pollution anxiety prevalence health effects environmental exposure respiratory health psychological impact pollution levels cardiovascular disease inflammatory response neurological disorders exposure fine particulate matter air pollution anxiety prevalence health effects environmental factors respiratory health mental health particulate matter PM2.5 cardiovascular disease inflammation neuroinflammation epidemiology cohort studies case-control studies clinical trials risk factors public health urban areas rural areas seasonal variations long-term exposure short-term exposure dose-response relationship biomarkers psychological impact socioeconomic status occupational exposure geographic information systems GIS spatial analysis temporal trends air quality indices AQI air pollution sources traffic emissions industrial emissions biomass fine particulate matter air pollution anxiety prevalence health effects pollutant exposure mental health epidemiology environmental factors
279	Commelina yellow mottle virus' (ComYMV) genome consists of 7489 baise pairs. Commelina yellow mottle virus' (ComYMV) genome consists of 7489 baise pairs. Commelina yellow mottle virus' (ComYMV) genome consists of 7489 baise pairs. Commelina yellow mottle virus' (ComYMV) genome consists of 7489 baise pairs. Commelina yellow mottle virus' (ComYMV) genome consists of 7489 baise pairs. ComYMV genome length viral genome plant virus genetic material RNA virus molecular biology virology gene sequence Commelina yellow mottle virus genome base pairs sequence genetics plant virology Commelina yellow mottle virus genome base pairs molecular biology plant virology genetics maximize search utility relevant expansion phrases Commelina yellow mottle virus ComYMV genome base pairs genetic sequence plant virus molecular biology viral genome analysis RNA virus virology research Commelina yellow mottle ComYMV genome base pairs virus genome genetic material nucleotide sequence molecular biology plant virus ComYMV genome size viral genome base pairs plant virus molecular biology genetic material viral genetics Commelina yellow mottle virus ComYMV genome length base pairs molecular biology plant virus genetic material RNA virus Commelina yellow mottle virus ComYMV genome base pairs sequence genetic information Commelina yellow mottle virus ComYMV genome length base pairs viral genetics plant virus molecular biology virology RNA virus genetic material
1014	Rapamycin decreases the concentration of triacylglycerols in fruit flies. Rapamycin decreases the concentration of triacylglycerols in fruit flies. Rapamycin decreases the concentration of triacylglycerols in fruit flies. Rapamycin decreases the concentration of triacylglycerols in fruit flies. Rapamycin decreases the concentration of triacylglycerols in fruit flies. Rapamycin triacylglycerols fruit flies lifespan extension metabolic effects calorie restriction aging genetics diet pharmacology rapamycin fruit flies triacylglycerols longevity metabolism aging gene expression lipid metabolism nutritional response TOR pathway Rapamycin fruit flies triacylglycerols lifespan metabolism longevity diet genetic treatment intervention cholesterol lipid nutrition aging Rapamycin effects on lipid metabolism triacylglycerol reduction mechanisms fruit fly aging rapamycin diet interventions metabolic pathways affected by rapamycin calorie restriction mimetics gerontogen action on lipids Rapamycin triacylglycerols fruit flies longevity metabolism diet genetic modification lipid levels lifespan extension Rapamycin diet effect Rapamycin lipid metabolism Triacylglycerol reduction mechanism Rapamycin lifespan extension Fruit fly metabolic pathway Rapamycin fatty acid synthesis Gerontology and rapamycin Lipid homeostasis rapamycin Caloric restriction mimic rapamycin Rapamycin triacylglycerols fruit flies lipid metabolism mTOR aging senescence nematode模型错误，请重试. Rapamycin triacylglycerols fruit flies lifespan extension dietary intervention glycemic control molecular aging metabolic health Rapamycin triacylglycerols fruit flies longevity metabolism intervention aging lipid diet genetic treatment pharmacology biodiesel energy nutrition life span health senescence calorie restriction gerontology physiology pharmacodynamics molecular biology genetics biochemistry cell biology pharmacokinetics cardiovascular insulin diabetes cholesterol fatty acids gene expression protein synthesis transcription translation signaling apoptosis autophagy inflammation oxidative stress mitochondria adipose tissue liver pancreas heart kidney muscle brain Rapamycin triacylglycerols fruit flies dietary interventions longevity glycemic control metabolic syndrome senescence mTOR pathway
830	NF2 (Merlin) causes phosphorylation and subsequent cytoplasmic sequestration of YAP in Drosophila by activating LATS1/2 kinases. NF2 (Merlin) causes phosphorylation and subsequent cytoplasmic sequestration of YAP in Drosophila by activating LATS1/2 kinases. NF2 (Merlin) causes phosphorylation and subsequent cytoplasmic sequestration of YAP in Drosophila by activating LATS1/2 kinases. NF2 (Merlin) causes phosphorylation and subsequent cytoplasmic sequestration of YAP in Drosophila by activating LATS1/2 kinases. NF2 (Merlin) causes phosphorylation and subsequent cytoplasmic sequestration of YAP in Drosophila by activating LATS1/2 kinases. NF2 gene Merlin protein phosphorylation process YAP localization LATS1/2 kinases Drosophila model cell signaling pathways NF2 protein function Merlin signaling YAP phosphorylation LATS1/2 activation Drosophila model cell cycle regulation tumor suppressor pathways cytoplasmic localization kinase cascade genetic interaction molecular mechanism developmental biology oncogenesis NF2 gene Merlin protein phosphorylation process YAP localization LATS1 kinase LATS2 kinase Drosophila model signaling pathway tumor suppressor cell proliferation cytoplasmic transport molecular biology techniques NF2 gene function Merlin protein YAP phosphorylation LATS1 activation LATS2 kinase Drosophila signaling cytoplasmic YAP localization tumor suppressor pathway genetic mutation impact cell cycle regulation molecular biology techniques NF2 Merlin phosphorylation cytoplasmic sequestration YAP Drosophila LATS1 LATS2 kinases signal transduction tumor suppressor protein interaction genetic regulation NF2 mutation Merlin protein YAP phosphorylation LATS1 activation LATS2 kinase cytoplasmic localization Drosophila model signal transduction pathway cell proliferation regulation NF2 protein Merlin phosphorylation YAP cytoplasmic sequestration LATS1 LATS2 kinase activation Drosophila model signal transduction cellular localization molecular biology genetic regulation NF2 mutation Merlin protein YAP phosphorylation LATS1/2 activation cytoplasmic YAP localization Drosophila signaling tumor suppressor pathway Hippo pathway NF2 gene Merlin protein phosphorylation YAP cytoplasmic sequestration LATS1 LATS2 Drosophila model kinase activation signaling pathway molecular biology genetic disorder tumor suppressor cell cycle regulation NF2 gene mutation Merlin protein YAP phosphorylation LATS1 activation LATS2 kinase cytoplasmic localization Drosophila model signaling pathway tumor suppression cell proliferation
831	NF2 (Merlin) prevents phosphorylation and subsequent cytoplasmic sequestration of YAP in Drosophila. NF2 (Merlin) prevents phosphorylation and subsequent cytoplasmic sequestration of YAP in Drosophila. NF2 (Merlin) prevents phosphorylation and subsequent cytoplasmic sequestration of YAP in Drosophila. NF2 (Merlin) prevents phosphorylation and subsequent cytoplasmic sequestration of YAP in Drosophila. NF2 (Merlin) prevents phosphorylation and subsequent cytoplasmic sequestration of YAP in Drosophila. NF2 protein Merlin protein YAP phosphorylation cytoplasmic sequestration Drosophila development Hippo pathway cell proliferation tumor suppression genetic mutation signaling pathway NF2 gene function YAP protein Drosophila model cell signaling phosphorylation cytoplasmic localization molecular biology genetics research biology biological pathway signal transduction protein interaction molecular mechanism NF2 gene Merlin protein YAP phosphorylation cytoplasmic sequestration Drosophila model signaling pathway tumor suppression cellular localization molecular biology genetic regulation NF2 gene function Merlin protein role YAP phosphorylation mechanism cytoplasmic localization Drosophila signaling pathway tumor suppressor NF2 YAP regulation by NF2 Merlin-YAP interaction Drosophila cell biology NF2 mutation effects YAP nuclear translocation tumor suppressor mechanisms signal transduction pathways NF2 Merlin phosphorylation YAP cytoplasmic sequestration Drosophila gene regulation tumor suppressor signaling pathway cell proliferation protein interaction NF2 protein function Merlin role YAP phosphorylation cytoplasmic localization Drosophila signaling Hippo pathway tumor suppression genetic regulation cellular proliferation tissue homeostasis NF2 Merlin YAP phosphorylation cytoplasmic sequestration Drosophila tumor suppressor Hippo pathway NF2 gene Merlin protein YAP phosphorylation cytoplasmic sequestration Drosophila model cell signaling tumor suppressor Hippo pathway NF2 Merlin YAP phosphorylation cytoplasmic sequestration Drosophila signaling pathway tumor suppression gene interaction protein regulation NF2 protein function Merlin role YAP phosphorylation Drosophila signaling cytoplasmic localization gene interaction tumor suppression Hippo pathway fly model cellular localization protein complex formation
1012	Radioiodine treatment of non-toxic multinodular goitre reduces thyroid volume. Radioiodine treatment of non-toxic multinodular goitre reduces thyroid volume. Radioiodine treatment of non-toxic multinodular goitre reduces thyroid volume. Radioiodine treatment of non-toxic multinodular goitre reduces thyroid volume. Radioiodine treatment of non-toxic multinodular goitre reduces thyroid volume. radioiodine therapy non-toxic multinodular goiter thyroid size reduction iodine-131 treatment thyroid function assessment radioactive iodine therapy goitre management thyroidectomy alternative iodine therapy effectiveness radioiodine therapy non-toxic multinodular goitre thyroid volume reduction treatment outcomes efficacy side effects complications radioactive iodine thyroidectomy comparison long-term effects radioiodine therapy non-toxic multinodular goiter thyroid volume reduction iodine-131 treatment thyroid nodules thyroid function radioactive iodine thyroidectomy alternative management strategies endocrinology treatments radioiodine therapy non-toxic goiter thyroid reduction iodine-131 treatment thyroid nodules radioactive iodine therapy gland volume reduction hyperthyroidism prevention thyroid function tests radioactive iodine uptake radioiodine non-toxic multinodular goitre thyroid volume treatment efficacy side effects patient outcomes radioiodine therapy non-toxic multinodular goiter thyroidectomy iodine-131 treatment thyroid hormone levels complications efficacy patient outcomes radioiodine therapy non-toxic multinodular goiter thyroid gland reduction iodine-131 treatment thyroidectomy alternative gland size decrease hyperthyroidism prevention radioactive iodine therapy radioiodine therapy non-toxic multinodular goiter thyroid volume reduction thyroid nodules iodine-131 treatment thyroid function tests follow-up assessment thyroidectomy alternative long-term outcomes radioiodine therapy non-toxic multinodular goiter thyroid size reduction iodine-131 treatment thyroidectomy comparison long-term efficacy side effects radioactive iodine therapy management strategies endocrine disorders radioiodine therapy non-toxic goiter thyroid reduction iodine-131 gland size decrease thyroid nodules management radioactive iodine treatment
832	NFAT4 activation requires IP3R-mediated Ca2+ mobilization. NFAT4 activation requires IP3R-mediated Ca2+ mobilization. NFAT4 activation requires IP3R-mediated Ca2+ mobilization. NFAT4 activation requires IP3R-mediated Ca2+ mobilization. NFAT4 activation requires IP3R-mediated Ca2+ mobilization. NFAT4 signaling calcium influx IP3 receptor calcium oscillations calcium ions signal transduction intracellular calcium calcium release calcium binding proteins calcium signaling pathways NFAT4 activation IP3R-mediated Ca2+ mobilization calcium signaling NFAT transcription factors calcium release channels intracellular calcium IP3 receptors calcium ion influx signaling pathways cell signaling NFAT4 signaling calcium signaling IP3 receptor calcium mobilization calcium ions NFAT activation calcium binding proteins intracellular calcium calcium influx calcium signaling pathway NFAT4 signaling pathway IP3R function calcium signaling calcium mobilization calcium ions IP3 receptor calcium release channels NFAT transcription factors calcium signaling cascade intracellular calcium calcium regulation calcium binding proteins calcium signaling events calcium homeostasis calcium signaling mechanisms NFAT4 activation IP3R Ca2+ mobilization signaling pathway regulation calcium ions intracellular signaling proteins immune response transcription因子 NFAT4 protein calcium signaling IP3 receptor gene expression signaling pathway calcium mobilization immunology cell biology calcium ions calcium signaling pathway calcium release calcium entry intracellular calcium calcium homeostasis NFAT transcription factors immune response calcium signaling cascade calcium signaling molecules calcium sensing receptors NFAT4 activation IP3R-mediated Ca2+ mobilization calcium signaling NFAT transcription factors IP3 receptors calcium ions signal transduction intracellular calcium release calcium-dependent protein kinases calcium/calmodulin-dependent kinases NFAT4 IP3R Ca2+ mobilization signaling pathway regulation mechanism calcium intracellular immunology transcription activation cell biology physiology NFAT4 activation IP3R Ca2+ mobilization signaling pathway regulation mechanism calcium ion translocation immune response transcription factors intracellular signaling pathways calcium signaling immune response regulation NFAT4 signaling NFAT4 signaling calcium ions IP3 receptors gene expression immune response calcium mobilization calcium influx calcium signaling NFAT family calcium-regulated transcription
834	NOX2-independent pathways can generate peroxynitrite by reacting with nitrogen intermediates. NOX2-independent pathways can generate peroxynitrite by reacting with nitrogen intermediates. NOX2-independent pathways can generate peroxynitrite by reacting with nitrogen intermediates. NOX2-independent pathways can generate peroxynitrite by reacting with nitrogen intermediates. NOX2-independent pathways can generate peroxynitrite by reacting with nitrogen intermediates. NOX2 peroxynitrite nitrogen intermediates reactive nitrogen species oxidative stress nitric oxide superoxide signaling pathways NOX2 peroxynitrite nitrogen intermediates oxidative stress enzymatic reactions biological pathways molecular mechanisms NOX2 peroxynitrite nitrogen intermediates reactive nitrogen species nitric oxide superoxide enzyme-independent nitration oxidative stress signaling pathways NOX2 alternative peroxynitrite generation nitrogen intermediates reactions cellular oxidant production nitric oxide metabolism reactive nitrogen species formation NOX2 peroxynitrite nitrogen intermediates reactive nitrogen species nitric oxide superoxide enzyme-independent nitration oxidative stress signaling pathways query expansion natural language processing NOX2 peroxynitrite generation nitrogen intermediates bioinformatics chemical reactions oxidative stress molecular biology pathway analysis NOX2 peroxynitrite nitrogen intermediates enzymatic pathways reactive nitrogen species NADPH oxidase nitric oxide superoxide biological pathways oxidative stress molecular biology immunology free radicals redox reactions NOX2 peroxynitrite nitrogen intermediates pathways reactive nitrogen species NADPH oxidase superoxide nitric oxide enzymatic reactions cellular signaling oxidative stress biological processes molecular mechanisms NOX2 peroxynitrite nitrogen intermediates alternative pathways nitric oxide reactive nitrogen species NADPH oxidase superoxide enzymatic reactions biochemistry antioxidant defenses cellular signaling NOX2 alternatives peroxynitrite production nitrogen intermediates oxidative stress markers nitric oxide derivatives redox reactions antioxidant defense mechanisms
956	Pleiotropic coupling of GLP-1R to intracellular effectors promotes distinct profiles of cellular signaling. Pleiotropic coupling of GLP-1R to intracellular effectors promotes distinct profiles of cellular signaling. Pleiotropic coupling of GLP-1R to intracellular effectors promotes distinct profiles of cellular signaling. Pleiotropic coupling of GLP-1R to intracellular effectors promotes distinct profiles of cellular signaling. Pleiotropic coupling of GLP-1R to intracellular effectors promotes distinct profiles of cellular signaling. GLP-1R agonists intracellular signaling pathways cellular responses glucose-dependent insulinotropic polypeptide receptor metabolic signaling pharmacology diabetes treatment hormone receptors signal transduction beta cell function regulatory mechanisms GLP-1R signaling pathways intracellular effectors pleiotropy cellular signaling GLP-1 receptor signal transduction hormone action metabolic effects insulin secretion G-protein coupled receptors cAMP production protein kinase A adiponectin inflammation cardiovascular benefits GLP-1R function intracellular signaling pathways pleiotropy GLP-1 receptor cellular responses signal transduction receptor coupling metabolic signaling peptide hormones glycagon-like peptide-1 cell signaling mechanisms GLP-1R signaling pathways intracellular effectors role pleiotropic effects GLP-1R cellular signaling mechanisms GLP-1 receptor function glucose-dependent insulinotropic polypeptide receptor downstream signaling cascades metabolic signaling pathways diabetes treatment targets hormone receptor interactions signal transduction mechanisms GLP-1R mediated responses GLP-1R intracellular effectors cellular signaling pleiotropy receptor coupling signaling pathways metabolic effects hormone action drug targets GLP-1R signaling pathways intracellular effectors list pleiotropic effects GLP-1R cellular signaling mechanisms GLP-1 receptor function regulatory mechanisms GLP-1R GLP-1R pharmacology intracellular signaling pathways GLP-1R GLP-1R biological roles GLP-1R molecular interactions GLP-1R function intracellular pathways cellular signaling networks glucose-dependent insulinotropic polypeptide receptor biological signaling mechanisms molecular interactions hormone receptor coupling metabolic signaling downstream signaling cascades cell response modulation GLP-1R function intracellular signaling pathways cellular responses pleiotropy GIPR comparison signaling networks metabolic effects pharmacological targets therapeutic potential signal transduction receptor coupling GLP-1R signaling pathways intracellular effectors list pleiotropy examples cellular signaling networks GLP-1 receptor functions metabolic effects GLP-1R downstream effectors GLP-1 signal transduction GLP-1R glucose-dependent insulinotropic polypeptide receptor cell signaling mechanisms GLP-1R mediated responses intracellular pathways GLP-1R distinct signaling profiles GLP-1R activation regulatory mechanisms GLP-1R GLP-1R activation intracellular signaling pathways cellular response diversity glucose-dependent insulin secretion 肠肽受体 signaling networks metabolic regulation β-cell function therapeutic targets diabetes treatment
50	AIRE is expressed in some skin tumors. AIRE is expressed in some skin tumors. AIRE is expressed in some skin tumors. AIRE is expressed in some skin tumors. AIRE is expressed in some skin tumors. AIRE tumors skin cancer expression gene molecular biology autoimmunity immunology thymus AIRE tumors skin cancer gene expression autoimmune diseases immunology molecularbiology AIRE autoimmunity cancer dermatology transcription factor immune tolerance skin cancer tumor immunity endogenous peptide presentation AIRE expression skin tumors AIRE gene skin cancer AIRE protein skin lesions AIRE function immune response AIRE upregulation tumor development AIRE tumors skin cancer gene expression autoimmunity thymus AIRE tumor expression AIRE skin cancer AIRE immune response AIRE autoimmunity AIRE gene function AIRE protein localization AIRE tumor immunity AIRE skin diseases AIRE immunology AIRE genetic variation AIRE autoimmune polyendocrine syndrome autoimmune diseases tumor microenvironment immunology endogenous peptide presentation epithelial cells dermatology cancer immunology lymphoid tissue AIRE tumors skin cancers immune tolerance autoimmunity gene expression melanoma lymphoma AIRE tumors skin cancer expression immune tissue disease genes autoimmunity AIRE tumor expression autoimmune diseases skin cancer types immune response skin tumors AIRE gene function tumor immunology autoimmunity and cancer AIRE protein localization
715	Low expression of miR7a does represses target genes and exerts a biological function in ovaries. Low expression of miR7a does represses target genes and exerts a biological function in ovaries. Low expression of miR7a does represses target genes and exerts a biological function in ovaries. Low expression of miR7a does represses target genes and exerts a biological function in ovaries. Low expression of miR7a does represses target genes and exerts a biological function in ovaries. miR7a microRNA ovaries target genes biological function expression levels molecular biology genetic regulation transcription factor mRNA stability miR7a miRNA ovarian function gene repression biological role microRNA expression miR7a expression miRNA function ovarian gene regulation target gene repression microRNA effect ovaries biology miR7a mechanism miR7a regulation miR7a targets miR7a function miR7a expression ovarian gene repression miRNA targeting miR7a biological role miR7a mechanism miR7a low expression target genes biological function ovaries microRNA gene regulation reproductive biology miR7a function miR7a target genes miR7a expression miR7a regulation miR7a ovaries miR7a biological role miR7a gene expression miR7a ovarian function miR7a molecular mechanism miR7a genetic regulation miR7a miRNA ovaries target genes biological function expression microRNA regulation genetic repression biomarker ovarian biology miR7a function ovaries target genes expression effects biological role microRNA regulation miR7a miRNA ovarian genes gene repression biological function microRNAexpression target genes regulation ovaries biology miR7a regulation target gene repression ovarian biology microRNA function mRNA expression levels molecular mechanism
957	Podocytes are motile and migrate in the presence of injury. Podocytes are motile and migrate in the presence of injury. Podocytes are motile and migrate in the presence of injury. Podocytes are motile and migrate in the presence of injury. Podocytes are motile and migrate in the presence of injury. Podocyte motility injury响应 migration renal pathology Podocytes motility injury response migration renal cells tissue repair cell behavior Podocyte motility migration injury response kidney cell movement glomerulus biological process epithelial cells fasciculat actin slit diaphragm kidney injury cell migration podocyte function glomerular disease biomarkers therapeutic intervention renal physiology proteinuria mechanobiology inflammation response Podocyte motility injury response migration renal disease cell biology angiogenesis treatment search optimization motile cells injury response migration biology podocyte function relevant queries biological motility medical search Podocyte injury response cell migration renal disease fascin podocin nephrin slit diaphragm 足细胞 迁移 肾小球损伤 Podocyte migration injury response motile cells kidney injury microvilli movement cellular adaptation podocyte motility injury migration biochemistry cellular response microscopy glomerulus kidney disease Podocyte migration injury response kidney repair cellular adhesion integrins extracellular matrix angiopoietinangiopoietin receptor signaling chemokines inflammation tubuloglomerular feedback
51	ALDH1 expression is associated with better breast cancer outcomes. ALDH1 expression is associated with better breast cancer outcomes. ALDH1 expression is associated with better breast cancer outcomes. ALDH1 expression is associated with better breast cancer outcomes. ALDH1 expression is associated with better breast cancer outcomes. ALDH1A1 breast cancer prognosis oxidative stress metabolite clearance chemotherapy response survival rate tumor heterogeneity genetic marker epithelial-mesenchymal transition ALDH1 breast cancer prognosis ALDH1 expression prognosis ALDH1 gene breast cancer ALDH1 biomarker breast cancer ALDH1 levels breast cancer outcomes ALDH1A1 breast cancer prognosis oncology research tumor markers survival analysis genetic biomarkers clinical trials cancer biology metabolic pathways chemotherapy response prognostic factor molecular biology cancer genetics gene expression profiling ALDH1 enzyme ALDH1A1 gene breast cancer prognosis tumor markers survival rates oncology research genetic markers cancer biology biomarkers therapeutic targets ALDH1 breast cancer prognosis biomarker survival oncology tumor marker genetic mutation treatment response clinical trial molecular biology epidemiology ALDH1 biomarker ALDH1 gene expression ALDH1 breast cancer prognosis ALDH1 protein levels ALDH1 and cancer survival ALDH1A1 breast cancer prognosis oncogenes tumor markers survival rates genetic markers cancer biology molecular diagnostics ALDH1 breast cancer prognosis ALDH1 gene expression ALDH1 and breast cancer survival ALDH1 biomarker breast cancer ALDH1 protein levels breast cancer ALDH1A1 breast cancer prognosis oncogenes tumor markers chemotherapy response metastasis survival rates gene expression biomarkers cancer biology molecular diagnostics ALDH1A1 breast cancer prognosis oncogenes tumor suppressors chemotherapy response survival rates genetic markers molecular biology cancer research biomarkers
716	Low expression of miR7a exerts a biological function in testis. Low expression of miR7a exerts a biological function in testis. Low expression of miR7a exerts a biological function in testis. Low expression of miR7a exerts a biological function in testis. Low expression of miR7a exerts a biological function in testis. miR7a expression testis biology function microRNA role microRNA regulation testicular gene expression biological impact miR7a miR7a function microRNA miR7a testis miR7a testis function expression biological microRNA regulation male reproduction miR7a expression testis biology functional genomics microRNA role reproductive health molecular biology genetic regulation testicular miRNAs miR7a expression testis functional role testicular biology microRNA function testis development molecular biology biological impact microRNA regulation testis specific gene expression microRNA target analysis miR7a testis low expression biological function microRNA spermatogenesis gene regulation fertility RNA biology miR7a function testis miR7a expression effects miR7a roles testicular biology miR7a regulation sperm development miR7a biological significance testes miR7a microRNA-7a testis biology gene regulation sperm development reproductive function RNA expression molecular biology genetic influence miR7a testis function biological expression efficacy keywords search优化 miR7a testis low expression biological function microRNA sperm development gene regulation fertility reproductive biology miR7a function testis biology miRNA role sperm development microRNA expression reproductive health
837	NR5A2 is important in development of endometrial tissues. NR5A2 is important in development of endometrial tissues. NR5A2 is important in development of endometrial tissues. NR5A2 is important in development of endometrial tissues. NR5A2 is important in development of endometrial tissues. NR5A2 function endometrial development gene expression endometrium physiology NR5A2 role female reproductive health NR5A2 function endometrial tissue development genetic role NR5A2 gene expression endometrium biology developmental importance NR5A2 NR5A2 gene function endometrium development female reproduction reproductive system hormones transcription factor uterus tissue differentiation molecular biology endothelial cells NR5A2 gene function endometrial tissue development genetic factors in uterus nr5a2 receptor uterine health uterine biology developmental genetics endometrium physiology NR5A2 function endometrial tissue development genes involved endometrium biology NR5A2 gene endometrial development gene function reproductive health hormone regulation uterine tissue embryo implantation transcription factor NR5A2 function NR5A2 gene expression NR5A2 role endometrial development endometrial tissues regulation NR5A2 signaling NR5A2 protein reproductive system development hormonal influences NR5A2 function endometrial development genes involved endometrium physiology NR5A2 role in biology NR5A2 function endometrial tissue development genetic factors endometrium biology steroid hormone receptors NR5A2 function endometrial development female reproduction genetic role molecular biology endometrium physiology
53	ALDH1 expression is associated with poorer prognosis in breast cancer. ALDH1 expression is associated with poorer prognosis in breast cancer. ALDH1 expression is associated with poorer prognosis in breast cancer. ALDH1 expression is associated with poorer prognosis in breast cancer. ALDH1 expression is associated with poorer prognosis in breast cancer. ALDH1A1 breast cancer prognosis oncogene metastasis chemotherapy resistance survival rate tumor marker ALDH1 breast cancer prognosis ALDH1 expression breast cancer outcomes ALDH1 biomarker breast cancer ALDH1 genetic marker breast cancer ALDH1 oncology research ALDH1 cancer study ALDH1 tumor marker ALDH1 clinical trials ALDH1 survival rate breast cancer ALDH1 risk factor breast cancer ALDH1A1 breast cancer prognosis oncogenes tumor markers metastasis survival rates genetic markers prognostic factors cancer subtype epithelial-mesenchymal transition chemotherapy resistance apoptosis gene expression profiling ALDH1 activity ALDH1 gene expression breast cancer prognosis cancer progression tumor biology oncology research genetic markers survival rates therapeutic targets cancer subtypes ALDH1A1 breast cancer prognosis tumor markers genetic expression oncology research survival rate biomarkers cancer progression therapeutic target breast cancer prognosis ALDH1 role cancer progression markers prognosis indicators oncology research gene expression analysis tumor biomarkers breast cancer subtypes ALDH1 function cancer survival rates ALDH1A1 breast cancer prognosis oncogenes tumor markers metastasis risk survival rates genetic markers epigenetic modifications therapeutic targets molecular biology cancer research epidemiology clinical outcomes ALDH1 breast cancer prognosis ALDH1 expression breast cancer ALDH1 biomarker breast cancer ALDH1 genetic marker breast cancer ALDH1 diagnosis breast cancer ALDH1 treatment outcomes breast cancer ALDH1 prognostic factor breast cancer ALDH1A1 breast cancer prognosis tumor markers gene expression oncology survival rates cancer biology cancer genetics molecular diagnostics therapeutic targets ALDH1A1 breast cancer prognosis tumor markers genetic markers oncology research cancer biomarkers cancer prognosis factors ALDH1 function cancer stem cells
718	Low nucleosome occupancy correlates with low methylation levels across species. Low nucleosome occupancy correlates with low methylation levels across species. Low nucleosome occupancy correlates with low methylation levels across species. Low nucleosome occupancy correlates with low methylation levels across species. Low nucleosome occupancy correlates with low methylation levels across species. low nucleosome occupancy methylation species evolutionary bioinformatics chromatin genomics histone modification patterns trends nucleosome occupancy methylation levels species comparison genetic regulation chromatin structure evo-devo biomarker transcription factor binding DNA methylation nucleosome dynamics low nucleosome occupancy methylation levels species epigenetics chromatin DNA histone genome biology genetics evolution epigenome genomic sequencing analysis correlation bioinformatics nucleosome positioning DNA methylation patterns epigenetic modifications chromatin structure gene expression regulation species comparison molecular biology techniques genomic analysis histone modifications genetic variation evolutionary biology bioinformatics tools nucleosome occupancy methylation species epigenetics chromatin DNA histone genomic regions evolution regulation transcription genes bioinformatics sequencing analysis comparative genomics nucleosome positioning chromatin structure epigenetics DNA methylation species comparison genomic regions transcription factor binding histone modification gene expression molecular biology techniques bioinformatics analysis low nucleosome high methylation epigenetics species comparison chromatin structure DNA modification gene expression histone modification epigenetic marks genomic regions genome analysis bioinformatics molecular biology genetics research nucleosome dynamics methylation patterns evolutionary biology genomic regions epigenetics histone modification species comparison chromatin structure low nucleosome occupancy methylation levels species comparison epigenetics chromatin structure DNA methylation genomic regions transcriptional activity histone modification evolutionary biology enhance search outcomes recommendations beneficial expansion/terms low nucleosome occupancy correlates low methylation levels species bioinformatics genomics epigenetics databases analysis molecular biology
839	Nanoparticles can be targeted against specific cell types by incorporating aptamers into lipid nanoparticles. Nanoparticles can be targeted against specific cell types by incorporating aptamers into lipid nanoparticles. Nanoparticles can be targeted against specific cell types by incorporating aptamers into lipid nanoparticles. Nanoparticles can be targeted against specific cell types by incorporating aptamers into lipid nanoparticles. Nanoparticles can be targeted against specific cell types by incorporating aptamers into lipid nanoparticles. Nanoparticles aptamers lipid nanoparticles cell targeting specific cell types molecular recognition drug delivery biocompatibility Nanoparticles aptamers lipid nanoparticles targeted therapy cancer treatment drug delivery biomedical applications specific cell targeting molecular recognition nanoparticles aptamers lipid nanoparticles targeted therapy specific cell types molecular recognition bioconjugates DNA aptamers drug delivery systems Nanoparticles targeting aptamer technology lipid nanoparticle design cell type specificity biomolecular targeting nanotechnology applications drug delivery systems biocompatibility nanomedicine personalized medicine genetic therapies Nanoparticles aptamers lipid nanoparticles targeted therapy cancer treatment molecular recognition drug delivery biomedical applications nanoparticles aptamers lipid nanoparticles targeting cellular targeting nanoparticles nanotechnology in medicine specific cell therapy biomolecular recognition nanoparticles drug delivery systems nanoparticles Nanoparticles aptamers lipid nanoparticles cell targeting molecular recognition biocompatibility treatment delivery theranostics specificity DNA aptamers RNA aptamers nanoparticles aptamers lipid nanoparticles targeted therapy specific cell types molecular targeting bioconjugates drug delivery systems molecular recognition biocompatibility nanoparticles aptamers cell targeting lipid nanoparticles molecular recognition specificity bioconjugates drug delivery molecular biology nanomedicine nanoparticle targeting aptamer-lipid nanoparticles specific cell delivery therapeutic nanoparticles molecular recognition biocompatible nanoparticles cancer treatment drug delivery systems
54	AMP-activated protein kinase (AMPK) activation increases inflammation-related fibrosis in the lungs. AMP-activated protein kinase (AMPK) activation increases inflammation-related fibrosis in the lungs. AMP-activated protein kinase (AMPK) activation increases inflammation-related fibrosis in the lungs. AMP-activated protein kinase (AMPK) activation increases inflammation-related fibrosis in the lungs. AMP-activated protein kinase (AMPK) activation increases inflammation-related fibrosis in the lungs. AMPK activation inflammation fibrosis lungs metabolic stress oxidative stress signaling pathways inflammatory response chronic obstructive pulmonary disease diabetes obesity AMPK activation inflammation fibrosis lungs molecular mechanisms signaling pathway metabolic stress chronic lung disease inflammatory response tissue repair gene expression oxidative stress therapeutic target cell signaling AMPK activation inflammation fibrosis lungs metabolic stress oxidative stress signaling pathways inflammation response pulmonary fibrosis kinase inhibitors gene expression inflammatory cytokines AMPK activation lung fibrosis AMPK role in fibrosis inflammation and fibrosis connection AMPK and lung health fibrotic processes triggered by AMPK AMPK inflammation fibrosis lungs signaling pathway metabolic stress oxidative stress mechanistic target of rapamycin (mTOR) peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) AMPK activation inflammation fibrosis lungs molecular targets therapeutic interventions metabolic stress oxidative stress signaling pathways gene expression inflammatory response chronic lung diseases pulmonary fibrosis kinase inhibitors biomarkers clinical trials pharmacology cellular mechanisms AMPK activation inflammation fibrosis lungs metabolic stress energy sensing mTOR inhibition p53 pathway autophagy inflammatory cytokines oxidative stress mechanistic target of rapamycin AMPK activators cell signaling chronic lung disease tissue repair fibrogenesis immune response tissue remodeling adiponectin liraglutide metformin AMPK activation inflammation fibrosis lungs molecular mechanisms signaling pathways therapeutic targets metabolic stress oxidative stress inflammation modulation fibrotic diseases AMPK activation inflammation fibrosis lungs signaling pathways metabolic stress oxidative stress inflammatory cytokines tissue repair cellular metabolism mechanistic target of rapamycin (mTOR) peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1alpha) AMPK activation inflammation fibrosis lungs molecular mechanisms signaling pathways metabolic stress oxidative stress inflammation resolution therapeutic targets
56	APOE4 expression in iPSC-derived neurons increases AlphaBeta production and tau phosphorylation causing GABA neuron degeneration. APOE4 expression in iPSC-derived neurons increases AlphaBeta production and tau phosphorylation causing GABA neuron degeneration. APOE4 expression in iPSC-derived neurons increases AlphaBeta production and tau phosphorylation causing GABA neuron degeneration. APOE4 expression in iPSC-derived neurons increases AlphaBeta production and tau phosphorylation causing GABA neuron degeneration. APOE4 expression in iPSC-derived neurons increases AlphaBeta production and tau phosphorylation causing GABA neuron degeneration. APOE4 iPSC neurons AlphaBeta tau phosphorylation GABA differentiation genetic modification neurodegeneration pathway microarray transcriptomics APOE4 iPSC nurons AlphaBeta tau phosphorylation GABA neuron degeneration genetics research neuroscience molecularbiology neuraldevelopment cellculture stemcells APOE4 iPSC nuerogenesis AlphaBeta protein tau protein GABA neuron degeneration molecular biology genetics neurodegeneration Alzheimer's stem cells neural differentiation protein expression cell culture neuroscience research techniques APOE4 genetic variant iPSC technology nervous system modeling neuronal differentiation AlphaBeta peptide tau protein modification GABAergic neurons neurodegeneration pathways stem cell research neuroscience experiments molecular biology techniques neural network function neurodegenerative diseases parkinson's disease alzheimer's disease synaptic dysfunction cellular pathology biomarker discovery neuroprotection strategies APOE4 iPSC neurons AlphaBeta tau phosphorylation GABA degeneration research genetics neuroscience molecular biology stem cells protein expression neurodegeneration/pathogenesis APOE4 gene expression iPSC technology neuronal cells AlphaBeta protein tau protein GABA neurons neuron degeneration genetic factors stem cell research neurodegenerative diseases DNA mutations APOE4 iPSC neurons AlphaBeta tau phosphorylation GABA degeneration molecular biomarker genetic neurodegeneration stem cells differentiation protein expression neuroscience biological/pathway aging Alzheimer's disease research clinical application APOE4 iPSC neurons AlphaBeta tau phosphorylation GABA neurons degeneration stem cells neurodegeneration molecular biology genetics DNA expression APOE4 iPSC network dysfunction neurodegeneration tauopathy genetic predisposition neural differentiation transcription regulation neurotransmission biomarker therapy prediction APOE4 iPSC-derived neurons AlphaBeta protein tau phosphorylation GABA neurons neuronal degeneration stem cells dementia Alzheimer's disease genetic risk factor molecular biology neurodegeneration/pathogenesis
57	APOE4 expression in iPSC-derived neurons increases AlphaBeta production and tau phosphorylation, delaying GABA neuron degeneration. APOE4 expression in iPSC-derived neurons increases AlphaBeta production and tau phosphorylation, delaying GABA neuron degeneration. APOE4 expression in iPSC-derived neurons increases AlphaBeta production and tau phosphorylation, delaying GABA neuron degeneration. APOE4 expression in iPSC-derived neurons increases AlphaBeta production and tau phosphorylation, delaying GABA neuron degeneration. APOE4 expression in iPSC-derived neurons increases AlphaBeta production and tau phosphorylation, delaying GABA neuron degeneration. APOE4 iPSC neurons AlphaBeta tau phosphorylation GABA neuron degeneration genetic predisposition research stem cells molecular biochemistry neuroscience Alzheimer's protein expression neurotransmitter differentiation biomarker therapeutics clinical study translational biology genomics neurodegeneration neuroscience research neural development aging genetics neuroprotection neuroinflammation neurotransmission neuroscience neur APOE4 iPSC differentiation GABA neurons AlphaBeta tau phosphorylation GABAergic degeneration microglia inflammation stem cells neurodegeneration amyloid plaque beta amyloidogenesis APOE4 iPSC neurons AlphaBeta tau phosphorylation GABA neuron degeneration microRNA genetic modification stem cells cognitive decline neurodegeneration model amyloid-beta APOE4 iPSC-derived neurons AlphaBeta production tau phosphorylation GABA neuron degeneration molecular mechanisms neurodegeneration research iPSC technology APOE4 genetics DNA methylation protein expression stem cell biology neuroscience studies tau pathology GABAergic dysfunction APOE4 iPSC neurons AlphaBeta tau phosphorylation GABA degeneration effects genetic neurodegeneration stem cells research molecular biology neuroscience biotechnology APOE4 iPSC-derived neurons AlphaBeta production tau phosphorylation GABA neuron degeneration relevant expansion phrases elevate search performance genetic factors molecular biology cognitive decline neurodegenerative diseases DNA methylation transcriptional regulation APOE4 iPSC-derived neurons AlphaBeta protein tau phosphorylation GABA neurons neuron degeneration molecular biology genetics neuroscience stem cells APOE4 iPSC-derived neurons AlphaBeta production tau phosphorylation GABA neuron degeneration neuron function stem cell research genetic factors neurodegeneration markers tau protein neural differentiation cellular biology molecular mechanisms novel therapies biomedical research neuroscience APOE4 iPSC-derived neurons AlphaBeta production tau phosphorylation GABA neuron degeneration molecular biology neurodegeneration research techniques genetics stem cells APOE4 iPSC-derived neurons AlphaBeta protein tau phosphorylation GABA neurons neuron degeneration molecular mechanisms neurodegeneration Alzheimer's disease research studies genetic factors stem cell technology neurotransmitter dysfunction neural differentiation
1274	The tip of the inner tube of the toxic type VI secretion system (T6SS) antibacterial effector in Escherichia coli (E. coli) carries toxic effector proteins. The tip of the inner tube of the toxic type VI secretion system (T6SS) antibacterial effector in Escherichia coli (E. coli) carries toxic effector proteins. The tip of the inner tube of the toxic type VI secretion system (T6SS) antibacterial effector in Escherichia coli (E. coli) carries toxic effector proteins. The tip of the inner tube of the toxic type VI secretion system (T6SS) antibacterial effector in Escherichia coli (E. coli) carries toxic effector proteins. The tip of the inner tube of the toxic type VI secretion system (T6SS) antibacterial effector in Escherichia coli (E. coli) carries toxic effector proteins. tip inner tube toxic type VI secretion system T6SS antibacterial effector proteins Escherichia coli E. coli protein structure bacterial defense secretion mechanism tip inner tube toxic T6SS antibacterial effector proteins Escherichia coli E. coli structure function mechanism microbiology bacteria secretion system molecular biology genetics immunity pathogenesis toxicity bacterial defense T6SS structure E. coli proteins effector mechanisms microbiology antimicrobial defenses protein function bacterial communication virulence factors inner tube T6SS antibacterial effectors E. coli toxic effector proteins T6SS structure E. coli T6SS bacterial secretion systems antibacterial mechanisms E. coli T6SS function E. coli defense mechanisms bacterial protein delivery T6SS components Escherichia coli T6SS type VI secretion system bacterial warfare T6SS tip structure tip inner tube T6SS antibacterial effector toxic proteins Escherichia coli E. coli bacterial defense secretion system molecular biology microbiology tip inner tube toxic type VI secretion system T6SS antibacterial effectors Escherichia coli E. coli toxic effector proteins bacterial defense mechanisms microbial secretion systems tip inner tube toxic type VI secretion system T6SS antibacterial effector Escherichia coli E. coli protein structure mechanism bacterial defense virulence factor toxic type VI secretion system T6SS antibacterial effector Escherichia coli E. coli inner tube toxic effector proteins bacterial defense protein delivery microbial warfare toxic T6SS Escherichia coli antibacterial effector inner tube tip toxin proteins molecular biology bacterial defense proteins secretion system inner管 T6SS效应蛋白 Escherichia coli毒力 抗菌效应器 内毒素蛋白 细胞膜穿透复合体
1395	p16INK4A accumulation is  linked to an abnormal wound response caused by the microinvasive step of advanced Oral Potentially Malignant Lesions (OPMLs). p16INK4A accumulation is  linked to an abnormal wound response caused by the microinvasive step of advanced Oral Potentially Malignant Lesions (OPMLs). p16INK4A accumulation is  linked to an abnormal wound response caused by the microinvasive step of advanced Oral Potentially Malignant Lesions (OPMLs). p16INK4A accumulation is  linked to an abnormal wound response caused by the microinvasive step of advanced Oral Potentially Malignant Lesions (OPMLs). p16INK4A accumulation is  linked to an abnormal wound response caused by the microinvasive step of advanced Oral Potentially Malignant Lesions (OPMLs). p16INK4A microinvasive tumor suppression Oral Potentially Malignant Lesions wound healing cancer progression molecular biology cytokines stroma response prognosis p16INK4A microinvasive advanced OPML oral cancer abnormal wound response biomarker molecular mechanism p16INK4A wound healing microinvasion OPML oral cancer dysplasia precancerous lesion epithelial dysregulation tumor suppressor immune response angiogenesis apoptosis p16INK4A expression wound healing impairment microinvasion process OPML progression oral mucosa damage cellular dysregulation cancer risk factor epithelial cell senescence inflammatory response tissue repair failure p16INK4A microinvasive advanced Oral Potentially Malignant Lesions OPML wound response abnormal terms expand query evidence biomarker cancer risk signaling pathway molecular diagnosis therapy prediction prevention clinical genetic environmental exposure histopathology stroma angiogenesis inflammation cellular dysplasia migration metastasis survival prognosis virulence host immune regulation mechanism biological p16INK4A expression wound healing microinvasion OPML progression dysregulation oncogenesis cellular proliferation genomic instability precancerous lesions cancer risk factors p16INK4A wound healing microinvasion Oral Potentially Malignant Lesions OPML cell cycle regulation epithelial dysplasia cancer progression tissue repair oncogenes tumor suppressors p16INK4A microinvasive OPML wound response oral cancer malignant potential p16INK4A wound healing microinvasion advanced OPMLs oral cancer cellular senescence tissue repair dysplasia premalignancy biomarker oncology pathology microinvasive advanced OPMLs p16INK4A wound healing oral cancer dysplasia precancerous biomarker treatment prognosis
1273	The sliding activity of kinesin-8 protein Kip3 promotes bipolar spindle assembly. The sliding activity of kinesin-8 protein Kip3 promotes bipolar spindle assembly. The sliding activity of kinesin-8 protein Kip3 promotes bipolar spindle assembly. The sliding activity of kinesin-8 protein Kip3 promotes bipolar spindle assembly. The sliding activity of kinesin-8 protein Kip3 promotes bipolar spindle assembly. kinesin-8 function bipolar spindle formation Kip3 role microtubule dynamics cell division process motor protein activity sliding mechanism kinesin-8 function bipolar spindle formation Kip3 role cell division process sliding motion kinesin proteins spindle assembly bipolar spindle kip3 function microtubule dynamics cell division kinesin-8 mechanism sliding mechanism kinesin-8 function bipolar spindle formation Kip3 role microtubule dynamics cell division process protein interaction chromosome segregation motor protein activity synaptic vesicle transport sliding activity kinesin-8 protein Kip3 bipolar spindle assembly microtubule dynamics cell division mitosis syneasthesia homolog saccharomyces cerevisiae dynein interaction kinesin-8 function bipolar spindle formation protein Kip3 role sliding activity impact microtubule dynamics chromosomal segregation process cell division regulation sliding motion kinesin proteins bipolar spindles spindle assembly Kip3 function protein dynamics microtubule interaction kinesin-8 mechanism sliding activity kinesin-8 protein Kip3 bipolar spindle assembly protein function spindle formation microtubule dynamics kinesin family cell division biological motor proteins sliding activity kinesin-8 Kip3 spindle assembly bipolar spindle effect of kinesin-8 on spindle kinesin motors cell division microtubule dynamics protein function sliding mechanism kinesin-8 function bipolar spindle formation Kip3 role microtubule dynamics
1272	The single flash-evoked ERG b-wave is generated by activity of ON-bipolar cells. The single flash-evoked ERG b-wave is generated by activity of ON-bipolar cells. The single flash-evoked ERG b-wave is generated by activity of ON-bipolar cells. The single flash-evoked ERG b-wave is generated by activity of ON-bipolar cells. The single flash-evoked ERG b-wave is generated by activity of ON-bipolar cells. flash-evoked_ERG b-wave ON-bipolar_cells retinal_function electroretinography neuroscience vision_research single_cell_activity retina_biology flash-evoked_ERG b-wave ON-bipolar_cells retinal_function electroretinography nerve_potential visual_pathway single_unit_response flash-evoked ERG b-wave ON-bipolar cells retina neuroscience electrophysiology vision photoreceptors ganglion neurons flash-evoked ERG ON-bipolar cells retinal function electrophysiology visual pathway photoreceptor response neural signaling ocular physiology neurobiology ophthalmology vision science flash-evoked ERG b-wave ON-bipolar cells retina vision neuroscience electrophysiology photoreceptor synaptic transmission flash-evoked ERG b-wave ON-bipolar cells retinal function electrophysiology visual pathway photoreceptor response neurobiology ophthalmology neuroscience flash-evoked ERG b-wave ON-bipolar cells retinal function visual pathway electrophysiology photoreceptor response neurobiology ophthalmology sensory neuroscience flash-evoked ERG ON-bipolar cells b-wave generation retinal function electrophysiology visual pathway neural response phototransduction flash-evoked_ERG b-wave ON-bipolar_cells optic_nerve functional_imaging retinal_disease neuroscience visual_system electroretinography retinal_cell_types nerve_conduction VEPs VEPs_vs_ERGs flash-evoked ERG ON-bipolar cells retinal function visual pathway electrophysiology photoreceptor response neurobiology ocular health biomedical research sensory neurons
1150	Tetraspanin-3 is a causative factor in the development of acute myelogenous leukemia Tetraspanin-3 is a causative factor in the development of acute myelogenous leukemia Tetraspanin-3 is a causative factor in the development of acute myelogenous leukemia Tetraspanin-3 is a causative factor in the development of acute myelogenous leukemia Tetraspanin-3 is a causative factor in the development of acute myelogenous leukemia Tetraspanin 3 acute myeloid leukemia oncogene cancer progression hematopoietic cells signaling proteins immune evasion chemotherapy resistance genetic mutation stem cells Tetraspanin-3 acute myelogenous leukemia cancer biology protein function oncogenesis hematopoietic cells molecular mechanisms genetic markers biomarkers clinical implications immunology tumor microenvironment signaling pathways Tetraspanin-3 acute myelogenous leukemia oncogenic factors cell signaling hematological malignancies cancer biomarkers immune evasion metastasis therapeutic targets Tetraspanin-3 role in AML Tetraspanin-3 AML research Tetraspanin-3 function in leukemia Tetraspanin-3 genetic link AML Tetraspanin-3 protein expression AML Tetraspanin-3 and leukemia development Tetraspanin-3 AML biomarker Tetraspanin-3 mechanisms in AML Tetraspanin-3 clinical relevance AML Tetraspanin-3 AML therapy Tetraspanin-3 AML prognosis Tetraspanin-3 acute myelogenous leukemia cancer biomarker cell signaling leukemia progression oncology research genetic mutation immune response therapeutic target Tetraspanin-3 leukemia acute myelogenous leukemia treatment leukemia risk factors Tetraspanin-3 function cancer genetics leukemia prevention oncology research biomarker discovery hematopoietic malignancies molecular biology Tetraspanin-3 acute myelogenous leukemia cancer biomarker leukemia progression molecular biology oncology gene expression protein function cell signaling hematopoietic stem cells tumor suppression Tetraspanin-3 acute myelogenous leukemia cancer biomarker cell signaling leukemia progression oncology research molecular biology gene expression therapeutic target Tetraspanin-3 acute myelogenous leukemia oncology biomarker cancer research genetic factors leukemia treatment cellular signaling Tetraspanin-3 leukemia acute myeloid leukemia cancer progression oncogenic roles hematological malignancies cell signaling immune evasion therapeutic targets gene expression biomarkers
1271	The severity of cardiac involvement in amyloidosis can be described by the degree of transmurality of late gadolinium enhancement in MRI. The severity of cardiac involvement in amyloidosis can be described by the degree of transmurality of late gadolinium enhancement in MRI. The severity of cardiac involvement in amyloidosis can be described by the degree of transmurality of late gadolinium enhancement in MRI. The severity of cardiac involvement in amyloidosis can be described by the degree of transmurality of late gadolinium enhancement in MRI. The severity of cardiac involvement in amyloidosis can be described by the degree of transmurality of late gadolinium enhancement in MRI. cardiac amyloidosis MRI late gadolinium enhancement transmural involvement cardiac involvement amyloidosis severity amyloidosis MRI transmurality late gadolinium enhancement cardiac involvement cardiac amyloidosis MRI severity cardiac MRI cardiac transmurality gadolinium enhancement cardiac MRI analysis cardiac involvement assessment cardiac amyloidosis MRI techniques late gadolinium enhancement myocardial involvement transmural extent cardiovascular amyloidosis imaging modalities cardiac MRI analysis amyloidosis types cardiac function assessment cardiac amyloidosis MRI techniques late gadolinium enhancement transmural involvement cardiac involvement severity amyloidosis types cardiac MRI analysis myocardial impairment assessment cardiac involvement amyloidosis late gadolinium enhancement MRI transmurality severity assessment cardiovascular disease cardiac amyloidosis imaging techniques diagnostic imaging myocardial involvement cardiac amyloidosis MRI late gadolinium enhancement transmurality severity assessment cardiovascular involvement cardiac amyloidosis MRI late gadolinium enhancement transmural involvement cardiac function imaging markers cardiovascular amyloidosis myocardial impairment cardiac amyloidosis transmurality late gadolinium enhancement MRI severity assessment cardiovascular involvement myocardial amyloidosis imaging markers cardiac function diagnostic criteria cardiac amyloidosis transmurality late gadolinium enhancement MRI cardiac involvement severity assessment cardiovascular amyloidosis imaging modalities cardiac MRI techniques amyloidosis types cardiac amyloidosis stages MRI techniques gadolinium enhancement significance transmural involvement cardiac function in amyloidosis clinical outcomes of cardiac amyloidosis diagnostic imaging of amyloidosis treatment options for cardiac amyloidosis
1270	The risk of male prisoners harming themselves is ten times that of female prisoners. The risk of male prisoners harming themselves is ten times that of female prisoners. The risk of male prisoners harming themselves is ten times that of female prisoners. The risk of male prisoners harming themselves is ten times that of female prisoners. The risk of male prisoners harming themselves is ten times that of female prisoners. male prisoners self-harm risk female prisoners incarceration mental health statistics prison conditions male prisoners self-harm female prisoners risk frequency incidence statistics criminal justice prison conditions safety measures male prisoners self-harm female prisoners risk factor mortality incarceration mental health risk assessment prisoner suicide incarceration safety male vs female inmates self-harm statistics prison mental health inmate behavior analysis correctional facilities security gender differences in prisons suicide prevention in prisons male prisoners risk harming themselves female prisoners statistics incarceration mental health prison conditions male prisoners self harm female prisoners self harm risk prison self harm statistics inmate self harm rates gender difference self harm prisons male prisoners self-harm female prisoners self-harm prison suicide rates inmate mental health prison population demographics self-harm statistics prisoners male vs female prisoner risks male prisoners self-harm female prisoners risk risk factors incarceration prison population mental health male prisoners self-harm risk female prisoners incarceration male inmate suicide rates female inmate homicide statistics prison environment mental health incarcerations male prisoners self-harm female prisoners risk factors augmentative searchterms incarceration mortality mental health
163	Bariatric surgery has a positive impact on mental health. Bariatric surgery has a positive impact on mental health. Bariatric surgery has a positive impact on mental health. Bariatric surgery has a positive impact on mental health. Bariatric surgery has a positive impact on mental health. bariatric surgery mental health weight loss psychological outcomes obesity treatment benefits improvement depression anxiety bariatric surgery mental health positive impact obesity psychological outcomes b益处 减肥手术 心理健康 体重管理 bariatric surgery mental health weight loss surgeries effectiveness benefits potential risk mental health improvement bariatric surgery benefits psychological well-being weight loss surgery effects obesity and mental health surgical intervention outcomes bariatric surgery mental health positive effect obesity weight loss surgical procedure psychological outcomes mental health improvement psychological benefits bariatric surgery effects weight loss and mood surgical intervention psychology obesity and mental wellbeing weight_loss surgical_intervention psychological_benefits obesity_treatment mood_improvement depression_reduction quality_of_life_improvement postoperative_outcomes bariatric surgery mental health positive impact keywords expansion efficacy bariatric surgery mental health obesity depression anxiety wellness quality life suggestions improvement effects benefits psychological therapy nutrition diabetes morbidity mortality weight loss satisfaction comorbidities bariatric surgery mental health weight loss surgeries outcomes benefits obesity treatment improvement
1029	Reduced responsiveness to interleukin-2 in regulatory T cells is associated with greater resistance to autoimmune diseases such as Type 1 Diabetes. Reduced responsiveness to interleukin-2 in regulatory T cells is associated with greater resistance to autoimmune diseases such as Type 1 Diabetes. Reduced responsiveness to interleukin-2 in regulatory T cells is associated with greater resistance to autoimmune diseases such as Type 1 Diabetes. Reduced responsiveness to interleukin-2 in regulatory T cells is associated with greater resistance to autoimmune diseases such as Type 1 Diabetes. Reduced responsiveness to interleukin-2 in regulatory T cells is associated with greater resistance to autoimmune diseases such as Type 1 Diabetes. interleukin-2 regulatory T cells autoimmune diseases Type 1 Diabetes immune response inflammation immunotherapy cytokines T-regulatory cells immune tolerance antigen presentation T-cell activation interleukin-2 regulatory T cells autoimmune diseases Type 1 Diabetes immune response inflammation cytokines immunology Tregs IL-2 signaling immune tolerance immune regulation T cell activation immune system immunopathology adaptive immunity innate immunity T helper cells Treg function T cell subset cytokine signaling immune checkpoint inhibitors regulatory T cells interleukin-2 responsiveness autoimmune diseases Type 1 Diabetes immune tolerance cytokines Treg function inflammation immune response modulation immune checkpoint inhibitors immune regulation cytokine function T cell activation autoimmunity mechanisms inflammatory response immunotherapy approaches gene expression analysis immune checkpoint inhibitors Treg cell dynamics cytokine signaling pathways interleukin-2 regulatory T cells autoimmune diseases Type 1 Diabetes immune response inflammation cytokines immunosuppression immune tolerance Treg cells IL-2 receptor T-cell activation regulatory T cells interleukin-2 autoimmune diseases Type 1 Diabetes immune response inflammation cytokines Tregs immunotherapy immunosuppression immune regulation T cell function immune tolerance immune checkpoint inhibitors adaptive immunity innate immunity autoimmunity immunology research biological markers therapeutic targets clinical trials immune system immunopathology interleukin-2 regulatory T cells autoimmune diseases Type 1 Diabetes immune response inflammation cytokines Treg function immunology pathology interleukin-2 regulatory T cells reduced responsiveness autoimmune diseases Type 1 Diabetes immune system inflammation cytokines Tregs immunotherapy biomarkers therapeutic targets regulatory T cells interleukin-2 responsiveness autoimmune diseases Type 1 Diabetes immunology inflammation cytokines immune tolerance T cell function adaptive immunity chronic inflammation interleukin-2 receptors regulatory T cell function autoimmune disease mechanisms Type 1 Diabetes treatment immune response modulation cytokine signaling
960	Polymeal nutrition reduces cardiovascular mortality. Polymeal nutrition reduces cardiovascular mortality. Polymeal nutrition reduces cardiovascular mortality. Polymeal nutrition reduces cardiovascular mortality. Polymeal nutrition reduces cardiovascular mortality. polymeal nutrition cardiovascular disease mortality health diets food heart wellness research science benefits study effectiveness prevention analysis evaluation impact comparison comparison studies meta-analysis polymeal nutrition cardiovascular mortality diet health heart diabetes weight management elderly fatigue polymeal nutrition cardiovascular mortality diet health cardiovascular disease meal replacement food combination effectiveness benefits polymeal diet benefits polymeal nutrition facts polymeal and heart health polymeal vs balanced diet polymeal research studies polymeal nutritional value polymeal impact on cardiovascular disease Polymeal nutrition cardiovascular mortality health benefits diet diabetes heart disease elderly diets meal replacement Polymeal diet nutritional benefits cardiovascular health meal planning dietary fiber polyphenols antioxidants heart disease prevention meal replacement balanced nutrition Polymer nutrition dietary fiber cardiovascular disease mortality rate nutritional supplements polyphenols antioxidant properties heart health chronic diseases dietary patterns health outcomes polymeal nutrition cardiovascular mortality dietary benefits polyphenols antioxidants heart disease dietitian clinical trials meal replacement plant-based Polymeal nutrition cardiovascular mortality dietary patterns polyphenols antioxidants heart disease diet quality chronic diseases food combinations nutritional epidemiology metabolic syndrome inflammation longevity health outcomes dietary diversity lifestyle factors polymer nutrition meal frequency cardiovascular disease prevention dietary fiber nutritional supplements meal timing cardiometabolic health diet quality nutrient density chronic diseases prevention
1389	mTORC2 regulates intracellular cysteine levels through xCT inhibition. mTORC2 regulates intracellular cysteine levels through xCT inhibition. mTORC2 regulates intracellular cysteine levels through xCT inhibition. mTORC2 regulates intracellular cysteine levels through xCT inhibition. mTORC2 regulates intracellular cysteine levels through xCT inhibition. mTORC2 cysteine xCT regulation inhibition protein synthesis metabolism signaling pathway mTORC2 xCT intracellular cysteine regulation proteins enzymes biochemistry metabolism signaling pathway mTORC2 function cysteine metabolism xCT protein cellular signaling cysteine transport mTORC2 activation intracellular redox proteins involved in cysteine regulation mTORC2 mechanism xCT inhibitor regulatory mechanisms cysteine homeostasis mTORC2 function cysteine metabolism xCT protein cell signaling pathways intracellular trafficking molecular mechanisms cancer biology protein synthesis regulation signal transduction mTORC2 cysteine xCT cell signaling proteins inhibition regulation metabolism mTORC2 function cysteine metabolism xCT protein intracellular amino acids mTORC2 signaling mTORC2 cysteine xCT inhibition regulation protein metabolism cellular biochemistry mTORC2 xCT intracellular cysteine regulation protein synthesis biosynthesis metabolism signaling enzymes gene expression molecular biology cellular homeostasis mTORC2 function xCT regulation cysteine biochemistry signaling pathway metabolism proteins enzymes cellular processes mTORC2 function cysteine metabolism xCT protein cell signaling cysteine deprivation oxidative stress molecular biology proteins interactions metabolic pathways
1146	Teaching hospitals do not provide better care than non-teaching hospitals. Teaching hospitals do not provide better care than non-teaching hospitals. Teaching hospitals do not provide better care than non-teaching hospitals. Teaching hospitals do not provide better care than non-teaching hospitals. Teaching hospitals do not provide better care than non-teaching hospitals. teaching hospital vs non-teaching hospital quality of care patient outcomes medical education impact hospital resources specialty training clinical skills healthcare efficacy comparative studies medical standards teaching hospital care quality non-teaching hospital comparison patient outcomes medical education impact hospital type effectiveness teaching hospitals vs non-teaching hospitals care quality differences medical education impact hospital resources comparison patient outcomes research training programs effectiveness teaching hospital vs non-teaching hospital outcomes teaching hospital care quality non-teaching hospital patient satisfaction comparative analysis teaching vs non-teaching hospitals teaching hospital efficiency non-teaching hospital medical advancements teaching hospital resources allocation non-teaching hospital training programs teaching hospital patient volume non-teaching hospital specialized care teaching hospital care quality non-teaching hospital evidence-based research patient outcomes medical educationimpact clinical training specializationavailability resource allocation geographical location patient demographics quality metrics evaluation methods study comparisons healthcare efficacy teaching hospital benefits non-teaching hospital drawbacks care quality comparison medical education impact hospital type effectiveness teaching hospitals care quality non-teaching hospitals patient outcomes research focus clinical training resources allocation evidence-based care medical errors mortality rates readmission rates teaching hospital benefits non-teaching hospital comparison patient care quality medical education impact hospital accreditation differences teaching hospitals vs non-teaching hospitals care quality patient outcomes medical education impact hospital resources clinical experience patient volume staff qualifications teaching hospital advantages non-teaching hospital strengths healthcare research clinical training programs teaching hospital vs non-teaching hospital patient outcomes quality of care medical education impact hospital accreditation clinical training effectiveness healthcare standards patient satisfaction comparative studies hospital types medical errors rate research environment patient volume specialty training long-term patient care community hospitals academic hospitals
1024	Recurrent mutations occur frequently within CTCF anchor sites adjacent to oncogenes. Recurrent mutations occur frequently within CTCF anchor sites adjacent to oncogenes. Recurrent mutations occur frequently within CTCF anchor sites adjacent to oncogenes. Recurrent mutations occur frequently within CTCF anchor sites adjacent to oncogenes. Recurrent mutations occur frequently within CTCF anchor sites adjacent to oncogenes. recurring mutations CTCF anchor sites oncogenes genomic variants cancer genome regions recurrentmutations CTCFanchorsites oncogenes genomicinstability cancergenetics transcriptionfactorbinding epigenetics chromatinstructure geneexpression mutationallandscape regulatoryregions tumorbiology recurrent mutations CTCF anchor sites oncogenes genomic instability chromatin regulation transcription factor binding cancer genetics epigenetics DNA methylation gene expression regulation recurrent mutations Ctcf anchor sites oncogenes genetic variations mutation frequency cancer genetics molecular biology genomic instability Oncogene regulation transcription factors genome stability CTCF protein recurrentmutations ctcfanchorites oncogenes geneticvariants cancerbiology moleculargenetics genomeanalysis biomedicalresearch mutationrates genomicstability tumorgenomics transcriptionfactors mutation patterns cancer genetics genomic instability epigenetic regulation transcription factor binding chromatin architecture oncogene activation DNA repair mechanisms mutational hotspots gene regulation networks recurrent mutations CTCF anchor sites oncogenes genomic regions gene regulation DNA binding proteins cancer genetics epigenetics transcription factors cancer genomics recurrent mutations CTCF anchor sites oncogenes genomic instability transcription factor binding cancer genetics epigenetic regulation chromatin structure gene expression cancer biology recurrent mutations CTCF anchor sites oncogenes genomic instability transcription factor binding cancer genetics epigenetic regulation gene expression DNA repair chromatin structure oncogene activation genetic predisposition mutation frequency biomarker therapeutic target recurringmutations ctcfanchorites oncogenes geneticvariants molecularbiology cancergenetics genomics mutationrates transcriptionfactors DNAelements
1266	The risk of breast cancer among parous women increases with placental weight of pregnancies, and this association is strongest for premenopausal breast cancer. The risk of breast cancer among parous women increases with placental weight of pregnancies, and this association is strongest for premenopausal breast cancer. The risk of breast cancer among parous women increases with placental weight of pregnancies, and this association is strongest for premenopausal breast cancer. The risk of breast cancer among parous women increases with placental weight of pregnancies, and this association is strongest for premenopausal breast cancer. The risk of breast cancer among parous women increases with placental weight of pregnancies, and this association is strongest for premenopausal breast cancer. breast_cancer parous_women placental_weight pregnancies premenopausal risk_factors oncology obstetrics epidemiology hormonal_impact pregnancy_outcomes breast_cancer_risk parous_women placental_weight pregnancy_outcomes premenopausal_cancer maternal_factors oncology_research reproductive_history obstetric_history epidemiology_studies breast_cancer_risk parous_women placental_weight pregnancy premenopausal_cancer reproductive_history obstetric_history oncology epidemiology pregnancy_outcomes breast cancer risk factors parous women health pregnancy outcomes placental weight impact premenopausal breast cancer risk reproductive history and cancer maternal health research obstetric data analysis prenatal factors breast cancer pregnancy complications and cancer breast cancer parous women placental weight premenopausal pregnancy outcomes oncology epidemiology risk factors breast cancer risk factors parous women health placental weight impact premenopausal breast cancer analysis pregnancy outcomes and cancer maternal health indicators reproductive history cancer association breast cancer parous women placental weight premenopausal pregnancy outcomes oncology epidemiology risk factors breast_cancer parous_women placental_weight pregnancies premenopausal_breast_cancer risk_factors oncology epidemiology breast cancer parous women placental weight pregnancies premenopausal risk factors oncology epidemiology breast_cancer_risk parous_women placental_weight pregnancy_outcomes premenopausal_cancer reproductive_history maternal_factors oncology epidemiology
721	Lupus-prone mice infected with curliproducing bacteria have higher autoantibody titers compared to controls. Lupus-prone mice infected with curliproducing bacteria have higher autoantibody titers compared to controls. Lupus-prone mice infected with curliproducing bacteria have higher autoantibody titers compared to controls. Lupus-prone mice infected with curliproducing bacteria have higher autoantibody titers compared to controls. Lupus-prone mice infected with curliproducing bacteria have higher autoantibody titers compared to controls. Lupus-susceptible mice autoimmunity bacteria infection antibody titer curls LPS immunity microbial gut microbiota Lupus-prone mice bacteria autoantibody titers immune response curliproducing bacteria microbial infection autoimmunity models mouse strains Lupus-prone mice curliproducing bacteria autoantibody titers immune response infection model immunology Lupus-prone mice research autoantibody titers measurement curliproducing bacteria properties lupus mouse models immune response in lupus-prone mice bacterial infection effects on autoimmunity lupus autoantibodies microbial influence on lupus development murine lupus studies autoimmunity mechanisms exploration Lupus lupus-prone mice autoantibodies curliproducing bacteria control group immune response inflammation genetics immunology mouse models autoimmune disorders Lupus-prone mice bacteria infection autoantibody titers curliproducing bacteria lupus modeling mouse models autoimmune diseases Lupus-prone mice curliproducing bacteria autoantibody titers controls infection model research immunity disease serology genetics immunology Lupus-prone mice curliproducing bacteria autoantibody titers immune response infection model genetics disease progression Lupus-prone mice curliproducing bacteria autoantibody titers immune response microbiome inflammation lupus models antigen presentation pathogenesis genetic susceptibility bacterial strains autoimmune diseases Lupus-prone mice bacteria infection autoantibody titers curliproducing bacteria immune response microbial influence Autoimmunity models
1144	Taxation of sugar-sweetened beverages had no effect on the incidence rate of type II diabetes in India. Taxation of sugar-sweetened beverages had no effect on the incidence rate of type II diabetes in India. Taxation of sugar-sweetened beverages had no effect on the incidence rate of type II diabetes in India. Taxation of sugar-sweetened beverages had no effect on the incidence rate of type II diabetes in India. Taxation of sugar-sweetened beverages had no effect on the incidence rate of type II diabetes in India. sugar-sweetened beverages diabetes India effect taxation population studies research public health economicimpact taxation sugar-sweetened beverages incidence type II diabetes India effect population study public health policy Taxation sugar-sweetened beverages incidence type II diabetes India public health policy epidemiology nutrition socioeconomic factors Taxation sugar-sweetened beverages incidence rate type II diabetes India public health policy economic impact dietary habits epidemiology obesity rates Taxation sugar-sweetened beverages incidence type II diabetes India public health epidemiology economic policy taxation sugar-sweetened beverages incidence type II diabetes India public health nutrition policy epidemiology taxation sugar-sweetened beverages incidence type II diabetes India public health epidemiology policy nutrition obesity metabolic syndrome economic impact health outcomes intervention observational study longitudinal study clinical trial health economics public opinion government policy healthcare system Taxation effectiveness sugar-sweetened beverages type II diabetes India research public health policy economics health outcomes taxation sugar-sweetened beverages type II diabetes India effect incidence population study research trends public health policy economics consumption intake socioeconomic factors ethnicity age gender prevalence meta-analysis controlled trial longitudinal observational taxation policies sugar-sweetened beverages type II diabetes India epidemiological studies public health outcomes alternative interventions
723	Ly49Q directs the organization of neutrophil migration to inflammation sites by regulating membrane raft functions. Ly49Q directs the organization of neutrophil migration to inflammation sites by regulating membrane raft functions. Ly49Q directs the organization of neutrophil migration to inflammation sites by regulating membrane raft functions. Ly49Q directs the organization of neutrophil migration to inflammation sites by regulating membrane raft functions. Ly49Q directs the organization of neutrophil migration to inflammation sites by regulating membrane raft functions. Ly49Q neutrophils inflammation membrane rafts migration immune response cytokines chemokines signaling pathways immune cells tissue repair Ly49Q neutrophils inflammation membrane rafts immune response chemotaxis innate immunity leukocyte recruitment cytokines signal transduction trafficking macrophages natural killer cells adhesion molecules Ly49Q protein neutrophil migration membrane rafts inflammation response immune system cellular adhesion innate immunity leukocyte trafficking cytokine signaling chemotaxis Ly49Q receptor neutrophil migration inflammation sites membrane rafts immune response innate immunity leukocyte function chemotaxis immune cell trafficking cytokine regulation signal transduction pathways cellular adhesion tissue inflammation immunology research leukocyte activation Ly49Q neutrophil migration inflammation sites membrane rafts immune response leukocyte recruitment cytokines chemokines signaling pathways Ly49Q function neutrophil migration membrane rafts inflammation sites immune response gene regulation cell signaling innate immunity leukocyte activation chemotaxis Ly49Q neutrophil migration inflammation sites membrane rafts immune response signaling pathways cell adhesion innate immunity Ly49Q neutrophil migration inflammation sites membrane rafts immune response innate immunity cytokine signaling leukocyte recruitment adaptive immune system cellular trafficking chemokine receptors antigen presentation natural killer cells Ly49Q neutrophil migration inflammation sites membrane rafts immune response signaling pathways leukocyte recruitment cytokines chemokines adaptive immunity innate immunity gene expression cell adhesion molecules inflammatory processes Ly49Q proteins neutrophil mobilization membrane rafts inflammation response immune system regulation cell adhesion molecules chemotaxis factors innate immunity leukocyte recruitment signaling pathways cytokines inflammatory mediators
845	Neutrophil extracellular traps (NETs) are released by ANCA-stimulated neutrophils. Neutrophil extracellular traps (NETs) are released by ANCA-stimulated neutrophils. Neutrophil extracellular traps (NETs) are released by ANCA-stimulated neutrophils. Neutrophil extracellular traps (NETs) are released by ANCA-stimulated neutrophils. Neutrophil extracellular traps (NETs) are released by ANCA-stimulated neutrophils. neutrophils extracellular traps NETs ANCA stimulation autoimmune disease inflammation biology medical research immune response mechanisms ANCA neutrophils NETs inflammation autoimmune bacteria DNA citrullination pathology immune response infection clinical mechanisms therapy diagnosis Neutrophils extracellular traps ANCA inflammation autoimmune bacteria mechanisms pathology genetics treatment therapy immunology cytokines microbiome neutrophil functions ANCA associated diseases NET formation mechanisms inflammatory responses autoimmunity markers granulocyte activation immune defense mechanisms medical research advances Neutrophils extracellular traps ANCA stimulated release mechanisms autoimmune inflammation pathology biology genetics treatment diagnostics Neutrophils ANCA extracellular traps NETosis autoimmune disease inflammation immunology biomedical research therapeutic targets infection defense Neutrophils extracellular traps ANCA stimulated inflammation autoimmune disease mechanism biology medical research immune response neutrophils extracellular traps NETs ANCA stimulated inflammatory response autoimmune diseases infection microbiome immunology biomedicine pathology neutrophil extracellular traps ANCA stimulated inflammatory response autoimmune disease mechanism biology pathology immunology neutrophils ANCA extracellular traps mechanisms inflammation disease pathogenesis antibodies immune response
967	Pretreatment with the Arp2/3 inhibitor CK-666 affects lamelliopodia formation. Pretreatment with the Arp2/3 inhibitor CK-666 affects lamelliopodia formation. Pretreatment with the Arp2/3 inhibitor CK-666 affects lamelliopodia formation. Pretreatment with the Arp2/3 inhibitor CK-666 affects lamelliopodia formation. Pretreatment with the Arp2/3 inhibitor CK-666 affects lamelliopodia formation. pretreatment Arp2/3 inhibitor CK-666 lamellipodia formation cellular dynamics actin polymerization biological mechanism research study experiment microscopy molecular biology cell science Arp2/3 inhibitor CK-666 lamellipodia formation cell migration actin polymerization inhibitor effects molecular biology cellular response microscopy analysis biological pathway Pretreatment Arp2/3 inhibitor CK-666 lamellipodia actin polymerization cell migration biological response microscopy dynamics regulation Pretreatment methods Arp2/3 inhibition CK-666 effects lamellipodia development cell migration actin polymerization biological response analysis molecular biology techniques biochemical assays microscopy imaging signal transduction pathways cellular dynamics pharmacological intervention biological mechanisms experimental design scientific research methodologies Arp2/3 complex CK-666 lamellipodia inhibitor cell migration actin polymerization molecular biology biochemistry cellular response drug effect biological pathway microscopy analysis gene expression protein interaction query expansion Arp2/3 inhibitor CK-666 lamellipodia cellular response actin polymerization biological assay microscopy analysis molecular mechanism cell migration CK-666 Arp2/3 inhibitor lamellipodia formation cell migration actin polymerization molecular biology biophysics microscopy scientific research cellular response Arp2/3 inhibitor CK-666 lamellipodia formation pretreatment effects cellular dynamics actin polymerization microscopy analysis molecular biology cell morphology Pretreatment Arp2/3 inhibitor CK-666 lamellipodia formation cell migration actin polymerization molecular biology biochemistry microscopy cell morphology biophysics Arp2/3 inhibition CK-666 effects lamellipodia development actin polymerization cell migration impacts inhibitor assays cytoskeletal dynamics biological response modifiers
847	New drugs for tuberculosis often do not penetrate the necrotic portion of a tuberculosis lesion in high concentrations. New drugs for tuberculosis often do not penetrate the necrotic portion of a tuberculosis lesion in high concentrations. New drugs for tuberculosis often do not penetrate the necrotic portion of a tuberculosis lesion in high concentrations. New drugs for tuberculosis often do not penetrate the necrotic portion of a tuberculosis lesion in high concentrations. New drugs for tuberculosis often do not penetrate the necrotic portion of a tuberculosis lesion in high concentrations. tuberculosis drug penetration TB treatment efficacy necrotic tissue drug delivery tuberculosis lesions treatment anti-TB drug absorption tuberculosis drug penetration tuberculosis necrotic tissue drug delivery tuberculosis tuberculosis lesion treatment anti-tuberculosis medication absorption tuberculosis lesion treatment drug penetration tuberculosis necrotic tissue drug delivery anti-tuberculosis drug efficacy tuberculosis drug absorption tuberculosis lesion drug distribution drug targeting tuberculosis lesions tuberculosis drug penetration tuberculosis treatment efficacy anti-tuberculosis drug delivery tuberculosis necrotic tissue tuberculosis lesion drug distribution new tuberculosis therapies tuberculosis infection management tuberculosis drug resistance tuberculosis lesion characteristics tuberculosis treatment options tuberculosis lesions drug penetration necrotic tissue tuberculosis treatment anti-tubercular drugs pharmacokinetics tuberculosis infection drug delivery systems tuberculosis drug penetration anti-tuberculosis treatment efficacy drug delivery systems tuberculosis tuberculosis lesion characteristics enhancing drug absorption tuberculosis tuberculosis lesions drug delivery systems antibiotic penetration necrotic tissue tuberculosis treatment advancements tuberculosis drug efficacy antimicrobial agents antibiotic delivery drug permeability lung tissue bioavailability infection treatment pharmaceutical formulation targeted therapy TB drug resistance drug absorption chronic infection management tuberculosis lesion composition drug delivery systems tuberculosis anti-tuberculosis drug penetration necrotic tissue drug absorption tuberculosis treatment efficacy advanced tuberculosis therapy tuberculosis drug resistance enhancing drug penetration tuberculosis TB drug delivery lung tissue penetration tuberculosis treatment advancements antibiotic efficacy bioavailability issues pharmacokinetics tuberculosis drug-resistant TB novel TB therapies
727	Ly6C hi monocytes have a lower inflammatory capacity compared to their Ly6C lo counterparts. Ly6C hi monocytes have a lower inflammatory capacity compared to their Ly6C lo counterparts. Ly6C hi monocytes have a lower inflammatory capacity compared to their Ly6C lo counterparts. Ly6C hi monocytes have a lower inflammatory capacity compared to their Ly6C lo counterparts. Ly6C hi monocytes have a lower inflammatory capacity compared to their Ly6C lo counterparts. inflammatory response monocyte subtypes immune system Ly6C expression macrophage polarization inflammation regulation leukocyte biology Ly6C monocytes inflammatory capacity comparison function cytokines immune response phenotype mouse human tissue role regulation activation differentiation markers genetics pathology physiology inflammatory response monocyte subtypes immune system cytokines innate immunity cell markers biological functions ly6c hi monocytes function ly6c hi monocyte characteristics ly6c hi vs ly6c lo monocytes inflammatory response of ly6c hi monocytes ly6c hi monocytes role ly6c hi monocytes properties comparative analysis ly6c hi and lo monocytes ly6c hi monocytes vs inflammation ly6c hi and lo monocytes comparison immunology ly6c hi monocytes inflammation levels in ly6c hi monocytes Ly6C expression monocyte subtypes inflammatory response immune cells macrophage differentiation innate immunity leukocytes cytokines phagocytosis tissue repair blood monocytes search optimization keyword expansion medical research immune system inflammation monocytosis biomarkers immunology cell differentiation biotechnology clinical applications monocyte subsets inflammation immune response Ly6C markers cell phenotype inflammatory capacity monocytes Ly6C expression immune response macrophage polarization cytokine production tissue repair phagocytosis infection defense hematopoiesis immunology research Ly6C expression monocyte subsets inflammatory response immune function macrophage differentiation immune cells inflammation markers leukocyte migration immunology research cell biology inflammatory response monocyte subpopulations immune function tissue repair cytokine production phagocytosis immune cell differentiation gene expression immunology research biomedical science
728	Ly6C hi monocytes have a lower inflammatory capacity than Ly6C lo monocytes. Ly6C hi monocytes have a lower inflammatory capacity than Ly6C lo monocytes. Ly6C hi monocytes have a lower inflammatory capacity than Ly6C lo monocytes. Ly6C hi monocytes have a lower inflammatory capacity than Ly6C lo monocytes. Ly6C hi monocytes have a lower inflammatory capacity than Ly6C lo monocytes. inflammatory response monocyte subtypes immune function macrophage development cytokine production blood cells innate immunity cell markers Ly6C monocytes inflammatory capacity comparison immune cells function biology research markers physiology inflammatory response monocyte subtypes immune system leukocytes macrophage differentiation innate immunity cytokines phagocytosis hematopoiesis inflammatory response monocyte subtypes immune system function lymphocyte markers innate immunity blood cell types cytokine production macrophage differentiation inflammatory markers monocytic lineage Ly6C monocytes inflammatory capacity immune cells differentiation function biology research markers monocyte subtypes inflammation immune response leukocytes biological markers cellular differentiation inflammatory response monocyte subtypes immune function cytokine production tissue residency phagocytosis rate activation markers Ly6Chi Ly6Clow monocyte subsets inflammation immune response differential functionality biological markers Ly6Chi Ly6Clow monocyte subsets inflammation immune response differential capacity immune cells cytokine production tissue distribution developmental stage macrophage polarization immune surveillance expansion terms monocyte subsets inflammatory response immune cells regulatory mechanisms biological markers cell phenotypes innate immunity
729	Lymphadenopathy is observed in knockin mouse lacking the SHP-2 MAPK pathway. Lymphadenopathy is observed in knockin mouse lacking the SHP-2 MAPK pathway. Lymphadenopathy is observed in knockin mouse lacking the SHP-2 MAPK pathway. Lymphadenopathy is observed in knockin mouse lacking the SHP-2 MAPK pathway. Lymphadenopathy is observed in knockin mouse lacking the SHP-2 MAPK pathway. Lymphadenopathy knockin mice SHP-2 MAPK pathway immune response gene knockout lymph node enlargement signaling molecules Lymphadenopathy knockin mouse SHP-2 MAPK pathway mouse model immunology molecular biology MMP pathway knockout mouse immune response Lymphadenopathy knockin mouse SHP-2 MAPK pathway immunology mouse model genetic modification immune response inflammation Lymphadenopathy symptoms knockin mouse model SHP-2 function MAPK pathway impact immunological response analysis genetic modification effects mouse lymph node examination signaling pathway disruption immune system changes disease model development Lymphadenopathy knockin mouse SHP-2 MAPK pathway immune response cancer models signaling pathway immunology genetic modification disease modeling Lymphadenopathy symptoms SHP-2 function knockin mice MAPK pathway effects immune response modulation gene knockout models lymph node enlargement causes signal transduction inhibitors immunology research mouse model diseases Lymphadenopathy knockin mice SHP-2 MAPK pathway immunology pathology genetic model immune response cancer signaling Lymphadenopathy knockin mouse SHP-2 MAPK pathway immunology genetic model pathology oncology immune response signal transduction biomedical research lymphadenopathy knockin mice SHP-2 MAPK pathway immunology genetics pathology knockout mice immune system oncology signal transduction Lymph node swelling SHP-2 deficiency knockout mouse model MAPK signaling Cancer predisposition Autism spectrum disorders
1163	The DdrB protein from Deinococcus radiodurans is an alternative SSB. The DdrB protein from Deinococcus radiodurans is an alternative SSB. The DdrB protein from Deinococcus radiodurans is an alternative SSB. The DdrB protein from Deinococcus radiodurans is an alternative SSB. The DdrB protein from Deinococcus radiodurans is an alternative SSB. DdrB Deinococcus radiodurans alternative SSB nucleotide binding protein radiation repair bacterial DNA protection stress survival Deinococcus radiodurans DdrB protein alternative SSB DNA repair radiation resistance protein function bacterial protein single-strand break nucleotide binding DDR250 DNA repair radiation resistance single-strand binding protein extremophile bacterial proteomics Deinococcus radiodurans genetics DDRB protein Deinococcus radiodurans SSB alternative single-strand binding protein DNA repair radiation resistance bacterial protein function SSB protein structure DNA damage tolerance protein biochemistry radiotolerance mechanism DDRB protein Deinococcus radiodurans alternative SSB DNA repair radiation resistance bacterial proteins single-strand binding protein DDRB protein Deinococcus radiodurans SSB alternative single-strand binding protein radiation resistance protein DNA repair mechanism DdrB protein Deinococcus radiodurans alternative SSB DNA repair radiation resistance protein function single-strand breaks DDRB protein Deinococcus radiodurans alternative SSB DNA repair radiation resistance protein function bacterial survival single-strand breaks nucleic acid binding DdrB protein function Deinococcus radiodurans DNA repair alternative single-strand binding protein SSB protein structure radiation resistance mechanism bacterial survival strategies Deinococcus radiodurans DNA repair DdrB function alternative single-strand binding protein radiation resistance mechanism protein structure DdrB
1041	Replacement of histone H2A with H2A.Z slows gene activation in yeasts by stabilizing +1 nucleosomes. Replacement of histone H2A with H2A.Z slows gene activation in yeasts by stabilizing +1 nucleosomes. Replacement of histone H2A with H2A.Z slows gene activation in yeasts by stabilizing +1 nucleosomes. Replacement of histone H2A with H2A.Z slows gene activation in yeasts by stabilizing +1 nucleosomes. Replacement of histone H2A with H2A.Z slows gene activation in yeasts by stabilizing +1 nucleosomes. histone modification chromatin structure gene expression regulation yeast genetics nucleosome stabilization molecular biology epigenetics histone modification yeast genetics gene regulation nucleosome stability H2A.Z replacement effects RNA polymerase transcription initiation histone modification gene regulation yeast biology nucleosome stability chromatin structure transcriptional control H2A.Z variant histone variants eukaryotic gene expression histone modification chromatin structure gene regulation nucleosome dynamics yeast genetics epigenetics transcriptional repression molecular biology evolutionary biology genomics histone modification gene regulation yeasts nucleosome stability H2A.H2A.Z substitution silent chromatin transcriptional repression histone modification chromatin structure gene expression regulation nucleosome stability yeast genetics molecular biology epigenetics transcriptional control genomic imprinting protein interactions histone modification gene expression yeast biology nucleosome stability chromatin dynamics H2A.Z protein transcription regulation histone modification chromatin structure gene regulation nucleosome stability yeast genetics epigenetics transcriptional repression molecular biology genomics epigenomic modification histone modification chromatin structure gene regulation yeast genetics nucleosome stability transcription initiation epigenetics molecular biology genetic engineering DNA packaging histone modifications chromatin structure transcriptional regulation yeast genetics epigenetics nucleosome dynamics gene expression evolutionary biology molecular mechanisms
171	Basophils counteract disease development in patients with systemic lupus erythematosus (SLE). Basophils counteract disease development in patients with systemic lupus erythematosus (SLE). Basophils counteract disease development in patients with systemic lupus erythematosus (SLE). Basophils counteract disease development in patients with systemic lupus erythematosus (SLE). Basophils counteract disease development in patients with systemic lupus erythematosus (SLE). basophils immune response systemic lupus erythematosus SLE inflammation autoimmunity therapeutic targets immunology cytokines mast cells antigen presentation basophils SLE counteract disease immune response inflammation autoimmunity clinical implications research therapy viral infections bacterial infections basophils systemic lupus erythematosus SLE immune response inflammation autoimmunity immunotherapy cytokines allergic reactions hematopoiesis immune cells basophilic role SLE treatment effects of basophils inflammatory response modulation autoimmune diseases immune system support basophil functions Disease progression inhibition Basophils systemic lupus erythematosus SLE immune response inflammation autoimmune diseases cytokines antinuclear antibodies hematopoiesis immunotherapy lupus SLE basophils immune response inflammation autoimmune diseases therapy treatment biomarkers clinical trials basophils systemic lupus erythematosus SLE immune response inflammation autoimmunity cytokines therapeutic targets clinical implications basophils immunity SLE treatment autoimmune response inflammation regulation immune cells function lupus therapy allergic reactions immunotherapy inflammatory diseases leukocyte role basophils immune response systemic lupus erythematosus SLE inflammatory markers therapeutic targets autoimmunity clinical implications immunology research basophils systemic lupus erythematosus immune response inflammation autoimmune diseases therapeutic targets clinical outcomes immunology biological markers
1282	Therapeutic use of the drug Dapsone to treat pyoderma gangrenous is based on anecdotal evidence. Therapeutic use of the drug Dapsone to treat pyoderma gangrenous is based on anecdotal evidence. Therapeutic use of the drug Dapsone to treat pyoderma gangrenous is based on anecdotal evidence. Therapeutic use of the drug Dapsone to treat pyoderma gangrenous is based on anecdotal evidence. Therapeutic use of the drug Dapsone to treat pyoderma gangrenous is based on anecdotal evidence. Dapsone pyoderma gangrenosum anecdotal evidence therapy drug efficacy clinical study dermatology Dapsone pyoderma gangrenosum anecdotal evidence therapeutic effectiveness treatment options clinical trials immunomodulatory effects dermatology medical research drug efficacy therapeutic evidence drug Dapsone pyoderma gangrenous anecdotal effectiveness research clinical trials potential benefits risk safety mechanism action alternative therapies comparison meta-analysis review clinical guidelines case studies patients outcomes side effects dosage frequency population age gender ethnicity genetics interactions monitoring management prevention treatment progress update publication accessibility availability cost economic impact quality control standard therapeutic evidence pyoderma gangrenosum dapsone clinical trials anecdotal pharmacology mechanism action skin infections Dapsone pyoderma gangrenosum anecdotal evidence therapeutic use antimicrobial immuneresponse therapeutic evidence pyoderma gangrenosum dapsone anecdotal pharmacology skin infection treatment clinical benefits Dapsone pyoderma gangrenosum evidence-based medicine anecdotal evidence drug therapy dermatology treatment options Dapsone benefits Dapsone therapy Dapsone effectiveness pyoderma gangrenosum treatment anecdotal evidence support therapeutic drug Dapsone Dapsone for skin conditions Dapsone dosage for pyoderma gangrenosum Dapsone pyoderma gangrenosum anecdotal evidence therapeutic application skin infections immunosuppressive drugs clinical trials dapsone efficacy pyoderma gangrenosum research anecdotal evidence validation drug effectiveness studies
1281	The ureABIEFGH gene cluster is induced by nickel (II) ion. The ureABIEFGH gene cluster is induced by nickel (II) ion. The ureABIEFGH gene cluster is induced by nickel (II) ion. The ureABIEFGH gene cluster is induced by nickel (II) ion. The ureABIEFGH gene cluster is induced by nickel (II) ion. ureAB gene cluster nickel induction heavy metal resistance gene expression bacterial genes nickel tolerance genetic regulation environmental response genes ureAB gene cluster nickel stress response metal-induced gene expression nickel tolerance gene regulation heavy metal resistance ureAB gene cluster nickel induction metal-responsive genes environmental stress response genetic regulation gene expression heavy metals microbial metabolism transcription factors ureAB gene cluster nickel response gene induction microbial metabolism heavy metal resistance bacterial gene expression metallomics transcription factors nickel toxicity genetic regulation ureAB gene cluster nickel (II) ion induction microbial response gene expression metalloremediation biofilm formation ureAB gene cluster nickel induction metal-responsive genes gene regulation environmental stress response bacterial resistance transcription factors metal ions genetic engineering microbial metabolism ureAB gene cluster nickel response metal induction gene expression environmental stress bacterial metabolism genetic regulation bioinformatics analysis transcription factors resistance mechanisms ureAB gene cluster nickel induction gene regulation metalloresponsive genes heavy metal tolerance bioinformatics analysis gene expression profiling ureAB gene cluster nickel induction microbial response nickel ions gene regulation metal tolerance transcriptomics microbial genetics GIS database bioremediation ureAB gene cluster nickel stress response heavy metal tolerance transcription factors gene expression microbial resistance environmental adaptation
294	Crossover hot spots are not found within gene promoters in Saccharomyces cerevisiae. Crossover hot spots are not found within gene promoters in Saccharomyces cerevisiae. Crossover hot spots are not found within gene promoters in Saccharomyces cerevisiae. Crossover hot spots are not found within gene promoters in Saccharomyces cerevisiae. Crossover hot spots are not found within gene promoters in Saccharomyces cerevisiae. Crossover hotspots gene promoters Saccharomyces cerevisiae yeast genetic recombination chromosomal crossover molecular biology genetics epigenetics DNA genome analysis Crossover hotspots Saccharomyces cerevisiae gene promoters chromosome segregation homologous recombination biogenetics molecular biology genetic variation genome analysis cell division crossover hotspots gene promoters Saccharomyces cerevisiae yeast genetic recombination DNA chromatin epigenetics transcription genome molecular biology genetics microbiology bioinformatics genomics genetics research yeast biology Crossover analysis Saccharomyces cerevisiae genome genetic recombination gene expression yeast genetics chromosomal crossover promoter region genetic mapping DNA sequence analysis epigenetics yeast strains molecular biology techniques genetic variability crossover frequency genetic loci yeast cells genetic markers genetic interactions bioinformatics tools genetic regulation Crossover hotspots gene promoters Saccharomyces cerevisiae genetics molecular biology chromosome yeast crossover analysis Saccharomyces cerevisiae gene promoter chromosomal crossover genetic recombination yeast genome bioinformatics tools genomic regions molecular biology techniques genetic markers DNA sequence analysis Crossover hotspots gene promoters Saccharomyces cerevisiae genetic recombination meiosis DNA chromatin yeast molecular biology genetics epigenetics genome analysis bioinformatics genetic variation crossover analysis Saccharomyces cerevisiae genome gene promoter regions genetic recombination热点 homologous recombination sites yeast genetics研究 crossover hotspots gene promoters Saccharomyces cerevisiae yeast genetic variation molecular biology genome biotechnology chromosome genetics microbiology epigenetics transcription regulation DNA sequence analysis bioinformatics genomics chromatin genetic markers Crossover analysis Saccharomyces cerevisiae gene regulation chromosomal crossover homologous recombination promoter region biological crossover GIS mapping genetic loci
1280	The ureABIEFGH gene cluster encodes urease maturation proteins : UreD/UreH, UreE, UreF, and UreG. The ureABIEFGH gene cluster encodes urease maturation proteins : UreD/UreH, UreE, UreF, and UreG. The ureABIEFGH gene cluster encodes urease maturation proteins : UreD/UreH, UreE, UreF, and UreG. The ureABIEFGH gene cluster encodes urease maturation proteins : UreD/UreH, UreE, UreF, and UreG. The ureABIEFGH gene cluster encodes urease maturation proteins : UreD/UreH, UreE, UreF, and UreG. urease maturation proteins ureD ureH ureE ureF ureG gene cluster bacteria enzymatic function structure regulation urease maturation genes ureD ureH ureE ureF ureG bacterial protein function enzyme biosynthesis nitrogen metabolism microbiology urease maturation proteins UreD UreH UreE UreF UreG gene cluster bacteria function expression regulation microbiology enzyme biogenesis ureagenesis urease mature gene cluster proteins UreD UreH UreE UreF UreG ureABIEFGH biotechnology microbiology enzymes ammonification nitrogen metabolism genetics expression transcription translation functionality enzymology ureAB gene cluster urease maturation UreD UreH UreE UreF UreG protein encoding gene function bacterial metabolism nitrogen fixation urea hydrolysis gene cluster recommendation search performance relevant expansion phrases UreD/UreH UreE UreF UreG urease maturation urease maturation proteins UreD UreH UreE UreF UreG gene cluster bacteria enzyme function biotic proteinase activity biosynthesis ureAB gene cluster urease maturation UreD protein UreH protein UreE protein UreF protein UreG protein urease proteins gene encoding microbial urease ureAB gene cluster urease maturation UreD UreH UreE UreF UreG urease protein gene function bacterial metabolism nitrogen fixation enzyme regulation urease maturation genes ureD ureH ureE ureF ureG bacterial protein function ureagenesis
295	Crosstalk between dendritic cells (DCs) and innate lymphoid cells (ILCs) is important in the regulation of intestinal homeostasis. Crosstalk between dendritic cells (DCs) and innate lymphoid cells (ILCs) is important in the regulation of intestinal homeostasis. Crosstalk between dendritic cells (DCs) and innate lymphoid cells (ILCs) is important in the regulation of intestinal homeostasis. Crosstalk between dendritic cells (DCs) and innate lymphoid cells (ILCs) is important in the regulation of intestinal homeostasis. Crosstalk between dendritic cells (DCs) and innate lymphoid cells (ILCs) is important in the regulation of intestinal homeostasis. crosstalk dendritic cells innate lymphoid cells intestinal homeostasis immune response inflammation immunology microbiome cytokines immune regulation crosstalk dendritic cells innate lymphoid cells intestinal homeostasis immune response inflammation microbiome signaling pathways immunology cytokines immune regulation crosstalk dendritic cells DCs innate lymphoid cells ILCs intestinal homeostasis immune response inflammation microbiome cytokines immune regulation gut immunity crosstalk DCs ILCs regulation intestinal homeostasis mechanisms DCs ILCs intestinal immunity dendritic cells function innate lymphoid cells role intestinal microenvironment inflammation immune response intestinal mucosal immunity immune cell interaction Crosstalk dendritic cells innate lymphoid cells intestinal homeostasis immune response signaling pathways inflammatory response microbiome interaction antigen presentation cytokines immune tolerance Crosstalk dendritic cells innate lymphoid cells intestinal homeostasis immune response inflammatory pathways microbial interaction antigen presentation cytokine production gut immunity immune tolerance immunological synapse dendritic cells DCs innate lymphoid cells ILCs intestinal homeostasis immune response cytokines signaling pathways microbiome inflammatory response immunology gut immunity Crosstalk dendritic cells innate lymphoid cells intestinal homeostasis immune response cytokines signaling pathways microbiome immune regulation inflammation immunology Crosstalk dendritic cells innate lymphoid cells intestinal homeostasis immune response inflammatory bowel disease immunology microbiome cytokines signaling pathways crosstalk dendritic cells innate lymphoid cells intestinal homeostasis immune response inflammation signaling pathways microbiomeinteraction immune regulation cytokines antigen presentation immune tolerance
298	Cytochrome c is released from the mitochondrial intermembrane space to cytosol during apoptosis. Cytochrome c is released from the mitochondrial intermembrane space to cytosol during apoptosis. Cytochrome c is released from the mitochondrial intermembrane space to cytosol during apoptosis. Cytochrome c is released from the mitochondrial intermembrane space to cytosol during apoptosis. Cytochrome c is released from the mitochondrial intermembrane space to cytosol during apoptosis. cytochrome apoptosis mitochondria intermembrane cytosol release signaling pathway death mechanism cytochrome c release mechanism mitochondrial apoptosis signaling intermembrane space cytosis apoptosis cytochrome c localization cytosolic cytochrome c detection cytochrome c apoptosis mitochondria intermembrane space cytosol cell death release mechanism signaling cytochrome c release mechanism mitochondrial intermembrane space apoptosis process cellular death mechanisms cytosol entry pathways Cytochrome mitochondria apoptosis intermembrane cytosol release oxidative stress signaling cytochrome c release mitochondrial apoptosis intermembrane space cytosol transfer caspase activation apoptotic signaling mitochondrial membrane apoptosis process caspase activation cell death mechanisms intermembrane space cytosolic release oxidative stress mitochondrial permeability transition Bcl-2 family proteins Cytochrome c release apoptosis process mitochondrial intermembrane space cytosol transfer programmed cell death caspase activation apoptosis signaling cytochrome c release mitochondrial intermembrane space apoptosis signaling cellular death markers cytochrome c release mitochondrial apoptosis caspase activation mitochondria outer membrane permeabilization apoptosis signaling mitochondrial membrane potential loss pro-apoptotic proteins
179	Birth-weight is positively associated with breast cancer. Birth-weight is positively associated with breast cancer. Birth-weight is positively associated with breast cancer. Birth-weight is positively associated with breast cancer. Birth-weight is positively associated with breast cancer. birth weight fetal growth breast cancer risk obesity pregnancy outcomes oncology epidemiology maternal health neonatal weight long-term health birth weight breast cancer epidemiology birth weight breast cancer risk low birth weight breast cancer high birth weight breast cancer prenatal nutrition breast cancer birth size breast cancer fetal growth breast cancer birth weight infant birth weight maternal health breastfeeding prenatal nutrition childhood obesity breast cancer risk oncology epidemiology demographics birth weight breast cancer risk low birth weight and breast cancer socioeconomic status and birth weight birth weight and breast cancer incidence maternal factors affecting birth weight birth weight breast cancer epidemiology risk factors infant health adult outcomes statistical analysis cohort studies longitudinal research public health birth weight breast cancer correlation low birth weight breast cancer risk high birth weight breast cancer infant birth weight and breast cancer elevated birth weight breast cancer association birth weight breast cancer risk infant birth weight adult cancer epidemiological study oncology research maternal health fetal development birth weight breast cancer risk factor epidemiology oncology infant birth weight adult health outcomes birth weight breast cancer risk prenatal nutrition maternal health infant health outcomes epidemiological studies genetic factors environmental influences lifestyle choices early life development oncology research birth weight prenatal nutrition maternal health infant mortality long-term outcomes epidemiological studies risk factors tumor development genetic predisposition hormonal influences
971	Primary cervical cancer screening with HPV detection has higher longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2. Primary cervical cancer screening with HPV detection has higher longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2. Primary cervical cancer screening with HPV detection has higher longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2. Primary cervical cancer screening with HPV detection has higher longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2. Primary cervical cancer screening with HPV detection has higher longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2. cervical_cancer_screening HPV_detection cervical_intraepithelial_neoplasia grade_2 longitudinal_sensitivity conventional_cytology cervical_cancer_screening HPV_detection longitudinal_sensitivity cytology cervical_intraepithelial_neoplasia CIN_2 cancer_prevention gynecological_screening HPV_test cervical_dysplasia oncology gynecology public_health medical_research healthcare_practice diagnostic_tests cervical_cancer_screening HPV_detection longitudinal_sensitivity conventional_cytology cervical_intraepithelial_neoplasia_grade_2 CIN2 detection_effectiveness pap_smear genital_warts vaccination_history hpv_genotypes screening_intervals lesion_detection early_detection risk_factors malignancy_assessment biopsy cellular_abnormalities screening_programs public_health prevention_strategies cervical_cancer_screening HPV_detection sensitivity_analysis cytology_vs_HPV cervical_intraepithelial_neoplasia grade_2 DNA_methylation microbiome_analysis persistent_HPV_infection early_detection_strategies clinical_trials new_screening_techniques genomic_markers immunohistochemistry biomarker_discovery screening_interventions public_health_implications comparative_study_design cervical_cancer_screening HPV_detection longitudinal_sensitivity conventional_cytology cervical_intraepithelial_neoplasia_grade_2 medical_screening test_efficiency population_health molecular_biology disease_prevention public_health research_studies healthcare_quality clinical_trials cervical_cancer_screening HPV_detection sensitivity conventional_cytology CIN_2 disease_prevention medical_research clinical_practice gynecological_care public_health health_policy vaccination_programs disease_mechanisms diagnostic_tests therapeutic_interventions biomarkers epidemiology healthcare_quality patient_outcomes research_methods publicity_campaigns screening_programs health_screening medical_treatment health_information healthcare_services health_systems healthcare_delivery healthcare_economics healthcare_policy cervical_cancer_screening HPV_detection sensitivity conventional_cytology CIN2 disease_prevention molecular_biomarkers early_detection neoplasia risk_factors biopsy clinical_guidelines public_health_strategies cervical_cancer_screening HPV_detection longitudinal_sensitivity conventional_cytology CIN2 detection_efficacy pap_smear hpv_test neoplasia_grade_2 primary_screening cervical_health malignancy_screening test_accuracy clinical_benefit cervical_cancer_screening HPV_detection longitudinal_sensitivity conventional_cytology cervical_intraepithelial_neoplasia_grade_2 screening_techniques molecular_testing pap_smear HIV_association lesion_detection risk_factors clinical_outcomes early_detection persistent_infection viral_load immune_response public_health_impact diagnostic_accuracy biomarker_discovery genetic_tests health_policy evidence_based_medicine quality_improvement patient_outcomes healthcare_economics global_health pilot_study random cervical cancer HPV testing cytology neoplasia early detection cervical health oncology gynecology cancer screening HPV infection cervical precancer medical research clinical trials diagnostic accuracy public health women's health pathology virology epidemiology oncogenes genotyping biomarkers
1279	The treatment of cancer patients with co-IR blockade precipitates adverse autoimmune events. The treatment of cancer patients with co-IR blockade precipitates adverse autoimmune events. The treatment of cancer patients with co-IR blockade precipitates adverse autoimmune events. The treatment of cancer patients with co-IR blockade precipitates adverse autoimmune events. The treatment of cancer patients with co-IR blockade precipitates adverse autoimmune events. cancer therapy immune checkpoint inhibitors autoimmune reactions co-inhibition treatment outcomes cancer therapy immune checkpoint inhibitors autoimmune reactions immunotherapy side effects clinical trials oncology biomarkers precision medicine tumor microenvironment cancer therapy immune checkpoint inhibitors autoimmune reactions co-inhibitory receptors treatment strategies adverse effects immunotherapy clinical outcomes biomarkers therapeutic targets cancer immunotherapy immune-related adverse events co-inhibitory receptors checkpoint inhibitors autoimmune disorders tumor microenvironment clinical trial outcomes inflammatory response tumor immunology therapeutic strategies oncology treatments cancer treatment co-IR blockade adverse events autoimmune response immunotherapy clinical trials immune checkpoint inhibitors tumor immunity inflammation biomarkers cancer treatment co-IR blockade autoimmune events immunotherapy side effects clinical trials biomarkers inflammation oncology immunomodulation cancer treatment co-IR blockade autoimmune events immunotherapy side effects clinical trials immune checkpoint inhibitors oncology inflammatory response therapeutic strategies cancer treatment co-IR blockade autoimmune events immunotherapy side effects clinical trials immune response oncology inflammation immunosuppression biomarkers cancer therapy immune checkpoint inhibitors autoimmune reactions treatment strategies clinical outcomes immunotherapy side effects co-inhibitory molecules tumor immunology precision medicine biomarkers clinical trials oncology research cancer immunotherapy immune-related adverse events co-inhibitory receptors checkpoint inhibitors autoimmune reactions tumor microenvironment inflammation clinical trials biomarkers therapeutic strategies
1278	The treatment of cancer patients with co-IR blockade does not cause any adverse autoimmune events. The treatment of cancer patients with co-IR blockade does not cause any adverse autoimmune events. The treatment of cancer patients with co-IR blockade does not cause any adverse autoimmune events. The treatment of cancer patients with co-IR blockade does not cause any adverse autoimmune events. The treatment of cancer patients with co-IR blockade does not cause any adverse autoimmune events. cancer therapy immune checkpoint inhibitors adverse effects autoimmune disorders co-inhibition blockade clinical trials immunotherapy side effects analysis cancer treatment immune checkpoint blockade adverse events autoimmune response clinical trials immunotherapy oncology tumor immunity inflammatory response pharmacology cancer therapy immune checkpoint inhibitors adverse effects autoimmune diseases treatment outcomes clinical trials immunotherapy side effects analysis treatment options cancer therapy co-IR blockade immune response cancer immunotherapy adverse events autoimmune reactions clinical trials safety profile immune checkpoint inhibitors cancer treatment co-IR blockade autoimmune events immunotherapy side effects clinical trials immune response oncology molecular biology cancer treatment co-IR blockade autoimmune events clinical trials immunotherapy side effects oncology research immune response patient outcomes pharmacology cancer therapy immune checkpoint inhibitors adverse effects autoimmune reactions clinical outcomes immunotherapy safety co-inhibitory molecules cancer treatment co-IR blockade autoimmune events beneficial expansion keywords treatment efficacy cancer treatment co-IR blockade autoimmune events immunotherapy side effects clinical trials immune response oncology biotechnology pharmaceuticals cancer immunotherapy immune checkpoint inhibitors co-inhibitory molecules autoimmune response clinical trials side effects oncology treatments
852	Non-invasive ventilation use should be decreased if there is inadequate response to conventional treatment. Non-invasive ventilation use should be decreased if there is inadequate response to conventional treatment. Non-invasive ventilation use should be decreased if there is inadequate response to conventional treatment. Non-invasive ventilation use should be decreased if there is inadequate response to conventional treatment. Non-invasive ventilation use should be decreased if there is inadequate response to conventional treatment. non-invasive ventilation response conventional treatment efficacy alternatives benefits risks non-invasive ventilation inadequacy conventional treatment limitations ventilation response monitoring respiratory therapy adjustment criteria clinical guidelines non-invasive ventilation non-invasive ventilation inadequate response conventional treatment respiratory therapy guidelines efficacy pulmonary disorders ICU home care non-invasive ventilation alternatives inadequate response treatments conventional therapy failure wean non-invasive ventilation increase invasive ventilation manage respiratory distress alternative therapies respiratory ventilation strategy changes non-invasive ventilation inadequate response conventional treatment respiratory therapy clinical guidelines non-invasive ventilation alternatives conventional treatment outcomes ventilation response assessment decrease ventilation criteria non-invasive ventilation inadequate response conventional treatment respiratory therapy clinical guidelines mechanical ventilation alternatives patient monitoring respiratory support methods therapeutic efficacy pulmonary care non-invasive ventilation inadequate response conventional treatment efficacy keywords expansion medical therapy respiratory support ventilator weaning patient monitoring clinical guidelines respiratory failure non-invasive ventilation inadequate response conventional treatment optimize search keywords expansion terms non-invasive ventilation alternatives conventional treatment failure respiratory support methods inadequate patient response mechanical ventilation transition clinical guidelines update
975	Primary pro-inflammatory cytokines induce secondary pro- and anti-inflammatory mediators. Primary pro-inflammatory cytokines induce secondary pro- and anti-inflammatory mediators. Primary pro-inflammatory cytokines induce secondary pro- and anti-inflammatory mediators. Primary pro-inflammatory cytokines induce secondary pro- and anti-inflammatory mediators. Primary pro-inflammatory cytokines induce secondary pro- and anti-inflammatory mediators. primary cytokines pro-inflammatory response secondary mediators anti-inflammatory factors cytokine induction immune response modulation inflammation cascade primary cytokines pro-inflammatory response secondary mediators immune response inflammation markers cytokine network immune mediators inflammatory cascade biomarkers cytokine signaling primary cytokines pro-inflammatory response secondary mediators anti-inflammatory cytokines immune response inflammatory cascade cytokine network immunology innate immunity adaptive immunity primary cytokines pro-inflammatory response secondary mediators anti-inflammatory cytokines immune response mechanisms cytokine network inflammation cascade immunology terms biological signaling primary cytokines pro-inflammatory secondary mediators anti-inflammatory immune response signaling pathways gene expression inflammatory cascade primary cytokines inflammatory response secondary mediators immune system pro-inflammatory anti-inflammatory cytokine network immune response regulation inflammation mechanisms primary cytokines pro-inflammatory response secondary mediators anti-inflammatory cytokines immune response inflammation cascade cytokine network immune regulation inflammatory signaling primary pro-inflammatory cytokines secondary mediators anti-inflammatory cytokines immune response inflammation pathway molecular signaling primary pro-inflammatory cytokines secondary mediators inflammatory response cytokine induction immune response regulation primary cytokines secondary mediators inflammation response immune response TNF-alpha IL-1 IL-6 anti-inflammatory cytokines MMPs COX-2
613	Increased microtubule acetylation repairs LRRK2 Roc-COR domain mutation induced locomotor deficits. Increased microtubule acetylation repairs LRRK2 Roc-COR domain mutation induced locomotor deficits. Increased microtubule acetylation repairs LRRK2 Roc-COR domain mutation induced locomotor deficits. Increased microtubule acetylation repairs LRRK2 Roc-COR domain mutation induced locomotor deficits. Increased microtubule acetylation repairs LRRK2 Roc-COR domain mutation induced locomotor deficits. microtubule stabilization LRRK2 protein function Roc-COR domain structure neurodegenerative diseases cell signaling pathways locomotor disorders acetylation process genetic mutations therapeutic targets neuronal health molecular biology techniques protein interaction networks microtubule acetylation LRRK2 mutation Roc-COR domain locomotor deficits neurodegeneration Parkinson's disease protein function cellular repair molecular biology genetic mutation therapeutic targets microtubule stabilization LRRK2 function Roc-COR domain neurodegeneration protein acetylation cellular repair Parkinson's disease model locomotor function genetic mutation impact Increased microtubule acetylation mechanisms LRRK2 Roc-COR domain function neurodegenerative disease treatment microtubule dynamics locomotor dysfunction acetylation therapy parkinsonism LRRK2 mutations effect of LRRK2 on microtubules microtubule stabilization techniques cellular repair strategies LRRK2 protein structure microtubule stabilization LRRK2 protein Roc-COR domain neuronal function Parkinson's disease model neurodegeneration acetylation enzymes motor dysfunction cellular repair mechanisms microtubule stabilization LRRK2 protein Roc-COR domain function locomotor disorders acetylation therapy neurodegenerative diseases cellular repair mechanisms protein mutations neuroprotection strategies molecular biology techniques microtubule stability acetylation process LRRK2 protein Roc-COR domain locomotor function neurodegenerative diseases cellular repair mechanisms genetic mutations microtubule stabilization LRRK2 dysfunction Roc-COR domain neurodegeneration synaptic function Parkinson's disease cellular repair mechanisms acetylation enzymes gene therapy neuroscience research protein aggregation microtubule stabilization LRRK2 dysfunction Roc-COR domain neurodegenerative diseases locomotor disorders acetylation therapy Parkinson's disease cellular repair mechanisms genetic mutations protein function neuroscience research microtubule stabilization LRRK2 function Roc-COR domain neurodegenerative diseases protein acetylation cellular repair mechanisms Parkinson's disease gene mutation impact motor neuron health therapeutic interventions
70	Activation of PPM1D suppresses p53 function. Activation of PPM1D suppresses p53 function. Activation of PPM1D suppresses p53 function. Activation of PPM1D suppresses p53 function. Activation of PPM1D suppresses p53 function. Activation PPM1D p53 function regulation mechanisms cancer signaling pathway PPM1D p53 function cellular response molecular biology cancer research signal transduction kinase activity PPM1D enzyme protein phosphatase p53 regulation tumor suppression cellular stress response cancer biology gene expression molecular mechanisms oncology research cellular signaling PPM1D enzyme p53 protein cellular signaling tumor suppression genetic regulation cancer biology phosphatase activity oncology research molecular mechanisms biological pathways PPM1D p53 cell cycle regulation protein phosphatase apoptosis tumor suppression molecular biology cancer research somatic mutations genetic regulation PPM1D inhibition p53 activation cellular stress response anti-apoptotic mechanism molecular biology techniques PPM1D enzyme p53 protein cellular stress response tumor suppression phosphatase activity genetic mutations cancer development PPM1D enzyme p53 protein cellular stress response tumor suppression phosphatase activity genetic mutations cancer development apoptosis regulation PPM1D enzyme p53 protein tumor suppression phosphorylation cancer biology genetic mutation cellular signaling oncology research PPM1D inhibitor p53 pathway cell cycle regulation cancer therapy mutations impact
72	Activator-inhibitor pairs are provided dorsally by Admpchordin. Activator-inhibitor pairs are provided dorsally by Admpchordin. Activator-inhibitor pairs are provided dorsally by Admpchordin. Activator-inhibitor pairs are provided dorsally by Admpchordin. Activator-inhibitor pairs are provided dorsally by Admpchordin. search effectiveness expansion terms activator-inhibitor pairs dorsal Admp chordin embryonic development molecular biology signaling pathways activator-inhibitor developmental biology Admp chordin dorsalization signaling pathway morphogenesis gene expression embryonic development molecular biology Activator-inhibitor model developmental biology Dorsal gradient Admp Chordin morphogenetics signaling pathways GDF11 bone morphogenetic proteins molecular biology embryonic development activator-inhibitor model Admp gene chordin dorsal-ventral patterning morphogen gradient signaling pathways embryonic development molecular biology gene interaction biological processes search efficiency keyword expansion activator-inhibitor pairs Admp chordin dorsal patterning molecular biology developmental biology query expansion relevant phrases search performance activator-inhibitor pairs Admp chordin dorsal region biological signaling gene expression developmental biology activator-inhibitor model Admp chordin dorsal patterning developmental biology signaling pathways Activator-inhibitor模型 Admp Chordin 背部发育 增强搜索关键词 生物发育机制 演化生物学关键词 activator-inhibitor模型 Admp chordin 背部发育 信号分子 转录调控 胚胎生物学 基因互作 Activator-inhibitor model Admp Chordin dorsalization morphogen gradient developmental biology gene expression signaling molecules
859	Normal expression of RUNX1 has tumor-promoting effects. Normal expression of RUNX1 has tumor-promoting effects. Normal expression of RUNX1 has tumor-promoting effects. Normal expression of RUNX1 has tumor-promoting effects. Normal expression of RUNX1 has tumor-promoting effects. RUNX1 protein function tumor suppression RUNX1 mutations cancer biology leukemia risk factors RUNX1 role in oncogenesis RUNX1 function tumor suppressor RUNX1 mutations cancer biology RUNX1 role in cancer RUNX1 transcription factor tumor progression RUNX1 function tumor-suppressing factors genetic regulation cancer biology molecular mechanisms RUNX1 mutations tumor microenvironment expression profiling RUNX1 protein structure RUNX1 gene expression tumor suppressor role RUNX1 mutations cancer risk assessment RUNX1 protein function RUNX1 function tumor suppressor cancer types cell differentiation molecular biology genetic regulation RUNX1 oncogenic roles RUNX1 in leukemia RUNX1 gene function RUNX1 cancer association RUNX1 protein expression RUNX1 protein function tumor_suppression cancer_genetics molecular_biology genetic_variants leukemia pathway_analysis RUNX1 oncogenic role RUNX1 cancer promotion RUNX1 tumor biology RUNX1 genetic impact RUNX1 carcinogenesis RUNX1 function RUNX1 mutation RUNX1 role in cancer RUNX1 transcription factor RUNX1 and leukemia RUNX1 protein expression RUNX1 tumor suppressor RUNX1 gene regulation RUNX1 clinical significance RUNX1 molecular biology RUNX1 tumor promotion RUNX1 genetic variants RUNX1 protein function RUNX1 cancer types RUNX1 signaling pathway RUNX1 epigenetics RUNX1 transcription regulation
619	Increased vessel density along with a reduction in fibrosis decreases the efficacy of chemotherapy treatments. Increased vessel density along with a reduction in fibrosis decreases the efficacy of chemotherapy treatments. Increased vessel density along with a reduction in fibrosis decreases the efficacy of chemotherapy treatments. Increased vessel density along with a reduction in fibrosis decreases the efficacy of chemotherapy treatments. Increased vessel density along with a reduction in fibrosis decreases the efficacy of chemotherapy treatments. vessel密度 纤维化减少 化疗效果 血管生成 肿瘤治疗效率 vessel density fibrosis chemotherapy efficacy tumor angiogenesis drug delivery cancer treatment biomarkers oncology research therapeutic resistance vessel_density fibrosis chemotherapy effectiveness tumor_growth microenvironment cancer_treatment angiogenesis inhibition tumor_progression vessel density impact fibrosis chemotherapy interaction tumor angiogenesis effect chemotherapy efficacy reduction fibrotic tissue impact vessel_count fibrosis chemotherapy effectiveness tumorangiogenesis microenvironment vascularization vessel density analysis fibrosis impact chemotherapy effectiveness angiogenesis inhibition tumor microenvironment fibrotic tissue reduction vessel normalization chemo resistance biomarker identification angiogenic factors vessel density fibrosis chemotherapy tumor angiogenesis cancer treatment drug efficacy tumor microenvironment vascularization proangiogenic factors fibrotic response vessel_density fibrosis chemotherapy efficacy tumor_growth angiogenesis microenvironment cancer_treatment biomarker therapeutic_response vessel_density fibrosis chemotherapy efficacy biomarkers molecular_markicators angiogenesis stroma tumor_microenvironment prognostic_factors vessel_reduction fibrosis_treatment chemotherapy_effectiveness vessel_formation inhibitors angiogenesis阻断剂 tumor_growth抑制剂 fibrotic_tissue阻断
75	Active H. pylori urease has a polymeric structure that compromises two subunits, UreA and UreB. Active H. pylori urease has a polymeric structure that compromises two subunits, UreA and UreB. Active H. pylori urease has a polymeric structure that compromises two subunits, UreA and UreB. Active H. pylori urease has a polymeric structure that compromises two subunits, UreA and UreB. Active H. pylori urease has a polymeric structure that compromises two subunits, UreA and UreB. H.pylori urease polymeric subunits UreA UreB bacterial enzyme composition H.pylori urease subunits UreA UreB polymeric structure bacterial enzyme microbiology active Helicobacter pylori urease subunits polymeric enzyme structure UreA protein UreB protein bacterial urease composition H.pylori urease composition urease subunit function polymeric enzyme structure bacterial urease mechanism H.pylori infection enzymes urease catalytic activity bacterial metabolism urease H.pylori urease mechanism H. pylori urease polymeric subunits UreA UreB protein structure bacterial enzyme microbiology gastric infection active H.pylori urease subunits polymeric structure urease UreA protein function UreB protein role H.pylori infection markers urease activity mechanism bacterial urease composition H.pylori urease subunits UreA UreB polymeric protein enzyme bacterial microbiology Active H.pylori urease polymeric structure UreA subunit UreB subunit bacterial urease microbial enzymes protein subunits molecular biology stomach bacteria gastric infection microbiology research active H.pylori urease polymeric structure UreA subunit UreB subunit protein composition bacterial enzyme gastric infection microbiology biomedical research active H.pylori urease subunits polymeric structure UreA UreB functionality enzymatic activity protein structure bacterial infections stomach ulcers molecular composition urease mechanism
1175	The PPR MDA5 has two N-terminal CARD domains. The PPR MDA5 has two N-terminal CARD domains. The PPR MDA5 has two N-terminal CARD domains. The PPR MDA5 has two N-terminal CARD domains. The PPR MDA5 has two N-terminal CARD domains. PPR protein MDA5 protein CARD domain nucleotide-binding oligomerization domain interferon regulatory factor innate immunity PPR protein MDA5 protein N-terminal CARD domain RNA binding innate immunity molecular structure tandem repeats genetic disorders PPR protein MDA5 protein CARD domain RNA binding protein interferon regulatory factor 3 innate immunity antiviral response PPR protein MDA5 protein CARD domain RNA binding innate immunity viral recognition molecular structure tandem repeats biological function signaling pathway PPR protein MDA5 N-terminal CARD domains RNA binding immune response signaling molecule molecular structure genetic regulation PPR protein MDA5 protein CARD domains nucleotide-binding oligomerization domain RNA recognition plant defense response signaling pathway molecular structure domain function PAMP-triggered immunity PPR protein MDA5 protein N-terminal CARD domain RNA binding protein innate immunity viral recognition molecular structure tandem repeats PPR protein MDA5 N-terminal CARD domains molecular recognition RNA binding innate immunity viral detection structural analysis plant defense PPR protein MDA5 protein CARD domain nucleotide-binding oligomerization domain RNA recognition motif immune system viral sensing innate immunity PPR protein MDA5 protein CARD domain RNA binding innate immunity viral recognition molecular structure protein function genetic regulation
180	Blocking the interaction between TDP-43 and respiratory complex I proteins ND3 and ND6 leads to increased TDP-43-induced neuronal loss. Blocking the interaction between TDP-43 and respiratory complex I proteins ND3 and ND6 leads to increased TDP-43-induced neuronal loss. Blocking the interaction between TDP-43 and respiratory complex I proteins ND3 and ND6 leads to increased TDP-43-induced neuronal loss. Blocking the interaction between TDP-43 and respiratory complex I proteins ND3 and ND6 leads to increased TDP-43-induced neuronal loss. Blocking the interaction between TDP-43 and respiratory complex I proteins ND3 and ND6 leads to increased TDP-43-induced neuronal loss. TDP-43 respiratory complex I ND3 ND6 neuronal loss interaction protein mechanism pathology mitochondria neurodegeneration ALS motor neurons oxidative stress signaling TDP-43 respiratory complex ND3 ND6 neurodegeneration protein-protein interaction neuronal loss pathology mechanism mitochondria oxidative phosphorylation ALS motor neuron disease model therapeutic target TDP-43 respiratory complex I ND3 ND6 neurodegeneration protein-protein interaction neuroscience mitochondria pathology ALS motor neurons oxidative stress mechanism therapeutic targets biomarkers TDP-43 interaction respiratory complex I ND3 protein ND6 protein neurodegenerative disease neuronal cell death molecular biology gene regulation proteomics therapeutic target oxidative phosphorylation mitochondrial dysfunction ALS frontotemporal dementia TDP-43 respiratory complex proteins ND3 ND6 neuronal loss interaction mechanism mitochondria oxidative stress neurodegeneration pathology TDP-43 respiratory complex I ND3 ND6 neuronal loss protein interaction therapeutic target neurodegeneration oxidative phosphorylation molecular biology genetic mutation mitochondrial dysfunction ALS frontotemporal dementia TDP-43 respiratory complex ND3 ND6 neuronal loss interaction blocking protein neurodegeneration mitochondria pathology RNA binding dysfunction TDP-43 respiratory complex I ND3 ND6 neuronal loss protein interaction neurodegeneration mitochondrial dysfunction ALS RNA binding protein TDP-43 respiratory complex ND3 ND6 neuronal loss interaction enhancement therapy mechanism pathology neurodegeneration mitochondrial function genetics biomarker treatment TDP-43 respiratory complex I ND3 ND6 neuronal loss protein interaction neurodegeneration oxidative stress mitochondrial dysfunction ALS frontotemporal dementia
183	Bone marrow cells contribute to adult macrophage compartments. Bone marrow cells contribute to adult macrophage compartments. Bone marrow cells contribute to adult macrophage compartments. Bone marrow cells contribute to adult macrophage compartments. Bone marrow cells contribute to adult macrophage compartments. bone marrow progenitor hematopoietic stem cells macrophage differentiation mononuclear phagocyte system immune response inflammation stem cell biology tissue repair aging cytokines chemokines bone marrow stem cells macrophage development adult hematopoiesis microenvironment immune response bone marrow progenitors macrophage development stem cells differentiation microenvironment immune response regeneration hematopoiesis bone marrow derived macrophages hematopoietic stem cells myeloid lineage monocyte differentiation innate immune system macrophage biology stem cell niche progenitor cells inflammatory response tissue repair bone marrow stem cells hematopoiesis macrophage differentiation mononuclear phagocyte system immune response inflammation angiogenesis cytokines chemokines hematopoietic niche microenvironment bone marrow-derived cells macrophage development adult hematopoiesis immune response modulation MMP production stem cell niches bone marrow progenitor cells microenvironment hematopoiesis monocytic lineage differentiation factors stem cells immune response phagocytosis marrow niche bone marrow stem cells macrophage development adult hematopoiesis microenvironment single cell analysis immune response regulation bone marrow-derived cells microenvironment stem cells hematopoiesis macrophage differentiation mouse models human studies aging renewal regeneration bone marrow progenitor cells microenvironment hematopoiesis stem cells Differentiation monocytes immunology molecular biology regulation transplantation
1292	There is no association between HNF4A mutations and diabetes risks. There is no association between HNF4A mutations and diabetes risks. There is no association between HNF4A mutations and diabetes risks. There is no association between HNF4A mutations and diabetes risks. There is no association between HNF4A mutations and diabetes risks. HNF4A diabetes genetic mutation risk factor association study research HNF4A mutations diabetes risk genetic association study research epidemiology liver function pancreatic insulin glucose metabolic syndrome type1 type2 hereditary prevalence incidence HNF4A mutations diabetes risk factors genetic association study research epidemiology pancreatic liver transcription.factor protein.function metabolic.disorders HNF4A gene mutation diabetes risk factors genetic predisposition to diabetes HNF4A and pancreatic function diabetes mellitus types diabetes genetics research pancreatic beta cells genetic variants and disease susceptibility diabetes heritability HNF4A diabetes genetic mutation risk factor association study renal cysts diabetes syndrome HNF4A function pancreatic development HNF4A gene diabetes risk factors genetic mutations pancreatic function glucose metabolism renal cysts intrahepatic cholestasis beta cell dysfunction type 2 diabetes type 1 diabetes genetic testing epidemiological studies molecular biology endocrinology research HNF4A gene diabetes risk factors genetic mutations pancreatic diseases insulin resistance metabolic syndrome type 1 diabetes type 2 diabetes genetic predisposition epidemiology研究 biomarkers HNF4A function diabetes risk genetic polymorphism association study evidence MODY transcription factor genevariant HNF4A gene diabetes risk factors genetic mutation analysis pancreatic beta cells insulin secretion metabolic syndrome type 2 diabetes genetic predisposition epidemiological studies clinical trials molecular biology genetic counseling biomarker discovery genotype-phenotype correlation glycemic control diabetes prevention genetic testing hereditary diabetes endocrine disorders metabolic diseases gene expression profiling population genetics genetic polymorphisms HNF4A diabetes risk factors genetic mutations pancreatic disease liver disease metabolic syndrome clinical genetics epidemiology gene expression insulin resistance Type 2 diabetes Type 1 diabetes
185	Breast cancer development is determined exclusively by genetic factors. Breast cancer development is determined exclusively by genetic factors. Breast cancer development is determined exclusively by genetic factors. Breast cancer development is determined exclusively by genetic factors. Breast cancer development is determined exclusively by genetic factors. genetics epigenetics environment lifestyle hereditary risk factors mutation tumor oncogenes suppressor genes genetic factors environment influence risk mutations epigenetics inheritance environmental hormones genetic predisposition environmental hormonal risk factors inheritance mutation study research epidemiology breast cancer genetics hereditary breast cancer environmental factors breast cancer genetic testing breast cancer lifestyle and breast cancer gene mutations breast cancer tumor suppressor genes breast cancer oncogenes breast cancer epigenetics breast cancer multifactorial inheritance breast cancer breast cancer genetic factors environmental influences epigenetics tumor suppressor genes oncogenes lifestyle predisposition risk factors hormonal influence hereditary cancer syndromes genetic factors breast cancer environmental influences breast cancer lifestyle and breast cancer hereditary breast cancer tumor suppressor genes breast cancer breast cancer risk factors epigenetics breast cancer genetic factors environmental influences lifestyle choices tumor suppressor genes oncogenes epigenetics hormonal factors radiation exposure infectious agents family history molecular biology clinical genetics epidemiology genetic factors breast cancer development exclusivity genetic predisposition breast cancer genetic factors environmental influences hormonal factors lifestyle mutations inheritance risk factors epidemiology molecular biology genetic predisposition environmental factors risk mutations inheritance hormones therapy prevention
1290	There is an inverse relationship between hip fractures and statin use. There is an inverse relationship between hip fractures and statin use. There is an inverse relationship between hip fractures and statin use. There is an inverse relationship between hip fractures and statin use. There is an inverse relationship between hip fractures and statin use. inverse relationship hip fractures statin use cholesterol lowering drugs bone density cardiovascular disease elderly bone health pharmacotherapy epidemiology clinical trial risk factor preventive medicine inverse relationship hip fractures statin use studies research epidemiology medication cholesterol cardiovascular benefits risk analysis population clinical trials correlation hip fractures statin use inverse relationship bone health cholesterol elderly medication epidemiology clinical trial risk factor prevention skeletal integrity hip fracture prevention statins benefits bone density and statins cholesterol medication effects elderly bone health statin usage analysis fracture risk reduction statins and osteoporosis cholesterol lowering drugs bone strength improvement hip fractures statin use inverse relationship bone health cholesterol elderly osteoporosis medication cardiovascular clinical studies epidemiology inverse relationship hip fractures statin use pharmacotherapy bone health elderly risk factors medication benefits cholesterol levels bone density cardiovascular disease prevention clinical trials epidemiology medical research inverse relationship hip fractures statin use medication impact bone health cholesterol lowering drugs osteoporosis prevention elderly health clinical studies epidemiology research inverse relationship hip fractures statin use beneficial expansion keywords medical research bone health cholesterol lowering elderly population pharmaceuticals bone density cardiovascular disease prevention inverse relationship hip fractures statin use pharmacotherapy bone health cholesterol elderly osteoporosis medication clinical trial epidemiology cardiovascular disease bone density prescription drugs risk factors preventive care healthcare public health medical research aging population inverse relationships statins hip fracture prevention bone health supplements cholesterol medication osteoporosis risk elderly bone density cardiovascular drugs impact prescription medications and fractures
1049	Ribosomopathies have a low degree of cell and tissue specific pathology. Ribosomopathies have a low degree of cell and tissue specific pathology. Ribosomopathies have a low degree of cell and tissue specific pathology. Ribosomopathies have a low degree of cell and tissue specific pathology. Ribosomopathies have a low degree of cell and tissue specific pathology. Ribosomes protein synthesis cellular stress genetic disorders tissue specificity pathology molecular biology ribosomal biogenesis congenital disorders Ribosomopathies cell specificity tissue specificity genetic disorders protein synthesis molecular biology pathology cellular stress ribosome function clinical manifestations genetic mutations hematopoietic disorders developmental disorders Ribosome pathology genetic mutations cell tissue specificity diseases molecular biology medicine diagnostics symptoms treatments Ribosomopathies symptoms Ribosomopathies causes Ribosomopathies types Ribosomopathies diagnosis Ribosomopathies treatment Ribosomopathies genetics Ribosomopathies examples Ribosomopathies prevalence Ribosomopathies cell specificity tissue pathology molecular mechanisms disease phenotypes genetic disorders RNA processing Ribosomopathies symptoms Ribosomopathies causes Ribosomopathies diagnosis Ribosomopathies treatment Ribosomopathies types Ribosome pathology cell tissue specificity genetic diseases protein synthesis disorders molecular biology mutations clinical manifestations treatment diagnosis Ribosomopathies cell specificity tissue specific pathology genetic disorders molecular biology translation errors microRNA mitochondrial dysfunction chromosome instability leukemia skeletal dysplasia Ribosomes pathogenesis genetic mutations cellular stress protein synthesis tissue specificity molecular biology medical genetics immunology bioinformatics transcriptomics proteomics Ribosome biology genetic mutations cellular stress response tissue specificity pathogenic mechanisms molecular genetics RNA metabolism
982	Proteins synthesized at the growth cone are ubiquitinated at a higher rate than proteins from the cell body. Proteins synthesized at the growth cone are ubiquitinated at a higher rate than proteins from the cell body. Proteins synthesized at the growth cone are ubiquitinated at a higher rate than proteins from the cell body. Proteins synthesized at the growth cone are ubiquitinated at a higher rate than proteins from the cell body. Proteins synthesized at the growth cone are ubiquitinated at a higher rate than proteins from the cell body. proteins growthcone ubiquitination cellbody molecularbiology synthesized preservation enzymology nucleus synthesis rates signaling microscopy neuroscience protein synthesis growth cone ubiquitination cell body neurobiology molecular biology synaptic plasticity neuronal development protein synthesis growth cone ubiquitination cell body molecular biology neuroscience biological process membrane protein signal transduction ubiquitination process growth cone biology protein synthesis regulation cell body comparison gene expression at growth cones molecular mechanisms of protein modification ubiquitination growth cone cell body protein synthesis gene expression molecular biology ubiquitination growth cone protein synthesis cell body relevant expansion phrases proteins growth cone cell body ubiquitination molecular biology nervous system synaptic development proteins growth cone ubiquitination cell body synthesized efficacy keywords protein synthesis growth cone ubiquitination cell body molecular biology neuroscience ubiquitination growth cone cell body proteins synthesis gene expression molecular biology nervous system development
742	Macrolides have no protective effect against myocardial infarction. Macrolides have no protective effect against myocardial infarction. Macrolides have no protective effect against myocardial infarction. Macrolides have no protective effect against myocardial infarction. Macrolides have no protective effect against myocardial infarction. macrolides myocardial infarction protective effect antibiotics cardiovascular drug efficacy macrolides myocardial infarction protection macrolide antibiotics cardiovascular antibiotic effectiveness myocardial infarction macrolide drug myocardial infarction protective effect macrolides heart disease macrolide antibiotics myocardial infarction prevention cardiovascular protection antimicrobial drugs statins aspirin heart attack risk clinical trials pharmacology antibiotic resistance macrolides myocardial infarction protection macrolides cardiovascular risk antibiotic myocardial infarction prevention macrolides heart attack protection macrolides and cardiac events macrolides side effects on heart macrolides cardioprotective efficacy macrolides myocardial ischemia macrolides and myocardial infarction research macrolides heart disease risk macrolides myocardial infarction protective effect cardiovascular disease antibiotic resistance clinical trial mechanism of action inflammation clinical evidence macrolides myocardial infarction protection macrolides heart disease prevention antibiotics myocardial infarction relation macrolides cardiovascular impact protective effects macrolides myocardial infarction antibiotic classes and myocardial infarction macrolide antibiotics myocardial infarction prevention cardiac protection drug efficacy cardiovascular health anti-inflammatory effects bacterial infections clinical trials pharmacodynamics risk factors macrolides myocardial infarction protective effect cardiovascular risk antibiotic efficacy clinical trials drug mechanism macrolides myocardial infarction protection macrolide antibiotics heart disease macrolides cardiovascular risk macrolides myocardial infarction clinical trial macrolides cardioprotection research macrolide antibiotics myocardial infarction prevention cardiovascular risk antibiotic efficacy heart attack protection anti-inflammatory effects lipid metabolism clinical trials pharmacology cardiac health infection control
501	Headaches are not correlated with cognitive impairment. Headaches are not correlated with cognitive impairment. Headaches are not correlated with cognitive impairment. Headaches are not correlated with cognitive impairment. Headaches are not correlated with cognitive impairment. headaches cognitive impairment correlation studies research brain function symptoms treatments neuroscience headaches cognitive impairment correlation research studies brain function symptoms treatment prevention headaches cognitive impairment research studies evidence correlation neurological conditions diseases migraines tension pain therapy treatment prevalence prevention headaches cognitive function headaches brain health cognitive decline headaches headache severity and cognition cognitive performance headaches headaches cognitive impairment correlation research studies evidence neurology migraines pain symptoms brain functioning headaches cognition headaches brain function cognitive function and headaches cognitive health headaches neurological correlation headaches headaches cognitive impairment research studies correlation analysis evidence pain memory thinking symptoms neurological conditions headaches cognitive impairment correlation studies research symptoms brain function neurology migraine headaches cognitive impairment correlation research studies evidence symptoms prevalence mild major neurological patients clinical findings headache causes headache symptoms cognitive function brain health neurological disorders
743	Macrolides protect against myocardial infarction. Macrolides protect against myocardial infarction. Macrolides protect against myocardial infarction. Macrolides protect against myocardial infarction. Macrolides protect against myocardial infarction. macrolides antibiotic heart attack prevention cardiovascular protection antibiotic class inflammation reduction cholesterol management cardiac health antimicrobial resistance therapeutic efficacy macrolides myocardial infarction antibiotics cardiovascular protection clinical trials mechanism bacteria inflammation lipid metabolism macrolide antibiotics cardiovascular protection myocardial ischemia antimicrobial drugs inflammation reduction heart disease prevention antibiotic effects clinical trials drug efficacy Macrolides antibiotic properties macrolides cardiovascular benefits macrolides reduce inflammation macrolides and heart health macrolides mechanism of action macrolides clinical trials macrolides versus statins macrolides safety profile macrolides myocardial infarction antibiotics cardiovascular protection bacterial infection inflammation clinical trial pharmacology macrolide antibiotics myocardial infarction prevention antibiotic therapy cardiovascular protection macrolides mechanism anti-inflammatory effects bacterial infection prevention heart disease treatment Macrolide antibiotics myocardial infarction prevention cardiovascular health antimicrobial effects inflammation reduction clinical trials pharmacology cardioprotective properties macrolides myocardial infarction antibiotic protection cardiovascular health pharmacology infection prevention inflammation reduction cardioprotection antimicrobial effects macrolides antibiotics myocardial infarction prevention cardiovascular benefits antibiotic classes inflammation reduction clinical trials macrolide antibiotics heart disease protection bacterial infection treatment pharmacological effects macrolide antibiotics cardiovascular protection myocardial ischemia anti-inflammatory effects bacterial infection prevention heart disease reduction therapeutic benefits
985	Pseudogene PTENP1 regulates the expression of PTEN by functioning as an miRNA decoy. Pseudogene PTENP1 regulates the expression of PTEN by functioning as an miRNA decoy. Pseudogene PTENP1 regulates the expression of PTEN by functioning as an miRNA decoy. Pseudogene PTENP1 regulates the expression of PTEN by functioning as an miRNA decoy. Pseudogene PTENP1 regulates the expression of PTEN by functioning as an miRNA decoy. pseudogene PTENP1 PTEN miRNA decoy gene regulation RNA interference oncogene tumor suppressor pseudogene PTENP1 PTEN miRNA decoy gene regulation RNA biology oncogene tumor suppressor genetic regulation Pseudogene PTENP1 PTEN miRNA regulation decoy RNA oncogene tumor suppression alternative splicing gene expression molecular biology genetic regulation pseudogene regulation miRNA decoy mechanism PTEN expression modulation gene function analysis RNA biology genetic regulation studies molecular biology research PTENP1 miRNA interaction pseudogene PTENP1 PTEN miRNA decoy gene regulation expression调控 RNA biology non-coding RNA molecular biology pseudogene PTENP1 PTEN miRNA decoy gene regulation expression modulation RNA biology oncogenes tumor suppressors pseudogene PTENP1 PTEN miRNA decoy microRNA decoy RNA interference expression regulation molecular biology genetic regulation non-coding RNA pseudogene PTENP1 PTEN miRNA decoy gene regulation expression调控 RNA interference molecular biology genetic regulatory mechanisms pseudogene PTENP1 PTEN miRNA decoy gene regulation RNA function oncogenes tumor suppression pseudogene regulation miRNA decoy mechanism PTEN gene expression RNA interference non-coding RNA function genetic regulation pathways epigenetic modifiers transcriptional control elements molecular biology techniques genetic counseling applications
502	Healthcare delivery efficiency in crowded delivery centers is impaired by improving structural, logistical, and interpersonal elements. Healthcare delivery efficiency in crowded delivery centers is impaired by improving structural, logistical, and interpersonal elements. Healthcare delivery efficiency in crowded delivery centers is impaired by improving structural, logistical, and interpersonal elements. Healthcare delivery efficiency in crowded delivery centers is impaired by improving structural, logistical, and interpersonal elements. Healthcare delivery efficiency in crowded delivery centers is impaired by improving structural, logistical, and interpersonal elements. healthcare optimization crowded hospitals logistics management interpersonal communication structural improvements patient flow analysis waiting time reduction resource allocation clinical workflow technology integration healthcare workflow patient flow management hospital infrastructure logistics optimization staff training interdisciplinary collaboration waiting room design appointment scheduling technological solutions patient satisfaction operational inefficiencies resource allocation emergency department overcrowding telemedicine integration staffing levels patient triage facility layout process improvement quality of care healthcare analytics healthcare optimization crowded hospitals strategic planning logistics management interpersonal communication wait time reduction equipment utilization patient flow analysis staff training resource allocation telemedicine application software workflow design pilot programs evidence-based practices quality improvement systematic evaluation technology integration capacity planning patient satisfaction supply chain efficiency workplace ergonomics behavioral interventions operational research clinical workflow staffing models patient navigation informatics solutions lean management continuous improvement cultural competency patient throughput health information exchange hospital design process mapping patient education community partnerships public healthcare optimization operational efficiency patient flow management staffing strategies technology integration wait time reduction facility design workflow analysis interdisciplinary collaboration resource allocation emergency room optimization telemedicine implementation supply chain management patient satisfaction healthcare policy healthcare economics healthcare management healthcare innovation healthcare technology trends healthcare optimization crowded hospitals logistics management structural improvements interpersonal communication equipment allocation patient flow wait time reduction staff training technological integration healthcare optimization crowded clinics logistical improvements structural enhancements interpersonal communication patient flow management resource allocation waiting time reduction staff training technology integration healthcare optimization crowded clinics logistics improvement strategic planning patient flow management staff training equipment allocation space utilization interdepartmental collaboration technology integration operational efficiency waiting time reduction queue management systems resource allocation patient satisfaction workflow analysis clinical workflow staffing models telemedicine application of AI process automation space design 等候时间 资源配置 临床工作流程 healthcare optimization crowded hospital management logistical workflow interpersonal communication structural improvements patient flow analysis wait time reduction hospital layout design staff training technology integration patient satisfaction metrics queue management systems telemedicine solutions resource allocation strategies operational efficiency healthcare policy systemic improvements healthcare optimization logistics management patient flow staffing strategies technological integration space utilization wait time reduction interdisciplinary collaboration healthcare infrastructure operational efficiency healthcare optimization crowded hospitals strategic planning logistics improvement interpersonal communication patient flow analysis resource allocation equipment management staff training wait time reduction triage process emergency department management
623	Individuals with low serum vitamin D concentrations have increased risk of multiple sclerosis. Individuals with low serum vitamin D concentrations have increased risk of multiple sclerosis. Individuals with low serum vitamin D concentrations have increased risk of multiple sclerosis. Individuals with low serum vitamin D concentrations have increased risk of multiple sclerosis. Individuals with low serum vitamin D concentrations have increased risk of multiple sclerosis. low vitamin D serum vitamin D levels vitamin D deficiency multiple sclerosis risk serum D concentration MS risk factors low vitamin D serum multiple sclerosis risk factors vitamin D deficiency serum vitamin D levels MS and vitamin D autoimmune diseases vitamin D low vitamin D symptoms vitamin D and immune system serum vitamin D multiple sclerosis vitamin D supplementation MS vitamin D deficiency multiple sclerosis risk fatty liver disease vitamin D insufficiency autoimmune disorders VDR gene polymorphism sunlight exposure osteoporosis calciferol immune response D3 D2 vitamin D deficiency multiple sclerosis vitamin D levels serum vitamin D low vitamin D MS risk Vit D deficiency Vit D levels Vitamin D supplementation serum 25(OH)D multiple sclerosis prevalence vitamin D deficiency multiple sclerosis risk factors serum levels immune system vitamin D supplementation epidemiology neurology vitamin D deficiency multiple sclerosis risk factors serum vitamin D levels MS vitamin D deficiency low vitamin D and MS vitamin D supplementation benefits autoimmune diseases vitamin D inflammatory response vitamin D vitamin D deficiency multiple sclerosis vitamin D levels serum vitamin D low vitamin D MS risk VitD deficiency VitD levels vitamin D deficiency multiple sclerosis vitamin D levels serum vitamin D low vitamin D MS risk VitD deficiency low serum vitamin D multiple sclerosis risk vitamin D deficiency autoimmune diseases neurodegenerative diseases epidemiology biomarkers inflammation genetics environmental factors clinical trials longitudinal studies vitamin D deficiency multiple sclerosis risk factors serum vitamin D levels MS prevalence autoimmune disorders nutritional supplementation epidemiological studies genetic predisposition sunlight exposure geographic distribution immune system function
744	Macropinocytosis contributes to a cell's supply of amino acids via the intracellular uptake of protein. Macropinocytosis contributes to a cell's supply of amino acids via the intracellular uptake of protein. Macropinocytosis contributes to a cell's supply of amino acids via the intracellular uptake of protein. Macropinocytosis contributes to a cell's supply of amino acids via the intracellular uptake of protein. Macropinocytosis contributes to a cell's supply of amino acids via the intracellular uptake of protein. macropinocytosis mechanism amino acid uptake intracellular process protein ingestion cell nutrition endocytosis types biological absorption nutrient intake cellular metabolism molecular transport macropinocytosis mechanism amino acid uptake cellular process intracellular trafficking protein internalization macropinosome aminoaciduptake cellmembrane endocytosisprocess proteintransport intracellulartrafficking biologicaluptake nutrientacquisition vesicleformation receptormediatedendocytosis fluidphaseendocytosis macropinocytosis mechanism amino acid absorption intracellular process protein uptake cellular nutrition endocytosis types nutrient acquisition biological transport macromolecule internalization Macropinocytosis amino acids protein uptake intracellular cell biology molecular transport macropinocytosis mechanism intracellular protein uptake amino acid acquisition cell nutrient transport endocytic process macropinosome formation receptor-independent engulfment cellular physiology biologic uptake mechanisms Macropinocytosis intracellular uptake amino acids protein absorption cellular nutrient acquisition endocytosis fluid-phase endocytosis cell metabolism biological transport nutrient influx Macropinocytosis process intracellular protein uptake amino acid absorption cellular nutrient acquisition membrane ruffling endocytosis mechanism cell metabolism nutrient transport biological uptake processes macropinocytosis intracellular uptake amino acids protein absorption cellular process nutrient intake biological transport membrane invagination endocytosis physiological function macropinosome receptor-mediated endocytosis nutrient acquisition fluid phase endocytosis amino acid transport cellular uptake mechanisms biological transport processes
507	Helminths interfere with immune system control of macrophages activated by IL-4 favor Mycobacterium tuberculosis replication. Helminths interfere with immune system control of macrophages activated by IL-4 favor Mycobacterium tuberculosis replication. Helminths interfere with immune system control of macrophages activated by IL-4 favor Mycobacterium tuberculosis replication. Helminths interfere with immune system control of macrophages activated by IL-4 favor Mycobacterium tuberculosis replication. Helminths interfere with immune system control of macrophages activated by IL-4 favor Mycobacterium tuberculosis replication. helminths immune system macrophages IL-4 Mycobacterium tuberculosis infection inflammation cytokines immunity pathogenesis parasitology immunomodulation helminths immune system macrophages IL-4 Mycobacterium tuberculosis parasite infection immunity cytokines inflammation pathogen host defense chronic infection immunomodulation helminths immune system macrophages IL-4 Mycobacterium tuberculosis parasite inflammation infection immunity microbiome cytokines pathogen hostdefense Helminth infections immune modulation macrophage function IL-4 signaling tuberculosis pathogenesis cytokine interactions parasite-host relationships immunological evasion chronic infection progression Th2 response granuloma formation helminths immune system macrophages IL-4 Mycobacterium tuberculosis cytokines Th2 response inflammation infection pathogenesis parasite-host interaction immunosuppression granuloma formation T-helper cells Helminths immune system macrophages IL-4 Mycobacterium tuberculosis infectionimmune modulationparasite interactionbiological response helminths immune system macrophages IL-4 Mycobacterium tuberculosis cytokines infection immunomodulation parasite-host interaction inflammation pathogenesis Helminths immune system macrophages IL-4 Mycobacterium tuberculosis reproductive interference immune evasion parasite-host interaction inflammation T-helper cells Tregs helminths immune system macrophages IL-4 Mycobacterium tuberculosis parasitic infection immune evasion cytokines Th2 response chronic infection host-pathogen interaction Helminth infections immune evasion macrophage activation IL-4 signaling tuberculosis pathology cytokine interactions immunomodulation parasite-host relationship Th2 response granuloma formation
628	Infection of human T-cell lymphotropic virus type 1 is most frequent in individuals of African origin. Infection of human T-cell lymphotropic virus type 1 is most frequent in individuals of African origin. Infection of human T-cell lymphotropic virus type 1 is most frequent in individuals of African origin. Infection of human T-cell lymphotropic virus type 1 is most frequent in individuals of African origin. Infection of human T-cell lymphotropic virus type 1 is most frequent in individuals of African origin. T-lymphotropic virus African origin HTLV-1 infections HIV immune system retrovirus RNA viral burden clinical symptoms African descent HIV HTLV-1 prevalence ethnic background infectious diseases T-cell lymphotropic virus epidemiology African population viral infections genetic predisposition infection human T-cell lymphotropic virus type 1 african origin prevalence epidemiology risk factors transmission diagnosis treatment Infection human T-cell lymphotropic virus African origin prevalence epidemiology risk factors clinical manifestations diagnosis treatment Infection human T-cell lymphotropic virus African origin prevalence epidemiology HTLV-1 infection human T-cell lymphotropic virus African origin prevalence HTLV-1 epidemiology tropical regions immunodeficiency leukemia myelopathy infection T-cell lymphotropic virus African origin HIV HTLV-1 symptoms prevalence risk factors Infectious diseases African descent HVTL-1 HTLV-1 infection T-cell lymphotropic virus African population Virus transmission Immune response HIV/AIDS relation Infection Human T-cell Lymphotropic Virus African Origin Clinical Symptoms Epidemiology Therapy infectious diseases African epidemiology T-lymphotropic virus strains clinical manifestations
508	Hematopoietic Stem Cell purification reaches purity rate of up to 50%. Hematopoietic Stem Cell purification reaches purity rate of up to 50%. Hematopoietic Stem Cell purification reaches purity rate of up to 50%. Hematopoietic Stem Cell purification reaches purity rate of up to 50%. Hematopoietic Stem Cell purification reaches purity rate of up to 50%. Hematopoietic Stem Cells purification techniques methods biotechnology advancements research isolation protocols efficiency medical applications clinical biomarkers Hematopoietic Stem Cell isolation Hematopoietic Stem Cell separation Hematopoietic Stem Cell enrichment Stem Cell purification techniques Stem Cell yield improvement Advanced Hematopoietic purification methods Hematopoietic Stem Cell purification techniques methods isolation techniques biotechnology medical research advancements efficiency protocols hematopoiesis stemness cellularity oncology immunology biomedical regenerativemedicine Hematopoietic Stem Cell isolation Hematopoietic Stem Cell enrichment Hematopoietic Stem Cell separation Hematopoietic Stem Cell techniques Hematopoietic Stem Cell protocols Stem Cell purification methods Stem Cell separation techniques Blood stem cell purification Advanced Hematopoietic Stem Cell enrichment Hematopoietic Stem Cell yield improvement Hematopoietic Stem Cell Purification Technique Purity Rate Biotechnology Isolation Method Blood Cancer Research Clinical Application Hematopoietic Stem Cell isolation Hematopoietic Stem Cell separation Hematopoietic Stem Cell enrichment Stem Cell purification techniques Stem Cell isolation efficiency Hematopoietic Stem Cell收获纯度 Advanced Hematopoietic Stem Cell purification methods Hematopoietic Stem Cell isolation purification techniques cellular biology bioengineering stem cell research biotechnology medical science immunology blood cell production scientific methods laboratory procedures clinical applications genetic engineering cancer treatment regenerative medicine Hematopoietic Stem Cell Purification Techniques Purity Rate Biotechnology Medical Research Methods Isolation Enhancements Efficiency Hematopoietic Stem Cell isolation Hematopoietic Stem Cell separation stem cell purification techniques high purity stem cells advanced cell sorting methods Hematopoietic Stem Cell isolation purification techniques advanced cell sorting high-purity stem cells stem cell enrichment methods cellular biomarkers biotechnology advancements clinical applications research methodologies
1187	The YAP1 and TEAD complex tanslocates into the nucleus where it interacts with transcription factors and DNA-binding proteins that modulate target gene transcription. The YAP1 and TEAD complex tanslocates into the nucleus where it interacts with transcription factors and DNA-binding proteins that modulate target gene transcription. The YAP1 and TEAD complex tanslocates into the nucleus where it interacts with transcription factors and DNA-binding proteins that modulate target gene transcription. The YAP1 and TEAD complex tanslocates into the nucleus where it interacts with transcription factors and DNA-binding proteins that modulate target gene transcription. The YAP1 and TEAD complex tanslocates into the nucleus where it interacts with transcription factors and DNA-binding proteins that modulate target gene transcription. YAP1 TEAD nuclear translocation transcription factors DNA-binding proteins gene transcription signaling pathway organogenesis oncogene Hippo pathway YAP1 TEAD nuclear translocation transcription factors DNA-binding proteins gene transcription signaling pathway cell proliferation organ development mechanistic basis biological process regulatory mechanism YAP1 TEAD nuclear translocation transcription factors DNA-binding proteins gene regulation signaling pathway molecular biology cell nucleus transcriptional activation YAP1 TEAD nuclear translocation transcription factors DNA-binding proteins target gene transcription cellular signaling gene expression regulation organ development Hippo pathway protein interactions biological processes molecular mechanisms YAP1 TEAD nucleus transcription factors DNA-binding proteins gene regulation signaling pathway hepatocellular carcinoma mechanistic insights biology YAP1 TEAD nuclear translocation transcription factors DNA-binding proteins target gene regulation cellular signaling oncogenic pathways gene expression modulation protein interactions YAP1 TEAD nuclear translocation transcription factors DNA-binding proteins target gene regulation signaling pathway gene expression cellular process molecular biology YAP1 TEAD nucleus transcription factors DNA-binding target genes modulation molecular biology cell signaling mRNA transcription protein interaction gene expression biological pathway translocation nuclear localization YAP1 TEAD nuclear translocation transcription factors DNA-binding proteins gene transcription regulatory proteins signaling pathway cellular response molecular interactions YAP1 TEAD nuclear translocation transcription factors DNA-binding proteins gene transcription cellular signaling biological regulation molecular interaction
1185	The US health care system can save up to $750 million if 7% of patients waiting for kidney transplants participate in the optimized national kidney paired donation program. The US health care system can save up to $750 million if 7% of patients waiting for kidney transplants participate in the optimized national kidney paired donation program. The US health care system can save up to $750 million if 7% of patients waiting for kidney transplants participate in the optimized national kidney paired donation program. The US health care system can save up to $750 million if 7% of patients waiting for kidney transplants participate in the optimized national kidney paired donation program. The US health care system can save up to $750 million if 7% of patients waiting for kidney transplants participate in the optimized national kidney paired donation program. healthcare cost savings kidney transplant waiting list national kidney paired donation optimization programs patient participation healthcare system improvements organ donation efficiency medical cost reduction transplantation medicine public health solutions US health care cost savings kidney transplant waiting list optimized donation program national kidney paired donation patient participation impact healthcare efficiency improvement transplant optimization program public health savings medical resource allocation healthcare reform kidney transplant optimization national kidney program paired donation patient wait times healthcare cost savings organ donation improvement medical efficiency transplant waiting list reduction healthcare cost savings kidney transplant waiting list optimize organ donation national kidney paired donation program benefits increase kidney transplant success rate reduce healthcare expenditure improve patient outcomes maximize organ donation efficiency enhance transplant programs public health economics healthcare efficiency kidney transplant waiting optimized national kidney paired donation cost savings patient participation medical optimization transplant programs healthcare economics health care optimization kidney transplant waiting list national kidney paired donation program benefits cost savings in healthcare patient participation impact medical cost reduction transplant efficiency improvement health care cost savings kidney transplant waiting list optimized kidney paired donation national organ sharing patient wait times healthcare optimization medical cost reduction transplant program efficiency healthcare cost savings kidney transplant waitlist optimized donation programs national kidney paired donation efficacy improvement patient participation healthcare efficiency surgical optimization organ allocation reform healthcare cost savings kidney transplant waiting list optimize organ donation national kidney paired donation program patient participation impact healthcare efficiency improvement transplant program enhancement cost reduction strategies medical resource optimization healthcare optimization kidney transplant waiting list national kidney paired donation program benefits patient participation savings potential medical resource allocation
1062	S-nitrosylated GAPDH physiologically transnitrosylates histone deacetylases. S-nitrosylated GAPDH physiologically transnitrosylates histone deacetylases. S-nitrosylated GAPDH physiologically transnitrosylates histone deacetylases. S-nitrosylated GAPDH physiologically transnitrosylates histone deacetylases. S-nitrosylated GAPDH physiologically transnitrosylates histone deacetylases. S-nitrosylation GAPDH histone deacetylases physiology nitric oxide pathway molecular biology tissue specificity enzymatic activity post-translational modification S-nitrosylation GAPDH histone deacetylases physiological processes nitric oxide molecular mechanisms tissue specificity disease association research methods S-nitrosylation GAPDH histone deacetylases physiological processes nitric oxide protein modifications enzymatic activity molecular mechanisms nuclear proteins cell signaling S-nitrosylation GAPDH histone deacetylases physiological processes nitric oxide signaling molecular mechanisms biochemistry research techniques proteomics enzymology cellular function S-nitrosylation GAPDH histone deacetylases physiological nitric oxide proteomics methylation detection techniques enzymology S-nitrosylation GAPDH histone deacetylases transnitrosylation physiological processes protein modifications enzymatic activity molecular biology nitric oxide signaling epigenetics transcription regulation S-nitrosylation GAPDH histone deacetylases physiological nitric oxide proteomics post-translational modification enrichment/terms biological processes molecular interactions S-nitrosylation GAPDH histone deacetylases physiological nitrosylation efficacy keywords biological process enzymatic activity molecular modification proteomics nitric oxide biology S-nitrosylation GAPDH histone deacetylases physiological processes nitric oxide protein modification transnitrosylation molecular biology enzymology S-nitrosylation GAPDH histone deacetylases physiology transnitrosylation proteomics molecular biology nitric oxide enzymology
1180	The PRR MDA5 is a sensor of RNA virus infection. The PRR MDA5 is a sensor of RNA virus infection. The PRR MDA5 is a sensor of RNA virus infection. The PRR MDA5 is a sensor of RNA virus infection. The PRR MDA5 is a sensor of RNA virus infection. PRR sensors RNA recognition molecular innate immunity viral sensing pathogen recognition receptors MDA5 function RNA viruses detection mechanisms inflammation response DNA damage response PRR sensors RNA viruses infection mechanisms MDA5 function viral detection molecular biology virus recognitionimmune response RNA sensing innate immunity viral detection molecular biology cytokine response antiviral mechanism virology immune signaling PRR sensors RNA virus detection MDA5 function immunology research viral infection response PRR sensors RNA viruses infection detection MDA5 function Viral recognition molecular biology immunology virology cell signaling antiviral defense host-pathogeninteraction RNA sensing viral infection response innate immunity MDA5 function RNA recognition PRR mechanism virus detection immune activation molecular biology virology research PRR sensors RNA recognition molecular markers viral detection immune response antiviral defense MDA5 function immunology virology signaling pathway PRR sensors RNA viruses MDA5 function viral sensing molecular immunity RNA detection immunology keywords VISA protein antiviral response PRR proteins MDA5 protein RNA virus detection innate immunity viral sensing interferon induction pathogen recognition receptors PRR sensors RNA viruses MDA5 function antiviral response infection pathways viral RNA detection DNA sensors immune response
198	CCL19 is absent within dLNs. CCL19 is absent within dLNs. CCL19 is absent within dLNs. CCL19 is absent within dLNs. CCL19 is absent within dLNs. CCL19 dendritic lymph nodes expression immune cells absence localization CCL19 dendritic cells lymph nodes lymph node dLNs immune response lymphocyte trafficking chemokine immunology T cells HIV inflammation CCL19 dendritic lymph nodes immune response chemokine antigen presentation inflammation migration T cells CCL19 expression dLNs function lymph node development CCL19 role in immune response chemokine receptors CCL21 interaction CCL19 knockout models CCL19 deficiency effects CCL19 dendritic cells lymph nodes immune response chemokine lymph node function antigen presentation CCL19 dendritic cells lymph node immunology chemokine T cells antigen presentation inflammation lymphocyte trafficking CCL19 dendritic cells lymph nodes immune response lymphocyte trafficking chemokines inflammation CCL19 dLNs lymph node immunology absence biomarker immune response inflammation lymphocyte trafficking CCL19 dendritic cells lymph node lymphatic tissue immune response inflammation lymphocyte trafficking chemokine receptor CCR7 immunology tumor microenvironment CCL19 lymph nodes dendritic cells lymphatic vessels chemokine receptors immune response inflammation tumor microenvironment immunotherapy lymph node sequestration
870	Obesity decreases life quality. Obesity decreases life quality. Obesity decreases life quality. Obesity decreases life quality. Obesity decreases life quality. obesity health life expectancy quality of life overweight fatness medical conditions nutrition exercise mortality fitness obesity health life expectancy quality of life weight management overweight metabolic disorders cardiovascular disease diabetes mortality rate obesity life quality health mortality longevity obesity rates quality of life obesity health effects lifestyle factors body mass index obesity complications obesity risks obesity health impacts obesity and longevity lifestyle obesity obesity mortality risk obesity life quality health mortality weight BMI diet exercise metabolic disorders cardiovascular diseases weight management healthy lifestyle diet plans fitness exercises metabolic rate body mass index obesity risks longevity factors nutritional advice physical activity benefits obesity health life expectancy quality of life overweight metabolic disorders cardiovascular disease nutrition exercise obesity rates fat percentage obesity life quality health risks weight management obesity complications longevity metabolic disorders diet impact exercise mortality rates obesity life quality health mortality complications nutrition exercise overweight fatness chronic diseases metabolic disorders obesity health impacts obesity mortality rates lifestyle changes for obesity obesity and cardiovascular disease obesity mental health
993	Pyridostatin destabilizes the G - quadruplex in the telomeric region. Pyridostatin destabilizes the G - quadruplex in the telomeric region. Pyridostatin destabilizes the G - quadruplex in the telomeric region. Pyridostatin destabilizes the G - quadruplex in the telomeric region. Pyridostatin destabilizes the G - quadruplex in the telomeric region. Pyridostatin G-quadruplex telomeric region telomeres anticancer drug molecular stability DNA structure Pyridostatin G-quadruplex telomeric region DNA stability telomeres molecular biology chromosomal ends pharmacodynamics antitumor activity pyridostatin telomere g-quadruplex anti-cancer molecular biology DNA stability telomeric DNA chromosome end pyridostatin G-quadruplex interaction telomere stability anti-cancer drug mechanism telomerase inhibition G-quadruplex forming sequences telomere structure pyridostatin mechanism of action G-quadruplex recognition anticancer therapy telomere function Pyridostatin G-quadruplex telomeric region DNA stability molecular biology drug mechanism pyridostatin telomeres pyridostatin G-quadruplex telomeric DNA stability pyridostatin mechanism quadruplex formation anti-telomerase activity Pyridostatin G-quadruplex telomeric region telomeres DNA stability binding affinity molecular dynamics structure formation Pyridostatin telomeric region G-quadruplex destabilization molecular biology biophysics drug mechanism anti-cancer therapy pyridostatin telomeric G-quadruplex structural destabilization molecular biology chromosomal stability cancer treatment anticancer drug genetic research synthetic biology pyridostatin mechanisms telomeric DNA stability G-quadruplex structure anti-cancer potential biological assays
873	Obesity is determined solely by environmental factors. Obesity is determined solely by environmental factors. Obesity is determined solely by environmental factors. Obesity is determined solely by environmental factors. Obesity is determined solely by environmental factors. obesity environmental factors determinants genetics caloric intake physical activity metabolism hormones genetics lifestyle metabolism diet exercise hormones socioeconomic cultural psychological obesity genetic factors diet physical activity metabolism socioeconomic status urbanization obesity prevalence lifestyle choices geneticFactors lifestyleChoices metabolicRate socioeconomicStatus dietQuality physicalActivity hormonalInfluences psychologicalFactors genetics metabolism diet exercise lifestyle socioeconomic culture genetics hormonal pharmaceutical intervention prevention public health obesity environment obesity genetic factors lifestyle choices metabolic rate diet impact exercise influence hormonal factors obesity prevention environmental impact public health genetics diet physical activity metabolism socioeconomic status urbanization sedentary behavior nutrition obesity prevalence public health geneticFactors metabolismRate lifestyleChoices dietaryHabits physicalActivityLevel hormonalInfluences socioeconomicStatus genetics lifestyle diet physical activity socioeconomic status metabolic rate hormonal influences epigenetics urbanization fast food sedentary behavior pollution stress sleep patterns genetic predisposition lifestyle diet exercise hormones
1179	The PRR MDA5 has a central DExD/H RNA helices domain. The PRR MDA5 has a central DExD/H RNA helices domain. The PRR MDA5 has a central DExD/H RNA helices domain. The PRR MDA5 has a central DExD/H RNA helices domain. The PRR MDA5 has a central DExD/H RNA helices domain. PRR proteins MDA5 function RNA recognition DExD/H box innate immunity viral detection molecular structure PRR proteins MDA5 function RNA recognition immune response helicase domain innate immunity viral detection molecular biology biochemistry immunology PRR proteins innate immunity RNA recognition viral detection helicase domain MDA5 function immune response molecular biology virology signaling pathway PRR protein function RNA recognition domain innate immunity viral detection MDA5 structure helicase activity antiviral response RNA binding motif PRR MDA5 DExD/H RNA domain innate immunity antiviral signaling query expansion keyword recommendation RNA recognition viral sensing innate immunity molecular function PRR domain MDA5 protein PRR proteins MDA5 function RNA recognition DExD/H box innate immunity viral detection signaling pathway PRR proteins RNA recognition MDA5 function DExD/H domain RNA binding domains immunologyKeywords Innate immunity Viral detection Molecular biology PRR proteins MDA5 function RNA recognition DExD/H box immune response viral detection signaling pathway PRR proteins RNA recognition molecular function antiviral response DExD/H box MDA5 domain
1298	Thigh-length graduated compression stockings (GCS) did not reduce deep vein thrombosis in patients admitted to hospital who are immobile because of acute stroke. Thigh-length graduated compression stockings (GCS) did not reduce deep vein thrombosis in patients admitted to hospital who are immobile because of acute stroke. Thigh-length graduated compression stockings (GCS) did not reduce deep vein thrombosis in patients admitted to hospital who are immobile because of acute stroke. Thigh-length graduated compression stockings (GCS) did not reduce deep vein thrombosis in patients admitted to hospital who are immobile because of acute stroke. Thigh-length graduated compression stockings (GCS) did not reduce deep vein thrombosis in patients admitted to hospital who are immobile because of acute stroke. compression therapy immobility stroke patients DVT prevention medical stockings thrombosis risk hospitalization leg support vein health circulation improvement thigh-length GCS deep vein thrombosis acute.stroke immobile hospital patients reduction clinical.trial evidence prevention treatment thrombosis stroke immobilization compression therapy DVT hospitalization rehabilitation leg compression acute illness medical compression袜子 血栓 中风 不活动 压力袜 深静脉血栓 医院治疗 thigh-length compression stockings GCS therapy deep vein thrombosis prevention acute stroke rehabilitation immobile patients hospital-acquired DVT compression garments efficacy thromboembolism risk reduction vascular health support post-stroke complications management compression therapy stroke recovery thrombosis prevention immobility risks hospital-acquired conditions medical garments clinical trials patient outcomes vascular health rehabilitation stockings compression therapy acute stroke recovery thrombosis prevention immobile patients hospital acquired conditions leg compression medical garments DVT risk rehabilitation aids patient mobility healthcare products deep vein thrombosis immobility acute stroke hospitalization compression therapy thrombosis prevention clinical trial vascular health medical compression garments venous insufficiency blood flow improvement medical evaluation patient outcomes compression therapy acute stroke prevention hospital immobility DVT risk therapeutic socks medical compression garments search optimize keywords deep vein thrombosis hospitalized immobile acute stroke compression stockings clinical trial prevention recovery rehabilitation patient management effectiveness risk factors outcomes deep vein thrombosis immobile patients acute stroke compression therapy thrombosis prevention medical garments clinical trial results vascular health hospital-acquired conditions patient mobility
513	High cardiopulmonary fitness causes increased mortality rate. High cardiopulmonary fitness causes increased mortality rate. High cardiopulmonary fitness causes increased mortality rate. High cardiopulmonary fitness causes increased mortality rate. High cardiopulmonary fitness causes increased mortality rate. cardiovascular health mortality risk fitness levels pulmonary function health outcomes exercise impact onset of diseases cardiovascular health mortality risk pulmonary function fitness levels health outcomes aerobic capacity exercise tolerance cardiovascular health mortality risk pulmonary function fitness levels health outcomes cardiovascular health respiratory function longevity exercise impact fitness levels mortality risk factors physical activity benefits heart health lung capacity endurance training effects cardiovascular health mortality risk factors fitness levels pulmonary function health outcomes cardiovascular health mortality risk pulmonary function fitness levels health outcomes physical activity cardiovascular health pulmonary function mortality risk fitness levels health outcomes aerobic capacity endurance-training mortality studies exercise intensity physiological fitness cardiovascular health mortality risk pulmonary function fitness levels health outcomes aerobic capacity exercise tolerance physiological fitness life expectancy cardiopulmonary fitness mortality rate exercise endurance health risk factors cardiovascular disease pulmonary function longevity physical activity mortality risk fitness levels cardiac function pulmonary health exercise frequency aerobic capacity mortality survival rate fitness cardiorespiratory mortality analysis fitness mortality physical fitness respiratory function mortality study cardiopulmonary exercise fitness and mortality pulmonary circulation cardiovascular health fitness levels and mortality exercise physiology cardiopulmonary health mortality and fitness physical activity levels fitness and health outcomes mortality and physical fitness cardiopulmonary fitness cardiovascular health mortality risk fitness levels pulmonary function health outcomes exercise intensity lifetime expectancy
514	High dietary calcium intakes are unnecessary for prevention of secondary hyperparathyroidism in subjects with 25(OH)D levels above 75 nmol/liter. High dietary calcium intakes are unnecessary for prevention of secondary hyperparathyroidism in subjects with 25(OH)D levels above 75 nmol/liter. High dietary calcium intakes are unnecessary for prevention of secondary hyperparathyroidism in subjects with 25(OH)D levels above 75 nmol/liter. High dietary calcium intakes are unnecessary for prevention of secondary hyperparathyroidism in subjects with 25(OH)D levels above 75 nmol/liter. High dietary calcium intakes are unnecessary for prevention of secondary hyperparathyroidism in subjects with 25(OH)D levels above 75 nmol/liter. calcium supplementation vitamin D secondary hyperparathyroidism bone health kidney function osteoporosis nutrition metabolism clinical guidelines epidemiology bone density chronic kidney disease metabolic bone disease dietary calcium hyperparathyroidism prevention vitamin D calcium intake secondary hyperparathyroidism 25(OH)D levels bone health renal disease osteoporosis nutritional guidelines metabolic bone disease calcium supplementation vitamin D levels secondary hyperparathyroidism bone health kidney function osteoporosis dietary guidelines mineral absorption nutritional recommendations metabolic bone disease high calcium intake 25(OH)D levels secondary hyperparathyroidism prevention vitamin D sufficiency parathyroid hormone dietary calcium necessity bone health renal function osteoporosis risk calcitriol production metabolic bone disease calcium supplementation vitamin D secondary hyperparathyroidism bone health kidney function osteoporosis metabolic bone disease nutritional guidelines renal impairment end-stage renal disease bone mineral density calcium supplements vitamin D levels hyperparathyroidism risk bone health nutritional advice parathyroid function calcium absorption dietary guidelines secondary hyperparathyroidism prevention 25(OH)D sufficiency nutritional recommendations calcium intake safety metabolic bone disease osteoporosis prevention calcium supplementation vitamin D secondary hyperparathyroidism bone health nutritional guidelines kidney disease osteoporosis prevention mineral metabolism calcium supplementation vitamin D hyperparathyroidism bone health metabolic bone disease osteoporosis nutrition epidemiology endocrinology dietary guidelines calcium supplementation vitamin D levels secondary hyperparathyroidism bone health renal function osteoporosis prevention nutritional guidelines metabolic bone disease parathyroid hormone dietary recommendations mineral metabolism secondaryhyperparathyroidism 25(OH)D vitaminD calciumsupplementation osteoporosis renalfailure bonehealth metabolicbone疾病 parathyroidhormone nutritionalguidelines endocrinology preventivecare
756	Many proteins in human cells can be post-translationally modified at lysine residues via acetylation. Many proteins in human cells can be post-translationally modified at lysine residues via acetylation. Many proteins in human cells can be post-translationally modified at lysine residues via acetylation. Many proteins in human cells can be post-translationally modified at lysine residues via acetylation. Many proteins in human cells can be post-translationally modified at lysine residues via acetylation. post-translational modification lysine acetylation protein acetylation acetyltransferase histone acetylation non-histone acetylation post-translational modification acetylation lysine human cells proteomics protein function epigenetics histone acetylation molecular biology post translational modification lysine acetylation protein acetylation ubiquitination SUMOylation phosphorylation protein modifications histone acetylation acetyltransferase deacetylase proteomics epigenetics cellular signaling post-translational modification lysine acetylation proteomics epigenetics protein function histone acetylation signaling pathways mass spectrometry biochemical assays genetic regulation proteins post-translational modification lysine acetylation human cells research biological processes molecular biology enzymes substrates modification sites enzymology proteins lysine residues acetylation post-translational modifications human cells molecular biology biochemistry ubiquitination histone acetylation signal transduction protein function regulation post-translational modification lysine acetylation protein acetylation acetyltransferase deacetylase epigenetics proteomics histone acetylation regulatory mechanism post-translational modification lysine acetylation protein acetylation acetyltransferase deacetylase acetylated proteins proteomics epigenetics histone acetylation ubiquitination glycosylation phosphorylation post-translational modification lysine acetylation protein acetylation ubiquitination SUMOylation phosphorylation human proteome acetyltransferase deacetylase proteomics post-translational modification acetylation lysine residues protein function regulatory mechanisms proteomics epigenetics cellular signaling
636	Inositol lipid 3-phosphatase PTEN converts Ptdlns(3,4)P 2 into phosphatidylinositol 4-phosphate. Inositol lipid 3-phosphatase PTEN converts Ptdlns(3,4)P 2 into phosphatidylinositol 4-phosphate. Inositol lipid 3-phosphatase PTEN converts Ptdlns(3,4)P 2 into phosphatidylinositol 4-phosphate. Inositol lipid 3-phosphatase PTEN converts Ptdlns(3,4)P 2 into phosphatidylinositol 4-phosphate. Inositol lipid 3-phosphatase PTEN converts Ptdlns(3,4)P 2 into phosphatidylinositol 4-phosphate. PTEN function lipid metabolism phosphoinositide 3-kinase PI3K pathway inositol phosphates cell signaling tumor suppressor PIP2 hydrolysis PI4P production phosphatase activity PTEN enzyme function PtdIns(3 4)P2 PIP4 lipid metabolism tumor suppressor phosphatidylinositol 3-kinase pathway PTEN function lipid metabolism phosphatidylinositol PtdIns(3 4)P2 PI4P tumor suppressor signaling pathway cell growth regulation autophagy insulin signaling PTEN function lipid metabolism phosphatase activity cellular signaling PIP2 conversion PI4P production tumor suppression phosphoinositide metabolism cancer research lipid kinase inhibitors PTEN inositol lipid 3-phosphatase Ptdlns(3 4)P 2 phosphatidylinositol 4-phosphate enzyme substrate metabolism molecular biochemistry mechanism cell signaling PTEN function lipid metabolism inositol phosphates phosphatase activity PtdIns(3 4)P2 PI(4)P conversion signaling pathway tumor suppression cellular signaling metabolic enzymes PTEN enzyme function inositol lipid metabolism PtdIns(3 4)P2 regulation PI4P production phosphatase activity cellular signaling pathways PTEN function lipid metabolism phosphoinositide regulation cell signaling pathways PIP2 conversion inositol lipids PTEN protein phosphatidylinositol 4-phosphate production PtdIns(3 4 5)P3 breakdown PTEN function inositol lipids phosphatidylinositol 4-phosphate PtdIns(3 4)P2 lipid metabolism tumor suppression signaling pathways PTEN function inositol lipid metabolism phosphoinositide 3-kinase PI3K pathway lipid signaling PIP2 degradation tumor suppression autophagy regulation insulin signaling cell proliferation
516	High levels of CRP reduces the risk of exacerbations in chronic obstructive pulmonary disease (COPD). High levels of CRP reduces the risk of exacerbations in chronic obstructive pulmonary disease (COPD). High levels of CRP reduces the risk of exacerbations in chronic obstructive pulmonary disease (COPD). High levels of CRP reduces the risk of exacerbations in chronic obstructive pulmonary disease (COPD). High levels of CRP reduces the risk of exacerbations in chronic obstructive pulmonary disease (COPD). CRP levels COPD exacerbations inflammation markers cardiac risk pulmonary function immune response clinical outcomes CRP levels COPD exacerbations inflammation cardiovascular risk pulmonary function anti-inflammatory therapy risk factors clinical outcomes CRP levels COPD exacerbations inflammation pulmonary disease risk factors chronic obstructive pulmonary disease cardiovascular health inflammatory markers therapeutic interventions CRP testing COPD management COPD inflammation CRP levels pulmonary disease treatment chronic obstructive pulmonary disease complications reduce COPD exacerbations inflammation markers in COPD CRP COPD exacerbations inflammation proteins risk factors clinical evidence CRP testing COPD management Inflammation markers COPD complications CRP measurement Pulmonary health assessments CRP levels COPD exacerbations inflammation markers chronic obstructive pulmonary disease acute exacerbations cardiovascular risk immune response pulmonary function tests biomarkers clinical outcomes CRP levels COPD exacerbations inflammation markers chronic obstructive pulmonary disease risk reduction acute exacerbations cardiovascular health inflammatory response pulmonary function clinical outcomes CRP levels COPD exacerbations inflammation cardiac risk pulmonary health chronic obstructive pulmonary disease markers CRP testing COPD management inflammation markers chronic lung disease pulmonary health exacerbation prevention inflammatory response
637	Input from  mental and physical health care professionals is effective at decreasing homelessness. Input from  mental and physical health care professionals is effective at decreasing homelessness. Input from  mental and physical health care professionals is effective at decreasing homelessness. Input from  mental and physical health care professionals is effective at decreasing homelessness. Input from  mental and physical health care professionals is effective at decreasing homelessness. mental health professionals physical health care input effectiveness reducing homelessness healthcare providers的意见 社区卫生工作者 心理健康专家 全科医生 健康护理贡献 支持服务 临床心理学家 精神卫生护士 多学科团队合作 咨询师 康复治疗师 mental health professionals physical health care effective interventions homelessness prevention healthcare providers social work counseling services psychiatric care primary care community health therapy techniques health policy public health patient care clinical practice healthcare integration mental health disorders substance abuse chronic illness healthcare access mental health stigma health education patient outcomes health disparities interdisciplinary care healthcare systems home health care healthcare economics healthcare technology healthcare quality healthcare utilization healthcare delivery healthcare innovation healthcare management healthcare ethics healthcare reform healthcare equity healthcare disparities healthcare accessibility healthcare impact healthcare effectiveness mental health professionals physical health care providers healthcare input decreasing homelessness strategies professional perspectives health care effectiveness mental health interventions physical health contributions healthcare professional roles reducing homelessness methods mental health interventions physical health integration healthcare professional collaboration homelessness prevention strategies psychological support services medical care access holistic health approach therapeutic environments professional input impact healthcare system improvements mental health care physical health care professional input homelessness prevention effective strategies healthcare providers social services public health community health health care systems policy recommendations clinical practice patient outcomes homelessness impact health disparities integrated care health care access behavioral health chronic illness management health literacy socioeconomic factors health equity public health interventions mental health interventions physical health care professional input homelessness reduction effective strategies healthcare collaboration mental health disorders substance abuse treatment chronic illness management social services integration patient outcomes housing support interdisciplinary approach public health measures mental health professionals physical health care providers healthcare input decreasing homelessness strategies professional perspectives effective interventions health care contributions reducing homelessness interdisciplinary approach social health impact mental health professionals physical health care input effective interventions decreasing homelessness interdisciplinary approach healthcare providers social work input psychological counseling medical expertise public health strategies community health workers mental health professionals physical health care providers effective interventions decreasing homelessness interdisciplinary approach healthcare integration mental health services physical health services professional input homelessness prevention clinical perspectives social care integration health care professionals public health community health workers patient outcomes healthcare collaboration mental health disorders physical health conditions healthcare access mental health treatment physical health screening homecare services healthcare policy healthcare systems health equity healthcare disparities health promotion health education healthcare utilization healthcare financing health outcomes health status health care delivery health care quality health care effectiveness health care accessibility mental health interventions physical health integration healthcare provider perspectives homelessness prevention professional collaboration mental illness treatment substance abuse counseling chronic disease management telehealth services community support networks
879	Occupancy of ribosomes by IncRNAs do not make functional peptides. Occupancy of ribosomes by IncRNAs do not make functional peptides. Occupancy of ribosomes by IncRNAs do not make functional peptides. Occupancy of ribosomes by IncRNAs do not make functional peptides. Occupancy of ribosomes by IncRNAs do not make functional peptides. IncRNAs functional peptides ribosome occupation mRNA translation non-coding RNA protein synthesis biological translation translational regulation RNA interference ribosome occupancy IncRNAs functional peptides mRNA transcription translation RNA biology ribosome IncRNAs functional peptides RNA protein translation molecular biology transcriptomics gene expression biological process RNA interference non-coding ribosome Occupancy IncRNAs function non-coding RNA roles peptide production inhibition translational control mechanisms RNA interference techniques gene expression regulation molecular biology processes ribosomal occupancy analysis ribosome IncRNAs functional peptides RNA binding translation inhibition gene regulation mRNA interaction IncRNAs ribosomes occupancy functional peptides non-coding RNA translation molecular biology gene expression RNA interference mRNA protein synthesis ribosome occupancy IncRNAs non-coding RNA peptide synthesis translation RNA function molecular biology gene expression ribosomal binding ribosome占用 IncRNAs功能 非蛋白质编码 翻译调控 基因表达 ribosome IncRNAs functional peptides transcription translation RNA protein biotechnology microbiology molecular biology gene expression ribosome occupancy IncRNAs functional peptides mRNA translation transcriptional regulation RNA biology microRNAs lncRNAs RNA sequencing protein synthesis
517	High levels of copeptin decrease risk of diabetes. High levels of copeptin decrease risk of diabetes. High levels of copeptin decrease risk of diabetes. High levels of copeptin decrease risk of diabetes. High levels of copeptin decrease risk of diabetes. copeptin diabetes hormone glucose insulin cardiovascular electrolytes kidney metabolic endocrine copeptin diabetes risk factors copeptin levels and diabetes copeptin measurement diabetes copeptin role in diabetes prevention copeptin and pancreatic health copeptin testing for diabetes copeptin insulin relationship copeptin glucose metabolism copeptin hormone function copeptin endocrine system high copeptin copeptin levels diabetes risk factors copeptin and diabetes copeptin measurement hormone copeptin vasopressin copeptin diabetes prevention glucose regulation endocrine system insulin resistance cardiovascular markers metabolic syndrome diabetes types copeptin levels diabetes risk factors hormone copeptin glucose regulation endocrine system pancreatic function diabetes prevention copeptin testing blood sugar management insulin resistance copeptin diabetes risk factors glucose insulin hormones endocrinology biomarkers pancreatic function kidney health cardiovascular disease copeptin levels diabetes risk factors hormone copeptin glucose regulation endocrine system insulin resistance pancreatic function cardiovascular health metabolic syndrome peptide hormones copeptin blood测试 血液检测 糖尿病风险 临床指标 生物标志物 垂体压 血管加压素 copeptin diabetes risk factors hormonal regulation glucose levels endocrinology biomarkers insulin resistance pancreatic function cardiovascular health copeptin diabetes hormonal regulation peptide hormones cardiovascular health insulin resistance endocrine system glucose metabolism biomarkers metabolic syndrome copeptin diabetes risk factors pancreatic beta cells glucose regulation hormone balance cardiovascular health insulin resistance endocrine system biomarkers metabolic syndrome
759	Mathematical models predict that using Artemisinin-based combination therapy over nongametocytocidal drugs have a dramatic impact in reducing malaria transmission. Mathematical models predict that using Artemisinin-based combination therapy over nongametocytocidal drugs have a dramatic impact in reducing malaria transmission. Mathematical models predict that using Artemisinin-based combination therapy over nongametocytocidal drugs have a dramatic impact in reducing malaria transmission. Mathematical models predict that using Artemisinin-based combination therapy over nongametocytocidal drugs have a dramatic impact in reducing malaria transmission. Mathematical models predict that using Artemisinin-based combination therapy over nongametocytocidal drugs have a dramatic impact in reducing malaria transmission. mathematical modeling artemisinin-based combination therapy nongametocytocidal drugs malaria transmission reduction drug efficacy parasitic infection treatment public health impact Artemisinin combination therapy nongametocytocidal malaria transmission mathematical modeling drug efficacy public health epidemiology tropical medicine antimalarial drugs mathematical modeling malaria transmission Artemisinin-based combination therapy nongametocytocidal drugs effective treatments malaria prevention modeling malaria drug efficacy Artemisinin-based combination therapy benefits nongametocytocidal drugs comparison malaria transmission reduction strategies mathematical modeling in malaria control antimalarial drug effectiveness analysis gametocyte clearance rates public health interventions vector-borne disease management epidemiological models drug resistance impacts Artemisinin combination therapy nongametocytocidal drugs malaria transmission predictive modeling public health anti-malarial resistance treatment efficacy drug effectiveness vector control disease spread modeling Artemisinin-based combination therapy malaria transmission reducing malaria modeling combination therapies effective treatments nongametocytocidal drugs therapeutic efficacy molecular biology public health strategies antimalarial drugs drug resistance mosquito transmission health policy Artemisinin combination therapy nongametocytocidal drugs malaria transmission predictive modeling public health impact antimalarial drugs transmission dynamics drug efficacy Artemisinin combination therapy nongametocytocidal drugs malaria transmission predictive models mathematical modeling public health drug efficacy parasite life cycle vector control Artemisinin combination therapy nongametocytocidal drugs malaria transmission mathematical modeling drug efficacy public health impact parasite lifecycle drug resistance vector control Artemisinin combination therapy nongametocytocidal drugs malaria transmission epidemiology public health drug efficacy disease modeling parasitology clinical trials vector control endemic regions global health treatment outcomes drug resistance health policy vector biology
94	Albendazole is used to treat lymphatic filariasis. Albendazole is used to treat lymphatic filariasis. Albendazole is used to treat lymphatic filariasis. Albendazole is used to treat lymphatic filariasis. Albendazole is used to treat lymphatic filariasis. lymphatic diseases filariasis treatment medication parasites drugs health medicine lymphatic_filariasis_treatment albendazole_dosage filariasis_prevention antifilarial_medications albendazole_side_effects albendazole lymphatic filariasis antiparasitic medication treatment disease tropical parasitic infection lymphatic filariasis treatment albendazole dosage albendazole side effects lymphatic filariasis prevention albendazole overdose filariasis symptoms albendazole effectiveness lymphatic filariasis causes albendazole lymphatic filariasis treatments medication parasitic infection tropical diseases lymphatic filariasis treatment albendazole dosage albendazole side effects lymphatic filariasis symptoms filariasis prevention antifilarial drugs albendazole dosage lymphatic filariasis filariasis infection albendazole filariasis treatment lymphatic filariasis lymphatic_filariasis treatment antihelminthic medication parasitic_infection drug_name health_care lymphatic_filariasis_treatment albendazole_medication worm_infestation_cure antifilarial_drug parasite_elimination albendazole lymphatic filariasis antiparasitic treatment drug parasitology helminthiasis public health lymphatic filariasis symptoms albendazole dosage albendazole side effects lymphatic filariasis treatment antifilarial drugs
99	Alizarin forms hydrogen bonds with residues involved in PGAM1 substrate binding. Alizarin forms hydrogen bonds with residues involved in PGAM1 substrate binding. Alizarin forms hydrogen bonds with residues involved in PGAM1 substrate binding. Alizarin forms hydrogen bonds with residues involved in PGAM1 substrate binding. Alizarin forms hydrogen bonds with residues involved in PGAM1 substrate binding. alizarin hydrogen bonds PGAM1 substrate binding residues protein interactions structural biology biochemistry alizarin hydrogen bonds PGAM1 substrate binding amino acid residues protein structure molecular interactions alizarin compounds hydrogen bonds PGAM1 protein substrate binding sites biochemistry terms molecular interactions alizarin molecules residue types ligand binding structural biology alizarin structure alizarin chemical properties alizarin hydrogen bonding PGAM1 protein PGAM1 substrate residues involved substrate binding mechanism molecular interactions biochemical processes structural biology protein-ligand interactions Alizarin hydrogen bonds PGAM1 substrate binding residues alizarin hydrogen bonds PGAM1 substrate binding residues protein structure drug binding site molecular interaction biochemical process alizarin hydrogen bonds PGAM1 substrate binding residue interactions structural biology biochemistry molecular recognition Alizarin hydrogen bonds PGAM1 substrate binding residues biochemistry molecular interactions Alizarin hydrogen bonds PGAM1 substrate binding protein interactions residue types alizarin structure hydrogen bond donors PGAM1 protein substrate recognition molecular interactions binding sites biochemical functions alizarin pigment residue types enzyme mechanisms
1197	The availability of safe places to study is not effective at decreasing homelessness. The availability of safe places to study is not effective at decreasing homelessness. The availability of safe places to study is not effective at decreasing homelessness. The availability of safe places to study is not effective at decreasing homelessness. The availability of safe places to study is not effective at decreasing homelessness. safe study spaces homelessness solutions educational accessibility affordable housing community centers public libraries safe zones shelter proximity learning environments poverty reduction safe study spaces homelessness reduction housing options educational accessibility urban planning community resources shelter availability student well-being policy impact social services safe study spaces homelessness prevention educational accessibility housing options community resources academic support urban planning public spaces poverty alleviation social services safe study spaces homeless prevention strategies community resources affordable housing options educational accessibility public space safety urban planning solutions after-school programs mental health support socioeconomic factors safe spaces homelessness prevention study environments affordable housing community centers educational resources public libraries urban planning social services inequality accessibility safe study spaces homelessness solutions community centers affordable housing student well-being public libraries urban planning educational resources socio-economic factors poverty reduction safe study spaces homeless reduction educational accessibility housing resources community centers libraries urban planning poverty alleviation social services public funding data analysis policy impact youth homelessness adult homelessness long-term solutions short-term interventions safe study spaces homelessness prevention community centers libraries educational accessibility housing resources urban planning social services public spaces poverty reduction youth shelters mental health support city development volunteer opportunities safe study spaces homelessness prevention community resources educational accessibility shelter proximity student well-being urban planning public spaces safety housing initiatives educational facilities location safe_spaces study_havens homelessness_prevention strategy effective_solutions education_access community_centers youth_shelters social_services urban_design public_policy
1196	The availability of safe places to study is effective at decreasing homelessness. The availability of safe places to study is effective at decreasing homelessness. The availability of safe places to study is effective at decreasing homelessness. The availability of safe places to study is effective at decreasing homelessness. The availability of safe places to study is effective at decreasing homelessness. safe study spaces homelessness prevention community resources educational accessibility shelter options learning environments housing solutions public spaces safety safe study spaces homeless prevention educational facilities community resources shelter access learning environments housing support academic success poverty reduction urban planning social services youth homelessness educational outcomes public policy inclusive education mental health economic development neighborhood stability literacy programs after-school programs safe study spaces homelessness prevention community learning centers affordable study areas youth shelters with study rooms educational housing options safe havens for students safe study spaces homeless prevention strategies community learning centers educational accessibility sheltered study areas reducing homelessness inclusive education environments safe harbor for students study environment impact academic resource centers safe study spaces homelessness prevention educational accessibility affordable housing community resources youth homelessness urban planning public libraries campus safety socioeconomic factors safe study spaces homelessness prevention community learning centers accessible study areas reducing homelessness educational resources shelter for students affordable study locations impact on homelessness study hub safety safe study spaces homeless reduction community learning centers affordable study areas youth shelters with study zones educational facilities in low-income areas safe study spaces homelessness prevention community learning centers educational shelters youth safe havens affordable study areas housing support services accessible study locations poverty reduction through education social welfare programs safe study spaces homeless reduction community learning centers educational accessibility shelter with study areas youth homelessness prevention affordable learning environments safe study spaces affordable housing community centers after-school programs educational resources urban planning public libraries poverty reduction youth shelters crime prevention
1194	The arm density of TatAd complexes is due to structural rearrangements within Class1 TatAd complexes such as the 'charge zipper mechanism'. The arm density of TatAd complexes is due to structural rearrangements within Class1 TatAd complexes such as the 'charge zipper mechanism'. The arm density of TatAd complexes is due to structural rearrangements within Class1 TatAd complexes such as the 'charge zipper mechanism'. The arm density of TatAd complexes is due to structural rearrangements within Class1 TatAd complexes such as the 'charge zipper mechanism'. The arm density of TatAd complexes is due to structural rearrangements within Class1 TatAd complexes such as the 'charge zipper mechanism'. TatAd complexes charge zipper mechanism structural rearrangements protein transport bacterial secretion class1 TatAd molecular dynamics electron microscopy proton motive force TatAd complexes charge zipper mechanism structural rearrangements protein transport bacterial Tat pathway membrane proteins molecular dynamics protein conformation ion transport Tat signal sequence protein translocation class1 Tat system membrane insertion protein folding bacterial secretion protein trafficking molecular biology techniques electron microscopy X-ray crystallography bioinformatics analysis Tat signal recognition TatAd complexes structural rearrangements charge zipper mechanism protein transport bacterial secretion molecular dynamics ion conductivity protein conformation translocation process TatAd complexes charge zipper mechanism structural rearrangements class1 TatAd protein transport bacterial secretion molecular dynamics cryo-electron microscopy Tat pathway membrane protein insertion TatAd complexes charge zipper mechanism structural rearrangements Class1 TatAd protein transport bacterial secretion molecular dynamics cryo-EM ion binding protein conformation TatAd complexes charge zipper mechanism structural rearrangements arm density Class1 TatAd complexes TatAd complexes charge zipper mechanism structural rearrangements protein transport bacterial secretion molecular dynamics ion conductance Tat pathway bacterial Tat system TatAd complexes charge zipper mechanism structural rearrangements Class1 TatAd protein transport bacterial secretion molecular dynamics ion channel energy coupling translocase complex TatAd complexes charge zipper mechanism structural rearrangements protein transport bacterial secretion Tat pathway ion coupling proton motive force TatAd complexes charge zipper mechanism structural rearrangements protein transport bacterial secretion molecular dynamics ion binding protein folding Tat pathway E.coli transport machinery
1191	The amount of publicly available DNA data doubles every 10 years. The amount of publicly available DNA data doubles every 10 years. The amount of publicly available DNA data doubles every 10 years. The amount of publicly available DNA data doubles every 10 years. The amount of publicly available DNA data doubles every 10 years. genetic data biotechnology growth pubmed genome sequence databases sequencing rate DNA storage genetic data growth biotechnology advancement genomic information expansion genetic sequencing increase bioinformatics trend public DNA database growth genetic information doubling genomics data rate DNA genetic sequencing biotechnology genomics data storage doubling trend analysis bioinformatics publicly available DNA data growth DNA data doubling time genetic data increase genomic data expansion biotechnology data trend DNA information doubling genetic research data growth DNA genomics biotechnology genetic_data exponential_growth bioinformatics publicly_available_data scientific_research genetic_information genomic_data DNA data growth genetic information expansion genomic data increase public DNA database exponential genetic data doubling time DNA genomic data proliferation DNA data growth genomic information increase genetic data exponential rise biogenetic data doubling time public genetic database expansion DNA data growth pUBLICLY AVAILABLE GENOME DATA GENOME DATA DOUBLING TEN YEAR DATA DOUBLING GROWTH RATE OF GENOMIC DATA DNA storage genetic data growth biotechnology trends genomic information doubling scientific data increase genetic sequencing advancements big data in genetics public DNA databases genetic data exponential growth genomic data doubling time DNA sequencing genomics genetic data bioinformatics genetic information molecular biology genetic databases genomic analysis genetic research biotechnology
880	Occupancy of ribosomes by IncRNAs mirror 5 0-UTRs Occupancy of ribosomes by IncRNAs mirror 5 0-UTRs Occupancy of ribosomes by IncRNAs mirror 5 0-UTRs Occupancy of ribosomes by IncRNAs mirror 5 0-UTRs Occupancy of ribosomes by IncRNAs mirror 5 0-UTRs IncRNAs function ribosomes 5' UTR mRNA translation effectiveness expansion terms search optimization mirroring biological mechanism IncRNAs ribosomes occupancy 5'UTRs mRNA transcription translation biology genetic regulation RNA biology molecular biology gene expression Ribosome occupancy IncRNAs 5'UTRs RNA binding translational regulation gene expression molecular biology transcriptomics ribosomal profiling occupancy ribosomes IncRNAs 5' UTRs mRNA translation regulation biology RNA genetic interaction molecular genetics bioinformatics expression transcriptomics sequencing biochemistry IncRNAs ribosomes occupancy mirror 5′-UTRs mRNA transcription translation genetic regulation bioinformatics omics data analysis cell biology microRNAs lncRNAs novel RNA ribosome occupancy IncRNAs 5'UTRs mRNA translation genetic regulation RNA binding molecular biology bioinformatics gene expression transcriptomics ribosome occupancy IncRNAs 5' UTRs mRNA translation RNA binding proteins gene expression transcriptomics molecular biology biotechnology genetic regulation Ribosome occupancy IncRNAs 5' UTRs mRNA translation gene expression RNA binding proteins molecular biology transcriptomics biotechnology genetic regulation ribosome occupancy IncRNAs 5' UTRs RNA binding transcriptional regulation molecular biology gene expression RNA structure biological markers IncRNAs ribosomes 5'UTRs mRNA synthesis transcription regulation biomarkers microRNAs translation eukaryotes nucleus expression
882	Omnivores produce less trimethylamine N-oxide from dietary I-carnitine than vegetarians. Omnivores produce less trimethylamine N-oxide from dietary I-carnitine than vegetarians. Omnivores produce less trimethylamine N-oxide from dietary I-carnitine than vegetarians. Omnivores produce less trimethylamine N-oxide from dietary I-carnitine than vegetarians. Omnivores produce less trimethylamine N-oxide from dietary I-carnitine than vegetarians. dietary I-carnitine omnivores vegetarians trimethylamine N-oxide metabolic differences gut microbiota dietary patterns nutrition science biochemistry health impacts dietary I-carnitine omnivores vegetarians trimethylamine N-oxide metabolic differences gut microbiome dietary patterns nutritional factors biomarkers dietary composition digestive processes dietary I-carnitine trimethylamine N-oxide omnivores vegetarians metabolism bacteria gut microbiome diet effect biological markers dietary I-carnitine omnivores versus vegetarians trimethylamine N-oxide production nutritional impact metabolic differences dietary habits health implications vegetarian diet omnivorous diet I-carnitine metabolism dietary I-carnitine omnivores vegetarians trimethylamine N-oxide metabolic differences gut microbiota nutritional impact dietary patterns dietary I-carnitine omnivores vegetarians trimethylamine N-oxide metabolic differences nutritional impact gut microbiome dietary habits biomarker analysis health implications dietary I-carnitine trimethylamine N-oxide omnivores vegetarians metabolism biomarker health nutrition study research dietary I-carnitine trimethylamine N-oxide omnivores vegetarians digestive process bioavailability carnitine metabolism food types diet impact metabolic differences dietary I-carnitine trimethylamine N-oxide omnivores vegetarians digestive process biochemistry food intake microbial metabolism intestinal bacteria metabolic differences health implications dietary I-carnitine omnivores vegetarians trimethylamine N-oxide gut microbiome metabolic differences nutritional impact bioavailability digestion dietary habits dietary composition
641	Insomnia can be effectively treated with cognitive behavioral therapy. Insomnia can be effectively treated with cognitive behavioral therapy. Insomnia can be effectively treated with cognitive behavioral therapy. Insomnia can be effectively treated with cognitive behavioral therapy. Insomnia can be effectively treated with cognitive behavioral therapy. sleeplessness cognitive interventions therapy strategies psychological treatment-Methods cognitive behavioral therapy treats insomnia sleep disorders mental health sleeping problems therapy effects sleeplessness cognitive interventions therapy strategies sleeping disorders treatment-Methods psychological cognitive behavioral therapy insomnia insomnia treatment methods insomnia cognitive behavioral therapy effectiveness cognitive behavioral therapy for insomnia symptoms insomnia management techniques cognitive behavioral therapy sleep disorders insomnia treatment effects population meta-analysis clinical cognitive therapy insomnia treatment behavioral techniques sleep disorders psychotherapy benefits insomnia treatment cognitive behavioral therapy sleep disorders psychology health mind body cognitive behavioral therapy insomnia treatment effective sleep disorders cognitive behavioral therapy treatment sleep disorders insomnia coping strategies psychology health management techniques cognitive behavioral therapy sleep disorders insomnia treatment strategies techniques management benefits
521	High-sensitivity cardiac troponin T (HSCT-T) dosage may not be diagnostic if the onset of symptoms occurs less than 3 hours before acute myocardial injury (AMI). High-sensitivity cardiac troponin T (HSCT-T) dosage may not be diagnostic if the onset of symptoms occurs less than 3 hours before acute myocardial injury (AMI). High-sensitivity cardiac troponin T (HSCT-T) dosage may not be diagnostic if the onset of symptoms occurs less than 3 hours before acute myocardial injury (AMI). High-sensitivity cardiac troponin T (HSCT-T) dosage may not be diagnostic if the onset of symptoms occurs less than 3 hours before acute myocardial injury (AMI). High-sensitivity cardiac troponin T (HSCT-T) dosage may not be diagnostic if the onset of symptoms occurs less than 3 hours before acute myocardial injury (AMI). high_sensitivity_cardiac_troponin_t hsct_t myocardial_injury am_i symptom_onset_time diagnostic_threshold cardiac_care troponin_levels acute_myocardial_injury time_to_diagnosis cardiac troponin T hsctt myocardial injury AMI symptoms dosage diagnostic time window high_sensitivity_cardiac_troponin_t hsct_t dosage acute_myocardial_injury ami symptoms onset_time diagnostic_value cardiac_troponin_test myocardial_injury_diagnosis time_window clinical_guidelines cardiac troponin hsct-t dosage symptoms onset acute myocardial injury ami time窗限 high_sensitivity_cardiac_troponin_T HSCT_T dosage diagnostic symptom_onset acute_myocardial_injury AMI time_window 3_hours cardiac troponin AMI dosage symptoms diagnostic time窗格 acute myocardial injury high-sensitivity cardiac troponin T 3 hours high_sensitivity_cardiac_troponin_T hsct_t myocardial_injury am_i symptom_onset diagnostic_test myocardial_injury_timeframe cardiac_marker troponin_levels early_myocardial_injury troponin_tassay high_sensitivity_cardiac_troponin_T HSCT_T dosage_guidelines acute_myocardial_injury AMI symptom_onset diagnostic_value time_window cardiac_care troponin_test heart_attack medical_diagnosis cardiac,troponin,T,dosage,AMI,symptoms,diagnosis,time窗口自动截断了内容，请稍简短重写或分词： 高敏心脏肌钙蛋白T,AMI,症状,诊断,时间窗,剂量 cardiac troponin AMI diagnosis dosage symptoms acute myocardial injury high-sensitivity clinical guidelines
644	Insulin increases risk of severe kidney failure. Insulin increases risk of severe kidney failure. Insulin increases risk of severe kidney failure. Insulin increases risk of severe kidney failure. Insulin increases risk of severe kidney failure. insulin kidney complications diabetes insulin kidney severe kidney disease diabetes insulin side effects kidneys diabetes mellitus kidney failure diabetes glucose nephropathy complications end-stagerenal hypertension treatment prevention epidemiology diabetes glucose pancreas complications end-stage dialysis treatment prevention studies symptoms insulin kidney disease insulin side effects kidneys insulin and renal failure risks of insulin therapy kidneys insulin impact on kidneys insulin kidney failure diabetes glucose glycemic control renal function complications end-stage renal disease metabolic syndrome hypertension proteinuria dialysis insulin resistance pancreatic beta cells nephropathy type 2 diabetes chronic kidney disease medication side effects glucose tolerance renal impairment search optimization keyword expansion health queries medical conditions kidney disease insulin side effects diabetes complications severe outcomes healthcare search medical research diabetes glycemic control kidney disease renal function glucose levels long-term complications metabolic syndrome insulin kidney failure risk factors insulin severe kidney complications diabetes insulin kidney health insulin treatment and kidney damage glucose control kidney function insulin dosage kidney impact type 2 diabetes kidney risk insulin side effects kidneys managing insulin to prevent kidney failure long-term insulin use kidney insulin diabetes insulin side effects insulin kidney disease severe kidney failure causes diabetes complications glycemic control impact insulin therapy risks diabetes glycemic control renal function insulin types long-term effects nephropathy glucose levels treatment options clinical studies prevention methods
887	Only a minority of cells survive development after differentiation into stress-resistant spores. Only a minority of cells survive development after differentiation into stress-resistant spores. Only a minority of cells survive development after differentiation into stress-resistant spores. Only a minority of cells survive development after differentiation into stress-resistant spores. Only a minority of cells survive development after differentiation into stress-resistant spores. cell survival stress resistance differentiation spores minority cells developmental biology microbial survival stressors microbial spores survival development differentiation stress-resistant spores minority cells cell survival differentiation process stress resistance spore formation minority cells developmental biology microbial survival cell survival stress resistance spore formation developmental biology minority cells survival rate differentiation process resilient spores cellular adaptation stress tolerance biological survival cell survival differentiation stress-resistant spores minority cells stress-resistant spores development cell survival rates differentiation process spore formation minority cells biological resilience cell survival differentiation process stress-resistant spores minority cells developmental biology microbial survival strategies cell survival differentiation process stress-resistant spores minority cells developmental biology microbial spores survival mechanisms environmental stress resistance cellular adaptation sporulation process cell survival differentiation stress resistance spores microbial development cell survival differentiation process stress resistance spore formation minority cells biological adaptation
525	Histone demethylase recruitment and a transient decrease in histone methylation is necessary for ligand-dependent induction of transcription by nuclear receptors. Histone demethylase recruitment and a transient decrease in histone methylation is necessary for ligand-dependent induction of transcription by nuclear receptors. Histone demethylase recruitment and a transient decrease in histone methylation is necessary for ligand-dependent induction of transcription by nuclear receptors. Histone demethylase recruitment and a transient decrease in histone methylation is necessary for ligand-dependent induction of transcription by nuclear receptors. Histone demethylase recruitment and a transient decrease in histone methylation is necessary for ligand-dependent induction of transcription by nuclear receptors. Histone demethylases nuclear receptors transcription induction ligand binding chromatin modification gene regulation epigenetics transient methylation changes histone demethylases nuclear receptors transcription induction ligand binding chromatin modification gene regulation epigenetics molecular biology histone methylation transcription factors histone demethylases nuclear receptors ligand-dependent activation transcription induction histone methylation dynamics chromatin remodeling gene expression regulation epigenetic modifications transcription factors epigenetics chromatin structure transcriptional activation DNA binding proteins epigenetic changes histone modification enzymes gene regulation mechanisms chromatin accessibility molecular biology epigenomic landscape histone lysine demethylases transcription initiation epigenetic inheritance epigenetic memory chromatin modification gene silencing epigenetic signaling chromatin fibers histone code histone demethylation Histone demethylase function nuclear receptor activation ligand-induced gene expression chromatin modification transcriptional regulation epigenetic changes histone methylation dynamics gene induction mechanism protein-DNA interaction epigenetics in transcription histone modification enzymes transcription factor binding chromatin remodeling epigenetic marks transcription initiation process Histone demethylases ligand-dependent transcription nuclear receptors histone methylation transcription induction chromatin modification gene regulation epigenetics transcription factors epigenetic modifiers ligand binding chromatin structure gene expression protein-DNA interaction Histone demethylase activity nuclear receptors ligand-dependent transcription histone methylation transcription induction pharmacological inhibition eukaryotic gene expression molecular mechanism chromatin modification Histone Ligand Nuclear receptors Transcription De methylation RNA binding proteins Molecular biology Epigenetics Gene regulation Signaling pathways Mechanisms DNA binding Histone demethylases nuclear receptors ligand-dependent transcription histone methylation timing of gene expression transcription factors chromatin modification histone demethylase ligand-dependent transcription nuclear receptors histone methylation gene regulation chromatin modification transcription factors epigenetics signaling pathway molecular biology epigenetic modifications histone modification nuclear receptor activation transcriptional regulation epigenetics ligand binding chromatin remodeling gene expression molecular biology epigenetic modifier DNA binding protein transcription factor activity
768	Mercaptopurine is anabolized into the inactive methylmercaptopurine by thiopurine methyltrasnferase (TPMT). Mercaptopurine is anabolized into the inactive methylmercaptopurine by thiopurine methyltrasnferase (TPMT). Mercaptopurine is anabolized into the inactive methylmercaptopurine by thiopurine methyltrasnferase (TPMT). Mercaptopurine is anabolized into the inactive methylmercaptopurine by thiopurine methyltrasnferase (TPMT). Mercaptopurine is anabolized into the inactive methylmercaptopurine by thiopurine methyltrasnferase (TPMT). Mercaptopurine anabolized inactive methylmercaptopurine thiopurine methyltransferase TPMT metabolism drug biochemistry pharmacology Mercaptopurine anabolism thiopurine methylmercaptopurine TPMT metabolism pharmacology biochemistry Mercaptopurine TPMT thiopurine methylmercaptopurine anabolism metabolism pharmacology drug metabolism enzyme activity Mercaptopurine metabolism TPMT function thiopurine methyltransferase anabolism pathways inactive metabolites drug metabolism enzymes Mercaptopurine TPMT thiopurine methyltrasnferase anabolism metabolism inactive metabolite methylmercaptopurine query expansion pharmacogenetics TPMT mercaptopurine metabolism anabolism drug metabolism enzyme activity therapeutic drugs genetic variation metabolic pathway Mercaptopurine TPMT thiopurine methyltrasnferase methylmercaptopurine anabolism drug metabolism Mercaptopurine anabolized methylmercaptopurine thiopurine methyltrasnferase TPMT metabolic pathway drug metabolism inactive metabolite mercaptopurine anabolism thiopurine methylmercaptopurine thiopurine methyltransferase TPMT drug metabolism Mercaptopurine metabolism TPMT activity thiopurine methyltransferase drug metabolism anabolism metabolic pathway inactive metabolites medication interactions pharmacogenomics therapeutic outcomes
527	Homozygous deletion of murine Sbds gene from osterix-expressing mesenchymal stem and progenitor cells (MPCs) prevents oxidative stress. Homozygous deletion of murine Sbds gene from osterix-expressing mesenchymal stem and progenitor cells (MPCs) prevents oxidative stress. Homozygous deletion of murine Sbds gene from osterix-expressing mesenchymal stem and progenitor cells (MPCs) prevents oxidative stress. Homozygous deletion of murine Sbds gene from osterix-expressing mesenchymal stem and progenitor cells (MPCs) prevents oxidative stress. Homozygous deletion of murine Sbds gene from osterix-expressing mesenchymal stem and progenitor cells (MPCs) prevents oxidative stress. Homozygous deletion murine Sbds gene osteogenesis mesenchymal stem cells progenitor cells ostérix oxidative stress molecular biology genetic modification cancer research cellular biology mouse models Homozygous deletion murine Sbds gene ostérix expressing mesenchymal stem cells progenitor cells MPCs prevents oxidative stress mouse model cell biology genetic modification stem cell research progenitor cells function osteogenesis apoptosis cellular senescence Homozygous deletion murine Sbds gene osteogenesis mesenchymal stem cells MPCs oxidative stress ostiogenesis impairment Sbds knockout stem cell research genetic deletion experiment cellular biology molecular genetics Homozygous deletion murine Sbds gene osterix-expressing mesenchymal stem cells progenitor cells MPCs prevents oxidative stress genetic modification cell biology molecular genetics stem cell research protein function gene expression cellular senescence DNA damage repair immunology oncology cardiovascular disease aging therapeutic targeting gene editing CRISPR biotechnology cellular metabolism Homozygous deletion murine Sbds gene osteix expressing mesenchymal stem cells progenitor cells oxidative stress mouse model molecular biology genetic modification stem cell research cell lineage biomedical science microbial genetics apoptosis cellular senescence Homozygous deletion murine Sbds gene osterix-expressing mesenchymal stem cells progenitor cells prevents oxidative stress gene knockout cellular biology genetic engineering stem cell research molecular biology biochemistry genetics cellular function oxidative damage DNA repair Sbds protein MPCs osteogenesis immunology pharmacology biotechnology scientific studies experimental design gene expression protein function cellular signaling DNA mutations cellular pathology genetic disorders genetic modification cellular response cellular metabolism Homozygous deletion murine Sbds gene osteogenesis mesenchymal stem cells progenitor cells MPCs oxidative stress osteriexpressing cells mouse model gene knockout cellular function stem cell biology genetic modification biomolecular research Homozygous deletion murine Sbds gene osteric-expressing mesenchymal stem cells progenitor cells MPCs prevents oxidative stress keyword expansion efficacy biological research molecular biology genetic modification stem cell research Homozygous deletion murine Sbds gene osteriexpressing mesenchymal stem progenitor cells MPCs oxidative stress genetic modification stem cell research progenitor cell biology cellular response genetic deletion experiments mouse models biological pathways apoptosis mitochondrial function Homozygous deletion murine Sbds gene osteriexpressing mesenchymal stem progenitor cells MPCs prevents oxidative stress biochemistry genetics molecular biology cellular function stem cell research oxidative stress mechanisms SBDS protein
528	Human T-lymphotropic virus type-I-associated myelopathy / tropical spastic paraparesis (HAM/TSP) patients produce Immunoglobulin G (IgG) antibodies which cross-react with an immunodominant epitope in Tax. Human T-lymphotropic virus type-I-associated myelopathy / tropical spastic paraparesis (HAM/TSP) patients produce Immunoglobulin G (IgG) antibodies which cross-react with an immunodominant epitope in Tax. Human T-lymphotropic virus type-I-associated myelopathy / tropical spastic paraparesis (HAM/TSP) patients produce Immunoglobulin G (IgG) antibodies which cross-react with an immunodominant epitope in Tax. Human T-lymphotropic virus type-I-associated myelopathy / tropical spastic paraparesis (HAM/TSP) patients produce Immunoglobulin G (IgG) antibodies which cross-react with an immunodominant epitope in Tax. Human T-lymphotropic virus type-I-associated myelopathy / tropical spastic paraparesis (HAM/TSP) patients produce Immunoglobulin G (IgG) antibodies which cross-react with an immunodominant epitope in Tax. Human_T_lymphotropic_virus HTLV-1 myelopathy tropical_spastic_paraparesis HAM/TSP Immunoglobulin_G IgG antibodies Tax_protein epitope immune_response HTLV_I neurological_disorders viral_infection immune_system viral_antigens Human T-lymphotropic virus HTLV-1 Tax protein immunodominant epitope IgG antibodies HAM/TSP neurological symptoms immune response antibody production viral proteins clinical manifestations Human T-lymphotropic virus type I HAM/TSP Immunoglobulin G antibodies Tax protein immunodominant epitope viral infection neurological symptoms immune response virology immunology clinical symptoms Human T-lymphotropic virus type I HAM/TSP diagnosis IgG antibodies production Tax protein immunodominant epitope virus-induced neurological disorders virology research neuroimmunology antibody cross-reaction viral latency markers Human T-lymphotropic virus type-I HAM/TSP immunoglobulin G antibodies Tax protein epitope cross-reactivity neurological disorder viral infection immune response Human T-lymphotropic virus type 1 HAM/TSP Tax protein IgG antibodies epitope recognition viral infection neurological symptoms diagnostic markers antibody production viral latency immune response virology research neuroimmunology Human T-lymphotropic virus HTLV-1 myelopathy tropical spastic paraparesis HAM/TSP Immunoglobulin G IgG antibodies Tax protein immunodominant epitope immune response viral infection neurology virology autoimmune reaction Human T-lymphotropic virus type-I HAM/TSP immunoglobulin G antibodies Tax protein immunodominant epitope cross-reaction Human T-lymphotropic virus type I HAM/TSP IgG antibodies Tax protein immunodominant epitope viral infection neurological disorder antibody production viral antigen immune response viral proteins Tax protein immune response cross-reactivity neurological symptoms HAM/TSP diagnosis antibody production viral epitopes immunoglobulin subclasses
649	Integrating classroom-based collaborative learning with Web-based collaborative learning leads to subpar class performance Integrating classroom-based collaborative learning with Web-based collaborative learning leads to subpar class performance Integrating classroom-based collaborative learning with Web-based collaborative learning leads to subpar class performance Integrating classroom-based collaborative learning with Web-based collaborative learning leads to subpar class performance Integrating classroom-based collaborative learning with Web-based collaborative learning leads to subpar class performance collaborative learning methods web-based learning classroom performance blended learning educational technology student engagement online collaboration tools face-to-face interaction digital literacy learning outcomes technology integration instructional strategies e-learning platforms hybrid learning environments classroom collaboration web-based collaboration blended learning student performance educational technology learning outcomes digital tools interactive learning online collaboration face-to-face interaction collaborative learning strategies web-based collaboration classroom effectiveness blended learning approaches student engagement technology integration educational outcomes online collaboration tools hybrid learning methods learning management systems digital collaboration platforms collaborative learning benefits web-based learning classroom integration student engagement technology in education learning outcomes online collaboration tools blended learning methods educational effectiveness group dynamics online collaborative learning web-based learning classroom performance technology integration student engagement online platforms blended learning educational outcomes group dynamics digital tools collaborative learning benefits web integration e-learning effectiveness classroom dynamics student engagement online collaboration tools hybrid learning learning outcomes technological integration pedagogical strategies collaborative learning strategies web-based tools classroom activities student engagement performance metrics technology integration educational outcomes collaborative learning strategies web-based learning classroom integration educational technology student engagement performance metrics online collaboration tools hybrid learning environments blended learning digital literacy skills classroom collaboration web-based learning hybrid learning student engagement performance metrics educational technology learning outcomes blended learning online collaboration tools face-to-face interaction digital divide educational effectiveness pedagogical strategies classroom collaboration web-based collaboration blended learning student engagement performance metrics technology integration educational outcomes online discussion forums hybrid learning environments collaborative tools learning management systems
1088	Silencing of Bcl2 is important for the maintenance and progression of tumors. Silencing of Bcl2 is important for the maintenance and progression of tumors. Silencing of Bcl2 is important for the maintenance and progression of tumors. Silencing of Bcl2 is important for the maintenance and progression of tumors. Silencing of Bcl2 is important for the maintenance and progression of tumors. Bcl2 inhibition tumor suppression cancer therapy molecular biology oncology Bcl2 protein function tumor growth regulation survivin Bcl2 family members cancer cell survival apoptosis regulation Bcl2 gene expression tumor suppression apoptosis regulation cancer biology oncology research Bcl2 inhibition tumor suppression molecular biology cancer therapy apoptosis regulation ONCOGENE BCL2 anti-apoptotic proteins treatment strategies cell death mechanisms Bcl2 inhibition cancer treatment tumor suppression apoptosis induction oncology research therapeutic targets cancer biology cell death mechanisms anti-tumor effects Bcl2 protein function treatment therapy molecular biology apoptosis cancer research genetic modification cell survival anti-apoptotic factor tumor抑制因子 oncology apoptosis regulation cancer therapy gene silencing techniques Bcl2 inhibition tumor suppression molecular targeting apoptosis induction cancer therapy anti-Bcl2 drugs Bcl2 protein expression Bcl2 inhibition tumor suppression cancer therapy apoptosis induction oncogene regulation cell survival cancer biology gene expression cancer biology apoptosis oncology gene silencing tumor suppression Bcl-2 protein cell death molecular mechanisms cancer therapy genetic regulation Bcl2 gene tumor suppression apoptosis regulation oncology research cancer therapy molecular biology tumor growth genetic modification chemotherapy resistance cell survival Bcl2 inhibition tumor suppression molecular therapy cancer treatment apoptosis induction anti-tumor effect Bcl2 protein Bcl2 overexpression tumor growth regulation
1086	Sildenafil improves erectile function in men who experience sexual dysfunction as a result of the use of SSRI antidepressants. Sildenafil improves erectile function in men who experience sexual dysfunction as a result of the use of SSRI antidepressants. Sildenafil improves erectile function in men who experience sexual dysfunction as a result of the use of SSRI antidepressants. Sildenafil improves erectile function in men who experience sexual dysfunction as a result of the use of SSRI antidepressants. Sildenafil improves erectile function in men who experience sexual dysfunction as a result of the use of SSRI antidepressants. sildenafil erectile function SSRI antidepressants sexual dysfunction treatment interaction side effects Sildenafil SSRI antidepressants sexual dysfunction erectile function male sexuality pharmacology treatment options drug interaction ED management antidepressant side effects sildenafil SSRI sexual dysfunction erectile function men antidepressants drug interaction viagrɑ priɑgra tadalafil sildenafil SSRIs sexual dysfunction sildenafil alternative to SSRIs SSRI-induced erectile dysfunction PDE5 inhibitors for SSRI users sildenafil effectiveness on SSRI side effects ED treatment with SSRIs sildenafil vs other ED treatments managing SSRI-related ED SSRI and erectile dysfunction solutions Sildenafil SSRI antidepressants erectile dysfunction sexual health pharmacology pharmaceuticals sexual performance male sexual function drug interactions Sildenafil SSRI antidepressants erectile dysfunction sexual health ED treatment antidepressant side effects male sexuality pharmaceuticals sexual performance medication interactions Sildenafil SSRI antidepressants sexual dysfunction erectile function improvement pharmacotherapy drug interaction vasodilation 勃起功能障碍 抗抑郁药影响 Sildenafil SSRI antidepressants sexual dysfunction erectile function improvement pharmacological intervention sexual health medication interaction male sexual dysfunction PDE5 inhibitors antidepressant side effects sildenafil erectile function SSRI antidepressants sexual dysfunction treatment mechanism effectiveness clinical trials interactions dosage recommendations SSRIs antidepressants side effects erectile dysfunction treatments Sildenafil alternatives sexual health medications
770	Metastatic colorectal cancer treated with a single agent fluoropyrimidines resulted in reduced efficacy and lower quality of life when compared with oxaliplatin-based chemotherapy in elderly patients. Metastatic colorectal cancer treated with a single agent fluoropyrimidines resulted in reduced efficacy and lower quality of life when compared with oxaliplatin-based chemotherapy in elderly patients. Metastatic colorectal cancer treated with a single agent fluoropyrimidines resulted in reduced efficacy and lower quality of life when compared with oxaliplatin-based chemotherapy in elderly patients. Metastatic colorectal cancer treated with a single agent fluoropyrimidines resulted in reduced efficacy and lower quality of life when compared with oxaliplatin-based chemotherapy in elderly patients. Metastatic colorectal cancer treated with a single agent fluoropyrimidines resulted in reduced efficacy and lower quality of life when compared with oxaliplatin-based chemotherapy in elderly patients. elderly patients metastatic colorectal cancer fluoropyrimidines oxaliplatin chemotherapy quality of life treatment efficacy elderly patients metastatic colorectal cancer fluoropyrimidines oxaliplatin chemotherapy quality of life treatment efficacy elderly patients metastatic colorectal cancer fluoropyrimidines oxaliplatin-based chemotherapy efficacy quality of life treatment outcomes comparative analysis oncology clinical trials elderly patients metastatic colorectal cancer fluoropyrimidines efficacy oxaliplatin-based chemotherapy benefits quality of life elderly metastatic colorectal single agent treatment outcomes comparative chemotherapy effectiveness elderly metastatic colorectal cancer treatment options chemotherapy side effects elderly patients metastatic colorectal cancer fluoropyrimidines oxaliplatin elderly patients efficacy quality life chemotherapy single agent metastatic colorectal cancer fluoropyrimidines oxaliplatin elderly patients efficacy quality life chemotherapy recommendation phrases search performance elevate metastatic colorectal cancer fluoropyrimidines oxaliplatin elderly patients efficacy quality life chemotherapy benefit risk single agent treatment outcome metastatic colorectal cancer fluoropyrimidines oxaliplatin elderly patients efficacy quality of life chemotherapy comparison beneficial expansion keywords metastatic colorectal cancer fluoropyrimidines oxaliplatin elderly patients efficacy quality of life chemotherapy single agent comparative study clinical trials survival risk factors population ageing disease stage treatment outcomes meta-analysis review systematic therapy histological types biomarkers prognosis randomized controlled trials RCT side effects dosage regimen adverse reactions pharmacokinetics pharmacodynamics elderly patients metastatic colorectal cancer fluoropyrimidines oxaliplatin-based chemotherapy efficacy quality of life treatment outcomes cancer therapy age-related factors
410	Febrile seizures increase the threshold for development of epilepsy. Febrile seizures increase the threshold for development of epilepsy. Febrile seizures increase the threshold for development of epilepsy. Febrile seizures increase the threshold for development of epilepsy. Febrile seizures increase the threshold for development of epilepsy. febrile seizures epilepsy threshold development risk factors pediatric neurological disorders seizure types brain function genetic predisposition neurodevelopment fever management seizure frequency long-term outcomes febrile seizures epilepsy threshold childhood seizures neurological disorders seizure threshold epilepsy risk febrile seizure epilepsy long-term outcomes pediatric epilepsy febrile seizures epilepsy seizure threshold pediatric epilepsy fever-induced seizures neurological disorders brain development seizure disorders pediatric neurology long-term outcomes febrile seizures epilepsy risk factors febrile seizures and long-term outcomes febrile seizure incidence epilepsy febrile seizures vs epilepsy febrile seizure diagnosis epilepsy febrile seizures and neurological disorders febrile seizures and genetic predisposition febrile seizures and brain development febrile seizures and pediatric epilepsy febrile seizures treatment epilepsy prevention febrile seizures epilepsy seizure threshold childhood seizures fever-induced seizures long-term epilepsy risk seizure triggers pediatric epilepsy febrile seizures epilepsy risk factors febrile seizures and long-term outcomes seizure threshold epilepsy development febrile seizures vs epilepsy fever-induced seizures epilepsy connection febrile seizure prevention epilepsy childhood febrile seizures epilepsy link febrile seizures epilepsy seizure threshold pediatric seizures neurological disorders brain development fever-induced seizures epilepsy risk seizure triggers neurodevelopmental disorders febrile seizures epilepsy threshold developmental risk seizure types pediatric epilepsy fever-induced seizures neurological disorders seizure thresholds childhood febrile seizures long-term epilepsy risk seizure threshold elevation seizure management fever and seizures febrile seizures epilepsy seizure threshold childhood seizures long-term epilepsy risk fever-induced seizures neurological conditions pediatric epilepsy brain development seizure frequency genetic factors fever management seizure prevention neurodevelopmental disorders febrile seizures epilepsy risk factors pediatric seizures neurological disorders seizure threshold long-term prognosis brain development genetic predisposition seizure frequency
411	Febrile seizures reduce the threshold for development of epilepsy. Febrile seizures reduce the threshold for development of epilepsy. Febrile seizures reduce the threshold for development of epilepsy. Febrile seizures reduce the threshold for development of epilepsy. Febrile seizures reduce the threshold for development of epilepsy. febrile seizures epilepsy seizure threshold fever neurological disorders pediatric seizures brain function inflammation genetic factors brain development seizure triggers febrile seizures epilepsy threshold development risk factors pediatric brain neurological seizures epilepsy association fever childhood seizure threshold febrile seizures epilepsy seizure threshold pediatric seizures fever-induced seizures brain development neurological disorders childhood seizures seizure risk factors epilepsy prevention febrile seizures epilepsy risk factors febrile seizures and brain development genetic predisposition febrile seizures febrile seizures seizure threshold early febrile seizures epilepsy connection febrile seizures long-term effects fever-induced seizures and epilepsy febrile seizures neurodevelopmental outcomes febrile seizures and future epilepsy role of fever in epilepsy development febrile seizures epilepsy seizure threshold pediatric epilepsy brain development fever neurological disorders genetic factors brain inflammation seizure duration fever management pediatric seizures febrile seizures epilepsy risk factors febrile seizures and brain development fever-induced seizures early onset epilepsy seizure types in children fever and epilepsy risk febrile seizures severity pediatric epilepsy risk seizure threshold lowering fever seizure triggers febrile seizures epilepsy seizure threshold pediatric seizures neurological disorders brain development fever childhood seizures epilepsy risk seizure triggers febrile seizures epilepsy seizure threshold neurological disorders pediatric seizures brain development seizure triggers epilepsy risk fever-induced seizures febrile seizures epilepsy seizure threshold developmental epilepsy febrile illness brain development neurology pediatric seizures seizure disorders neurological conditions febrile seizures epilepsy seizure threshold pediatric epilepsy febrile illness neurological disorders brain development seizure types risk factors long-term outcomes
532	Hyperfibrinogenemia decreases rates of femoropopliteal bypass thrombosis. Hyperfibrinogenemia decreases rates of femoropopliteal bypass thrombosis. Hyperfibrinogenemia decreases rates of femoropopliteal bypass thrombosis. Hyperfibrinogenemia decreases rates of femoropopliteal bypass thrombosis. Hyperfibrinogenemia decreases rates of femoropopliteal bypass thrombosis. hyperfibrinogenemia thrombosis femoropopliteal bypass fibrinogen clotting surgery blood flow vascular treatment prevention risk factor condition management hyperfibrinogenemia thrombosis femoropopliteal bypass clinical trial treatment outcome blood clot vascular surgery cardiovascular anticoagulation risk factor prevention hyperfibrinogenemia thrombosis femoropopliteal bypass clotting factor genetics treatment outcomes prevention vascular surgery clinical studies incidence risk factors management hyperfibrinogenemia treatment hyperfibrinogenemia management hyperfibrinogenemia symptoms hyperfibrinogenemia causes hyperfibrinogenemia diagnosis hyperfibrinogenemia complications hyperfibrinogenemia risk factors hyperfibrinogenemia prevention hyperfibrinogenemia patient outcomes femoropopliteal bypass surgery femoropopliteal bypass thrombosis femoropopliteal bypass procedures femoropopliteal bypass complications thrombosis prevention thrombosis treatment thrombosis management hyper hyperfibrinogenemia thrombosis femoropopliteal bypass fibrinogen blood clotting vascular surgery clinical trials treatment outcomes risk factors Hyperfibrinogenemia treatment hyperfibrinogenemia benefits fibrinogen levels femoropopliteal bypass surgery thrombosis prevention hyperfibrinogenemia risk fibrinolytic therapy blood clot formation vascular surgery hyperfibrinogenemia management hyperfibrinogenemia thrombosis femoropopliteal bypass fibrinogen blood clotting vascular surgery clinical trial treatment effectiveness hyperfibrinogenemia thrombosis femoropopliteal bypass beneficial keywords efficacy vascular surgery clot prevention blood coagulation fibrinogen levels hyperfibrinogenemia thrombosis femoropopliteal bypass fibrinogen blood clotting vascular surgery treatment outcomes thromboembolism cardiovascular disease clot formation anticoagulation therapy blood thinners clinical trials patient prognosis hyperfibrinogenemia treatments thrombosis prevention femoropopliteal surgery blood clot reduction fibrinogen levels vascular procedures clinical outcomes surgical risks thrombolytic therapy anticoagulation management
533	Hyperfibrinogenemia increases rates of femoropopliteal bypass thrombosis. Hyperfibrinogenemia increases rates of femoropopliteal bypass thrombosis. Hyperfibrinogenemia increases rates of femoropopliteal bypass thrombosis. Hyperfibrinogenemia increases rates of femoropopliteal bypass thrombosis. Hyperfibrinogenemia increases rates of femoropopliteal bypass thrombosis. hyperfibrinogenemia thrombosis femoropopliteal bypass clotting risk factors treatment diagnosis hyperfibrinogenemia thrombosis femoropopliteal bypass clinical risk factor studies treatment outcomes diagnosis hyperfibrinogenemia thrombosis femoropopliteal bypass clotting factor blood viscosity treatment prevention risk analysis hyperfibrinogenemia treatment hyperfibrinogenemia diagnosis hyperfibrinogenemia symptoms hyperfibrinogenemia risk factors femoropopliteal bypass complications thrombosis prevention thrombosis management hyperfibrinogenemia prevalence hyperfibrinogenemia causes femoropopliteal bypass surgery hyperfibrinogenemia thrombosis femoropopliteal bypass clotting factors blood coagulation vascular surgery clinical outcomes diagnostic markers treatment options preventive measures femoropopliteal bypass complications hyperfibrinogenemia treatment thrombosis risk factors vascular surgery outcomes blood clot prevention fibrinogen levels impact surgical procedures complications hyperfibrinogenemia thrombosis femoropopliteal bypass clotting factors blood coagulation vascular surgery cardiovascular risk fibrinogen levels thromboembolism vascular diseases hemostasis hyperfibrinogenemia thrombosis femoropopliteal bypass blood clotting fibrinogen levels vascular surgery cardiovascular disease clot risk factors hypercoagulability hyperfibrinogenemia thrombosis femoropopliteal bypass clot formation vascular surgery blood coagulation fibrinogen levels cardiovascular risk surgical complications thromboembolism vascular disease hypercoagulability medical conditions treatment outcomes hyperfibrinogenemia treatment hyperfibrinogenemia management femoropopliteal bypass thrombosis prevention thrombosis risk factors hyperfibrinogenemia symptoms hyperfibrinogenemia diagnosis hyperfibrinogenemia complications thrombosis incidence vascular surgery
775	Mice defective for deoxyribonucleic acid (DNA) polymerase I (polI) reveal increased sensitivity to ionizing radiation (IR). Mice defective for deoxyribonucleic acid (DNA) polymerase I (polI) reveal increased sensitivity to ionizing radiation (IR). Mice defective for deoxyribonucleic acid (DNA) polymerase I (polI) reveal increased sensitivity to ionizing radiation (IR). Mice defective for deoxyribonucleic acid (DNA) polymerase I (polI) reveal increased sensitivity to ionizing radiation (IR). Mice defective for deoxyribonucleic acid (DNA) polymerase I (polI) reveal increased sensitivity to ionizing radiation (IR). DNA repair mouse model Ionizing radiation single-strand breaks POLI DNA damage response mice DNA polI sensitivity ionizing radiation genetics molecular biology cancer biology radiobiology mutagenesis radioresistance mice DNA polI sensitivity ionizing radiation genetics molecular biology biological response radiation sensitivity mouse models DNA repair DNA polymerase I polI deficiency ionizing radiation sensitivity mice model genetic mutation DNA repair radiation biology genotoxicity cell survival biomolecular research radiation response mice DNA polI sensitivity ionizing radiation molecular biology research model organisms genomics radiobiology DNA polymerase I polI mice ionizing radiation IR genetic defect radiation sensitivity DNA repair genomic instability gene knockout radiation biology DNA polymerase I polI mice ionizing radiation IR genetic defect DNA repair radiation sensitivity genomics molecular biology genetics radiobiology DNA polymerase I polI mice ionizing radiation IR genetic defect radiosensitivity DNA repair gene function radiation biology mice DNA polI sensitivity ionizing radiation molecular biochemistry cancer genetics radiobiology genome stability mutagenesis homologous recombination cell damagerepair mice DNA polymerase I polI sensitivity ionizing radiation genetic models molecular biology cancer susceptibility radiotherapy response cellular repair mechanisms
1199	The benefits of colchicine were achieved with effective widespread use of secondary prevention strategies such as high-dose statins. The benefits of colchicine were achieved with effective widespread use of secondary prevention strategies such as high-dose statins. The benefits of colchicine were achieved with effective widespread use of secondary prevention strategies such as high-dose statins. The benefits of colchicine were achieved with effective widespread use of secondary prevention strategies such as high-dose statins. The benefits of colchicine were achieved with effective widespread use of secondary prevention strategies such as high-dose statins. colchicine benefits secondary prevention strategies high-dose statins widespread use cardiovascular health cholesterol management risk reduction clinical outcomes treatment efficacy colchicine benefits secondary prevention strategies high-dose statins widespread use cardiovascular health cholesterol management clinical outcomes pharmacological interventions colchicine therapy secondary prevention high-dose statins cardiovascular benefits cholesterol management inflammatory reduction clinical trials treatment efficacy colchicine therapy secondary prevention strategies high-dose statins cardiovascular benefits reducing inflammation cholesterol management preventative medicine long-term health outcomes colchicine treatment lipid-lowering drugs colchicine secondary prevention strategies high-dose statins benefits disease management cardiovascular risk reducing inflammation colchicine benefits secondary prevention strategies high-dose statins widespread use cardiovascular health inflammation reduction gout treatment clinical outcomes colchicine benefits secondary prevention high-dose statins widespread use cardiovascular health cholesterol reduction clinical trials risk management pharmacotherapy inflammatory response colchicine benefits secondary prevention strategies high-dose statins widespread use cardiovascular health inflammation reduction gout treatment cholesterol management clinical trials risk reduction therapeutic efficacy colchicine therapy secondary prevention high-dose statins cardiovascular benefits lipid management inflammatory response clinical outcomes pharmacotherapy preventative care treatment efficacy colchicine therapy secondary prevention high-dose statins cardiovascular risk reduction inflammation control clinical trial outcomes lipid management arterial plaque stabilization
535	Hypertension is frequently observed in type 1 diabetes patients. Hypertension is frequently observed in type 1 diabetes patients. Hypertension is frequently observed in type 1 diabetes patients. Hypertension is frequently observed in type 1 diabetes patients. Hypertension is frequently observed in type 1 diabetes patients. Hypertension type 1 diabetes comorbidity cardiovascular risk blood pressure insulin resistance kidney disease complications management treatment prevalence hypertension type1diabetes comorbidities renaldisease cardiovasculardisease insulinresistance glycemiccontrol hormonalimbalances hypertension type1diabetes cardiovascularrisk glucosecontrol insulintherapy kidneyfailure hypertensionmanagement comorbidities diabeticnephropathy bloodpressure监测 hypertension complications type 1 diabetes management blood pressure control diabetes hypertension risk treatment options hypertension diabetes hypertension and insulin resistance diabetes patient monitoring cardiovascular risks diabetes hypertension hypertension prevention strategies diabetes and high blood pressure Hypertension type 1 diabetes comorbidities risk factors clinical symptoms prevalence management treatment complications Hypertension type 1 diabetes complications hypertension management in diabetes diabetes and blood pressure type 1 diabetes cardiovascular risk hypertension treatment plans diabetes hypertension symptoms hypertension prevention in diabetes hypertension type 1 diabetes comorbidity blood pressure cardiovascular risk glucose control kidney complications hypertension type 1 diabetes comorbidity blood pressure cardiovascular risk glucose control renal function complications treatment management prevalence symptoms hypertension type1diabetes comorbidities cardiovascularrisk frequentassociation clinicaloutcomes Hypertension type 1 diabetes complications hypertension management type 1 diabetes diabetes mellitus type 1 hypertension risk hypertension treatment type 1 diabetes comorbidities hypertension type 1 diabetes
415	Female carriers of the Apolipoprotein E4 (APOE4) allele have increased risk for dementia. Female carriers of the Apolipoprotein E4 (APOE4) allele have increased risk for dementia. Female carriers of the Apolipoprotein E4 (APOE4) allele have increased risk for dementia. Female carriers of the Apolipoprotein E4 (APOE4) allele have increased risk for dementia. Female carriers of the Apolipoprotein E4 (APOE4) allele have increased risk for dementia. ApoE4 dementia risk female genetics Alzheimer's cognitive decline brain health genetic predisposition Apolipoprotein E4 APOE4 allele female dementia risk female carriers dementia genetics genetic predisposition Alzheimer's disease APOE4 dementia symptoms genetic factors neurodegeneration ApoE4 dementia female risk factors genetics neurodegeneration alzheimer symptoms prevalence association studies research 流行病学 干预措施 Apolipoprotein E4 genetic risk female dementia risk factors APOE4 and cognitive decline genetic predisposition to dementia APOE4 carriers dementia prevention in APOE4 carriers APOE4 and Alzheimer's disease genetic testing for APOE4 APOE4 and brain health APOE4 mutation impact ApoE4 dementia risk female genetics neurodegeneration alzheimer biomarkers epidemiology symptoms prevention therapy ApoE4 dementia risk female genetics research biomarkers neurodegeneration molecular biology genomic studies ApoE4 dementia female risk factors genetics neurodegeneration aging haplotype susceptibility Alzheimer's disease ApoE4 dementia female risk factors genetics alzheimer carrier increased susceptibility Apolipoprotein E4 dementia risk factors genetic population studies female carriers neurodegeneration alzheimer's disease ApoE4 dementia female risk factors genetics neurodegeneration age alzheimer's disease vascular dementia
536	Hypocretin neurones induce panicprone state in rats. Hypocretin neurones induce panicprone state in rats. Hypocretin neurones induce panicprone state in rats. Hypocretin neurones induce panicprone state in rats. Hypocretin neurones induce panicprone state in rats. Hypocretin orexin anxiety stress rats neurobiology panic neurotransmitters sleep behavior corticotropin adrenocorticotropic hormone Hypocretin neurons panic-prone rats neurobiology anxiety sleep orexin stress behavior neurotransmitters Hypocretin neuroneurons panic-prone rats stress anxiety sleep orexin neurobiology neuroscience behavior physiology Hypocretin function panic-prone behavior rat study neurochemical response stress reaction sleep deprivation anxiety levels neurotransmitter role panic disorder models brain arousal systems Hypocretin panicprone rats neurobiology fear anxiety sleep dreaming stress neuroscience neurotransmitters hypocretin panic rats neuroscience anxiety neurochemistry behavior sleep stress brain corticotropin releasing hormone Hypocretin neurobiology panic-prone rats stress anxiety sleep neurotransmitters brain behavior neuroscience Hypocretin neurobiology panic rats stress anxiety neuroscience neurochemicals hypocretin neurons panic-prone rats stress anxiety neuroscience neurobiology neurotransmitters sleep depression corticotropin-releasing hormone Hypocretin receptors anxiety fear responses rodent models stress neurobiology neurotransmitters panic disorders brain mechanisms neuroimaging genetic factors behavioral tests cortisol levels sleep deprivation conditioned fear reward system
659	Ivermectin is used to treat lymphatic filariasis. Ivermectin is used to treat lymphatic filariasis. Ivermectin is used to treat lymphatic filariasis. Ivermectin is used to treat lymphatic filariasis. Ivermectin is used to treat lymphatic filariasis. ivermectin treatment lymphatic filariasis management antiparasitic drugs filarial infection therapy public health treatment ivermectin treatment lymphatic filariasis management filariasis cure antiparasitic drugs ivermectin dosage ivermectin treatments lymphatic filariasis symptoms ivermectin dosage filariasis prevention ivermectin side effects lymphatic filariasis causes ivermectin efficacy filariasis prevalence ivermectin administration lymphatic filariasis cure ivermectin treatments ivermectin dosage ivermectin side effects ivermectin for scabies ivermectin resistance Ivermectin lymphatic filariasis parasitic infection treatment dosage efficacy side effects public health malaria onchocerciasis ivermectin lymphatic filariasis treatment ivermectin side effects ivermectin dosage lymphatic filariasis ivermectin resistance ivermectin effectiveness ivermectin alternative treatments ivermectin medication safety ivermectin clinical trials ivermectin lymphatic filariasis treatment medication parasitic infection efficacy dosage side effects Ivermectin lymphatic filariasis treatment antiparasitic drugs malaria prevention onchocerciasis scabies treatment parasitic infections tropical diseases public health vector control medication efficacy ivermectin treatment lymphatic filariasis symptoms ivermectin dosage ivermectin side effects lymphatic filariasis prevention ivermectin for onchocerciasis public health ivermectin ivermectin efficacy ivermectin treatments ivermectin dosage lymphatic filariasis symptoms lymphatic filariasis stages ivermectin side effects
539	Hypoglycemia increases the risk of dementia. Hypoglycemia increases the risk of dementia. Hypoglycemia increases the risk of dementia. Hypoglycemia increases the risk of dementia. Hypoglycemia increases the risk of dementia. hypoglycemia dementia risk factors study evidence association diabetes neurodegeneration hypoglycemia dementia risk factors association research studies diabetes glycemic控制 levels neurological impacts elderly prevalence complications management treatment prevention mechanisms clinical observations hypoglycemia dementia risk factors study evidence association diabetes age severity treatment hypoglycemia dementia prevention hypoglycemia and cognitive decline glucose levels and dementia low blood sugar dementia risk managing hypoglycemia to reduce dementia hypoglycemia severity dementia connection diabetes control and dementia long-term hypoglycemia dementia link intermittent hypoglycemia and brain health hypoglycemia duration and dementia risk hypoglycemia dementia risk factors diabetes glucose neurodegeneration cardiovascular metabolic symptoms prevention treatment association research study clinical evidence hypoglycemia dementia risk factors hypoglycemia and cognitive decline glucose levels and dementia low blood sugar dementia connection managing hypoglycemia to prevent dementia hypoglycemia severity and dementia chronic hypoglycemia dementia link diabetes hypoglycemia dementia relationship hypoglycemia dementia risk factors study evidence association diabetes glucoselevels brainfunction aging neurodegeneration cardiovascularhealth metabolicsyndrome hypoglycemia dementia risk factors diabetes neurodegeneration glucose memory impairment cognitive decline age symptoms prevention treatment links beneficial expansions search terms medical research clinical studies hypoglycemia dementia risk factors association research studies diabetes glucose age neurodegeneration mortality hypoglycemia dementia diabetes memory impairment neurodegeneration glucose levels cardiovascular disease stroke alzheimer's disease
1099	Statins decrease blood cholesterol. Statins decrease blood cholesterol. Statins decrease blood cholesterol. Statins decrease blood cholesterol. Statins decrease blood cholesterol. statins blood cholesterol lowering lipid metabolism dyslipidemia hypolipidemic molecules atherosclerosis statins blood cholesterol reduce lower health effects benefits risk disease medications dosage facts sides statins blood cholesterol medicine treatment lowering health cardiovascular disease population prescription side effects Statins side effects statins benefits how statins work statins dosage statins diet interaction Statins blood cholesterol lowering effects health benefits risk heart disease medicine population studies research statin benefits cholesterol levels heart health lipid management side effects statin types dietary changes exercise impact cardiovascular disease prevention statins blood cholesterol lowering molecules health treatment medications diet effectiveness Statins cholesterol cardiovascular health benefits side effects lipid management prevention medication statins blood cholesterol health effectiveness medication diet side effects population prevention statin benefits cholesterol management lipid-lowering drugs cardiovascular risk reduction side effects statins
660	Ivermectin is used to treat onchocerciasis. Ivermectin is used to treat onchocerciasis. Ivermectin is used to treat onchocerciasis. Ivermectin is used to treat onchocerciasis. Ivermectin is used to treat onchocerciasis. Ivermectin onchocerciasis river blindness parasitic treatment antiparasitic drugs ivermectin treatment onchocerciasis management anti-parasitic drugs malaria prevention tropical diseases public health drug efficacy ivermectin treatment onchocerciasis medication anti-parasitic drugs tropical diseases skin conditions eye health public health ivermectin treatment onchocerciasis symptoms ivermectin dosage ivermectin side effects onchocerciasis transmission ivermectin administration ivermectin resistance ivermectin efficacy ivermectin onchocerciasis malaria scabies lymphatic filariasis parasitic worms antiparasitic drugs tropical diseases vector-borne diseases ivermectin treatment onchocerciasis management anti-parasitic drugs onchocerciasis symptoms ivermectin dosage onchocerciasis causes ivermectin treatment onchocerciasis medication parasitic infection skin condition eye disease dosing ivermectin ivermectin side effects onchocerciasis symptoms Ivermectin onchocerciasis treatment benefits medication dosage side effects prevalence controlprograms Ivermectin onchocerciasis treatment medicine parasite infection drug usage efficacy ivermectin dosage ivermectin side effects onchocerciasis symptoms ivermectin mechanism of action ivermectin administration methods
781	Mice that lack Interferon-γ or its receptor exhibit high resistance to experimental autoimmune myocarditis. Mice that lack Interferon-γ or its receptor exhibit high resistance to experimental autoimmune myocarditis. Mice that lack Interferon-γ or its receptor exhibit high resistance to experimental autoimmune myocarditis. Mice that lack Interferon-γ or its receptor exhibit high resistance to experimental autoimmune myocarditis. Mice that lack Interferon-γ or its receptor exhibit high resistance to experimental autoimmune myocarditis. Interferon-gamma IFN-g immune response myocarditis mouse models genetic knockout cytokines inflammatory response heart disease autoimmunity Mice Interferon-γ receptor experimental autoimmune myocarditis resistance immune response inflammation cardiovascular disease genetic knockout cytokines Interferon-gamma IFN-g immune response heart inflammation autoimmune diseases mice models cytokines antigen presentation T cells Th1 response Interferon-gamma deficiency receptor knockout myocarditis susceptibility immune response modulation cytokine function inflammatory reaction cardiac autoimmunity gene knockout models pathogenesis investigation immunology research Interferon-gamma receptor deficiency autoimmune myocarditis mouse model immune response inflammation cardiac disease immunology Interferon-gamma Interferon-gamma receptor experimental autoimmune myocarditis immune response modulation mouse models cytokine function inflammatory diseases genetic knockout cardiac inflammation Interferon-gamma Interferon-g immune response myocarditis mouse model autoimmune disease gene knockout cardiac inflammation Interferon-γ deficiency receptor knockout myocarditis susceptibility immune response modulation T-cell activation cytokine function inflammatory pathways antigen presentation adaptive immunity innate immunity pathogen recognition cardiac inflammation Mice Interferon-γ receptor experimental autoimmune myocarditis immune response gene knockout cardiovascular disease inflammation immunology biochemistry pathology mouse models cytokines T cells macrophages antigen presentation adaptive immunity innate immunity Interferon-gamma interferon gamma receptor autoimmune myocarditis mouse models immune response cardiac inflammation Th1 cells cytokines gene knockout pathogenesis
540	Hypothalamic glutamate neurotransmission is crucial to energy balance. Hypothalamic glutamate neurotransmission is crucial to energy balance. Hypothalamic glutamate neurotransmission is crucial to energy balance. Hypothalamic glutamate neurotransmission is crucial to energy balance. Hypothalamic glutamate neurotransmission is crucial to energy balance. neurotransmitters hypothalamus metabolism appetite obesity neurons signaling peptides regulation homeostasis neurotransmitters hypothalamus glutamate metabolism obesity appetite neurobiology signaling homeostasis diet neuroscience weight regulation neurotransmitters hypothalamus energy metabolism appetite regulation neurobiology metabolic homeostasis obesity neuroendocrinology neural circuits signaling pathways Hypothalamus function glucose metabolism neuroendocrine regulation appetite control obesity research neurotransmitter dynamics metabolic signaling synaptic plasticity diet-induced thermogenesis neuronal network analysis Hypothalamus glutamate neurotransmission energy balance metabolism obesity appetite homeostasis neurotransmission hypothalamus energy balance glutamate neurobiology metabolism appetite regulation neuroscience neurochemicals homeostasis neurotransmitters hypothalamus energy metabolism appetite regulation metabolic hormones neurobiology synaptic transmission neuronal signaling metabolic homeostasis obesity leptin corticotropin-releasing hormone hypothalamus glutamate neurotransmission energy balance metabolism appetite regulation obesity homeostasis neuronal signaling hypothalamus glutamate neurotransmission energy balance metabolic regulation homeostasis obesity appetite insulin leptin hypothalamus glutamate metabolism appetite obesity neurotransmission neurons homeostasis reward signaling diet hormones insulin leptin neuropeptide Y agouti-related peptide
783	Mice without IFN-γ or its receptor are resistant to EAM induced with α-MyHC/CFA. Mice without IFN-γ or its receptor are resistant to EAM induced with α-MyHC/CFA. Mice without IFN-γ or its receptor are resistant to EAM induced with α-MyHC/CFA. Mice without IFN-γ or its receptor are resistant to EAM induced with α-MyHC/CFA. Mice without IFN-γ or its receptor are resistant to EAM induced with α-MyHC/CFA. Mice IFN-γ receptor EAM α-MyHC CFA resistance immune response inflammation tissue injury autoimmunity Mice IFN-γ receptor EAM α-MyHC CFA resistance immune response inflammation disease model Mice IFN-γ receptor EAM α-MyHC CFA resistance immune response inflammation T-cell antibody autoimmunity transgenic knockout murine model biology immunology molecular biology protein expression cell signaling mice IFN-γ receptor resistance EAM α-MyHC/CFAimmune response T-cell activation autoimmune encephalomyelitis innate immunity MHC class II expression immune tolerance bone marrow transplantation lymph node analysis antibody response Mice IFN-γ receptor EAM α-MyHC CFA resistance immunity biology medicine virology Elevate search performance recommend relevant expansion phrases query Mice IFN-γ receptor resistant EAM α-MyHC/CFA immunology inflammation cytokines immune response Mice IFN-γ receptor EAM α-MyHC CFA resistance immune response inflammation Mice IFN-γ receptor EAM α-MyHC CFA resistance immune response inflammation disease model molecular biology immunology Mice IFN-γ receptor EAM α-MyHC CFA resistance virus mouse model immune response Mice IFN-γ receptor EAM α-MyHC/CFA resistance immunology inflammation autoimmune mice models immune response
300	Cytosolic proteins bind to iron-responsive elements on mRNAs coding for DMT1. Cytosolic proteins bind to iron-responsive elements on mRNAs coding for proteins involved in iron uptake. Cytosolic proteins bind to iron-responsive elements on mRNAs coding for DMT1. Cytosolic proteins bind to iron-responsive elements on mRNAs coding for proteins involved in iron uptake. Cytosolic proteins bind to iron-responsive elements on mRNAs coding for DMT1. Cytosolic proteins bind to iron-responsive elements on mRNAs coding for proteins involved in iron uptake. Cytosolic proteins bind to iron-responsive elements on mRNAs coding for DMT1. Cytosolic proteins bind to iron-responsive elements on mRNAs coding for proteins involved in iron uptake. Cytosolic proteins bind to iron-responsive elements on mRNAs coding for DMT1. Cytosolic proteins bind to iron-responsive elements on mRNAs coding for proteins involved in iron uptake. Cytosolic proteins iron responsive elements mRNA DMT1 iron uptake transcription translation regulation genetics biochemistry cellular metabolism iron-responsive elements cytosolic proteins mRNA binding DMT1 iron uptake transferrin receptor ferritin iron metabolism RNA binding proteins cellular iron homeostasis iron transport proteins cytosolic proteins iron responsive elements mRNA DMT1 iron uptake transcription regulation translation genetics biochemistry molecular biology cellular function mechanisms cytosolic proteins iron-responsive elements mRNAs DMT1 iron uptake translational regulation metal transporters hemochromatosis ferroportin hepcidin iron metabolism mRNA binding proteins transcription factors iron homeostasis Cytosolic proteins iron-responsive elements mRNAs DMT1 iron uptake protein binding translational regulation iron metabolism Cytosolic proteins iron-responsive elements DMT1 iron uptake mRNAs protein binding translational regulation iron metabolism Cytosolic proteins iron-responsive elements mRNAs DMT1 iron uptake transcription factors regulation cellular iron homeostasis cytosolic proteins iron-responsive elements mRNAs DMT1 iron uptake protein binding translational regulation iron metabolism cytosolic proteins iron responsive elements mRNAs DMT1 iron uptake transport genes regulation transcription translation metabolism ferritin transferrin transferrin receptor hepcidin cytosolic proteins iron-responsive elements mRNAs DMT1 iron uptake translational regulation iron metabolism protein binding mRNA stabilization mRNA localization
421	Flexible molecules experience greater steric hindrance in the tumor microenviroment than rigid molecules. Flexible molecules experience greater steric hindrance in the tumor microenviroment than rigid molecules. Flexible molecules experience greater steric hindrance in the tumor microenviroment than rigid molecules. Flexible molecules experience greater steric hindrance in the tumor microenviroment than rigid molecules. Flexible molecules experience greater steric hindrance in the tumor microenviroment than rigid molecules. steric hindrance molecules tumor microenvironment rigidity drug delivery flexible molecules rigid molecules diffusion synthesis biophysics chemical structure flexible molecules steric hindrance tumor microenvironment rigid molecules molecular flexibility tumor environment chemical structure drug delivery biomolecules molecular dynamics flexible molecules steric hindrance tumor microenvironment rigid molecules molecular flexibility cancer cells biomolecular interactions drug delivery molecular dynamics chemical structure tumor environment molecular rigidity biochemical factors steric hindrance flexible molecules rigid molecules tumor microenvironment chemical flexibility molecular rigidity bioavailability drug molecules molecular dynamics tumor environment synthetic biology biophysical properties steric hindrance flexible molecules rigid molecules tumor microenvironment molecular flexibility chemical structure solubility penetration drug delivery steric hindrance flexible molecules rigid molecules tumor microenvironment drug delivery molecular flexibility chemical properties biomolecular interactions steric hindrance molecules tumor microenvironment rigidity drug delivery molecular flexibility steric hindrance flexible molecules rigid molecules tumor microenvironment molecular flexibility drug delivery efficacy biophysics molecular dynamics therapeutic agents flexible molecules steric hindrance tumor microenvironment rigid molecules molecular flexibility cancer cells biomolecular interactions drug delivery molecular dynamics chemical structure steric hindrance flexible molecules rigid molecules tumor microenvironment drug delivery molecular flexibility molecular rigidity cancer biology chemical kinetics
784	MicroRNA is involved in the regulation of Neural Stem Cell (NSC) differentiation and proliferation dynamic homeostasis MicroRNA is involved in the regulation of Neural Stem Cell (NSC) differentiation and proliferation dynamic homeostasis MicroRNA is involved in the regulation of Neural Stem Cell (NSC) differentiation and proliferation dynamic homeostasis MicroRNA is involved in the regulation of Neural Stem Cell (NSC) differentiation and proliferation dynamic homeostasis MicroRNA is involved in the regulation of Neural Stem Cell (NSC) differentiation and proliferation dynamic homeostasis microRNAs neural stem cells differentiation proliferation homeostasis gene expression cellular biology neurogenesis molecular regulation MicroRNA Neural Stem Cell differentiation proliferation homeostasis gene expression molecular biology neurogenesis stem cell research RNA interference biological pathways cellular dynamics microRNA function neural stem cell biology differentiation process proliferation dynamics homeostasis mechanisms gene expression regulation RNA molecules neurogenesis molecular biology cellular metabolism MicroRNA function neural stem cell development gene expression regulation cellular metabolism molecular biology neurogenesis RNA silencing biological pathway stem cell maintenance transcriptome analysis signaling pathways molecular mechanisms neurodevelopment disorders MicroRNA Neural Stem Cell differentiation proliferation homeostasis regulatory mechanism gene expression cellular biology neuroscience molecular biology stem cell research RNA function MicroRNA regulation Neural Stem Cell function differentiation process proliferation dynamics homeostasis maintenance gene expression control stem cell biology molecular mechanisms neurogenesis miRNA roles MicroRNA Neural Stem Cell differentiation proliferation homeostasis gene expression cellular metabolism molecular biology neuroscience stem cell research regulatory mechanisms microRNA function NSC biology stem cell regulation molecular mechanisms homeostasis maintenance gene expression调控 cell cycle control neurogenesis process RNA binding proteins signaling pathways epigenetic modification MicroRNA Neural Stem Cell differentiation proliferation homeostasis regulatory network gene expression stem cell biology molecular mechanisms neurogenesis MicroRNA regulation neural stem cell differentiation factors proliferation control homeostasis maintenance molecular mechanisms developmental biology genetic regulation cellular dynamics bioinformatics analysis RNA interference stem cell research neurological disorders gene expression profiling
785	Microarray results from culture-amplified mixtures of serotypes correlate poorly with microarray results from uncultured mixtures. Microarray results from culture-amplified mixtures of serotypes correlate poorly with microarray results from uncultured mixtures. Microarray results from culture-amplified mixtures of serotypes correlate poorly with microarray results from uncultured mixtures. Microarray results from culture-amplified mixtures of serotypes correlate poorly with microarray results from uncultured mixtures. Microarray results from culture-amplified mixtures of serotypes correlate poorly with microarray results from uncultured mixtures. microarray culture-amplification serotypes correlation uncultured microbiome pathogen_detection gene_expression microarray culture-amplification serotypes uncultured correlation microbiology genomics diagnostics virology bacteriology fungi transcriptomics microarray analysis serotype identification culturing effects microbial mixture correlation analysis gene expression pathogen detection microbiome研究 single nucleotide polymorphism RNA profiling microarray analysis culture-amplified samples serotype mixture correlation studies uncultured samples microbiome diversity pathogen identification genetic variability microbial community analysis molecular diagnostics microarray serotypes culture-amplified uncultured correlation efficiency terms expand query microarray analysis culture-amplified samples serotype correlation uncultured samples microbial diversity gene expression bioinformatics pathogen detection molecular biology microbiome profiling microarray culture-amplified serotypes uncultured correlation bacterial mixture molecular biology pathogen detection gene expression bioinformatics microbiology microarray analysis culturing bacteria serotype identification microbial mixture gene expression diagnostic accuracy microbiome analysis pathogen detection molecular biology techniques bioinformatics tools microarray culture-amplified serotypes uncultured correlation molecular biology infectious disease genetic analysis microbiology bioinformatics pathogen identification gene expression diagnostic tools microarray analysis culturing methods serotype diversity microbial community genetic variability pathogen identification sample preparation bioinformatics tools cross-validation techniques molecular diagnostics
544	IFIT1 restricts viral replication by sequestrating mis-capped viral RNAs. IFIT1 restricts viral replication by sequestrating mis-capped viral RNAs. IFIT1 restricts viral replication by sequestrating mis-capped viral RNAs. IFIT1 restricts viral replication by sequestrating mis-capped viral RNAs. IFIT1 restricts viral replication by sequestrating mis-capped viral RNAs. IFIT1 viral replication mis-capped viral RNAs interferon-induced protein antiviral defense sRNA capping machinery Virus-host interaction RNA interference Virus infection molecular biology immunology virology biomedical research genetics protein function antiviral mechanism cellular response IFIT1 function viral RNA modification viral infection response mis-capped RNA antiviral mechanism VSR interaction host-virus interaction RNA interference IFIT1 viral replication mis-capped RNA antiviral response RNA interference innate immunity virology molecular biology immune evasion RNA modifications IFIT1 function viral RNA recognition antiviral response mis-capped RNA IFIT1 mechanism RNA modification viral replication inhibition innate immunity virology research gene expression regulation IFIT1 viral replication mis-capped viral RNAs immune response molecular mechanism VIPRE protein promotes antiviral defense interferon-induced protein with tetratricopeptide repeats IFIT1 function viral RNA interaction antiviral mechanism cap structure recognition protein-RNA binding IFIT1 viral replication mis-capped RNA antiviral response innate immunity RNA interference viral infection molecular biology virology immune evasion capsid modification viral capsid RNA processing interferon induction IFIT1 viral replication mis-capped viral RNAs antiviral mechanism RNA interference molecular biology virus-host interaction viral RNA processing immunology cellular defense/response IFIT1 viral replication mis-capped RNAs antiviral mechanism interferon-induced protein sRNA biology virus-host interaction immunology VIPERI IFIT1 function viral RNA interference mis-capped RNA antiviral response viral replication inhibition RNA modification VISA protein VLPs interferon signaling
303	DMRT1 is a sex-determining gene that is epigenetically regulated by the MHM region. DMRT1 is a sex-determining gene that is epigenetically regulated by the MHM region. DMRT1 is a sex-determining gene that is epigenetically regulated by the MHM region. DMRT1 is a sex-determining gene that is epigenetically regulated by the MHM region. DMRT1 is a sex-determining gene that is epigenetically regulated by the MHM region. sex determination epigenetics DMRT1 function MHM region gene regulation sexual development sex determination epigenetics DMRT1 function MHM region gene regulation sex chromosome epigenetic modification developmental biology genetic regulation sex determination pathway DMRT1 gene sex determination epigenetics MHM region genetic regulation sex chromosome gene expression epigenetic modification sex determination genes DMRT1 function sex determination genes epigenetic regulation DMRT1 function MHM region impact sex chromosome interaction gene expression in sex determination epigenetics in sex development sex determination mechanism genetic factors in sex determination regulatory regions of genes DMRT1 sex determination epigenetics MHM region gene regulation sex determination epigenetics DMRT1 function MHM region gene regulation sexual differentiation DMRT1 sex-determination epigenetics MHM gene regulation sexual development chromatin modification transcription factor sex determination epigenetics MHM region gene regulation DMRT1 function sexual differentiation genetic regulation epigenetic markers DMRT1 gene sex determination epigenetic regulation MHM region sex hormones chromatin modification transcription factor genetic regulation sexual development gene expression epigenetics sex chromosome avian species mammalian genes sex determination epigenetics MHM region gene regulation DMRT1 function chromatin modification sex chromosome gene expression genetic regulation
1089	Smc5/6 engagment drives the activation of SUMO E3 ligase Mms21 by ATP-dependent remolding. Smc5/6 engagment drives the activation of SUMO E3 ligase Mms21 by ATP-dependent remolding. Smc5/6 engagment drives the activation of SUMO E3 ligase Mms21 by ATP-dependent remolding. Smc5/6 engagment drives the activation of SUMO E3 ligase Mms21 by ATP-dependent remolding. Smc5/6 engagment drives the activation of SUMO E3 ligase Mms21 by ATP-dependent remolding. Smc5/6 complex SUMOylation Mms21 protein ATP-dependent remodeling E3 ligase activity chromosomal maintenance SUMO E3 ligase engagement chromosomal cohesion cell cycle regulation DNA repair process SMC5/6 complex SUMOylation Mms21 protein ATP remodeling chromatin structure DNA repair cell cycle regulation histone modification SUMO E3 ligase activity SMC5/6 function SUMO pathway protein ubiquitination chromosomal maintenance molecular biology genetic regulation SUMO conjugation chromosomal proteins ATPase activity transcriptional activation gene expression DNA damage response protein-protein interactions cellular proliferation epigenetics SMC5/6 complex mechanism SUMO modification SUMO ligase recruitment chromosomal dynamics SUM SMC5/6 complex SUMOylation Mms21 protein ATP remodeling chromatin modification cell cycle regulation SUMO E3 ligase activity DNA repair process SMC5/6 complex SUMOylation process ATP binding Mms21 protein chromosomal maintenance cell cycle regulation DNA repair mechanism histone modification protein conjugation SUMO E3 ligase activity chromatin remodeling molecular biology terms SMC5/6 complex SUMOylation ATPase activity Mms21 protein chromatin remodeling cell division DNA repair ubiquitin-like proteins protein-protein interaction molecular dynamics biochemical assay query expansion SMC5/6 SUMOylation Mms21 ATP-dependent remodeling chromatin structure DNA repair protein complexinteraction SUMO E3 ligase activation molecular biology cellular processes SMC5/6 complex SUMOylation Mms21 protein ATP-dependent remodeling cell division chromatin structure protein interaction SUMO E3 ligase activity Smc5/6 complex SUMO E3 ligase Mms21 protein ATP-dependent remodeling molecular engagement SUMOylation process chromatin modification cell cycle regulation DNA repair mechanism Smc5/6 complex SUMOylation Mms21 protein ATP-dependent remodeling chromatin structure cell cycle regulation DNA repair protein-protein interaction SUMO E3 ligase activity molecular biology techniques genetic interactions epistasis analysis yeast model system histone modification post-translational modification SMC5/6 complex SUMOylation ATPase activity chromatin remodeling Mms21 interaction protein modification cell division DNA repair molecular biology techniques SUMO E3 ligase function
549	IRG1 has antiviral effects against neurotropic viruses. IRG1 has antiviral effects against neurotropic viruses. IRG1 has antiviral effects against neurotropic viruses. IRG1 has antiviral effects against neurotropic viruses. IRG1 has antiviral effects against neurotropic viruses. IRG1 function antiviral mechanisms neurotropic viruses viral infection immune response gene expression protein interaction viral replication antiviral therapy virology research IRG1 antiviral neurotropic viruses immune response protein infection protection mechanisms pathogen IRG1 protein antiviral mechanisms neurotropic viruses viral infection prevention immune response virology research gene function antiviral therapy neurological viruses innate immunity IRG1 antiviral properties IRG1 neurotropic viruses IRG1 viral defense mechanism IRG1 virus interaction IRG1 gene function IRG1 immune response IRG1 therapeutic potential IRG1 virus treatment IRG1 virology research IRG1 antiviral efficacy IRG1 antiviral neurotropic viruses immune response gene protein mechanism infection protection virology neuroscience immunity viral defense IRG1 antiviral properties IRG1 virus defense neurotropic virus treatment IRG1 mechanism of action IRG1 viral infection response antiviral genes IRG1 gene function neurotropic viruses treatment IRG1 and antiviral activity viral resistance IRG1 IRG1 protein antiviral mechanisms neurotropic viruses viral infection gene expression immune response viral replication antiviral therapy viral pathogenesis innate immunity IRG1 antiviral properties neurotropic viruses treatment immune response enhancement viral infection prevention antiviral mechanisms IRG1 function analysis viral neurotropism innate immunity stimulation virus-specific defense virology research advancements IRG1 antiviral properties neurotropic viruses viral infection host defense viral pathogenesis interferon response gene expression viral entry replication inhibitors IRG1 function neurotropic viruses types antiviral mechanisms viral entry inhibition interferon response gene expression analysis viral replication inhibitors
551	ITAM phosphorylation prevents the transfer of the T cell receptor (TCR) signal from the echo-domain to the cytoplasmic tail of the T cell receptor (TCR). ITAM phosphorylation prevents the transfer of the T cell receptor (TCR) signal from the echo-domain to the cytoplasmic tail of the T cell receptor (TCR). ITAM phosphorylation prevents the transfer of the T cell receptor (TCR) signal from the echo-domain to the cytoplasmic tail of the T cell receptor (TCR). ITAM phosphorylation prevents the transfer of the T cell receptor (TCR) signal from the echo-domain to the cytoplasmic tail of the T cell receptor (TCR). ITAM phosphorylation prevents the transfer of the T cell receptor (TCR) signal from the echo-domain to the cytoplasmic tail of the T cell receptor (TCR). ITAM phosphorylation TCR signal transduction echo-domain cytoplasmic tail immunology T cell biology ITAM phosphorylation TCR echo-domain cytoplasmic tail immunology T cell signaling protein interaction cellular biology ITAM phosphorylation TCR cytoplasmic tail echo-domain T cell receptor signal transduction immunology molecular biology immune system protein interaction cellular signaling ITAM function TCR signaling pathway immunology research T cell activation molecular biology signal transduction immune system kinase activity cellular communication biological pathways TCR structure immunology concepts T cell biology protein phosphorylation ITAM phosphorylation TCR echo-domain cytoplasmic tail signal transfer ITAM function TCR signaling pathway cytoplasmic domain immune synapse formation T cell activation protein kinase activity immunology research signal transduction cellular immunology biological regulation molecular mechanisms ITAM phosphorylation T cell receptor TCR echo-domain cytoplasmic tail signal transduction immunology molecular biology ITAM phosphorylation TCR echo-domain cytoplasmic tail signal transduction immunology T cell biology ITAM phosphorylation TCR echo-domain cytoplasmic tail signal transfer immunology T cell biology ITAM function TCR signaling cellular immunology lymphocyte activation immunophosphorylation signal transduction immune synapse TCR complex lymphocyte biology
793	Mitochondria are uninvolved in apoptosis. Mitochondria are uninvolved in apoptosis. Mitochondria are uninvolved in apoptosis. Mitochondria are uninvolved in apoptosis. Mitochondria are uninvolved in apoptosis. mitochondria apoptosis role mitochondrial function in cell death apoptosis mitochondrial involvement uninvolved mitochondria mechanism mitochondria apoptosis involvement mitochondrial role in cell death apoptosis mechanism mitochondria function in programmed cell death uninvolved in apoptosis evidence mitochondria and necrosis mitochondria vs apoptosis mitochondrial membrane and apoptosis mitochondrial apoptosis role function cell death regulation genetics biology mitochondria programmed organelle mitochondria apoptosis function mitochondrial role in cell death involvement mitochondria apoptosis mitochondria and programmed cell death mitochondria apoptosis mechanism mitochondria apoptosis function apoptosis regulation mitochondrial membrane potential apoptotic signaling pathways cardiomyocytes apoptosis neurons apoptosis mitochondrial role apoptosis mechanism cell death process uninvolved factors mitochondrial function programmed cell death mitochondria apoptosis role mitochondrial function in cell death uninvolved in programmed cell death mitochondria and apoptosis mechanisms mitochondrial_role_apoptosis mitochondria_function apoptosis_mechanism uninvolved_in_apoptosis mitochondrial_debate_apoptosis mitochondria apoptosis mechanism mitochondrial role in cell death uninvolved mitochondria apoptosis apoptosis independent mitochondria mitochondrial dysfunction apoptosis mitochondrial dysfunction apoptosis mechanisms caspase activation cell death types mitochondrial membrane potential
431	FoxO3a activation in neuronal death is mediated by reactive oxygen species (ROS). FoxO3a activation in neuronal death is mediated by reactive oxygen species (ROS). FoxO3a activation in neuronal death is mediated by reactive oxygen species (ROS). FoxO3a activation in neuronal death is mediated by reactive oxygen species (ROS). FoxO3a activation in neuronal death is mediated by reactive oxygen species (ROS). FoxO3a neuronal death reactive oxygen species ROS apoptosis oxidative stress neurodegeneration signaling pathway inflammation gene expression FoxO3a neuronal death reactive oxygen species ROS signaling pathway apoptosis oxidative stress neurodegeneration molecular mechanism cell death inflammation gene expression FoxO3a neuronal death reactive oxygen species ROS apoptosis oxidative stress neurodegeneration signaling pathway gene expression antioxidant defense inflammation FoxO3a signaling neuronal apoptosis oxidative stress ROS production neurodegeneration mechanisms FoxO3a pathway antioxidant defense redox regulation neuroprotective strategies gene expression modulation neuronal survival factors ROS-induced damage FoxO3a neuronal death reactive oxygen species ROS apoptosis oxidative stress signaling pathway neurodegeneration inflammation FoxO3a signaling neuronal apoptosis oxidative stress ROS regulation neurodegeneration mechanisms transcription factor FoxO3a redox signaling FoxO3a neuronal death reactive oxygen species ROS oxidative stress apoptosis signaling pathway neurodegeneration redox regulation gene expression FoxO3a neuronal death reactive oxygen species ROS oxidative stress apoptosis signaling pathway neurodegeneration redox regulation gene expression molecular biology FoxO3a neuronal death reactive oxygen species ROS apoptosis oxidative stress neurodegeneration signaling pathway molecular mechanism gene expression antioxidant defense FoxO3a signaling neuronal apoptosis oxidative stress ROS pathways neurodegeneration mechanisms redox imbalance cellular senescence mitochondrial dysfunction inflammation response gene expression regulation
552	IgA plasma cells that are specific for transglutaminase 2 accumulate in the duodenal mucosa on commencement of a gluten-free diet. IgA plasma cells that are specific for transglutaminase 2 accumulate in the duodenal mucosa on commencement of a gluten-free diet. IgA plasma cells that are specific for transglutaminase 2 accumulate in the duodenal mucosa on commencement of a gluten-free diet. IgA plasma cells that are specific for transglutaminase 2 accumulate in the duodenal mucosa on commencement of a gluten-free diet. IgA plasma cells that are specific for transglutaminase 2 accumulate in the duodenal mucosa on commencement of a gluten-free diet. IgA plasma cells transglutaminase 2 duodenal mucosa gluten-free diet celiac disease immunology gastroenterology antigen-specific immunity IgA plasma cells transglutaminase 2 duodenal mucosa gluten-free diet celiac disease immunology gastrointestinal pathology autoimmunity IgA antibodies transglutaminase 2 duodenal biopsy gluten sensitivity celiac disease mucosal inflammation gluten-free diet impact immune response gastrointestinal symptoms IgA plasma cells transglutaminase 2 duodenal mucosa gluten-free diet celiac disease intestinal immunity immunoglobulin A mucosal inflammation food allergy autoimmunity gastrointestinal tract antigen-specific response IgA plasma cells transglutaminase 2 duodenal mucosa gluten-free diet celiac disease immunoglobulins gluten sensitivity IgA plasma cells transglutaminase 2 duodenal mucosa gluten-free diet celiac disease autoimmune response intestinal biopsy gluten sensitivity IgA plasma cells transglutaminase 2 duodenal mucosa gluten-free diet celiac disease immune response gluten sensitivity IgA plasma cells transglutaminase 2 duodenal mucosa gluten-free diet celiac disease markers IgA plasma cells transglutaminase 2 duodenal mucosa gluten-free diet celiac disease antigen-specific immunity intestinal inflammation immunoglobulin A IgA plasma cells transglutaminase 2 duodenal mucosa gluten-free diet celiac disease autoimmunity intestinal inflammation
674	LDL cholesterol has no involvement in the development of cardiovascular disease. LDL cholesterol has no involvement in the development of cardiovascular disease. LDL cholesterol has no involvement in the development of cardiovascular disease. LDL cholesterol has no involvement in the development of cardiovascular disease. LDL cholesterol has no involvement in the development of cardiovascular disease. LDL cholesterol cardiovascular disease metabolism genetics inflammation atherosclerosis risk factors prevention LDL cholesterol cardiovascular disease role mechanism research evidence prevention treatment LDL cholesterol cardiovascular disease metabolic genetics inflammation atherosclerosis epidemiology prevention treatment cardiovascular health lipid profile analysis cholesterol management atherosclerosis risk metabolic syndrome triglycerides levels high density lipoprotein statin therapy heart disease prevention dietary fats impact LDL cholesterol cardiovascular disease metabolism genetics diet inflammation atherosclerosis risk factors reducing LDL cholesterol cardiovascular prevention diet lifestyle genetic factors inflammation LDL cholesterol cardiovascular disease inflammation plaque metabolism genetics lifestyle diet exercise LDL cholesterol cardiovascular disease metabolism genetics inflammation atherosclerosis prevention treatment LDL cholesterol cardiovascular disease prevention genetics diet lifestyle treatment risk factors cardiovascular health lipid profile atherosclerosis triglycerides HDL cholesterol inflammatory markers genetic factors
312	De novo assembly of sequence data has more specific contigs than unassembled sequence data. De novo assembly of sequence data has more specific contigs than unassembled sequence data. De novo assembly of sequence data has more specific contigs than unassembled sequence data. De novo assembly of sequence data has more specific contigs than unassembled sequence data. De novo assembly of sequence data has more specific contigs than unassembled sequence data. de novo assembly techniques specific contigs unassembled sequence data genome assembly bioinformatics tools contig analysis sequencing technologies genetic mapping next-generation sequencing assembly algorithms de novo assembly contigs unassembled sequence data genome assembly next-generation sequencing bioinformatics sequencing technologies assembly algorithms de novo assembly techniques contig quality unassembled reads genome assembly methods sequence data analysis bioinformatics tools genetic sequencing technologies de novo assembly benefits specific contig advantages unassembled sequence limitations genomic assembly techniques contig quality comparison sequence data analysis de novo assembly contigs unassembled sequence data genome assembly bioinformatics sequencing technologies genetic sequences molecular biology computational biology next-generation sequencing de novo assembly techniques specific contigs benefits unassembled sequence challenges bioinformatics tools genome sequencing methods assembly quality improvement genetic data analysis next-generation sequencing assembly algorithms contig length comparison de novo assembly contigs sequence data unassembled data genetic assembly bioinformatics genome sequencing molecular biology next-generation sequencing DNA assembly de novo assembly contigs unassembled sequence data specificity genetic sequencing bioinformatics genome assembly molecular biology computational biology de novo assembly contigs unassembled sequences bioinformatics genome assembly next-generation sequencing DNA sequencing molecular biology computational biology genetic information de novo assembly benefits specific contigs generation unassembled data comparison genomic sequencing techniques assembly quality improvement sequence analysis tools biological sequence assembly genome assembly methods
554	Immune complex triggered cell death leads to extracellular release of neutrophil protein HMGB1. Immune complex triggered cell death leads to extracellular release of neutrophil protein HMGB1. Immune complex triggered cell death leads to extracellular release of neutrophil protein HMGB1. Immune complex triggered cell death leads to extracellular release of neutrophil protein HMGB1. Immune complex triggered cell death leads to extracellular release of neutrophil protein HMGB1. immune complexes cell death extracellular release neutrophils HMGB1 inflammatory response cytokines apoptosis necrosis innate immunity immune complex cell death extracellular release neutrophil protein HMGB1 inflammatory response apoptosis necrosis cytokines inflammation immunology biochemistry pathophysiology immune complexes cell death mechanisms extracellular signals neutrophils HMGB1 protein inflammatory response immune regulation cytokines innate immunity apoptosis necrosis immune complex formation cell death mechanisms extracellular release neutrophil proteins HMGB1 function inflammatory response immunology research biological pathways medical conditions immune system disorders immune complex cell death extracellular release neutrophil HMGB1 inflammation cytokines signaling pathways immune response apoptosis necrosis immune response cell apoptosis inflammatory cascade neutrophil extracellular traps cytokine release immunology biomarkers innate immunity molecular biology clinical applications immune complex cell death extracellular release neutrophil HMGB1 cytokine inflammation apoptosis necrosis signaling pathways immune response immune complex cell death extracellular release neutrophil HMGB1 cytokine inflammation apoptosis necrosis immune response immune complex cell death extracellular release neutrophil HMGB1 cytokines inflammation immunology biomarkers immune complex formation cell apoptosis extracellular signals neutrophil activation HMGB1 release inflammatory response cytokine production immune surveillance autoimmunity tissue damage markers
314	Deamination of cytidine to uridine on the minus strand of viral DNA results in catastrophic G-to-A mutations in the viral genome. Deamination of cytidine to uridine on the minus strand of viral DNA results in catastrophic G-to-A mutations in the viral genome. Deamination of cytidine to uridine on the minus strand of viral DNA results in catastrophic G-to-A mutations in the viral genome. Deamination of cytidine to uridine on the minus strand of viral DNA results in catastrophic G-to-A mutations in the viral genome. Deamination of cytidine to uridine on the minus strand of viral DNA results in catastrophic G-to-A mutations in the viral genome. deamination cytidine uridine viral DNA minus strand G-to-A mutations catastrophic mutations virus mutation V RNA editing RNA virusmutations DNA methylation transcription errors viral replication cycle viral genome stability deamination cytidine uridine viral DNA minus strand G-to-A mutations catastrophic genome RNA virus DNA virus mutagenesis epigenetics virology molecular biology deamination cytidine uridine viral DNA minus strand G-to-A mutations RNA editing mutagenesis retroviruses epitranscriptomics deamination process viral DNA mutation cytidine deamination uracil incorporation G to A mutation viral replication errors DNA modification viral genetic instability viral RNA editing mutagenesis mechanisms viral evolution deamination cytidine uridine viral DNA minus strand G-to-A mutations genome efficiency expand query valuable terms DNA modification viral mutation epigenetics RNA interference gene editing mutagenesis virology base editing genetic variation molecular biology deamination cytidine uridine viral DNA minus strand G-to-A mutations genome RNA editing mutagenesis viral replication epigenetics nucleotide modification deamination cytidine uridine viral DNA minus strand G-to-A mutations genome RNA editing mutagenesis epigenetics molecular biology virology genetic variation deamination cytidine uridine viral DNA minus strand G-to-A mutations genome RNA virus HIV hepatitis B epigenetics mutagenesis replication fidelity antiviral therapy genetic drift deamination cytidine uridine viral DNA minus strand G-to-A mutations genome RNA editing mutagenesis antiviral therapy molecular biology virology
436	Free histones are degraded by a Rad53-dependent mechanism once DNA has been replicated. Free histones are degraded by a Rad53-dependent mechanism once DNA has been replicated. Free histones are degraded by a Rad53-dependent mechanism once DNA has been replicated. Free histones are degraded by a Rad53-dependent mechanism once DNA has been replicated. Free histones are degraded by a Rad53-dependent mechanism once DNA has been replicated. histone degradation Rad53 protein DNA replication post-replicative processes chromatin remodeling cell cycle regulation molecular biology techniques genetic pathways proteasome function epigenetics transcription factors histone degradation Rad53 protein DNA replication molecular biology cell cycle regulation chromatin structure genetic repair mechanisms protein function biochemical pathways histone degradation Rad53 protein DNA replication histone turnover cell cycle regulation chromatin dynamics protein kinase repair pathway molecular biology techniques DNA replication histone degradation Rad53 protein cell cycle regulation chromatin dynamics post-replicative modification histone turnover DNA damage response protein kinase activity genetic repair mechanisms free histones Rad53-dependent DNA replication degradation mechanism rad53 protein function dna replication histone degradation molecular biology cell cycle regulation histone degradation Rad53 protein DNA replication post-replication processes histone modifications cell cycle regulation free histones degradation process Rad53-dependent DNA replication molecular biology keywords cell cycle regulation protein breakdown genetic information processing biochemical pathways epigenetics research scientific inquiry genetic material maintenance biological function analysis molecular mechanisms genetic information flow cellular metabolism biochemistry DNA repair gene expression regulation chromatin dynamics cellular processes biological sciences scientific methods genetic studies molecular genetics protein function genetic regulation biological systems genetic research molecular interactions scientific experiments genetic information storage genetic information transmission cellular components scientific exploration genetic analysis biological evolution genetic variability free histones Rad53 protein DNA replication degradation pathway cell cycle regulation histone degradation Rad53 protein DNA replication post-replicative modification chromatin dynamics histone turnover cell cycle regulation protein kinase activity
437	Functional consequences of genomic alterations due to Myelodysplastic syndrome (MDS) are poorly understood due to the lack of an animal model. Functional consequences of genomic alterations due to Myelodysplastic syndrome (MDS) are poorly understood due to the lack of an animal model. Functional consequences of genomic alterations due to Myelodysplastic syndrome (MDS) are poorly understood due to the lack of an animal model. Functional consequences of genomic alterations due to Myelodysplastic syndrome (MDS) are poorly understood due to the lack of an animal model. Functional consequences of genomic alterations due to Myelodysplastic syndrome (MDS) are poorly understood due to the lack of an animal model. genomic alterations Myelodysplastic syndrome animal models functional consequences hematopoietic disorders genetic mutations stem cell abnormalities bone marrow failure blood cancer cellular biology molecular mechanisms experimental models oncology research clinical implications genomic alterations MDS animal models functional consequences stem cells cancer genetics 血液病 分子机制 functional genomics MDS models animal models genomic alterations hematopoietic dysfunction gene expression epigenetic modifications cancer genetics stem cell biology hematological disorders molecular mechanisms genomic alterations MDS animal model functional consequences myelodysplastic syndrome relevant expansion phrases lack of understanding research gaps stem cell biology transgenic models molecular mechanismsclinical implications genomic alterations Myelodysplastic syndrome functional consequences animal models hematopoietic dysfunction genetic mutations bone marrow failure cellular proliferation differentiation defects epigenetic modifications cancer genetics stem cell biology transcription factors gene expression profiling molecular mechanisms clinical outcomes genomic alterations MDS functional consequences animal model research limitations clinical implications biological pathways disease modeling translational research molecular mechanisms genomic alterations functional consequences Myelodysplastic syndrome MDS animal model hematopoietic stem cells leukemia genetic mutations cellular function bone marrow failure clinical outcomes molecular biology oncology genetic modeling stem cell research blood disorders genomic alterations MDS functional consequences animal model research limitations molecular mechanisms hematopoietic disorders cancer genomics stem cell biology transgenic models clinical implications somatic mutations therapeutic targets genomic alterations Myelodysplastic syndrome animal models functional consequences hematopoietic disorders gene expression cellular biology cancer genetics molecular mechanisms hematopoiesis genomic alterations Myelodysplastic syndrome animal models functional consequences hematopoietic stem cells transcription factors epigenetic modifications cancer biology genetic predisposition clinical outcomes
439	Fz/PCP-dependent Pk localizes to the anterior membrane of neuroectoderm cells during zebrafish neuralation Fz/PCP-dependent Pk localizes to the anterior membrane of neuroectoderm cells during zebrafish neuralation Fz/PCP-dependent Pk localizes to the anterior membrane of neuroectoderm cells during zebrafish neuralation Fz/PCP-dependent Pk localizes to the anterior membrane of neuroectoderm cells during zebrafish neuralation Fz/PCP-dependent Pk localizes to the anterior membrane of neuroectoderm cells during zebrafish neuralation Fz/PCP Planar Cell Polarity PK protein Zebrafish development Neuralation Neuroectoderm cells Membrane localization Signal transduction Embryonic patterning Morphogenesis Fz/PCP planar cell polarity neuroectoderm cells zebrafish neuralation anterior membrane protein localization developmental biology embryonic cells Fz/PCP planar cell polarity neuroectoderm zebrafish development neuralation anterior membrane protein localization embryonic cells signaling pathways Fz/PCP signaling Pk protein zebrafish embryonic development neuralation process neuroectoderm cells anterior membrane localization planar cell polarity gene expression analysis cellular localization studies zebrafish model neurogenesis Fz/PCP Pk protein zebrafish neuralation neuroectoderm anterior membrane cell localization developmental biology molecular biology Fz/PCP signaling neuroectoderm development zebrafish embryogenesis cell membrane localization neuralation process Fz/PCP planar cell polarity neuroectoderm zebrafish development neuralation anterior membrane protein localization embryo biology Fz/PCP Pk protein neuroectoderm cells zebrafish neuralation anterior membrane localization planar cell polarity developmental biology Fz/PCP Pk protein neuroectoderm cells zebrafish development neuralation cell membrane localization planar cell polarity Fz/PCP Pk protein zebrafish development neuralation neuroectoderm cells anterior membrane planar cell polarity
560	Immune responses result in the development of inflammatory Th17 cells and anti-inflammatory iTregs. Immune responses result in the development of inflammatory Th17 cells and anti-inflammatory iTregs. Immune responses result in the development of inflammatory Th17 cells and anti-inflammatory iTregs. Immune responses result in the development of inflammatory Th17 cells and anti-inflammatory iTregs. Immune responses result in the development of inflammatory Th17 cells and anti-inflammatory iTregs. immune responses Th17 cells iTregs inflammation immune regulation cytokines T-helper cells regulatory T-cells immune tolerance autoimmune diseases immunology immune responses Th17 cells iTregs inflammation regulatory T cells cytokines immune regulation autoimmune diseases immune tolerance immunology immune responses Th17 cells anti-inflammatory iTregs cytokines T helper cells immune regulation immune tolerance adaptive immunity immune response mechanisms immune responses inflammatory Th17 cells anti-inflammatory iTregs immune system T helper cells regulatory T cells immune inflammation cytokines adaptive immunity immune response mechanisms immunology immune cell types T cell subsets immune regulation autoimmune diseases immune tolerance immune signaling immune responses Th17 cells iTregs inflammation regulatory T cells cytokines immune homeostasis autoimmune diseases chronic inflammation adaptive immunity immune responses Th17 cells iTregs inflammation immune system T helper cells regulatory T cells cytokines immune tolerance autoimmune diseases immunology immune responses Th17 cells iTregs inflammation immune system cytokines T helper cells regulatory T cells immune tolerance immune responses Th17 cells iTregs inflammation immune system cytokines T helper cells regulatory T cells immune response mechanisms immune regulation adaptive immunity immunology cytokine production cell signaling autoimmune diseases chronic inflammation immune responses Th17 cells iTregs inflammation regulatory T cells cytokines immune tolerance autoimmune diseases immunology T helper cells immune response mechanisms immune regulation inflammation mechanisms Th17 cells function iTregs role immune homeostasis cytokine production adaptive immunity processes immune cell differentiation
440	Fz/PCP-dependent Pk localizes to the anterior membrane of notochord cells during zebrafish neuralation. Fz/PCP-dependent Pk localizes to the anterior membrane of notochord cells during zebrafish neuralation. Fz/PCP-dependent Pk localizes to the anterior membrane of notochord cells during zebrafish neuralation. Fz/PCP-dependent Pk localizes to the anterior membrane of notochord cells during zebrafish neuralation. Fz/PCP-dependent Pk localizes to the anterior membrane of notochord cells during zebrafish neuralation. Fz/PCP signaling zebrafish development neuralation notochord cells anterior membrane localization planar cell polarity Fz/PCP Pk protein zebrafish development neuralation notochord cells anterior membrane molecular biology embryology gene expression cell signaling Fz/PCP Pk protein zebrafish development neuralation notochord cells anterior membrane signaling pathway gene expression embryonic stages cell polarization Fz/PCP signaling Pk protein localization zebrafish development neuralation process notochord cells analysis embryonic patterning cell membrane定位 molecular biology techniques gene expression during neuralation zebrafish embryology研究 Fz/PCP Pk protein zebrafish neuralation notochord anterior membrane localization developmental biology genetics embryo Fz/PCP signaling zebrafish development neuralation process notochord cells membrane localization protein localization gene expression analysis embryonic patterning cell polarity molecular biology techniques Fz/PCP planar cell polarity zebrafish neuralation notochord cell membrane localization developmental biology genetics Fz/PCP Pk protein notochord cells zebrafish development neuralation anterior membrane cell localization molecular biology embryonic development Fz/PCP Pk protein zebrafish development neuralation notochord cells anterior membrane cell localization gene expression embryonic stage molecular biology developmental biology Fz/PCP signaling zebrafish development notochord functional genomics neuralation molecular biology cell localization
1303	Tirasemtiv has no effect on fast-twitch muscle. Tirasemtiv has no effect on fast-twitch muscle. Tirasemtiv has no effect on fast-twitch muscle. Tirasemtiv has no effect on fast-twitch muscle. Tirasemtiv has no effect on fast-twitch muscle. tirasemtiv muscle type slow-twitch faster testing clinical trials effectiveness neurodegenerative diseases tirasemtiv muscle fibers efficacy slow-twitch clinical trials neurodegeneration ALS therapeutic effects tirasemtiv muscle type slow-twitch clinical trial effectiveness ALS skeletal muscle fiber type tirasemtiv clinical trials tirasemtiv side effects tirasemtiv benefits tirasemtiv dosage tirasemtiv approval status tirasemtiv fast-twitch muscle efficacy clinical trial neurology myotonic dystrophy drug response tirasemtiv fast-twitch muscle effectiveness clinical trials neurological disorders treatment pharmacology myopathies clinical outcomes neuromuscular diseases tirasemtiv fast-twitch muscle efficacy clinical trial neurological disorder treatment therapy pharmacology muscle type drug response tirasemtiv fast-twitch muscle efficacy clinical trial neurological disorder treatment myotonic dystrophy pharmacology muscle type therapeutic index tirasemtiv fast-twitch muscle efficacy clinical trial neurodegenerative disease treatment pharmacology myotonic dystrophy therapeutic response mechanism tirasemtiv benefits slow-twitch muscle clinical trials muscle types therapeutic effects
684	Lack of clpC does not affect sporulation efficiency in Bacillus subtilis cells. Lack of clpC does not affect sporulation efficiency in Bacillus subtilis cells. Lack of clpC does not affect sporulation efficiency in Bacillus subtilis cells. Lack of clpC does not affect sporulation efficiency in Bacillus subtilis cells. Lack of clpC does not affect sporulation efficiency in Bacillus subtilis cells. Lack clpC Bacillus subtilis sporulation effectiveness genes proteins microbiology molecularbiology clpC protein function Bacillus subtilis sporulation sporulation process protein role in bacteria clpC gene effect clpC protein Bacillus subtilis sporulation bacterial sporulation gene function genetic mutation protein role bacteria cell cycle sporulation process bacterial physiology clpC homologs Lack of clpC Bacillus subtilis clpC protein function sporulation process Bacillus subtilis clpC gene deletion bacterial sporulation efficiency clpC role in sporulation Bacillus subtilis cell biology spore formation Bacillus subtilis clpC homologs bacterial stress response Lack clpC Bacillus subtilis sporulation effect genes microbiology clpC function Bacillus subtilis sporulation sporulation efficiency gene clpC protein role clpC protein Bacillus subtilis sporulation gene function bacterial spore formation genetic mutation impact sporulation process bacterial genetics clpC role Lack clpC Bacillus subtilis sporulation effectiveness keywords biological microbiology genetic factor clpC protein Bacillus subtilis sporulation bacterial spore formation genetic mutation impact sporulation efficiency analysis Clp protease family clpC protein function Bacillus subtilis sporulation sporulation efficiency factors ClpC role in bacteria sigma factor regulation Bacillus subtilis genetics molecular biology of sporulation Bacterial protein roles
443	GATA-3 is important for hematopoietic stem cell (HSC) function. GATA-3 is important for hematopoietic stem cell (HSC) function. GATA-3 is important for hematopoietic stem cell (HSC) function. GATA-3 is important for hematopoietic stem cell (HSC) function. GATA-3 is important for hematopoietic stem cell (HSC) function. GATA3 hematopoietic stem cells function transcription factor immune system differentiation maintenance regulation development GATA3 hematopoietic.stem.cell function stem.cells research regulation differentiation molecular.biology transcription.factor immune.system GATA3 hematopoietic.stem.cell function regulation transcription.factors maintenance differentiation immune.response tcell.development GATA-3 role GATA-3 function GATA-3 hematopoietic stem cells GATA-3 gene expression GATA-3 protein GATA-3 regulation GATA-3 signaling GATA-3 mutation GATA-3 knockout GATA-3 mechanism GATA-3 hematopoietic stem cell function transcription factor maintenance differentiation regulation immune system development GATA-3 role HSC development GATA-3 gene expression Hematopoiesis regulation HSC maintenance GATA-3 knockout HSC differentiation HSC biology GATA3 hematopoietic stem cells function stem cell biology molecular biology transcription factors immune system cell differentiation microRNA regulatory elements GATA-3 HSC function stem cells immune system differentiation maintenance regulation transcription factor cell biology immunology GATA3 hematopoietic.stem.cell function regulation transcription.factors mouse.experiments human.studies DNA.bindings promoter.regulation cell.differentiation GATA3 hematopoiesis stem cells immune system transcription factor Th17 development gene expression lymphopoiesis
324	Deleting Raptor reduces G-CSF levels. Deleting Raptor reduces G-CSF levels. Deleting Raptor reduces G-CSF levels. Deleting Raptor reduces G-CSF levels. Deleting Raptor reduces G-CSF levels. search effectiveness expansion terms query medical pharmacology hematopoietic stem cells immunology therapy treatment side effects clinical studies database analysis literature review Raptor medication G-CSF therapy bone marrow suppression myeloid progenitor cells immune response modification hematopoiesis process deleting raptor g-csf levels immune response myeloid cells cytokines hematopoiesis bone marrow clinical trials therapeutic impact query expansion relevant phrases medical conditions pharmacology treatment effects clinical implications hematopoietic growth factors bone marrow stimulation immune response modulation Deleting Raptor Raptor inhibition G-CSF regulation hematopoiesis myeloid cells signaling pathways clinical trials pharmacodynamics immune response bone marrow function search optimization keyword expansion medical queries pharmacology terms G-CSF reduction Raptor treatment search accuracy query expansion medical terminology pharmacology bone marrow neutropenia cytokines hematopoiesis immunology clinical trials side effects drug interactions blood cells immune system therapeutic targets biotechnology oncology patient outcomes clinical symptoms Deleting Raptor G-CSF levels therapeutic target bone marrow hematopoiesis immune response clinical trial biomarker cytokine myeloid cells immunosuppression Deleting Raptor Raptor inhibition G-CSF reduction myeloid cells cytokine production bone marrow function hematopoiesis immune response clinical trials pharmacodynamics signaling pathways cancer therapy hematologic disorders immune modulation drug effects biomarkers therapeutic targets search outcomes enhancement keyword recommendation medical biology pharmacology cytokines bone marrow hematopoiesis
327	Deletion of αvβ8 does not result in a spontaneous inflammatory phenotype. Deletion of αvβ8 does not result in a spontaneous inflammatory phenotype. Deletion of αvβ8 does not result in a spontaneous inflammatory phenotype. Deletion of αvβ8 does not result in a spontaneous inflammatory phenotype. Deletion of αvβ8 does not result in a spontaneous inflammatory phenotype. αvβ8 integrin inflammatory response gene deletion spontaneous inflammation immune system cytokines thrombospondin-1 cell adhesion bone marrow hematopoiesis Deletion αvβ8 integrin spontaneous inflammation knockout mouse model immune response cytokine production gene editing innate immunity adaptive immunity αvβ8 integrin inflammation knockout immune response cytokines gene deletion spontaneous disease inflammatory phenotype cell adhesion fibrosis αvβ8 integrin inflammatory phenotype immune response gene deletion cell adhesion thrombospondin binding bone marrow hematopoietic cells macrophages cytokine production immune modulation angiogenesis wound healing cancer progression autoimmune diseases αvβ8 integrin inflammatory response knockout mice spontaneous inflammation immune system gene deletion inflammatory phenotype inflammatory response αvβ8 integrin immune system knockout model cytokine production tissue repair cell adhesion wound healing innate immunity adaptive immunity αvβ8 integrin inflammatory response spontaneous inflammation gene deletion knockout model immune system cytokines macrophages fibroblasts vascular development thrombosis risk Deletion αvβ8 integrin inflammatory phenotype spontaneous inflammation gene knockout immune response mice model collagen deposition bone marrow hematopoietic cells angiogenesis wound healing Deletion αvβ8 integrin spontaneous inflammation knockout mice inflammatory phenotype immune response tissue repair gene function cytokine production hematopoietic cells endothelial cells signaling pathways molecular biology immunology pathology αvβ8 integrin inflammation knockout immune response mice tissue repair wound healing cytokines genetics immunology cell adhesion pathology
569	In adult tissue, most T cells are memory T cells. In adult tissue, most T cells are memory T cells. In adult tissue, most T cells are memory T cells. In adult tissue, most T cells are memory T cells. In adult tissue, most T cells are memory T cells. adult tissue T cells memory T cells immunology lymphocytes hematopoiesis immune response adult tissue T cells memory T cells immunology immune response human body T cell development tissue-specific immunity adult tissue T cells memory T cells immunology hematopoiesis immune response adult tissue memory T cells immune system T cell development immunology research tissue-specific immunity adaptive immunity T cell subsets lymphocyte function antigen-specific immunity adult tissue memory T cells immune system lymphocytes antigen experience adaptive immunity T cell subsets immunology research cellular biology T cell memory adult immune system tissue-specific T cells T cell activation adaptive immunity in adults adult tissue memory T cells immune system lymphocytes antigen experience immunology adaptive immunity T cell subsets T memory cells tissue-resident memory T cells adult tissue T cells memories T cells immune response longevity memory cells tissue-specific immunity adult tissue memory T cells immune response antigen exposure lymphocyte development immunology adaptive immunity T cell subsets cellular immunity immune system structure adult tissue T cells memory T cells immunology immune response lymphocytes antigen presentation vaccine response B cells
208	CHEK2 is not associated with breast cancer. CHEK2 is not associated with breast cancer. CHEK2 is not associated with breast cancer. CHEK2 is not associated with breast cancer. CHEK2 is not associated with breast cancer. CHEK2 breast cancer mutation CHEK2 function breast cancer genetic testing breast cancer risk factors CHEK2 protein BRCA1 BRCA2 breast cancer prevention tumor suppressor genes CHEK2 breast cancer association studies CHEK2 genetic testing CHEK2 mutation analysis CHEK2 cancer risk CHEK2 tumor biology CHEK2 clinical significance CHEK2 epidemiology CHEK2 cancer genetics CHEK2 oncology research CHEK2 pathogenicity CHEK2 gene breast cancer risk genetic testing cancer susceptibility tumor suppressor gene BRCA1 BRCA2 comparison hereditary cancer syndrome genomic analysis oncology research genetic counseling mutation prevalence CHEK2 gene function CHEK2 and cancer types CHEK2 mutation analysis CHEK2 breast cancer risk CHEK2 genetic testing CHEK2 inheritance pattern CHEK2 gene function mutation risk factor brca1 brca2 cancer types hereditary predisposition study findings clinical significance genetic testing cancer risk hereditary factors mutation analysis breast cancer screening test results interpretation clinical genetics CHEK2 gene breast cancer risk tumor suppressor gene genetic testing cancer susceptibility BRCA1 and BRCA2 hereditary cancer syndromes genomic testing oncology medical genetics cancer predisposition genetic counseling cancer biomarkers CHEK2 genetic test CHEK2 mutation breast cancer risk tumor suppressor gene BRCA1 and BRCA2 comparison CHEK2 clinical significance CHEK2 breast cancer genetics CHEK2 mutation analysis breast cancer risk factors CHEK2 protein function BRCA1 BRCA2 comparison genetic testing for breast cancer CHEK2 clinical significance breast cancer genetic testing CHEK2 function cancer predisposition genes BRCA1 BRCA2 comparison
690	Less than 10% of the gabonese children with Schimmelpenning-Feuerstein-Mims syndrome (SFM) had a plasma lactate of more than 5mmol/L. Less than 10% of the gabonese children with Schimmelpenning-Feuerstein-Mims syndrome (SFM) had a plasma lactate of more than 5mmol/L. Less than 10% of the gabonese children with Schimmelpenning-Feuerstein-Mims syndrome (SFM) had a plasma lactate of more than 5mmol/L. Less than 10% of the gabonese children with Schimmelpenning-Feuerstein-Mims syndrome (SFM) had a plasma lactate of more than 5mmol/L. Less than 10% of the gabonese children with Schimmelpenning-Feuerstein-Mims syndrome (SFM) had a plasma lactate of more than 5mmol/L. Schimmelpenning-Feuerstein-Mims syndrome SFM plasma lactate Gabonese children disease rare condition metabolism gabonese population SFMS plasma lactate levels symptoms prevalence genetic disorder growth development Schimmelpenning-Feuerstein-Mims SFM Gabon children plasma lactate syndrome prevalence metabolic disorders neurological Schimmelpenning-Feuerstein-Mims SFM plasma lactate Gabon children syndrome electrolyte imbalance metabolic disorder neurological symptoms genetic condition pediatric diagnostic markers Schimmelpenning-Feuerstein-Mims syndrome Gabon children plasma lactate level prevalence Schimmelpenning-Feuerstein-Mims SFM Gabon plasma lactate syndrome children Schimmelpenning-Feuerstein-Mims syndrome gabonese children plasma lactate level percentage Schimmelpenning-Feuerstein-Mims SFM Gabonese children plasma lactate syndrome metabolic disorder pediatric condition electrolyte imbalance Schimmelpenning-Feuerstein-Mims Gabon plasma lactate syndrome children prevalence metabolic disorder Schimmelpenning-Feuerstein-Mims Gabon children plasma lactate syndrome epidemiology metabolism
691	Leukemia associated Rho guanine nucleotide-exchange factor represses RhoA in response to SRC activation. Leukemia associated Rho guanine nucleotide-exchange factor represses RhoA in response to SRC activation. Leukemia associated Rho guanine nucleotide-exchange factor represses RhoA in response to SRC activation. Leukemia associated Rho guanine nucleotide-exchange factor represses RhoA in response to SRC activation. Leukemia associated Rho guanine nucleotide-exchange factor represses RhoA in response to SRC activation. Leukemia RhoGDP exchange factor RhoA SRC kinase gene expression oncology signal transduction molecular biology cancer therapy Leukemia Rho guanine nucleotide-exchange factor RhoA SRC activation gene expression signaling pathway oncology hematopoiesis cell biology Leukemia RhoGDI2 RhoA SRC signaling gene expression oncology pathology bioinformatics molecular biology cancer research hematopoiesis Leukemia RhoGAP RhoA SRC activation signaling pathway gene expression cancer biology cell regulation molecular mechanism oncology research Leukemia Rho guanine nucleotide-exchange factor RhoA SRC activation gene expression oncology signal transduction cellular biology molecular mechanism leukemia Rho guanine nucleotide-exchange factor RhoA SRC activation gene expression oncology signaling pathways molecular biology cancer research Leukemia Rho guanine nucleotide-exchange factor RhoA SRC activation gene expression oncology signaling pathway cancer biology molecular biology cell regulation Leukemia Rho guanine nucleotide-exchange factor RhoA SRC activation gene expression signaling pathway oncology hematopoietic disorders molecular biology cancer research Leukemia Rho guanine nucleotide-exchange factor RhoA SRC activation gene expression oncology signaling pathway molecular biology cancer research bioinformatics Leukemia Rho guanine nucleotide-exchange factor RhoA SRC activation gene expression oncology molecular biology signal transduction cancer therapy cellular regulation
692	Leuko-increased blood increases infectious complications in red blood cell transfusion. Leuko-increased blood increases infectious complications in red blood cell transfusion. Leuko-increased blood increases infectious complications in red blood cell transfusion. Leuko-increased blood increases infectious complications in red blood cell transfusion. Leuko-increased blood increases infectious complications in red blood cell transfusion. leukocytes blood transfusion infectious complications erythrocytes white blood cells leukocytes transfusion infection risk clinical studies evidence mortality treatment management leukocytes transfusion infection risk complications red blood cells white blood cells immune response leukocyte reduction techniques infectious diseases risk factors transfusion medicine clinical implications blood transfusion safety white blood cells leukocytes blood transfusion infectious complications erythrocytes white blood cells transfusion medicine leukocytes blood transfusion infectious risk immune response transfusion medicine leukocytes blood transfusion infectious diseases complications immune response leukocyte reduction transfusion risk complications infectious disease prevention therapy leukocyte transfusion infection risk factor clinical treatment prevention hematopoiesis immuneresponse leukocyte risk factors transfusion-associated guidelines infectious diseases clinical trials
1316	Transferred UCB T cells acquire a memory-like phenotype in recipients. Transferred UCB T cells acquire a memory-like phenotype in recipients. Transferred UCB T cells acquire a memory-like phenotype in recipients. Transferred UCB T cells acquire a memory-like phenotype in recipients. Transferred UCB T cells acquire a memory-like phenotype in recipients. Transduced UCB T cells Memory phenotype acquisition Transplantation immunology Lymphocyte function Immune memory induction Hematopoietic stem cell transplantation T cell differentiation Immune response modulation Stem cell biology Adoptive cell transfer immune response transplantation immunology T cell function memory T cells lymphocyte migration adaptive immunity chimeric antigen receptor gene editing cytokine production immune response memory T cells transplantation immune tolerance cytokine production clonal expansion antigen specificity lymphocyte trafficking adaptive immunity immune activation immune response transplantation immunology T cell function adaptive immunity lymphocyte trafficking cytokine production antigen presentation immune memory formation transplant rejection immunosuppression T cells memory-like phenotype transferred cells UCB recipients immune response lymphocytes transplantation immunology adaptive immunity stem cells chimerism inflammation UCB cells memory T cells transferred immunity adaptive immune response immunology research cellular therapy immune memory T cell activation stem cell transplantation graft-versus-host disease immune response antigen presentation lymphocyte activation adaptive immunity cellular therapy immunology research T cell function gene editing immune memory clinical trial outcomes Transplantation Immune Response Lymphocytes Adaptive Immunity Stem Cells Gene Therapy Immunology Biotechnology Cell Therapy Clinical Trials immune response transplantation immunology T cell function adaptive immunity memory T cells graft-versus-host cellular therapy immunological memory immune reconstitution T-cell memory immune response transplantation adaptive immunity cytokines antigen presentation lymphocyte activation immunology clinical trial immunotherapy stem cell transplantation
693	Leuko-reduced blood reduces infectious complications in red blood cell transfusion. Leuko-reduced blood reduces infectious complications in red blood cell transfusion. Leuko-reduced blood reduces infectious complications in red blood cell transfusion. Leuko-reduced blood reduces infectious complications in red blood cell transfusion. Leuko-reduced blood reduces infectious complications in red blood cell transfusion. leukoreduced blood transfusion infectious complications red blood cells white blood cell transfusion safety hematology clinical trial immunology leuko-reduction blood transfusion infectious complications red blood cells white blood cells transfusion medicine hematopoiesis cellular therapy medical research clinical trials transfusion safety leukocytes immune response blood products hematology leukoreduced leukocyte transfusion complications infection blood products therapeutic treatment clinical trial efficacy safety hematological donor recipient immunology therapy biochemistry pathology leuko-reduction technique leukoreduced blood benefits infectious complications prevention red blood cell safety blood transfusion infection risk leukocyte reduced products clinical applications leukoreduction blood component therapy transfusion-associated graft-versus-host disease immunological advantages leuko-reduction blood transfusion infectious complications red blood cells white blood cells clinical trial transfusion medicine hematopoietic stem cell transplantation infection prevention blood product safety leuko-reduced blood benefits leuko-reduced blood safety leukocyte-reduced blood advantages reduced leukocytes transfusion leukoreduced blood infections leukoreduction process leukoreduced blood efficacy leukocyte-reduced blood transfusion leuko-reduction blood transfusion infectious complications white blood cells transfusion safety blood processing techniques leuko-reduction blood transfusion infectious complications red blood cells therapeutic apheresis blood processing techniques clinical efficacy medical treatments hematology transfusion medicine leuko-reduction blood transfusion infectious complications red blood cells clinical trials patient outcomes immune compatibility storage conditions transplantation immunology leuko-reduction blood transfusion infectious complications white blood cells transfusion safety hematopoietic stem cells immunocompromised patients
452	Gene expression does not vary appreciably across genetically identical cells. Gene expression does not vary appreciably across genetically identical cells. Gene expression does not vary appreciably across genetically identical cells. Gene expression does not vary appreciably across genetically identical cells. Gene expression does not vary appreciably across genetically identical cells. gene regulation cellular consistency genetic identicality molecular biology cell variability gene regulation cellular consistency molecular biology genetic identicality cell homogeneity transcriptomics biological variability molecular variation epigenetics gene regulation transcriptional variability cellular homogeneity genetic clones molecular biology techniques epigenetics stochastic gene expression gene regulation cellular heterogeneity epigenetics transcriptional variation identical twins molecular biology gene function genetic similarity biological consistency cell differentiation gene regulation cellular consistency genetic clones transcriptional stability identical twins molecular biology epigenetics genetic variation cellular heterogeneity molecular biology RNA expression identical twins gene regulation biological variance gene regulation cell homogeneity molecular biology genetic identicality transcriptional consistency gene stability cellular uniformity molecular consistency identical cells expression genetic identicality impacts gene regulation cellular heterogeneity epigenetics transcriptional variability identical twins molecular biology genetic identicality gene regulation transcriptional control cellular heterogeneity epigenetics stochastic processes
212	CR is associated with higher methylation age. CR is associated with higher methylation age. CR is associated with higher methylation age. CR is associated with higher methylation age. CR is associated with higher methylation age. CR methylation age longevity dietary restriction aging senescence human studies model organisms gene expression longevity markers CR methylation age longevity caloric restriction epigenetics human aging research biomarker senescence geroscience CR methylation age dietary restriction longevity epigenetics nutrition human aging molecular biology genetic factors life span effects of diet CR methylation age longevity aging dietary restriction human aging model organisms epigenetic age biomarkers of aging genetic factors environmental factors CR methylation age longevity aging dietary restriction senescence human studies model organisms epigenetic clock CR methylation age aging process longevity dietary restriction epigenetic markers CR methylation age longevity dietary restriction aging senescence gene expression epigenetics human studies mouse models CR methylation age longevity aging caloric restriction dietary restriction epigenetics human aging model organisms mouse studies biomarker biological age genetic factors environmental factors life span chronological age CR methylation age longevity aging dietary restriction epigenetics human aging model organisms nutrition genetic factors biomarkers CR methylation age longevity aging dietary restriction epigenetic age genetic factors lifestyle factors healthspan
575	In domesticated populations of Saccharomyces cerevisiae, whole chromosome aneuploidy is very uncommon. In domesticated populations of Saccharomyces cerevisiae, whole chromosome aneuploidy is very uncommon. In domesticated populations of Saccharomyces cerevisiae, whole chromosome aneuploidy is very uncommon. In domesticated populations of Saccharomyces cerevisiae, whole chromosome aneuploidy is very uncommon. In domesticated populations of Saccharomyces cerevisiae, whole chromosome aneuploidy is very uncommon. Saccharomyces cerevisiae genetics chromosome abnormalities yeast genomics common genetic variations chromosomal instability yeast biology aneuploidy prevalence genomic stability Saccharomyces cerevisiae chromosome structure Saccharomyces cerevisiae genetics whole chromosome aneuploidy frequency yeast chromosome variations common genetic mutations Saccharomyces cerevisiae genomic stability aneuploidy occurrence domesticated yeast chromosomes genetic abnormalities in yeast yeast chromosome instability Saccharomyces cerevisiae genome analysis Saccharomyces cerevisiae genetics chromosome abnormalities yeast genome variation aneuploidy prevalence domesticated yeasts chromosomal mutations Saccharomyces cerevisiae evolution Saccharomyces cerevisiae genome analysis yeast chromosome variation genetic diversity in yeast common yeast chromosome abnormalities yeast population genetics chromosome aneuploidy frequency Saccharomyces cerevisiae genetic stability yeast chromosomal mutations whole genome sequencing in yeast yeast chromosome structurevariation Saccharomyces cerevisiae whole chromosome aneuploidy domesticated populations genetic variability yeast genetics chromosome abnormalities evolutionary biology molecular genetics yeast genomics Saccharomyces cerevisiae chromosome variations common chromosome alterations Saccharomyces cerevisiae genetic stability yeast chromosome aneuploidy frequency domesticated yeast genetic changes Saccharomyces cerevisiae whole chromosome aneuploidy domesticated populations genetic variation yeast biology chromosomal abnormalities genetic stability genomic imprinting gene dosage effects Saccharomyces cerevisiae chromosome aneuploidy domesticated yeast genetic stability chromosomal abnormalities yeast genetics rare chromosomal alterations genomic instability Saccharomyces cerevisiae biology yeast domestication common genetic variations Saccharomyces cerevisiae whole chromosome aneuploidy domesticated populations genetic variation yeast aneuploidy evolutionary biology chromosomal abnormalities Saccharomyces cerevisiae genetics Saccharomyces cerevisiae whole chromosome aneuploidy domesticated populations yeast genetics chromosomal abnormalities genetic variation common genetic patterns molecular biology evolutionary genetics
213	CRP is not predictive of postoperative mortality following Coronary Artery Bypass Graft (CABG) surgery. CRP is not predictive of postoperative mortality following Coronary Artery Bypass Graft (CABG) surgery. CRP is not predictive of postoperative mortality following Coronary Artery Bypass Graft (CABG) surgery. CRP is not predictive of postoperative mortality following Coronary Artery Bypass Graft (CABG) surgery. CRP is not predictive of postoperative mortality following Coronary Artery Bypass Graft (CABG) surgery. CRP postoperative mortality CABG coronary artery bypass predictive factors surgical outcomes CRP postoperative mortality CABG coronary artery bypass predictive factors surgery outcomes CRP inflammatory markers postoperative outcomes CABG cardiovascular surgery mortality risk predictive factors surgical complications CRP levels CABG surgery postoperative mortality predictive factors cardiovascular surgery inflammation markers clinical outcomes CRP postoperative mortality CABG coronary artery bypass predictive factors surgical outcomes CRP levels postoperative complications CABG surgery outcomes mortality risk factors cardiovascular surgery inflammatory markers CRP postoperative mortality Coronary Artery Bypass Graft CABG predictive factors surgery outcomes inflammation markers cardiovascular surgery risk assessment clinical indicators CRP levels CABG surgery postoperative mortality predictive factors cardiovascular surgery inflammatory markers CRP levels postoperative complications CABG surgery inflammatory markers mortality risk cardiac surgery outcomes predictive factors surgical interventions CRP levels postoperative complications CABG success inflammatory markers surgical outcomes mortality risk factors cardiac surgery recovery clinical prognosis
577	In mice, P. chabaudi parasites are able to proliferate faster early in infection when inoculated at lower numbers than when inoculated at high numbers. In mice, P. chabaudi parasites are able to proliferate faster early in infection when inoculated at lower numbers than when inoculated at high numbers. In mice, P. chabaudi parasites are able to proliferate faster early in infection when inoculated at lower numbers than when inoculated at high numbers. In mice, P. chabaudi parasites are able to proliferate faster early in infection when inoculated at lower numbers than when inoculated at high numbers. In mice, P. chabaudi parasites are able to proliferate faster early in infection when inoculated at lower numbers than when inoculated at high numbers. mice P. chabaudi parasite proliferation inoculation number infection timing parasitic adaptation immune response infection dynamics mice P. chabaudi infection dynamics parasite proliferation viral load immune response inoculation dose effect of number P. chabaudi mice infection parasite proliferation inoculation dosage immune response infection kinetics parasitic load host response P. chabaudi infection dynamics parasite proliferation rates inoculation density effects malaria parasite behavior early infection stages immune response latency virulence factors host-microbe interaction immunology research parasitology studies P. chabaudi mice parasite proliferation infection dynamics inoculation quantity immune response P. chabaudi parasites proliferation infection dynamics inoculation numbers mouse models parasite expansion rates immune response influence host factor impact virulence factors parasitic load early infection phase immune system engagement infectious dose effects P. chabaudi parasites proliferation infection inoculation mouse model parasite load immune response virulence factors P.chabaudi parasite proliferation mouse infection inoculation dose early infection parasite adaptation immunological response virulence factors P. chabaudi parasite proliferation mouse infection inoculation dose early infection phase parasite growth rate immunological response malaria parasites mouse models infection dynamics parasite inoculation viral load effect of dosage onset of infection
578	In mouse models, the loss of CSF1R facilitates MOZ-TIF2-induced leuekmogenesis. In mouse models, the loss of CSF1R facilitates MOZ-TIF2-induced leuekmogenesis. In mouse models, the loss of CSF1R facilitates MOZ-TIF2-induced leuekmogenesis. In mouse models, the loss of CSF1R facilitates MOZ-TIF2-induced leuekmogenesis. In mouse models, the loss of CSF1R facilitates MOZ-TIF2-induced leuekmogenesis. mouse models CSF1R MOZ-TIF2 leuekmogenesis cancer development immune response hematopoiesis genetic mutation mouse models CSF1R loss facilitation MOZ-TIF2 leukemogenesis genetic modifications cancer development hematopoietic cells immune system impact oncogenic mechanisms CSF1R knockout mouse model MOZ-TIF2 leukemia development stem cell differentiation cancer biology immune response MPO expression myeloid lineage CSF1R function MOZ-TIF2 interaction leukemia development mouse genetics hematopoietic stem cells oncogenic pathways immune response modulation myeloid lineage differentiation gene expression analysis cancer biology research genetic models of disease mouse models CSF1R MOZ-TIF2 leukemogenesis immune response microenvironment stem cells cancer biology genetic modifications mouse models CSF1R loss MOZ-TIF2 leukemia genetic models oncogenesis hematopoietic malignancy stem cell differentiation immune system signaling pathways mouse models CSF1R loss MOZ-TIF2 leukemogenesis gene expression cancer development hematopoiesis stem cells oncology research immune system signaling pathways protein interactions CSF1R knockout mouse models MOZ-TIF2 leukemia induction immune response modulation cancer progression bone marrow cells microenvironmentinteraction mouse models CSF1R MOZ-TIF2 leukaemogenesis hematopoiesis gene expression cancer progression immunology oncology stem cells mouse models CSF1R MOZ-TIF2 leuekmogenesis genetic modification hematopoietic stem cells cancer development immune response modulation gene expression analysis oncogenic pathways
216	CX3CR1 on the Th2 cells impairs T cell survival CX3CR1 on the Th2 cells impairs T cell survival CX3CR1 on the Th2 cells impairs T cell survival CX3CR1 on the Th2 cells impairs T cell survival CX3CR1 on the Th2 cells impairs T cell survival CX3CR1 Th2 cells T cell survival immunology inflammation cytokines genetics mouse models immune response adaptive immunity innate immunity CX3CR1 Th2 cells T cell survival immunology cytokines inflammation mouse models human studies immune response adaptive immunity innate immunity cell signaling gene expression pathology allergic diseases asthma autoimmune disorders CX3CR1 Th2 cells T cell survival immunology cytokines gene expression allergic responses inflammation immune regulation monocytic chemokine receptors CX3CR1 Th2 cells immunology CX3CR1 Th2 cells T cell survival CX3CR1 Th2 immune response CX3CR1 Th2 T cell interaction CX3CR1 Th2 regulatory function CX3CR1 Th2 signaling pathways CX3CR1 Th2 inflammation CX3CR1 Th2 cytokine production CX3CR1 Th2 T cell differentiation CX3CR1 Th2 T cell activation CX3CR1 Th2 cells T cell survival immune response inflammation cytokines gene expression immunology adaptive immunity cellular communication biological markers CX3CR1 Th2 cells T cell survival CX3CR1 Th2 immune response Th2 cell function CX3CR1 CX3CR1 T cell interaction Th2 cell CX3CR1 role CX3CR1 immunology Th2 T cell survival mechanisms CX3CR1 CX3CR1 gene expression Th2 CX3CR1 Th2 inflammation Th2 CX3CR1 signaling CX3CR1 Th2 cells T cell survival immune response inflammation cytokines gene expression immunology cell signaling allergic diseases asthma immune tolerance CX3CR1 Th2 cells T cell survival immunity immune response inflammation cytokines molecular markers immune regulation CX3CR1 Th2 cells T cell survival immunology cytokines gene expression inflammation allergy asthma immune response regulatory T cells antigen presentation CX3CR1 Th2 cells T cell survival immune response inflammation cytokines gene expression immune modulation immunotherapy allergic reactions autoimmune diseases
217	CX3CR1 on the Th2 cells promotes T cell survival CX3CR1 on the Th2 cells promotes T cell survival CX3CR1 on the Th2 cells promotes T cell survival CX3CR1 on the Th2 cells promotes T cell survival CX3CR1 on the Th2 cells promotes T cell survival CX3CR1 Th2 cells T cell survival immune response cytokines gene expression inflammation allergy asthma immunology biomarker cell signaling CX3CR1 Th2 cells T cell survival immunology molecular biology inflammation immune response cell signaling CX3CR1 Th2 T cell survival immune response cytokines chemokines inflammation gene expression signaling pathways immunology cell biology CX3CR1 signaling Th2 cell activation T cell proliferation immune response regulation CX3CL1 interaction adaptive immunity enhancement cytokine production immunological synapse formation CX3CR1 Th2 cells T cell survival immune response cytokines signaling pathways inflammation antigen presentation adaptive immunity gene expression immunology molecular biology CX3CR1 Th2 cells T cell survival immunology inflammation cytokines gene expression immune response lymphocytes adaptive immunity innate immunity cell signaling allergic reactions chronic inflammation immune checkpoint inhibitors monoclonal antibodies CX3CR1 Th2 cells T cell survival immunology cytokines chemokines immune response inflammation gene expression cell signaling CX3CR1 Th2 cells T cell survival immunology cytokines chemokines gene expression immune response inflammation allergy asthma autoimmune disorders T helper cells signaling pathways CX3CR1 Th2 cells T cell survival immune response inflammation cytokines gene expression immunology biomarker allergy asthma multiple sclerosis adaptive immunity innate immunity CX3CR1 Th2 cells T cell survival immune response cytokines chemokines inflammation immunology adaptive immunity cellular interactions gene expression protein function allergy asthma autoimmune disorders lymphocyte activation
338	Dexamethasone decreases risk of postoperative bleeding. Dexamethasone decreases risk of postoperative bleeding. Dexamethasone decreases risk of postoperative bleeding. Dexamethasone decreases risk of postoperative bleeding. Dexamethasone decreases risk of postoperative bleeding. Dexamethasone corticosteroids postoperative complications bleeding risk surgical outcomes inflammation reduction anesthesia interaction steroid therapy surgery recovery dexamethasone postoperative bleeding surgical bleeding risk reduction anesthesia surgery type dosage effect inflammation reduction corticosteroid therapy dexamethasone postoperative bleeding surgical outcomes corticosteroids anesthesia recovery时间 dexamethasone surgery postoperative care guidelines perioperative dexamethasone bleeding risk reduction anesthetic interaction inflammation control surgical bleeding prevention dexamethasone dosage for surgery dexamethasone postoperative bleeding surgery anesthesia inflammatory response corticosteroid surgical patients risk reduction medical interventions Dexamethasone surgical benefits postoperative recovery time anti-inflammatory effects surgery risk reduction operations dexamethasone use anesthesia postoperative complications prevention steroid usage surgery perioperative management strategies dexamethasone postoperative bleeding surgical bleeding steroid effects inflammation reduction anesthesia interactions surgical recovery risk reduction medical outcomes Dexamethasone postoperative bleeding surgical outcomes anti-inflammatory corticosteroid hemorrhage reduction risk factor anesthesia interaction surgical preparation recovery time dexamethasone postoperative bleeding risk reduction surgical bleeding corticosteroids anesthesia inflammation recovery time dexamethasone surgery dexamethasone anesthesia postoperative complications surgical bleeding prevention anti-inflammatory drugs surgery glucocorticoids surgery
218	CX3CR1 on the Th2 cells promotes airway inflammation. CX3CR1 on the Th2 cells promotes airway inflammation. CX3CR1 on the Th2 cells promotes airway inflammation. CX3CR1 on the Th2 cells promotes airway inflammation. CX3CR1 on the Th2 cells promotes airway inflammation. CX3CR1 Th2 cells airway inflammation immune response allergy asthma cytokines chemokines mouse model human study inflammatory pathways CX3CR1 Th2 cells airway inflammation immune response allergy asthma cytokines chemokines mouse model human study immunology respiratory system inflammation mechanisms gene expression cell signaling allergens eosinophils macrophages T-helper cells pulmonary function bronchial hyperreactivity CX3CR1 Th2 cells airway inflammation immune response cytokines asthma allergic reactions gene expression immune cells lung function immunology CX3CR1 Th2 cells inflammation CX3CR1 signaling Th2 cells CX3CR1 expression in Th2 cells CX3CR1 role in asthma CX3CR1 Th2 cell interaction CX3CR1 and immune response CX3CR1 gene Th2 cells CX3CR1 activation Th2 cells CX3CR1 Th2 cell mechanism CX3CR1 Th2 cell pathway CX3CR1 Th2 cells airway inflammation immune response asthma cytokines chemokines allergic reactions lung function immune regulation gene expression CX3CR1 Th2 cells airway inflammation immune response asthma inflammation markers cytokines chemokines allergic reactions immunology lung health cell signaling molecular biology genetic factors disease mechanisms therapeutic targets CX3CR1 Th2 cells airway inflammation immune response asthma cytokines gene expression allergic reactions lung function immunology CX3CR1 Th2 cells airway inflammation immune response asthma eosinophils cytokines allergic reaction lung inflammation T helper cells inflammatory pathways CX3CR1 Th2 cells airway inflammation immunology cytokines allergic asthma T helper cells chemokine receptors lung pathology immune response CX3CR1 Th2 cells airway inflammation immune response cytokines asthma allergy immunology gene expression biomarkers
219	CX3CR1 on the Th2 cells suppresses airway inflammation. CX3CR1 on the Th2 cells suppresses airway inflammation. CX3CR1 on the Th2 cells suppresses airway inflammation. CX3CR1 on the Th2 cells suppresses airway inflammation. CX3CR1 on the Th2 cells suppresses airway inflammation. CX3CR1 Th2 cells airway inflammation immune response asthma cytokines allergy immunology lung health inflammatory diseases CX3CR1 Th2 cells airway inflammation immunology allergy asthma immune response cytokines signaling genetics mouse models human studies therapeutic targeting CX3CR1 Th2 cells airway inflammation immunology cytokines allergic responses asthma immune regulation inflammation markers immune cells T helper cells lung health allergens immune response modulation gene expression allergic disorders inflammatory diseases immune signaling immune checkpoint allergy management cellular interactions CX3CR1 function Th2 cells role airway inflammation mechanism immune response regulation inflammatory cytokines asthma treatment allergic reaction suppression immunology research biomarker identification therapeutic targets CX3CR1 Th2 cells airway inflammation immunology cytokines asthma allergy immune response gene expression allergic inflammation antigen presentation T helper cells inflammation regulation molecular biology CX3CR1 Th2 cells airway inflammation immune response regulatory T cells allergic asthma cytokine production immunosuppression lung function eosinophils CX3CR1 Th2 cells airway inflammation immune response cytokines asthma allergy immunology lung tissue repair inflammatory mediators CX3CR1 Th2 cells airway inflammation immune response regulatory T cells cytokines asthma allergic reactions immunology molecular biology antigen presentation inflammatory pathways CX3CR1 Th2 cells airway inflammation immune response regulatory T cells asthma cytokines gene expression immunology allergic reactions CX3CR1 Th2 cells airway inflammation immune response allergic reactions asthma immunology cytokines gene expression biomarkers
1319	Transplanted human glial cells can differentiate within the host animal. Transplanted human glial cells can differentiate within the host animal. Transplanted human glial cells can differentiate within the host animal. Transplanted human glial cells can differentiate within the host animal. Transplanted human glial cells can differentiate within the host animal. transplantation glial cells differentiation host animal neurobiology stem cells xenograft grafting neuroscience tissue engineering transplantation neuroscience gliosis neurogenesis xenograft host response cell differentiation neural transplantation glial cell function stem cells tissue compatibility stem cells neural transplantation gliogenesis brain repair neurogenesis cell therapy bioscience research biotechnology neuroscience xenotransplantation transplanted human neural cells differentiation process host animal response glial cell function neuroscience research human-animal chimeras stem cell transplantation gene expression analysis brain tissue compatibility transplantation human glial cells differentiation host animal neurobiology neuroscience stem cells xenotransplantation biocompatibility regeneration neuroregeneration gliogenesis brain nervous system neural transplantation glial cell differentiation host animal compatibility stem cell therapy neuroregeneration tissue engineering cellular transplantation brain repair stem cells in neuroscience gliosis response transplanted human cells glial cell differentiation host animal response neural stem cells xenotransplantation neurogenesis immune rejection gene expression analysis neural plasticity transplantation biology transplantation glial cells differentiation host animal neuroscience neurobiology stem cells biomedical research neural regeneration tissue engineering transplantation glial cells differentiation host animal neuroscience stem cells regeneration biocompatibility xenotransplantation neurobiology neural stem cells gliogenesis xenotransplantation neuroregeneration astrocytes oligodendrocytes brain plasticity immune response survival rate functional recovery
100	All hematopoietic stem cells segregate their chromosomes randomly. All hematopoietic stem cells segregate their chromosomes randomly. All hematopoietic stem cells segregate their chromosomes randomly. All hematopoietic stem cells segregate their chromosomes randomly. All hematopoietic stem cells segregate their chromosomes randomly. hematopoietic stem cells chromosome segregation random mitosis genetics biology oncology hematopoietic.stem.cells chromosome.segregation random.mitosis cell.division genetic.diversity stem.cell.research oncology molecular.biology genomics biomedical.science hematopoietic.stem.cells chromosome.segregation mitosis binary.fission stochastic.processes gene.expression cell.division somatic.mutation population.genetics molecular.biology hematopoietic stem cell biology chromosome segregation process genetic diversity mitosis in stem cells random assortment during cell division stem cell differentiation genetic variation in blood cells molecular mechanisms of randomness hematopoiesis overview chromosome distribution accuracy hematopoiesis chromosome segregation stem cell division mitosis genetic diversity clonal expansion blood cell development hematopoietic stem cell division chromosome segregation process genetic diversity mitotic spindle orientation random karyokinesis hematopoietic.stem.cells chromosome.segregation random.mechanism stem.cell.division molecular.biology genetics somatic.cells hematopoietic stem cells chromosome segregation random distribution genetic diversity cell division meiosis mitosis oncogenesis cellular biology molecular genetics biomedical research stem cell differentiation hematopoietic.stem.cells chromosome.segregation random.mechanism cell.division genetic.diversity stem.cell.research molecular.biology oncology hematopoiesis genetic.inheritance hematopoiesis stem cell division chromosomal segregation genetic diversity blood cell development meiosis mitosis oncogenesis stem cell biology molecular genetics
1204	The combination of H3K4me3 and H3K79me2 is found in quiescent hair follicle stem cells. The combination of H3K4me3 and H3K79me2 is found in quiescent hair follicle stem cells. The combination of H3K4me3 and H3K79me2 is found in quiescent hair follicle stem cells. The combination of H3K4me3 and H3K79me2 is found in quiescent hair follicle stem cells. The combination of H3K4me3 and H3K79me2 is found in quiescent hair follicle stem cells. H3K4me3 H3K79me2 quiescent hair follicle stem cells epigenetics methylation qHSCs H3K4me3 H3K79me2 quiescent hair follicle stem cells chromatin markers genetics biology molecular patterns quiescent cells stem cell biology epigenetics chromatin modifications hair follicle development gene expression regulation histone modifications transcription factors cell cycle quiescent hair follicle stem cells H3K4me3 H3K79me2 chromatin modification gene regulation stem cell biology epigenetics follicle development quiescent state transcription factors cellular differentiation H3K4me3 H3K79me2 quiescent hair follicle stem cells chromatin modification epigenetics H3K4me3 H3K79me2 quiescent hair follicle stem cells chromatin modifications gene regulation epigenetics cellular differentiation follicle stem cell markers histone modifications H3K4me3 H3K79me2 quiescent hair follicle stem cells epigenetics methylation chromatin regulation DNA modifications H3K4me3 H3K79me2 quiescent hair follicle stem cells genetic markers chromatin modifications DNA methylation transcription regulation H3K4me3 H3K79me2 quiescent hair follicle stem cells chromatin markers methylation regulation DNA expression proteomics transcription factor regulator genetics biomarker euchromatin heterochromatin H3K4me3 H3K79me2 quiescent hair follicle stem cells DNA methylation chromatin expression regulation transcription factors cell cycle
343	Diabetic patients with acute coronary syndrome experience increased short-term and long-term risk for bleeding events. Diabetic patients with acute coronary syndrome experience increased short-term and long-term risk for bleeding events. Diabetic patients with acute coronary syndrome experience increased short-term and long-term risk for bleeding events. Diabetic patients with acute coronary syndrome experience increased short-term and long-term risk for bleeding events. Diabetic patients with acute coronary syndrome experience increased short-term and long-term risk for bleeding events. diabetes acute coronary syndrome bleeding complications cardiovascular disease long-term effects short-term risks diabetes acute coronary syndrome bleeding risk factors cardiovascular complications thrombocytopenia anticoagulants platelet function mortality comorbidities pharmacotherapy management prognosis diabetes diabetic complications acute coronary syndrome bleeding risk cardiovascular disease thrombocytopenia anticoagulation therapy hypertension hyperglycemia mortality myocardial infarction stroke kidney failure retinopathy neuropathy platelet function antiplatelet agents vitamin K antagonists novel oral anticoagulants bleeding outcomes clinical trials epidemiology prevention strategies management guidelines patient education comorbidities prognosis diabetes acute coronary syndrome bleeding events diabetic patients cardiovascular risk factors acute coronary syndrome management in diabetics long-term complications of diabetes and ACS bleeding risks in diabetic ACS patients diabetic patients with ACS bleeding risk analysis short-term bleeding outcomes in diabetics with ACS differentiating bleeding risk in diabetic vs non-diabetic ACS acute coronary syndrome in diabetes treatment considerations increased bleeding risk in diabetic ACS population diabetes acute coronary syndrome bleeding risk factors long-term complications short-term effects diabetes acute coronary syndrome bleeding risk factors diabetes ACS bleeding complications diabetic ACS patient outcomes diabetic ACS bleeding management diabetic ACS bleeding prevention diabetic ACS bleeding incidence diabetic ACS long-term prognosis diabetic ACS short-term risks diabetes acute coronary syndrome bleeding risk short-term complications long-term effects diabetic cardiovascular disease thrombocytopenia anticoagulation management hypoglycemia vascular complications diabetes acute coronary syndrome bleeding risk short-term risk long-term risk diabetic patients cardiovascular events thrombosis anticoagulation hemodynamics complications diabetes acute coronary syndrome bleeding risk long-term complications short-term effects diabetic cardiomyopathy thrombocytopenia anticoagulation therapy hypertension hyperglycemia cardiovascular mortality diabetes acute coronary syndrome bleeding risk cardiovascular complications diabetic cardiomyopathy thrombocytopenia anticoagulation therapy antiplatelet agents mortality morbidity clinical trials retrospective studies pharmacotherapy glycemic control cardiovascular events bleeding incidence comorbid conditions medication management preventive strategies
1202	The center of the granuloma in an immune cell induces a pro-inflammatory immune response. The center of the granuloma in an immune cell induces a pro-inflammatory immune response. The center of the granuloma in an immune cell induces a pro-inflammatory immune response. The center of the granuloma in an immune cell induces a pro-inflammatory immune response. The center of the granuloma in an immune cell induces a pro-inflammatory immune response. granuloma formation immune cell types pro-inflammatory cytokines immune response mechanisms granuloma formation immune cell activation pro-inflammatory cytokines tissue inflammation immune response mechanisms granuloma formation immune cell types inflammatory mediators immune response mechanisms pro-inflammatory cytokines granuloma formation immune response mechanisms inflammatory cytokines immune cell types infection-induced inflammation tissue granuloma development granuloma formation immune cell activation pro-inflammatory cytokines immune response mechanisms granuloma formation immune cell activation pro-inflammatory cytokines immune response mechanism inflammatory center identification granuloma formation immune cell types pro-inflammatory cytokines immune response mechanisms antigen presentation macrophage activation T-cell involvement cytokine production inflammatory mediators immune surveillance granuloma center immune cell function pro-inflammatory response immune response induction granuloma formation granuloma formation immune cell types pro-inflammatory cytokines immune response mechanisms inflammatory mediators granuloma formation immune response mechanisms inflammatory cytokines macrophage activation pathogen recognition receptors
587	In transgenic mice harboring green florescent protein under the control of the Sox2 promoter, less than ten percent of the cells with green florescent colocalize with cell proliferation markers. In transgenic mice harboring green florescent protein under the control of the Sox2 promoter, less than ten percent of the cells with green florescent colocalize with cell proliferation markers. In transgenic mice harboring green florescent protein under the control of the Sox2 promoter, less than ten percent of the cells with green florescent colocalize with cell proliferation markers. In transgenic mice harboring green florescent protein under the control of the Sox2 promoter, less than ten percent of the cells with green florescent colocalize with cell proliferation markers. In transgenic mice harboring green florescent protein under the control of the Sox2 promoter, less than ten percent of the cells with green florescent colocalize with cell proliferation markers. transgenic mice Sox2 promoter green fluorescent protein cell proliferation markers colocalization stem cells neural progenitors gene expression fluorescence microscopy developmental biology genetic engineering transgenic mice green fluorescent protein Sox2 promoter cell proliferation colocalization stem cells neural progenitors gene expression fluorescence microscopy bioluminescence epigenetics developmental biology transgenic mice green fluorescent protein Sox2 promoter cell proliferation markers colocalization stem cells neural progenitors gene expression fluorescence microscopy developmental biology regenerative medicine transgenic mice Sox2 promoter green fluorescent protein cell proliferation markers colocalization gene expression stem cells neuroscience research genetic engineering fluorescence microscopy biological markers molecular biology stem cell markers transgenic mice green fluorescent protein Sox2 promoter cell proliferation markers colocalization transgenic mice Sox2 promoter green fluorescent protein cell proliferation markers colocalization gene expression stem cells neurogenesis fluorescence microscopy transgenic mice Sox2 promoter green fluorescent protein cell proliferation markers colocalization gene expression stem cells neuroscience biotechnology genetic engineering fluorescence microscopy transgenic mice green fluorescent protein Sox2 promoter cell proliferation colocalization gene expression stem cells neuroscience biotechnology genetic engineering fluorescence microscopy transgenic mice green fluorescent protein Sox2 promoter cell proliferation markers colocalization stem cells neural progenitors gene expression fluorescence microscopy biosciences genetic engineering transgenic mice Sox2 promoter green fluorescent protein cell proliferation markers colocalization stem cells neural progenitors gene expression fluorescence microscopy developmental biology regenerative medicine
1200	The binding orientation of the ML-SA1 activator at hTRPML2 is different from the binding orientation of the ML-SA1 activator at hTRPML1. The binding orientation of the ML-SA1 activator at hTRPML2 is different from the binding orientation of the ML-SA1 activator at hTRPML1. The binding orientation of the ML-SA1 activator at hTRPML2 is different from the binding orientation of the ML-SA1 activator at hTRPML1. The binding orientation of the ML-SA1 activator at hTRPML2 is different from the binding orientation of the ML-SA1 activator at hTRPML1. The binding orientation of the ML-SA1 activator at hTRPML2 is different from the binding orientation of the ML-SA1 activator at hTRPML1. binding orientation ML-SA1 activator hTRPML2 hTRPML1 protein structure ligand binding channel activation molecular dynamics pharmacology ion channels binding site hTRPML2 hTRPML1 activator orientation ML-SA1 protein different binding ion channel structural biology ligand binding analysis binding site hTRPML2 activator ML-SA1 binding orientation differentiation trpml1 structure comparison binding orientation analysis ML-SA1 activator hTRPML2 hTRPML1 receptor binding sites activation mechanism comparison molecular docking simulation pharmacological targeting ion channel function signaling pathway differences binding orientation ML-SA1 activator hTRPML2 hTRPML1 structural differences ion channels protein binding ligand specificity binding orientation ML-SA1 activator hTRPML2 hTRPML1 molecular dynamics receptor activation pharmacology ion channel protein structure ligand binding biological mechanism binding site hTRPML2 hTRPML1 activator orientation structural difference Martin-Sapienza Activator 1 binding orientation ML-SA1 activator hTRPML2 hTRPML1 molecular dynamics ligand binding protein structure ion channel pharmacology biochemical assay binding orientation ML-SA1 activator hTRPML2 hTRPML1 molecular dynamics crystal structure pharmacodynamics ion channel activation mechanism protein-ligand interaction binding site hTRPML2 activator orientation differentiation ion channel ML-SA1
589	In young and middle-aged adults, current or remote uses of ADHD medications do not increase the risk of serious cardiovascular events. In young and middle-aged adults, current or remote uses of ADHD medications do not increase the risk of serious cardiovascular events. In young and middle-aged adults, current or remote uses of ADHD medications do not increase the risk of serious cardiovascular events. In young and middle-aged adults, current or remote uses of ADHD medications do not increase the risk of serious cardiovascular events. In young and middle-aged adults, current or remote uses of ADHD medications do not increase the risk of serious cardiovascular events. ADHD medications cardiovascular risk young adults middle-aged adults serious cardiac events medication use psychiatric drugs heart problems long-term effects short-term effects ADHD medications cardiovascular risk young adults middle-aged adults serious events medication use cardiovascular health psychiatric medications long-term effects short-term effects cardiac events cognitive enhancers stimulants non-stimulants side effects clinical trials epidemiological studies drug safety mental health medications prescription drugs ADHD medications cardiovascular events young adults middle-aged adults serious cardiac issues medication use psychiatric drugs heart problems long-term effects short-term risks ADHD medications cardiovascular safety long-term ADHD medication use ADHD drug cardiovascular side effects ADHD treatment heart risks young adult ADHD medication safety middle-aged ADHD medication impact ADHD therapy cardiovascular outcomes ADHD stimulant heart event risk ADHD non-stimulant cardiac safety ADHD medication long-term effects ADHD medications cardiovascular events risk adults current remote use association study outcomes ADHD medications cardiovascular risk young adults middle-aged adults serious events medication use cardiac events psychiatric medications long-term effects ADHD medications cardiac events young adults middle-aged cardiovascular risk medication use serious events psychiatric drugs long-term effects short-term effects ADHD medications cardiovascular risk young adults middle-aged adults serious events medication use long-term effects ADHD medications cardiovascular risk young adults middle-aged adults serious events medication use cardiac outcomes psychiatric medications long-term effects short-term effects ADHD medications cardiovascular risk young adults middle-aged adults serious events medication use psychiatric drugs cardiac outcomes long-term effects short-term effects
1320	Transplanted human glial progenitor cells are incapable of forming a neural network with host animals' neurons. Transplanted human glial progenitor cells are incapable of forming a neural network with host animals' neurons. Transplanted human glial progenitor cells are incapable of forming a neural network with host animals' neurons. Transplanted human glial progenitor cells are incapable of forming a neural network with host animals' neurons. Transplanted human glial progenitor cells are incapable of forming a neural network with host animals' neurons. transplanted cells glial progenitor neural network host animals neuron compatibility neurological integration brain cells tissue engineering stem cells neuroregeneration transplantation glial progenitor cells neural network host animals incapable function biology neuroscience neurology transplantation rejection integration failure cellular communication transplanted human glial progenitor cells incapable forming neural network host animals neurons neuroscience neurology biology transplantation stem cells connectivity synaptic formation brain integration transplantation neuroscience glial cells function neural connectivity stem cell research neuroregeneration synaptic formation neurogenesis brain repair biocompatibility neurological disorders transplanted cells glial progenitor cells neural network formation host animals neuron connectivity biological transplantation neurological research cell biology neuroscience neurogenesis neural network formation glial progenitor cells transplanted neurons host animal neurons cellular communication neurogenesis synaptic connectivity neural connectivity glial integration host neuron interaction cell transplantation neurogenesis transplanted cells neural network formation glial progenitor cells host neurons incapability synaptic connections neurogenesis brain integration cellular communication neuroanatomy neuroscience research transplanted cells neural network formation host neurons glial progenitor cells brain transplantation synaptic connectivity neuroregeneration neurobiology neuroscience stem cell research transplantation neurogenesis synaptic connectivity gliogenesis neural plasticity brain repair stem cell therapy neuroinflammation xenograft neuronal integration
903	PD-1 triggering on monocytes reduces IL-10 production by monocytes. PD-1 triggering on monocytes reduces IL-10 production by monocytes. PD-1 triggering on monocytes reduces IL-10 production by monocytes. PD-1 triggering on monocytes reduces IL-10 production by monocytes. PD-1 triggering on monocytes reduces IL-10 production by monocytes. PD-1 ligands monocyte function immunosuppression cytokine regulation T-cell activation PD-1 receptor monocyte function IL-10 cytokine immune response modulation innate immunity adaptive immunity interaction cancer immunotherapy monocyte activation immune checkpoint inhibitors PD-1 ligands monocyte activation IL-10 regulation immune checkpoint inhibitors cytokine production T-cell suppression tumor immunity monocytic PD-1 pathway PD-1 receptor activation monocyte function immunosuppression inflammation cytokine regulation T-cell inhibition chronic infection cancer immunotherapy adaptive immunity innate immunity immune checkpoint inhibitors monocyte IL-10 production immune modulation antigen presentation immune response modulation PD-L1 interaction tumor microenvironment immune tolerance autoimmunity vaccine development clinical trials biomarker discovery PD-1 monocytes IL-10 immunotherapy cytokines tumor immune evasion checkpoint inhibitors inflammatory response adaptive immunity innate immunity PD-1 ligands monocyte function immune checkpoint inhibitors IL-10 suppression tumor immunity inflammatory response T cell activation cancer immunotherapy monocyte biology PD-1 pathway cytokine regulation PD-1 ligands monocyte activation IL-10 suppression immune checkpoint inhibitors innate immunity cytokine production T cell signaling inflammation response PD-1 ligands monocyte activation IL-10 suppression immune checkpoint inhibitors innate immunity cytokine regulation tumor immunology PD-1 receptor monocyte activation IL-10 cytokine immune checkpoint inflammatory response immunotherapy monocyte function immune modulation T-cell interaction cancer immunology PD-1 ligands monocyte activation IL-10 suppression immunotherapy cytokine regulation T-cell inhibition immune checkpoint inhibitors
904	PDPN promotes efficient motility along stromal surfaces by activating the C-type lectin receptor to rearrange the actin cytoskeleton in dendritic cells. PDPN promotes efficient motility along stromal surfaces by activating the C-type lectin receptor to rearrange the actin cytoskeleton in dendritic cells. PDPN promotes efficient motility along stromal surfaces by activating the C-type lectin receptor to rearrange the actin cytoskeleton in dendritic cells. PDPN promotes efficient motility along stromal surfaces by activating the C-type lectin receptor to rearrange the actin cytoskeleton in dendritic cells. PDPN promotes efficient motility along stromal surfaces by activating the C-type lectin receptor to rearrange the actin cytoskeleton in dendritic cells. PDPN motility stromal surfaces C-type lectin receptor actin cytoskeleton dendritic cells cell migration immune response signaling pathway protein function PDPN C-type lectin receptor dendritic cells actin cytoskeleton motility stromal surfaces PDPN C-type lectin receptor actin cytoskeleton dendritic cells motility stromal surfaces protein interactions immune response cell migration signaling pathways PDPN function C-type lectin receptor activation actin cytoskeleton rearrangement dendritic cell motility stromal surface interaction molecular mechanism analysis immune system dynamics PDPN C-type lectin receptor actin cytoskeleton dendritic cells motility stromal surfaces PDPN function motility enhancement C-type lectin receptor activation actin cytoskeleton rearrangement dendritic cell movement stromal interaction immune response modulation signal transduction pathways cell adhesion molecules inflammation process PDPN motility stromal actin cytoskeleton C-type lectin receptor dendritic cells immune response cell migration PDPN motility stromal surfaces C-type lectin receptor actin cytoskeleton dendritic cells keyword expansion efficacy biological process PDPN motility dendritic cells C-type lectin receptor actin cytoskeleton stromal surfaces molecular mechanism cell migration immune response PDPN C-type lectin receptor actin cytoskeleton dendritic cells motility stromal surfaces
1207	The composition of myosin-II isoform switches from the polarizable B isoform to the more homogenous A isoform during hematopoietic differentiation. The composition of myosin-II isoform switches from the polarizable B isoform to the more homogenous A isoform during hematopoietic differentiation. The composition of myosin-II isoform switches from the polarizable B isoform to the more homogenous A isoform during hematopoietic differentiation. The composition of myosin-II isoform switches from the polarizable B isoform to the more homogenous A isoform during hematopoietic differentiation. The composition of myosin-II isoform switches from the polarizable B isoform to the more homogenous A isoform during hematopoietic differentiation. myosin-II isoforms hematopoietic differentiation cellular differentiation B isoform A isoform muscle protein isoforms cytoskeletal proteins biological isoforms myosin-II switch cellular development myosin-II isoforms hematopoietic differentiation cell differentiation cytoskeletal proteins B isoform A isoform muscle protein switching biological isoforms developmental biology molecular biology cellular biology biochemistry protein function gene expression cellular differentiation tissue development molecular mechanisms myosin-II isoform hematopoietic differentiation B isoform A isoform cell differentiation muscle protein isoforms molecular biology cytoskeletal proteins developmental biology gene expression cellular dynamics biochemistry protein switching biological isoforms myosin-II isoform switch hematopoietic differentiation process cell migration changes cytoskeletal reorganization muscle protein dynamics A isoform characteristics B isoform functions cellular differentiation stages protein isoform regulation biological phase transition myosin-II isoform B isoform A isoform hematopoietic differentiation polarizable more homogenous switch composition myosin-II isoform switch hematopoietic differentiation B isoform A isoform cell differentiation protein isoforms biological differentiation myosin composition change myosin-II isoforms polarizable B isoform homogenous A isoform hematopoietic differentiation molecular biology cell differentiation biological sciences microscopy techniques gene expression analysis protein structure changes myosin-II isoform B isoform A isoform hematopoietic differentiation polarizable homogenous differentiation process cellular differentiation isoform switching myosin-II isoform polarizable B isoform homogenous A isoform hematopoietic differentiation cellular differentiation muscle protein isoforms molecular biology biophysics protein structure gene expression cellular morphology myosin-II isoforms hematopoietic differentiation cell polarity molecular biology muscle cells biophysics gene expression protein function cellular dynamics stem cell development