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 altered expression tumor-suppressing DNA repair gene regulation biomarker molecular cancer pathogenesis PGE2 intestinal tumors PGE2 gene expression PGE2 tumor suppression PGE2 DNA repair prostaglandin E2 intestinal cancer tumor promoting factors gene regulation tumors inflammation tumor growth PGE2 prostaglandin E2 intestinal neoplasms gene expression tumor suppressor genes DNA repair inflammation cancer progression gastrointestinal tumors epigenetics signaling pathways PGE2 intestinal tumors PGE2 gene expression PGE2 tumor suppression PGE2 DNA repair PGE2 oncogenesis PGE2 gastrointestinal cancers PGE2 cancer progression PGE2 intestinal inflammation PGE2 molecular mechanisms PGE2 tumor microenvironment PGE2 intestinal tumor growth tumor suppressor DNA repair genes expression PGE2 intestinal tumors gene expression alteration PGE2 role in cancer tumor suppressor genes regulation DNA repair gene modulation PGE2 and oncogenesis gastrointestinal cancer promotion prostaglandin E2 effects PGE2 intestinal tumors gene expression tumor suppressors DNA repair genes inflammation oncogenesis gastrointestinal cancer prostaglandin E2 cancer progression PGE2 intestinal tumor growth tumor suppressing genes DNA repair PGE2 intestinal tumor growth tumor suppressing genes DNA repair expression molecular mechanisms cancer biology intestinal epithelial cells prostaglandin E2 genetic regulation PGE2 intestinal cancer DNA repair genes tumor suppressor genes gut inflammation stem cell proliferation eicosanoids cancer progression intestinal epithelial cells prostaglandin E2 genetic expression profiling
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 factor IF3 tRNA discrimination translation initiation elongation tRNAs initiation tRNAs molecular biology protein synthesis genetic code biochemical processes RNA functions translation initiation factor IF3 function tRNA discrimination elongation tRNA initiator tRNA protein synthesis molecular biology genetic code translation process biochemical reaction translation initiation factor IF3 function tRNA types initiation tRNA elongation tRNA molecular biology protein synthesis genetic code ribosome binding aminoacyl-tRNA mRNA binding discrimination mechanism translation initiation factor IF3 function tRNA roles in translation initiation vs elongation tRNAs tRNA selection during translation role of IF3 in translation initiation tRNA specificity elongation tRNA recognition translation factors involvement tRNA discrimination process discrimination initiation factor elongation tRNA translation IF3 molecular biology biochemistry protein synthesis cellular processes translation initiation factor IF3 tRNA discrimination initiation tRNA elongation tRNA molecular recognition translation process genetic code ribosomal function aminoacyl-tRNA start codon recognition mRNA binding protein synthesis regulation translation initiation factor IF3 discriminator role tRNA types initiation tRNA elongation tRNA molecular biology protein synthesis translation process biochemical factors discrimination initiator tRNA elongation tRNA translation initiation factor IF3 molecular biology protein synthesis cellular processes biochemistry discrimination initiator elongation tRNAs translation initiation factor IF3 molecular biology protein synthesis genetic code ribosome binding mRNA recognition biochemical assay sequence specificity translation initiation factor IF3 tRNA discrimination initiation tRNA elongation tRNA molecular biology genetic translation biochemistry cellular processes protein synthesis molecular 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. alcohol aldehyde dehydrogenase deficiency carriers non-carriers drinking habits genetic mutation alcohol metabolism liver enzymes epidemiology genetics biochemistry alcohol aldehyde dehydrogenase deficiency carriers non-carriers drinking genetics metabolism alcoholism genetic predisposition mutation Lee ADH1B genetics drinking behavior ASD1 ALDH2 ethnicity EastAsian riskfactor metabolism study prevalence alcohol dehydrogenase deficiency genetic mutation liver function alcohol metabolism health impact gene carriers drinking habits genetic testing medical genetics epidemiology研究 酒精代谢障碍 遗传因素影响 健康行为学 alcohol aldehyde dehydrogenase deficiency carriers non-carriers drinking genetics ethanol代谢 acetaldehyde累积 饮酒量 基因突变 alcohol dehydrogenase deficiency carriers mutation reduced alcohol consumption genetic mutation impact liver metabolism ethanol tolerance Asian flushing reaction ALDH2 deficiency alcohol dehydrogenase deficiency carriers non-carriers genetic mutation drinking habits enzyme function allele frequency risk factors metabolic rate alcohol tolerance alcohol aldehyde dehydrogenase deficiency carriers non-carriers drinking habits genetic mutation epidemiology metabolic disorder liver function ethanol metabolism alcohol aldehyde dehydrogenase deficiency carriers non-carriers drinking genetics ethanol代谢 acetaldehyde累积 酒精耐受性 基因突变 alcoholism risk genetic mutation ALDH2 deficiency drinking behavior population studies epidemiology metabolite accumulation health outcomes genetic counseling screening methods public health
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. heart failure incidence women 1979 trends medical research statistics health improvement female cardiovascular disease reduction analysis heart failure incidence women 1979 statistics trends cardiovascular disease public health epidemiology heart_failure_prevalence women_health_outcomes cardiovascular_disease_trends public_health_improvements aging_population medical_treatment_advancements diabetes_prevalence hypertension_control obesity_rates smoking_rates heart failure rates gender differences cardiovascular health trends female heart health incidence reduction cardiac disease statistics women's health improvement cardiac mortality decrease healthcare outcomes analysis heart failure incidence women 1979 health statistics cardiovascular disease epidemiology heart failure incidence women 1979 trends gender differences in heart failure rates cardiovascular health improvements women heart failure reduction female population cardiac health trends females heart failure women incidence statistics medical research health trends cardiovascular disease epidemiology demographic changes heart failure incidence women 1979 decrease female heart failure incidence trend heart failure reduction women heart failure rates women 1979 present cardiac disease女性 发病率 减少 cardiovascular health female improvement heartfailure incidence gender trends cardiovasculardisease statisticalanalysis medicalresearch epidemiology publichealth gendergap healthinequality heart failure incidence gender differences cardiovascular health trends women's health medical research public health data epidemiology risk factors statistical analysis population health
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 domain TMEM27 cleavage human beta cells insulin processing protease diabetes molecular biology pancreatic extracellular region TMEM27 beta cells cleavage process human pancreas molecular biology protein processing endocytosis signal peptides diabetes research cellular localization extracellular region TMEM27 protein beta cell processing cleavage sites human pancreas protein domains signal peptide glycosylation membrane protein exports extracellular region TMEM27 protein beta cell processing cleavage sites glucose metabolism insulin secretion membrane protein function proteolytic cleavage signaling pathways molecular biology techniques diabetes research cellular localization glycoproteins endogenous cleavage posttranslational modifications extracellular domain TMEM27 human beta cells cleavage glycoproteins endoprotease processing beta cell function cell signaling extracellular region TMEM27 protein beta cell function cleavage process signaling pathway glucose metabolism diabetes research membrane protein processing extracellular region TMEM27 protein human beta cells cleavage process glycoproteins signal peptides enzymes protein processing B-cell differentiation extracellular region TMEM27 beta cells cleavage human pancreas molecular biology endopeptidase signal peptide proteolytic processing extracellular TMEM27 human beta cells cleavage protein domain insulin secretion diabetes research molecular biology signal peptide proteolysis glucose metabolism extracellular proteolysis TMEM27 cleavage beta cell signaling glucose response mechanisms membrane protein processing insulin secretion pathways
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. Ubiquitin ligase UBC13 K63 polyubiquitin PCNA K164 protein modification pathway mechanism biology DNA repair ubiquitination Ubiquitination PCNA K164 protein stability DNA damage response E3 ligase polyubiquitination signal transduction molecular biology oncology cell cycle regulation Ubiquitination polyubiquitin chain K63 linkage PCNA DNA repair proteasome ubiquitin conjugation E3 ligase protein modification cell cycle regulation Ubiquitination PCNA modification K63 linkage protein degradation DNA repair E3 ligase polyubiquitin chain cell cycle regulation Ubiquitin ligase UBC13 K63 polyubiquitin PCNA K164 protein modification DNA damage response cell cycle regulation polyubiquitin K63-linked PCNA K164 ubiquitin ligase UBC13 recommendation search performance query expansion ubiquitin ligase UBC13 K63-linked polyubiquitin PCNA K164 protein complex ubiquitination DNA damage response cell cycle regulation Ubiquitination PCNA modification K63 linkage polyubiquitin chain E3 ligase protein conjugation DNA damage response Ubiquitin UBC13 K63 polyubiquitin PCNA K164 protein degradation DNA repair E3 ligase Ubiquitination PCNA modification protein degradation K63 ubiquitin chain Ubc13-Ube2v1 complex polyubiquitin assembly K164 site cell cycle regulation
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 trachoma blindness Southern Sudan eye disease public health tropical diseases vision impairment medical conditions ophthalmology infectious diseases Cataract treatment trachoma epidemiology Southern Sudan health prevalence vision blindness population medical causes eye disease risk factors control prevention cataract treatment trachoma prevention blindness causes Southern Sudan health eye disease vision impairment tropical diseases ophthalmology Africa Cataract treatment trachoma prevention blindness causes Southern Sudan health eye disease prevalence Cataract trachoma blindness Southern Sudan eye disease public health tropical diseases ophthalmology vision impairment eye diseases Southern Sudan blinding diseases ophthalmology public health Vision loss Cataract trachoma blindness Southern Sudan eye disease public health vision impairment tropical diseases healthcare access infectious diseases Cataract trachoma blindness Southern Sudan eye disease public health vision impairment tropical diseases healthcare access Cataract treatment trachoma prevalence Southern Sudan eye disease blindness health causes vision impairment malnutrition diagnosis preventive measures public healthcare awareness Cataract treatment trachoma prevention blindness causes Southern Sudan health eye diseases tropical ophthalmology public eye health visual impairment ocular infections global blindness
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 cells TCR transplantation immune system diversity stem cells bone marrow autoimmune response UCB stem cells transplantation TCR immune system diversity T cells hematopoietic immunology oncology bone marrow lymphocytes immunotherapy clinical trial UCB cells T cell receptor transplantation outcomes immune system stem cell transplant T cell diversity hematopoietic stem cells immunology research clinical trials transplantation immunology UCB stem cells T cell receptor transplantation outcomes immune system response hematopoietic stem cells TCR repertoire cellular immunology post-transplantation immunity T cell function immune reconstitution TCR gene diversity UCB T cells TCR transplantation immune system stem cells diversity immune response bone marrow hematopoiesis UCB cells T cell receptor transplantation impact immune system stem cells T cell diversity bone marrow transplantation immunology research T cell function immune response modification UCB cells T cell receptors transplantation dendritic cells immunology hematopoietic stem cells immune system TCR repertoires alloreactivity tolerance induction UCB cells T cell receptor transplantation outcomes immune system response stem cell transplant T cell diversity immunology research hematopoietic stem cells immune reconstitution UCB cells T cells TCR diversity transplantation immunology hematopoietic stem cells immune system bone marrow transplantation T cell receptor immune response stem cell transplantation UCB cells T cell receptor transplantation outcomes immune system stem cell transplant T cell function post-transplant immunity TCR repertoire hematopoietic stem cells immunotherapy alloreactivity T cell depletion immune reconstitution
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. cell autonomy sex determination somatic cells Galliformes avian biology genetics sex chromosomes developmental biology cell autonomous sex determination Galliformes somatic cells sex determination Galliform birds genetics reproduction avian biology sex chromosomes sexual development sex determination mechanisms somatic cells Galliformes avian sex determination cell autonomy genetic sex determination somatic sex determination cell non-autonomous sex determination Galliformes sex chromosome Galliformes somatic cells sex determination mechanisms somatic cell sex determination avian sex determination genetic sex determination somatic sex differentiation Galliformes genetics sex chromosomes function Cell autonomous sex determination Galliformes somatic cells sex chromosomes genetic mechanisms avian sex determination cell autonomous sex determination somatic cells Galliformes relevant expansion phrases query refinement search optimization biological sex determination avian biology genetic mechanisms sex determination somatic cells Galliformes birds genetic mechanisms developmental biology sex chromosomes gene expression epigenetics cell autonomous sex determination Galliformes somatic cells sex determination机制 avian biology cell autonomous sex determination somatic cells Galliformes birds sex chromosomes genetic mechanisms Wnt signaling female development germ cells heterogametic sex autocrine signaling Sex Determination Genes Gallus gallus DNA methylation sex determination systems Gallus gallus DNA methylation somatic cell reprogramming gene expression analysis pituitary gland hormonal regulation RNA editing
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. Scribble protein cell transformation mammary tumorigenesis cell signaling tumor suppression protein localization oncogenesis genetic mutation cellular proliferation cancer biology Downregulation Scribble mislocalization cancer cell transformation mammary tumorigenesis molecular biology mouse models genetics protein localization tumor suppression downregulation Scribble protein cell transformation mammary tumorigenesis cell signaling tumor suppressor protein localization genetic mutation cancer biology oncology research cellular pathology cell transformation mammary tumorigenesis Scribble protein epithelial cells cancer prevention cell signaling oncogenes tumor suppressors genetic mutations cellular localization cell adhesion cancer biology oncogenic pathways Downregulation mislocalization Scribble cell transformation mammary tumorigenesis molecular biology cancer biology genetics tumor suppression Scribble protein function cell polarity tumor suppression oncogene activation Scribble gene regulation Scribble mutation impact Scribble localization importance cell transformation mechanisms mammary gland cancer Scribble protein expression Scribble signaling pathway cancer prevention mechanisms downregulation mislocalization Scribble cell transformation mammary tumorigenesis protein localization cancer biology tumor suppression cell signaling molecular biology genetics biological pathways cellular transformation proteins cell biology downregulation Scribble mislocalization cell transformation mammary tumorigenesis cancer prevention molecular biology tumor suppressor cell signaling pathways microscopy analysis genetic manipulation protein localization downregulation Scribble mislocalization cell transformation mammary tumorigenesis molecular biology cancer research genetics protein localization tumor suppression cell signaling pathways downregulation mislocalization Scribble cell transformation mammary tumorigenesis cancer biology molecular biology tumor suppressor proteins protein localization GTPases signal transduction pathways
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. glycometabolism cellular metabolism energy production 糖酵解 anaerobic respiration metabolic pathway biochemistry glucose breakdown ATP synthesis glycolysis primary glycometabolic pathways cells metabolic biochemistry cellular energy process glycolysis pathway glycometabolic processes cellular metabolism energy production sugar breakdown anaerobic respiration glucose oxidation metabolic pathway biochemistry concepts glycometabolic pathways explanation glycolysis process steps glycolysis cellular respiration glycolysis chemical reactions glycometabolism overview glycolysis importance in cells glycolysis energy production glycolytic enzymes function glycolysis primary glycometabolic pathways cells glucose metabolic process cellular energy reaction biosynthesis glycometabolism cellular respiration glucose breakdown metabolic pathway energy production biochemistry enzymatic reactions anaerobic metabolism ATP generation metabolic disorder glycometabolism cellular metabolism energy production metabolic pathway 糖酵解 phosphoglycerate kinase Glycometabolic pathways glycolysis definition glycolysis process glycolysis importance glycolysis products glycolysis stages glycolysis regulation glycolysis enzymes glycolysis vs Krebs cycle glycolysis role in cells glycolysis glycometabolic pathways cellular metabolism energy production glucose breakdown biochemistry metabolic pathway cellular respiration ATP production metabolic processes Glycometabolic pathways cellular respiration glucose metabolism energy production metabolic pathway diagram enzymatic reactions ATP production anaerobic respiration
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 ACE inhibitors renal failure kidney function side effects medication hypertension cardiovascular diabetes angiotensin renin-angiotensin system ACE inhibitors kidney failure drug side effects renal function hypertension treatment medication risks angiotensin ACE inhibitors kidney function renal failure side effects medication hypertension cardiovascular drug interactions clinical trials long-term use angiotensin kidney function medication side effects renal failure ACE inhibitors drug therapy hypertension treatment clinical outcomes pharmacotherapy kidney disease cardiovascular health therapeutic options medical research drug interactions patient monitoring therapeutic efficacy Angiotensin ACE inhibitors renal function kidney failure medication side effects hypertension treatment Angiotensin ACE inhibitors kidney function renal impairment medication side effects Angiotensin ACE inhibitors kidney failure renal dysfunction side effects hypertension cardiovascular diuretics dialysis diabetes medication pharmacology nephrology clinical trials renal function tests renal disease drug interaction medication management renal protection angiogenics inhibitors risk renal insufficiency diseases atherosclerosis hypertension guidelines effectiveness safety angiotensin converting enzyme inhibitors renal insufficiency side effects hypertension treatment kidney function medication cardiovascular disease clinical trials patients outcomes angiogenesis inhibitors renoprotective agents kidney function tests ACE inhibitor side effects renal failure risk factors cardiovascular outcomes hypertension treatment complications
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 cells TCR diversity transplantation immune system immunology stem cells bone marrow transplant adaptive immunity T cell receptor UCB cells T cell receptor transplantation outcomes immune system stem cells TCR diversity hematopoietic stem cells immunology research transplantation immunology UCB stem cells T cell receptor transplantation outcomes immunodiversity alloreactivity hematopoietic stem cells T cell development TCR repertoire diversity hematopoietic transplantation thymic selection T cell homeostasis T cell receptor diversity immune reconstitution transplantation outcomes adaptive immunity T cell function TCR repertoire immune response dynamics transplantation immunology lymphocyte development immune surveillance UCB stem cells TCR transplantation immune system lymphocytes immunotherapy bone marrow immune reconstitution T cell diversity hematopoietic stem cells adaptive immunity allogeneic transplantation immune response immunodiversity TCR diversity UCB cells transplantation outcomes immune system stem cell transplants T cell function immunotherapy post-transplant immunity TCR repertoires UCB cells T cell receptor transplantation outcomes immune response diversity stem cell transplantation TCR repertoire hematopoietic stem cells adaptive immunity immunotherapy T cell development UCB transplantation T cell diversity TCR repertoire immune reconstitution stem cell transplant immunotherapy adaptive immunity hematopoietic stem cells antigen receptor diversity T cell receptor repertoire immune system recovery UCB cells T cells TCR diversity transplantation immune system stem cells hematopoietic stem cells immune reconstitution bone marrow transplantation thymus T cell development immunology transplantation medicine immune response UCB cells T cell receptor repertoire transplantation outcomes immune reconstitution stem cell transplantation TCR diversity maintenance hematopoietic stem cells immunological memory chimeric antigen receptors
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_rates cervical_cancer_prevalence cervical_cancer_statistics cervical_cancer_trends cancer_screening_effectiveness public_health_strategies cervical_health_data cervical_cancer_decreased_reasons cervical_cancer incidence_rates health_statistics cancer_screening prevention_methods medical_trends public_health gynecological_cancer cervical_cancer_prevalence trends cervical_screening effectiveness HPV_vaccination population_data public_health_strategies cervical_cancer_decrease factors_in_cervical_cancer_decrease prevention_of_cervical_cancer early_detection_cervical_cancer vaccination_effect_on_cervical_cancer screening_impact_cervical_cancer cervical_cancer incidence_rates cancer_screening prevention_strategies public_health_measures healthcare_access age_groups geographic_locations smoking_status HPV_vaccination treatment_outcomes cervical_cancer_decreased factors_in_cervical_cancer_decrease screening_impact_cervical_cancer prevention_methods_cervical_cancer vaccination_effect_cervical_cancer cervical_cancer incidence_rates cancer_screening prevention_strategies public_health_measures vaccination_programs early_detection mortality_rates cervical_cancer_rates cervical_cancer_prevalence cancer_incidence women_health oncology_trends screening_effectiveness health_statistics medical_research public_health_improvement treatment_outcomes cervical_cancer incidence_rates trends prevention_methods screening_programs vaccination public_health_strategies epidemiology treatment_advancements demographic_factors cervical_cancer_screening HPV_vaccination_rates public_health_strategies cancer_mortality_rates preventive_care_access
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. monocyte activation inflammatory diseases immune response cytokines chronic inflammation monocyte function innate immunity inflammatory mediators immune dysregulation monocyte activation inflammatory diseases immune response cytokines macrophages chronic inflammation pathophysiology biomarkers treatment options therapeutic targets monocyte activation inflammatory diseases immune response cytokines chronic inflammation cardiovascular disease autoimmune disorders inflammatory markers monocyte function innate immunity monocyte activation inflammatory diseases immune response chronic inflammation cytokine production macrophage function autoimmune disorders cardiovascular disease immunology research biomarker discovery monocyte activation inflammatory diseases deregulation prolonged response immune system cytokines inflammation monocyte function disease progression immune response modulation monocyte activation inflammatory diseases immune response chronic inflammation monocyte function cytokine release pathogenesis immune cell activation disease progression immune system dysfunction monocyte activation inflammatory diseases immune response chronic inflammation cytokines immune cells pathological processes immune dysfunction monocyte activation inflammatory diseases deregulation prolonged inflammation immune response cytokines pathology therapeutic targets biomarkers clinical outcomes monocyte activation inflammatory diseases immune response cytokines chronic inflammation monocyte function immunology inflammation mechanisms monocyte activation inflammatory diseases chronic inflammation cytokines immune response pathological processes immune cells inflammation mechanisms monocyte function disease progression
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_screening uterine_cervix_cancer cytology_tests cervical_cancer_prevalence screening_program_effectiveness cervical_cancer_risk_factors Pap_smear_tests cervical_dysplasia HPV_infection cervical_cancer_mortality cervical_cancer_incidence cervical_cancer incidence_rates screening_programs cytology uterine_cervical_cancer public_health gynecology oncology HPV_vaccination early_detection epidemiology health_policy cervical_screening cancer_prevention medical_screening cancer_rates gynecological_cancer cervical_dysplasia healthcare_policy cervical_cancer incidence_rates screening_programs cytology uterine_cervical_cancer healthcare_screening cancer_detection public_health cervical_dysplasia HPV_infection cervical_treatment gynecological_screening cervical_prevention medical_screening cancer_screening_programs cervical_carcinoma screening_effectiveness cervical_cancer_screening uterine_cervical_cancer_prevention cytology_tests cervical_cancer_risk_factors screening_program_effectiveness cervical_dysplasia_detection HPV_testing_cervical_cancer cervical_cancer_statistics cervical_cancer_mortality_rate cervical_cancer_screening_recommendations cervical_cancer incidence_rates screening_programs cytology uterine_cervical_cancer early_detection public_health oncology gynecology epidemiology cervical_cancer_screening uterine_cervical_cancer cytology_tests incidence_rates screening_programs_effectiveness cervical_cancer incidence_rates screening_programs cytology uterine_cervical_cancer early_detection public_health oncology gynecology epidemiology cervical_cancer incidence_rates screening_programs cytology uterine_cervical_cancer public_health diagnostic_tests prevention_strategies gynecological_cancer health_policy medical_screening oncology epidemiology incidence cervical cancer screening programs cytology uterine detection rates publichealth prevention epidemiology healthcare population mortality screening_tests screeningprograms cytology uterine cervicalcancer incidencerates nationwide detection mortalityrates vaccination paptests hpvtesting
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 spores disposal methods handling containment decontamination biological safety anthrax survival dispersal decontamination bioterrorism spore killing sterilization storage anthrax survival dispersal decontamination sterilization biological warfare cleaning killing spore kiln incineration anthrax_disposal_methods anthrax_spore_elimination biohazard_waste_management safe_spore_destruction spore_disinfection_techniques anthrax_containment_procedures anthrax sppores dispersal contamination disposal easy methods biological safety hazard anthrax disposal methods safe anthrax spore handling anthrax decontamination techniques how to remove anthrax spores anthrax spore cleanup services proper anthrax disposal procedures anthrax spore removal methods effective anthrax spore disposal anthrax survival temperature killing sterilization disinfection biological hazard spore preservation decontamination anthrax spstypes dispersalmethods decontaminationtechniques easydisposal sporecharacteristics safetymeasures anthrax spores disposal methods safety containment biohazard cleanup protocols treatment anthrax survival temperature killing sterilization storage contamination decontamination
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 sex determination somatic cells Passeriformes genetic mechanism avian biology sexual differentiation molecular biology genetics research cell autonomy somatic cells sex determination Passeriformes birds molecular biology genetics evolutionary biology sexual dimorphism chromosomes Y chromosome X chromosome cell biology somatic genetics sex determination molecular biology birds Passeriformes genetic regulation somatic sex differentiation avian genetics cell autonomous sex determination somatic cells Passeriformes avian biology reproductive biology molecular genetics sex chromosomes genetic determination animal behavior phenotypic plasticity cell biology sex determination somatic cells Passeriformes genetics avian biology developmental biology epigenetics gene regulation evolutionary biology cell autonomous sex determination somatic cells Passeriformes genetic mechanisms sexual development avian biology gene expression sex chromosomes epigenetics evolutionary biology molecular genetics cell autonomous sex determination somatic cells Passeriformes avian genetics sex chromosomes gene expression sexual differentiation molecular biology epigenetics cell autonomous sex determination somatic cells Passeriformes avian genetics sex determination mechanisms somatic sex determination avian biology genetic sex determination Passeriformes biology cell autonomous sex determination somatic cells Passeriformes birds genetic mechanism sexual differentiation molecular biology avian biology sex determination mechanisms somatic cells birds genetics Passeriformes avian biology chromosomal sex determination hormonal sex determination molecular biology genomic research
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-cells differentiation anergy Ca2+ cytosol immune response calcium signaling T-cell development Golli-proteins T-cells differentiation anergy Ca2+ cytosol immune response calcium signaling T-cell activation T-regulatory cells Golli proteins T-cells anergy Ca2+ signaling adaptive immunity immune response cytosolic calcium t-cell differentiation Golli proteins T-cell differentiation anergy Ca2+ signaling adaptive immunity molecular mechanisms T-cell activation T-cell function T-cell development Ca2+ cytosol Golli-TNF pathway Golli-deficiency effects Golli-proteins T-cells anergy adaptive immune response Ca2+ cytosol immunology cell signaling immune regulation Golli protein T-cell differentiation anergy calcium signaling immune response adaptive immunity immunology T-cell activation immune regulation Golli-proteins T-cell differentiation anergy Ca2+ cytosol immune response adaptive immunity immunology cell signaling molecular biology Golli proteins T-cell differentiation anergy Ca2+ signaling adaptive immunity immune response Ca2+ cytosol Golli-deficient cells Golli-proteins T-cells differentiation anergy Ca2+ cytosol immune response adaptive immunity molecular mechanisms Golli proteins T-cell differentiation anergy Ca2+ signaling adaptive immune response
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 alpha pro inflammatory cytokines IL 6 IL 10 inhibition tumor necrosis factor alpha inhibitors interleukin 1 receptor antagonists pro-inflammatory response cytokine network inflammatory bowel disease rheumatoid arthritis acute phase reactants immune response modulation chronic inflammation biomarkers cytokine signaling tumor necrosis factor pro-inflammatory cytokines IL-6 inhibition IL-10 regulation immune response inflammation markers cytokine network immune modulation chronic inflammation inflammatory diseases tumor necrosis factor alpha effects interleukin 1 function pro-inflammatory cytokines roles IL-6 inhibition mechanisms IL-10 suppression cytokine network inflammatory response regulation TNF-α biological actions IL-1 biological functions immune system cytokines cytokine signaling pathways inflammatory cytokines list cytokine interactions immunology research inflammation mechanisms Tumor necrosis factor alpha TNF-α interleukin 1 pro-inflammatory cytokines inhibit IL-6 IL-10 inflammation molecular biochemistry immuneresponse signaling/pathways Tumor necrosis factor alpha inhibitors interleukin 1 inhibitors pro-inflammatory cytokines effects IL-6 inhibition IL-10 regulation inflammation pathways cytokine balance immune response modulation TNF-alpha blockers cytokine network inflammatory mediators Tumor necrosis factor alpha cytokines pro-inflammatory IL-6 IL-10 inhibition immune response inflammation tumor necrosis factor IL-1 pro-inflammatory cytokines IL-6 IL-10 inhibition immune response Tumor necrosis factor IL-1 pro-inflammatory cytokines IL-6 IL-10 inhibit enhance query expansion terms pro-inflammatory cytokines immune response inflammation inhibit IL-6 IL-10 TNF-α TLR4 signaling pathway molecular biology
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. Bacillus subtilis sporulation clpC protein cell division gene function sporulation process bacterial spore formation clpC protein function Bacillus subtilis sporulation sporulation process Bacillus subtilis genetics Clp protease Bacillus subtilis cell biology sporulation Bacillus_subtilis clpC_protein heat_shock_response protein_degradation genetic_defect bacterial_sporulation Clp protease bacterial_sporeFormation sporulation process Bacillus subtilis clpC protein functional analysis defective sporulation cellular stress response protein degradation clpC protein Bacillus subtilis sporulation bacterial sporulation Clp protease Bacillus subtilis genetics sporulation defect protein degradation bacterial physiology gene function bacterial survival Bacillus subtilis sporulation clpC protein function cell division process bacterial spore formation genetic mutation effects sporulation Bacillus subtilis clpC protein cell development gene function bacterial sporulation genetic defect protein degradation cellular differentiation sporulation Bacillus subtilis clpC protein genetic defect bacterial spore formation proteolytic activity heat shock response protein degradation transcription regulation clpC protein Bacillus subtilis sporulation gene knockout sporulation process protein degradation Clp protease bacterial spore formation genetic defect cellular machinery sporulation efficiency Bacillus subtilis genetics sporulation Bacillus subtilis clpC protein genetic mutation regulatory genes protein degradation bacterial spores gene function microbiology bacterial development
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 miRNAs activation molecular biology cancer metabolism nutrition cells methionine restriction microRNAs activation mRNA expression metabolism signaling pathway genetic regulation methionine deprivation miRNA induction cell starvation sulfur amino acid restriction gene expression modulation metabolic stress response epigenetic regulation methionine restriction effects miRNAs activation cellular response metabolic restriction gene expression regulation protein synthesis reduction nutritional deprivation epigenetic changes cell signaling pathways transcriptome analysis cells methionine restriction miRNAs activation molecular biochemistry genetics metabolism signaling pathways microRNAexpression biological responses health outcomes methylotrophic bacteria methionine starvation miRNA regulation sulfur amino acid deprivation cancer therapy proliferation inhibition microbial response microbiome impact metabolic stress methionine restriction cells miRNAs microRNAs gene expression metabolic stress aging cancer nutrition epigenetics Cells methionine restriction miRNAs activation search efficacy keyword expansion beneficial keywords cells methionine restriction miRNAs microRNAs activation expression regulation gene synthesis metabolism therapy dietary biological molecular bioinformatics transcription translation nucleic acids DNA RNA biomarkers cancer aging proteomics microbial environmental therapeutic diagnostic mechanisms signaling signalling networks interactions interaction potential study analysis research clinical application impact evaluation effectiveness validation prediction modeling model computational methionine restriction effects miRNAs activation cell metabolism gene expression protein synthesis nutritional limitation epigenetic regulation cellular stress response antioxidant defense apoptosis autophagy
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 infection resistance microbiota probiotics prebiotics dysbiosis therapy treatment antibiotics gut microbiota Clostridium difficile infection therapy resistance microbiome dysbiosis probiotics prebiotics metagenomics intestinal flora antibiotics gut microbiota Clostridium difficile infection resistance development microbiome diversity probiotics fecal transplantation antibiotic stewardship antibiotics gut microbiota microbial diversity probiotics supplementation antibiotic-associated diarrhea Clostridium difficile infection fecal microbiota transplantation gut flora imbalance antimicrobial stewardship gut microbiome modulation microbial ecology changes antibiotics gut microbiota Clostridium difficile infection resistance diversity therapy bacteria dysbiosis prebiotics probiotics symbiosis metagenomics antibiotics gut microbiota Clostridium difficile infection microbial diversity probiotics treatment fecal microbiota transplantation antibiotic stewardship microbiome resilience microbial ecology gut flora imbalance antimicrobial resistance antibiotics gut microbiota Clostridium difficile inflammation metabolism resistance mechanisms bacterial diversity probiotics fecal transplant treatment options antibiotics gut microbiota Clostridium difficile inflammation resistance diversity bacterial strains intestinal flora dysbiosis probiotics metagenomics therapy effectiveness prevalence immunity virulence factors antibiotics gut microbiota Clostridium difficile infections resistance therapy prevalence diversity probiotics fecal transplants metagenomics antibiotics gut microbiota Clostridium difficile inflammation probiotics dysbiosis therapy resistance mechanisms metagenomics prebiotics
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. cell biology senescence skin aging telomere shortening free radicals oxidative stress genomic instability epigenetic changes cellular repair mitochondrial dysfunction cellular老化 telomere缩短 DNA损伤累积 衰老机制 细胞功能衰退 皮肤老化 基因表达变化 cellular aging skin ageing facial biological aging wrinkles photoaging senescence damage molecules gene-expression cellular老化 ageing机制 端粒缩短 自由基损伤 遗传因素 环境影响 皮肤老化 生物年龄评估 衰老生物学 细胞代谢变化 cellular老化 telomere缩短 DNA损伤累积 蛋白质稳态失衡 端粒酶活性降低 自噬作用减弱 基因表达变化 氧化应激反应 cellular aging factors telomere shortening senescent cells free radicals DNA damage genetic mutations aging skin wrinkles sagging skin age-related diseases cellular老化 telomere缩短 DNA损伤累积 细胞分裂限制 端粒酶活性 cellular senescence telomere shortening oxidative stress genomic instability senescent cells chronological aging biological age aging mechanisms skin aging longevity markers cellular老化 senescence chronological年龄 DNA损伤 端粒缩短 衰老标志物 表观遗传学改变 自由基理论 基因表达变化 cellular degeneration telomere shortening senescence oxidative stress genomic instability mitochondrial dysfunction aging skin 皱纹 biological age DNA damage
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 mouse models pain receptors neuroscience gene expression molecular biology PKG-la pain hypersensitivity PGK-la knockout mice gene expression mouse model nociception analgesia signaling pathway neuroscience research pain mechanisms pain sensitivity knockout mice PKG-la function mouse genetics nociception pain model gene expression sensory neurons neurobiology analgesia molecular biology pain mechanism PKGLA knockout pain sensitivity genetic knockout pain hypersensitivity mechanisms PKGLA function mouse models pain gene expression pain PKGLA protein pain research knockout mice studies sensory neuron pain pain pathway modulation PKG-la pain hypersensitivity PGK-la knockout mice genetic knockout model effectiveness biological role neuroscience research关键词结束 PKGLA gene pain sensitivity knockout mice pain hypersensitivity genetic knockout pain signaling PKGLA protein nociception mouse models pain research genetic modification pain mechanism PKGLA function PKG-la pain hypersensitivity PGK-la knockout mice molecular mechanisms gene function pain research neuroscience genetic models PKG-la pain hypersensitivity PGK-la knockout mice gene knockout nociception mouse model pain signaling analgesia genetic knockout sensory neurons inflammation pain pathways molecular biology genetic knockout models pain research nociceptive behavior genetic manipulation pain mechanisms PKG enzyme knockout technology PKG-la pain hypersensitivity PGK-la knockout mice molecular mechanisms neuroscience research methodology genetic models pain pathways pain sensitivity PGK-la knockout gene expression nociception sensory neurons inflammation analgesia transcription factors pain model molecular mechanisms
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 dimers lipid regulation PPAR RXRs inhibitors PPAR ligands effects PPAR-RXR pathway PPAR activation RXR antagonism PPAR agonists PPAR signaling RXR ligands nuclear receptors transcription factors lipid metabolism diabetes research cardiovascular disease PPAR-RXR coactivators antagonists ligand binding nuclear receptors transcription factors fatty acids thiazolidinediones retinoids synthetic ligands gene expression signaling pathways PPAR RXRs inhibitors PPAR ligands effects PPAR-RXR signaling PPAR RXR interaction PPAR agonists PPAR target genes PPAR RXR complex PPAR pathway regulation PPAR-RXR nuclear receptors PPAR inhibitor drugs PPAR-RXR inhibition PPAR ligands nuclear receptors transcription factors signaling pathways PPAR RXRs inhibition PPAR ligands function PPAR-RXR pathway nuclear receptors regulation ligand binding proteins PPAR RXRs ligands inhibition drug interactions transcription factors metabolism PPAR-RXRs inhibition PPAR ligands molecular biology drug mechanisms transcription factors signaling pathways gene expression metabolic disorders PPAR-RXRs PPAR ligands coactivators corepressors transcription factors fatty acids synthetic agonists antagonists gene expression metabolic disorders PPAR activators RXR activation PPAR heterodimers nuclear receptors ligand binding domains transcription factors lipid metabolism adipogenesis cardiovascular diseases
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 activators nuclear receptors ligand activation transcription factors fatty acids retinoids thyroid hormones PPAR RXRs ligands activation genetics molecular biochemistry signaling potential therapeutics interaction disease model expression PPAR agonists RXR activators ligand activation nuclear receptors transcription factors fatty acids thiazolidinediones retinoid-X-receptors PPAR RXR activation PPAR ligands function RXR ligands list PPAR signaling pathway PPAR target genes RXR dimerization PPAR agonists examples PPAR-RXR heterodimer nuclear receptor ligands lipid metabolism PPAR RXR protein structure PPAR-RXR ligands activation nuclear receptors transcription factors PPAR-RXR activation PPAR ligands nuclear receptors transcription factors fatty acids synthetic agonists gene expression metabolic diseases drug targets cholesterol regulation PPAR-RXR ligands activators nuclear receptors transcription factors fatty acids synthetic agonists gene expression metabolic disorders PPAR agonists RXR activation ligand binding transcription factors metabolic disorders cardiovascular health gene regulation lipid metabolism nuclear receptors drug targets signaling pathways PPAR RXRs ligands activators dimers retinoid x fatty acids transcription factors PPAR agonists RXR activation ligand binding transcription factors metabolic syndrome cardiovascular disease adipogenesis anti-inflammatory agents
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 efficacy accuracy complications imaging techniques ultrasound_guidance needle_insertion traumatic_procedures medical_imaging minimally_invasive diagnostic_imaging procedural_safety healthcare_technology puncture_techniques image_guided_procedure ultrasound guided needle insertion ultrasound imaging in procedures trauma reduction techniques medical ultrasound applications real-time ultrasound guidance ultrasound guidance benefits ultrasound guidance techniques ultrasound guidance needle insertion traumatic procedures reduction ultrasound imaging guidance needle insertion accuracy ultrasound guidance applications ultrasound technology in medicine medical ultrasound guidance traumatic injuries prevention ultrasound guidance traumatic procedures needle insertion accuracy safety imaging minimally invasive ultrasound guidance benefits ultrasound guidance techniques ultrasound guidance accuracy ultrasound guidance applications ultrasound guidance importance ultrasound guidance advantages ultrasound guided needle insertion trauma reduction needle procedures ultrasound imaging for needle placement accuracy in needle insertion minimally invasive ultrasound guidance ultrasound guidance needle insertion traumatic procedures medical imaging procedural success minimally invasive diagnostic imaging real-time guidance clinical efficacy patient safety ultrasound guidance traumatic procedures needle insertion accuracy minimally invasive imaging technique 成功率 安全性 精度 介入技术 ultrasonic imaging needle localization minimally invasive procedures real-time guidance procedural success rates medical imaging techniques trauma reduction diagnostic ultrasound needle insertion accuracy surgical assistance technologies
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 causes pregnancy infants perinatal mortality low birth weight factors pregnancy infants complications nutrition prematurity healthcare prevention perinatal mortality low birth weight factors pregnancy infants complications newborn epidemiology obstetrics perinatal mortality factors low birth weight causes perinatal health indicators birth weight effects mortality rates analysis perinatal mortality low birth weight factors infants complications pregnancy neonatal epidemiology risk conditions perinatal mortality factors low birth weight causes pregnancy outcomes lifestyle impacts on birth weight maternal health and perinatal outcomes perinatal mortality low birth weight infant health pregnancy preterm babies gestational age complications perinatal mortality low birth weight beneficial keywords expansion research evidence-based prevalence causes publichealth perinatal mortality low birth weight infant premature delivery factors risk pregnancy perinatal low birth weight mortality factors prevalence infant health pregnancy risk identification screening causes
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 chronic disease predictive factors diet quality malnutrition health outcomes nutritional status obesity diabetes cardiovascular disease immune function micronutrients macronutrients suboptimal nutrition chronic disease prediction diets health outcomes factors prevalence risks assessment food quality vitamins minerals obesity cardiovascular diabetes cancer age socioeconomic environment genetics mechanisms preventive management effects impact studies research population clinical associations trends markers prognosis screening education public awareness prevention mitigation complications symptoms treatment prevalence incidence suboptimal nutrition factors chronic disease prediction nutritional deficiencies diet quality health outcomes malnutrition indicators long-term health effects dietary patterns nutrient intake epidemiological studies nutrition quality dietary habits health outcomes chronic conditions nutritional status diet diversity malnutrition indicators nutritional deficiencies diet and disease diet impact nutritional risk factors nutrition quality dietary patterns chronic illness prediction nutritional deficiencies long-term health outcomes diet diversity micronutrient intake epidemiological studies biomarker analysis lifestyle factors nutrition assessment chronic diseases risk dietary habits malnutrition indicators nutritional deficiencies diet quality health outcomes prediction dietary patterns analysis nutrition dietary habits diet quality food intake malnutrition chronic diseases health outcomes nutritional status dietary patterns diet diversity nutritional deficiencies suboptimal nutrition chronic diseases predictive factors nutritional deficiencies health outcomes dietary patterns food insecurity malnutrition risk assessment public health evidence-based medicine nutrition quality dietary habits chronic illness risk nutritional deficiencies diet diversity long-term health outcomes food intake patterns malnutrition indicators health conditions diet quality metrics nutrition assessment diet quality dietary patterns nutritional deficiencies chronic diseases risk epidemiological studies public health indicators dietary diversity micronutrient intake food security malnutrition markers lifestyle factors genetic predisposition
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 cytokine release neuroinvasion inflammation upregulation mosGCTL-1 West Nile virus infection immune response viral infection protein expression cellular response virus-host interaction biomarker upregulation mosGCTL-1 West Nile viral infection immune response gene expression cytokines inflammation pathogen recognition signaling pathway upregulation mosGCTL-1 West Nile virus infection immune response gene expression viral infection cellular response pathogen detection innate immunity upregulation mosGCTL-1 West Nile virus infection immune response gene expression cellular response viral infection pathogenesis upregulation mosGCTL-1 West Nile virus infection gene expression viral infection immune response cellular response pathogen recognition molecular biology virology immunology upregulation mosGCTL-1 West Nile virus infection immune response gene expression viral infection cytokines immune system pathogen response upregulation mosGCTL-1 West Nile virus infection gene expression immune response viral infection cellular response molecular biology virology upregulation mosGCTL-1 West Nile virus infection gene expression immune response viral infection pathogenesis molecular biology virology upregulation mosGCTL-1 West Nile virus infection gene expression immune response viral infection neuroinvasion inflammation cell signaling protein expression
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. antibody response activated B cells paracortical areas oxysterol stromal cells immune response lymph node structure B cell migration antigen presentation adaptive immunity immune activation early antibody response activated B cells migration paracortical areas oxysterol accumulation stromal cells immune response B cell activation antigen presentation lymph node structure immune system adaptive immunity immunology antibody production cellular trafficking antibody response activated B cells migration paracortical areas oxysterol stromal cells immune response lymph node structure B cell activation immunology antibody production antibody production immune response B cell activation paracortex stromal cells oxysterol biosynthesis antigen presentation lymph node architecture adaptive immunity B cell migration immune synapse formation immunology research antibody diversity plasma cell differentiation T-B cell interaction immune memory development antibody response activated B cells migration paracortical areas oxysterol accumulation stromal cells antibody production B cell activation paracortical regions oxysterol biosynthesis stromal cell function immune response mechanisms early antibody response activated B cells migration paracortical areas oxysterol accumulation stromal cells immunology adaptive immunity lymph node structure early antibody response activated B cells migration paracortical areas oxysterol accumulation stromal cells beneficial keywords efficacy query expansion early antibody response activated B cells migration paracortical areas oxysterol accumulation stromal cells immunology lymph node structure immune response mechanisms early antibody response activated B cells paracortical areas oxysterol accumulation stromal cells immune response lymph node structure antigen presentation B cell activation immunology research adaptive immunity
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 browning process cold exposure adipose tissue thermogenesis white fat brown fat beige fat lipid metabolism cold adaptation energy expenditure metabolic rate fat cells cryolipolysis adipocyte differentiation subcutaneous fat browning process cold exposure adipose tissue differentiation thermogenesis white fat brown fat beige fat molecular mechanisms metabolism obesity health impact therapeutic potential subcutaneous fat depots browning processes cold exposure adipose tissue thermogenesis white fat brown fat lipid metabolism cryolipolysis cold adaptation fat mobilization energy expenditure subcutaneous fat depots browning process cold exposure adipose tissue metabolism thermogenic adipocytes white fat browning energy expenditure fat tissue metabolism cryolipolysis treatment effects metabolic health benefits subcutaneous fat browning cold exposure adipose tissue thermogenesis white fat brown fat lipid metabolism energy expenditure temperature regulation cold exposure effects subcutaneous fat browning adipose tissue metabolism thermogenic fat depots brown adipose tissue induction subcutaneous fat browning process cold exposure adipose tissue thermogenesis white fat brown fat metabolic rate lipid metabolism adiponectin uncoupling protein 1 thermogenic genes energy expenditure obesity metabolic syndrome cold exposure browning process subcutaneous fat adipose tissue cryolipolysis thermogenic fat white fat brown fat beige fat energy metabolism temperature regulation fat metabolism cellular adaptation biological response thermoregulation metabolic switching subcutaneous fat browning process cold exposure adipose tissue thermogenesis lipolysis metabolism insulation energy expenditure white fat brown fat beige fat cryotherapy temperature regulation obesity metabolic syndrome cold exposure browning process subcutaneous fat adipose tissue cryolipolysis molecular changes thermogenic genes white fat brown fat transformation
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. biomaterials dimensionality inductive tissue engineering bioactive nanomaterials scaffold regenerativemedicine nanobiomaterials bioactive glasses hydrogels nanofibers tissue engineering biomineralization stem cells osteoconductivity inductivity biomimetic materials biomaterials inductive properties 0-dimensional nanomaterials tissue engineering scaffold biocompatibility stimuli-responsive microstructure applications regenerativemedicine materialscience biomaterials properties 0-dimensional materials biomaterial science inductive biomaterials nanobiomaterials bioactive materials tissue engineering biomaterial applications nanomaterials in biology biomaterial induction biomaterials inductive properties dimensionality nanomaterials cell induction bioactive materials surface chemistry molecular recognition biomaterials properties bioinductive materials nanomaterials applications 0D biomaterials biomaterial science tissue engineering materials inductive biomaterials advanced biomaterials biomaterial research medical biomaterials biomaterials inductive properties 0D bioengineering nanomaterials scaffolds molecular recognition tissue engineering biocompatibility 0-dimensional biomaterials inductive properties nanomaterials bioactive stimuli-responsive theranostics biomedical applications biomaterials 0-dimension inductive properties nanomaterials bioinduction biocompatibility biomedical applications materials science biomaterials 0-dimensional inductive properties nanomaterials conductive biomimetic tissue engineering regenerative medicine applications biocompatibility synthesis fabrication
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. TET protein function biological consequences myeloid cancers gene dysregulation epigenetic modifications cancer development oncology genomic instability tumor suppression DNA methylation TET protein function myeloid cancers DNA methylation epigenetic regulation cancer biology gene expression oncology stem cells tumor suppressor chromatin modification TET1 TET2 TET3 biological functions cancer risk epigenetics DNA methylation leukemia malignancy genetic disorders stem cell biology TET protein function epigenetic modifications cancer development myeloid malignancies gene expression regulation DNA methylation oncogenic pathways chromatin remodeling stem cell differentiation tumor suppressor genes TET protein epigenetics DNA methylation cancer risk myeloid diseases gene function biological impact TET protein function biological consequences myeloid cancers gene mutation epigenetic changes cancer risk factors oncology research DNA methylation stem cell biology cancer prevention TET protein function epigenetics cancer risk myeloid diseases gene expression DNA methylation oncogenesis biological impact TET protein function myeloid cancers gene expression regulation DNA methylation cancer biology epigenetic modifications oncogenesis cellular differentiation genomic instability tumor suppressor genes TET protein function myeloid cancers biological consequences TET gene mutation TET protein role cancer risk TET protein dysregulation DNA methylation genetic mutations TET protein biology epigenetics DNA methylation cancer development myeloid diseases gene function impact
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 prior use risk comparison thrombosis management anticoagulation therapy stroke patients direct oral anticoagulants warfarin in-hospital mortality risk comparison stroke treatment anticoagulation therapy hemorrhagic stroke ischemic stroke clinical outcomes stroke patients direct oral anticoagulants warfarin in-hospital mortality risk comparison thrombosis bleeding management treatment outcomes stroke recovery anticoagulant efficacy hospital outcomes thrombosis prevention hemorrhagic conversion atrial fibrillation management stroke rehabilitation pharmacotherapy effectiveness cardiovascular health stroke prognosis stroke prior use direct oral anticoagulants warfarin in-hospital mortality risk factors clinical outcomes hematology cardiology vascular surgery neurology stroke patients direct oral anticoagulants warfarin in-hospital mortality risk prior use comparative analysis stroke patients direct oral anticoagulants warfarin in-hospital mortality risk prior use clinical trial thromboembolism bleeding events efficacy safety healthcare outcomes stroke direct oral anticoagulants warfarin in-hospital mortality prior use efficacy beneficial expansion keywords stroke direct oral anticoagulants warfarin in-hospital mortality prior use risk comparison thrombosis bleeding stroke treatment anticoagulation therapy stroke outcomes direct oral anticoagulants warfarin comparison in-hospital mortality stroke patient management anticoagulant efficacy
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. rs647161 genetic variant colorectal cancer susceptibility polymorphism gene mutation oncology epidemiology bioinformatics medical research locus rs647161 colorectal cancer genetic marker colorectal carcinoma polymorphism colorectal cancer variant rs647161 colorectal tumor susceptibility cancer predisposition gene genetic risk factor colorectal rs647161 genetic variant colorectal cancer polymorphism susceptibility gene mutation oncology biomarker epidemiology tumor development DNA marker hereditary cancer cancer genetics genomic analysis rs647161 genetic variant colorectal cancer risk factors genetic predisposition to colorectal cancer colorectal carcinoma genetics rs647161 and cancer associations between rs647161 and colorectal cancer rs647161 polymorphism colorectal cancer genetic markers rs647161 and disease susceptibility rs647161 in colorectal cancer locus rs647161 colorectal carcinoma genetic variant association cancer predisposition mutation epidemiology genetics oncology biomarker DNA chromosome risk因素 clinical research database locus rs647161 colorectal cancer genetic markers colorectal carcinoma SNP rs647161 colorectal tumor risk rs647161 association study colorectal cancer genetics cancer susceptibility gene rs647161 colorectal cancer genetic marker cancer risk genomic locus colorectal carcinoma genetics locus rs647161 colorectal carcinoma risk genetic marker cancer susceptibility polymorphism epidemiology oncology biomedicine genomic association tumor development locus rs647161 colorectal carcinoma genetic association study mutations variant analysis cancer genetics genomic research biomarkers molecular biology single nucleotide polymorphism SNP effects of genetic variants rs647161 colorectal cancer genetic markers tumor susceptibility polymorphism cancer risk factors
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 strata HIV infection treatment prevalence efficacy risk reduction clinical trials epidemiology antiretroviral tuberculosis CD4 strata effectiveness prevalence risk factors viral load clinical trials public health immunology AIDS HIV antiretroviral tuberculosis CD4 therapy effectiveness hIV virus rates populations strata demographics reduction prevalence clinical studies research prevention immunosuppression co-infection public health antiretroviral treatment HIV tuberculosis coinfestation CD4 count tuberculosis prevention viral load suppression HIV/AIDS treatment TB incidence reduction immune reconstitution inflammatory syndrome ART efficacy tuberculosis prevalence antiretroviral therapy tuberculosis CD4 strata HIV infection prevention efficacy clinical study treatment 流行病学 耐药性 免疫重建炎性疾病 antiretroviral therapy tuberculosis CD4 strata treatment efficacy HIV infection antiretroviral therapy tuberculosis CD4 strata HIV treatment prevention effectiveness immunology epidemiology antiretroviral therapy tuberculosis CD4 strata HIV infectious disease prevention efficacy treatment immunology 流行病学 antiretroviral therapy tuberculosis CD4 strata HIV treatment efficacy prevention infection risk reduction clinical studies outcomes antiretroviral drugs tuberculosis prevention CD4 count hIV treatment effectiveness studies public health interventions
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 genomic research genetic sequencing population genetics variant mapping genomics projects geneticvariation rarevariants penetrance commonvariants humangenomeproject sequencingtechnologies populationgenetics single nucleotidepolymorphisms associationstudies geneexpression genetictesting bioinformatics medicalgenetics epigenetics transcriptomics phylogenetics molecularbiology eugenics biostatistics publichealthgenomics cancergenomics neurogenomics pharmacogenomics geneticcounseling ethicsgenetics genomewideassociationstudy gwas wholeexomesequencing wholegenomesequencing genetic variation mapping techniques rare variants penetrance common variants genetic sequencing 1000 genomes project genetic variation mapping techniques rare variants penetrance effects common variants genomic research genetic sequencing biomedical genetics human genetic diversity single nucleotide polymorphisms SNP analysis genetic variation mapping common variants rare variants penetrance 1 000 genomes project genetic variation rare variants larger penetrance common variants genome mapping genetic sequencing genetic research genomics genetic disorders population genetics variant discovery sequencing technologies genetic variation analysis genetic screening genetic testing genome-wide association studies genetic data analysis 1000 Genomes Project rare variants larger penetrance genetic sequence variation common variants mapping genomics research genetic diversity genetic variation mapping 1000 Genomes Project rare variants penetrance common variants genetic sequencing efficacy beneficial keywords research genomics geneticvariation rarevariants populationgenetics molecularbiology sequencingtechniques populationgenomics pangenomestudies geneticpenetrance variantanalysis geneticmapping geneticdiversity biologicalinformatics genetic variation mapping techniques rare variants penetrance common variants genetic sequencing biological databases human genome research variant analysis genetic disorders
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. upregulation p53 pathway molecular events cancer resistance shortened lifespan senescent cells accelerated aging mutation tumor suppressor genetic alteration cell cycle regulation apoptosis oxidative stress aging process genome stability upregulation p53 pathway molecular-events cancer-resistance senescent-cells accelerated-aging lifespan-shortening molecular-biology cancer-genetics cell-signaling genetic-mutations tumor-suppressors RNA-expression microRNAs protein-interactions nuclear-translocation methylations DNA-repair somatic-mutations multi-gene-interactions molecular-networks prognostic-markers therapeutic-targets biomarkers anti-apoptotic-pathways apoptosis aging-mechanisms upregulation p53 pathway molecular events cancer resistance shortened lifespan senescent cells accelerated aging genetic factors therapy treatment biomarkers mechanisms signaling networks clinical impact biology prognosis mutation expression interactions therapeutics genomics epigenetics up-regulation p53 pathway molecular events cancer resistance shortened lifespan senescent cells accelerated aging genetic factors microenvironment tumor suppression cell cycle regulation apoptosis induction oxidative stress angiogenesis inhibition microbial infection chronic inflammation therapy resistance stem cell dysfunction damage response genome stability survival analysis prognostic marker therapeutic target multi-factorial cause population genetics network biology systems biology molecular biology cancer genomics aging research biomarker discovery cell signaling signal transduction protein interaction p53 up-regulation cancer resistance molecular events senescent cells accelerated aging lifespan缩短 肿瘤耐药性 p53 pathway regulation cancer resistance mechanisms molecular events in cancer senescent cells organismal aging up-regulation effects lifespan reduction cellular senescence p53 and cancer molecular biology of aging cancer therapy resistance up-regulation p53 pathway molecular events cancer resistance senescent cells accelerated aging shortened lifespan molecular biology cancer research aging mechanisms p53 pathway up-regulation cancer resistance molecular events senescent cells shortened lifespan accelerated aging oncogenes tumor suppressors DNA damage apoptosis genetic instability cellular senescence telomere shortening oxidative stress inflammation up-regulation p53 pathway molecular events cancer resistance shortened lifespan senescent cells accelerated aging molecular biology cancer research genetic factors tumor suppression cellular senescence microRNAs chromatin modification apoptosis survival rate aging mechanisms genomic instability somatic mutations cell signaling pathways therapeutic targets biomarkers clinical trials prevention strategies age-related diseases DNA damage response mitochondrial function oxidative stress nuclear receptors transcription factors stem cell衰老 端粒缩短 表观遗传学 p53 up-regulation cancer resistance molecular events senescent cells accelerated aging lifespan reduction tumor suppression genetic mutations apoptosis induction oncogene inhibition
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. prion disease uk prevalence neurodegenerative disorder brain pathology scrapie cjd genetic prion disease 1/2000 UK abnormal PrP positivity neurological disease epidemiology prion transmission prevalence prion disease uk prevalence abnormal prion protein neurodegenerative disorders spongiform encephalopathy brain pathology genetic prion disease transmissible spongiform encephalopathy variant cjd 1/2000 UK PrP positivity 1/2000 UK abnormal PrP PrP positivity UK statistics 1/2000 UK cattle PrP 1/2000 UK sheep PrP PrP positivity UK disease 1/2000 UK BSE PrP 1/2000 UK CWD PrP PrP positivity UK prevalence 1/2000 UK scrapie PrP abnormal_prion_protein UK_disease_prevalence 1_2000_ratio prion_disease_prevalence abnormal_prP_positivity prion_diseases_uk cjd_risk_factors prion_disease_prevalence neurodegenerative_disorders Uk PrPSc prion disease CJD vCJD sCJD genetic prion disease abnormal PrP prion positivity UK prevalence neurological disorders prion protein brain pathology neurodegenerative diseases PrPsc variant Creutzfeldt-Jakob disease vCJD prion disease UK surveillance cattle prions human prion infection scrapie genetic prion disease PrPSc variant Creutzfeldt-Jakob disease vCJD epidemiology neurodegenerative diseases bovine spongiform encephalopathy BSE surveillance diagnostic tests brain tissue protein misfolding genetics prion diseases public health veterinary science neuroscience medical research healthcare systems UK statistics neurological disorders prion protein infectious diseases PrPSc prion disease neurodegenerative scrapie variant CJD genetic prion disorders diagnostic tests prevalence epidemiology neurological symptoms brain pathology protein misfolding transmissible spongiform encephalopathies TSE prion research brain biopsy MRI EEG diagnostic criteria
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 interaction EB1 microtubules tumor synthesis filament binding domain cellular proteins structure function biological mechanism arginine p150grip EB1 protein interaction molecular biology cell division filament association biochemical function structural role arginine residue p150grip protein interaction EB1 microtubules binding domain structure function cell biology biochemistry arginine 90 mutation p150glued EB1 protein integer phosphoprotein protein interaction domains microtubule binding Arginine p150grip EB1 protein interaction molecular biology cellular process structural biology biochemistry cell motility cytoskeleton arginine p150n EB1 protein interaction molecular biology cellular process amino acid structural role arginine p150grip EB1 protein interaction structural biology molecular dynamics biochemical function cell biology molecular recognition arginine p150n EB1 protein interaction molecular biology cell division microtubules biomolecule binding structural protein cellular transport arginine residue p150grip protein interaction EB1 microtubules molecular biology cell division structural role function dynamics arginine p150grip EB1 protein interaction molecular biology cell division microscopy biochemical function
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. Chenodeoxycholic acid energy expenditure metabolism hepatic bile hormones thermogenesis chenodeoxycholic acid treatment energy expenditure metabolism obesity weight loss fatty liver disease clinical study mechanism effect human animal dose response Chenodeoxycholic acid metabolism liver fat digestion obesity weight loss bile hormones thermogenesis fatty acids diet exercise calorieburning Chenodeoxycholic acid benefits chenodeoxycholic acid metabolism chenodeoxycholic acid weight loss chenodeoxycholic acid thermogenesis chenodeoxycholic acid clinical trials chenodeoxycholic acid obesity treatment chenodeoxycholic acid mechanism of action chenodeoxycholic acid calorie burn chenodeoxycholic acid dietary impact chenodeoxycholic acid hormone regulation Chenodeoxycholic acid energy expenditure metabolism liver obesity bile salts fat digestion thermogenesis weight loss hepatobiliary pathway Chenodeoxycholic acid benefits cholesterol metabolism liver function weight loss mechanisms fatty acid oxidation thermogenesis hepatobiliary effects metabolic syndrome obesity treatment lipid absorption bile acid regulation calorie burn metabolic rate enhancement chenodeoxycholic acid energy metabolism obesity treatment fatty acid bile acid weight loss thermogenesis Chenodeoxycholic acid energy expenditure treatment metabolic effects obesity metabolism liver bile acids thermogenesis Chenodeoxycholic acid energy expenditure metabolic rate bile acid obesity lipid metabolism weight loss thermogenesis liver function bile acids metabolism weight loss fat oxidation thermogenesis obesity treatment lipid metabolism
1100	Statins increase blood cholesterol. Statins increase blood cholesterol. Statins increase blood cholesterol. Statins increase blood cholesterol. Statins increase blood cholesterol. statins blood cholesterol effects medication dosage side effects population benefits risk factors statins blood cholesterol effect medication disease treatment lowering health impact statins blood cholesterol effectiveness dosage factors interactions population risk benefits statin side effects statin benefits cholesterol lowering drugs lipid profile improvement heart disease prevention statin dosage statin alternatives statins blood cholesterol lipid profile cardiovascular risk hyperlipidemia pharmacology medication efficacy clinical trials side effects dosage statin side effects statins benefits cholesterol levels and statins how statins work statins diet interactions statin cholesterol medication lipid treatment heart disease side effect liver function dosage interaction patient management statins blood cholesterol lower effectiveness benefits risk heart disease levels treatment statins blood cholesterol lowering effects medication dosage guidelines research studies population risks benefits Statins side effects statins mechanism cholesterol types lipid profile test statin dosage statins diet interaction statin alternatives
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 cancer genetics mutations oncology biomarkers genomic aberrations metastases primary tumor cancer mutations oncology genetics pathology biomarkers genomic aberrations metastases primary tumor oncology mutations cancer genetics biomarkers epigenetics transcriptomics genomic aberrations metastases primary tumor similarities cancer genomics metastasis tumor progression genomics genetic mutations metastasis genomic alterations metastases oncology genomics metastasis cancer genetics metastatic tumors molecular biology metastasis tumor genomics metastases genomic aberrations metastases primary tumor similarity oncogenes suppressor genes chromosomal alterations genomic alterations matastases primary tumor similar aberrations genetic mutations genomic aberrations metasastes primary tumor similarities mutations genetic changes cancer progression genomic aberrations metastases primary tumor similarity oncogenes mutations epigenetics cancer progression genomic aberrations metastases primary tumor similarity cancer genetics mutations oncology biomarkers genomic profiling molecular markers tumor heterogeneity cancer genetics mutations somatic alterations ploidy analysis allele frequency variants genetic testing
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. arteriole diameter venule lumen vascular effectiveness search terms expansion population vessel size comparison arteriole vessel diameter venule anatomy capillaries blood vessels vasculature human body structure biology arteriole diameter venule lumen anatomy circulatory system vasculature blood vessels angiography arteriole characteristics venule characteristics blood vessel comparison vascular anatomy lumen sizedifference circulatory system components arteriole diameter venule lumen anatomy vasculature circulatory system arteriole diameter venule lumen anatomy vascular physiology pulse hypertension arteriole lumen diameter venule vasculature anatomy vascular system arteriole lumen diameter venule anatomy circulatory系统 arteriole diameter venule lumen vascular dilation vasculature human anatomy capillaries vessel size vascular system arteries diameter venules vascular anatomy biology tissue circulation
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. Chenodeoxycholic acid energy expenditure treatment hepatic fatty acid metabolism liver obesity diet effectiveness chenodeoxycholic acid treatment energy expenditure metabolism obesity liver bile acids diet fat absorption thermogenesis clinical studies mechanism effects clinical trials Chenodeoxycholic acid energy expenditure hepatic fat breakdown metabolism obesity liver functions treatment effectiveness therapeutics pharmacology clinical study review meta-analysis chenodeoxycholic acid energy metabolism fatty acid synthesis bile acid obesity treatment metabolic rate lipid absorption hepatobiliary function cholesterol management weight loss mechanisms Chenodeoxycholicacid energyexpenditure weightmanagement liverfunction bileacids Chenodeoxycholic acid energy metabolism liver function bile acids obesity lipid absorption metabolic rate hepatobiliary disease fat digestion cholesterol regulation Chenodeoxycholic acid metabolic rate obesity fat metabolism liver bile acids thermogenesis Chenodeoxycholic acid energy expenditure treatment metabolism liver bile fats digestion obesity cholesterol diet pharmacology hepatology Chenodeoxycholic acid energy metabolism weight loss fatty liver bile acids obesity metabolic syndrome Chenodeoxycholic acid metabolic rate fat metabolism liver function bile acids obesity treatment weight loss lipid absorption
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 traditional journals citation likelihood scholarly articles accessibility publication formats open access traditional journals citation frequency scholarly articles publishing formats academic impact accessibility peer review scientific communication journal impact factor openaccess journals citation impact factor traditional journal peer-reviewed publishing model science academia research popularity availability readership impact analysis comparison study paper trends publication process quality scope coverage dissemination effectiveness prominence visibility accessibility popularity metrics evaluation review comparison comparison study comparison study comparison study comparison study comparison study comparison study comparison study comparison study comparison study comparison study comparison open access journals citation advantage traditional scholarly articles publishing impact academic dissemination free article access research visibility impact factor digital publishing trends open access journal impact funding sources citation advantage publishing models research visibility peer review process accessibility issues article dissemination academic publishing trends open access journals citation rates traditional journals article impact peer-reviewed articles online publications academic dissemination accessibility and citation OA journals impact openaccess journals traditional journalism citation effectiveness academic publishing model research popularity impact factor availability accessibility scholarly dissemination impactfactor OA journalimpact articleimpact open access articles citation rate journal impact factor traditional journals peer-reviewed publications academic dissemination online publication accessibility and citation article metrics scientific communication OA vs traditional journals open access journal impact freely available research visibility published articles citation rates academic publishing timing of publication article metrics online availability accessibility and citations openaccess journalcitation traditionaljournals researchdissemination accessmodels citationindices peerreviewimpact OApublishing trends
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 neurodegeneration telomere shortening senescence synaptic plasticity epigenetics brain aging neurogenesis gene expression chromatin modification DNA methylation histone modification senescence cognitive decline telomere length synaptic plasticity aging research neurological disorders epigenetics brain aging neurogenesis gene expression epigenetic modifications aging process molecular biology DNA methylation histone modification RNA editing epigenetic modifications neurogenesis regulation brain aging processes gene expression changes chromatin remodeling age-related cognitive decline DNA methylation histone modification aging neurons epigenetic therapies epigenetics brain aging neurogenesis gene expression chromatin modification DNA methylation histone modification telomere length senescence cognitive decline epigenetic modifications brain aging neurogenesis genes gene expression aging process cognitive decline DNA methylation histone modification chromatin remodeling longevity genes epigenetic modification brain aging neurogenesis genes gene expression chromatin modification DNA methylation histone modification transcription factors neuronal plasticity senescence markers epigenetics brain aging neurogenesis gene expression epigenome modification DNA methylation histone modification molecular biology genetic regulation natural aging process epigenetics brain aging neurogenesis gene expression epigenomic modification aging process molecular biology genetic regulation nucleosome dynamics histone modification RNA editing DNA methylation chromatin remodeling epigenetics neurogenesis aging brain genes chromatin modification gene expression telomeres DNA methylation histone modification senescence
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. physical activity cognitive functioning health benefits six months improvement mental health exercise effects six_months_physical_activity cognitive_functioning physical_exercise b益处 大脑健康 运动对认知的影响 长期锻炼效果 physical_activity cognitive_functioning six_months improvement elderly population benefits research study effects health exercise intelligence memory brain_function mental_health physical activity benefits cognitive improvement six month exercise mental health activity impact brain function improvement exercise routine health benefits six_months physical_activity cognitive_functioning improvement benefits mental_health exercise fitness sports research studies effects physical activity cognitive functioning six months improve memory brain health exercise benefits mental clarity fitness programs physical activity cognitive functioning six months exercise brain health fitness program mental performance endurance training strength training cardiovascular health neuroplasticity memory improvement attention span brain stimulation healthy lifestyle exercise regimen aerobic activities resistance training six_months_physical_activity cognitive_functioning benefits_of_exercise improved_cognition physical_therapy mental_health exercise_regimen activity_levels cognitive_performance health_improvement six_months_physical_activity cognitive_functioning exercise_effects intelligence_improvement health_benefits activity_regimen cognitive_health mind_body_connection fitness_programs mental_clarity physical锻炼 六个月 认知功能改善 健身活动类型 心理健康benefits 运动频率 年龄影响 性别差异 社会影响因素
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 stable partnerships relationship status progression rate sexual health long-term relationships partnership types HIV AIDS stable partnerships progression patients relationship status sexual partnerships long-term relationships chronic illness management HIV AIDS partnership stable relationships progression infection immunity treatment support lifestyle risk factors HIV/AIDS progression stable relationships partnership impact sexual health viral load immune system antiretroviral therapy long-term prognosis relationship status infectious disease management HIV AIDS partnership relationship stable progression infection transmission immune system duration health status HIV/AIDS stable relationships partnership impact disease progression chronic infections immune system public health treatment outcomes viral load sexual health epidemiology medical research HIV AIDS stable partnerships relationship status progression rate immune system medical research virology epidemiology public health HIV/AIDS progression stable relationships partnership impact infectious diseases immune system health outcomes viral load CD4 count treatment access sexual health public health epidemiology HIV AIDS stable partnerships relationship status progression rate sexual health partnership duration viral load immune system response medical outcomes chronic illness management HIV AIDS partnership relationship stable progression risk factors treatment outcome support prevention
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 cancer metastasis therapeutic targets immunotherapy protein inhibitors monoclonal antibody therapy N-cadherin inhibition metastasis prevention cancer treatment protein targeting immunotherapy metastatic suppression biologic agent tumor biology monoclonal antibodies N-cadherin cancer metastasis therapeutic targets biomarkers cell adhesion immunotherapy protein function gene expression tumor growth monoclonal antibodies treatment N-cadherin function cancer metastasis prevention therapeutic antibody development cell adhesion modulation clinical monoclonal antibody therapy metastatic disease inhibition N-cadherin targeted therapy antibody drug mechanism tumor growth suppression monoclonal antibodies N-cadherin metastasis inhibitors cancer therapy biochemistry molecular biology immunotherapy tumor growth cell adhesion monoclonal antibodies N-cadherin inhibition cancer metastasis therapeutic targets biomarkers cancer immunotherapy cell adhesion molecules tumor growth suppression monoclonal antibodies cancer metastasis N-cadherin function biological inhibitors immunotherapy cell adhesion molecules molecular targeting anti-metastatic therapy prognostic markers clinical applications monoclonal antibodies N-cadherin inhibits metastasis anticancer therapy tumor progression cancer immunotherapy biotherapy molecular targeted therapy clinical trial effectiveness analysis monoclonal antibodies N-cadherin metastasis inhibition cancer therapy biomarkers clinical trials immunotherapy cell adhesion tumor progression oncology research cancer therapy biotechnology immunotherapy biomarker clinical trial drug development protein interaction cell adhesion tumor suppression genetic modification
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 genetic processes Okazaki fragments DNA replication termination events sequence specificity molecular biology genetic processes biochemistry scientific research primer extension DNA polymerase Okazaki fragments DNA replication sequence specificity termination events nucleotide sequences genetic processes Okazaki fragments termination mechanisms DNA replication process sequence-specific endonucleases Okazaki fragment processing enzymes RNA primers removal methods Okazaki fragments DNA replication termination events sequence specificity molecular biology genetic processes biochemical reactions Okazaki fragments termination DNA replication sequence specificity molecular biology terms genetic events biosynthesis process scientific queries Okazaki fragments DNA replication termination events sequence specificity molecular biology genetic processes biochemical reactions biotechnology cellular mechanisms Okazaki fragments DNA replication termination events sequence specificity biochemical processes molecular biology genetic mechanisms Okazaki fragments DNA replication termination events sequence specificity molecular biology genetic processes Okazaki fragment synthesis DNA replication RNA primers lagging strand strand displacement DNA polymerase molecular biology techniques genetic mutations biopolymer assembly chromosome maintenance
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. synaptogenesis neurotrophins dendritic spines neurotransmission synaptic plasticity BDNF receptors neuronal differentiation synaptic plasticity neurotrophic factors dendritic spines BDNF release neuronal communication neurotransmission neural plasticity synaptic signaling neurogenesis molecular neuroscience neuronal activity synaptic plasticity neurotrophins dendritic spines neurotransmitters neuronal differentiation BDNF receptors neurogenesis synaptic transmission neuromodulation synaptic vesicles synaptic plasticity neurotrophic factors dendritic spines neurotransmitter release neural development cognitive function synaptic signaling BDNF receptors neuronal growth neurogenesis synaptic activity local release brain derived neurotrophic factor postsynaptic dendrites neurotrophic factors neuronal signaling synaptic plasticity neurotransmitters neuronal growth cognitive function neural communication synaptic plasticity neurotrophic factors dendritic spines BDNF release neurotransmission enhancement neural growth synaptic mechanisms neurotrophic factors dendritic spines neural plasticity neurotransmission molecular biology neuroscience learning memory neurogenesis synaptic mechanisms neurotrophic factors dendritic spines BDNF release neural plasticity neurotransmission synaptic signaling neuronal growth synaptic mechanisms brain derived neurotrophic factor postsynaptic signaling dendritic release neurotrophic factors synaptic plasticity neurotransmission neurogenesis molecular mechanisms neurobiology neuroscientific research synaptic plasticity neurotrophic factors dendritic spines neurotransmitters neuron growth cognitive function synaptic transmission neural regeneration learning processes memory formation
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. venule arteriole blood vessel endothelium capillary anatomy physiology diameter lumen structure circulation microcirculation blood flow venules smooth muscle arterioles vessel layers endothelial cells venule smooth muscle arteriole lumen blood vessel wall endothelial internodal thickness venules structure venules characteristics venules vs arterioles blood vessel layers endothelial lining vascular system comparison venules arterioles smooth muscle blood vessels capillaries diameter endothelium venules structure venules characteristics venule smooth muscle arteriole comparison vascular anatomy venules smooth muscle arterioles endothelium blood vessels vasculature human anatomy vascular structure vascular physiology venules arterioles smooth muscle blood vessels capillaries endothelium diameter lumen circulatory system venules smooth muscle arterioles endothelium vasculature anatomy lymphatics vasculogenesis venule anatomy microcirculation endothelial cells capillary structure blood vessel types vascular smooth muscle
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. myocardium cardiac progenitors mesoderm development cardiomyocytes cardiac progenitors mesodermal cells myocardial development cardiomyocytes embryonic heart stem cells cardiac differentiation molecular biology cardiovascular system embryology cardiac progenitor cells mesoderm tissue engineering cardiology stem cells myocardial regeneration differentiation embryonic development cardiac progenitors mesodermal origin myocardial differentiation stem cells cardiomyocyte development embryonic heart myocardium formation cardiac progenitors mesodermal origin myocardial lineage differentiation cardiomyocytes stem cells embryonic development cardiac progenitors mesodermal development myocardial cells cardiomyocyte differentiation cardiac lineage specification embryonic heart formation mesoderm biology myocardial cells cardiac progenitors mesoderm cardiomyocytes developmental biology heart development myocardial development cardiac progenitors mesodermal origin cardiovascular lineage stem cells heart formation embryonic development cardiomyocyte differentiation cardiac progenitors mesodermal origin myocardial development stem cells cardiology research cardiac progenitors mesodermal development myocardial differentiation embryonic cardiomyocytes cardiac stem cells
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. blood vessels anatomy circulatory system arteriole classification diameter vasculature venules lumen diameter arterioles anatomy vessel size biology vasculature capillaries venules diameter arterioles lumen capillaries vasculature human blood vessels anatomy physiology venule arteriole lumen diameter circulatory system blood vessel anatomy physiology venules arterioles lumen diameter capillaries vessel type anatomy vasculature search optimization keyword expansion relevant phrases venules comparison arterial system anatomy keywords venules arterioles lumen diameter vascular anatomy physiology biology medical terminology venules arterioles lumen diameter vasculature anatomy blood vessels angiography endothelium venules arterioles lumen diameter vascular human body anatomy physiology angiography endothelium venule arteriole blood vessel capillary anatomy physiology diameter lumen circulation
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 mellitus genetic mutation juvenile diabetes pancreatic function beta cells genetic testing disease onset gene expression metabolic syndrome HNF4A diabetes genetic mutation carrier onset age 14 years pancreatic dysfunction congenital hyperglycemia liver disease kidney dysfunction transcription factor HNF4A gene diabetes mellitus genetic mutation juvenile diabetes pancreatic dysfunction congenital disorder metabolic syndrome liver disease renal failure transcription factor HNF4A gene mutations diabetes onset genetic predisposition early diabetes pancreatic beta cells congenital hyperinsulinism liver disease kidney dysfunction genetic testing mutation carriers juvenile diabetes HNF4A diabetes mutant carriers age 14 genetic mutation pancreatic dysfunction transcription factor HNF4A gene mutations diabetes in youth genetic predisposition pancreatic beta cells early onset diabetes hepatocyte nuclear factor 4 alpha HNF4A gene diabetes mellitus genetic mutation juvenile diabetes beta cell function pancreatic islets congenital anomalies glycemic control liver diseases kidney dysfunction HNF4A gene diabetes diagnosis genetic mutation juvenile diabetes pancreatic function carrier risk genetic testing metabolic disorder liver disease kidney dysfunction HNF4A mutations diabetes mutant carriers age 14 years genetic disorder pancreatic dysfunction liver disease kidney disease HNF4A gene diabetes diagnosis early onset diabetes genetic testing pancreatic dysfunction metabolic syndrome carrier risk genetic mutations diabetes prevalence juvenile diabetes
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 t Traditional journals impact factor availability readership publishing model scientific communication effectiveness dissemination peer review online accessibility research popularity impact score publications paywall boundaryless science repository sharing free publishing models discovery metrics openaccess journals citation impact factors publishing model research popularity availability dissemination openaccess journal citation effectiveness research publishing model impact frequency availability quality open access journals traditional scholarly articles citation advantage academic publishing trends accessible research papers open access impact scholarly communication peer-reviewed open access article metrics journal impact factors openaccess citation effectiveness traditionaljournals researchvisibility publishingmodels open access articles citation advantage traditional journals scholarly communication digital publishing academic impact accessible research peer-reviewed articles scholarly impact factor open access journal articles citation frequency traditional journals academic publishing article impact因子 OA articles peer-reviewed journals accessibility and citations open access traditional journals citation frequency scholarly articles digital dissemination academic publishing accessibility impact scientific communication peer-reviewed papers open access journal/articles citation publishing model academic impact article metrics peer review process dissemination of knowledge impact factor research visibility publication type accessibility scientific communication OA journals traditional publishing open access journals citation advantage research dissemination academic impact free access publications peer-reviewed articles impact factor online journal access article visibility OA vs traditional journals
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 anti-inflammatory medication pain relief COX enzyme aspirin inhibitors prostaglandin E2 anti-inflammatory mechanism action medication pain relief clinical research biochemistry aspirin inhibitors prostaglandin E2 COXenzyme anti-inflammatory pain thrombosis fever Aspirin pain relief anti-inflammatory aspirin aspirin mechanism action aspirin medication uses aspirin drug effects prostaglandin synthesis inhibition NSAIDs function aspirin medical benefits aspirin PGE2 inhibition anti-inflammatory cyclooxygenase COX medication effectiveness aspirin pain relief aspirin anti-inflammatory aspirin medication mechanism prostaglandin inhibitors nonsteroidal anti-inflammatory drugs aspirin side effects aspirin dosage aspirin health benefits aspirin nonsteroidalanti-inflammatorydrugs cyclooxygenase prostaglandins inflammation pain fever aspirin PGE2 inhibition nonsteroidal anti-inflammatory drugs COX enzyme reduction inflammation pain relief aspirin nonsteroidal抗炎药 prostaglandin E2 COX inhibitors inflammation pain relief thrombosis prevention clinical applications pharmacodynamics dose-response关系 aspirin mechanisms prostaglandins COX enzyme anti-inflammatory pain relief thrombosis prevention
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 PI(3 4)P2 Src nonreceptor tyrosine kinase focal adhesion cell invasion signal transduction tumor metastasis assembly invadopodia phosphatidylinositol-3 4-biphosphate Src nonreceptor tyrosine kinase focal generation signal transduction cell invasion biophysics biochemical pathways molecular biology cancer metastasis phosphatidylinositol-3 4-biphosphate synthesis Src activation invadopodia formation focal adhesion kinase PI3K signaling matrix metalloproteinase secretion actin polymerization tumor cell invasion phosphoinositide 3-kinase cell migration integrin signaling phosphatidylinositol-3 4-biphosphate synthesis Src activation molecular mechanisms invadopodia formation focal adhesion kinase FAT10 interaction Rac1 activation VPS35 role PIK3CA enzyme assembly invadopodia phosphatidylinositol-3 4-biphosphate Src tyrosine kinase focal adhesion signaling pathway cancer metastasis assembly proteins phosphatidylinositol-3 4-biphosphate synthesis Src activation invadopodia formation cell invasion pathways focal adhesion kinase PI3K signaling assembly invadopodia phosphatidylinositol-3 4-biphosphate Src tyrosine kinase cellular invasion focal adhesion signaling pathway cell motility tumor metastasis assembly invadopodia phosphatidylinositol-3 4-biphosphate Src nonreceptor tyrosine kinase focal generation signaling pathway cell invasion biophospholipids cell motility molecular biology cancer metastasis assembly invadopodia phosphatidylinositol-3 4-biphosphate Src tyrosine kinase focal adhesion cell migration matrix degradation PI3K signaling pathway assembly proteins phosphatidylinositol-3 4-biphosphate generation Src activation invadopodia formation signaling pathways cell migration cancer metastasis biomarkers molecular mechanisms
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 smoking cessation effectiveness long-term treatment clinical trial comparison quit smoking varenicline nicotine replacement therapy bupropion smoking cessation effectiveness treatment duration clinical trial quit smoking cessation success rates varenicline nicotine replacement therapy bupropion smoking cessation effectiveness long-term treatment duration comparison study results varenicline efficacy nicotine replacement therapy bupropion combination smoking cessation treatment long-term varenicline benefits smoking cessation outcomes pharmacotherapy comparison quit smoking aids smoking cessation methods varenicline maintenance therapy smoking cessation effectiveness analysis varenicline effectiveness nicotine replacement therapy bupropion treatmentduration smokingcessation varenicline effectiveness nicotine replacement therapy comparison cessation success rates long-term quit smoking analysis pharmacotherapy outcomes varenicline nicotine replacement therapy bupropion smoking cessation effectiveness treatment duration comparison therapy types quit smoking varenicline monotherapy efficacy comparison nicotine replacement bupropion duration smoking cessation clinical trial quit rate varenicline monotherapy effectiveness nicotine replacement bupropion long-term treatment smoking cessation clinical trial comparison efficacy duration varenicline effectiveness nicotine replacement therapy bupropion smoking cessation long-term treatment comparative efficacy
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 visual acuity geriatric care preventive medicine eye exams aging population healthcare outcomes elderly health visual screening asymptomatic conditions vision improvement aging population eye examination geriatric care preventive medicine ocular health diagnostic tests elderly health vision tests asymptomatic conditions screening programs visual acuity aging population eye examination geriatric care diagnostic accuracy public health initiatives elderly eye health asymptomatic vision issues aging population screening visual acuity tests geriatric eye exams early detection blindness non-invasive eye screening elderly visual function asymptomatic visual problems age-related eye diseases asymptomatic visual impairment screening elderly populations improved vision public health ocular diseases prevention healthcare geriatrics eye exams diagnosis elderly care vision screening health outcomes elderly eye health asymptomatic vision test geriatric eye screening vision impairment detection elderly visual acuity检查 preventive ophthalmology age-related vision issues asymptomatic visual impairment elderly populations screening improved vision ocular health diagnostic tests prevention eye conditions diagnosis geriatric ophthalmology detection chronic diseases public health intervention risk factors symptoms treatment management elderly health visual screening asymptomatic conditions eye examination aging population vision assessment preventive care geriatric ophthalmology diagnostic accuracy public health strategy asymptomatic visual impairment screening elderly populations outcomes intervention benefits diagnostic tests healthcare public policy aging eye disease prevention quality vision treatment geriatrics ophthalmology epidemiology risk factors complications management longitudinal studies meta-analysis systematic review clinical guidelines elderly health screenings asymptomatic conditions visual acuity tests aging population health preventive ophthalmology geriatric eye care vision assessment methods public health interventions ocular disease detection long-term visual outcomes
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 severity genetic allele minor G variant inflammatory bowel disease genetic susceptibility symptom manifestation FOXO3 gene Crohn's Disease severity gene variant G allele genetic factor inflammation immune response genetics研究 炎症机制 免疫基因alogy FOXO3 gene Crohn's Disease severity genetic polymorphism inflammation markers immune response genes susceptibility alleles gastrointestinal symptoms genetic variants Crohn's disease genetics FOXO3 gene variation Crohn's Disease severity genetic factors in Crohn's FOXO3 and inflammation allelic variations Crohn's disease genetic markers G allele impact Crohn's symptomatology genetics FOXO3 G allele Crohn's Disease symptoms genetic factor severity variant association study FOXO3 gene Crohn's Disease symptoms G allele genetic factor variant impact genetic predisposition immune response FOXO3 gene Crohn's Disease severity G allele effects genetic susceptibility inflammatory bowel disease markers FOXO3 gene Crohn's Disease symptom severity G allele genetic factor variant association研究关键词：FOXO3基因 Crohn's病 症状严重程度 G等位基因 遗传因素 变异关联 FOXO3 gene Crohn's Disease genetic variation symptom severity allele expansion major allele comparison genetic predisposition disease progression FOXO3 gene variant Crohn's Disease severity G allele impact inflammation markers genetic predisposition disease progression symptom manifestation
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 vitamin C neurotransmitters antioxidant metabolism genetics neuroscience metabolic disorder mutant mice SVCT2 ascorbic acid brain adrenals genetic modification vitamin C neurological effects adrenal glands metabolic pathways mutant mice SVCT2 ascorbic acid brain adrenals vitamin C neurotransmitters antioxidant gene deletion neurological disorders adrenalin production mutant mice research SVCT2 function ascorbic acid brain levels adrenals vitamin C genetic modification effects neurobiology studies antioxidant role analysis mouse model experiments mutant mice SVCT2 ascorbic acid brain adrenals vitamin C oxidative stress nicotinamide mononucleotide NMN neuroprotection molecular biology genetics metabolism neuroscience mutant mice SVCT2 ascorbic acid brain adrenals genetic modification vitamin C neurological function adrenal function gene knockout antioxidant defense metabolic pathway mutant mice SVCT2 ascorbic acid brain adrenals vitamin C solute carrier neuroscience molecular biology endocrine system mutant mice SVCT2 ascorbic acid brain adrenals beneficial expansion keywords efficacy search optimization mutant mice SVCT2 ascorbic acid brain adrenals vitamin C neurological function adrenal gland gene expression oxidative stress antioxidant defense mutant mice SVCT2 gene ascorbic acid brain adrenals antioxidant defense vitamin C neurological function adrenal gland genetic modification metabolic pathway
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 GNB2 cancers loss interaction G-alpha subunits AKT activation pathway genetics oncology molecular biology cell signaling proteins diseases biomarkers tumor development signaling pathways DNA alterations mutations G-Beta protein GNB2 cancers loss of interaction G-alpha subunits AKT pathway molecular biology oncology molecular genetics signal transduction pathway activation cancer genomics cancer research molecular targets genetic mutations cancer mutation profiling cancer genetics GNB2 mutations G-alpha subunits AKT pathway protein interactions cancer research molecular biology tumor development mutation effects mutations G-beta protein GNB2 cancers loss interaction G-alpha subunits concomitant activation AKT pathway GNB2 mutations cancer genetics AKT pathway activation mechanisms G-alpha subunit interactions GNB2 protein function cancer genetic mutations signal transduction pathways cancer molecular biology Mutations G-Beta protein GNB2 cancers loss interaction G-alpha subunits AKT activation pathway cancer mutations GNB2 G-alpha subunits AKT pathway relevant phrases genetic alterations protein interactions biological pathways molecular biology cancer research molecular genetics tumor development signal transduction mutations G-Beta protein GNB2 cancers loss of interaction G-alpha subunits AKT pathway genetic alterations oncology molecular biology cancer genetics signal transduction biomarkers mutations G-Beta gnb2 cancers G-alpha AKT interaction activation genetic Oncology signaling pathways mutations G-Beta GNB2 cancers loss integration G-alpha subunits AKT activation pathway geneticvariants cellsignaling molecularbiology tumorogenesis diseaseassociation proteinteractions molecularpathways biomarkers mutationimpact signaltransduction cancer genomics G-protein signaling AKT activation oncogenic mutations GNB2 function cellular signaling pathways cancer genetics molecular biology oncology research
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 oxidative stress cytokines signaling pathways peroxynitrite formation nitration process TCR/CD8 complex immune response oxidative stress protein modification cell signaling peroxynitrite nitration TCR CD8 immune response signaling inflammation oxidative stress cell signaling Peroxynitrite formation nitration process TCR/CD8 function immune response regulation oxidative stress signaling pathway biological mechanism molecular interaction immunology research protein modification Peroxynitrite nitration TCR CD8 immune response signaling oxidative stress inflammation Peroxynitrite generation nitration process TCR activation CD8 role immune response mechanisms protein modification enzymes Peroxynitrite nitration TCR CD8 immune response signaling inflammation Peroxynitrite nitration TCR CD8 antibody staining cellular signaling molecular mechanism peroxynitrite nitration TCR CD8 immune response protein modification inflammation oxidative stress immunology biochemistry cell signaling Peroxynitrite formation nitration process TCR complex CD8 molecule oxidative stress immune response protein modification inflammatory signaling molecular mechanism redox biology
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 blood tests folate deficiency vitamin B12 deficiency homocysteine levels neurological symptoms malabsorption vegetarian diet lack symptoms risk factors treatment causes vitamin B12 deficiency homocysteine levels neurological symptoms blood test megaloblastic anemia vitamin B12 deficiency symptoms homocysteine levels vitamin B12 B12 deficiency effects vitamin B12 importance low B12 symptoms homocysteine and B12 deficiency increase B12 absorption B12 deficiency causes B12 supplementation benefits homocysteine B12 relationship vitamin B12 deficiency homocysteine levels malnutrition neurological symptoms anemia blood tests dietary sources 补充词汇:营养不良 神经症状 贫血 血液检测 维生素B12来源 vitamin B12 deficiency homocysteine levels neurological symptoms B12 supplements megaloblastic anemia vitamin B12 deficiency homocysteine levels neurological symptoms anemia methylcobalamin coenzymeb12 RBC size vitamin B12 deficiency homocysteine levels neurological symptoms blood tests megaloblastic anemia supplements dietary sources RNA synthesis vitamin B12 deficiency homocysteine levels neurological symptoms megaloblastic anemia dietary sources B12 absorption medical conditions treatment options health risks vitamin B12 deficiency homocysteine levels neurological symptoms malabsorption supplements dietary sources RNA metabolism MTHFR mutation
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 signal transduction immune response antigen recognition lymphocyte activation TCR CD3 microdomains immunologic synapse T cell activation immune response signaling proteins cell communication adaptive immunity antigen recognition TCR CD3 microdomains immunologic synapse T cells signal transduction immune response protein interactions immunology cell biology antigen recognition immune activation lymphocyte activation TCR complex assembly CD3 signaling pathways immunological synapse formation T cell activation mechanisms membrane microdomains role TCR/CD3 clusters immune response initiation adaptive immunity processes T cell receptor dynamics molecular interactions in T cells TCR CD3 microdomains immunologic synapse T cells immune activation signaling complex immune response antigen recognition TCR complex components CD3 signaling pathways immunological synapse formation T cell activation mechanisms microdomain roles in immunity TCR CD3 microdomains immunologic synapse T cell activation signaling complexes immunology cell biology immune response molecular interactions antigen recognition TCR CD3 microdomains immunologic synapse T cells immune activation signaling complexes cell communication antigen recognition adaptive immunity TCR CD3 microdomains immunologic synapse T cells activation signaling immune response antigen recognition cell biology immunology protein interaction immune system T cell receptor adaptive immunity TCR/CD3 complex immunologic synapse formation T cell activation signaling microdomains immune response induction protein-protein interactions adaptive immunity cell communication antigen recognition immune synapse dynamics
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 tTregs αvβ8 integrin immune suppression inflammatory response immune tolerance T-cell activation immunosuppressive function autoimmune diseases inflammation T regulatory cells αvβ8 integrin pathogenic T-cell suppression active inflammation immune regulation immunology T cell biology inflammatory diseases Treg function immune tolerance regulatory T cells αvβ8 integrin inflammation suppression immune regulation T-cell activation cytokine production autoimmune diseases immune tolerance immune response modulation adaptive immunity T regulatory cells αvβ8 integrin pathogenic T-cell suppression active inflammation immune regulation inflammatory response T-cell function immunology research cell biology adaptive immunity cytokine production antigen presentation immune tolerance chronic inflammation T regulatory cells Tregs αvβ8 integrin suppress pathogenic T-cells active inflammation molecular markers immune regulation T regulatory cells αvβ8 integrin pathogenic T-cell suppression inflammation immune regulation autoimmune diseases immunology cell biology medical research therapeutic targets T regulatory cells tTregs αvβ8 integrin inflammation immune suppression T-cell responses cytokines immune tolerance autoimmune diseases cancer immunotherapy T regulatory cells Tregs αvβ8 integrin suppression pathogenic T-cells inflammation immune response immunosuppression regulatory T cells anti-inflammatory activity Treg αvβ8 inflammation immune suppression pathogenic T-cells cytokines immune tolerance autoimmune diseases immunotherapy cell signaling regulatory T cells αvβ8 integrin inflammation suppression immune tolerance autoimmune diseases cytokine production antigen presentation lymphocyte activation immune response regulation
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. viral infection inflammatory response chemokine production lung inflammation immune response viral load pulmonary infection cytokine release innate immunity viral clearance enhanced early production inflammatory chemokines viral control lung infection immune response cytokine storm antiviral mechanisms innate immunity respiratory system gene expression viral load immunology inflammation biochemistry molecular biology pulmonary function virus replication pathogenesis clinical trials treatment strategies pharmacology virology epidemiology molecular markers therapeutic targets viral infection inflammatory response chemokine production lung inflammation immune response cytokine release respiratory tract viral load innate immunity pulmonary infection host defense inflammatory response enhancement viral infection treatment strategic cytokine induction lung inflammation reduction immune system boost chemokine upregulation techniques viral load decrease innate immunity stimulation inflammatory response viral infection chemokine production pulmonary inflammation virus control early immune response immune system activation viral infection treatment immune response enhancement inflammation reduction lung health improvement chemokine therapy early inflammation management respiratory virus control immune system boost inflammatory cascade modulation viral load decrease enhanced early production inflammatory chemokines viral control lung infection immune response cytokine release innate immunity pathogen clearance acute inflammation respiratory virus interferon response antigen presentation neutrophil recruitment airway inflammation viral load reduction immune cell activation enhanced early production inflammatory chemokines viral control lung infection immune response cytokine storm respiratory virus innate immunity pathogenesis antiviral defense immunology molecular biology virology pulmonary inflammation chemokine receptors interferon response immune evasion viral load clinical outcome inflammatory response chemokine production viral infection lung inflammation immune response cytokine induction antiviral defense immune activation pathogen control immunology research inflammatory response chemokine production viral infection lung inflammation immunological response cytokine release host defense pathogen clearance immune activation innate immunity antiviral 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 maternal nutrition fetal development sunlight exposure supplements genetics epidemiology public health obstetrics vitamin D birth weight epidemiology nutrition prenatal supplementation sunshine genetic socioeconomic dietary maternal fetal development vitamin D birth weight deficiency evidence research factors prenatal nutrition study analysis association vitamin D supplementation birth weight factors maternal nutrition prenatal vitamins Vitamin D levels during pregnancy Vitamin D and infant health vitamin D birth weight evidence study metaanalysis prevalence risk factor pregnancy nutrition health outcome Vitamin D supplementation birth weight impacts Vitamin D levels prenatal Vitamin D Vitamin D during pregnancy vitamin D birth weight prenatal vitamins nutrition maternal health infant development supplementation sunshine exposure calcium absorption immune system bone density growth factors vitamin D birth weight nutritional deficiency prenatal vitamins maternal nutrition fetal development health outcomes epidemiology nutritional science public health Vitamin D birth weight pregnancy supplementation sunlight genetics nutrition epidemiology public health prenatal care vitamin D supplementation birth weight factors maternal nutrition prenatal vitamins 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 endurance training endothelial dysfunction vasodilation nitric oxide cardiovascular health aerobic conditioning physical activity endothelial nitric oxide effectiveness of exercise chronic exercise endothelial function vasodilation nitric oxide aerobic training cardiovascular health physiological response long-term effects exercise physiology endothelium-dependent relaxation chronic exercise endothelial dysfunction aerobic training vasodilation NO synthase nitric oxide cardiovascular health exercise physiology endothelial nitric oxide production chronic aerobic exercise benefits endothelial function improvement vasodilation mechanisms nitric oxide role exercise and cardiovascular health long-term aerobic training effects endothelial dysfunction treatment chronic exercise endothelial function vasodilation NO microvascular response aerobic training endothelial dysfunction exercise physiology chronic aerobic benefits endothelial function improvement NO vasodilation exercise impact cardiovascular health enhancement chronic aerobic exercise endothelial function vasodilation nitric oxide NO cardiovascular health physical activity long-term exercise blood flow vascular endothelium athletic training exercise physiology chronic exercise endothelial function vasodilation nitric oxide aerobic exercise cardiovascular health athletic performance endothelium NO signaling chronic exercise endothelial function vasodilation NO molecular mechanisms aerobic training cardiovascular health endothelial dysfunction aerobic exercise benefits vasodilation mechanisms NO production endurance training effects
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 cognition perception sensory integration therapy neurofeedback mindfulness music brainwaves auditory entrainment visual audio synchronization neurofeedback brainwaves stimulation pacedreading music timing sensoryintegration auditory entrainment visual audio synchronization neurofeedback brainwave therapy music patterns stimulation sensory consistency synchronization timing phaselocking Auditory entrainment visual congruence information brain synchronization neuroscience sensory perception therapy meditation technology enhancement cognitive psychology auditory entrainment visual information synchronization brainwave modulation therapy patterns frequency auditory entrainment techniques visual stimuli impact congruent sensory input mindfulness practices synchrony effects audio-visual therapy hemispheric synchronization virtual reality applications neurofeedback training auditory entrainment visual audio synchronization coherence stimulation neural rhythm phaselocking perception auditory entrainment visual audio synchronization consistency stimulation cognition mindfulness therapy brainwave modulation auditory entrainment visual audio synchronization stimulation consistency cognition perception sensory integration neurofeedback brainwave modulation effects enhancement therapy mindfulness Auditory entrainment visual audio synchronization therapy brainwave modulation power naps learning relaxation
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. autologous transplantation mesenchymal stem cells opportunistic infections induction therapy anti-interleukin-2 receptor antibodies immune response clinical outcomes stem cell therapy immunosuppression cytokine regulation transplant complications mesenchymal stem cells autologous transplantation opportunistic infections anti-interleukin-2 receptor antibodies induction therapy comparative analysis immunosuppression stem cell therapy clinical trials immune response modification tissue regeneration cellular biology autologous transplantation mesenchymal stem cells opportunistic infections anti-interleukin-2 receptor antibodies immune system clinical trials transplant rejection cytokine therapy immune modulation stem cell therapy organ transplant immune response biologic agents immunosuppression autologous transplantation mesenchymal stem cells opportunistic infections anti-interleukin-2 receptor antibodies immune response clinical outcomes treatment efficacy stem cell therapy immune modulation transplant complications immunosuppression inflammatory response mesenchymal stem cells autologous transplantation opportunistic infections anti-interleukin-2 receptor antibodies induction therapy immunosuppression stem cell transplantation immune response modulation graft-versus-host disease cytokine release syndrome autologous transplantation mesenchymal stem cells opportunistic infections anti-interleukin-2 receptor antibodies induction therapy immune response stem cell therapy immunosuppression clinical outcomes biomarkers infection risk therapeutic comparison cellular therapy immune modulation regenerative medicine autologous transplantation mesenchymal stem cells opportunistic infections anti-interleukin-2 receptor antibodies immune response stem cell therapy infection risk immunosuppression clinical trial biologic therapy immunomodulation autologous transplantation mesenchymal stem cells opportunistic infections anti-interleukin-2 receptor antibodies induction therapy immune response stem cell therapy infection risk biological therapy clinical outcome autologous transplantation mesenchymal stem cells opportunistic infections anti-interleukin-2 receptor antibodies immune response stem cell therapy transplantation complications cytokine regulation immunosuppression clinical outcomes mesenchymal stem cells autologous transplantation opportunistic infections anti-interleukin-2 receptor antibodies induction therapy immune response stem cell therapy transplant complications cytokine release immunosuppression clinical outcomes treatment efficacy graft-versus-host disease
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 low-income countries health economics disease prevalence socioeconomic factors public health burden of disease epidemiology noncommunicable diseases low income health economics prevalence global health socioeconomic factors disease burden developing countries public health epidemiology noncommunicable diseases economic settings low income health burden prevalence socio-economic factors global health public health disease distribution Epidemiology noncommunicable diseases socioeconomic factors disease burden low-income regions health statistics non-communicable diseases prevalence economic status and health outcomes epidemiology noncommunicable diseases low economic settings disease prevalence health economics public health socioeconomic factors global health disparities epidemiology noncommunicable diseases economic settings disease burden low income countries public health prevalence risk factors healthcare access socioeconomic status epidemiology noncommunicable diseases economic settings low income health disparities disease prevalence public health socio-economic factors morbidity mortality global health developing countries Epidemiology Noncommunicable diseases Low income Economic impact Disease prevalence Public health Global health Risk factors Healthcare access Demographics Epidemiology noncommunicable diseases low-income countries health economics disease prevalence socioeconomic factors public health burden of disease healthcare access demographic data risk factors mortality rates morbidity rates epidemiology noncommunicable diseases economic status low-income countries health disparities disease prevalence socioeconomic factors public health outcomes
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 immune response therapy comparison stem cell therapy immunosuppression infection prevention mesenchymal stem cells autologous transplantation opportunistic infections anti-interleukin-2 receptor antibodies induction therapy immune response clinical trials regenerative medicine immunosuppression cell therapy comparative analysis autologous transplantation mesenchymal stem cells opportunistic infections anti-interleukin-2 receptor antibodies immune response stem cell therapy organ transplant immune system biological therapy clinical trial autoimmune disorders tissue engineering autologous transplantation mesenchymal stem cells opportunistic infections anti-interleukin-2 receptor antibodies immune response therapeutic alternatives clinical outcomes immunosuppression cell therapy regenerative medicine cytokine inhibition mesenchymal stem cells autologous transplantation opportunistic infections anti-interleukin-2 receptor antibodies immune response clinical outcomes immunosuppression regenerative medicine cellular therapy mesenchymal stem cells autologous transplantation opportunistic infections anti-interleukin-2 receptor antibodies immune response clinical outcomes regenerative medicine cell therapy immunosuppression biotechnology autologous transplantation mesenchymal stem cells opportunistic infections anti-interleukin-2 receptor antibodies immune response clinical trial immunomodulation stem cell therapy treatment efficacy autologous transplantation mesenchymal stem cells opportunistic infections anti-interleukin-2 receptor antibodies immune response clinical trial regenerative medicine immunosuppression stem cell therapy biomedicine transplantation outcomes mesenchymal stem cells autologous transplantation opportunistic infections anti-interleukin-2 receptor antibodies immune response clinical trials regenerative medicine cell therapy immunosuppression mesenchymal stem cells autologous transplantation anti-interleukin-2 receptor antibodies opportunistic infections therapeutic outcomes immune response modulation clinical trials regenerative medicine immunosuppression stem cell therapy benefits infection risk reduction
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 modulating agents antitumor immune response cancer model therapeutic potential gene expression immune modulation oncology immunotherapy chromatin modification epigenetics cancer treatment immune response tumor suppression chemotherapy gene expression immunotherapy molecular biology pharmacology oncology clinical trial drug development epigenetics modulating agents antitumor immune response cancer model therapeutic targets gene expression immunotherapy oncology molecular biology epigenetics modulating agents antitumor immunity cancer models gene expression immune response modulation epigenetic therapy tumor microenvironment immunotherapy cancer treatment epigenetic modifications epigenetics modulating agents antitumor immune response cancer model immune modulation molecular biology tumor suppression genetic regulation immunotherapy epigenetics cancer treatment immune response modulation EMA mechanisms tumor biology therapeutic targets gene expression modification immunotherapy pharmacology molecular biology epigenetics modulating agents antitumor immune response cancer model gene expression immunotherapy chromatin modification cancer treatment molecular biology tumor microenvironment epigenetic therapy immune checkpoint inhibitors epigenetics modulating agents antitumor immune response cancer model therapeutic targets gene expression immunotherapy epigenetic modifications cancer treatment molecular biology tumor microenvironment epigenetics modulation tumor immune response cancer model system agents therapy immunotherapy single cell analysis gene expression methylation acetylation deacetylation proteomics genomics clinical trial preclinical study mechanism of action drug development anti-tumor activity single nucleotide polymorphism(SNP) microRNAs MiRNAS non-coding RNA RNA interference RNAi CRISPR CpG islands chromatin remodeling cell line animal model patient sample biomarker therapeutic target pipeline epigenetics immune response cancer therapy drug efficacy gene expression immunomodulation tumor microenvironment molecular biology clinical trials biomarkers
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 intravenous therapy nursing errors pharmacology patient safety errors peripheral IV drug administration bolus multiple-step medication preparation infusion complications nursing pharmacology patient safety clinical practice medical errors errors peripheral IV drug administration bolus multiple-step medication preparation infusion nursing complications healthcare pharmacology dosage accuracy medication safety intravenous medical errors pharmacology errors medication administration techniques IV therapy complications nursing practice guidelines infusion safety drug preparation procedures healthcare quality improvement patient safety measures errors peripheral IV drug administration bolus multiple-step medication preparation infusion complications healthcare medication safety nursing clinical practice medical errors peripheral IV complications bolus administration errors multiple-step medication risks drug preparation mistakes patient safety in IV therapy IV infusion issues pharmacy practices clinical pharmacy advice errors peripheral IV drug administration bolus multiple-step medication preparation infusion complications nursing patient safety medical errors healthcare intravenous medication management peripheral IV complications bolus administration errors multiple-step medication risks drug preparation mistakes IV therapy issues polypharmacy IV infusion safety peripheral IV best practices errors peripheral IV drug administration bolus multiple step medicine preparation pharmacology nursing clinical medication safety healthcare infusion complications peripheral IV complications bolus administration risks multiple-step preparation errors drug infusion issues pharmacy safety guidelines IV therapy mistakes medication administration errors
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 deficiency pregnancy childbirth gestational period prenatal health maternal vitamin D fetal development delivery duration preterm birth birth complications Vitamin D pregnancy outcomes childbirth prenatal health maternal vitamin D fetal development labor duration postpartum complications calcium absorption bone health immune function gestational period prenatal vitamins maternal nutrition neonatal health vitamin D pregnancy outcomes childbirth prenatal vitamin D maternal vitamin D fetal development pregnancy complications gestational period childbirth duration prenatal care obstetrics perinatal health vitamin D supplementation birth outcomes Vitamin D deficiency during pregnancy impact of vitamin D on childbirth role of vitamin D in gestation period vitamin D levels and delivery timing effect of low vitamin D on pregnancy outcome vitamin D supplementation and preterm birth vitamin D pregnancy childbirth gestational period bone health immunity neonatal outcomes prenatal care vitamin D supplementation maternal vitamin D levels prenatal vitamin D vitamin D during pregnancy impact of vitamin D on delivery vitamin D and gestational length vitamin D and childbirth outcomes vitamin D deficiency in pregnancy vitamin D and preterm birth vitamin D pregnancy outcomes childbirth prenatal health neonatal development maternal nutrition bone health immunity gestational period fetal growth Vitamin D deficiency pregnancy impact of Vitamin D on delivery Vitamin D during pregnancy Vitamin D and childbirth outcomes prenatal Vitamin D benefits Vitamin D pregnancy outcomes childbirth gestational period prenatal health maternal vitamin D fetal development calcium absorption bone health immune function vitamin D deficiency pregnancy vitamin D supplementation during pregnancy impact of vitamin D on gestation role of vitamin D in childbirth vitamin D levels and pregnancy outcomes
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. mesenchymal stem cells autologous transplantation rejection rates anti-interleukin-2 immunotherapy stem cell therapy organ transplantation immune response biologics clinical trials mesenchymal stem cells autologous transplantation anti-interleukin-2 receptor antibodies induction therapy immune rejection clinical outcomes regenerative medicine stem cell therapy immune tolerance transplant immunology autologous transplantation mesenchymal stem cells lower rejection rates induction therapy anti-interleukin-2 receptor antibodies immune response stem cell therapy tissue regeneration immunosuppression clinical application therapeutic efficacy autologous transplantation mesenchymal stem cells lower rejection rates induction therapy anti-interleukin-2 receptor antibodies clinical applications immune response stem cell therapy regenerative medicine transplant success immunosuppression alternatives biologic treatments medical research mesenchymal stem cells autologous transplantation rejection rates induction therapy anti-interleukin-2 receptor antibodies immune response clinical application stem cell therapy biomedicine tissue engineering immunology mesenchymal stem cells autologous transplantation rejection rates induction therapy anti-interleukin-2 receptor antibodies stem cell therapy immune response clinical applications tissue regeneration immunosuppression autologous stem cells mesenchymal transplantation rejection rates anti-interleukin therapy immune response stem cell therapy biotherapy immunomodulation clinical applications autologous transplantation mesenchymal stem cells lower rejection rates induction therapy anti-interleukin-2 receptor antibodies immunotherapy stem cell therapy tissue engineering regenerative medicine clinical applications mesenchymal stem cells autologous transplantation rejection rates anti-interleukin-2 receptor antibodies immunotherapy regenerative medicine clinical trials biological therapy immune response modification mesenchymal stem cells malignancy treatment immune response clinical trials transplantation outcomes biological therapies rejection rate regenerative medicine
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 tolerance bacterial stress response IBP gene protein expression bacterial adaptation ethanol impact transcription factors stress proteins metabolic stress ethanol stress bacterial response IBP protein gene expression bacteria stress tolerance ethanol impact bacterial genes Ethanol tolerance bacterial stress response IBP proteins gene expression bacterial survival alcohol impact stress genes ethanol metabolism Ethanol tolerance bacterial stress response IBP regulation gene expression analysis ethanol metabolism bacterial adaptation stress proteins microbial physiology bioethanol impact Ethanol stress bacterial IBP gene expression microbiology metabolic response transcriptomics proteomics ethanol tolerance bacterial stress response IBP gene regulation metabolic stress ethanol metabolism bacterial adaptation protein synthesis inhibition gene expression analysis ethanol stress bacterial response IBP protein gene expression microbiology bacterial adaptation stress proteins cellular stress transcriptomics bioinformatics Ethanol tolerance bacterial stress response IBP gene regulation ethanol impact on bacteria stress proteins in bacteria ethanol-induced gene expression bacterial survival mechanisms IBP downregulation ethanol metabolism in bacteria Ethanol stress bacterial response IBP gene expression levels microbial adaptation Biosynthesis pathways SOS response Ethanol tolerance bacterial stress response IBP protein gene expression analysis microbiology research bioinformatics tools microbial metabolism stress proteins transcriptomics molecular biology techniques
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 tolerance thermogenesis adipose tissue metabolic rate energy expenditure winter survival brown fat activation non-shivering thermogenesis cold adaptation chilly environment fat metabolism calorie burning heat production cold tolerance BAT activation thermogenesis pubic bone fat shivering thermogenesis non-shivering thermogenesis cold stress BAT activation thermogenic response temperature regulation fatigue resistance metabolic rate adipose tissue hypothermia resistance cold tolerance thermogenesis brown adipose tissue metabolic rate calorie burning energy expenditure non-shivering thermogenesis adaptive thermogenesis chilly environment cold adaptation fat metabolism weight loss techniques obesity prevention temperature regulation Cold tolerance BAT activation thermogenesis energy metabolism Winter acclimation cold tolerance thermogenesis adaptive brown fat metabolic rate 寒暴露 脂肪贝塔招募 低温适应 棕色脂肪细胞增加 冷应激 cold tolerance brown adipose tissue thermogenesis energy metabolism non-shivering thermogenesis hypothermia resistance cold tolerance bat activation body temperature thermal regulation hypothermia resistance winter survival negative calorie burn metabolic rate enhancement energy expenditure fat mobilization cold stress BAT activation body temperature thermogenesis energy metabolism CIDEA protein expression cold tolerance thermogenesis metabolic rate brown fat activation 寒暴露 冷应激 非寒性冷刺激
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 effects population control measures economic impacts of one-child policy one-child policy history one-child policy history one-child policy effects population control measures one-child policy success family planning policy China population growth one-child policy history one-child policy effects one-child policy consequences population control measures policy impacts on society population growth rates China demographic changes population control demographic impact birth rates social consequences economic effects family planning China's economy cultural changes one-child policy population control demographic transition China's policy fertility rates social impact economic consequences one-child policy effects impact of one-child policy population control methods policy on population growth one-child policy history one-child policy effects population control strategies China demographics one-child policy consequences one-child policy effects population control strategies economic impact of one-child policy one-child policy history population growth rates one-child policy history one-child policy effects population control strategies one-child policy China one-child policy outcomes one-child policy history population control measures effects of one-child policy alternative population policies one-child policy replacement
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. age-related autophagy decline senescence autophagy cellular aging autophagy autophagy reduction elderly age induced autophagy decrease autophagy aging senescence cellular degradation lifespan aging process mitochondrial function protein turnover aging research autophagy mechanism age-related diseases ageing senescence cellular_degradation lifespan mitochondrial_function metabolic_rate protein_homeostasis inflammation apoptosis free_radicals autophagy process age-related autophagy decline autophagy function in aging senescent cell autophagy autophagy mechanisms in elderly declining autophagy over time age-associated autophagy reduction autophagy and longevity autophagy mechanisms aging process cellular degradation senescence markers mitochondrial function protein turnover gene expression regulation metabolic changes lifespan extension autophagy inhibitors age-related diseases autophagy aging age-related autophagy decline aging process autophagy reduction in elderly aged cells senescence and autophagy ageing and autophagy connection autophagy mechanism age-related decline senescence cellular aging autophagy dysfunction aging process autophagy regulation gerontology lifespan reduction biological aging Autophagy aging senescence mechanisms cellular degradation longevity factors mitochondrial function gene expression aging protein turnover lifespan extension age-related diseases autophagy stimulation metabolic changes aging age-related changes autophagic flux senescence cellular aging mitochondrial function lysosomal activity gene expression protein degradation metabolic rate oxidative stress autophagy mechanisms age-related decline cellular aging autophagy regulation senescence markers mitochondrial autophagy neurodegeneration senolytics lifespan extension autophagy activators
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 thermogenesis brown adipose tissue non-shivering hypothermia cold acclimation metabolic rate energy expenditure fat metabolism adaptive thermogenesis cold tolerance BAT activation thermogenic response fat metabolism cryogenics hypothermia thermal regulation hormesis metabolism stimulation energy expenditure cold stress thermogenesis brown adipose tissue metabolic rate acclimation hypothermia non-shivering thermogenesis adaptive thermogenesis Cold tolerance thermogenesis enhancement metabolic rate increase adipose tissue activation brown fat stimulation non-shivering thermogenesis promotion cold adaptation benefits cold tolerance bat activation thermogenesis adipose tissue metabolism regulation hypothermia resistance endocrine response Cold tolerance thermogenesis adipose tissue metabolic rate heat production energy expenditure brown fat activation temperature regulation cold acclimation non-shivering thermogenesis cold temperature thermogenesis brown adipose tissue metabolic rate non-shivering thermogenesis calorie burning fat metabolism energy expenditure chilly environment adaptive thermogenesis cold tolerance thermogenesis adipose tissue metabolic rate brown fat activation hypothermia resistance energy expenditure non-shivering thermogenesis cold acclimation temperature regulation cold temperature thermogenesis adipose tissue metabolic rate energy expenditure brown fat activation non-shivering thermogenesis cold acclimation temperature sensitivity fat metabolism Cold tolerance thermogenesis metabolic rate adipose tissue non-shivering diet impact exercise influence aging effect genetic factors
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 cleavage sitesidentification RNA processing molecular biology techniques bioinformatics tools chromatin structure transcription factor binding N-terminal cleavage transcription start sites proteomics biomarker detection enzymatic processing mass spectrometry genomics alternative splicing N terminal cleavage protein digestion mass spectrometry transcription start site gene expression analysis proteomics cleavage site identification peptide mapping RNA sequencing proteolytic cleavage N-terminal proteolysis transcription initiation RNA polymerase binding chromatin structure gene expression analysis splicing variants epigenetic modifications transcript mapping bioinformatics tools genome editing next-generation sequencing N terminal proteolysis transcription initiation peptide sequencing RNA binding proteins chromatin structure gene expression profiling splice variants DNA-protein interactions bioinformatics tools mass spectrometry analysis N terminal cleavage transcription start sites protein processing genetic engineering bioinformatics molecular biology proteomics RNA analysis gene expression sequence analysis N-terminal cleavage transcription start sites proteomics mass spectrometry peptide sequencing bioinformatics gene expression RNA processing N terminal cleavage transcription start sites protein digestion sequencing accuracy proteomics RNA processing gene expression analysis N-terminal cleavage transcription start sites enhance query expansion terms protein processing molecular biology research genetics DNA sequencing analysis biotechnology biological omics transcriptional regulation eukaryotic prokaryotic N terminal cleavage transcription start sites proteomics mass spectrometry RNA processing gene expression protein modification peptide sequencing molecular biology techniques
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 localization Arabidopsis embryo VPS9a protein localization plant biology embryogenesis cellular localization Arabidopsis thaliana endomembrane system PIN1 protein Arabidopsis thaliana VPS9a protein embryo development subcellular localization plant biology cellular compartments protein interactions gene function embryogenesis PIN1 protein Arabidopsis thaliana embryo development localization VPS9a protein plant cell biology trafficking endomembrane system Golgi apparatus localization mechanisms protein interaction PIN1 localization Arabidopsis embryo development VPS9a function plant cell biology embryo patterning localized protein distribution Arabidopsis genetics endomembrane system PIN1 vesicle trafficking PIN1 localization Arabidopsis embryo VPS9a protein trafficking plant cell biology endomembrane system Golgi apparatus subcellular localization gene expression developmental biology PIN1 localization Arabidopsis embryo VPS9a requirement plant hormone signaling embryo development protein localization subcellular localization PIN proteins plant biology gene function cell biology PIN1 protein localization Arabidopsis embryo development VPS9a function plant cell biology embryogenesis process subcellular localization plant hormone transport auxin distribution molecular biology techniques genetic analysis protein interaction cellular compartmentalization PIN1 localization Arabidopsis embryo VPS9a dependency plant cell biology embryo development protein localization molecular biology Arabidopsis thaliana cellular compartments PIN1 Arabidopsis embryo localization VPS9a protein transport cell biology plant science endomembrane system subcellular定位 生物学 植物学 内膜系统 PIN1 protein Arabidopsis thaliana embryo development localization mechanisms VPS9a protein endomembrane system cellular trafficking molecular biology plant cell biology genetic analysis biochemical functions
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 transcription start sites proteomics sequencing mass spectrometry RNA processing bioinformatics regulation genomics N terminal cleavage proteomics transcription start sites protein digestion mass spectrometry RNA sequencing chromatin immunoprecipitation transcription factors gene expression molecular biology techniques N-terminal cleavage reduces success identifying transcription start sites proteomics bioinformatics mass spectrometry gene expression regulation RNA sequencing genome analysis protein processing N-terminal proteolysis transcription initiation gene expression analysis RNA sequencing cleavage assays splice variants regulatory regions chromatin immunoprecipitation transcript mapping protein modification techniques N terminal cleavage transcription start sites proteomics mass spectrometry RNA processing gene expression regulatory regions N terminal cleavage impact transcription start site identification challenges proteomics analysis methods RNA processing steps gene expression regulation N terminus modifications transcript mapping accuracy protease specificity for N-terminal cleavage N-terminal cleavage transcription start sites proteomics mass spectrometry RNA sequencing bioinformatics gene expression regulation molecular biology epigenetics chromatin structure transcriptional initiation promoter motif analysis database annotation genome mapping N terminal cleavage transcription start sites proteomics sequencing techniques peptide fragmentation RNA processing molecular biology bioinformatics gene expression analysis protein modification mass spectrometry N terminal cleavage protein processing transcription start site proteomics gene expression analysis peptide sequencing RNA-Seq alternative splicing biological pathways molecular biology techniques N terminal cleavage transcription start site identification proteomics RNA sequencing protein digestion gene expression analysis bioinformatics tools molecular biology techniques peptide mapping transcriptome 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 protein localization Arabidopsis root development VPS9a function plant cell biology molecular localization techniques Arabidopsis thaliana endomembrane system protein trafficking PIN1 protein Arabidopsis roots VPS9a dependency localization mechanism plant cell biology endomembrane system protein trafficking PIN1 Arabidopsis localization roots VPS9a protein trafficking plant biology subcellular localization endomembrane system molecular biology plant cell biology PIN1 protein localization Arabidopsis root development VPS9a function plant cell biology endomembrane trafficking gene expression analysis subcellular localization molecular biology techniques plant hormone transport receptor signaling pathways PIN1 localization Arabidopsis roots VPS9a protein trafficking endomembrane system Golgi apparatus yeast two-hybrid fluorescence microscopy PIN1 protein Arabidopsis roots localization process VPS9a dependency cellular localization plant biology gene function molecular biology protein interactions PIN1 localization Arabidopsis roots VPS9a protein transport endomembrane system plant cell biology auxin transport membrane trafficking PIN1 localization Arabidopsis roots VPS9a protein localization plant cell biology localization requirements biochemical pathways gene function molecular biology plant hormones PIN1 localization Arabidopsis roots VPS9a protein trafficking cellular localization plant biology endomembrane system Golgi apparatus yeast two-hybrid genetic analysis confocal microscopy PIN1 protein Arabidopsis roots VPS9a dependency localization mechanism plant cell biology endomembrane system subcellular distribution biochemical function molecular biology techniques genetic analysis cellular trafficking
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 mutation drug resistance mechanisms antiretroviral therapy N348I mutation zidovudine resistance AZT resistance HIV drug resistance mutagenesis studies antiretroviral therapy N348I mutation zidovudine resistance AZT resistance HIV mutations antiretroviral therapy resistance N348I mutation zidovudine resistance AZT resistance HIV drug resistance antiretroviral therapy failure N348I mutation zidovudine resistance AZT N348I mutations zidovudine resistance AZT resistance mutation effects Antiretroviral therapy mutational analysis HIV treatment N348I mutation zidovudine resistance AZT resistance HIV mutation antiretroviral therapy drug resistance markers N348I mutation zidovudine resistance AZT resistance HIV drug resistance Mutation effects N348I mutation zidovudine resistance AZT resistance HIV mutation drug resistance antiretroviral therapy N348I mutation zidovudine resistance AZT resistance HIV treatment Viramune
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. high microerythrocyte count homozygous alpha (+)-thalassemia severe anemia erythrocyte size alpha thalassemia trait hemoglobin levels red blood cell indices genetic disorder hematological vulnerability iron deficiency anemia thalassemia screening microcytosis anemia risk factors high microerythrocyte count homozygous alpha(+)-thalassemia severe anemia thalassemia trait erythrocyte size hemoglobin levels genetic disorder hematological risk因素 clinical symptoms diagnostic markers high microerythrocytosis alpha plus thalassemia anemia susceptibility erythrocyte size genetic predisposition hemoglobin levels thalassemia major red blood cell morphology hematological parameters iron deficiency anemia hemolytic anemia high microerythrocyte count severe anemia homozygous alpha (+)-thalassemia erythrocyte size genetic disorder hemoglobin levels red blood cell count thalassemia major iron deficiency blood transfusions hemolytic anemia pediatric anemia hematopoietic stem cells bone marrow failure chronic anemia management microerythrocyte count homozygous alpha (+)-thalassemia severe anemia vulnerability erythrocyte size alpha thalassemia hemoglobin levels genetic disorder red blood cell morphology anemia risk factors thalassemia types hematological parameters microerythrocytosis alpha thalassemia anemia risk red blood cells hemoglobin deficiency genetic disorder hematological condition blood transfusion necessity iron supplementation healthcare management microerythrocytosis alpha thalassemia thalassemia major hemoglobin red blood cells anemia risk genetic disorder hematological condition blood transfusions iron supplementation bone marrow diagnostic tests microerythrocyte count homozygous alpha (+)-thalassemia severe anemia erythrocyte size thalassemia traits red blood cell abnormalities genetic predisposition hemoglobin levels hematological disorders microerythrocytosis alpha thalassemia severe anemia homozygous erythrocyte genetic disorder hematological condition blood disorder hemoglobinopathy anemia risk red blood cell size thalassemia major hemoglobin A2 levels iron deficiency blood transfusion genetic counseling microerythrocytosis alpha thalassemia hemoglobinopathy genetic predisposition anemia risk blood disorder red blood cell abnormalities hematological condition medical genetics genetic counseling clinical diagnosis
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 infection population transmission risk prevalence study asymptomatic vCJD UK statistics prevalence vCJD UK vCJD infection symptoms UK vCJD cases UK investigation asymptomatic vCJD transmission UK asymptomatic vCJD infection UK population spread prevalence detection risk factors genetics transmission clinical variants asymptomatic vCJD cases vCJD infection spread vCJD transmission methods prevalence vCJD UK vCJD symptoms absent vCJD diagnosis asymptomatic vCJD risk factors asymptomatic vCJD UK infection population studies research cases detection prevalence search optimization query expansion vCJD asymptomatic carriers UK statistics infectious diseases public health epidemiology rare infections asymptomatic vCJD vCJD infection UK vCJD prevalence UK vCJD symptoms absence variant Creutzfeldt-Jakob disease asymptomatic asymptomatic vCJD vCJD infection UK vCJD carrier UK vCJD prevalence UK asymptomatic vCJD UK statistics vCJD infection prevalence UK vCJD cases asymptomatic vCJD diagnosis vCJD incubation period vCJD UK research vCJD symptomatology vCJD transmission methods vCJD epidemiology UK asymptomatic vCJD UK statistics vCJD transmission vCJD prevalence UK prion disease research vCJD incubation period asymptomatic 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 function Dicer interaction pre-miRNA processing molecular biology techniques RNA editing enzymes ADAR1 Dicer pre-miRNA cleavage molecular biology RNA editing RNA processing miRNA maturation enzymology biological pathway genetic regulation transcriptional regulation ADAR1 function Dicer interaction pre-miRNA processing molecular biology techniques miRNA maturation RNA editing ADAR1 function Dicer interaction miRNA processing RNA binding proteins pre-miRNA cleavage mechanisms RNA interference gene regulation molecular biology techniques RNA structure small RNA pathway ADAR1 Dicer pre-miRNA cleavage molecular biology RNA editing ADAR1 function Dicer interaction miRNA processing RNA editing gene regulation molecular biology pre-miRNA cleavage enzymatic activity RNA binding protein RNA metabolism ADAR1 function ADAR1 Dicer interaction pre-miRNA processing RNA binding proteins miRNA maturation RNA interference molecular biology techniques ADAR1 Dicer pre-miRNA cleavage molecular biology RNA editing miRNA processing enzyme interaction microRNAs adenosine deaminase ADAR1 function Dicer interaction pre-miRNA processing molecular biology techniques miRNA maturation process RNA editing enzymes ADAR1 function Dicer interaction pre-miRNA processing RNA editing miRNA maturation ADAR1 mutation impact Dicer substitutes RNA binding proteins miRNA biogenesis pathways
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 expansion weak ligand alternatives signal enhancement techniques ligand binding affinity signalling pathway strengthening cSMAC mechanisms protein interaction analysis cSMAC mechanism cSMAC protein ligand binding affinity signaling pathway protein interaction molecular biology signaling molecules cellular response biochemistry weak signals receptor activation signal transduction biological pathways cSMAC expansion ligand binding enhancement molecular interactions signalling pathways protein complexes biochemistry research ligand affinity improvement cSMAC protein function cSMAC mechanism of action cSMAC and signaling pathways cSMAC role in cell signaling cSMAC interaction with ligands cSMAC enhancement mechanisms cSMAC biological significance cSMAC in drug development cSMAC research applications cSMAC molecular structure cSMAC protein complex weak ligands signaling pathways molecular interactions receptor binding signal transduction biochemistry pharmacology cell biology cSMAC expansion phrases ligand binding enhancement protein complex formation signaling pathway improvement molecular interaction strengthening cellular response amplification cSMAC protein complex apoptosis IAPs caspase activation ligand binding signaling pathways molecular interactions biological processes cell death mechanisms cSMAC molecular chaperone protein aggregation ligand binding signalling pathway biological process pharmacology medicine research therapeutics cell biology cSMAC apoptosis caspase IAPs ligand binding signaling pathways protein complex cell death molecular biology signal transduction weak signals therapeutic targets cSMAC protein ligand binding signal transduction molecular interactions receptor activation biochemical pathways cellular response pharmacology bioinformatics molecular dynamics simulation
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. Rapid up-regulation interferon-induced genes reduce survival granule cell neurons infected West Nile virus immune response inflammation neuroinvasion pathogenesis innate immunity rapid up-regulation interferon-induced genes granule cell neurons West Nile virus survival gene expression neurological impact viral infection neuroinflammation innate immunity cytokine response neuronal death interferon-induced genes rapid up-regulation basal expression granule cell neurons West Nile virus neuroinvasion inflammation viral load neuronal death innate immune response antiviral defenses interferon-induced genes expression rapid up-regulation West Nile virus infection granule cell neurons survival rates viral neuroinvasion immune response gene regulation neurotropism inflammatory cytokines interferon-induced genes rapid up-regulation basal expression granule cell neurons West Nile virus viral infection neuronal survival immune response gene expression virology neuroscience interferon response West Nile virus infection neuron survival gene expression analysis viral neuropathogenesis immune response modulation antiviral defense interferon-induced genes rapid up-regulation basal expression granule cell neurons West Nile virus viral infection gene expression survival rates neuroinvasion innate immunity RNA viruses Rapid up-regulation interferon-induced genes granule cell neurons West Nile virus survival reduction viral infection gene expression neuroinflammation neuronal apoptosis antiviral response Rapid up-regulation interferon-induced genes survival granule neuron West Nile virus immune response molecular pathway neuroinflammation viral infection neurotropic host microenvironment West Nile virus infection interferon-induced genes neuronal survival gene expression viral neuropathy immune response neuroinflammation RNA interference antiviral defense neurodegeneration
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-stimulated genes West Nile virus infection neuronal survival innate immune response viral neuropathy gene expression analysis neuroinflammation antiviral defense neurological disorders Rapid up-regulation interferon-induced genes survival granule cell neurons West Nile virus immune response neuroprotection inflammation gene expression viral infection neuronal survival interferon pathway viral genes neuroinflammation interferon-inducible genes West Nile virus infection neuronal survival immune response antiviral defense gene expression profiling neuroinflammation neuron vulnerability Rapid up-regulation mechanisms interferon-induced genes function survival benefits granule cell neurons West Nile virus infection gene expression enhancement viral neuroinvasion response immune system activation neuroprotection strategies Rapid up-regulation interferon-induced genes survival granule cell neurons infected West Nile virus immune response viral infection neuroprotection gene expression inflammation neuronal survival interferon-induced genes West Nile virus granule cell neurons rapid up-regulation basal expression survival rates viral infection response neurological impact genetic factors interferon-induced genes rapid up-regulation basal expression granule cell neurons West Nile virus survival rates viral infection response immune system neuroprotection gene expression analysis RNA interference cytokine production interferon-induced genes rapid up-regulation basal expression granule cell neurons West Nile virus survival rate immune response viral infection neuroprotection interferon-induced genes West Nile virus granule cell neurons rapid up-regulation higher basal expression survival rate viral infection neuroprotection gene expression analysis immune response interferon-stimulated genes WNV infection neurological outcome granulocytes immune response viral load survival rate gene expression profiling
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 editing DNA repair mechanisms double strand break repair human genome editing genetic engineering techniques gene editing accuracy CRISPR Cas9 complications Cas9 repair mechanisms human DNA damage genome editing errors Cas9 double strand break repair non-homologous end joining NHEJ CNN repair process HDR efficiency Cas9 enzyme function DNA repair mechanisms double strand break repair human cell biology genetic engineering techniques CRISPR-Cas9 system molecular biology processes genetic mutation rates gene editing accuracy genome stability maintenance Cas9 induced DNA damage homology directed repair efficiency non-homologous end joining process double strand break repair mechanisms gene editing errors CRISPR off-target effects Cas9 protein DNA repair mechanisms genome editing技术 base editing技术 non-homologous end joining NHEJ homology-directed repair HDR Cas9 induced double strand breaks DNA repair mechanisms CRISPR Cas9 accuracy genetic engineering errors gene editing complications molecular biology techniques genomic stability maintenance Cas9 repair mechanisms human DNA damage Cas9 editing errors genome repair pathways DNA repair proteins Cas9 off-target effects DNA double strand break repair CRISPR-Cas9 accuracy Cas9 repair mechanisms human DNA damage Cas9 double strand breaks efficacy of DNA repair 精准基因编辑错误 CRISPR Cas9 off-target effects DNA修复途径 双链断裂修复机制 基因编辑安全性 Cas9 repair mechanisms human DNA damage double strand break repair non-homologous end joining homologous recombination gene editing errors CRISPR-Cas9 accuracy DNA repair pathways genetic engineering techniques Cas9 efficiency DNA repair mechanisms double strand break repair human genome editing gene editing 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. α-tocopherol vitamin E prostate health cancer prevention antioxidant α-tocopherol vitamin E prostate cancer prevention dosage supplements health benefits antioxidant vitamin_e cancer_prevention prostate_health antioxidants diet_supplements health_benefits α-tocopheryl acetate benefits prostate cancer prevention methods alpha tocopherol advantages 400mg vitamin E efficacy dietary supplements for prostate health α-tocopherol vitamin E prostate health cancer prevention antioxidant properties α-tocopheryl acetate benefits prostate cancer prevention methods vitamin E and prostate health supplementation for cancer prevention α-tocopherol dosage prostate anti-oxidants for prostate health α-tocopherol vitamin E prostate health cancer prevention antioxidant supplements dosage benefits α-tocopheryl acetate benefits prostate cancer prevention vitamin E dosage cancer risk reduction supplements for prostate health antioxidant supplements α-tocopheryl acetate benefits prostate cancer prevention strategies dietary supplements for prostate health vitamin E and prostate cancer α-tocopherol effectiveness α-tocopherol vitamin E prostate health cancer prevention antioxidant dosage supplementation clinical studies risk reduction
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 glutamine metabolism cancer signal proliferation therapy resistance aPKCz tumour glutamine metabolism cancer signal transduction pathway cell growth proliferation aPKCz tumor enhancement glutamine metabolism cancer cell proliferation oncogenic signaling metabolic reprogramming cancer metabolism amino acid metabolism protein kinase C zeta cancer biology tumor growth metabolic pathways cancer metabolism regulation aPKCz tumor enhancement aPKCz glutamine metabolism aPKCz cancer growth aPKCz metabolic pathway aPKCz oncogenesis aPKCz cellular metabolism aPKCz cancer metabolism aPKCz signaling pathways aPKCz tumor biology aPKCz metabolic reprogramming aPKCz tumour glutamine metabolism cancer biomarker therapy signal transduction proliferation aPKCz tumour enhancement aPKCz cancer promotion aPKCz glutamine metabolism aPKCz cell proliferation aPKCz metabolic reprogramming aPKCz oncogenic signaling aPKCz cancer metabolism aPKCz tumor growth aPKCz metabolic pathway aPKCz cancer biology aPKCz tumour enhancement glutamine metabolism cell signaling cancer biology molecular oncology metabolic reprogramming aPKCz tumour enhancement glutamine metabolism pathway cell proliferation molecular biology cancer research metabolic reprogramming aPKCz tumour glutamine metabolism cancer enzymes signal transduction gene expression therapy biomarker aPKCz tumor oncogenic role aPKCz glutamine metabolism cancer metabolic reprogramming tumor aPKCz signaling tumor growth factors cancer metabolism aPKCz cancer research glutaminase activation metabolic pathway alteration
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 therapy nicotine replacement nicotine cessation abstinence rates varenicline bupropion tobacco cessation smoking cessation therapy comparison quitting smoking pharmacotherapy clinical trials effectiveness smoking cessation treatments nicotine replacement therapies varenicline bupropion abstinence rates 52 weeks monotherapy smoking cessation meta analysis clinical trial systematic review effectiveness comparison treatment options outcomes duration efficacy quit smoking cessation methods strategies quitting smokingcessation pharmaceuticals pharmacological interventions tobacco addiction health benefits risks guidelines smokers nicotine dependence cessation success factors variables predictors metaanalysis clinicaltrials systematicreview randomized controlled studies nicotine replacement therapy nicotine gum nicotine patch combining medications long-term smoking cessation varenicline benefits bupropion use smoking cessation outcomes 52-week study quit smoking aids nicotine replacement therapy combinations varenicline and bupropion together long-term smoking cessation quit smoking aids abstinence maintenance dual therapy for nicotine addiction extended treatment options smoking cessation success rates quit smoking support methods long-term smoking cessation outcomes nicotine replacement therapies varenicline bupropion abstinence rates long-term smoking cessation clinical trial quit smoking addiction treatment 戒烟疗法 长期戒断成功率 nicotine replacement therapies varenicline bupropion abstinence rates long-term smoking cessation combination therapy quitting smoking smoking cessation treatments quit rates tobacco cessation dual therapy multi-modal therapy nicotine replacement therapies varenicline bupropion abstinence rates long-term 52 weeks monotherapy smoking cessation addiction treatment clinical trial meta-analysis quit smoking relapse prevention pharmacotherapy dual therapy combination therapy nicotine replacement abstinence rates varenicline bupropion 52 weeks smoking cessation nicotine replacement therapies varenicline bupropion abstinence rates 52 weeks monotherapy smoking cessation clinical trial quit smoking 戒烟疗法 长期戒断 吸烟辅助治疗 nicotine replacement therapy nicotine patches nicotine gum bupropion monotherapy combination therapy abstinence rates long-term cessation varenicline efficacy
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 regulatory mechanisms protein kinases bacterial signaling molecular biology genetic switches phosphotransferase two-component signaling bacterial response protein phosphorylation signal transduction enzymatic kinetics genetic regulation biosensor technology molecular biology microbiology phosphorylation two-component signaling bacterial response signal transduction protein phosphorylation regulatory proteins enzyme kinetics molecular biology gene expression cellular signaling phosphotransfer mechanisms two component signaling protein phosphorylation bacterial signal transduction genetic regulatory systems enzymatic phosphorylation rates signal amplification sensory adaptation proteins phosphorelay pathways intracellular communication phosphorylation signal transduction bacterial systems protein modification sensory histidine kinases response regulators molecular mechanisms enzymatic kinetics genetic regulation biochemical pathways phosphotransfer mechanisms two-component signaling enzymatic phosphorylation signal transduction pathways bacterial response regulation protein modification rates cellular communication processes sensory histidine kinases phosphorelay systems gene expression regulation phosphorylation signal transduction enzymatic kinetics bacterial signaling protein modification gene regulation molecular biology signal amplification sensory adaptation transcriptional control phosphotransferases signaling pathways bacterial communication genetic regulation kinase activity protein modification signal transduction two-component regulatory system molecular biology enzymology phosphorelay signal transduction bacterial communication protein phosphorylation regulatory networks two-component signaling phosphorylation signal transduction bacterial regulation kinase activity transcriptional control protein modification molecular biology signal cascade enzymatic reaction genetic switch
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 drug combination therapy oncology research signal transduction inhibitors targeted therapy molecular targeting tumor suppression phosphatidylinositide 3-kinase inhibitors MEK 1/2 inhibitors KRAS mutant tumors cancer treatment drug combination therapy oncology research signaling pathways targeted therapies clinical trials molecular biology pharmacology tumor suppression phosphatidylinositide 3-kinase inhibitors MEK 1/2 inhibitors KRAS mutant tumors cancer treatment oncology research drug combination therapy signal transduction inhibitors cell proliferation阻断剂 phosphatidylinositide 3-kinase inhibitors MEK 1/2 inhibitors KRAS mutant tumors cancer treatment therapeutic combination oncology research signaling pathways drug efficacy precision medicine targeted therapy molecular biology phosphatidylinositide 3-kinase MEK 1/2 inhibitors KRAS mutant tumors cancer therapy efficacy drug combination anti-cancer treatment signaling pathway阻断剂 phosphatidylinositide 3-kinase inhibitors MEK 1/2 inhibitors KRAS mutant tumors cancer treatment therapeutic combinations oncology research signaling pathways drug efficacy targeted therapy molecular biology phosphatidylinositide 3-kinase inhibitors MEK 1/2 inhibitors KRAS mutant tumors cancer treatment drug combination therapy signaling pathways oncology research targeted therapy tumor suppression phosphatidylinositide 3-kinase inhibitors MEK 1/2 inhibitors KRAS mutant tumors cancer treatment targeted therapy oncology drug combination signaling pathways therapeutic efficacy cancer research clinical trials molecular biology phosphatidylinositide 3-kinase inhibitors MEK 1/2 inhibitors KRAS mutant tumors cancer treatment drug combination therapy oncology research therapeutic efficacy signal transduction inhibitors targeted cancer therapies phosphatidylinositide 3-kinase inhibitors MEK 1/2 inhibitors KRAS mutant tumors cancer treatment targeted therapy oncology research clinical trials pharmacodynamics drug resistance tumor suppression signaling pathways
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 drug response metabolic rate gene expression chemotherapy resistance breast cancer tamoxifen metabolism genetic factors treatment outcome pharmacogenetics gene expression drug response oncology personalized medicine molecular biology clinical trials breast cancer tamoxifen metabolism genetic factors treatment response pharmacogenetics gene expression oncology drug efficacy breast cancer tamoxifen metabolism genetic factors treatment outcome pharmacogenetics gene expression metabolic pathway clinical trial drug response oncology research personalized medicine breast cancer tamoxifen metabolic capacity genetic factors treatment outcome breast cancer tamoxifen metabolism genetic factors treatment outcome pharmacogenetics drug response gene-drug interaction oncology metabolizing capacity breast cancer tamoxifen metabolism genetic factors treatment outcome pharmacogenomics enzyme activity genetic polymorphism drug response metabolic pathway breast cancer patient tamoxifen metabolism genetic makeup treatment outcome pharmacogenetics oncology drug response gene variants therapeutic efficacy personalized medicine breast cancer tamoxifen metabolism genetic factors treatment outcome pharmacogenetics oncology gene expression drug response personalized medicine clinical trials biomarkers breast cancer genomics tamoxifen metabolism genetic polymorphisms pharmacogenetics treatment response oncology genetics drug efficacy metabolizing enzymes genetic markers
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 glioblastoma cancer expression molecular biology genetics prognosis therapy biomarker study analysis research clinical mechanism activation downregulation upregulation promoter microRNA RNA interference CRISPR genomic variant mutation association correlation disease model stem cells treatment immunotherapy nano technology diagnosis prevalence risk factor signaling pathway protein interaction cellular regulation angiogenesis inflamm TNFAIP3 glioblastoma tumor suppressor genetic factor cancer biology molecular mechanisms prognosis differential expression clinical relevance genetics research TNFAIP3 tumor suppressor function glioblastoma metastasis TNFAIP3 gene expression glioblastoma immune response TNFAIP3 protein levels glioblastoma prognosis TNFAIP3 mutation impact glioblastoma therapy resistance TNFAIP3 function TNFAIP3 role TNFAIP3 gene glioblastoma suppression glioblastoma tumor suppressor TNFAIP3 protein TNFAIP3 mechanism TNFAIP3 expression TNFAIP3 mutation TNFAIP3 pathway TNFAIP3 glioblastoma tumor suppressor molecular biology cancer immunology genetic factor prognosisMarkers TNFAIP3 function glioblastoma suppression relevant gene queries prognostic marker glioblastoma TNFAIP3 pathway analysis glioblastoma therapy target TNFAIP3 expression levels tumor suppressor genes in glioblastoma TNFAIP3 gene function tumor suppressor glioblastoma biomarker molecular biology cancer research genetics RNF5 interaction NFKB inhibition TNFAIP3 glioblastoma tumor suppressor genetic factor molecular biology cancer research oncology biomedical science protein function clinical application genetics RNA expression DNA methylation microenvironmentinteraction TNFAIP3 glioblastoma tumor suppressor inflammation genetic mutation cancer progression biomarker gene expression oncology neuro-oncology molecular biology TNFAIP3 function glioblastoma prognosis TNFAIP3 mutation TNFAIP3 expression glioblastoma treatment tumor suppressor genes glioblastoma immunotherapy TNFAIP3 regulation 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 risk factors epidemiology obesity genetics pregnancy outcomes birth weight breast cancer women likelihood epidemiology studies risk factors birthweight breastcancer epidemiology obesity genetics prenatalnutrition fetaldevelopment riskfactors birth weight and cancer risk breast cancer epidemiology maternal birth weight adult health outcomes prenatal factors cancer high birth weight implications birth weight breast cancer women likelihood adulthood birth weight cancer risk female health breast cancer epidemiology infant mortality adult diseases birth weight breast cancer risk maternal health fetal development cancer outcomes obesity genetics epidemiology birth weight breast cancer women risk factors epidemiology developmental origins health oncology mortality rates birthweight breastcancer infanthealth adultdiseases prenatalcare economics status nutrition genetics obstetrics gynecology birth weight breast cancer risk maternal health infant mortality oncology epidemiology genetic factors nutrition prenatal care long-term health
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. fine particulate matter air pollution anxiety mental health epidemiology risk factors public health environmental exposure respiratory health cardiovascular disease neurological impact air quality pollution levels health outcomes exposure fine particulate air pollution anxiety prevalence epidemiology health correlation studies research environmental risk factors mental health effects fine particulate matter air pollution anxiety prevalence health impact pollutants mental health particulate matter PM2.5 environmental exposure fine particulate matter health impact air pollution mental health connection particulate matter exposure anxiety environmental pollution effects on anxiety fine particles and psychological disorders pollution and mental health links PM2.5 and anxiety air quality and mental health particulate matter and stress indoor air pollution anxiety exposure fine particulate air pollution anxiety prevalence health effects association risk factors environmental mental illness studies research statistics correlation air pollution particulate matter anxiety mental health environmental factors risk assessment public health respiratory issues cardiovascular disease stress inflammation air pollution fine particulates anxiety mental health exposure epidemiology risk factors respiratory health cardiovascular disease inflammation exposure fine particulate matter air pollution anxiety prevalence health effects environmental factors mental health pollution exposure risk factors exposure fine particulate matter air pollution anxiety prevalence epidemiology health effects respiratory pollution psychological impact environmental factors public health risk assessment fine particulate matter air pollution anxiety mental health epidemiology risk factors public health environmental exposure health outcomes respiratory pollution
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. Commelina yellow mottle virus genome base pairs sequence structure genetics plant virology RNA length ComYMV genome length plant virus genetic sequence molecular biology virology RNA virus gene content Commelina yellow mottle virus genome base pairs sequence genetics plant virology Commelina yellow mottle virus genome structure Commelina yellow mottle virus replication Commelina yellow mottle virus symptoms Commelina yellow mottle virus host range Commelina yellow mottle virus transmission Commelina yellow mottle virus symptoms in plants Commelina yellow mottle virus genetic analysis Commelina yellow mottle virus comparison with other viruses Commelina yellow mottle virus sequence analysis Commelina yellow mottle virus vector identification Commelina yellow mottle virus ComYMV genome base pairs RNA plant virus virus genome analysis genetic sequence nucleotide composition molecular biology techniques plant virus study ComYMV characteristics Commelina yellow mottle ComYMV genome base pairs genetic material viral genome molecular biology ComYMV genome length viral genome base pairs plant virus molecular biology genetic material RNA virus plant pathology Commelina yellow mottle virus genome base pairs genetic structure RNA Commelina yellow mottle virus genome length ComYMV genetic sequence plant virus genome viral nucleic acid molecular biology virus genomic analysis biological virus characteristics
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 metabolism longevity diet genetic modification lipid levels Rapamycin fruit flies triacylglycerols longevity metabolism lifespan lipid diet genetics treatment intervention calorie restriction aging Rapamycin triacylglycerols fruit flies lifespan metabolism aging diet genetic treatment intervention biomarkers lipid regulation longevity pharmacology Rapamycin effects on lipid metabolism triacylglycerol reduction mechanisms Rapamycin dietary impact longevity and triacylglycerols Rapamycin gene expression analysis Rapamycin metabolic pathways fruit fly lipid profile changes Rapamycin intervention studies aging and triacylglycerol levels Rapamycin clinical trials overview Rapamycin triacylglycerols fruit flies lifespan metabolism aging diet genetic modification lipid levels Rapamycin metabolism Rapamycin diet Triacylglycerols reduction Fruit fly genetics Rapamycin lifespan Triacylglycerol biosynthesis Rapamycin treatment Fruit fly nutrition Metabolic effects Rapamycin Triacylglycerol regulation Rapamycin triacylglycerols fruit flies lipid metabolism longevity geroscience mTOR senescent cells Rapamycin metabolism triacylglycerols reduction fruit fly lifespan longevity genes calorie restriction effect metabolic pathways aging research diet intervention genetic modification lipid homeostasis rapamycin treatment Rapamycin triacylglycerols fruit flies longevity metabolism intervention dietary restriction aging gene expression lipid metabolism insulin signaling Rapamycin lifespan extension Rapamycin metabolic effects Triacylglycerol reduction mechanisms Fruit fly nutrition Calorie restriction mimetics
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 YAP transcription factor cytoplasmic localization LATS1 kinase LATS2 kinase Drosophila model signal transduction pathway cancer research molecular biology cell signaling NF2 gene Merlin protein YAP phosphorylation LATS1/2 kinases cytoplasmic sequestration Drosophila model signal transduction tumor suppressor cellular localization molecular mechanisms NF2 protein Merlin function YAP phosphorylation LATS1 activation LATS2 kinase Drosophila signaling cytoplasmic localization tumor suppressor cellular proliferation genetic regulation cell cycle control molecular biology neurofibromatosis type 2 signal transduction protein interaction gene expression cellular pathway biological process genetic mutation NF2 protein function Merlin signaling pathway YAP phosphorylation mechanism LATS1/2 activation cytoplasmic sequestration process Drosophila cellular response NF2-YAP-LATS1/2 interaction genetic regulation analysis cell cycle control tumor suppressor role molecular biology techniques biochemistry pathways NF2 Merlin phosphorylation YAP cytoplasmic sequestration LATS1/2 Drosophila kinase activity NF2 mutation YAP protein LATS1 kinase Drosophila model phosphorylation process cytoplasm localization molecular biology research techniques genetic regulation kinase activation NF2 Merlin YAP phosphorylation cytoplasmic sequestration LATS1 LATS2 Drosophila kinase signaling pathway molecular biology genetics protein interaction cell cycle regulation NF2 gene Merlin protein YAP phosphorylation LATS1/2 kinases cytoplasmic sequestration Drosophila model molecular signaling pathway tumor suppressor function cell proliferation regulation NF2 Merlin phosphorylation YAP cytoplasmic sequestration LATS1 LATS2 Drosophila kinase activation gene regulation signal transduction cellular localization molecular biology oncogenesis NF2 mutation Merlin protein YAP phosphorylation LATS1 activation LATS2 kinase Drosophila signaling cytoplasmic localization Hippo pathway tumor suppressor 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 function YAP phosphorylation cytoplasmic localization Drosophila signaling Hippo pathway tumor suppressor gene regulation cell proliferation fly model biological pathway molecular mechanism NF2 gene Merlin protein YAP phosphorylation cytoplasmic sequestration Drosophila model cell signaling tumor suppressor Hippo pathway RNA expression genetic mutation NF2 protein Merlin function YAP phosphorylation cytoplasmic localization Drosophila signaling tumor suppressor Yap1 protein Hippo pathway genetic regulation cell proliferation cancer biology NF2 protein function Merlin protein interaction YAP phosphorylation mechanism cytoplasmic sequestration process Drosophila signaling pathway YAP protein localization NF2 gene expression cellular proliferation regulation fly model biology NF2 Merlin YAP phosphorylation cytoplasmic sequestration Drosophila gene regulation signaling pathway tumor suppressor Hippo pathway NF2 gene function YAP protein regulation Drosophila model YAP phosphorylation mechanism cell signaling pathways MERLIN protein role biological pathways analysis NF2 protein Merlin protein YAP phosphorylation cytoplasmic sequestration Drosophila model signal transduction molecular biology tumor suppressor NF2 gene Merlin protein YAP phosphorylation cytoplasmic sequestration Drosophila model signaling pathway tumor suppression genetic regulation cell proliferation NF2 protein Merlin YAP phosphorylation cytoplasmic sequestration Drosophila signaling pathway tumor suppressor genetic mutation cell proliferation organ size regulation NF2 protein function Merlin role YAP regulation Drosophila signaling cytoplasmic localization phosphorylation mechanism tumor suppression gene interaction cell proliferation
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 volume reduction iodine-131 treatment thyroid nodules hyperthyroidism risk radioisotope therapy thyroid function tests long-term outcomes thyrotoxicosis prevention radioiodine therapy non-toxic multinodular goiter thyroid volume reduction thyroid hormone levels side effects long-term outcomes patient selection treatment efficacy follow-up care comparative studies radioiodine therapy non-toxic multinodular goiter thyroidectomy thyroid function radioactive iodine gland volume reduction iodine-131 thyrotoxicosis treatment outcomes hyperthyroidism management radioiodine therapy non-toxic goiter thyroid reduction iodine-131 treatment multinodular goitre management thyroidectomy alternative radioactive iodine therapy radiotherapy for goiter thyroid function assessment iodine therapy benefits radioiodine treatment non-toxic multinodular goitre thyroid volume efficacy side effects patient outcomes radioisotope therapy thyroidectomy comparison radioactive iodine radioactive isotopes gland size reduction nuclear medicine endocrinology clinical trial results follow-up assessments radioiodine therapy non-toxic goitre thyroid reduction nuclear medicine iodine-131 thyroid nodules radioactive iodine treatment hyperthyroidism prevention thyroidectomy alternative long-term efficacy radioiodine therapy non-toxic multinodular goiter thyroid size reduction iodine-131 treatment thyroid function analysis radioactive iodine therapy thyroid nodule management radiotherapy for thyroid Radioiodine therapy non-toxic multinodular goitre thyroid volume reduction iodine-131 treatment thyroid nodules radioactive iodine thyroidectomy alternative gland size decrease endocrine treatment thyroid function assessment radioiodine treatment non-toxic multinodular goitre thyroid volume reduction efficacy clinical outcomes thyroiditis hyperthyroidism management radioactive iodine ablation follow-up complications radioiodine therapy non-toxic goitre thyroid reduction iodine-131 treatment thyroidectomy alternative long-term efficacy side effects patient selection criteria follow-up management
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 activation IP3R-mediated Ca2+ mobilization calcium signaling nuclear factor of activated T-cells calcium release-activated channels intracellular calcium immune response signal transduction calcium ions gene expression calcium flux NFAT4 calcium signaling IP3R Ca2+ mobilization transcription factor signaling pathway cellular response gene expression immunology physiology NFAT4 signaling calcium influx IP3 receptors calcium oscillations Ca2+ entry calcium release channels intracellular calcium calcium signaling IP3 signaling NFAT transcription factors calcium binding proteins calcium sensors cytosolic calcium levels membrane calcium channels NFAT4 activation process NFAT4 signaling pathway IP3R function Ca2+ mobilization mechanism calcium signaling in cells NFAT4 regulation IP3R types Ca2+ release channels calcium ions role signaling molecules interaction cellular response to calcium NFAT4 activation IP3R Ca2+ mobilization signaling pathway calcium ions immune response transcription factors NFAT4 regulation calcium signaling IP3 receptor function calcium mobilization transcription factor activation signaling pathways calcium ions gene expression immune response cellular metabolism NFAT4 activation IP3R Ca2+ mobilization signaling pathway calcium ions regulation immune response transcription factors cellular biology NFAT4 IP3R Ca2+ mobilization signaling pathway regulation calcium ion cells transcription factor immune response NFAT4 activation IP3R-mediated Ca2+ mobilization calcium signaling NFAT transcription factors intracellular calcium immune response signaling pathways gene expression calcium release channels calcium ions cell signaling calcium signaling pathway calcium regulation calcium homeostasis calcium-dependent processes NFAT4 signaling calcium ions IP3 receptors cellular response transcription factor calcium mobilization immune regulation gene expression signaling pathway calcium signaling
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 nitric oxide superoxide enzymatic reactions signaling pathways oxidative stress biological processes molecular mechanisms NOX2 peroxynitrite nitrogen intermediates oxidative stress enzymatic reactions biological pathways nitric oxide superoxide reactive nitrogen species antioxidant defense cellular signaling NOX2 peroxynitrite nitrogen intermediates reactive nitrogen species nitric oxide superoxide enzymatic pathways non-enzymatic pathways oxidative stress signaling pathways redox regulation NOX2 alternative peroxynitrite generation nitrogen intermediates reactions enzymatic NOX2-independent peroxynitrite formation nitric oxide metabolism reactive nitrogen species production cellular redox regulation peroxynitrite biosynthesis alternatives biological nitrogen intermediates antioxidant defense mechanisms oxidative stress pathways NOX2 peroxynitrite nitrogen intermediates pathways reactive nitrogen species ROS RNS query expansion NOX2 peroxynitrite nitrogen intermediates redox reactions biological pathways reactive nitrogen species enzymatic mechanisms molecular biology biochemistry NOX2 peroxynitrite nitrogen intermediates enzymatic pathways reactive nitrogen species nitric oxide superoxide antioxidant defense biological oxidation redox reactions NOX2 peroxynitrite nitrogen intermediates oxidative stress enzymatic reactions nitric oxide reactive nitrogen species molecular mechanisms biological pathways NOX2 peroxynitrite nitrogen intermediates pathway expansion search optimization biochemical reactions NOX2 alternative mechanisms peroxynitrite generation nitrogen intermediates reaction oxidase independent pathways nitric oxide metabolism reactive nitrogen species production
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 insulin secretion incretin effects cell signaling pathways cAMP production pancreatic beta cells metabolic regulation drug targets diabetes treatment signaling cascades G protein-coupled receptors GLP-1R signaling intracellular pathways cellular responses metabolic effects insulin secretion incretin hormones diabetes treatment molecular mechanisms signal transduction pharmacology therapeutic targets GLP-1R agonists cellular signaling pathways incretin hormones pancreatic beta cells cAMP production downstream effectors diabetes treatment hormone action mechanisms pharmacological targets glucose-dependent insulin secretion signal transduction metabolic regulation GLP-1R function intracellular signaling pathways cellular response variation pleiotropy effects GPCR signaling hormone action mechanisms signal transduction metabolic regulation therapeutic targets biological signaling networks Pleiotropy GLP-1R intracellular effectors cellular signaling molecular biochemistry diabetes metabolism endocrinology GLP-1R signaling pathways intracellular effectors list pleiotropic effects database cellular signaling networks GLP-1 receptor agonists signaling pathway analysis intracellular signaling mechanisms glucose-dependent insulinotropic polypeptide receptors downstream effectors identification signal transduction pathways pharmacological targets exploration cellular response diversity GLP-1R therapeutic applications GLP-1R function intracellular signaling pathways cellular response variation pleiotropy effects GPCRs signaling mechanisms GLP-1R function intracellular signaling pathways cellular response variation pleiotropy GLP-1 receptor mechanisms hormonal signaling impact metabolic effects signal transduction physiological outcomes diabetes treatment insights Pleiotropic effects GLP-1R activation intracellular signaling pathways cellular response modulation hormone action mechanisms metabolic signaling beta cell function insulin secretion pharmacological targets therapeutic interventions GLP-1R activation intracellular signaling pathways cellular responses metabolic effects insulin secretion 肠上皮细胞 beta cell function G protein-coupled receptors signaling molecules pharmacological interventions
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 immunology molecular biology autoimmunity expression gene regulation immune tolerance AIRE autoimmunity immune tolerance skin cancers transcription factor dendritic cells thymus peripheral tolerance autoimmune diseases organ-specific tolerance AIRE autoimmune polyendocrine syndrome skin cancer tumor immunity endogenous peptide thymus autoimmunity immune tolerance gene expression dermatology oncology immunology AIRE expression cancer AIRE skin tumor types AIRE gene activation AIRE protein function AIRE autoimmune disease connection AIRE immunology role AIRE diagnostic marker AIRE therapeutic target AIRE tumors skin cancer gene autoimmunity expression immune tolerance organ-specific autoimmune diseases AIRE tumor expression AIRE skin cancer AIRE autoimmune diseases AIRE gene function AIRE protein localization AIRE immune tolerance AIRE mutation analysis AIRE immunohistochemistry AIRE molecular biology AIRE diagnostic markers AIRE autoimmune polyendocrine syndrome skin cancer tumor microenvironment autoimmunity transcription factor immune tolerance melanoma dermatology oncology AIRE tumors skin cancers immunology molecular markers autoimmunity immune tolerance AIRE autoimmunity skin tumors immune tolerance gene expression tumor microenvironment immunology endogenous peptide presentation autoimmune polyendocrine syndrome organ-specific autoimmune diseases AIRE tumor expression AIRE autoimmunity AIRE gene function AIRE immune tolerance AIRE protein localization AIRE skin diseases AIRE cancer research AIRE immunology AIRE pathology AIRE genetic variation
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 expression target genes repression biological function ovaries research microRNA role miR7a function ovaries target genes low expression repression biological role microRNA regulation genetic expression Ovary biology miRNA function miR7a miRNA ovaries gene repression target genes biological function microRNA expression ovarian biology RNA molecules molecular biology genetic regulation miR7a regulation miR7a target genes miR7a biological function miR7a ovarian expression miR7a downregulation effect miR7a genetic impact miR7a gene repression miR7a ovarian role miR7a functional significance miR7a ovarian influence miR7a microRNA ovaries target genes biological function expression level repression molecular biology mRNA regulation RNA interference miR7a function miRNA targeting ovarian gene regulation miR7a expression target gene repression miRNA biological role ovaries miRNA miR7a microRNA ovaries target genes biological function expression level molecular biology RNA interference miR7a function ovaries target genes expression effect repression biological function microRNA regulation miR7a miRNA ovarian function gene repression biological role microRNA expression target genes reproductive biology miR7a regulation miR7a target genes miR7a ovarian function miR7a expression levels miR7a biological role miR7a genetic analysis miR7a molecular mechanism miR7a ovarian development miR7a gene expression miR7a pathway involvement
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 response migration renal tissue repair differentiation angiogenesis Podocyte motility injury response migration renal disease biology cellular Podocyte migration injury response renal cell biology cellular motility glomerular filtration tubulointerstitial disease kidney injury model molecular mechanisms cytoskeletal dynamics signal transduction pathways Kidney injury cellular migration podocyte function glomerular damage renal disease biomarkers therapeutic intervention biological response Podocytes motility injury response migration glomerular filtration neuropodium cell specialization motility podocytes injury migration relevant phrases search performance Podocyte migration injury response motility markers microenvironment signaling glomerular damage cellular adhesion motility podocytes injury migration renal.cells biological.response cellmovement glomerular.disease Podocyte motility injuryresponse migration tissuerepair glomerulardisease cellbehavior renalpathology Kidney injury motility biochemistry cell migration glomerular disease specialized cells renal pathology
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 cancer biomarkers tumor markers survival rates genetic markers oncology research cancer biology cancer genetics clinical outcomes ALDH1 breast cancer prognosis ALDH1 expression level ALDH1 biomarker ALDH1 gene ALDH1 protein ALDH1 in breast cancer ALDH1 role ALDH1 prognosis ALDH1 markers ALDH1 research ALDH1A1 ALdehyde dehydrogenase breast cancer prognosis oncology markers survival rates tumor biomarkers genetic predisposition cancer therapy response molecular biology clinical trials epidemiology cancer research diagnostic tools genomic analysis ALDH1 activity breast cancer prognosis metabolism markers cancer survival outcome prediction genetic markers expression levels tumor markers prognostic factors ALDH1 breast cancer prognosis biomarker survival oncology research gene expression therapeutic target ALDH1 activity ALDH1 gene breast cancer prognosis cancer cell metabolism oxidative stress resistance survival rate tumor aggressiveness biomarker relevance ALDH1A1 ALDH1L1 breast cancer prognosis oncology markers tumor biology survival rates genetic markers cancer research molecular biology biomarkers ALDH1 breast cancer prognosis ALDH1 positive breast cancer cells ALDH1 biomarker breast cancer ALDH1 gene expression breast cancer ALDH1 protein expression breast cancer ALDH1 and breast cancer survival ALDH1 levels in breast cancer ALDH1 role in breast cancer ALDH1 breast cancer risk ALDH1 breast cancer subtype ALDH1A1 breast cancer prognosis metabolic markers tumor heterogeneity survival rates genetic markers oncology research biomarkers chemotherapy response epithelial cells ALDH1A1 breast cancer prognosis oncogenes tumor suppressors survival rates genetic markers therapeutic targets
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 microRNA function spermatogenesis genetic regulation reproductive health molecular biology RNA expression miR7a testis function biological expression regulation microRNA role research study genetic miR7a expression testis biology miRNA function reproductive health microRNA testis biological role miR7a miR7a function testis miR7a expression impact miR7a role testicular biology miR7a downregulation effect miR7a biological significance testes miR7a function testis expression biological microRNA male reproductive health genetic regulation miR7a function testis biology expression levels microRNA role testis health miR7a expression testis biology microRNA function male reproductive health gene regulation sperm development RNA expression profiling miR7a testis biological function low expression microRNA sperm production gene regulation fertility 睾丸 微小RNA 低表达 生物学功能 miR7a testis low expression biological function microRNA sperm development gene regulation reproductive biology RNA expression miR7a function testis biology low miRNA expression microRNA role testicular health MiR7a regulation
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 biology NR5A2 role NR5A2 gene endometrial development endometrium function uterine biology female reproductive health genetic role in menstruation NR5A2 function endometrial development genes involved female reproductive health endometrium biology NR5A2 function endometrial tissue development genetic role NR5A2 expression female reproductive health NR5A2 gene endometrial development uterine tissues regulation mechanisms female reproduction gene function biomarkeridentification molecular biology reproductive health NR5A2 function NR5A2 gene expression NR5A2 role endometrial development endometrial health NR5A2 protein molecular biology reproductive system hormone regulation gene regulation developmental biology NR5A2 gene endometrial development uterine tissue functional role gene expression reproductive biology NR5A2 function endometrial development gene role female reproductive health endometrium physiology NR5A2 function endometrial tissue development genetic factors endometrium physiology NR5A2 expression RNA analysis cellular biology endometrial health biomarker research NR5A2 function NR5A2 gene expression endometrial development endometrial health NR5A2 protein molecular biology reproductive health hormone regulation endometrial cancer gene therapy transcription factors
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 oncogenes tumor markers survival rate cancer progression genetic markers cancer subtypes ALDH1 breast cancer prognosis ALDH1 expression breast cancer ALDH1 positive breast cancer ALDH1 biomarker breast cancer ALDH1 prognostic factor ALDH1 gene breast cancer ALDH1 protein breast cancer ALDH1 level breast cancer ALDH1A1 ALDH1 expression level breast cancer prognosis oncology markers cancer progression survival rate gene expression tumor markers ALDH1 activity breast cancer outcomes prognostic markers cancer prognosis disease progression ALDH1 overexpression breast cancer subtypes biomarkers in breast cancer clinical implications of ALDH1 ALDH1A1 breast cancer prognosis oncogenes tumor markers survival rate genetic markers cancer progression biomarkers ALDH1 breast cancer prognosis ALDH1 gene expression ALDH1 positive breast cancer ALDH1 biomarker breast cancer ALDH1 protein expression ALDH1 and breast cancer outcome ALDH1A1 breast cancer prognosis cancer progression oncology research biomarker survival analysis genetic marker ALDH1 breast cancer prognosis ALDH1 expression levels ALDH1 positive breast cancer ALDH1 role in breast cancer ALDH1 biomarker breast cancer ALDH1 gene expression breast cancer ALDH1 prognosis prediction ALDH1 cancer progression ALDH1 and breast cancer survival ALDH1 biomarker significance ALDH1A1 breast cancer prognosis tumor markers survival analysis oncology genetic markers cancer biology biomarkers clinical outcomes ALDH1A1 breast cancer prognosis cancer biomarkers oncology research genetic markers survival rates tumor markers molecular biology cancer therapy response cancer subtypes
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. nucleosomes methylation species evolution epigenetics histones gene expression chromatin genomic regions biological function nucleosome occupancy methylation levels species comparison epigenetics chromatin structure genetic variation DNA methylation nucleosome dynamics genomic regions biological species genome-wide analysis nucleosome dynamics methylation patterns evolutionary conservation chromatin structure genomic regions species comparison genetic regulation epigenetics研究 表观遗传学 基因调控 nucleosome dynamics methylation patterns evolutionary conservation chromatin structure genomic regions Epigenetics species comparison transcriptional activity histone modifications nucleosome occupancy methylation species epigenetics chromatin genome DNA histone correlation evolutionary biology nucleosome occupancy methylation levels species comparison genetic correlation chromatin structure biological significance evo-devo genomic regions histone modification genetic variation transcription factor binding nucleosomes methylation species evolution epigenetics chromatin genomic regions DNA modification transcription regulation histones low nucleosome occupancy low methylation levels species comparison epigenetics nucleosome positioning methylation patterns genomic regions species evolution chromatin structure eukaryotic cells human genetics mouse genetics DNA methylation nucleosome dynamics nucleosome density methylation patterns evolutionary conservation chromatin structure genomic regions histone modification DNA methylation species comparison low nucleosome occupancy methylation levels species epigenetics chromatin regulation genetics biology DNA histone variation correlation genomic analysis molecular epigenomic
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 specific cell targeting molecular recognition drug delivery biomedical applications Nanoengineering Nanoparticles aptamers lipid nanoparticles specific cell targeting molecular recognition bioconjugates theranostics DNA aptamers RNA aptamers Nanoparticles aptamers lipid nanoparticles specific cell targeting molecular recognition drug delivery biocompatibility tumor targeting nanomedicine targeted drug delivery aptamer-lipid nanoparticles cellular targeting nanotechnology in medicine biomolecular recognition gene therapy nanoparticles cancer treatment nanoparticles personalized medicine nanoparticles RNA aptamers peptide aptamers Nanoparticles aptamers lipid nanoparticles targeted delivery cell types molecular recognition specificity bioconjugates drug delivery theranostics nanoparticles aptamers lipid nanoparticles targeted therapy cell targeting biomedical applications nanomedicine molecular recognition drug delivery systems Nanoparticles aptamers lipid nanoparticles cell targeting molecular recognition specificity bioconjugates drug delivery systems mRNA therapeutics Nanoparticles aptamers lipid nanoparticles targeted delivery specific cell types molecular recognition bioconjugates biomedical applications nanomedicine cancer therapy drug delivery systems Nanoparticles aptamers lipid nanoparticles specific cell targeting molecular recognition drug delivery biomedical applications Nanoparticle targeting aptamer-lipid nanoparticles cellular delivery biomolecular recognition cancer therapy gene delivery drug encapsulation biosensors immunotherapy nanotechnology applications
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 inflammation response lung diseases chronic inflammation fibrotic diseases kinase inhibitors gene expression inflammatory markers AMPK activation inflammation fibrosis lungs mechanism signaling therapy treatment gene expression metabolites oxidative stress cytokines adipose tissue metabolism diabetes obesity cardiopulmonary disease pharmacology biomarkers AMPK activation inflammation fibrosis lungs cellular metabolism energy sensing mTOR p53 autophagy oxidative stress cytokines epithelial-mesenchymal transition chronic lung diseases obesity diabetes smoking genetic factors pharmacological intervention signaling pathways AMPK activation effects lung fibrosis mechanisms inflammation and fibrosis AMPK role in fibrosis lung inflammation pathways fibrotic processes in lungs AMPK and inflammation molecular targets for fibrosis anti-fibrotic therapies AMPK signaling in fibrosis AMPK activation inflammation fibrosis lungs metabolism signaling pharmacology genetics regulation pathways mechanisms therapeutic targets AMPK activation inflammation fibrosis lungs relevant expansion phrases query refinement keyword expansion medical research molecular biology cellular response AMPK activation inflammation fibrosis lungs molecular mechanism metabolic stress cellular signaling inflammatory response tissue remodeling oxidative stress inflammatory mediators gene expression therapeutic targets AMPK inflammation fibrosis lungs activation molecular targets therapeutic intervention metabolic stress oxidative stress signaling pathways AMPK activation inflammation fibrosis lungs molecular mechanisms signaling pathways therapeutic targets metabolic stress oxidative stress gene expression inflammatory cytokines AMPK activation lung fibrosis inflammation protein kinase therapeutic targets metabolic stress oxidative stress cellular signaling gene expression inflammatory cytokines
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 degeneration genetics molecular biology neurodegeneration neuron function stem cells protein production APOE4 iPSC-derived neurons AlphaBeta protein tau phosphorylation GABA neurons neuron degeneration genetic factors stem cells disease modeling neurodegeneration mechanisms APOE4 iPSC neurons AlphaBeta tau phosphorylation GABA degeneration molecular biochemistry genetics neurodegeneration pathology research model cognition alzheimer disease neural differentiation stem cells transdifferentiation expression protein markers signaling promoter transcription regulation neurobiology biomarker therapy vulnerable cells neurotransmitter synapse mechanism study experiment validation clinical validation screening screening techniques methods APOE4 gene expression iPSC technology nervous system degeneration neuron function impairment GABA neurotransmission tau protein modification stem cell research neurodegenerative diseases biomarker discovery genetic predisposition analysis APOE4 iPSC differentiation neurons AlphaBeta tau phosphorylation GABA neuron degeneration microglia inflammation neurodegeneration amyloid APOE4 gene expression iPSC technology neuronal cells AlphaBeta protein tau protein GABAergic neurons neuron degeneration molecular biology genetic factors stem cell research neurodegeneration markers neuroscience studies APOE4 iPSC neurons AlphaBeta tau phosphorylation GABA neurons neuron degeneration genetic factor molecular biology neurodegeneration research stem cell technology biomedical science APOE4 iPSC-derived neurons AlphaBeta production tau phosphorylation GABA neuron degeneration neurodegeneration parkinson's disease alzheimer's disease stem cell research genetic factors molecular biology neuroscience bioinformatics neuronal function protein aggregation APOE4 iPSC-derived neurons AlphaBeta protein tau phosphorylation GABA neurons neuron degeneration molecular biology genetics neurodegeneration neural stem cells biomarkers disease modeling Alzheimer's disease neurotransmitters neuroscience research cellular biology stem cell technology APOE4 iPSC nurons AlphaBeta tau phosphorylation GABA differentiation neurodegeneration microscopy genetics neuroscience stem cells neuroinflammation proteinopathy
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 nurons AlphaBeta tau phosphorylation GABA neuron degeneration genetics molecular biochemistry neuroscience stemcells neurodegeneration Alzheimer symptoms mechanism research biologicalmarkers clinicalapplication APOE4 iPSC-derived neurons AlphaBeta protein tau phosphorylation GABA neuron degeneration microRNA regulation genetic modification neurodegenerative disease stem cell research neural differentiation protein aggregation APOE4 iPSC neurons AlphaBeta tau phosphorylation GABA degeneration molecular biochemistry genetics neurodegeneration stemcells DNA RNA proteinexpression neuroscience research clinical therapy virology bioinformatics neurotransmitters neuralcircuitry ageing cognitiveimpairment Alzheimer's synaptic function preservation neuronhealth biomarkers microglia astrocytes neuroinflammation mitochondria network differentiation pluripot APOE4 iPSC-derived neurons AlphaBeta production tau phosphorylation GABA neuron degeneration molecular mechanisms neurodegeneration parkinson's disease alzheimer's disease stem cell research genetic factors neuronal function APOE4 iPSC-derived neurons AlphaBeta protein tau phosphorylation GABA neurons neuron degeneration genetic markers molecular biology cognitive decline neurodegeneration APOE4 iPSC-derived neurons AlphaBeta production tau phosphorylation GABA neuron degeneration relevant expansion phrases neural stem cells molecular biology genetic factors neurodegenerative diseases stem cell research DNA analysis microarray analysis neuronal function genetic testing neuroscience biotechnology potential therapies clinical applications APOE4 iPSC neurons AlphaBeta tau phosphorylation GABA neuron degeneration genetic modification molecular biology neurodegeneration research stem cell technology APOE4 iPSC-derived neurons AlphaBeta protein tau phosphorylation GABA neurons neuron degeneration beneficial keywords search efficacy neural differentiation stem cells DNA methylation proteomics transcriptomics neurodegeneration Alzheimer's disease APOE4 iPSC nervous system differentiation GABA tau neurons AlphaBeta phosphorylation neuron degeneration stem cells microscopy genetics biochemistry neurodegeneration parkinsons cognitive decline amyloid-beta APOE4 iPSC-derived neurons AlphaBeta protein tau phosphorylation GABA neurons neuron degeneration genetic factors molecular mechanisms disease modeling stem cell research
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 microbial defense bacterial communication virulence factors toxic T6SS E. coli bacteria antibacterial effectors inner tube structure protein delivery bacterial defense mechanisms tip inner tube toxic type VI secretion system T6SS antibacterial effector proteins Escherichia coli E. coli bacterial toxins molecular biology microbial defense bacterial secretion protein structure bacterial communication virulence factors inner tube T6SS antibacterial effectors E. coli toxic effector proteins T6SS E. coli T6SS mechanism T6SS structure function T6SS effector delivery bacterial type VI secretion E. coli bacterial defense T6SS toxicity mechanisms bacterial secretion systems E. coli protein secretion tip inner tube T6SS antibacterial effector toxic proteins Escherichia coli E. coli T6SS antibacterial effector Escherichia coli toxic protein inner tube tip secretion system toxic type VI secretion system T6SS Escherichia coli E. coli antibacterial effectors inner tube protein structures bacterial defense mechanisms secretion system components effector proteins microbial toxins toxic type VI secretion system antibacterial effector Escherichia coli E. coli inner tube effector proteins bacterial defense protein delivery gram-negative bacteria bacterial pathogenesis molecular biology microbiology infection mechanism tip inner tube toxic type VI secretion system T6SS antibacterial effector proteins Escherichia coli E. coli molecular biology bacterial defense protein structure pathogenesis microbial physiology toxic type VI secretion system antibacterial effectors Escherichia coli E. coli T6SS effector proteins bacterial defense protein delivery microbial warfare bacterial toxins molecular biology Gram-negative bacteria bacterial communication
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 accumulation abnormal wound response microinvasive advanced Oral Potentially Malignant Lesions OPMLs carcinogenesis dysplasia epithelial tumor progression biomarker prognosis treatment prevention oncology pathology p16INK4A microinvasion abnormal wound response advanced OPMLs oral cancer precursors DNA damage cell cycle regulation tumor suppressor genes cancer progression biomarkers clinical diagnosis treatment options molecular biology genetic mutations p16INK4A accumulation abnormal wound response microinvasive advanced Oral Potentially Malignant Lesions OPMLs oral cancer precancerous tissue repair cellular dysregulation inflammation oncogenes tumor suppressor epithelial cells mucosa biopsies histopathology genetic mutations dysplasia carcinogenesis prognosis treatment risk factors molecular biology pathology epidemiology p16INK4A expression wound healing impairment microinvasion OPML progression dysregulation pathways oral precancerous lesions cellular senescence oncogenic transformation tissue repair mechanisms genetic alterations p16INK4A wound response microinvasion advanced OPMLs oral cancer precancerous lesions dysplasia epithelial changes cellular alterations p16INK4A accumulation symptoms p16INK4A and wound healing microinvasive cancer detection oral potentially malignant disorders OPML progression wound response abnormalities p16INK4A role in malignancy early OPML diagnosis wound healing impairment p16INK4A expression in OPML p16INK4A wound healing microinvasion Oral Potentially Malignant Lesions OPML cancer progression cellular response dysregulation epithelial cells oncology biomarker tumor suppressor genetic alteration clinical diagnosis pathogenesis p16INK4A microinvasive advanced OPMLs wound response malignant lesions cancerous progression dysplasia oral mucosa biomarker prognosis treatment outcome precancerous lesions molecular marker cellular dysregulation tumor suppressor gene DNA methylation Rb pathway virus infection genetic mutation survival rate angiogenesis metastasis risk fibroblast activity stroma remodeling chronic inflammation p16INK4A wound healing microinvasion OPML oral cancer dysplasia epithelial dysregulation tumor progression cellular senescence oncogenesis genetic alterations biomarkers clinical outcomes p16INK4A wound healing microinvasion oral cancer OPML dysplasia epithelial dysregulation tumor suppressor biomarker cellular senescence chronic inflammation
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. sliding mechanism kinesin-8 kip3 bipolar spindle assembly process microtubule interaction cell division polar microtubules sliding mechanism kinesin-8 function bipolar spindle formation Kip3 role microtubule interaction protein dynamics cell division cytokinesis motor proteins sliding mechanism kinesin proteins bipolar spindles spindle assembly Kip3 function microtubule dynamics kinesin-8 roles cell division process protein function analysis kinesin-8 function bipolar spindle formation Kip3 role sliding mechanism microtubule dynamics chromatin organization cell division process molecular motor protein spindle assembly checkpoint mitosis regulation sliding activity kinesin-8 protein Kip3 bipolar spindle assembly microtubule dynamics cell division mitosis taxonomical specificity motility mechanisms kinesin-8 function bipolar spindle formation Kip3 role protein sliding activity spindle assembly regulation sliding mechanism kinesin-8 Kip3 spindle assembly bipolar spindle formation microtubule dynamics cell division motor protein function sliding activity kinesin-8 protein Kip3 bipolar spindle assembly protein function microtubule dynamics cell division kinesin family spindle assembly regulation sliding activity kinesin-8 protein Kip3 bipolar spindle assembly protein dynamics microtubule interaction cell division kinesin motors mitosis suggestive search terms biological processes spindle formation kinesin-8 function bipolar spindle formation cell division process Kip3 role mitotic spindle assembly
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 potentials ERG b-wave ON-bipolar cells retinal function visual signaling neurobiology electrophysiology retina response photoreceptor interaction neural signaling single flash-evoked ERG b-wave ON-bipolar cells retinal function electrophysiology visual pathway neurobiology ophthalmology retina cells visual evoked potential flash-evoked ERG b-wave ON-bipolar cells retinal function visual pathway neurobiology electrophysiology retina cells photoreceptor response neural signaling visual evoked potential retinal function test ON-bipolar cell activity electroretinography single flash ERG b-wave generation retinal ganglion cells photoreceptor signaling flash-evoked ERG b-wave ON-bipolar cells retinal function neural response VIP neurons GABA signaling flash-evoked ERG ON-bipolar cells visual pathway retinal function electrophysiology neurology ocular health vision science sensory processing neurological disorders flash-evoked ERG b-wave ON-bipolar cells optic nerve functional vision test retina single cell response Omphalotin single flash-evoked ERG b-wave ON-bipolar cells retinal function visual pathway neurobiology electrophysiology retina physiology flash-evoked ERG b-wave ON-bipolar cells optimize search meaningful expansion terms enhance query vision science electroretinography bipolar cells neurophysiology retinal-function electrophysiology visual-pathway photoreceptor-interactions neurophysiology ocular-imaging retina-cell-types
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 myelogenous leukemia cancer biomarker oncology genetic mutation protein expression leukemia therapy cell signaling Tetraspanin-3 acute myelogenous leukemia cancer protein function gene expression oncology leukemia types biomarker therapeutic target Tetraspanin acute myeloid leukemia oncogene biomarker cancer protein expression stem cells bone marrow chemotherapy resistance signaling pathway immune evasion Tetraspanin-3 role Tetraspanin-3 function Tetraspanin-3 acute myelogenous leukemia Tetraspanin-3 oncogenicity Tetraspanin-3 mechanisms Tetraspanin-3 genetic factors Tetraspanin-3 treatment Tetraspanin-3 biomarker Tetraspanin-3 clinical significance Tetraspanin-3 pathway involvement Tetraspanin-3 acute myelogenous leukemia cancer biomarker signaling proteins leukemia progression oncology research gene expression molecular biology therapeutic target Tetraspanin-3 leukemia acute myelogenous leukemia causes Tetraspanin-3 function Tetraspanin-3 gene leukemia risk factors Tetraspanin-3 acute myelogenous leukemia cancer progression cellular signaling protein function leukemia subtypes gene expression oncogenesis biomarker immune response Tetraspanin-3 acute myelogenous leukemia cancer development molecular biology genetic markers oncology hematopoiesis cell signaling protein function biomarkers leukemia subtypes Tetraspanin-3 acute myelogenous leukemia cancer biology genetic factors leukemogenesis oncology molecular markers Tetraspanin-3 cancer leukemia treatment myelogenous leukemia progression oncogenic role Tetraspanin-3 tumor suppressor genes interaction leukemia diagnosis markers
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 involvement amyloidosis late gadolinium enhancement MRI transmurality severity cardiovascular imaging diagnosis myocardium echocardiography prognosis amyloidosis MRI cardiac amyloidosis late gadolinium enhancement myocardial involvement transmural extent cardiac magnetic resonance cardiac amyloidosis severity MRI techniques cardiac MRI analysis transmural myocardium cardiac involvement assessment amyloidosis cardiac MRI transmural myocardial fibrosis late gadolinium enhancement severity cardiac amyloidosis staging myocardial involvement grading cardiac MRI techniques amyloidosis types cardiac amyloidosis diagnosis MRI cardiac imaging cardiac involvement quantification cardiac amyloidosis MRI assessment late gadolinium enhancement myocardial involvement cardiac function transthoracic echocardiography cardiac MRI arrhythmias heart failure cardiac amyloidosis types cardiovascular symptoms cardiac involvement amyloidosis late gadolinium enhancement MRI transmurality severity cardiac amyloidosis MRI late gadolinium enhancement transmural involvement cardiac involvement severity amyloidosis diagnosis imaging techniques cardiac MRI analysis cardiac amyloidosis MRI late gadolinium enhancement transmural involvement myocardial impairment cardiac function imaging modalities arrhythmia risk clinical outcomes diagnostic accuracy cardiac amyloidosis transmural involvement MRI late gadolinium enhancement cardiac MRI severity assessment myocardial impairment amyloidosis cardiac MRI transmural involvement late gadolinium enhancement cardiac amyloidosis severity cardiac MRI analysis cardiac involvement quantification amyloidosis imaging markers cardiac amyloidosis transmurality MRI late gadolinium enhancement cardiac involvement severity assessment myocardial amyloidosis imaging techniques cardiovascular 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 female prisoners self harm prison suicide rates inmate mental health prison safety measures male prisoners self harm incarceration female prisoners suicide risk prison conditions mental health statistics incarceration rates male prisoners self-harm female prisoners risk frequency incidence mental health prison conditions statistics male prisoners self harm female prisoners self harm prison suicide rates inmate mental health incarceration risks prison safety measures psychological disorders in prisoners prison population demographics self harm statistics prisons inmate behavior analysis male prisoners self harm female prisoners incarceration risks suicide attempts prison population mental health incarceration conditions male prisoners self harm female prisoners self harm prison suicide rates inmate mental health prison safety measures solitary confinement effects incarceration risks male prisoners self-harm female prisoners self-harm prison suicide rates inmate mental health incarceration risks prison population statistics self-harm in prisons gender differences in prison prisoner mental health issues male prisoners self-harm female prisoners risk factors incarceration mental health statistics prison conditions male prisoners self-harm female prisoners risk frequency incarceration mortality behavioral health prison conditions gender differences male prisoners self-harm female prisoners risk_factors incarceration suicide_attempts population_differences mental_health prison_environment
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 surgical procedures wellness psychological benefits bariatric surgery mental health weight loss psychological outcomes benefits risk factors diabetes depression obesity therapy support complications effects bariatric surgery mental health weight loss depression anxiety psychological benefits support therapy obesity diabetes cardiovascular wellness mental health improvement bariatric surgery benefits psychological effects weight loss surgery mood obesity treatment mental surgical options for depression bariatric procedures mental health bariatric surgery mental health evidence research benefits obesity psychological outcomes quality lifestyle bariatric surgery mental health improvement psychological benefits bariatric surgery mental health outcomes after bariatric surgery bariatric surgery depression relief bariatric surgery anxiety reduction mental well-being post bariatric surgery psychological effects of bariatric surgery bariatric surgery mental health obesity depression anxiety weight_loss surgical_interventions psychological_benefits bariatric surgery mental health benefits obesity improvement wellness bariatric surgery mental health weight loss depression benefits psychological wellness surgical treatment mental health benefits surgical procedures obesity treatment psychological effects bariatric surgery outcomes weight loss and mental health surgical intervention and psychology
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 cytokines Tregs inflammation immunotherapy immune regulation T cell function cytokine production adaptive immunity chronic inflammation interleukin-2 regulation regulatory T cells function autoimmune diseases prevention type 1 diabetes mechanisms immune system response inflammation reduction cytokine signaling T cell activation immune tolerance chronic inflammation interleukin-2 receptors regulatory T cell function autoimmunity immune tolerance cytokines Treg cells immunosuppression type 1 diabetes mechanisms inflammation immune system regulation regulatory T cells function interleukin-2 mechanism autoimmune disease prevention type 1 diabetes risk factors immune system modulation T cell activation cytokine therapy immunotherapy approaches interleukin-2 regulatory T cells autoimmune diseases Type 1 Diabetes immune response cytokines Tregs immunosuppression inflammation regulatory T cells interleukin-2 responsiveness autoimmune diseases Type 1 Diabetes immune response T cell function inflammation immunotherapy cytokines Treg cells immune regulation chronic inflammation autoimmunity mechanisms regulatory T cells interleukin-2 responsiveness autoimmune diseases Type 1 Diabetes immunotherapy inflammation immune response cytokines T cell function adaptive immunity chronic inflammation regulatory T cells interleukin-2 responsiveness autoimmune diseases Type 1 Diabetes immunology cytokines immune tolerance Treg function inflammation immune response interleukin-2 regulatory T cells autoimmune diseases Type 1 Diabetes immune response cytokine therapy immunology Treg function inflammation immune regulation immune tolerance clinical trials biomarkers immune checkpoint inhibitors interleukin-2 receptors regulatory T cell function autoimmune disease mechanisms immune response modulation type 1 diabetes risk factors
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. polymer nutrition dietary fiber cardiovascular disease prevention meal replacement nutrient composition health benefits chronic disease management diet therapy nutritional supplements polymeal nutrition cardiovascular mortality diet health heart diabetes obesity atherosclerosis polymeal nutrition cardiovascular mortality healthy diet food heart health science research benefits risks study population analysis effects prevention statistics comparison evaluation impact factors variables polymeal benefits polymeal diet polymeal health polymeal components polymeal science polymeal study polymeal impact polymeal nutrition facts polymeal heart health polymeal lifestyle Polymeal nutrition cardiovascular mortality dietary patterns polyphenols fiber antioxidants inflammation metabolic syndrome heart disease diet diversity meal frequency Polymeal benefits polyprotein diet effects nutrition and heart health meal composition impact cardiovascular disease prevention balanced meals importance dietary patterns analysis polyphenol rich foods nutritional factors cardiovascular health PolyMeal nutrition cardiovascular mortality diet health heart disease food combinations meal composition cardioprotective factors Polymeal nutrition cardiovascular mortality dietary patterns health benefits meal combinations polyphenols antioxidants cardiovascular diseases diet quality nutritional science Polymeal nutrition cardiovascular mortality dietary patterns polyphenols antioxidants chronic diseases heart disease dietary fiber Mediterranean diet inflammatory markers Polymer nutrition cardiovascular health mortality reduction balanced diet nutritional supplements heart disease prevention dietary fiber antioxidant rich foods inflammation reduction metabolic syndrome management
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 xCT intracellular cysteine regulation signaling pathway metabolism mTORC2 cysteine xCT regulation inhibition cellular metabolism protein synthesis signal transduction biological pathways molecular mechanisms physiological functions mTORC2 function cysteine metabolism xCT protein cellular signaling protein synthesis inhibitors regulatory pathways biological pathways cell biology metabolism regulation mTORC2 function intracellular metabolism cysteine regulation xCT protein signaling pathways cellular signaling amino acid transport oxidative stress metabolic disorders cancer biology therapeutic targets mTORC2 cysteine xCT regulation cellular metabolism protein synthesis signaling pathway gene expression mTORC2 function cysteine metabolism xCT protein cell signaling protein synthesis regulatory mechanisms cancer biology biological pathways mTORC2 function intracellular cysteine xCT regulation inhibition proteins metabolism signaling molecular biology cellular processes mTORC2 function xCT protein cysteine metabolism cellular signaling protein regulation intracellular trafficking mTORC2 xCT intracellular cysteine regulation proteins metabolism signaling/pathway mTORC2 function intracellular metabolism cysteine transport xCT protein cellular signaling amino acid homeostasis redox regulation cancer metabolism therapeutic targets
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 benefits non-teaching hospital outcomes patient care quality medical education impact hospital training programs care effectiveness comparison teaching hospitals vs non-teaching patient outcomes hospital education medical training impact healthcare quality comparison teaching hospital vs non-teaching hospital patient outcomes medical education impact hospital resources specialized care availability resident physician influence clinical trial participation community hospital advantages healthcare quality metrics teaching hospital vs non-teaching hospital outcomes teaching hospital care quality comparison non-teaching hospital advantages patient care standards teaching vs non-teaching hospitals hospital education impact on patient care teaching hospital effectiveness evaluation non-teaching hospital patient satisfaction comparative analysis teaching vs non-teaching hospitals teaching hospital resource allocation non-teaching hospital medical training impact teaching hospitals care quality non-teaching hospitals medical education evidence-based medicine patient outcomes clinical training healthcare settings clinical skills academic institutions teaching hospital effectiveness non-teaching hospital comparison patient outcomes teaching vs non-teaching hospital type impact medical education influence on care teaching hospital vs non-teaching care quality teaching hospitals care quality non-teaching hospitals patient outcomes medical education evidence-based research hospital resources clinical skills student impact teaching hospitals vs non-teaching patient outcomes teaching hospitals non-teaching hospital care quality comparative hospital care efficiency teaching hospital benefits debate non-teaching hospital advantages hospital education impact on care teaching hospital effectiveness comparative healthcare quality analysis non-teaching hospital patient care teaching hospitals vs non-teaching hospitals care quality medical educationimpact patient outcomes hospital types clinical training best practices evidence-based medicine patient care quality teaching hospital effectiveness medical training impact hospital care standards healthcare outcomes comparison
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. recurrent mutations CTCF anchor sites oncogenes genomic instability transcription factor binding cancer genetics epigenetics chromatin regulation gene expression DNA repair recurrent mutations CTCF anchor sites oncogenes genomic regions DNA binding proteins transcriptional regulation cancer genetics epigenetics chromatin structure gene expression recurrent mutations CTCF anchor sites oncogenes genetic variation epigenetic regulation cancer genetics transcription factors chromatin structure genomic instability recurrent mutations CTCF anchor sites oncogenes genomic instability cancer genetics epigenetic regulation chromatin structure gene expression tumor suppressors DNA methylation transcription factors recurrent mutations CTCF anchor sites oncogenes genomic instability transcription factor binding cancer genetics epigenetics gene regulation mutation hotspots chromatin structure recurrent mutations CTCF anchor sites oncogenes genetic variations molecular biology cancer genetics genomic instability transcription factors Epigenetics somatic mutations recurrent mutations CTCF anchor sites oncogenes genomic regions chromatin structure gene regulation cancer genetics epigenetics DNA binding proteins transcriptional control genetic variations cancer biology recurrent mutations CTCF anchor sites oncogenes genomic instability cancer genetics molecular biology tumor suppressor genes genome regulation RNA binding proteins recurrent mutations CTCF anchor sites oncogenes genomic instability transcription factor binding cancer genetics epigenetic regulation chromatin structure gene expression regulation recurringmutations ctcfanchor sites oncogenes genomicinstability cancerbiology moleculargenetics mutationrates tumorgenesis
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 pregnancy premenopausal risk_factors breast_cancer parous_women placental_weight pregnancies premenopausal risk_factors epidemiology breast_cancer parous_women placental_weight pregnancies premenopausal risk_factors epidemiology oncology reproductive_health maternal_health pregnancy_outcomes hormonal_factors genetic_predisposition obesity lifestyle_factors breast cancer risk factors parous women health placental weight pregnancy premenopausal breast cancer risk pregnancy outcomes and cancer maternal health and cancer fetal programming cancer risk breast cancer prevention research breast_cancer parous_women placental_weight pregnancies premenopausal_breast_cancer risk_factors breast cancer parous women placental weight pregnancies premenopausal risk factors breast_cancer parous_women placental_weight pregnancies premenopausal risk_factors obstetric_history breast cancer parous women placental weight pregnancies premenopausal breast cancer risk factors oncology epidemiology breast cancer parous women placental weight pregnancy premenopausal breast cancer risk factors epidemiology Obstetrics gynecology oncology breast_cancer_risk parous_women placental_weight pregnancy_outcomes premenopausal_cancer reproductive_history oncology_research maternal_health cancer_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-prone mice bacteria infection autoantibodies curliproducing bacteria immunity response immune dysregulation Lupus-prone mice bacteria curliproducing autoantibody titers controls research immunology microbial infection Autoimmune disorders Lupus-prone mice curliproducing bacteria autoantibody titers immune response genetic models infectious agents autoimmune disorders microbial diversity inflammation immunology research mouse models pathogenesis antibody production Lupus-prone mice research curliproducing bacteria effects autoantibody titer increase immune response in lupus models microbiome and lupus lupus mouse models bacterial strains causing autoimmunity inflammation in lupus-prone mice Lupus lupus-prone mice autoantibodies curliproducing bacteria control group immune response autoimmune disease mouse model antibody titers Lupus prone mice curliproducing bacteria autoantibody titers immune response inflammatory markers genetic predisposition microbiome influence autoimmune diseases Lupus-prone mice curliproducing bacteria autoantibody titers control gene expression immunity/response immune system innate immunity adaptive immunity Lupus-prone mice curliproducing bacteria autoantibody titers controls infection model immunity Lupus-prone mice curliproducing bacteria autoantibody titers immune response genetic models microbiome autoimmune diseases inflammation immunology rheumatology mouse models pathogenesis antigen presentation T cells B cells Lupus-prone mice bacteria infection autoantibody titers curliproducing bacteria immunology mouse models lupus research autoimmune response
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. taxation sugar-sweetened beverages incidence type II diabetes India public health policy economic impact dietary habits obesity nutrition epidemiology taxation sugar-sweetened beverages incidence type II diabetes India public health policy epidemiology economic impact obesity nutrition dietary habits sugar-sweetened beverages tax incidence type II diabetes india public health policy epidemiology consumption obesity metabolic syndrome socio-economic factors intervention outcomes taxation policies sugar-sweetened beverages type II diabetes India economic impact health outcomes research studies population health public health policy SMB taxes socioeconomic factors Taxation sugar-sweetened beverages incidence type II diabetes India public health epidemiology economic policy obesity metabolic syndrome nutrition dietary habits healthcare costs relevance analysis impact epidemiology public health taxation政策 贝verages消费 糖尿病发病率 印度地区 经济措施 taxation sugar-sweetened beverages incidence type II diabetes India economic impact public health policy effect socioeconomic factors health outcomes taxation sugar-sweetened beverages type II diabetes India effectiveness studies research trends population health economic impact public policy taxation sugar-sweetened beverages incidence type II diabetes India public health economic impact policy nutrition epidemiology obesity health outcomes dietary habits Taxation effectiveness sugar-sweetened beverages type II diabetes India research studies policy economicimpact healthoutcomes
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 migration inflammation membrane rafts immune response cytokines chemokines signaling pathways immune cell trafficking NK cells Ly49Q neutrophil migration membrane rafts inflammation sites immune response leukocyte recruitment cytokines chemokines innate immunity cell adhesion signaling pathways Ly49Q neutrophil migration inflammation sites membrane rafts immune response cell signaling innate immunity biomarkers molecular interactions cytokines chemokines tissue repair immune surveillance Ly49Q protein function neutrophil migration regulation membrane raft signaling inflammation response immune cell trafficking innate immunity mechanisms leukocyte recruitment cytokine production chemokine receptors immune system activation cellular adhesion molecules inflammatory processes immune response modulation Ly49Q neutrophil migration inflammation sites membrane rafts immune response cell adhesion cytokines chemokines immune surveillance innate immunity leukocyte recruitment immune trafficking signal transduction query expansion relevant phrases neutrophil migration inflammation sites membrane rafts Ly49Q functions Ly49Q neutrophil migration inflammation sites membrane rafts immune response signaling pathways cytokines chemokines immune cell trafficking adaptive immunity innate immunity Ly49Q neutrophil migration inflammation sites membrane rafts immune response cellular adhesion chemotaxis cytokines innate immunity leukocyte trafficking immune cell activation signal transduction immunology biomedicine molecular biology Ly49Q neutrophil migration inflammation sites membrane rafts immune response signal transduction cytokines chemokines cell adhesion innate immunity immune cells leukocyte trafficking Ly49Q neutrophils inflammation membrane rafts migration immune response cytokines chemokines cell adhesion signaling pathways innate immunity
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 stimulated autoimmune inflammation infection biology medical pathology neutrophils extracellular traps NETs ANCA stimulated autoimmune inflammation mechanisms biology medicine research pathology neutrophils extracellular traps NETs ANCA inflammation autoimmune disease mechanism biology immunology pathology research clinical diagnosis treatment neutrophil extracellular trap formation ANCA associated vasculitis neutrophil function inflammation markers immune response mechanisms DNA-based antimicrobial defense neutrophil activation oxidative stress inflammatory disorders autoimmunity conditions Neutrophils extracellular traps ANCA stimulated autoimmune inflammation mechanism biology medical research neutrophil extracellular traps NETs ANCA stimulated inflammation autoimmune disease biology immunology mechanism medical research therapy diagnosis neutrophils extracellular traps ANCA stimulation autoimmune inflammation biology genetics immune response infection defense mechanism DNA histones antimicrobial proteins neutrophils ANCA NETs microbial infection inflammation biofilm killing extracellular traps autoimmune disease immuneresponse Neutrophils ANCA extracellular traps NETs inflammation autoimmune disease mechanism biology immuneresponse Neutrophils ANCA inflammation bacterial defense microbiology immune response angiitis disease mechanism antibodies oxidative stress
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 CK-666 lamellipodia inhibitor actin dynamics cellmigration polymerization regulation Arp2/3 inhibitor CK-666 lamellipodia formation cell migration actin polymerization molecular biology inhibitor effects cytoskeleton dynamics biophysics pharmacology CK-666 Arp2/3 inhibitor lamellipodia formation actin polymerization cell migration morphogenesis cellular response biological process modification microscopy analysis molecular biology techniques Pretreatment effects Arp2/3 inhibition CK-666 function lamellipodia development cell migration actin dynamics biological response inhibitor impact molecular biology cellular behavior biophysical chemistry Pretreatment Arp2/3 inhibitor CK-666 lamellipodia formation cell migration actin polymerization biomembrane dynamics molecular biology cytoskeleton biochemical assay Arp2/3 inhibitor effects CK-666 lamellipodia pretreatment cell migration actin polymerization inhibitors lamellipodia formation mechanisms cellular response inhibitors Arp2/3 complex CK-666 lamellipodia actin polymerization cell migration inhibitors biomolecular interactions Pretreatment Arp2/3 inhibitor CK-666 lamellipodia formation cell migration actin polymerization molecular biology cellular response inhibitor effects Pretreatment Arp2/3 inhibitor CK-666 lamellipodia formation cell migration actin polymerization molecular biology microscopy analysis Pretreatment Arp2/3 inhibitor CK-666 lamellipodia formation actin polymerization cell migration molecular biology biochemical assay microscopy signaling pathway
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 treatment drug penetration necrotic tissue tuberculosis lesion anti-tubercular drugs drug delivery systems tuberculosis therapy bacterial resistance tuberculosis infection tuberculosis drug penetration anti-tuberculosis therapy tuberculosis lesions necrotic tissue treatment drug delivery systems tuberculosis tuberculosis infection management tuberculosis treatment efficacy tuberculosis lesions drug penetration necrotic tissue tuberculosis treatment antitubercular drugs bacterial resistance lung infection tuberculosis pathology pharmacokinetics infectious diseases tuberculosis management tuberculosis lesion treatment drug penetration tuberculosis new tuberculosis medications anti-tuberculosis drug efficacy tuberculosis necrotic tissue TB drug delivery systems tuberculosis infection management enhancing drug penetration tuberculosis tuberculosis lesion composition drug delivery systems tuberculosis anti-tuberculosis drug penetration necrotic tissue drug response tuberculosis treatment efficacy tuberculosis lesion penetration drug delivery tuberculosis necrotic tissue treatment anti-tuberculosis medication efficacy tuberculosis treatment advances tuberculosis treatment drug penetration lung lesions anti-tuberculosis agents pharmacokinetics mycobacterium tuberculosis drug delivery systems necrotic tissue bacterial resistance tuberculosis therapy tuberculosis lesion penetration anti-tuberculosis drug delivery necrotic tissue treatment tuberculosis drug efficacy tuberculosis treatment advancements tuberculosis lesions drug penetration necrotic tissue TB treatment antimicrobial efficacy tuberculosis drug delivery tuberculosis infection management tuberculosis lesion penetration drug delivery systems tuberculosis new tuberculosis treatments anti-tuberculosis drug efficacy necrotic tissue drug absorption
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 subsets immune function inflammation markers macrophage differentiation immunology leukocyte biology immune cells Ly6Chi monocytes function Ly6Cl monocytes differences inflammation role regulation immune response biological markers inflammatory response immune cells macrophages cytokines innate immunity leukocytes biomarkers gene expression mouse models human samples immunology research inflammatory response immune cells monocytic subset innate immunity leukocyte markers cytokine production phagocytosis efficiency tissue distribution immune function signaling pathways Ly6C expression monocyte subsets inflammatory response immune cells macrophage polarization cytokine production phagocytosis innate immunity blood cells stem cell factor chemokines tissue repair cardiovascular disease infection response antigen presentation immune regulation gene expression signaling pathways Ly6C hi monocytes inflammatory capacity Ly6C lo monocytes immune response macrophage differentiation inflammatory markers immune system function monocyte subtypes monocyte subsets inflammatory response Ly6C markers immune function differential expression macrophage development ly6c hi monocytes function ly6c lo monocytes inflammatory response differences immune cells regulation biological markers immune function cell differentiation immunology monocyte subtypes innate immunity ly6c hi monocytes inflammatory capacity ly6c lo monocytes immune function macrophage polarization cytokine production innate immunity gene expression cell differentiation inflammation markers inflammatory response immune cells monocytic subsets cytokine production innate immunity leukocyte markers
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 Ly6C markers macrophage polarization ly6c hi phenotype ly6c lo phenotype monocyte subpopulations inflammatory capacity comparison immune cell function monocyte subsets inflammation response differences blood monocytes immunology research leukocyte markers inflammatory response monocyte subtypes immune system leukocytes macrophage differentiation cytokine production innate immunity circulatory system hematopoiesis ly6c hi monocytes function ly6c hi vs ly6c lo monocytes ly6c hi monocyte role ly6c hi monocyte properties inflammatory response comparison monocyte subtypes monocyte classification immunology terms immune system functions Ly6C expression monocyte subsets inflammatory response immune cells cytokine production tissue infiltration phagocytosis activation markers macrophage differentiation query expansion natural language processing bioinformatics immunology research monocyte subtypes inflammation markers genomic analysis cell biology Ly6C expression monocyte subsets inflammatory response immune cells differential functionality ly6c hi monocytes ly6c lo monocytes inflammatory capacity differential function immune response macrophage development innate immunity stem cell biology immune cell subsets Ly6C expression monocyte subpopulations inflammatory response immune cells biomarkers immunology innate immunity cell markers inflammation biology Ly6C expression monocyte subsets inflammation immune response cytokines macrophages leukocytes phagocytosis immunology differential function immune cells 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 mouse SHP-2 MAPK pathway mouse models immune system molecular biology genetic modification MMP pathway knockout mice LN enlargement Lymphadenopathy knockin mouse SHP-2 MAPK pathway immune response mouse model molecular biology genetics immunology tumor development Lymphadenopathy knockin mouse SHP-2 MAPK pathway immune response mouse model cancer signal transduction Lymphadenopathy causes knockin mice characteristics SHP-2 function MAPK pathway impact immune system response genetic modifications effects mouse model diseases signaling pathway disruption Lymphadenopathy knockin mouse SHP-2 MAPK pathway immunology genetics oncology pathology Lymphadenopathy causes MAPK pathway function knockin mice models SHP-2 role inflammation response mouse genetics molecular biology immunology disease modeling biological pathways lymph node enlargement SHP-2 deficiency MAPK pathway disruption genetic knockin model immune response alteration signaling pathway analysis lymphoid tissue pathology cancer susceptibility bone marrow examination T-cell development Lymphadenopathy knockin mouse SHP-2 MAPK pathway mouse model immune response signal transduction MALZ deficiency MKP3 knockout PTPN11 mutation Lymphadenopathy knockin mice SHP-2 MAPK pathway immunology genetics pathology molecular biology mouse models immune system Lymph nodes mouse models SHP-2 deficiency MAPK signaling immune response pathway disruption genetic knockout liver fibrosis cancer susceptibility
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 PROTEIN DEINOCOCCUS RADIODURANS ALTERNATIVE SSB DNA REPAIR RADIONUCLIDE RESISTANCE BACTERIAL PROTEINS DNA BINDING PROTEINS Deinococcus radiodurans DdrB protein function alternative SSB dna repair molecular biology radiation tolerance Deinococcus radiodurans DdrB alternative SSB DNA repair radiation resistance protein function bacterial proteins single-strand break survival mechanism DDRB protein alternative single-strand binding protein Deinococcus radiodurans SSB radiation repair protein DNA damage response protein function genomic stability bacterial stress resistance SSB proteins radiation survival mechanisms Deinococcus radiodurans DdrB protein alternative SSB DNA repair radiation resistance proteins bacterial survival stress response single-strand breaks DDR2110 protein radiation repair single-strand breaks DNA damage tolerance Deinococcus radiodurans genome protein function analysis SSB protein homologs bacterial survival mechanisms radiotolerance factors DdrB Deinococcus radiodurans SSB alternative single-strand binding protein DNA repair radiation resistance protein function molecular biology bacterial survival Deinococcus radiodurans DdrB protein Ssb alternative single-strand DNA binding protein radS homolog Deinococcus radiodurans DdrB protein alternative SSB DNA repair radiation resistance protein function bacterial survival DNA binding protein recombinase protein stress response Deinococcus radiodurans genome alternative single-strand binding protein DdrB function radiation resistance mechanisms 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 modifications chromatin structure gene expression regulation nucleosome stability yeast genetics epigenetics molecular biology genetic modification transcriptional control genomic context protein interactions genetic engineering epigenetic marks chromatin dynamics histone modification chromatin structure gene regulation yeast biology nucleosome stability transcriptional silencing epigenetics molecular biology genetic engineering cellular metabolism histone modification chromatin structure gene expression regulation yeast genetics nucleosome dynamics epigenetics transcriptional silencing genetic engineering molecular biology cellular processes histone modification chromatin structure gene regulation yeast genetics nucleosome stability transcription initiation epigenetics genetic modification molecular biology cellular processes histone modification gene expression yeast nucleosome stability H2A.Z transcription regulation histone modification chromatin structure gene regulation nucleosome stability yeast genetics epigenetics transcriptional repression molecular biology genomics DNA packaging histone modification chromatin structure gene regulation nucleosome stability transcriptional silencing yeast genetics epigenetics molecular biology genetic engineering DNA packaging histone modification chromatin structure gene regulation nucleosome stabilization yeast genetics epigenetics transcriptional control molecular biology genetic engineering biochemical assays histone modifications gene regulation yeast biology nucleosome stability H2A.H2A.Z replacement transcriptional control histone modifications gene expression regulation nucleosome stability transcriptional repression yeast genetics H2A.Z function gene activation 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 inflammation autoimmune diseases immunology medical research therapeutic targets clinical implications basophils role SLE treatment effectiveness of basophils immune response basophils SLE inflammation control basophil therapy SLE patient outcomes Basophils immune response systemic lupus erythematosus inflammation autoimmunity cytokines immunomodulation therapeutic targets immune cells basophils role in SLE basophils immune response SLE basophils disease modulation SLE basophils therapeutic potential SLE basophils inflammation control SLE basophils systemic lupus erythematosus SLE immune response inflammation autoimmune diseases therapeutic potential clinical significance basophilic cells SLE treatment mast cells disease modulation inflammatory response Lupus therapy elevated immune function anti-inflammatory effect basophils immune response systemic lupus erythematosus SLE inflammation autoimmune diseases immunology therapeutic targets biological markers basophils SLE immune response basophils role in lupus basophils disease fighting basophils inflammation reduction basophils autoimmunity basophils patient outcomes basophils therapeutic target basophils systemic lupus erythematosus SLE immune response inflammation autoimmune diseases therapeutic targets clinical implications immunology biomarkers Basophils Systemic Lupus Erythematosus SLE immune response inflammatory markers therapeutic targets autoimmunity immunology clinical significance
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. therapeutic evidence drug Dapsone pyoderma gangrenosum anecdotal research clinical study dermatology clinical trials efficacy mechanism side effects dosage patient outcomes evidence-based medicine dermatology antibiotic resistance immune response Dapsone pyoderma gangrenosum evidence-based medicine anecdotal evidence drug therapy treatment options immune system skin conditions therapeutic evidence drug Dapsone pyoderma gangrenous anecdotal pharmacology treatment clinical research Dapsone pyoderma gangrenosum anecdotal evidence therapy clinical application microbial infection immune response therapeutic evidence pyoderma gangrenosum dapsone application clinical case studies alternative approaches Dapsone therapy pyoderma gangrenosum treatment anecdotal evidence review drug efficacy skin disease management Dapsone therapy pyoderma gangrenosum treatment anecdotal efficacy therapeutic drug use dermatology treatments autoimmune skin conditions therapeutic evidence pyoderma gangrenosum Dapsone anecdotal clinical study dermatology microbial infection immune response clinical trials systematic review efficacy studies side effects patient outcomes treatment guidelines pharmacology dermatology evidence-based medicine
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 response heavy metal induction gene regulation nickel tolerance microbial metabolism environmental genetics bioinformatics analysis transcription factor binding ureAB gene cluster nickel response metal-induced genes gene regulation nickel toxicity genetic induction GFP assay RNA sequencing NIC2.1 gene ureAB gene cluster nickel stress response heavy metal induction gene regulation bacterial gene expression nickel toxicity metalloregulation genetic cluster environmental gene induction ureAB gene cluster nickel stress response metalloregulation gene induction microbial metabolism nickel toxicity metallic ions transcriptional regulation GISR genes NicR regulator ureAB gene cluster nickel response metal induction genetic regulation Gene regulatory networks nickel tolerance gene expression profiling microbial metabolism bioremediation ureAB gene cluster nickel response metal induction gene regulation microbial metabolism environmental stress genetic engineering bioinformatics metallotransport protein transcription factor ureAB gene cluster nickel stress response metallothionein transcription factors gene regulation environmental stress inducible genes bacterial metal resistance genomic context analysis molecular biology techniques ureABIEFGH nickel(II) ion gene regulation heavy metals bioremediation effectiveness microbial response environmental stress gene induction ureAB gene cluster nickel stress response metal induction genetic regulation environmental adaptation gene expression microbial metabolism bioremediation transcription factors regulatory networks ureAB gene cluster nickel stress response gene regulation mineral ion influence microbial metabolism genetic induction factoring in environmental stimuli metallotransformation pathway metallic cation impact
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 DNA genome biology genetics molecular biology genetics research chromosome epigenetics crossover hotspots gene promoters Saccharomyces cerevisiae yeast genetic recombination chromosome epigenetics molecular biology genetics research crossover hotspots gene promoters Saccharomyces cerevisiae yeast genetic recombination chromosome biology molecular biology genetics epigenetics crossover analysis yeast genetics gene regulation DNA recombination Saccharomyces cerevisiae genome chromosomal crossover frequency genetic promoters molecular biology techniques yeast genomics epigenetics research Crossover hotspots gene promoters Saccharomyces cerevisiae genetic recombination meiosis epigenetics yeast chromatin DNA molecular biology genetics genomics crossover analysis Saccharomyces cerevisiae gene promoters chromosomal crossover genetic research yeast genetics genomic regions molecular biology genetic mapping DNA crossover crossover analysis Saccharomyces cerevisiae gene promoters molecular biology recombination hotspots homologous recombination genetic mapping chromosome segregation DNA sequences Crossover hotspots gene promoters Saccharomyces cerevisiae chromosomal recombination yeast genetic analysis epigenetics Crossover hotspots gene promoters Saccharomyces cerevisiae genetic recombination yeast genome analysis epigenetics Crossover events gene regulation Saccharomyces genetics molecular biology recombinase activity
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 gene cluster maturation proteins UreD UreH UreE UreF UreG ureABIEFGH urease microbial proteins function gene cluster bacteria maturation enzymes ureD UreH UreE UreF UreG urease gene_cluster bacterial_metabolism maturation_proteins ureD ureH ureE ureF ureG nitrogen_fixation ammoniaoxidizing_bacteria protein_function molecular biology biochemistry microbiology genetic_engineering biotechnology urease microbiology gene function protein ureD UreH UreE UreF UreG urease maturation enzymology biochemistry bacterial genes metabolic process urease maturation genes UreD UreH UreE UreF UreG ureABIEFGH protein urease mature protein gene cluster ureD UreH UreE UreF UreG maturation enzyme function biological sequence expression metabolism bacterial ammonia nitrogen urease maturation proteins ureD ureH ureE ureF ureG gene cluster bacterial enzyme function urease maturation proteins gene cluster UreD UreH UreE UreF UreG ureABIEFGH ureAB gene cluster urease maturation UreD protein UreH protein UreE protein UreF protein UreG protein urease enzyme bacterial urease gene expression protein function microbial metabolism nitrogen fixation urea hydrolysis urease maturation genes ureD ureH ureE ureF ureG bacterial function protein synthesis enzyme cluster microbial activity expression regulation structure composition
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. dendritic cells innate lymphoid cells intestinal homeostasis immune response cytokines signaling pathways microbiome inflammation adaptive immunity innate immunity crosstalk dendritic cells innate lymphoid cells intestinal homeostasis immune response microbiome inflammation cytokines immune regulation gastrointestinal tract immune cell interaction immunology mucosal immunity Crosstalk Dendritic Cells Innate Lymphoid Cells Intestinal Homeostasis Immune Response Inflammation Gut Microbiota Immunology Cellular Interaction Immune Regulation Crosstalk mechanisms DCs functions ILCs interactions intestinal immune response homeostasis maintenance immunological synapse formation antigen presentation cytokine production microbial flora influence adaptive immunity initiation mucosal immunity inflammatory bowel disease immune tolerance induction crosstalk dendritic cells innate lymphoid cells intestinal homeostasis immune response inflammation microbiome cytokines immune regulation gut immunity immunology Crosstalk dendritic cells innate lymphoid cells intestinal homeostasis immune response inflammation microbial interaction antigen presentation cytokines gut microbiome immune regulation crosstalk dendritic cells innate lymphoid cells intestinal homeostasis immune response inflammatory signaling microbiomeinteraction immune regulation antigen presentation cytokines gut immunity Crosstalk dendritic cells innate lymphoid cells intestinal homeostasis immune response microbiomeinteraction inflammation immune regulation immunology cytokines adaptive immunity innate immunity Crosstalk dendritic cells innate lymphoid cells intestinal homeostasis immune response inflammation microbiome signaling pathways immunology gut immunity immune regulation crosstalk dendritic cells innate lymphoid cells intestinal homeostasis immune response inflammation microbiome signaling pathways immunology gut immunity immune regulation
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 c apoptosis mitochondria intermembrane space cytosol release signaling pathway cell-death mechanism cytochrome c release apoptosis mechanism mitochondrial intermembrane space cytosol translocation caspase activation mitochondrial outer membrane permeabilization apoptotic signaling programmed cell death Bcl-2 family proteins reactive oxygen species apoptosis induction mitochondrial dynamics mitochondria function cellular stress response cytochrome c mitochondria apoptosis cytosol intermembrane space release mitochondrial fission hormones oxidative stress cellular damage Cytochrome c release mechanism apoptosis mitochondrial intermembrane space cytosol apoptosis signaling cytochrome c role in apoptosis mitochondrial outer membrane permeabilization apoptosis cytochrome c pathway cytochrome c apoptosis regulation mitochondria cytochrome c release apoptosis caspase activation mitochondrial apoptosis function cytochrome c mitochondrial intermembrane space cytosol apoptosis cell death mitochondrial outer membrane permeabilization caspases programmed cell death apoptotic cascade cytochrome c release apoptosis mechanism mitochondrial outer membrane caspase activation cell death process intermembrane space cytosolic localization apoptotic signaling Cytochrome c release mitochondrial apoptosis intermembrane space caspase activation apoptotic signaling cytochrome c apoptosis mitochondrial membrane caspase activation apoptotic signaling intermembrane space cell death mechanisms cytosolic release oxidative stress cytochrome c release apoptosis process mitochondrial intermembrane space cytosol transfer cell death mechanisms cytochrome c release mitochondrial apoptosis caspase activation apoptosis signaling mitochondrial outer membrane permeabilization cell death mechanism intermembrane space cytosolic localization 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 size prenatal nutrition breastfeeding maternal health infant weight oncology epidemiology risk factors developmental origins adiposity birth weight breast cancer study birth weight and breast cancer risk low birth weight breast cancer high birth weight breast cancer research birth weight cancer association birth weight breast cancer risk infant weight adult cancer prenatal nutrition maternal health oncology research epidemiological studies childhood growth reproductive factors birth weight and breast cancer risk low birth weight breast cancer high birth weight and cancer prenatal nutrition and breast cancer intrauterine growth and breast cancer birth size and breast cancer incidence birth weight breast cancer epidemiology risk factors infant mortality maternal nutrition childhood outcomes prenatal care birth weight breast cancer risk low birth weight and breast cancer high birth weight breast cancer link infant birth weight breast cancer perinatal mortality birth weight breast cancer birth weight infant weight maternal nutrition prenatal care breast cancer risk obesity epidemiology cohort study statistical analysis public health birth weight breast cancer efficacy association expansion keywords research prevalence risks factors infant health mortality maternal health statistical analysis population studies clinical trials genetic predisposition environmental factors obstetric outcomes birth weight breast cancer epidemiology risk factors cohort studies case-control studies obesity nutrition prenatal care neonatal outcomes long-term health birth size infant health maternal nutrition long-term outcomes prenatal care genetic factors hormonal influences epidemiological studies statistical correlation risk factors
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 sensitivity conventional_cytology CIN2 detection_rate longitudinal_study cervical_neoplasia cervical_cancer_screening HPV_detection cervical_intraepithelial_neoplasia cytology_comparison longitudinal_sensitivity cervical_dysplasia cervical_cancer_screening HPV_detection longitudinal_sensitivity conventional_cytology cervical_intraepithelial_neoplasia_grade_2 detection_efficiency clinical_relevance sample_collection diagnostic_tests healthcare_quality public_health_strategies HPV testing cervical cancer cytology comparison longitudinal study cervical intraepithelial neoplasia grade 2 detection cancer screening oncology research gynecological examination early cervical cancer detection HPV infection cervical dysplasia cancer prevention medical diagnostics cervical health cervical precancer HPV prevalence cervical cancer screening methods HPV vaccination impact cervical_cancer_screening HPV_detection longitudinal_sensitivity conventional_cytology cervical_intraepithelial_neoplasia_grade_2 sensitivity_analysis early_detection precancerous_cervical_conditions health_screening biomarker_assessment viral_infection clinical_benefits cervical_cancer_screening HPV_detection sensitivity longitudinal_studies cervical_intraepithelial_neoplasia conventional_cytology neoplasia_grade_2 detection_techniques clinical_trials public_health_implications healthcare_quality medical_research vaccination_programs screening_interventions prevention_strategies biopsy_procedures diagnostic_tests health_policy cervical_cancer_screening HPV_detection sensitivity cytology CIN_2 detection_accuracy longitudinal_study neoplasia_grade_2 medical_screening public_health biomedical_science gynecology healthcare_quality clinical_research cervical_cancer_screening HPV_detection sensitivity conventional_cytology CIN2 detection efficacy longitudinal_analysis neoplasia primary cervical cancer HPV detection longitudinal sensitivity conventional cytology cervical intraepithelial neoplasia grade 2 screening oncology gynecology HPV cytology diagnostic accuracy epidemiology gynecological cancer neoplasia detection public health cervical health medical research HPV testing cervical intraepithelial neoplasia screening protocols longitudinal studies conventional cytology evidence-based medicine early detection cancer prevention vaccination programs population screening
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-related adverse events immunotherapy checkpoint inhibitors autoimmunity treatment strategies clinical outcomes immune modulation cancer therapy immune checkpoint inhibitors adverse effects autoimmunity clinical trials immunotherapy tumor immunology immune modulation biomarkers therapeutic strategies cancer immunotherapy immune-related adverse events checkpoint inhibitors autoimmune disorders treatment efficacy clinical outcomes immunomodulatory drugs oncology therapy biomarkers therapeutic strategies cancer immunotherapy immune-related adverse events co-inhibitory molecules checkpoint inhibitors autoimmune disorders treatment efficacy clinical trials oncology research tumor immunity immune modulation techniques cancer treatment immune response blockade autoimmune reactions clinical trials immunotherapy side effects biomarkers therapeutic strategies inflammation genetic factors cancer therapy immune checkpoint inhibitors adverse effects autoimmune response co-ir blockade treatment strategies clinical outcomes cancer therapy immune checkpoint inhibitors autoimmune reactions treatment outcomes clinical trials immunotherapy side effects management cancer treatment co-IR blockade autoimmune events immunotherapy side effects clinical trials immune response oncology inflammation biomarkers genetic factors therapeutic strategies cancer treatment immune-related side effects immunotherapy autoimmune disorders co-inhibitory molecules checkpoint inhibitors inflammation clinical trials oncology immunomodulation cancer immunotherapy immune checkpoint inhibitors autoimmune reactions treatment outcomes therapeutic strategies clinical trials side effects management
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 autoimmune reactions treatment outcomes clinical trials immunotherapy safety cancer therapy immune checkpoint inhibitors side effects autoimmune reactions clinical trials immunotherapy tumor treatment safety profile biomarkers long-term effects cancer treatment co-IR blockade adverse events autoimmune reactions immunotherapy clinical trials side effects tumor immunity checkpoint inhibitors cancer treatment co-IR blockade autoimmune events clinical trials immunotherapy side effects cancer immunology tumor therapy immune checkpoint inhibitors oncology research cancer treatment co-IR blockade adverse events autoimmune response immunotherapy clinical trial oncology immune checkpoint inhibitors side effects tumor immunology cancer treatment co-IR blockade adverse events immune-related side effects immunotherapy autoimmune disorders cancer immunology treatment efficacy clinical outcomes cancer therapy cancer treatment co-IR blockade autoimmune events immunotherapy side effects clinical trials immune checkpoint inhibitors tumor immunology oncology therapeutic strategies cancer treatment co-IR blockade adverse events autoimmune response therapeutic efficacy cancer treatment co-IR blockade adverse events autoimmune response immunotherapy clinical trial side effects tumor immunology immune checkpoint inhibitors cancer therapy immune checkpoint inhibitors adverse effects autoimmune diseases co-ir blockade benefits clinical trials patient outcomes
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 inadequate response conventional treatment efficacy alternatives respiratory therapy pulmonary care guidelines clinical outcomes non-invasive ventilation inadequate response conventional treatment criteria guidelines clinical effectiveness outcomes non-invasive ventilation inadequate response conventional treatment wean oxygen therapy respiratory failure mechanical ventilation outcomes efficacy Non-invasive ventilation alternatives inadequacy criteria respiratory therapy adjustments patient response monitoring ventilator weaning protocols non-invasive ventilation inadequate response conventional treatment respiratory therapy outcomes clinical guidelines non-invasive ventilation alternatives conventional treatment outcomes respiratory therapy adjustments prolonged non-invasive ventilation risks patient response monitoring non-invasive ventilation inadequate response conventional treatment respiratory therapy clinical guidelines criteria non-invasive ventilation inadequacy conventional treatment efficacy keywords expand respiratory therapy alternatives effectiveness clinical guidelines pulmonary symptoms non-invasive ventilation inadequate response conventional treatment optimize search expansion terms respiratory therapy clinical guidelines non-invasive ventilation alternatives wean patients ventilation weaning criteria responding to treatment conventional therapy outcomes
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 immune response inflammation markers cytokine induction immunology keywords inflammatory cascade primary cytokines secondary mediators inflammation response immune reaction cytokine cascade inflammatory mediators pro-inflammatory factors anti-inflammatory molecules primary cytokines pro-inflammatory response secondary mediators anti-inflammatory cytokines immune response inflammatory cascade cytokine network immune regulation inflammatory response regulation immune system activation cytokine signaling pathways inflammatory mediator classification innate immunity mechanisms chronic inflammation markers acute phase reaction indicators primary cytokines pro-inflammatory secondary mediators anti-inflammatory immune response inflammation markers cytokine network inflammatory cascade query expansion relevant phrases primary cytokines secondary mediators inflammatory response immune system bioscience medical research bioinformatics clinical applications primary pro-inflammatory cytokines secondary mediators inflammatory response cytokine induction immune response pro-inflammatory mediators anti-inflammatory cytokines inflammation cascade primary cytokines pro-inflammatory response secondary mediators anti-inflammatory cytokines immune response inflammation cascade cytokine network immune regulation primary pro-inflammatory cytokines secondary mediators inflammation cytokine response immune response interleukins tumor necrosis factor chemokines macrophages neutrophils adaptive immunity innate immunity primary cytokines pro-inflammatory response secondary mediators anti-inflammatory cytokines immune response inflammation Keywords Comma Separated List
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 Roc-COR domain neurodegenerative disease cellular repair mechanisms locomotor function genetic mutation acetylation process neuronal health protein function restoration microtubule acetylation LRRK2 Roc-COR domain locomotor deficits neurodegenerative diseases Parkinson's disease protein function cellular repair molecular biology genetic mutations neuroscience research cellular signaling microtubule stabilization LRRK2 protein function Roc-COR domain structure neuronal degeneration neurodegenerative diseases acetylation mechanisms cellular repair processes gene mutations neurological disorders protein dysfunction therapeutic targets molecular biology techniques pharmacological interventions microtubule stabilization LRRK2 function Roc-COR domain neurodegenerative diseases cell signaling locomotor dysfunction protein acetylation molecular biology techniques therapeutic targets neuronal health microtubule stability LRRK2 protein Roc-COR domain neuronal function genetic mutation locomotion disorders protein acetylation cellular repair mechanisms microtubule stabilization acetylation therapy LRRK2 protein Roc-COR domain function neurodegenerative diseases cellular repair mechanisms locomotor dysfunction genetic mutations molecular biology techniques neuroprotection strategies microtubule stability acetylation process LRRK2 protein Roc-COR domain locomotor function genetic mutation neuronal health protein function cellular repair mechanisms microtubule stabilization LRRK2 protein Roc-COR domain neurodegenerative disorders synaptic function autophagy Parkinson's disease cellular signaling therapeutic targets neuroscience research microtubule acetylation LRRK2 mutation Roc-COR domain locomotor function neurodegeneration Parkinson's disease protein acetylation cellular repair mechanisms molecular biology neurology genetic disorders synaptic dysfunction neuronal health therapeutic targets neuroscience research microtubule stabilization LRRK2 protein Roc-COR domain function neurodegenerative diseases locomotor dysfunction acetylation therapy Parkinson's disease cellular repair mechanisms
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. PPM1D enzyme function p53 protein cellular signaling genetic regulation molecular biology cancer research biological pathway phosphatase activity PPM1D p53 activation suppression molecular biochemistry cancer genetics pathway mechanism therapy treatment PPM1D enzyme p53 protein tumor suppression phosphatase activity cancer biology cellular response genetic regulation molecular interaction oncology research apoptosis induction PPM1D enzyme function p53 protein regulation cancer cell survival tumor suppression mechanisms phosphatase activity genetic mutations impact cell cycle control apoptosis induction oncogenic signaling pathways molecular biology research Activation PPM1D p53 function suppression molecular biology cancer genetics protein interaction signal transduction cell cycle regulation PPM1D enzyme p53 protein cell cycle regulation tumor suppression phosphorylation dephosphorylation cancer therapy genetic mutation transcription factor apoptosis induction PPM1D enzyme p53 protein cellular stress response tumor suppression phosphatase activity genetic mutations cancer development molecular biology oncology research Activation PPM1D p53 function suppression molecular biochemistry cancer therapy research genetics cell cycle apoptosis PPM1D p53 function activation inhibition molecular biology cancer genetics cell cycle apoptosis PPM1D inhibition p53 pathway cell cycle regulation cancer biology genetic mutation effects
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 provided dorsal Admp chordin embryonic development gene expression signaling molecules biological processes molecular biology tissue patterning activator-inhibitor模型 Admp蛋白 chordin蛋白 背部发育 转录调控 胚胎生物学 骨骼形成 activator-inhibitor model Admp chordin dorsalization developmental biology morphogen gradients gene expression embryonic patterning signaling pathways activator-inhibitor model Admp chordin dorsalization developmental biology signaling pathways morphogen gradients Activator-inhibitor model dorsal patterning Admp Chordin gene expression effectors mechanism activator-inhibitor model Admp protein chordin developmental biology gene regulation morphogen gradient embryonic development signaling pathways search accuracy expansion terms enrich query activator-inhibitor pairs Admp chordin dorsal patterning developmental biology gene expression morphogenesis Activator-inhibitor model Admp Chordin dorsalization embryonic development gene interaction morphogen gradient activator-inhibitor模型 Admp chordin 背侧化 演化发育生物学 信号传导 morphogen梯度 search outcomes beneficial expansion terms activator-inhibitor pairs Admp chordin dorsal development molecular signaling embryonic patterning gene expression morphogen gradients
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 function tumor biology RUNX1 role cancer genetics RUNX1 protein expression tumor suppression RUNX1 mutation tumor progression RUNX1 regulation RUNX1 tumor association RUNX1 tumor-promoting mechanisms RUNX1 genetic alterations RUNX1 role in cancer RUNX1 transcription factor function RUNX1 oncogenic activity RUNX1 mutation impact RUNX1 protein expression RUNX1 signaling pathways RUNX1 cancer research RUNX1 clinical implications RUNX1 function tumor suppressor genes cancer genetics molecular biology RUNX1 mutations RUNX1 regulation tumor progression RUNX1 protein expression leukemia development RUNX1 function tumor suppressor role expression patterns cancer biology genetic factors RUNX1 mutations tumor progression RNA expression biomarker potential RUNX1 protein RUNX1 function RUNX1 mutation RUNX1 role in cancer oncogenic RUNX1 RUNX1 tumor promotion RUNX1 role in cancer RUNX1 genetic expression RUNX1 cancer mechanisms RUNX1 oncogenic activity RUNX1 leukemia association RUNX1 transcription factors RUNX1 gene function RUNX1 protein expression RUNX1 molecular biology RUNX1 protein function tumor suppression RUNX1 genetic variants RUNX1 and cancer biology RUNX1 expression levels cancer progression markers RUNX1 role in oncogenesis RUNX1 tumor promotion RUNX1 cancer role RUNX1 oncogenic functions RUNX1 in leukemia RUNX1 gene function RUNX1 protein expression RUNX1 biological significance RUNX1 mutation impact RUNX1 genetic factors RUNX1 cellular mechanisms RUNX1 tumor-promoting mechanisms RUNX1 genetic variations RUNX1 protein function RUNX1 in cancer development RUNX1 regulatory elements RUNX1 transcriptional activity RUNX1 binding sites RUNX1 mutations impact RUNX1 and oncogenesis RUNX1 expression levels tumor correlation RUNX1 tumor suppression RUNX1 genetic variation RUNX1 role in cancer RUNX1 protein function RUNX1 gene expression analysis RUNX1 and leukemia RUNX1 mutation impact RUNX1 binding sites RUNX1 transcription regulation RUNX1 interactome
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_count fibrotic_changes chemotherapy_response vessel_density tumor_progression fibrosis_effect treatment_outcome vessel密度 纤维化减少 化疗效果 血管生成 药物输送效率 治疗响应性 vessel_count fibrotic_change chemotherapy_response vessel_growth fibrosis_level tumorangiogenesis chemo_effectiveness vascular_density fibrotic_tissue antineoplastic_agent vessel density impact fibrosis effect chemotherapy success tumor angiogenesis fibrotic response vascular density anti-angiogenic therapy chemotherapy resistance fibrosis treatment angiogenesis inhibitors vessel_count fibrosis_levels chemotherapy_response disease_progression tumor_microenvironment nanotherapy targeted_treatment vessel density fibrosis chemotherapy efficacy tumor angiogenesis drug delivery cancer treatment biomarkers therapeutic response oncology research vessel density fibrosis chemotherapy efficacy tumor angiogenesis microenvironment cancer progression vessel_density fibrosis chemotherapy efficacy beneficial_keywords reduction increased_density favorable_outcomes negative_impact clinical_relevance vessel_density fibrosis chemotherapy efficacy tumor_growth microenvironment angiogenesis prognosis biomarkers disease_progression vessel density fibrosis chemotherapy efficacy tumor angiogenesis cancer treatment outcomes biomarkers drug delivery tumor microenvironment
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 enzyme polymeric structure UreA UreB bacterial infection gastric ulcer microbiology protein subunits H.pylori urease subunits UreA UreB polymeric structure bacterial protein enzyme microbiology gastroenterology research function composition H.pylori urease enzyme polymeric composition subunit structure UreA UreB subunits bacterial urease molecular architecture Active H.pylori urease function Active H.pylori urease composition Active H.pylori urease subunits UreA protein structure UreB protein structure Polymeric enzyme structure H.pylori infection symptoms H.pylori treatment options Urease enzyme mechanism Active H.pylori urease polymeric structure UreA UreB subunits enzymatic function molecular composition H. pylori urease subunits urease structure bacterial urease UreA protein UreB protein polymeric enzyme bacterial infection gastric ulcer microbiology enzyme function active H.pylori urease polymeric structure UreA UreB urease subunits helicobacter pylori protein structure active H.pylori urease polymeric structure UreA subunit UreB subunit bacterial urease molecular composition active H.pylori urease polymeric structure UreA subunit UreB subunit protein structure bacterial urease bacterial infection stomach bacteria gastric ulcer H.pylori urease subunits polymeric enzyme bacterial metabolism gastric infection urea hydrolysis microbial physiology medical microbiology diagnostic markers
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 N-terminal CARD domain plant regulatory protein interferon induced protein antiviral response PPR protein MDA5 protein CARD domain nucleic acid binding RNA recognition immune response inflammation autoimmune disease molecular structure genetic regulation signaling pathway PPR protein MDA5 protein CARD domain nucleic acid binding RNA recognition immune response viral infection signaling molecule molecular structure tandem repeats protein function biological pathway PPR protein MDA5 protein CARD domain nucleotide-binding oligomerization domain innate immunity RNA binding protein autophagy interferon-induced protein viral recognition signaling pathway molecular structure bioinformatics analysis PPR protein MDA5 N-terminal CARD domains molecular recognition RNA binding innate immunity PPR protein MDA5 protein CARD domains RNA binding innate immunity molecular structure plant defense genetic regulation PPR protein MDA5 protein CARD domain nucleotide-binding oligomerization domain antiviral response interferon pathway PPR protein MDA5 protein CARD domain N-terminal domain molecular biologykeywords PPR protein MDA5 protein N-terminal CARD domains RNA binding immune response interferon signaling pathway PPR protein MDA5 protein CARD domains RNA binding immune response molecular structure 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 ND3 ND6 neurodegeneration protein-protein interaction neurotoxicity mitochondria ALS RNA-binding TDP-43 respiratory complex ND3 ND6 neuronal loss interaction mechanism pathology mitochondrial disease neurodegeneration protein regulation dysfunction therapeutic intervention biomarker RNA binding mutations oxidative stress aging ALS motor neurons mitochondria genetics proteomics signaling pathway transcription regulation cellular physiology treatment prevention screening diagnosis TDP-43 respiratory complex ND3 ND6 neurodegeneration protein-protein interaction mitochondria neuronal dysfunction pathology ALS Huntington's Parkinson's TDP-43 function respiratory complex I neurodegeneration protein interaction neuronal death genetic modification molecular biology mitochondrial dysfunction ALS research disease mechanism exploration TDP-43 respiratory complex ND3 ND6 neuronal loss interaction proteomics genetics mitochondria pathology therapeutic mechanism TDP-43 respiratory complex I ND3 ND6 neuronal loss protein interaction disease mechanism therapeutic target molecular biology neurodegeneration TDP-43 respiratory complex I ND3 ND6 neuronal loss proteininteraction neurodegeneration pathology mitochondria apoptosis RNA binding ALS motorneuron dysfunction TDP-43 respiratory complex I ND3 ND6 neuronal loss protein interaction neurodegeneration mitochondrial dysfunction ALS dementia blocking mechanism TDP-43 respiratory complex I ND3 ND6 neuronal loss protein interaction neurodegeneration mitochondrial dysfunction ALS pathology mechanism treatment biomarker TDP-43 respiratory complex I ND3 ND6 neuronal loss protein interaction neurodegeneration mitochondrial dysfunction ALS motor neuron disease oxidative stress gene regulation RNA binding protein cellular respiration
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 cells hematopoiesis macrophage development mononuclear phagocyte system stem cells myeloid differentiation immune response regenerative medicine cellular therapy biomedicine research bone marrow progenitor cells hematopoietic stem cells macrophage development monocyte-macrophage lineage myeloid differentiation innate immunity stem cell niches cytokines chemokines tissue macrophages bone marrow-derived cells macrophage development adult hematopoiesis monocyte-macrophage lineage bone marrow transplantation myeloid progenitor cells hematopoietic stem cells microenvironment innate immunity cellular trafficking bone marrow-derived macrophages hematopoietic stem cells myeloid progenitors macrophage differentiation monocyte recruitment tissue macrophages immunology research stem cell biology regenerative medicine cellular therapy inflammation response immune system blood cell development stem cell niches monocytic lineage macrophage polarization innate immunity hematopoiesis stem cell transplantation bone marrow stem cells microenvironment immune response murine models hematopoietic progenitor cells differentiation survival factors regulation aging transplantation studies bone marrow progenitor cells macrophage differentiation stem cell biology hematopoietic stem cells monocyte-macrophage lineage immune response regulation myeloid lineage development bone marrow progenitor cells hematopoiesis macrophage differentiation monocyte migration stem cells myeloid lineage immune system development tissue macrophages lymphoid organs phagocytosis bone marrow derived cells macrophage development adult hematopoiesis microenvironment blood stem cells differentiation immune response bone marrow progenitor cells macrophage development stem cell niches myeloid differentiation microenvironment factors bone marrow-derived cells microenvironment spleen lymph nodes myeloid progenitors differentiation migration stem cells hematopoiesis innate immunity
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 mutations diabetes risk factors genetic association studies research epidemiology pancreas transcription factor HNF4A diabetes genetic mutation risk factor pancreatic liver kidney glucose insulin epidemiology prevalence study research variant polymorphism HNF4A gene function diabetes type 2 genetic polymorphism study evidence association studies variants risk factors research meta-analysis clinical patients genotype prevalence HNF4A gene diabetes risk factors genetic mutation analysis pancreatic beta cells insulin production metabolic syndrome Type 1 diabetes Type 2 diabetes genetic predisposition epidemiological studies molecular biology genetic testing clinical trials genetic variations diabetes mellitus gene expression protein function hereditary conditions biomarkers genotype-phenotype correlation HNF4A diabetes genetic mutation risk factor association research study epidemiology HNF4A mutations diabetes risk factors genetic predisposition pancreatic function metabolic syndrome type 2 diabetes insulin resistance gene regulation liver disease renal failure HNF4A gene function diabetes types risk factors genetic mutations research studies evidence review clinical implications associated diseases HNF4A diabetes genetic mutation risk factor association research epidemiology genetics metabolic syndrome pancreatic beta cells insulin resistance hepatocyte nuclear factor 4 alpha HNF4A diabetes genetic mutation risk factor association study pancreatic disease liver disease transcription factor gene expression metabolic syndrome HNF4A gene function diabetes risk factor mutation study clinical evidence genetic association研究 prevalence diabetic complications variant analysis
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. breast cancer genetic factors development heredity inheritance gene mutations environmental influences lifestyle epigenetics breast cancer genetic factors environmental influences hormonal factors lifestyle epigenetics tumor development oncogenes susceptibility genes epidemiology breast cancer genetic factors environmental influences hormonal factors tumor development oncogenes tumor suppressor genes epigenetics lifestyle hereditary cancers BRCA1 BRCA2 genetic factors breast cancer environmental factors breast cancer lifestyle and breast cancer hereditary breast cancer gene mutations breast cancer risk factors breast cancer prevention breast cancer early detection breast cancer breast cancer treatment breast cancer symptoms genetic predisposition environmental factors hormonal mutations inheritance risk cells gene genetic factors breast cancer environmental factors breast cancer lifestyle and breast cancer hereditary breast cancer tumor suppressor genes breast cancer oncogenes breast cancer genetic testing breast cancer genetic factors environmental influences lifestyle choices tumor suppressor genes oncogenes epigenetics hormonal factors family history mutation rates risk assessment early detection preventive measures genetic factors breast cancer development exclusively determinants environmental influences hormonal factors aging ethnicity risk factors breast cancer genetic factors environmental influences hormonal factors epigenetics tumor suppressor genes oncogenes lifestyle epidemiology risk factors genetic factors environmental influences epigenetics hormonal factors age 生活方式 肥胖 家族史
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 medication bone density cardiovascular drugs geriatric medicine pharmacology epidemiology osteoporosis prevention inverse relationship hip fractures statin use epidemiology research studies clinical evidence association cholesterol medication prevention elderly bone health inverse relationship hip fractures statin use cholesterol lowering drugs bone density elderly cardiovascular disease cohort studies randomized controlled trials observational studies meta-analysis epidemiology hip fracture prevention statins benefits reverse correlation medicine statin therapy effects osteoporosis treatment and statins inverse relationship hip fractures statin use epidemiology medication bone health osteoporosis cholesterol cardiovascular disease inverse relationship hip fractures statin use medication impact bone health cholesterol lowering drugs fracture risk elderly population clinical research preventive care medical studies inverse relationship hip fractures statin use cholesterol medication bone density cardiovascular health elderly osteoporosis prevention drug efficacy medical research epidemiology studies inverse_relationship hip_fractions statin_use bone_density cholesterol_levels cardiovascular_health aging_population osteoporosis_risk medication_effectiveness inverse relationship hip fractures statin use epidemiology risk factors clinical trials meta-analysis bone health cholesterol levels aging population osteoporosis medication effectiveness pharmacotherapy healthcare outcomes hip fracture prevention statin efficacy bone health supplements cholesterol lowering drugs osteoporosis risk reduction statins and bone density inverse correlation studies medication impact on bones
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. Ribosome pathology cell tissue specificity genetic disorders translation proteins Ribosomopathies cell specificity tissue pathology molecular mechanisms genetic factors clinical manifestations ribosome biogenesis protein synthesis congenital disorders hematopoietic diseases bone marrow failure neurodevelopmental disorders immunodeficiency cancer predisposition gene mutations RNA processing transcription factors signaling pathways stem cell dysfunction epigenetics epidemiology treatment options diagnostic methods Ribosome pathology genetics disease protein synthesis specificity tissues cells Ribosomopathies symptoms Ribosomopathies genetic factors Ribosomopathies diagnosis Ribosomopathies treatment Ribosomopathies types Ribosomopathies research Ribosomopathies prevalence Ribosomopathies cell specificity tissue specificity molecular pathology genetic disorders ribosomal dysfunction disease phenotypes Ribosomopathies symptoms Ribosomopathies types Ribosomopathies causes Ribosomopathies treatment Ribosomopathies examples Ribosomopathies genetic Ribosomopathies diagnosis Ribosomopathies prevalence Ribosome pathology cell tissue specificity genetic diseases molecular biology translation protein synthesis genetics RNA mitochondria hematopoietic stem cells myelodysplastic syndrome anemia Ribosomopathies cell specificity tissue pathology genetic disorders molecular biology cancer leukemia developmental disorders mitochondrial dysfunction apoptosis ribosomal biogenesis RNA processing Ribosomes cell biology tissue specificity genetic disorders protein synthesis molecular pathology ribosome biogenesis pathophysiology molecular genetics medical genetics cellular stress response RNA processing translational fidelity disease mechanism genetic variation clinical manifestations biomarkers therapeutic targets ribosome biology genetic mutations cellular stress response tissue vulnerability pathogenesis mechanisms molecular genetics protein synthesis disorders rare diseases hematopoietic dysfunction neurodevelopmental disorders
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 geneexpression neuroscience molecularbiology proteins growth cone cell body ubiquitination molecular biology nervous system development growth cone proteomics ubiquitination rate synaptic proteins axonal transport protein synthesis neuronal development cellular localization molecular biology techniques proteins growth cone ubiquitination process cell body proteins protein synthesis neuronal development synaptic plasticity molecular biology techniques proteomics analysis ubiquitination growth cone cell body protein synthesis proteostasis microtubules nerve growth ubiquitination growth cone protein synthesis cell body proteomics molecular biology neuroscience signal transduction protein modification synaptic plasticity proteins growth cone ubiquitination cell body synthesized molecular biology neuroscience growth cone proteomics ubiquitination rates protein synthesis neuronal development synaptic plasticity molecular biology techniques proteins growth cone cell body ubiquitination molecular biology neuroscience protein synthesis proteolysis growth cone biology ubiquitination protein synthesis gene expression 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. macrolide antibiotics myocardial infarction prevention cardiac protection antibiotic efficacy cardiovascular risk macrolide drugs macrolides myocardial infarction antibiotic heart disease protective effect clinical trial cardiovascular medication treatment infection inflammation macrolide antibiotics myocardial infarction prevention cardiovascular effects antibiotic efficacy clinical trials pharmacology cardiac protection antimicrobial drugs inflammation response risk factors macrolides cardiovascular risk macrolide antibiotics myocardial infarction antibiotic effects on heart protective effects against heart attacks macrolides side effects heart myocardial infarction prevention medications macrolides myocardial infarction protective effect clinical trial antibiotics cardiovascular disease drug efficacy research treatment prevention Macrolides myocardial infarction protection macrolide antibiotics heart disease protective effects against MI macrolides clinical trial outcomes myocardial infarction prevention research antibiotic efficacy on heart conditions macrolide antibiotics myocardial infarction prevention cardiac protection antimicrobial drugs cardiovascular outcomes macrolides myocardial infarction protective effect cardiovascular disease antibiotic efficacy clinical trial heart attack antibiotic resistance macrolides myocardial infarction protection macrolides cardiovascular disease macrolide antibiotics myocardial infarction protective effects macrolides anti-inflammatory macrolides myocardial infarction macrolide antibiotics myocardial infarction prevention cardiac health pharmacological effects clinical trials adverse effects cardiovascular disease antibiotic resistance
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 research studies evidence paper analysis neurology brain functional tests mri symptoms headaches cognitive impairment correlation neurology memory function stroke dementia pain brain medicine research study analysis prevalence treatment evidence clinical patient headaches cognitive impairment research studies symptoms brain function neurology correlation clinical data analysis treatment prevention risk factors population demographics severity duration frequency headaches cognition headache correlation studies cognitive function and headaches impairment without headaches brain health and headaches headaches cognitive impairment correlation research studies evidence neurological conditions migraines symptoms pain brain functioning test results prevalence severity frequency treatment management impact quality life diagnosis prevention clinical patients symptomatology headache_impairment research_headache cognitive_function_headache headache_mechanisms correlation_headache_impairment headaches cognitive impairment brain function neurological disorders memory concentration pain symptoms studies research correlation analysis headaches cognitive impairment correlation neurological conditions evidence research study analysis headaches cognitive impairment correlation research studies neurology migraines pain symptoms brain function test analysis prevalence headaches cognition headaches brain function cognitive decline headaches neurological symptoms headaches
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 myocardial infarction antibiotic cardiovascular protection mechanism study research bacteria inflammation macrolides myocardial infarction protection mechanisms macrolides cardiovascular benefits macrolide antibiotics myocardial infarction macrolides and heart disease macrolides anti-inflammatory effects macrolides clinical trials myocardial infarction macrolide antibiotics myocardial infarction prevention cardiac protection antibiotic therapy cardiovascular disease macrolides efficacy macrolides antibiotic properties macrolides cardiovascular benefits macrolides and heart health macrolides reduce inflammation macrolides prevent heart attack macrolides mechanism of action macrolides clinical trials macrolides vs statins macrolides long-term effects macrolides and cholesterol management macrolides myocardial infarction antibiotics cardiovascular protection mechanism clinical trials inflammation lipid metabolism macrolide antibiotics cardiovascular protection myocardial ischemia antibiotic therapy macrolides mechanism anti-inflammatory effects cardiotonic drugs macrolide antibiotics myocardial infarction prevention cardiac protection antibiotic efficacy inflammation reduction cardiovascular health drug mechanism Macrolides cardiovascular benefits myocardial infarction prevention antibiotic cardioprotection erythromycin effects macrolide antibiotics heart attack reduction anti-inflammatory macrolides mechanism of cardioprotection macrolides and ischemia Macrolides myocardial infarction antibiotic therapy cardiovascular protection drug efficacy clinical trials inflammation reduction bacterial infection heart disease prevention macrolide antibiotics myocardial infarction prevention cardiovascular health antibiotic efficacy inflammation reduction bacterial infections heart disease risk 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 oncogenes tumor suppressor Pseudogene PTENP1 PTEN miRNA decoy gene regulation RNA biology oncogene tumor suppressor molecular mechanism genetic regulation pseudogene PTENP1 PTEN miRNA decoy gene regulation RNA function oncogene tumor suppression pseudogene regulation miRNA decoy mechanism PTEN expression genetic regulation RNA function miRNA sponge PTENP1 role gene interaction RNA biology oncogenes and pseudogenes Pseudogene PTENP1 PTEN miRNA decoy gene regulation RNA interference oncogene tumor suppressor pseudogene regulation miRNA decoy mechanism PTEN expression RNA interference genetic regulatory elements gene function analysis molecular biology techniques oncogenic pseudogenes non-coding RNA roles pseudogene PTENP1 PTEN miRNA decoy gene regulation RNA function expression调控 非编码RNA pseudogene PTENP1 PTEN miRNA decoy gene regulation RNA function molecular biology oncology genetic regulation Pseudogene PTENP1 regulates PTEN miRNA decoy gene expression RNA biology oncogenes tumor suppression pseudogene PTENP1 PTEN miRNA decoy gene regulation RNA biology oncogene tumor suppressor
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 logistical solutions structural improvements interpersonal communication wait time reduction patient flow management resource allocation hospital design equipment maintenance staff training technology integration queue management systems patient satisfaction operational efficiency emergency room management healthcare workflow patient flow management staffing optimization technology integration waiting room design appointment scheduling interdisciplinary collaboration resource allocation queuing theory telemedicine implementation infection control measures patient triage systems staff training programs facility layout adjustments healthcare optimization crowded hospitals supply chain management patient flow analysis interprofessional collaboration structural reforms logistical improvements hospital capacity planning wait time reduction patient satisfaction metrics healthcare workflow optimization crowded hospital management strategic healthcare planning logistical efficiency in healthcare structural improvements in healthcare interpersonal communication in healthcare healthcare resource allocation hospital layout redesign patient flow improvement staff training in healthcare healthcare optimization crowded clinics logistics improvement interpersonal communication structural changes efficiency metrics patient flow management time management strategies resource allocation wait time reduction healthcare optimization crowded hospital management logistical workflow interpersonal communication structural improvements patient flow analysis waiting room design hospital layout effective triage resource allocation strategies healthcare optimization crowded hospitals logistics management structural improvements interpersonal communication patient flow analysis resource allocation wait time reduction hospital layout design staff training technological integration healthcare optimization operational logistics patient flow management waiting time reduction staff training facility design technology integration workflow analysis resource allocation customer service improvement queue management systems interdisciplinary collaboration emergency room efficiency healthcare analytics telemedicine implementation healthcare optimization crowded hospitals logistical improvements structural changes interpersonal communication efficency metrics patient flow management hospital capacity staffing issues technology integration healthcare optimization patient flow management staff coordination facility layout technological integration wait time reduction operational workflow telemedicine implementation resource allocation customer service training
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. vitamin D deficiency multiple sclerosis vitamin D levels serum vitamin D low vitamin D MS risk factors vitamin D deficiency multiple sclerosis vitamin D levels serum vitamin D MS risk folate levels B12 deficiency sunlight exposure geographical location ethnicity age sex D3 supplementation D2 D dietary sources autoimmune diseases VitD deficiency vitamin D deficiency multiple sclerosis risk fatty liver disease VDR gene obesity autoimmune disorders calciferol 25-hydroxyvitamin D UVB exposure seasonal variation vitamin D deficiency multiple sclerosis risk factors serum vitamin D levels low vitamin D and MS vitamin D supplementation benefits vitamin D deficiency symptoms autoimmune diseases vitamin D vitamin D and neurological health vitamin D deficiency multiple sclerosis risk factors serum levels immunology epidemiology vitamin D supplementation autoimmune diseases vitamin D levels multiple sclerosis risk serum vitamin D low vitamin D MS vitamin D vitamin D deficiency autoimmune diseases neurological disorders dietary vitamin D vitamin D supplementation vitamin D deficiency multiple sclerosis vitamin D levels serum vitamin D low vitamin D MS risk Vitamin D insufficiency demyelinating diseases Vitamin D supplementation autoimmune disorders vitamin D deficiency multiple sclerosis vitamin D levels serum vitamin D low vitamin D MS risk vitamin D and MS vitamin D insufficiency vitamin D supplementation D3 and MS VitD and MS vitamin D deficiency multiple sclerosis risk factors serum levels clinical outcomes vitamin D supplementation immunological response genetic predisposition epidemiology nutritional health autoimmune diseases vitamin D deficiency multiple sclerosis risk factors serum 25-hydroxyvitamin D autoimmune diseases inflammatory response epidemiological studies supplementation benefits
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 process intracellular protein uptake amino acid absorption cell nutrient acquisition endocytic vesicle formation membrane invagination nutrient sensing pathways macropinocytosis mechanism amino acid uptake cellular process intracellular transport protein absorption biological uptake process macropinocytosis mechanism amino acid uptake cellular process intracellular transport molecular biology macropinocytosis mechanism amino acid uptake intracellular process protein absorption cellular nutrient acquisition endocytosis function biological transport cell metabolism nutritional sourcing molecular biology processes macropinocytosis amino acids intracellular uptake protein cell metabolism endocytosis nutrient acquisition membrane invagination fluid phase endocytosis lysosome signaling molecules macropinocytosis mechanism amino acid absorption cellular uptake processes protein internalization nutrient acquisition methods endocytosis types macromolecule ingestion biological transport mechanisms macropinocytosis intracellular amino acids protein uptake cellular process endocytosis nutrient acquisition biological transport cellular nutrition Macropinocytosis intracellular uptake amino acids protein absorption cellular nutrition endocytosis process nutrient acquisition macropinocytosis amino acids intracellular uptake protein cellular processes nutrient acquisition membrane invagination endocytosis cell biology biological transport cellular metabolism macropinocytosis mechanisms amino acid absorption cellular uptake processes protein intake endocytosis types nutrient acquisition biological transport cell metabolism receptor-independent endocytosis intracellular trafficking membrane invagination lysosomal processing
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 parasite interference Th2 response inflammation pathogen interaction immunomodulation helminths immune system macrophages IL-4 Mycobacterium tuberculosis parasitic worms infection immunology pathogen interaction cytokines immune response modulation helminths immune system macrophages IL-4 Mycobacterium tuberculosis Th2 response inflammation infection immunomodulation parasite/protozoan interactions cytokines antigen presentation granuloma formation helminth infection immune evasion macrophage activation IL-4 signaling tuberculosis pathology parasite-host interaction immunomodulation microbial replication Th2 response chronic infection helminths immune system macrophages IL-4 Mycobacterium tuberculosis cytokines inflammation parasite infection Th2 response antigen presentation cell signaling Helminths immune system macrophages IL-4 Mycobacterium tuberculosis infection immunity pathogenesis host-parasite interactions cytokines helminths immune system macrophages IL-4 Mycobacterium tuberculosis parasite interference inflammation immunology pathogen interaction cytokines Th2 response host defense chronic infection immune evasion helminths immune system macrophages IL-4 Mycobacterium tuberculosis parasite interference cytokine response immune evasion infection biology microbiology helminths immune system macrophages IL-4 Mycobacterium tuberculosis infection disease parasite immune response macrophage activation suggestive terms query expansion biological interaction immune modulation tuberculosis infection helminth infection parasitic infection immune evasion immune regulation immune dysfunction macrophage cytokine production immune signaling host defense immunology bioinformatics genetic factors microbial interactions molecular biology cellular immunity innate immunity adaptive immunity immune checkpoint inhibitors antigen presentation T cell activation B cell response helminth infections immune evasion macrophage activation IL-4 cytokine Mycobacterium tuberculosis Th2 response parasite interference granuloma formation chronic infection immunity modulation
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. infection human T-cell lymphotropic virus type 1 African origin prevalence epidemiology transmission risk factors infection human T-cell lymphotropic virus African origin frequency prevalence study population genetics transmission risk factors clinical manifestations Infection Human T-cell Lymphotropic Virus African Origin Epidemiology Prevalence Risk Factors Transmission Diagnosis Treatment infection human t-cell lymphotropic virus African origin frequency prevalence transmission risk factors epidemiology demographics genetics immunology virology health clinical population studies research diagnosis treatment preventive measures public health policy education awareness infection T-cell lymphotropic virus African origin HTLV-1 HIV AIDS HVTN retrovirus infectious diseases African ancestry T-lymphotropic virus HIV retrovirus lymphoma immunology Viral infections African populations Blood transfusion risks infection T-cell lymphotropic virus African origin HTLV-1 population frequency transmission risk factors epidemiology infection human T-cell lymphotropic virus African origin prevalence HTLV-1 HIV AIDS transmission risks immunology epidemiology clinical symptoms diagnosis treatment public health genetics race ethnicity 流行病学 免疫学 临床症状 诊断 治疗 公共卫生 遗传学 种族 ethnicity Infection human T-cell lymphotropic virus African origin prevalence epidemiology transmission HIV immunodeficiency subtype clinical manifestations risk factors infection human T-cell lymphotropic virus HTLV-1 African origin prevalence epidemiology risk factors transmission diagnosis treatment
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 purity rates stem cell research biotechnology cellular biology hematology cancer therapy molecular biology Hematopoietic Stem Cell Purification Techniques Methods Biotechnology Purity Rate Research Advances Clinical Applications Isolation Technologies Efficiency Hematopoietic Stem Cell Purification Techniques Methods Procedures Bioengineering Biotechnology Isolation Cancer Therapy Research Efficiency Technologies Advances Hematopoietic Stem Cell isolation Hematopoietic Stem Cell separation Hematopoietic Stem Cell enrichment Stem Cell purification techniques Stem Cell separation methods Hematopoietic Stem Cell yield improvement Hematopoietic Stem Cell harvesting Stem Cell technology advancements Hematopoietic Stem Cells purification techniques methods protocols biological research advancements biotechnology clinical applications isolation technologies efficiency enhancement medical oncology immunology Hematopoietic Stem Cell isolation Hematopoietic Stem Cell separation Hematopoietic Stem Cell enrichment Hematopoietic Stem Cell techniques Stem Cell purification methods High purity Hematopoietic Stem Cells Hematopoietic Stem Cell extraction Advanced Hematopoietic Stem Cell purification Hematopoietic Stem Cells purification techniques cell separation molecular markers flow cytometry affinity chromatography stem cell biology purity assessment biological research Hematopoietic Stem Cells purification techniques 50% purity cell separation molecular markers biological techniques hematology research methods clinical applications Hematopoietic Stem Cells purification techniques purity rate cell separation biotechnology medical research stem cell therapy hematology clinical applications Hematopoietic Stem Cell isolation Hematopoietic Stem Cell separation Hematopoietic Stem Cell enrichment Hematopoietic Stem Cell techniques Stem Cell purification methods Stem Cell yield improvement Blood stem cell extraction Hematopoietic Stem Cell technology advancements
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 regulation signaling pathway cellular response molecular biology oncology developmental biology YAP1 TEAD nuclear translocation transcription factors DNA-binding proteins gene transcription signaling pathway cellular proliferation organ development Hippo pathway YAP1 TEAD nuclear translocation transcription factors DNA-binding proteins gene regulation transcriptional complex cellular signaling biological pathways YAP1 TEAD nucleus translocation transcription factors DNA-binding proteins target gene transcription molecular biology signaling pathway gene regulation cell proliferation organ development Hippo pathway oncogenesis RNA binding proteins chromatin modification gene expression cellular response developmental biology epigenetics tissue homeostasis protein-protein interaction signaling network gene regulation mechanisms YAP1 TEAD nucleus transcription factors DNA-binding target genes modulation molecular biology cell signaling YAP1 TEAD nuclear translocation transcription factors DNA-binding proteins gene regulation signaling pathway cellular metabolism developmental biology organogenesis oncogenesis YAP1 TEAD nuclear translocation transcription factors DNA-binding proteins gene transcription regulatory proteins cellular signaling molecular biology oncogenes YAP1 TEAD nucleus transcription factors DNA-binding proteins target gene modulation complex integration regulation molecular biochemistry signaling YAP1 TEAD nucleus transcription factors DNA-binding target genes modulation molecular biology cell signaling GTPase protein interaction translocation mRNA expression biological pathway genome regulation organogenesis pulmonary fibrosis cancerbiology YAP1 TEAD nucleus transcription factors DNA-binding proteins gene transcription cellular signaling organ development stem cell biology cancer research
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 optimized kidney paired donation national kidney program patient participation impact healthcare efficiency improvements organ donation optimization medical cost reduction transplant program enhancement patient waitlist management healthcare cost savings kidney transplant waiting list optimized kidney paired donation patient participation organ donation program effectiveness healthcare efficiency medical cost reduction transplant waiting times national kidney program improvement healthcare optimization kidney transplant等候 program improvement national kidney paired donation nephrology efficiency patient wait time reduction medical cost savings transplant matching programs public health improvement health care cost savings kidney transplant waiting list optimize organ donation national kidney paired donation program benefits patient participation impact healthcare efficiency improvement transplant waiting times reduction organ donation optimization strategies US health care system optimization kidney transplants national kidney paired donation program savings patient wait time medical efficiency healthcare costs transplantation programs healthcare optimization kidney transplant waiting list national kidney paired donation patient participation savings potential transplant efficiency program effectiveness healthcare system kidney transplant optimization national kidney paired donation program savings patient waiting time organ donation program healthcare cost reduction health care cost savings kidney transplant optimization national kidney paired donation patient wait time reduction medical program efficiency healthcare cost reduction organ donation pairing healthcare system improvement transplant program enhancement healthcare cost savings kidney transplant waiting list optimized kidney paired donation national kidney program potential savings medical patient participation impact transplant optimization programs healthcare cost savings kidney transplant optimization national kidney paired donation program patient wait times healthcare efficiency organ donation matching medical cost reduction public health improvement transplantation programs healthcare policy improvement
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 physiological process nitric oxide protein modification molecular biology effectiveness suggestions query expansion S-nitrosylation GAPDH histone deacetylases physiology transnitrosylation nitric oxide molecular biology enzymology proteomics biomarkers research techniques S-nitrosylation GAPDH histone deacetylases physiology nitrosative stress molecular biology enzymatic activity protein-protein interaction cell signaling/pathways transnitrosylation post-translational modification S-nitrosylation GAPDH histone deacetylases physiological process nitric oxide signaling protein modification molecular mechanism S-nitrosylation GAPDH histone deacetylases physiological nitric oxide protein modification enzyme activity regulation molecular biology biomedical research S-nitrosylation GAPDH histone deacetylases physiological process nitric oxide proteomics molecular biology enzymology nitrosative stress S-nitrosylation GAPDH histone deacetylases physiological nitric oxide protein modification enzymatic activity nuclear receptors transcription regulation molecular biology biomedical research cellular signaling S-nitrosylation GAPDH histone deacetylases physiological nitrosylation efficacy keywords biological processes molecular mechanisms S-nitrosylation GAPDH histone deacetylases physiological processes nitric oxide protein modification enzymatic activity molecular biology transnitrosylation genetic regulation S-nitrosylation GAPDH histone deacetylases physiological process nitric oxide signaling molecular mechanism gene expression regulation biochemistry proteomics enzymology nitrosative stress transnitrosylation proteins modification cellular signaling
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 signaling RNA sensing MDA5 function Virus detection immunology rna viruses interferon pathway inflammation response PRR sensor RNA virus detection mechanism immunology viral sensing molecular biology MDA5 function RNA sensing innate immunity viral detection MDA5 function PRR role RNA virus response immunology keywords pathogen recognition molecular biology concepts PRR MDAs RNA virus detection innate immunity viral sensors MDA5 function RNA interference type I interferon response PRR signaling virus sensing molecules PRR MDA5 RNA virus infection immune response signaling pathogen recognition interferon PRR sensors RNA viruses MDA5 function infection response viral detection molecular recognition immune system activation PRR sensors RNA viruses MDA5 function antiviral response viral sensing mechanisms immunology host defense RNA helicases VIPERI pathway PRR MDA5 function RNA virus detection antiviral immunity MDA5 signaling RNA sensors infection response immunology RNA helicases virus recognition MHC presentation PRR sensors RNA viruses MDA5 function infection response Viral recognition immunology RNA helicases TIR domain proteins PRR proteins RNA sensing molecular biology viral detection immunology infection mechanisms MDBA5 protein RNA viruses immune response sensor molecules DNA damage 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 absence immunology chemokine immune response CCL19 dendritic lymph nodes lymphatic trafficking chemokine immune response antigen presentation inflammation T cells CCL19 dendritic lymph nodes expression immunology absence inflammation immune response chemokine T cells CCL19 dendritic cells lymph node immunology chemokine lymphocyte trafficking inflammation immune response lymphadenopathy lymphoma T cell recruitment CCR7 HIV autoimmunity CCL19 dendritic cells lymph node migration immune response inflammation chemokine antigen presentation CCL19 dendritic cells lymph nodes immune response chemokine lymph node function T cell trafficking CCL19 dendritic cells lymph nodes immune response inflammation chemokine lymphocyte trafficking antigen presentation CCL19 dLNs lymph nodes immune response inflammation chemokine lymphocyte trafficking CCL19 dendritic cells lymph node migration trafficking immune response lymphatic tissue chemokine inflammatory response CCL19 dendritic cells lymph node lymphatic tissue immune response inflammation antigen presentation chemokines T cells immunology lymphoid organs
870	Obesity decreases life quality. Obesity decreases life quality. Obesity decreases life quality. Obesity decreases life quality. Obesity decreases life quality. obesity life quality health mortality longevity diet exercise fat BMI metabolic complications obesity life quality health mortality weight management BMI obesity complications lifestyle factors diet exercise metabolic disorders obesity health lifespan quality of life weight management metabolic disorders cardiovascular disease diabetes mortality obesity prevalence obesity impact obesity impacts health obesity linked longevity obesity reduces lifespan obesity affects well-being obesity health risks obesity quality of life obesity mortality rate obesity life quality health longevity overweight fat medical conditions nutrition exercise mortality obesity index body mass index BMI metabolic disorders physical activity diet cardiovascular disease diabetes obesity prevalence public health health issues weight gain risk factors complications diet effects lifestyle choices obesity life quality health impact mortality risk chronic diseases physical fitness nutrition sedentary lifestyle metabolic syndrome obesity prevalence obesity life quality health impacts reduced longevity weight management obesity complications fitness level metabolic disorders physical activity dietary habits obesity life quality health nutrition physical activity BMI metabolic disorders longevity obesity prevention lifestyle changes dietary habits obesity health risk factors life expectancy diet exercise mortality rates impact diabetes cardiovascular
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 DNA stability molecular dynamics cancer therapy biomolecules chromosomal ends biophysics nucleic acids Pyridostatin G-quadruplex telomeric region DNA stability molecular dynamics biophysical properties nucleic acids anticancer drugs pyridostatin telomeric region G-quadruplex stability anticancer drug biological activity molecular structure therapeutic potential pyridostatin mechanism G-quadruplex structure telomeric DNA stability telomere function pyridostatin binding DNA quadruplex telomere biology pyridostatin research telomerase inhibition DNA conformation Pyridostatin telomeric region G-quadruplex search efficiency molecular targeted therapy telomerase inhibition biochemistry biophysics molecular biology pyridostatin G-quadruplex telomeric region chromosome ends molecular biology genetics anti-cancer drug specialized chemistry biomedical research Pyridostatin G-quadruplex telomeric region telomeres molecular dynamics biophysics nucleic acids stability binding affinity Pyridostatin telomeric region G-quadruplex destabilization therapy molecular biology antitumor activity Pyridostatin G-quadruplex telomeric region telomerase inhibition molecular dynamics single-stranded DNA stabilization anticancer agent biophysical techniques Pyridostatin mechanism G-quadruplex stabilization telomere function DNA structure anticancer drugs molecular dynamics chromosomal instability
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 genetics lifestyle diet exercise metabolism genetics lifestyle diet exercise metabolism socioeconomic cultural hormonal genetic predisposition urbanization genetics lifestyle metabolism socioeconomic nutrition physical activity epigenetics geneticFactors metabolicRate lifestyleChoices caloricIntake physicalActivity hormonalInfluences socioeconomicStatus dietQuality sleepPatterns stressLevels genetics diet exercise hormones metabolism obesogenic factors prevalence population studies research public health individual behavior biology obesity genetics obesity metabolism environmental impact obesity lifestyle and obesity genetic factors obesity genetics diet exercise metabolism lifestyle socioeconomic culture genetics epigenetics genetic Factors metabolic Rate lifestyle Choices dietary Habits physical Activity Level hormonal Influences socioeconomic Status obesity Epidemic public Health Measures individual Responsibility nutritional Education sedentary Behaviors obesity environmental factors diet genetics exercise study causes prevalence societalimpact genetics metabolism lifestyle diet physical activity socioeconomic status epigenetics
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 immune response viral detection signal transduction innate immunity molecular structure domain analysis PRR proteins RNA recognition molecular domain MDA5 function immunology RNA helicase DExD/H domain immune response viral detection RNA binding PRR proteins innate immunity RNA recognition helicase activity viral detection molecular function immunology pathogen recognition MDA5 protein RNA binding domain PRR proteins RNA recognition motif MDA5 function DExD/H box RNA binding domain Viral RNA detection Type I interferon response PRR MDA5 RNA helices domain immune recognition pattern binding PRR proteins innate immunity RNA recognition viral detection helicase domain interferon induction immune response molecular biology PAMP recognition antiviral defense PRR proteins MDA5 function RNA recognition immune system viral detection helical domains innate immunity molecular biology immunology PRR proteins RNA recognition molecular domains MDA5 function DExD/H box immune response viral detection RNA binding PRR proteins MDA5 function RNA recognition DExD/H box innate immunity viral detection molecular structure antigen receptors signaling pathways PRR proteins MDA5 function RNA recognition DExD/H box immune response viral detection signaling pathway
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. thigh-high GCS deep vein thrombosis acute stroke hospitalized patients mobility prevention evidence review clinical trial compression therapy immobility risk factors vascular health thigh length GCS deep vein thrombosis acute stroke immobile hospitalization evidence review clinical trial compression therapy RV thrombosis compression therapy deep vein thrombosis prevention stroke rehabilitation hospital-acquired conditions immobility risks thrombosis treatment clinical trials vascular health medical garments patient mobility hospital patients thrombophlebitis venous insufficiency compression socks thrombus formation preventive measures patient outcomes acute stroke management medical compression healthcare interventions compression stockings deep vein thrombosis acute stroke hospital admission immobility prevention clinical trial effectiveness patient outcomes thigh-length GCS deep vein thrombosis acute stroke immobile hospital evidence meta-analysis compression stockings deep vein thrombosis acute stroke immobile patients hospital admissions thrombosis prevention GCS efficacy medical compression garments thrombosis immobility acute stroke compression therapy DVT hospitalization rehabilitation leg support medical compression vascular health patient mobility clinical trial prevention methods thigh-length GCS deep vein thrombosis immobile acute stroke efficacy keyword expansion beneficial keywords thigh-length GCS deep vein thrombosis immobile acute stroke patients hospital compression stockings evidence meta-analysis clinical trials prevention venous stasis ultrasound prophylaxis randomized controlled treatment effectiveness compression garments acute stroke rehabilitation thrombosis prevention patient mobility medical compression socks hospital-acquired thrombosis immobilization risk venous insufficiency treatment clinical trial outcomes DVT reduction studies
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 risks pulmonary function fitness levels health outcomes aerobic capacity physical activity cardiovascular health mortality risk fitness levels exercise impact pulmonary function survival rates physical activity health outcomes cardiovascular health mortality risk fitness levels pulmonary function health outcomes exercise impact sports medicine physiological measures cardiovascular health mortality risks pulmonary function outcome analysis fitness levels health impact cardiopulmonary exercise life expectancy cardiorespiratory endurance longevity mortality exercise fitness cardiovascular pulmonary health survival physical activity cardiovascular health mortality risk pulmonary function fitness levels health outcomes cardiovascular health mortality risk pulmonary function fitness levels health outcomes physical activity cardiovascular health mortality risk fitness levels pulmonary function health outcomes research studies exercise impact physical activity cardiovascular health mortality risks pulmonary function outcome analysis fitness levels health impact研究方向 运动强度 生命质量 cardiovascular health respiratory function longevity exercise intensity endurance training mortality risk fitness levels physical activity health outcomes
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. dietary calcium hyperparathyroidism prevention vitamin D 25(OH)D levels bone health calcium absorption kidney function osteoporosis risk mineral metabolism nutritional guidelines calcium supplementation vitamin D levels hyperparathyroidism risk bone health nutritional guidelines renal disease osteoporosis prevention metabolic bone disease calciferol phosphorus metabolism renal function mineral homeostasis dietary recommendations secondary hyperparathyroidism management calcium supplementation vitamin D secondary hyperparathyroidism bone health renal function osteoporosis nutrition guidelines metabolic bone disease end-stage renal disease 25-hydroxyvitamin D parathyroid hormone dietary recommendations calcium supplementation vitamin D levels hyperparathyroidism risk bone health maintenance nutritional recommendations metabolic bone disease renal function osteoporosis prevention mineral absorption hormonal balance chronic kidney disease nutritional guidelines endocrine disorders calcium supplementation vitamin D secondary hyperparathyroidism bone health renal function osteoporosis nutrition guidelines calcium supplementation vitamin D secondary hyperparathyroidism bone health nutritional recommendations kidney disease osteoporosis prevention calcium supplementation vitamin D secondary hyperparathyroidism bone health nutritional requirements renal function osteoporosis prevention calcium intake secondary hyperparathyroidism vitamin D 25(OH)D levels bone health kidney function osteoporosis phosphorus balance renal impairment nutritional guidelines end-stage renal disease dietary recommendations calcium supplementation vitamin D levels secondary hyperparathyroidism bone health renal function osteoporosis risk nutritional guidelines metabolic bone disease mineral homeostasis hormonal regulation calcium supplementation vitamin D levels hyperparathyroidism risk bone health nutritional guidelines renal function osteoporosis prevention mineral metabolism dietary recommendations end-stage renal disease chronic kidney disease
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 acetylation lysine residues proteomics protein function molecular biology epigenetics ubiquitination histone acetylation post-translational modification acetylation lysine proteomics signaling pathways epigenetics molecular biology ubiquitination deacetylation mass spectrometry post-translational modification lysine acetylation protein acetylation acetyltransferase ubiquitination SUMOylation phosphorylation deacetylation histone acetylation proteomics post-translational modification lysine acetylation proteomics epigenetics protein function acetyltransferase deacetylase histone acetylation signaling pathways cellular metabolism post-translational modification lysine acetylation human cells proteins proteins post-translational modification lysine acetylation relevant phrases recommendation search performance elevate performance human cells molecular biology post-translational modification acetylation lysine human proteins biochemical modifications post-translational modification acetylation lysine residues protein modification human cells beneficial expansion keywords post-translational modification lysine acetylation protein acetylation ubiquitination SUMOylation phosphoacetylation acetyltransferase deacetylase proteomics mass spectrometry post-translational modification lysine acetylation proteomics epigenetics ubiquitination SUMOylation phosphorylation
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 enzyme inositol lipid metabolism PtdIns(3 4)P2 phosphatidylinositol 4-phosphate tumor suppressor PI3K pathway cellular signaling phosphatase activity PIP2 conversion lipid kinases PTEN function inositol lipid metabolism PIP2 conversion PI4P production phosphatase activity tumor suppressor lipid signaling cellular proliferation molecular biology genetic disorder cancer research biochemical pathway PTEN function phosphatase activity inositol lipids PtdIns(3 4)P2 PI(4)P signaling pathway tumor suppressor lipid metabolism cell growth regulation PTEN function inositol lipid metabolism PtdIns(3 4)P2 conversion phosphatidylinositol 4-phosphate tumor suppressor PTEN lipid signaling pathways PIP2 regulation PTEN activity lipid phosphatases PtdIns(3 4 5)P3 PI(4)P synthesis PTEN mutation cancer biology cellular signaling lipid second messengers PIP kinases lipidomics PTEN protein structure Inositol lipid PTEN Ptdlns(3 4)P phosphatidylinositol 4-phosphate enzyme metabolism molecular biochemistry research signaling pathway mechanism molecules biology cancer genetics cellular regulation diagnosis treatment PTEN function inositol lipid metabolism PtdIns(3 4)P2 phosphatidylinositol 4-phosphate tumor suppressor PI3K pathway lipid signaling cellular metabolism molecular biology cancer research inositol lipid PTEN Ptdlns(3 4)P phosphatidylinositol 4-phosphate molecular biochemistry enzymology cellular/signaling metabolism PTEN function phosphatase activity lipid metabolism PtdIns(3 4)P2 PI(4)P conversion tumor suppression PI3K pathway cellular signaling autophagy regulation lipid phosphate biosynthesis Inositol lipid PTEN phosphatase Ptdlns(3 4)P 2 phosphatidylinositol 4-phosphate molecular biochemistry enzymology research biology cellular signaling mechanism functions substrates kinases preservation pathway dynamics molecular biology protein function metabolism cell signaling signal transduction gene expression membrane cell biology genetics metabolic pathways enzyme activity biological processes biomolecules phosphorylation cellular components cell PTEN function lipid metabolism phosphatidylinositol PtdIns(3 4 5)P3 tumor suppression PI3K pathway cellular signaling PI(4)P production phosphatase activity
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 pulmonary health chronic respiratory disease risk factors CRP testing COPD complications chronic lung disease inflammation markers pulmonary health risk factors COPD management CRP levels COPD exacerbations inflammation markers chronic obstructive pulmonary disease risk factors inflammatory response cardiovascular health immune response CRP levels COPD complications COPD inflammation chronic obstructive pulmonary disease risk factors C-reactive protein pulmonary disease management reducing COPD exacerbations CRP and COPD chronic respiratory disease CRP COPD exacerbations inflammation pulmonary disease risk factors CRP levels COPD management chronic obstructive pulmonary disease inflammation markers reduced exacerbations CRP testing pulmonary health clinical outcomes inflammatory biomarkers COPD complications CRP levels COPD complications COPD management Inflammation markers COPD exacerbation prevention CRP testing COPD management chronic inflammation pulmonary health risk reduction exacerbation prevention CRP levels COPD exacerbations inflammation pulmonary health chronic obstructive pulmonary disease risk factors clinical outcomes CRP levels COPD management chronic inflammation pulmonary health risk factors reducing exacerbations inflammatory markers clinical outcomes
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 care physical health care professional input homelessness reduction healthcare providers social impact psychological support therapeutic interventions community health wellness programs mental health professionals physical health care input effectiveness decreasing homelessness strategies healthcare provider insights mental health interventions physical health contributions interdisciplinary approach healthcare professional opinions reducing homelessness methods mental health professionals physical health care input effectiveness reducing homelessness healthcare providers social work input psychological perspectives healthcare integration public health impacts therapeutic approaches mental health professionals physical health care providers healthcare input effective interventions decreasing homelessness strategies professional collaboration mental health care physical health impact reducing homelessness expert opinions healthcare effectiveness mental health care physical health care professional input homelessness reduction effective strategies health care providers social services community support public health intervention methods mental health interventions physical health care healthcare professional collaboration effective strategies homelessness reduction mental healthcare providers physical health services professional input homelessness prevention health care effectiveness mental health care physical health care professional input homelessness prevention effectiveness social care counseling therapy intervention strategies healthcare providers community support mental health disorders substance abuse chronic illnesses rehabilitation programs patient outcomes public health socioeconomic factors policy recommendations empirical evidence clinical practice case management supportive housing psychological well-being health services research homeless population long-term solutions interdisciplinary approach mental health professionals physical health care providers healthcare integration effective interventions homelessness reduction professional input health care collaboration clinical expertise social health impact patient outcomes mental health professionals physical health care providers healthcare integration homelessness reduction effective interventions professional collaboration social services patient perspectives community health workers psychiatric nurses psychologists counselors public health homelessness prevention mental health disorders substance abuse chronic illness management healthcare policy patient outcomes behavioral health home health care telehealth primary care holistic approach patient advocacy public health strategies health equity social determinants healthcare access interdisciplinary teams patient-centered care evidence-based practices health promotion preventive care health disparities health system reform health literacy health education health screenings patient mental health professionals physical health care providers healthcare integration homelessness prevention professional input effective interventions mental health care physical health contributions interdisciplinary approach healthcare professionals' role
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. ribosome IncRNAs non-coding RNA functional peptides translation mRNA protein synthesis IncRNAs ribosomes occupancy functional peptides translation RNA gene expression molecular biology non-coding RNA protein synthesis IncRNAs ribosomes occupancy functional peptides mRNA translation RNA binding molecular biology gene expression non-coding RNA protein synthesis ribosome Occupancy IncRNAs function RNA interference non-coding RNA role peptide production inhibition translational regulation ribosomal binding genetic expression impact molecular biology techniques Ribosomes IncRNAs functional peptides occupancy mRNA effect translation biology molecular genetics ribosome occupancy IncRNAs non-coding RNA translational efficiency peptide synthesis mRNA binding regulatory RNA IncRNAs ribosome occupancy functional peptides non-coding RNA translational initiation mRNA binding proteins ribosome IncRNAs functional peptides RNA occupancy translational efficiency non-coding RNA mRNA competition protein synthesis inhibition regulatory RNA ribosome IncRNAs non-coding RNA peptide synthesis translational occupancy gene expression RNA binding proteins post-transcriptional regulation molecular biology ribonucleoprotein transcriptomics IncRNAs ribosomes functional peptides mRNA translation bioinformatics genomics transcription ribonucleoprotein protein synthesis microRNA RNA interference
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. high copeptin copeptin levels diabetes risk glucose regulation endocrine system hormone function pancreatic health insulin resistance metabolic markers cardiovascular disease copeptin diabetes glucose insulin endocrinology biomarker cardiovascular electrolytes pancreatic inflammation high sensitivity copeptin diabetes risk factors insulin glucose levels cardiovascular endoocrine endocrinology copeptin diabetes risk factors copeptin levels and diabetes copeptin testing for diabetes copeptin and glucose regulation copeptin measurement in diabetes研究 copeptin role in diabetes prevention copeptin vs insulin resistance copeptin and beta cell function copeptin biomarker diabetes copeptin and type 2 diabetes copeptin diabetes glucose insulin endocrinology metabolic markers cardiovascular risk pancreatic function hormone regulation copeptin levels diabetes risk factors hormone regulation glucose metabolism endocrine system medical research biomarkers clinical guidelines copeptin blood test diabetes risk factors insulin resistance hormones prediabetes glycemiccontroldiabetes copeptin diabetes risk factors clinical markers blood test levels study evidence copeptin diabetes risk factors hormone pancreatic function glucose insulin resistance cardiovascular health endocrine system metabolic markers copeptin diabetes risk factors copeptin levels and diabetes copeptin measurement for diabetes copeptin and glucose regulation copeptin in pancreatic function copeptin test diabetes screening copeptin cardiovascular disease copeptin insulin interaction copeptin hormone relationship copeptin and 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. Artemisinin combination therapy nongametocytocidal drugs malaria transmission mathematical models efficacy public health antimalarial treatment epidemiology parasitology vector control clinical trials drug resistance mathematical modeling malaria transmission Artemisinin-based combination therapy nongametocytocidal drugs effectiveness public health population dynamics drug resistance disease modeling simulation studies mathematical modeling malaria treatment artemisinin combination therapy gametocytocidal drugs effective malaria control reducing malaria传播 疟疾传播_reduction 抗青蒿素联合疗法 非杀配子体药物 Artemisinin-based combination therapy benefits nongametocytocidal drugs comparison malaria transmission reduction strategies mathematical model applications public health interventions drug efficacy analysis parasite lifecycle impact healthcare policy recommendations long-term transmission dynamics clinical trial outcomes Artemisinin combination therapy nongametocytocidal drugs malaria transmission predictive modeling public health antimalarial efficacy drug resistance transmission dynamics Artemisinin-based combination therapy malaria transmission reduced nongametocytocidal drugs mathematical models predictive analysis effective treatment malaria control drug efficacy public health impact Artemisinin combination therapy nongametocytocidal drugs malaria transmission mathematical models drug efficacy public health parasitic infections antimalarial treatment vector control drug resistance clinical outcomes Artemisinin combination therapy nongametocytocidal drugs malaria transmission predictive modeling public health antimalarial treatment epidemiology drug resistance transmission dynamics Artemisinin combination therapy nongametocytocidal drugs malaria transmission predictive models public health drug efficacy parasitic infections treatment strategies epidemiology global health antimalarial drugs Artemisinin gametocytocidal malaria transmission drug efficacy predictive modeling public health intervention parasitic treatment
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 albendazole biological health effectiveness lymphatic filariasis treatment antiparasitic medications parasites buruli eczematoid dermal infection lymphatic diseases filariasis treatment medications parasites health symptoms cures prevention drugs side effects lymphatic filariasis treatment albendazole dosage albendazole side effects albendazole parasites filariasis management antifilarial drugs drug albendazole albendazole dosage lymphatic filariasis treatment filariasis albendazole lymphatic filariasis control albendazole lymphatic filariasis parasitic infections tropical diseases antihelminthic treatment medication efficacy side effects drug resistance lymphatic filariasis treatment Albendazole dosage side effects Albendazole Albendazole efficacy albendazole prescription lymphatic filariasis treatment Albendazole dosage Albendazole side effects lymphatic filariasis symptoms Albendazole medication guide lymphatic_filariasis_treatment albendazole_indications parasitic_infections antiparasitic_drugs filarial_disease_management lymphatic_filariasis treatment malaria parasitic_infections antiparasitic_drugs medication public_health drug_delivery global_health medical_treatment lymphatic filariasis treatment albendazole dosage parasitic infections filarial worms antihelminthic drugs public health tropical diseases
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 biochemistry molecular interactions structural biology protein function alizarin hydrogen bonds PGAM1 substrate binding residues protein structure biochemical interactions alizarin hydrogen bonds PGAM1 substrate binding residues biochemistry protein interactions molecular docking ligand binding structural biology Alizarin binding sites PGAM1 structure hydrogen bond interactions residue mapping substrate recognition protein-ligand interactions biochemical assays molecular dynamics simulations alizarin chemical properties PGAM1 function biochemical pathways Alizarin hydrogen bonds PGAM1 substrate binding residues Alizarin molecule hydrogen bond formation PGAM1 protein substrate interaction chemical residue bonding biochemical interactions molecular recognition ligand binding site Alizarin hydrogen bonds PGAM1 substrate binding residues protein interactions structural biology biochemistry molecular recognition Alizarin hydrogen bonds PGAM1 substrate binding molecular interactions alizarin hydrogen bonds PGAM1 substrate binding protein structure molecular interactions biochemistry residue specificity ligand binding site structural biology alizarin interactions hydrogen bond donors PGAM1 protein substrate binding sites molecular docking bioinformatics analysis structural biology enzyme inhibitors chemical compounds functional groups
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 prevention community centers affordable housing educational resources urban planning public libraries shelter access student support social services city policies youth homelessness safe spaces study areas homelessness solutions educational accessibility housing support community resources youth homelessness urban planning public spaces social services safe study spaces homelessness prevention educational resources housing accessibility community centers urban planning social services poverty levels education impact public facilities safe study spaces homelessness reduction affordable housing student accommodation community centers library resources urban planning public spaces safety education access poverty alleviation safe study spaces homelessness prevention educational resources affordable housing community centers university facilities public libraries urban planning socioeconomic factors mental health support safe study spaces homeless prevention strategies community resources educational accessibility housing support services urban planning public spaces safety student well-being homelessness statistics resource allocation neighborhood development safe study spaces homeless shelters affordable housing community centers educational resources poverty alleviation social services urban planning public libraries youth programs safe study spaces homelessness prevention educational accessibility community resources youth shelters affordable housing learning environments public libraries student safety urban planning social services safe study spaces homelessness prevention educational accessibility affordable housing community resources urban planning social equity learning environments public spaces poverty reduction safe_spaces studying_environments homelessness_reduction community_centers youth_shelters educational_facilities social_services urban_design public_policy mental_health_support crime_prevention access_to_resources student_wellbeing local_government_initiatives nonprofit_organizations education_accessibility cultural_background age_groups gender_issues disability_inclusivity mental_health physical_safety financial_assistance volunteer_programs emergency_shelter health_care job_training legal_assistance environmental_factors transportation_access
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 reduction educational accessibility shelter for students academic environments housing for learners learning facilities safety community resources for education safe study spaces homelessness prevention educational facilities community learning centers affordable workspaces sheltered study areas academic support hubs housing insecurity solutions safe study spaces homeless prevention educational facilities community resources affordable learning environments shelter access learning safety housing solutions safe study spaces homeless reduction strategies community learning centers affordable study areas educational facility access housing support programs urban study hubs safe study spaces homelessness prevention community resources educational support housing solutions youth shelters learning environments urban planning social services public spaces safe study spaces homeless prevention strategies community learning centers reducing homelessness accessible study areas educational resource hubs urban study spots affordable learning environments impact of study locations safe havens for students safe study spaces homeless prevention community resources educational accessibility shelter proximity learning environments poverty reduction urban planning social support networks safe study spaces homeless reduction community learning centers educational accessibility sheltered study areas poverty alleviation through education safe study spaces homelessness prevention community centers libraries affordable housing education accessibility urban planning social services youth shelters public spaces safety safe study spaces homeless reduction strategies community resources educational accessibility housing support programs learning environments safety urban planning solutions academic shelter options poverty alleviation techniques public space utilization
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 structural rearrangements charge zipper mechanism protein transport bacterial secretion molecular dynamics electrostatic interactions proton motive force class1 Tat system TatAd complexes charge zipper mechanism structural rearrangements Class1 TatAd protein transport bacterial secretion molecular dynamics ion binding membrane protein translocase E. coli Tat pathway TatAd complexes charge zipper mechanism structural rearrangements protein transport bacterial secretion molecular dynamics ion binding electrostatic interactions Class1 Tat pathway TatAd complexes charge zipper mechanism structural rearrangements arm density Class1 TatAd protein transport bacterial secretion molecular biology Tat pathway ion conductivity membrane protein interaction TatAd complexes charge zipper mechanism structural rearrangements Class1 TatAd complexes protein transport bacterial secretion molecular dynamics ion channel amino acid composition protein-protein interaction membrane protein electron microscopy cryo-EM biochemical assay TatAd complexes charge zipper mechanism structural rearrangements protein transport bacterial secretion molecular dynamics ion channels membrane insertion protein assembly biological transport arm density TatAd complexes structural rearrangements Class1 TatAd complexes charge zipper mechanism protein conformation ion binding molecular dynamics simulation cryo-EM structure bacterial transport system TatAd complexes charge zipper mechanism structural rearrangements Class1 TatAd complexes protein transport bacterial secretion molecular dynamics ion conductivity membrane interaction translocase complexes arm density TatAd complexes structural rearrangements Class1 TatAd complexes charge zipper mechanism protein transport translocase membrane protein insertion biophysical properties molecular dynamics ion channel formation TatAd complexes charge zipper mechanism structural rearrangements class1 TatAd protein transport bacterial secretion molecular dynamics cryo-EM ion binding sites proton translocation
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. publicly available DNA data growth trend biotechnology molecular genetics population sequencing archive storage surge biological DNA storage genetic data growth biotechnology advancement genomic information doubling effect scientific data increase bioinformatics genetic sequencing digital genetics DNA storage genomics growth biotechnology advancement genetic data doubling molecular biology trend publicly available DNA data growth genetic data expansion doubling time DNA data genetic information doubling exponential increase DNA data genomic data growth rate public genetic database expansion DNA data growth genetic information expansion biotechnology trends genomic data increase scientific data doubling bioinformatics progress DNA data growth genomic data explosion genetic information doubling biotechnology advancements next-generation sequencingincrease genetic data storage genomic research expansion public DNA database expansion genetic information accessibility DNA data growth pubmed database genomic data increase biological information expansion DNA sequencing speed DNA data growth genomic information expansion genetic data doubling public DNA repository genetic sequencing increase biotechnology data growth genomic data surge genetic information availability doubling time technology DNA data growth genetic information expansion genomic data doubling public genetic databases biological data increase genetic material availability genomic research data genetic.data.increase molecular.biology.research pubmed databases biological.sequenceinformatics genomics.trends DNA.archiving open.access.biological.data government.genome.projects
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 ribosome occupancy IncRNAs 5' UTRs RNA binding gene expression molecular biology transcriptomics IncRNAs ribosomes occupancy 5'-UTRs molecular biology RNA binding gene expression translational control RNA occupancy ribosome binding sites IncRNAs function 5' UTRs translational regulation RNA structure molecular biology gene expression bioinformatics transcriptomics ribosomal profiling ribosome occupancy IncRNAs 5' UTRs mRNA translation gene expression RNA binding molecular biology transcriptomics ribonucleoprotein complex biogenesis regulation genetic overlap RNA structure protein synthesis cellular function molecular interaction nucleic acid transcript stability regulatory RNA alternative splicing RNA interference transcriptional regulation ribosome occupancy IncRNAs 5'UTRs mRNA regulation RNA binding transcriptional control molecular biology gene expression ribosome occupancy IncRNAs 5'UTRs RNA binding gene expression transcriptomics molecular biology regulatory RNAs IncRNAs ribosomes 5'UTRs mRNA translational regulation occupancy eukaryotic cells molecular biology RNA sequencing genomics bioinformatics microRNAs nuclear RNAs messenger RNA transcription translation post-transcriptional regulation post-translational modification structural biology protein synthesis RNA-protein interactions IncRNAs ribosomes occupancy mirror 5'UTRs beneficial expansion keywords efficacy application research biology mRNA synthesis transcription translation genetics molecular biology biomarker interaction nucleic acids cellular processes microRNA ncRNA RNA biology biotechnology omics genomics proteomics therapeutics ribosome occupancy IncRNAs 5'UTRs mRNA regulation RNA binding transcriptomics gene expression biotechnology molecular biology IncRNAs ribosomes 5'UTRs mRNA transcription translation binding/sites evidence modulation function biological processes molecular interactions genomics transcriptomics novel non-coding RNAs expression profiling cellular machinery ribosome profiling biomarkers molecular biology RNA structure post-transcriptional regulation
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 gut microbiome metabolic differences nutritional impact dietary I-carnitine omnivores vegetarians trimethylamine N-oxide metabolic differences gut microbiome dietary habits nutritional science biomarkers dietary I-carnitine omnivores vegetarians trimethylamine N-oxide gut microbiome dietary patterns nutritional differences metabolic pathways dietary I-carnitine omnivores vegetarians trimethylamine N-oxide metabolic differences gut microbiome nutritional impact dietary habits health comparison biochemical processes dietary I-carnitine trimethylamine N-oxide omnivores vegetarians metabolism diet effect biomarker health impact nutrition science intestinal microbiota dietary I-carnitine omnivores vs vegetarians trimethylamine N-oxide metabolic differences gut microbiome dietary habits nutrition science biochemistry health comparison carnitine metabolism trimethylamine N-oxide dietary I-carnitine omnivores vegetarians microbiome digestion metabolism dietary patterns nutritional biochemistry trimethylamine N-oxide omnivores vegetarians I-carnitine dietary intake microbial metabolism gut microbiome nutritional factors health implications biomarker comparative study dietary I-carnitine trimethylamine N-oxide omnivores vegetarians metabolism digestion biotics probiotics gut microbiome nutrition health food science biochemistry biomedical research clinical studies diets food intake biological markers health outcomes scientific studies biological processes enzymes microbiota biological compounds chemical compounds biological reactions biological variations health differences biological factors biological conditions biological comparisons biological analysis biological indicators biological measurement dietary I-carnitine omnivores vegetarians trimethylamine N-oxide gut microbiome metabolic differences nutritional factors dietary habits microbial metabolism dietary composition bioavailability digestion nutrient absorption health outcomes
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. insomnia treatment cognitive behavioral therapy sleep disorders psychology health management insomnia cognitive behavioral therapy effective treatments sleep disorders psychology mental health cognitive behavioral therapy sleep disorders insomnia treatment methods effects benefits population studies research treatment options cognitive strategies sleep disorders insomnia remedies psychological therapy therapy effectiveness behavioral techniques insomnia management therapy types coping mechanisms insomnia cognitive behavioral therapy effective treatments sleep disorders mental health sleeping habits psychology symptoms management tips strategies cognitive behavioral therapy insomnia insomnia treatment methods cognitive therapy for insomnia behavioral therapy insomnia effective insomnia treatments cognitive behavioral techniques insomnia sleep disorders cognitive behavioral therapy cognitive behavioral therapy sleep disorders insomnia treatment methods effects benefits cognitive behavioral therapy insomnia treatment effective sleep disorders management improvement mental health counseling techniques cognitive behavioral therapy sleep disorders insomnia treatment techniques effects benefits cognitive behavioral therapy insomnia treatment sleep disorders psychology interventions counseling sessions
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 AMI symptom_onset_time diagnostic_value cardiac_markers troponin_levels acute_coronary syndromes cardiovascular_risk heart_attack chest_pain ECG treatment_delay prognostic_indicators high_sensitivity_cardiac_troponin_T HSCT_T dosage_guidelines acute_myocardial_injury AMI symptom_onset_time diagnostic_value cardiac_care myocardial_injury_assessment clinical_guidance cardiac troponin T HSCT AMI symptoms dosage time diagnostic acute myocardial injury onset hours cardiac troponin AMI dosage symptoms onset high-sensitivity diagnostic time coronary heart misdiagnosis clinical elevated myocardial injury patients acute measurement threshold evaluation risk factors management prevention therapy high_sensitivity_cardiac_troponin_t hsct_t dosage acute_myocardial_injury ami symptom_onset time_window diagnostic_value cardiac troponin AMI dosage symptoms time diagnostic test measurement heart clinical elevation health medicine recommendations cardiac troponin T hsct-t dosage acute myocardial injury AMI symptoms time-onset high_sensitivity_cardiac_troponin_t hsct_t dosage_guidelines acute_myocardial_injury onset_symptoms diagnostic_criteria myocardial_injury time_window cardiovascular_disease biomarkers heart_attack clinical_guidance emergency_medicine cardiology cardiovascular_risk diagnostic_test symptomatology medical_diagnosis high_sensitivity_cardiac_troponin_T hsct_t myocardial_injury am_i symptom_onset diagnostic_threshold time_window heart_attack chest_pain myocardium biomarkers cardiac_care emergency_medical cardiac_events acute_coronary_syndrome ischemia myocardial_ischemia cardiac troponin AMI dosage symptoms onset diagnostic timeinterval coronary ischemia cardiology myocardial injury therapy evaluation risk management clinical guidelines accuracy precision population study review association correlation prevalence prognosis complications therapeutics genetics epidemiology vascular atherosclerosis exercise trauma acute presenting signs syndrome chest pain electrocardiogram EKG Laboratory markers
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. diabetes glycemic control nephropathy insulin resistance renal function glucose levels end-stagerenal disease diabetes glucose nephropathy complications metabolic endocrine hypertension proteinuria insulin diabetes kidney disease complications glycemic control nephropathy insulin resistance chronic kidney disease metabolic syndrome glucose levels renal failure risk end-stage renal disease insulin kidney complications insulin side effects kidneys severe kidney issues insulin insulin treatment kidney health diabetes and kidney failure risk insulin dosage kidney impact long-term insulin use kidneys Insulin therapy diabetes mellitus kidney function renal failure glycemic control glucose levels long-term complications metabolic syndrome dialysis proteinuria hypertension recomended search terms medical research diabetes complications kidney disease prevention insulin side effects severe kidney failure causes diabetes management healthcare recommendations clinical studies patient outcomes insulin diabetes kidney disease risk factors glycemic control impact insulin types renal function glucose metabolism chronic kidney disease insulin therapy complications insulin kidney failure diabetes insulin kidney severe kidney disease diabetes insulin side effects kidneys high insulin levels kidney insulin treatment kidney failure insulin dosage kidney health glucose control kidney function type 2 diabetes kidney risk insulin therapy complications kidneys insulin diabetes insulin side effects insulin kidney disease severe kidney failure causes kidney failure risk factors diabetes and kidney complications insulin and nephropathy diabetes mellitus kidney insulin treatment side effects long-term insulin use diabetes glucose complications nephropathy treatment prevention symptoms management
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 process spore formation minority cells stress-resistant spores cell survival differentiation minority development cell survival stress resistance differentiation process spore formation minority cells developmental biology microbial survival adaptive responses cell survival stress resistance spore differentiation minority cells developmental biology microbial survival adaptive spores cell survival stress resistance differentiation spores minority cells cell survival stress resistance spore differentiation minority cells developmental biology microbial spores stressors resistance biological survival cell survival stress-resistant spores developmental biology minority cells differentiation process survival differentiation stress-resistant cells minority spores cell survival differentiation stress-resistant spores molecular mechanisms developmental biology apoptosis germination cell survival stress resistance differentiation process spore formation minority cells
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 transient methylation nuclear receptors ligand induction transcription factors chromatin modification gene expression epigenetics molecular biology signaling pathways histone demethylase function nuclear receptor signaling ligand-induced transcription histone methylation dynamics transcriptional activation pathways coactivators receptor-mediated gene expression chromatin remodeling transcription factors molecular mechanisms mRNA expression profiling histone modifications nuclear receptors ligand-dependent transcription demethylase activity transcription factors methylation levels gene expression protein binding time-dependent changes Histone demethylase activation transient histone methylation reduction nuclear receptor ligand response transcription initiation process epigenetic modifications gene expression regulation chromatin remodeling ligand-dependent transcription factor activity Histone demethylase ligand-dependent induction nuclear receptors transient methylation transcription regulation chromatin modification gene expression epigenetics hormone response protein interaction signaling pathway Histone demethylase function nuclear receptor signaling transcription initiation epigenetic modification ligand binding gene activation chromatin dynamics methylation state transcription factor binding gene expression regulation Histone demethylases nuclear receptors ligand-dependent transcription transient histone methylation gene expression regulation chromatin modification transcription factors epigenetic modifications Histone demethylase ligand-dependent induction nuclear receptors transcription activation methylation dynamics gene expression regulation chromatin remodeling molecular mechanism epigenetic modification Histone demethylase nuclear receptors ligand-dependent transcription induction histone methylation chromatin modification gene regulation epigenetics molecular biology signaling pathways histone modification chromatin remodeling transcription factor binding gene regulation epigenetics nuclear receptor signaling DNA binding domain protein-protein interaction RNA polymerase II recruitment chromatin accessibility
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 methylmercaptopurine thiopurine methyltrasnferase tpmt gene metabolism pharmacology drug metabolism mercaptourine isobutylmercaptopurine thiopurine methylmercaptopurine tpmt metabolism pharmacology enzymes drug metabolism Mercaptopurine TPMT thiopurine anabolism metabolism inactive metabolite methylmercaptopurine Mercaptopurine metabolism TPMT function anabolism pathways drug metabolism enzymes thiopurine methyltransferase activity inactive metabolites pharmacokinetics therapeutic drug monitoring genetic polymorphisms personalized medicine Mercaptopurine thiopurine methyltrasnferase TPMT methylmercaptopurine anabolism drug metabolism query expansion relevant phrases mercaptopurine metabolism thiopurine methyltransferase TPMT activity inactive metabolites drug metabolism anabolism pharmacogenetics therapeutic implications Mercaptopurine thiopurine methyltrasnferase TPMT methylmercaptopurine anabolism metabolism drug metabolism biochemistry enzyme activity Mercaptopurine anabolism methylmercaptopurine thiopurine methyltrasnferase TPMT drug metabolism biochemistry pharmacology Mercaptopurine anabolism thiopurine methyltrasnferase TPMT inactive metabolite methylmercaptopurine Mercaptopurine metabolism TPMT activity thiopurine methyltransferase drug metabolism anabolism inactive metabolites methylmercaptopurine formation
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 osteric expression MPCs oxidative stress molecular biology stem cell research genetic modification progenitor cells mouse models cellular physiology gene function skeletal development Homozygous deletion murine Sbds gene osterix-expressing mesenchymal stem cells progenitor cells MPCs prevents oxidative stress molecular biology genetic modification cellular senescence DNA damage cell signaling mouse models gene function stem cell research biological pathways genetic engineering biotechnology immunology cancer aging Homozygous deletion murine Sbds gene osterix-expressing mesenchymal stem cells progenitor cells MPCs prevents oxidative stress genetic modification cellular biology molecular genetics stem cell research progenitor cell function antioxidant defense gene expression cellular senescence inflammation DNA damagerepair Homozygous deletion benefits murine Sbds function osterix expressing cells MPCs properties oxidative stress prevention genetic manipulation effects stem cell research gene editing techniques cellular metabolism impact bone development study molecular biology applications Homozygous deletion murine Sbds gene osteriexpressing mesenchymal stem progenitor cells MPCs prevents oxidative stress bone development mouse model genetic modification skeletal system cellular biology biomedical research stem cell biology genomics oxidative stress response Homozygous deletion murine Sbds gene osterix-expressing mesenchymal stem cells progenitor cells prevents oxidative stress gene modification cellular biology genetic engineering molecular biology stem cell research antioxidant response genetic mutation cellular metabolism gene function biological stress response genetic screening cell culture techniques Homozygous deletion murine Sbds gene osteriexpressing mesenchymal stem cells progenitor cells oxidative stress genetic manipulation MPCs skeletal development apoptosis cellular senescence Homozygous deletion murine Sbds gene ostérix expressing mesenchymal stem cells MPCs prevents oxidative stress genetic modification stem cell biology progenitor cells oxidative stress resistance cellular senescence molecular biology genomics biomedical research mouse models cell lineage specification Homozygous deletion murine Sbds gene osteogenesis mesenchymal stem cells MPCs oxidative stress osteriexpressing genetic modification cell biology molecular genetics bone development Homozygous deletion murine Sbds gene osterix-expressing mesenchymal stem cells progenitor cells MPCs oxidative stress gene editing cellular biology genetic modification molecular biology cell therapy immunology oncology genetics research DNA repair biological function cell signaling stem cell research gene expression molecular mechanisms biological pathways genetic disorders cell biology cellular function DNA mutations gene knockout genetic engineering biotechnology medical research therapeutic targets biological processes genetic variations cell behavior gene regulation genetic screening cellular metabolism
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 type I HAM/TSP immunoglobulin G antibodies Tax protein epitope cross-reactivity neurological symptoms viral proteins immune response diagnostic markers Human T-lymphotropic virus type I HAM/TSP IgG antibodies Tax protein immunodominant epitope viral proteins autoimmune response neurological disorders immune response virology neurology antibody production Human T-lymphotropic virus HTLV-1 myelopathy tropical spastic paraparesis HAM/TSP Immunoglobulin G IgG antibodies Tax protein epitope immune response HTLV-1-associated disease neuroimmune virology immunology Human T-lymphotropic virus HAM/TSP diagnosis IgG antibodies Tax protein immunodominant epitope viral infection symptoms neurological manifestations antibody production virus-host interaction diagnostic markers viral proteins immune response analysis medical research virology neurology immunology epidemiology patient care therapeutic strategies molecular biology antigen-antibody reaction clinical trials pathogenesis treatment options disease management Human T-lymphotropic virus type-I HAM/TSP Immunoglobulin G antibodies Tax protein immunodominant epitope viral infection neuroimmune response diagnostic marker query expansion relevant phrases HAM/TSP Immunoglobulin G Tax protein immune response viral proteins antibody production epitope recognition neuroimmune disorders virology research medical immunology Human T-lymphotropic virus type I HAM/TSP Immunoglobulin G antibodies Tax protein immunodominant epitope viral infection neurological symptoms immune response Human T-lymphotropic virus Tax protein IgG antibodies HAM/TSP immunodominant epitope viral infection neurological disorder autoimmune response antibody production viral proteins neurological symptoms immune system viral-induced pathology T-cell activation Human T-lymphotropic virus type I HAM/TSP IgG antibodies Tax protein epitope recognition immune response neurological disorders viral infections antibody cross-reactivity T-cell lymphotropic virus Human T-lymphotropic virus Tax protein IgG antibodies Immunodominant epitope HAM/TSP diagnosis Virus-induced autoimmune response Antibody cross-reactivity Viral tax gene product Neurological manifestations Immune response to HTLV-1
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 technology integration educational strategies student collaboration online learning platforms blended learning instructional design digital tools academic outcomes classroom collaboration web-based learning hybrid learning student engagement performance metrics educational technology blended learning online collaboration tools face-to-face interaction digital divide synchronous learning asynchronous learning learning outcomes educational effectiveness technology integration pedagogical strategies student feedback teacher facilitation cognitive load motivation levels group dynamics technology barriers collaborativelearning webbasedlearning classperformance studentengagement technologyintegration educationalmethods blendedlearning onlinecollaboration facecollaboration effectivenessevaluation instructionalstrategies collaborative learning techniques web-based collaboration classroom integration student engagement technology in education online collaboration tools blended learning approaches group dynamics educational outcomes digital learning environments classroom collaboration web-based collaboration learning effectiveness student engagement technology integration educational outcomes blended learning online interaction face-to-face interaction hybrid learning environment collaborative learning strategies web-based learning classroom integration student engagement technology enhanced learning educational outcomes online collaboration blended learning methods learning effectiveness digital tools for education remote collaboration techniques collaborative learning techniques web-based learning classroom integration student engagement technology in education online collaboration tools blended learning educational outcomes group dynamics digital platforms classroom collaboration web-based learning hybrid learning model student engagement technology integration educational outcomes online collaboration tools blended learning group dynamics digital platforms learning effectiveness remote collaboration collaborative learning strategies web-based collaboration classroom integration student engagement technology in education online learning platforms blended learning educational outcomes learning effectiveness digital collaboration tools peer interaction virtual classrooms synchronous learning asynchronous learning educational technology instructional methods academic performance collaborative learning methods web-based learning classroom activities student engagement technology integration educational outcomes online collaboration tools blended learning peer interaction learning effectiveness
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 protein tumor suppression cancer progression apoptosis regulation oncology research gene expression cell survival therapeutic targets Bcl2 protein apoptosis regulation tumor suppression cancer therapy gene expression oncology research cellular survival chemotherapy resistance Bcl2 inhibition tumor suppression molecular mechanisms cancer therapy apoptosis regulation Oncology research anti-tumor activity Bcl2 family proteins Bcl2 inhibition tumor suppression mechanisms cancer therapy apoptosis induction oncogene regulation tumor growth inhibition Bcl2 protein function cancer biology chemotherapy resistance molecular targeted therapy Bcl2 protein tumor suppression apoptosis oncogenes cancer therapy gene expression cell survival chemotherapy resistance cancer biology molecular mechanisms cancer research apoptosis oncology genetic modification tumor suppression cell death therapeutic target biomarkers cancer biology gene expression Bcl2 inhibition tumor suppression apoptosis induction cancer therapy molecular biology cancer cell survival pro-apoptotic proteins Bcl2 family members treatment resistance genetic modification cancer biology apoptosis oncogenes tumor suppression gene silencing Bcl2 function cancer progression Bcl2 protein function treatment strategy mechanism expression therapy regulation cancer biology apoptosis cell survival Bcl2 inhibition tumor suppression molecular therapy cancer biology apoptosis induction anti-tumor effect genetic modification chemotherapy resistance pro-apoptotic proteins Bcl2 family members
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 SSRI antidepressants erectile dysfunction sexual dysfunction PDE5 inhibitors Sildenafil ED SSRI antidepressants sexual dysfunction 勃起功能障碍 抗抑郁药 SSRIs PDE5 inhibitors sildenafil erectile function SSRI antidepressants sexual dysfunction phosphodiesterase inhibitors dapoxetine vardenafil tadalafil sexual performance antidepressant side effects sildenafil SSRI antidepressants erectile dysfunction sexual dysfunction treatment options pharmaceutical solutions medication effectiveness male sexual health drug interactions ED improvement sildenafil erectile function SSRI antidepressants sexual dysfunction treatment mechanism effectiveness sildenafil SSRI interaction erectile dysfunction treatment antidepressants side effects sexual health improvement drug interactions Levitra PDE5 inhibitors sexual performance enhancement Sildenafil SSRI antidepressants erectile dysfunction sexual health drug interaction PDE5 inhibitor treatment options male sexual function sildenafil SSRI antidepressants sexual dysfunction erectile function treatment options medication interactions sexual health male fertility dosing instructions side effects clinical trials Sildenafil SSRI antidepressants sexual dysfunction erectile function treatment options pharmacology pharmaceuticals clinical efficacy drug interactions sexual health SSRI interference ED treatment antidepressant side effects phosphodiesterase inhibitors sexual health improvement male dysfunction remedies
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-based chemotherapy efficacy quality of life treatment outcomes age factor oncology clinical trials comparative analysis elderly patients metastatic colorectal cancer fluoropyrimidines oxaliplatin-based chemotherapy efficacy quality of life treatment outcomes clinical trials comparative analysis oncology senior citizens cancer therapies metastatic colorectal cancer elderly patients fluoropyrimidines oxaliplatin chemotherapy efficacy quality life single agent comparison clinical trials age impact benefit elderly patients metastatic colorectal cancer oxaliplatin-based chemotherapy fluoropyrimidines treatment efficacy quality of life comparison single agent therapy effectiveness metastatic colorectal cancer elderly patients fluoropyrimidines oxaliplatin chemotherapy efficacy quality life prognosis treatment comparison age factors risk benefit safety elderly patients metastatic colorectal cancer treatment efficacy oxaliplatin fluoropyrimidines quality of life chemotherapy comparison clinical trial outcomes elderly oncology elderly patients metastatic colorectal cancer fluoropyrimidines oxaliplatin-based chemotherapy treatment efficacy quality of life cancer therapy comparison elderly patients metastatic colorectal cancer fluoropyrimidines oxaliplatin-based chemotherapy efficacy quality of life treatment outcomes elderly patients metastatic colorectal cancer fluoropyrimidines oxaliplatin-based chemotherapy treatment efficacy quality of life clinical outcomes age-related factors cancer therapy comparison elderly patients metastatic colorectal cancer fluoropyrimidines oxaliplatin-based chemotherapy efficacy quality of life treatment outcomes clinical trials comparative analysis oncology chemotherapy regimens side effects
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 developmental threshold seizure history neurological risk childhood febrile illness febrile seizures epilepsy threshold risk factors pediatric seizures brain development seizure duration fever management neurological disorders febrile seizures epilepsy seizure threshold pediatric seizures neurological disorders brain development fever-induced seizures epilepsy risk childhood seizures neurological conditions febrile seizures epilepsy risk factors febrile seizures and brain damage febrile seizures long term effects febrile seizures genetic predisposition febrile seizures and neurological outcomes febrile seizures vs epilepsy febrile seizures brain function febrile seizures and seizures later in life febrile seizures and cognitive impairment febrile seizures and neuronal development febrile seizures epilepsy seizure threshold risk factors pediatric seizures neurological disorders brain development genetic predisposition fever management long-term outcomes search optimization query expansion relevant phrases febrile seizures epilepsy development medical research seizure frequency neurological conditions pediatric epilepsy seizure thresholds health information retrieval febrile seizures epilepsy seizure threshold child health neurological disorders fever impact brain development pediatric seizures long-term outcomes febrile seizures epilepsy threshold development children risk因素 临床表现 预后因素 febrile seizures epilepsy seizure threshold pediatric epilepsy fever-induced seizures neurological disorders risk factors brain development seizure types epilepsy prevention child health febrile seizures epilepsy seizure types developmental threshold neurological conditions pediatric seizures long-term risk brain development seizure duration fever management genetic factors brain injury 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 brain development fever neurological disorders febrile seizures epilepsy threshold brain children risk factors seizure fever neurological pediatric onset febrile seizures epilepsy seizure threshold pediatric epilepsy fever-induced seizures neurological disorders brain development seizure triggers neurodevelopment risk factors febrile seizures causes febrile seizures definition febrile seizures symptoms febrile seizures treatment febrile seizures risk factors febrile seizures and brain damage febrile seizures and genetic predisposition febrile seizures duration febrile seizures first aid febrile seizures vs epilepsy febrile seizures epilepsy seizure threshold brain development neurological disorders pediatric seizures fever-induced seizures long-term outcomes neurological risk factors febrile seizures epilepsy risk factors febrile seizures and brain development seizure types in children epilepsy prevention strategies child seizure management febrile seizure duration impact neurological development and febrile seizures long-term effects of febrile seizures febrile seizures epilepsy risk seizure triggers pediatric seizures brain development fever and seizures neurological conditions seizure threshold fever-induced seizures febrile seizures epilepsy seizure threshold pediatric seizures neurological disorders fever-induced seizures brain development genetic factors seizure prevention neurodevelopment seizure onset cerebral function pediatric epilepsy fever management brain plasticity neurological conditions seizure triggers childhood seizures fever and seizures epilepsy risk febrile seizure prognosis febrile seizures epilepsy seizure threshold pediatric seizures fever-induced seizures neurological disorders brain function genetic factors brain development childhood febrile episodes febrile seizures epilepsy seizure threshold neurological disorders pediatric seizures seizure risk factors brain development seizure types epilepsy prevention fever and seizures
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 treatment outcomes fibrinogen blood clotting vascular surgery clinical trials blood thinners risk factors hyperfibrinogenemia thrombosis femoropopliteal bypass clinical trial risk factor treatment outcomes vascular surgery hematology fibrinogen blood clotting Hyperfibrinogenemia thrombosis femoropopliteal bypass fibrinogen vascular surgery complications prevention blood coagulation factors hyperfibrinogenemia treatment hyperfibrinogenemia risk factors hyperfibrinogenemia symptoms hyperfibrinogenemia diagnosis hyperfibrinogenemia causes hyperfibrinogenemia complications hyperfibrinogenemia management hyperfibrinogenemia prevalence hyperfibrinogenemia patient outcomes femoropopliteal bypass surgery femoropopliteal bypass thrombosis hyperfibrinogenemia and cardiovascular health hyperfibrinogenemia clinical trials hyperfibrinogenemia genetic aspects hyperfibrinogenemia thrombosis femoropopliteal bypass fibrinogen blood clotting vascular surgery clinical trial risk factor treatment outcome Hyperfibrinogenemia treatment thrombosis prevention femoropopliteal bypass fibrinogen levels surgical outcomes blood clotting vascular surgery hypercoagulable state clinical trials medical research patient outcomes Hyperfibrinogenemia thrombosis femoropopliteal bypass fibrinogen blood clotting vascular surgery medical research clinical trials hematology hyperfibrinogenemia treatment femoropopliteal bypass thrombosis benefits keywords efficacy increase medical clinical hyperfibrinogenemia thrombosis femoropopliteal bypass fibrinogen levels surgical outcomes vascular surgery blood clot prevention hypercoagulability clinical trials angioplasty stents risk factors treatment efficacy hyperfibrinogenemia treatment thrombosis prevention femoropopliteal bypass surgery fibrinogen levels clinical trials patient outcomes vascular surgery blood clotting disorders genetic factors therapeutic interventions
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 factor blood vessel condition risk treatment surgery complication hyperfibrinogenemia thrombosis femoropopliteal surgery risk factor vascular condition complications treatment prevention clinical studies patients diagnosis hyperfibrinogenemia thrombosis femoropopliteal bypass clotting factor blood vessels risk conditions treatment surgery patients incidence complications prevention management hyperfibrinogenemia complications femoropopliteal bypass surgery thrombosis risk factors increased thrombotic events hypofibrinolysis treatment options hyperfibrinogenemia thrombosis femoropopliteal bypass blood clotting fibrinogen vascular surgery cardiovascular risk factors hemostasis thrombogenesis hyperfibrinogenemia complications femoropopliteal bypass surgery thrombosis risk factors vascular surgery outcomes fibrinogen levels and thrombosis hypofibrinolysis clinical impact Hyperfibrinogenemia thrombosis femoropopliteal bypass clotting factors blood coagulation vascular health medical research clinical studies diagnostic markers treatment options Hyperfibrinogenemia thrombosis femoropopliteal bypass beneficial expansion keywords medical fibrinogen vascular surgery blood clotting risk factors clinical outcomes Hyperfibrinogenemia thrombosis femoropopliteal bypass surgery clotting factors blood coagulation vascular disease cardiovascular risk fibrinogen levels thromboembolism surgical outcomes clinical trials epidemiology treatment options preventive measures hyperfibrinogenemia treatment femoropopliteal bypass thrombosis prevention clot formation fibrinogen levels vascular surgery complications thromboembolism risk hypercoagulable state vascular health blood clotting disorders
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 polymerase I polI mice ionizing radiation IR genetic defect DNA repair radiation sensitivity genotoxicity biomarker mutation cell survival apoptosis DNA polI mice sensitivity ionizing radiation molecular biology cancer genetics mutation radiation tolerance DNA polymerase polI mice ionizing radiation IR genetic defect radiosensitivity DNA repair genetic mutation radiobiology genome stability DNA polymerase I polI deficient mice ionizing radiation sensitivity DNA repair mechanisms gene knockout radiation biology genetic models DNA damage response radiation sensitivity assays mice DNA polI sensitivity ionizing radiation molecular biology research model organisms genetics mutation RNA editing DNA polymerase I polI mice irradiation ionizing radiation DNA repair radiation sensitivity genetic defect molecular biology radiation biology DNA polymerase I polI mice ionizing radiation IR genetic defect radiosensitivity genome stability DNA repair cellular response genetic model DNA polymerase I polI mice ionizing radiation IR genetic defect radiation sensitivity DNA repair genomic instability radiation biology cellular response genetics research molecular biology radiation sensitivity assay mice DNA polymerase I polI ionizing radiation IR sensitivity molecular biology genetics cancer research radiobiology mouse model mutation analysis DNA repair polI function IR sensitivity genomics radiation biology genetic model molecular biology radiation damage DNA damage response cell survival radiation sensitivity assays
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 high-dose statins widespread use cardiovascular health lipid management clinical outcomes therapeutic efficacy colchicine secondary prevention statins cardiovascular risk cholesterol management inflammation reduction clinical trials treatment efficacy preventative healthcare lipid lowering heart disease prevention colchicine benefits secondary prevention strategies high-dose statins cardiovascular health cholesterol management risk reduction clinical trials pharmacotherapy inflammatory response therapeutic efficacy colchicine therapy secondary prevention strategies high-dose statins cardiovascular health cholesterol reduction risk factor management clinical outcomes long-term benefits colchicine benefits secondary prevention strategies high-dose statins effective use widespread implementation colchicine treatment secondary prevention high-dose statins cardiovascular benefits inflammation reduction cholesterol management clinical outcomes colchicine benefits secondary prevention high-dose statins cardiovascular health reduction in risk cholesterol management clinical outcomes therapeutic strategies colchicine benefits secondary prevention strategies high-dose statins widespread use cardiovascular health reduced inflammation treatment efficacy cholesterol management clinical outcomes preventative medicine colchicine secondary prevention statins high-dose benefits cardiovascular disease cholesterol clinical trials efficacy treatment strategies colchicine therapy secondary prevention high-dose statins cardiovascular benefits reduction in inflammation clinical trial results long-term outcomes cholesterol management adverse effects treatment efficacy
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 type1diabetes complications comorbidity cardiovascularrisks glucosecontrol insulintherapy kidneydisease retinopathy neurologyimpact hypertension type1 diabetes diabetes complications renal disease hypertensive nephropathy vascular complications hypertension type1diabetes cardiovascularrisks glucosecontrol complications insulintherapy metabolicsyndrome bloodpressuremanagement hypertension type 1 diabetes management hypertension complications type 1 diabetes risk factors hypertension type 1 diabetes treatment hypertension type 1 diabetes hypertension monitoring type 1 diabetes lifestyle changes hypertension type 1 diabetes genetic links hypertension type 1 diabetes hypertension prevention type 1 diabetes cardiovascular risks hypertension type 1 diabetes Hypertension type 1 diabetes comorbidity cardiovascular risk glucose control kidney disease blood pressure management Hypertension type 1 diabetes complications hypertension management type 1 diabetes diabetes hypertension risk factors hypertension control in diabetes hypertension treatment type 1 diabetes type 1 diabetes and blood pressure hypertension in diabetes patients hypertension diagnosis type 1 diabetes hypertension prevention diabetes type 1 hypertension screenings for type 1 diabetes hypertension type 1 diabetes cardiovascular risk comorbidity blood pressure glucose control insulin resistance chronic conditions Hypertension type 1 diabetes comorbidity cardiovascular risk blood pressure glucose control complications chronic disease management renal function obesity genetics lifestyle factors hypertension type1diabetes cardiovascularrisks comorbidities glucosecontrol hypertensionprevalence diabetescomplications Hypertension complications type 1 diabetes management diabetes hypertension risk frequent hypertension in diabetes prediabetes hypertension connection
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. Apolipoprotein E4 dementia risk female carriers genetics alzheimer's disease Apolipoprotein E4 dementia female risk factors genetic population study clinical trials neurodegeneration prevalence association heredity age ethnicity brain health alzheimer's disease Apolipoprotein E4 dementia risk factors genetic predisposition female carriers age Alzheimer's disease neurodegeneration ApoE4 and dementia APOE4 genetics female dementia risk apolipoprotein E4 carriers APOE4 and Alzheimer's genetic factors dementia APOE4 and cognitive decline APOE4 prevalence dementia APOE4 female impact APOE4 and brain health Apolipoprotein E4 dementia risk female carriers genetic factor Alzheimer's disease cognitive decline hereditary predisposition APOE4 dementia risk female genetics alzheimer carrier mutation neurodegeneration aging prevalence biomarkers clinical symptoms preventive measures ApoE4 dementia risk factors genetic predisposition alzheimer's carrier gender neurodegeneration Apolipoprotein E4 dementia risk female carriers genetic factor neurodegeneration molecular biology genomics alzheimer's disease ApoE4 dementia female risk factors genetics neurodegeneration age symptoms prevalence cohorts clinical trials genome variant epidemiology brain health ApoE4 genetics dementia risk female health genetic factors dementia prevention APOE4 carriers neurodegenerative diseases aging research genetic testing 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 fear neuroscience rodent behavior neurochemical sleep depression Hypocretin neurons panic-prone rats neuroscience anxiety sleep hypocretin-1 orexin brain stress neurotransmitters behavior psychiatric disorders neurobiology rodent models neurochemicals hypocretin neurons panic-prone rats neurochemistry stress anxiety sleep orexin brain behavior physiology hypocretin neurons function hypocretin role in anxiety panic-prone rats mechanisms hypocretin-induced panic state neurochemical basis of panic hypocretin and stress response panic disorder animal models hypocretin neuron activation fear response in rats stress-induced panic state Hypocretin neurobiology panic rats neuroscience anxiety sleep dopamine Hypocretin function panicprone rats neuronal activity stress response hypothalamic peptides Hypocretin neurobiology panic rat studies stress response fear conditioning anxiety disorders neurotransmitters sleep deprivation brain imaging behavioral tests Hypocretin neurobiology panic rats stress neurotransmitters sleep anxiety brain neurochemicals hypocretin neurons panic-prone rats anxiety stress sleep hypocretin-1 orexin neurotransmitters behavior psychological neuroscience sleep-wake cycle corticotropin-releasing hormone CRH hypocretin neurobiology anxiety rat studies panic disorder neurotransmitters fear responses stress neuroscience sleep disorders
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 treatments lymphatic filariasis prevention onchocerciasis treatment ivermectin dosage filarial infection management ivermectin lymphatic filariasis treatment drug parasitic infection tropical diseases ivermectin treatment lymphatic filariasis symptoms ivermectin dosage lymphatic filariasis prevention ivermectin side effects lymphatic filariasis cure ivermectin efficacy lymphatic filariasis prevalence ivermectin treatments ivermectin dosage ivermectin side effects ivermectin for scabies ivermectin efficacy ivermectin mechanism of action ivermectin resistance ivermectin distribution lymphatic filariasis prevention lymphatic filariasis symptoms Ivermectin lymphatic filariasis parasitic infection treatment medication public health antiparasitic malaria tropical diseases vector-borne diseases ivermectin treatments lymphatic filariasis symptoms filariasis prevention ivermectin dosage lymphatic filariasis antifilarial drugs ivermectin side effects lymphatic filariasis Ivermectin treatment lymphatic filariasis medication antiparasitic drugs tropical diseases public health application Ivermectin lymphatic filariasis treatment medication antiparasitic dosage side effects prevention health parasites drugs medical malaria worms ivermectin treatments lymphatic filariasis symptoms ivermectin dosage ivermectin side effects lymphatic filariasis prevention ivermectin efficacy ivermectin administration lymphatic filariasis transmission ivermectin resistance lymphatic filariasis global prevalence lymphatic filariasis treatment ivermectin dosage ivermectin side effects lymphatic filariasis prevention ivermectin administration filariasis symptoms ivermectin efficacy lymphatic system antiparasitic drugs public health treatment
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 links study evidence diabetes brain health glycemic control hypoglycemia dementia risk factors connection research studies prevalence diabetes age severity comorbidities neurological effects hypoglycemia dementia risk factors diabetes brain function glucose mortality age severity chronicity hypoglycemia dementia prevention hypoglycemia dementia correlation hypoglycemia and cognitive decline links between hypoglycemia dementia hypoglycemia severity dementia risk managing hypoglycemia to reduce dementia hypoglycemia duration and dementia hypoglycemia frequency dementia connection hypoglycemia treatment dementia impact hypoglycemia management dementia预防 hypoglycemia与痴呆关系 糖尿病低血糖痴呆风险 hypoglycemia dementia risk factors diabetes glucose memory neurodegeneration elderly population studies research clinical hypoglycemia dementia risk factors hypoglycemia and cognitive decline glucose levels and dementia low blood sugar and brain function diabetes management and dementia hypoglycemia prevention dementia insulin use and dementia risk hypoglycemia dementia risk factors association medical research diabetes brain health endocrinology hypoglycemia dementia risk factors diabetes glucose brain health neurodegeneration elderly stroke cardiovascular health hypoglycemia dementia risk factors association studies diabetes elderly neurodegeneration vascular.health hypoglycemia dementia risk factors association research evidence prevention treatment complications
1099	Statins decrease blood cholesterol. Statins decrease blood cholesterol. Statins decrease blood cholesterol. Statins decrease blood cholesterol. Statins decrease blood cholesterol. statins cholesterol medication health cardiovascular benefits side effects lipid treatment prevention cholesterol_reduction lipid_regulators heart_disease_prevention statin_benefits lipid_profile_analysis hyperlipidemia_treatment statins blood cholesterol lowering effects dosage side medications diet lifestyle statin benefits statin side effects cholesterol levels lipid profile cardiovascular health cholesterol management statin prescription high cholesterol treatment statin dosage statin brands statins cholesterol cardiovascular drugs benefits side effects lipid profile prescription cholesterol_reduction lipid_controllers heart_disease_risk lipid_profile_analysis cholesterol_lowering_drugs statins cholesterol lipid medication cardiovascular health treatment reduction efficacy side effects Statins benefits cholesterol reduction lipid lowering medications cardiovascular health lipid profile hypercholesterolemia treatment statins cholesterol lowering drugs health benefits risk cardiovascular disease population prediction model clinical effects mechanism statin benefits statin side effects cholesterol levels lipid profile cardiovascular health stroke risk diabetes management statin alternatives dietary changes exercise impact
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 treatment onchocerciasis medication filariasis cure skin infections tropical diseases parasitic infections ivermectin onchocerciasis parasitic treatment medicine efficacy dosage side effects vector control public health ivermectin treatments onchocerciasis control anti-parasitic drugs tropical diseases malaria prevention skin infections parasitic worms public health measures ivermectin treatment onchocerciasis symptoms ivermectin dosage ivermectin side effects onchocerciasis prevention ivermectin mechanism ivermectin resistance Ivermectin onchocerciasis river blindness parasitic infection treatment medicine efficacy dosage side effects ivermectin treatment onchocerciasis management antiparasitic drugs tropical diseases skin conditions eye health medication efficacy Ivermectin onchocerciasis river blindness parasitic infection malaria tropical diseases drug treatment medical use Ivermectin treatment onchocerciasis prevention ivermectin dosage onchocerciasis symptoms ivermectin side effects onchocerciasis transmission ivermectin administration onchocerciasis infection ivermectin treatment onchocerciasis management anti-parasitic drugs onchocerciasis symptoms ivermectin dosage ivermectin treatment onchocerciasis prevention ivermectin dosage onchocerciasis symptoms ivermectin side effects onchocerciasis transmission ivermectin administration onchocerciasis prevalence
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 interferon-g receptor autoimmune myocarditis mouse model immune response cardiac inflammation cytokines gene knockout immune regulation T cells B cells adaptive immunity innate immunity Interferon-gamma Interferon-gamma receptor experimental autoimmune myocarditis mice genetic models immune response cardiovascular disease cytokines inflammatory response immunology research mouse strains pathogenesis gene knockout heart inflammation Interferon-gamma Interferon-gamma receptor Experimental autoimmune myocarditis Mice genetic models Immune response Cardiac inflammation Gene knockout Immunopathology Myocardial damage Adaptive immunity Innate immunity Interferon-gamma deficient mice receptor-deficient mice autoimmune heart disease innate immune response adaptive immunity cardiac inflammation Th1 cells cytokine production antigen presentation T-cell activation immune regulation disease susceptibility genetic models mouse models immunology research cardiac pathology inflammatory response immune deficiency myocarditis treatment gene knockout cytokine signaling Interferon-γ receptor deficiency experimental autoimmune myocarditis mouse model immune response inflammation cardiac function pathogenesis Interferon-gamma receptor deficiency autoimmune myocarditis mouse model immune response cardiovascular disease inflammation Interferon-gamma interferon gamma receptor experimental autoimmune myocarditis mice genetics immune response cardiovascular disease inflammatory response cytokines immune deficiency Interferon-γ deficient mice receptor knockout myocarditis immune response modulation inflammatory/autoimmune diseases cardiovascular pathology gene editing techniques cytokine function analysis adaptive immunity deficiency heart inflammation models Interferon-gamma interferon-g receptor experimental autoimmune myocarditis mouse model immune response inflammation cardiac disease genetic knockout cytokines autoimmune disorders Interferon-gamma immune response myocarditis gene knockout mouse models cytokines inflammation autoimmunity heart disease immunology
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 energy metabolism appetite regulation metabolic hormones neurobiology synaptic transmission metabolic homeostasis neurotransmitters hypothalamus glutamate energy metabolism obesity appetite regulation neuroscience neurobiology metabolic disorders hypothalamus glutamate neurotransmission energy balance metabolism appetite obesity homeostasis neurons signaling Hypothalamus energy metabolism neuropeptide Y regulation synaptic transmission obesity metabolic syndrome neurobiology appetite control mechanisms glutamate receptors role hypothalamic plasticity hunger hypothalamus glutamate neurotransmission energy balance metabolism appetite obesity homeostasis neurons neurotransmitters hypothalamus glutamate energy metabolism obesity appetite regulation neuroscience metabolic disorders synaptic transmission neurobiology hypothalamus glutamate neurotransmission energy balance metabolic regulation appetite control neurobiology neuroscience homeostasis obesity metabolism neuroendocrinology hypothalamus glutamate neurotransmission energy balance metabolic regulation appetite control neurology neuroscience biochemistry synaptic transmission Hypothalamus glutamate neurotransmission energy balance metabolism appetite regulation obesity neurobiology neuroscience metabolic hormones neurotransmitters hypothalamus metabolism appetite obesity diet neuronal signaling homeostasis neurology
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 immune response inflammation autoimmune transplantation genetics immunology Mice IFN-γ receptor EAM α-MyHC CFA resistance immune response inflammation tissue damage autoimmunity Mice IFN-γ receptor EAM α-MyHC CFA resistance immune response autoimmunity muscle inflammation Mice IFN-γ receptor EAM α-MyHC CFA immune response inflammation resistance autoimmune model antigen presentation cytokines genetic modification immunology pathology Mice IFN-γ receptor EAM α-MyHC CFA resistance immunity inflammation autoimmune response Mice IFN-γ receptor EAM α-MyHC/CFA immune response resistance inflammation immunology mice model autoimmune encephalomyelitis Mice IFN-γ receptor EAM α-MyHC CFA immune response inflammation resistance immunology mouse model Mice IFN-γ receptor EAM α-MyHC CFA resistance immune response viral infection murine model autoimmunity Mice IFN-γ receptor EAM α-MyHC CFA resistance immune response inflammation autoimmunity transgenic murine model Mice IFN-γ receptor EAM α-MyHC CFA resistance immunity autoimmune response B-cell murine model
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 mRNAs DMT1 iron uptake transcription translation regulation cellular biochemistry genetics molecularbiology iron-responsive elements mRNAs DMT1 iron uptake cellular iron homeostasis translational regulation protein binding molecular biology genetics RNA binding proteins iron transporters cytosolic proteins iron responsive elements mRNAs DMT1 iron uptake translation regulation ferritin transferrin transporters transcription expression metabolism biosynthesis cytosolic proteins iron-responsive elements mRNA DMT1 iron uptake transcription factors mRNA binding iron metabolism gene expression cellular iron homeostasis protein interaction RNA binding proteins Cytosolic proteins iron-responsive elements mRNAs DMT1 iron uptake translational regulation iron metabolism mRNA binding Cytosolic_proteins iron-responsive_elements mRNAs DMT1 iron_uptake protein_binding transcriptional regulation iron_metabolism post_transcriptional_regulation RNA_binding_proteins molecular_biology genetics cellular_maintenance iron_homeostasis Cytosolic proteins iron responsive elements mRNAs DMT1 iron uptake transporters transcription regulation cellular metabolism cytosolic proteins iron-responsive elements mRNAs DMT1 iron uptake protein binding translational regulation iron homeostasis cytosolic proteins iron responsive elements mRNA DMT1 iron uptake regulation transcription translation metabolism transport genes expression cellular function bioinformatics RNA binding mechanisms signaling cytosolic proteins iron-responsive elements DMT1 iron uptake mRNA protein binding iron metabolism translational regulation mRNA stability iron transport gene expression cellular iron homeostasis
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. flexible molecules steric hindrance tumor microenvironment rigid molecules molecular flexibility tumor environment biomolecules nanotechnology drug delivery molecular dynamics cancer therapy 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 molecular flexibility chemical rigidity biomolecular interactions cancer drug delivery molecular dynamics biophysics steric hindrance flexible molecules tumor microenvironment rigid molecules drug delivery molecular flexibility chemical structure biomolecular interactions therapeutic agents steric hindrance tumor microenvironment flexible molecules rigid molecules diffusion biomacromolecules molecular dynamics drug delivery steric hindrance molecules tumor microenvironment rigidity flexibility steric hindrance molecules tumor microenvironment rigid molecules flexible molecules drug delivery molecular flexibility steric hindrance tumor microenvironment molecular flexibility rigid molecules flexible molecules bioavailability cancer drugs molecular dynamics steric hindrance flexible molecules rigid molecules tumor microenvironment chemical flexibility molecular dynamics cancer therapy synthesis methods bioavailability steric hindrance molecules tumor microenvironment rigidity flexibility molecular dynamics drug delivery cancer biology
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 MicroRNA Neural Stem Cell differentiation proliferation homeostasis gene regulation neurogenesis stem cell biology molecular mechanisms microRNA regulation neural stem cell differentiation proliferation dynamics homeostasis mechanisms NSC microRNAs stem cell biology gene expression cellular metabolism molecular biology neurological disorders RNA interference biotechnology applications microRNA regulation Neural Stem Cell differentiation process proliferation dynamics homeostasis maintenance gene expression control cellular metabolism molecular biology neurogenesis RNA interference stem cell research biological pathways genetic regulation neuroscience biotechnology molecular mechanisms MicroRNA function neural stem cell development gene expression regulation stem cell biology RNA interference cellular differentiation proliferation control molecular mechanisms neurogenesis biogenesis process signaling pathways epigenetic modification transcriptome analysis cancer research neurological disorders MicroRNA Neural Stem Cell differentiation proliferation homeostasis regulatory mechanism gene expression molecular biology neurogenesis RNA interference MicroRNA function neural stem cell biology differentiation process proliferation control homeostasis maintenance gene expression regulation molecular mechanisms neurogenesis miRNA targets NSC dynamics MicroRNA regulation Neural Stem Cell differentiation proliferation dynamics homeostasis factors stem cell biology RNA function neurogenesis molecular biology genetic regulation MicroRNA regulation Neural Stem Cell differentiation proliferation dynamics homeostasis maintenance molecular biologykeywords RNA function neurogenesis process gene expression control stem cell research biological pathway analysis MicroRNA Neural Stem Cell differentiation proliferation homeostasis gene expression regulatory network neurogenesis stem cell biology molecular mechanisms RNA silencing microRNA functions NSC differentiation factors proliferation dynamics stem cell maintenance molecular mechanisms NPCs microRNAs neural development genes cellular homeostasis markers
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-amplified serotypes uncultured correlation microbiome pathogen detection gene expression molecular biology infectious diseases bioinformatics RNA analysis microarray serotypes culture-amplified uncultured correlation microbiology molecular biology pathogen detection gene expression diagnostic methods microarray serotypes culture-amplified uncultured correlation microbiology genomics pathogenidentification transcriptomics microarray analysis culture amplification serotype correlation uncultured samples microbiome diversity pathogen detection genetic variation diagnostic accuracy bioinformatics tools microbial community structure microarray serotypes culture-amplified uncultured correlation efficiency propose valuable terms microarray analysis serotype identification culture-dependent culture-independent microbiome bioinformatics genotyping infectious disease pathogen detection molecular diagnostics microarray culture-amplified serotypes uncultured correlation microbiology genomics transcriptomics bioinformatics pathogen identification microarray serotypes culture-amplified uncultured correlation efficacy keywords mixtures microarray culture-amplified serotypes uncultured correlation genetic microbiology infectious disease pathogen analysis bioinformatics microarray analysis culture-dependent culture-independent serotype diversity microbial communities gene expression molecular biology pathogen identification bioinformatics microbiome研究 cross-validation sensitivity specificity diagnostic accuracy
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 antiviral mechanism interferon-induced protein sRNA cap analogs viral infection response viral RNA modification IFIT1 viral replication mis-capped RNAs antiviral mechanism Viral infection immune response RNA interference interferon protein expression viral capsid molecular biology antiviral drug development host-virus interaction IFIT1 viral replication mis-capped RNA antiviral response innate immunity RNAse L activation viral RNA recognition IFIT family proteins cap structure modification viral infection resistance IFIT1 function viral RNA modification antiviral mechanism innate immunity response RNA cap structure virus infection process molecular biology terms IFIT1 viral replication mis-capped viral RNAs antiviral mechanism RNA cap sRNA regulation viral entry VISR host defense RNA interference RNA modification IFIT1 function viral RNA modification viral replication inhibition mis-capped RNA antiviral mechanism RNAse L activation VISA protein VINH domain IFIT1 viral replication mis-capped viral RNAs antiviral mechanism RNA interference protein function viral infection immune response IFIT1 viral replication mis-capped viral RNAs antiviral mechanism RNA interference broad spectrum antiviral pattern recognition receptors Viral RNA capping sRNA biology viral mRNA metabolism Virus-host interaction molecular virology RNA viruses host defense mechanisms immunology Virus restriction factors IFIT1 viral replication mis-capped viral RNAs antiviral mechanism RNA interference host defense virology restriction factor molecular biology immunology genetics biomedical research pubmed database protein function IFIT1 protein viral RNA capping antiviral response host-virus interaction gene expression regulation innate immunity RNA interference viral genome processing viral RNA recognition cellular defense mechanisms
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. DMRT1 gene sex determination epigenetics MHM region genetic regulation sex chromosome avian sex determination molecular biology gene expression sexual differentiation sex determination epigenetics DMRT1 function MHM region gene regulation sexual development chromatin modification epigenetic markers DMRT1 gene sex determination epigenetics MHM region sexual differentiation gene regulation chromatin modification sex chromosomes transcription factors sex determination genes epigenetic regulation DMRT1 function MHM region role sex determination mechanisms gene regulation examples epigenetics in sex determination DMRT1 expression sex chromosome influence genetic factors in sex determination DMRT1 sex determination epigenetics MHM region gene regulation sex chromosome transcription factor sex determination genes epigenetic regulation DMRT1 function MHM region impact sex chromosome interactions gene expression modulation genetic regulation mechanisms sex determination epigenetics DMRT1 function MHM region gene regulation DMRT1 gene sex determination epigenetic regulation MHM region genetic research sexual differentiation chromatin modification epigenetics sex hormones gene expression sexual development DMRT1 gene sex determination epigenetics MHM region transcription factor chromatin modification sexual development genetic regulation sex-linked genes molecular biology sex determination pathway sex determination epigenetics gene regulation DMRT1 function MHM region sexual differentiation genetic regulation epigenetic markers sex chromosome interactions gene expression 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 remodeling E3 ligase activity ATP-dependent remodeling SMC5/6 complex SUMO E3 ligase Mms21 activation chromatin structure cell cycle regulation DNA repair protein modification molecular biology epistasis analysis SUMOylation process Smc5/6 complex SUMOylation ATP-dependent remodeling Mms21 enzyme protein modification chromosomal maintenance cell cycle regulation DNA repair Smc5/6 complex function SUMOylation process Mms21 protein interaction ATP role in protein modification chromosomal maintenance cell cycle regulation DNA repair mechanism ubiquitination comparison protein remodeling techniques SUMO E3 ligase mechanism SMC5/6 complex SUMOylation Mms21 protein ATP-dependent remodeling E3 ligase activity SMC5/6 complex SUMOylation process ATP binding chromosomal stability MMS21 protein cell division regulation DNA repair mechanism protein modification enzymes molecular biology techniques SMC5 SMC6 SUMOylation Mms21 ATPase protein complex chromatin remodeling cell cycle DNA repair Smc5/6 complex SUMO E3 ligase Mms21 protein ATP-dependent remodeling SMC5/6 engagement SUMOylation process chromosomal maintenance cell cycle regulation protein modification DNA repair机制 Smc5/6 complex SUMOylation ATP-dependent remodeling Mms21 ligase chromosomal maintenance protein modification cellular senescence DNA repair SMC5/6 complex SUMOylation ATP-dependent remodeling Mms21 activation chromosomal maintenance cell division protein modification SUMO E3 ligase function DNA repair chromatin structure molecular biology techniques
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 gene antiviral properties neurotropic viruses viral infection resistance innate immunity response virus-specific defense mechanisms IRG1 protein function IRG1 antiviral neurotropic viruses immune response protein mechanism protection infection neuroscience virology cellular biology IRG1 function antiviral mechanisms neurotropic viruses virus infection immune response viral pathogenesis gene expression protein interaction drug target therapeutic potential IRG1 virus resistance IRG1 antiviral mechanism IRG1 neurotropic virus treatment IRG1 gene function IRG1 antiviral properties neurotropic virus infection IRG1 viral defense antiviral proteins IRG1 IRG1 and viral diseases IRG1 immune response IRG1 antiviral properties neurotropic viruses viral infection immune response virus inhibition gene function virology research molecular biology antiviral treatments IRG1 function neurotropic viruses types viral infection prevention gene expression analysis IRG1 protein antiviral properties neurotropic viruses viral infection defense innate immunity virus specificity gene function viral pathogenesis molecular biology virology research antiviral mechanisms IRG1 function antiviral mechanisms neurotropic viruses viral infection defense gene expression immune response enhancement viral replication inhibition cellular resistance IRG1 protein antiviral activity neurotropic viruses viral infection immune response gene function virology antiviral mechanisms neurological viruses IRG1 function antiviral mechanisms neurotropic viruses viral infection prevention innate immunity response viral replication inhibition neurovirology IRG1 activation antiviral therapy viral entry阻断
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 T cell receptor echo-domain cytoplasmic tail signal transduction immunology TCR protein phosphorylation ITAM phosphorylation TCR echo-domain cytoplasmic tail immunology signal transduction T cell biology adaptive immunity protein kinase lymphocyte activation ITAM phosphorylation TCR signal transduction cytoplasmic tail echo-domain immunology T cell receptors immune system protein tyrosine kinases adapter proteins ITAM function TCR signaling pathway cellular immunology immunophosphorylation lymphocyte activation molecular biology adaptive immune response antigen recognition cell signaling protein interaction biological regulation ITAM phosphorylation TCR echo-domain cytoplasmic tail signal transduction ITAM function TCR signaling immunology research molecular biology signal transduction T cell activation phosphorylation sites echo-domain role cytoplasmic domain interactions ITAM phosphorylation TCR echo-domain cytoplasmic tail signal transduction immunology T cell biology immune system protein interaction cellular signaling ITAM phosphorylation TCR signal transfer echo-domain cytoplasmic tail immunology T cell signaling molecular biology adaptive immunity kinase activation immune response regulation ITAM phosphorylation TCR echo-domain cytoplasmic tail immune synapse signaling cascade T cell activation immunology molecular biology signal transduction immune response protein interaction ITAM function T cell receptor signaling phosphorylation process cytosolic transmission Echo domain role
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 apoptosis regulation cell death mechanisms mitochondrial dysfunction apoptosis mitochondrial involvement uninvolved cellular processes mitochondria apoptosis role mitochondrial function in cell death apoptosis mitochondrial involvement mitochondria and programmed cell death uninvolved in apoptosis mechanisms mitochondria apoptosis involvement role mitochondria apoptosis apoptosis mitochondrial function mitochondrial dysfunction apoptosis mitochondrial role in cell death apoptosis without mitochondria apoptosis independent mitochondria mitochondria apoptosis function apoptosis regulation mitochondria role of mitochondria in cell death mitochondrial membrane potential and apoptosis apoptosis and mitochondrial damage mitochondrial dysfunction apoptosis regulation cell death mechanisms caspase activation Bcl-2 family proteins mitochondria apoptosis function mitochondrial role in cell death apoptosis regulation mitochondria mitochondrial dysfunction apoptosis apoptosis without mitochondria apoptosis mechanisms excluding mitochondria mitochondria apoptosis function apoptosis mechanism role of mitochondria in cell death mitochondrial dysfunction and apoptosis mitochondrial membrane potential apoptosis apoptosis signaling pathways mitochondria apoptosis function mitochondrial role in cell death apoptosis mitochondrial involvement uninvolved mitochondria mechanisms apoptosis without mitochondria mitochondrial dysfunction apoptosis mitochondria and programmed cell death mitochondria apoptosis function mitochondria role in cell death mitochondrial involvement in programmed cell death apoptosis mechanism mitochondria and caspase activation mitochondrial role apoptosis mechanisms cell death processes uninvolved factors mitochondrial dysfunction programmed cell death
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 molecular mechanism brain injury FoxO3a neuronal death reactive oxygen species ROS signaling pathway oxidative stress apoptosis neurodegeneration transcription factor cellular metabolism FoxO3a neuronal death reactive oxygen species ROS apoptosis oxidative stress signaling pathway neurodegeneration gene expression antioxidant inflammation FoxO3a signaling neuronal apoptosis oxidative stress ROS production neurodegeneration mechanisms FoxO3a pathway reactive oxygen species roles neuronal function impairment redox homeostasis cellular signaling pathways neuroprotection strategies FoxO3a neuronal death reactive oxygen species ROS signal transduction apoptosis oxidative stress neurodegeneration redox signaling FoxO3a neuronal death reactive oxygen species ROS apoptosis oxidative stress neurodegeneration signaling pathways gene expression antioxidant defense cell survival inflammation aging ischemia neuroprotection FoxO3a neuronal death reactive oxygen species ROS apoptosis oxidative stress signaling pathway neurodegeneration antioxidant gene expression FoxO3a neuronal death reactive oxygen species ROS molecular mechanism oxidative stress apoptosis neurodegeneration signaling pathway FoxO3a neuronal death reactive oxygen species ROS signaling pathway apoptosis oxidative stress neurodegeneration gene expression molecular biology aging neuroprotection FoxO3a neuronal death reactive oxygen species ROS oxidative stress apoptosis signaling pathway neurodegeneration molecular mechanism
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 autoimmune response gluten sensitivity gastrointestinal symptoms IgA plasma cells transglutaminase 2 duodenal mucosa gluten-free diet celiac disease intestinal immune response gliadin endomysial antibodies IgA plasma cells transglutaminase 2 duodenal mucosa gluten-free diet celiac disease autoimmune response gastrointestinal pathology immunoglobulin A endomysial antibodies intestinal permeability gluten sensitivity IgA plasma cells transglutaminase 2 duodenal mucosa gluten-free diet celiac disease immune response gastrointestinal tract wheat proteins autoimmune disorders enteropathy biopsy markers antigen-specific antibodies IgA plasma cells transglutaminase 2 duodenal mucosa gluten-free diet celiac disease immune response autoimmunity query expansion IgA plasma cells transglutaminase 2 duodenal mucosa gluten-free diet celiac disease autoimmune response immunology gastroenterology medical research diagnostic markers IgA plasma cells transglutaminase 2 duodenal mucosa gluten-free diet celiac disease autoimmune response intestinal biopsy gluten sensitivity immunoglobulin A intestinal inflammation gluten exposure antigen-specific antibodies IgA plasma cells transglutaminase 2 duodenal mucosa gluten-free diet autoimmune response celiac disease markers IgA plasma cells transglutaminase 2 duodenal mucosa gluten-free diet celiac disease autoimmune response intestinal biopsy immune system gliadin antigen-specific IgA antibodies transglutaminase 2 duodenal biopsy celiac disease gluten sensitivity intestinal mucosa dietary changes immune response markers
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 metabolic genetics inflammation atherosclerosis prevention diet treatment risk factors LDL cholesterol cardiovascular disease inflammation atherosclerosis genetics diet treatment prevention LDL cholesterol cardiovascular disease prevention genetics diet inflammation plaques arteries LDL cholesterol function LDL cholesterol heart health LDL cholesterol benefits LDL cholesterol management LDL cholesterol diet LDL cholesterol levels LDL cholesterol cardiovascular risk LDL cholesterol metabolism LDL cholesterol cardiovascular disease metabolism genetics diet inflammation atherosclerosis LDL cholesterol heart health role of cholesterol in heart disease cardiovascular health factors impact of LDL on heart cardiovascular disease risk factors LDL cholesterol cardiovascular disease inflammation atherosclerosis metabolism genetics diet lifestyle LDL cholesterol cardiovascular disease metabolism genetics inflammation atherosclerosis prevention treatment LDL cholesterol cardiovascular disease prevention mechanism clinical research genetics lifestyle treatment cardiovascular health cholesterol types atherosclerosis lipid profile statins diet impact genetic factors inflammatory markers
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 contigs unassembled sequence data genome assembly sequence analysis bioinformatics genetic sequencing molecular biology de novo assembly techniques contig quality unassembled data comparison genome assembly methods bioinformatics tools sequence data processing contig length assembly algorithms sequencing technologies genetic analysis molecular biology genomics applications de novo assembly techniques specific contigs benefits unassembled sequence limitations bioinformatics tools genome assembly methods contig accuracy improvement sequencing technologies impact genetic data organization assembly algorithm advantages de novo assembly benefits contig quality improvement unassembled data comparison genome assembly techniques sequence data analysis bioinformatics tools genetic contig generation molecular biology advancements next-generation sequencing impact de novo assembly contigs unassembled sequences genome assembly sequencing technologies bioinformatics tools sequence alignment genetic information computational biology de novo assembly techniques specific contigs benefits unassembled sequence challenges bioinformatics tools genome sequencing methods assembly software recommendations next generation sequencing assembly de novo assembly contigs sequence data unassembled data genome assembly bioinformatics genetic sequencing molecular biology genomics de novo assembly contigs sequence data unassembled sequences genome assembly bioinformatics genetic analysis molecular biology DNA sequencing de novo assembly contigs unassembled sequence data genome assembly bioinformatics next-generation sequencing DNA sequencing genetic assembly sequence analysis de novo assembly benefits specific contigs advantages unassembled sequence limitations bioinformatics techniques genome assembly improvements next-generation sequencing assembly algorithms sequence analysis tools
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 complex cell death extracellular release neutrophil HMGB1 inflammation cytokine apoptosis necrosis signaling pathway immune complexes cell death extracellular release neutrophils HMGB1 inflammation cytokines immunology biomedical research autoimmunity apoptosis necrosis immune complexes cell death mechanisms extracellular release neutrophils HMGB1 protein inflammatory response immunology molecular biology apoptosis cytokines innate immunity autoimmune diseases immune complex formation cellular apoptosis extracellular signal neutrophil activation HMGB1 release molecular mechanisms inflammatory response DNA damage signal transduction pathways immune surveillance nuclear factor activation immune complexes cell death extracellular release neutrophil HMGB1 inflammation cytokines apoptosis necrosis autoimmune diseases cancer infection immune response cell signaling inflammatory process molecular mechanisms immune modulation cytokine release innate immunity pathogen recognition immune surveillance adaptive immunity immune response cytokines inflammatory signaling apoptosis necroptosis cytokine release immune surveillance inflammatory cascade innate immunity cellular debris inflammation markers immune complex cell death extracellular release neutrophil HMGB1 cytokine inflammation apoptosis necrosis immunology biochemistry immune complexes cell death extracellular release neutrophils HMGB1 inflammation cytokines apoptosis necrosis innate immunity autoimmunity oncology pathology biomedicine immune complex resolution necroptosis pyroptosis NETs DAMPs inflammatory response cytokines chemokines immunology cell signaling proteomics bioinformatics medical research therapeutic targets
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 viral genome RNA editing AID APOBEC3G APOBEC3F deamination cytidine uridine viral DNA minus strand G-to-A mutations catastrophic mutations RNA virus DNA replication mutagenesis virology epigenetics genetic drift reverse transcription mutational hotspot viral evolution deamination cytidine uridine viral DNA minus strand G-to-A mutations catastrophic mutations viral replication error-prone replication V(D)J recombination mRNA editing AID enzyme TusB protein DNA repair base excisionrepair uracil N-glycosylase deaminase activity mutagenesis viral evolution Virus-host interaction deamination process viral DNA mutations uridine formation cytidine conversion G-to-A mutation viral replication accuracy viral genome stability DNA repair mechanisms viral evolution polymerase error rate viral adaptation deamination cytidine uridine viral DNA minus strand G-to-A mutations genome RNA editing mutagenesis retrovirus HIV mutation rate epigenetics virology molecular biology viral DNA repair deamination process uridine formation G-to-A mutations minus strand impact epigenetic changes viral genome stability mutagenesis mechanisms RNA interference reverse transcription errors deamination cytidine uridine viral DNA minus strand G-to-A mutations genomic instability RNA editing mutagenesis virology epigenetics deamination cytidine uridine viral DNA minus strand G-to-A mutations genome molecular biology epigenetics virology RNA interference mutagenesis genetic variation antiviral therapy viral evolution deamination cytidine uridine viral DNA minus strand G-to-A mutations genome RNA virus retrovirus HIV hepatitis B epigenetics molecular biology virology mutagenesis base modification epitranscriptomics deamination cytidine uridine viral DNA G-to-A mutations strand specificity RNA editing epigenetics virology molecular biology genetic drift mutagenesis
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 cell cycle regulation proteasome pathway chromatin dynamics molecular biology genomics epigenetics genetic regulation histone degradation Rad53 protein DNA replication post-replication cell cycle molecular biology genetic regulation protein function chromatin dynamics histone degradation Rad53 protein DNA replication chromatin dynamics cell cycle regulation molecular biology techniques postreplicative checkpoint epigenetics protein phosphorylation genetic pathways free histones degradation Rad53 protein function DNA replication aftermath histone turnover process cell cycle regulation post-replication events histone modification following replication Rad53 kinase activity chromatin dynamics after DNA replication histone degradation Rad53 protein DNA replication post-replicative modification cellular machinery chromatin maintenance molecular biology genetic regulation cell cycle protein function biochemical pathway histone degradation Rad53 protein DNA replication histone turnover chromatin maintenance cell cycle regulation free histones Rad53 protein DNA replication degradation process cell cycle regulation histone degradation Rad53 protein DNA replication cellular repair chromatin structure post-replicative maintenance proteasome pathway cell cycle regulation histone degradation Rad53 protein DNA replication post-replicative processes chromatin remodeling cell cycle regulation proteasome pathway molecular biology techniques histone degradation Rad53 protein DNA replication post-replicative modification chromatin dynamics cell cycle regulation
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 biology cancer genetics blood disorders molecular biology translational research genomic alterations MDS animal model functional consequences myelodysplastic syndrome research limitations molecular mechanisms cancer biology hematopoietic stem cells somatic mutations treatment options veterinary models stem cell disorders genomic alterations MDS functional consequences animal models molecular mechanisms clinical implications bioinformatics single cell analysis stem cells cancer genetics genomic alterations MDS functional consequences animal models biological pathways cancer research stem cell biology hematopoiesis molecular mechanisms clinical implications genomic alterations Myelodysplastic syndrome animal models functional consequences hematopoietic stem cells gene expression chromosomal abnormalities cellular proliferation leukemia risk epigenetic modifications transcriptomics proteomics stem cell biology hematopoiesis oncogenesis clinical outcomes genetic heterogeneity therapeutic targets disease progression mutation impact molecular mechanisms mouse models zebrafish models genetic screening gene knockouts patient-derived xenografts genomic alterations MDS animal model functional consequences myelodysplastic syndrome research limitations stem cell dysfunction treatment options genetic mutations clinical applications preclinical studies genomic alterations Myelodysplastic syndrome functional consequences animal models cellular mechanisms hematopoietic disorders genetic variations disease modeling biological pathways clinical implications genomic alterations MDS animal models functional consequences stem cell dysfunction leukemia risk pancytopenia immune response apoptosis chromosomal abnormalities mutation impact cellular biology cancer development genomic alterations Myelodysplastic syndrome animal models functional consequences hematopoietic dysfunction cellular mechanisms oncogenic mutations blood disorders gene expression stem cell biology cancer genetics genomic alterations MDS functional consequences animal models cancer genetics molecular biology hematopoiesis stem cell dysfunction somatic mutations DNA damage response 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 Pk protein zebrafish development neuroectoderm cells neuralation cell membrane localization planar cell polarity Fz/PCP Pk protein anterior membrane neuroectoderm cells zebrafish development neuralation planar cell polarity cell localization molecular biology developmental genetics Fz/PCP Planar Cell Polarity Protein Localization Zebrafish Embryology Neural Development Neuroectoderm Cells Planar Polarization Fz/PCP pathway Pk protein neuroectoderm cells zebrafish development neuralation process anterior membrane localization cell signaling pathways molecular biology techniques gene expression analysis zebrafish embryo developmental biology research Fz/PCP Pk protein neuroectoderm cells zebrafish neuralation anterior membrane cell localization developmental biology molecular biology genetics Fz/PCP Pk localization neuroectoderm cells zebrafish neuralation planar cell polarity embryonic development molecular biology genetics neuroscience Fz/PCP Pk protein neuroectoderm cells zebrafish development neuralation anterior membrane cell localization molecular biology embryonic patterning Fz/PCP Pk protein neuroectoderm cells zebrafish neuralation anterior membrane molecular localization developmental biology gene expression cell signaling Fz/PCP Pk protein neuroectoderm cells zebrafish development neuralation cell membrane localization planar cell polarity molecular biology embryology Fz/PCP signaling zebrafish neural development neuroectoderm cell differentiation polarization in embryos Pk protein localization
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 regulatory T cells cytokines immune tolerance adaptive immunity immune responses Th17 cells iTregs inflammation immune regulation cytokines T helper cells regulatory T cells immunology autoimmune diseases chronic inflammation adaptive immunity cell biology immunopathology immune tolerance immune responses Th17 cells iTregs inflammation immune regulation cytokines immune response types adaptive immunity immune tolerance immune response mechanisms Th17 cell induction iTreg function immune regulation inflammation process adaptive immunity cytokine production immune cell differentiation immunological tolerance T cell subsets immune system responses immune responses Th17 cells iTregs inflammation cytokines immune regulation autoimmune diseases T cell differentiation immunology adaptive immunity immune responses Th17 cells iTregs inflammation immune regulation cytokines T cell differentiation immune tolerance autoimmune diseases immunology adaptive immunity immune responses Th17 cells iTregs inflammation immune regulation cytokines T helper cells regulatory T cells immune tolerance immune responses Th17 cells iTregs inflammation immune system cytokines lymphocytes T-helper cells regulatory T cells immunology autoimmune diseases infection immune tolerance immune response Th17 cells iTregs inflammation cytokines T helper cells regulatory T cells immune regulation autoimmune diseases immune tolerance immune modulation immune regulation inflammation Th17 cells iTregs cytokines immune tolerance autoimmunity immune homeostasis adaptive immunity T 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 receptors PCP signaling zebrafish development notochord neuralation anterior membrane localization cell biology embryonic development molecular biology gene expression Fz/PCP Pk protein zebrafish development notochord cells neuralation cell membrane localization molecular biology embryonic patterning developmental genetics Fz proteins PCP signaling zebrafish development neuralation process notochord cells anterior membrane localization gene expression embryonic stages molecular biology morphogenesis Fz/PCP signaling zebrafish development notochord cells neuralation polarity proteins molecular biology cellular localization Fz/PCP Pk protein zebrafish development neuralation notochord anterior membrane cell localization gene expression embryonic stage molecular biology morphogenesis Fz/PCP signaling zebrafish development notochord cells neuralation anterior membrane localization Pk protein planar cell polarity gene expression analysis embryonic patterning morpholino knockdown fluorescent microscopy Fz/PCP Pk protein zebrafish development neuralation notochord cell membrane localization molecular biology embryonic development genetic markers Fz/PCP Pk protein zebrafish development neuralation notochord cells anterior membrane molecular localization embryonic patterning Fz/PCP Pk protein zebrafish development neuralation notochord anterior membrane cell localization molecular biology embryonic stage Fz/PCP Pk protein zebrafish development neuralation notochord cells anterior membrane planar cell polarity gene expression embryo stage cellular 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 fast-twitch muscle efficacy clinical trial neuromuscular disease treatment study symptoms tirasemtiv fast twitch muscle effect research studies trials clinical benefits side pharmacology neurology motor function atrophy symptoms treatment patients population study analysis comparison mechanism therapy clinical trial tirasemtiv fast-twitch muscle effectiveness clinical study research treatment therapy neurological disease symptoms improvement efficacy Tirasemtiv treatment outcomes slow-twitch muscle effects Tirasemtiv clinical trials muscle fiber type response Tirasemtiv mechanism of action Tirasemtiv fast-twitch muscle efficacy clinical trial neuromuscular disease myopathy skeletal muscle motor neurons pharmacodynamics clinical outcome therapeutic index tirasemtiv muscle fibers efficacy clinical trials slow-twitch pharmacology neuromuscular therapy treatments clinical outcomes tirasemtiv fast-twitch muscle effectiveness clinical trial neuroscience muscular dystrophy myopathy pharmacodynamics efficacy biomedical research tirasemtiv clinical trials slow-twitch muscle fibers muscle type specificity pharmacodynamics tirasemtiv fast-twitch vs slow-twitch muscle fiber research therapeutic effects muscle diseases tirasemtiv efficacy assessment muscle contraction mechanisms tirasemtiv fast-twitch muscle efficacy clinical trial neurology ALS muscular dystrophy pharmacology treatment symptoms improvement side effects tirasemtiv clinical trials slow-twitch muscle fibers muscular dystrophy treatment muscle atrophy research sarcoptic glycoprotein 3 neurodegenerative diseases muscle fiber types therapeutic efficacy muscle weakness studies drug efficacy analysis
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. clpC protein Bacillus subtilis sporulation genetic mutation bacterial spore formation gene function sporulation process clpC role bacterial genetics spore formation efficiency gene deletion effect clpC protein function Bacillus subtilis sporulation sporulation efficiency analysis genetic impact on sporulation clpC role in bacteria Lack clpC Bacillus subtilis sporulation effectiveness genetic modification protein expression microbiology clpC protein function Bacillus subtilis sporulation bacterial spore formation gene knock-out effect sporulation efficiency analysis clpC role in bacteria sporulation regulation genes clpC protein Bacillus subtilis sporulation process genetic mutation bacterial cell cycle gene function microbial physiology Lack of clpC sporulation efficiency Bacillus subtilis gene function protein degradation bacterial cell cycle transcription factors genetic mutation impact microbial physiology clpC protein Bacillus subtilis sporulation gene function bacterial spore formation sporulation process genetic knockout cell biology microbiology biological pathway analysis clpC protein Bacillus subtilis sporulation sporulation efficiency genetic mutation proteolysis regulator Lack clpC Bacillus subtilis sporulation effect molecular biology genetics proteolysis clpC function Bacillus subtilis sporulation gene expression protein degradation sporulation process bacterial spore formation genetic mutation impact biological pathway analysis
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.cell function stem.cell.differentiation molecular.biology T-cell.development immune.system regulation gene.expression microarrayanalysis transcription.factors developmental.biology GATA-3 hematopoietic stem cell function transcription factor molecular biology regulation immunology stem cell research cellular biology DNA binding GATA3 hematopoietic.stem.cell function stem.cell.differentiation molecular.biology gene.expression immune.system t-cell.development regulatory.factors transcription.factor GATA-3 role GATA-3 function hematopoietic stem cell maintenance GATA-3 gene hematopoiesis regulation HSC differentiation transcription factor GATA-3 GATA-3 protein expression hematopoietic development stem cell biology GATA-3 hematopoietic stem cell function transcription factor gene expression immune system differentiation regulatory T cells Th17 cells GATA-3 role HSC development GATA-3 gene functional importance Hematopoiesis stem cell maintenance GATA3 hematopoietic.stem.cell function regulation T-cell.development maintenance DNA.bindings promoter.activation molecular.biology stem.cell.research transcription.factors immunology bioinformatics microarray.technology genetic.mechanisms GATA-3 role HSC function blood development stem cell biology immune system regulation transcription factor activity GATA3 hematopoietic.stem.cell function molecular.gene.regulation immune.system stem.cells blood.formation differentiation transcription.factor cellular.processes GATA-3 regulation hematopoietic stem cell differentiation GATA-3 expression hematopoiesis GATA-3 knockout experiment hematopoietic lineage development
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 deleting raptor G-CSF levels clinical trial pharmacology biology hematopoiesis cytokines chemotherapy side effects deleting raptor gcsf levels immune response risk factors clinical trial biological markers deleting raptor g-csf levels hematopoietic growth factors myeloid lineage cytokine therapy bone marrow recovery immunosuppression hematopoiesis inflammation oncology treatment search optimization query expansion medical research hematopoietic cytokines pharmacological interventions clinical efficacy drug interactions biotechnology immunology therapeutic targets search efficiency expand query deleting raptor g-csf levels clinical study mechanisms impact treatment pharmacology immunology search optimization query expansion relevant phrases medical terms G-CSF levels Raptor treatment Deleting Raptor G-CSF levels gene editing cytokines hematopoiesis immune response oncology pharmacodynamics Deleting Raptor G-CSF levels pharmacological intervention immune response hematopoiesis clinical trial bone marrow inflammation therapeutic target cytokine regulation Deleting Raptor Raptor inhibition G-CSF levels myeloid progenitor cells immunosuppression inflammation bone marrow function cytokine production hematopoiesis therapeutic targets drug effects immune response modification deleting raptor gcsf levels immune modulation cytokines myeloid cells hematopoiesis pharmacodynamics
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. Deletion αvβ8 spontaneous inflammatory phenotype immune response fibrosis angiogenesis cytokines mice models pathology hematopoiesis αvβ8 integrin deletion experiment inflammatory response spontaneous inflammation gene knockout immune system mouse model cell adhesion biomarker therapeutic target inflammatory response αvβ8 integrin knockout model immune system gene deletion inflammatory phenotype immunology inflammation genetic modification biological response mouse model integrins cytokines leukocyte recruitment immune cells chronic inflammation acute inflammation tissue repair wound healing inflammatory response αvβ8 integrin deletion effects immune system mouse model gene knockout inflammation phenotype hematopoietic cells tissue repair signaling pathways αvβ8 integrin inflammatory phenotype knockout model spontaneous inflammation immune response bone marrow gut microbiota vascular permeability wound healing cancer progression angiogenesis immunology genetics mouse model αvβ8 integrin inflammatory response deletion effects spontaneous inflammation immune system gene knockout biomarkers cytokines cell adhesion tissue repair pharmacological intervention mouse model therapeutic target αvβ8 integrin inflammation knockout mice immune response cytokines hematopoietic cells vascular integrity wound healing cancer progression bone remodeling αvβ8 integrin inflammatory response knockout model spontaneous inflammation immune system gene deletion biological function tissue repair vascular development hematopoiesis αvβ8 integrin inflammatory phenotype deletion study immune response gene knockout inflammation autoimmune disorders immunology molecular biology cell signaling pathology αvβ8 integrin inflammatory response knockout mice immune system gene deletion cytokines inflammatory markers autoimmune diseases tissue repair blood vessels collagen-binding signaling pathways immune cells bone marrow embryonic development adult tissue cell adhesion angiogenesis cancer progression wound healing fibrosis thrombosis
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 memories T cells immune response lymphocytes adult tissue memory T cells immune system T cell types immunology lymphocytes adaptive immunity tissue-specific immunity adult tissue T cells Memory T cells immunology tissue types immune system T cell development memory T cells function T cell differentiation adult immune system T cell biology adaptive immunity T cell subtypes T cell longevity immunology research T cell activation adult tissue memory T cells T cell types immune system lymphocytes immunology adaptive immunity tissue specificity cellular immunity adult tissue memory T cells T cell types immune system response tissue specificity T cell subsets adaptive immunity lymphocyte function immunology research T cell development adult tissue memory T cells T cell types immune system tissue samples lymphocytes immunology adaptive immunity T cell subsets cellular biology adult tissue T cells memory T cells immune system cellular immunity B cells antigen presentation immune response adult tissue T cells memories T cells immune response vaccine response chronic infection ageing-immune-system adult tissue memory T cells immune system lymph nodes T cell subsets immunology adaptive immunity antigen presentation T cell development immune response duration
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 genetic mutation CHEK2 gene breast cancer risk factors CHEK2 protein function breast cancer predisposition tumor suppressor gene CHEK2 inheritance BRCA1 BRCA2 comparison genetic testing for breast cancer CHEK2 pathway involvement CHEK2 breast cancer association CHEK2 genetic testing CHEK2 mutation CHEK2 inheritance CHEK2 risk factors CHEK2 and cancer CHEK2 clinical significance CHEK2 prevalence CHEK2 cancer types CHEK2 epidemiology CHEK2 gene breast cancer risk genetic association cancer susceptibility BRCA1 BRCA2 hereditary breast cancer tumor suppressor gene breast cancer genetic testing CHEK2 function CHEK2 mutation analysis breast cancer risk factors tumor suppressor genes breast cancer prevention strategies CHEK2 gene function brca1 brca2 cancer risk family history symptoms prevention treatment mutations inheritance pattern clinical significance genetic counseling genetic testing cancer risk mutation analysis BRCA1/2 hereditary cancer predisposition tests CHEK2 gene function breast cancer risk family history genetic testing mutation association studies research population genetics CHEK2 gene function mutations risk factors hereditary predisposition brca1 brca2 differences cancer genetics testimonials research studies clinical trials genetic counseling prevention screening heritable traits genome analysis biological markers mutation impact prognosis treatment options public health genomics biotechnology medical advancements patient education clinical implications genetic testing precision medicine healthcare outcomes biomedical research public awareness genetic disorders medical genetics biological significance molecular biology genetic testing benefits genetic CHEK2 breast cancer genetic mutation BRCA1 BRCA2 cancer predisposition tumor suppressor gene clinical significance hereditary cancer syndromes oncogenes genetic testing cancer risk assessment breast cancer genetic testing CHEK2 function cancer risk factors breast cancer genetics gene mutation analysis
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 %5mmol/L less than 10% effectiveness search terms suggestions Schimmelpenning-Feuerstein-Mims SFM Gabon plasma lactate children prevalence symptoms genetics metabolic disorders Schimmelpenning-Feuerstein-Mims syndrome SFM plasma lactate Gabon children disease metabolism effectiveness query expansion keywords research pediatrics mortality risk frequency statistics Schimmelpenning-Feuerstein-Mims syndrome Gabonese children plasma lactate SFM neurological disorders pediatric conditions metabolic syndromes neurological symptoms blood lactate levels genetic disorders Schimmelpenning-Feuerstein-Mims syndrome Gabonese children lactate plasma pediatrics rare disease clinical biomarker Schimmelpenning-Feuerstein-Mims syndrome Gabon plasma lactate genetic disorders metabolic syndromes pediatric conditions neurological symptoms diagnostic markers Schimmelpenning-Feuerstein-Mims syndrome gabonese children plasma lactate 5mmol/L medical genetics rare diseases clinical manifestations Schimmelpenning-Feuerstein-Mims Gabon children plasma lactate syndrome prevalence metabolic disorder Schimmelpenning-Feuerstein-Mims syndrome Gabonese children lactate plasma disease rare metabolic Schimmelpenning-Feuerstein-Mims syndrome Gabonese children lactate plasma elevated percentage
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 RhoGAP RhoA SRC gene regulation oncology signal transduction cancer biology cellular response Leukemia Rho guanine nucleotide-exchange factor RhoA SRC activation gene expression signaling pathway oncology molecular biology hematopoietic disorders cancer research leukemia RhoGAP RhoA SRC oncology molecular biology signal transduction genetic factors cancer biology tumor suppressor leukemia RGNEF RhoA regulation SRC activation oncogenic signaling gene expression cancer biology cellular response molecular mechanisms leukemic cells Rho GTPases signal transduction pathways Leukemia Rho guanine nucleotide-exchange factor RhoA SRC activation gene expression signaling pathway oncology molecular biology cancer research Leukemia Rho guanine nucleotide-exchange factor RhoA SRC activation gene expression signal transduction oncology research molecular biology cancer therapy cellular response Leukemia Rho guanine nucleotide-exchange factor RhoA SRC activation gene expression signaling pathway oncology cellular biology molecular biology cancer research leukemia RhoGDI2 RhoA SRC gene expression signaling pathway oncology hematopoietic cells cancer biology molecular genetics Leukemia Rho guanine nucleotide-exchange factor RhoA SRC activation gene expression signaling pathway oncology molecular biology cancer research cellular regulation leukemia RhoGEF RhoA SRC gene expression signaling pathway cancer biology molecular genetics
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. leukocyte transfusion infection risk factor hematology immune reaction prevention treatment leukocyte transfusion infection risk increase hematopoietic stem cells immune response leukocytes transfusion-related infection immune response clinical outcomes white blood cells hematopoiesis immunocompromised blood compatibility cytokines leukocytes blood transfusion risks infectious disease prevention immune response white blood cells transfusion-associated complications clinical guidelines patient safety medical research hematological factors leukocytes blood transfusion infectious complications erythrocytes immune response hematology risk factors leukocyte risk factors transfusion complications immune response patients donor processing storage leukocyte transfusion infection complication blood cells immune response donor recipient neutrophils monocytes cytokines leukocyte risk factor transfusion associated infection complications therapeutic blood product safety leukocytes blood transfusion infectious complications transfusion medicine immune response white blood cells leukocyte reduction transfusion risk factors complications therapy evidence prevention
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. Transplantation Immunology Lymphocytes Memory Cells Immune Response Tissue Engineering Regenerative Medicine T cell memory transferred cells immune response memory T cells lymphocyte migration adaptive immunity immunology transplantation cellular therapy immune reconstitution chimeric antigen receptors TCR expression T cell activation antigen presentation T cell proliferation Transplantation Immunology Lymphocytes Adaptive Immunity Gene Therapy Host-Pathogen Interaction Immune Response Stem Cells Biomedical Research Clinical Trial Transplantation immune response gene editing immunotherapy adaptive immunity cytokine production antigen presentation T cell differentiation alloreactivity chronic infection cancer treatment transplantation immunology immunological memory stem cell transplantation T helper cells regulatory T cells cytotoxic T cells CD8+ T cells CD4+ T cells Transplantation Immune response Lymphocytes Adaptive immunity Memory cells Transcription factors Gene expression Immunology Stem cells Host-microbe interaction memory T cells transferred lymphocytes immune response modulation immunotherapy adaptive immunity cell transfer experiments T cell differentiation antigen-specific memory transplantation immunology adaptive immunity T cell differentiation memory T cells immune response lymphocyte trafficking cytokine production gene expression stem cell transplantation transferred UCB cells memory-like phenotype T cell differentiation immune response stem cells transplant immunity lymphocyte activation adaptive immunity cellular therapy immune response memory T cells transplantation immunology adaptive immunity lymphocytes antigen recognition cytokines T cell activation graft-versus-host immune memory T cell differentiation allogeneic移植细胞 immune response memory T cells transplantation immune tolerance chimeric抗原受体 alloreactivity
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 white blood cells transfusion safety hematology clinical trials medical research blood donation immune system healthcare treatment effectiveness leuko-reduction blood transfusion infectious complications red blood cells leukocytes transfusion medicine clinical trials hematopoiesis immune system medical research leukoreduced leukocyte transfusion infection complication blood treatment therapy patient risk reduction hospital clinical efficacy safety transfusion medicine hematology immunology pathology leuko-reduced blood benefits leuko-reduced blood safety leuko-reduced blood transfusion leukocyte-reduced blood advantages leukocyte-reduced blood infection reduced leukocytes in blood leukoreduced blood efficacy leuko-reduction blood transfusion infectious complications red blood cells white blood cells transfusion safety hematopoietic stem cell transplantation clinical trial blood product safety leuko-reduced blood benefits leuko-reduced blood safety leuko-reduced blood transfusion reduced infectious risk blood transfusion infections leukocyte-reduced blood leukoreduced blood advantages blood transfusion complications blood component therapy white blood cell filtration leukoreduced blood infectious complications red blood cell transfusion white cell reduction blood purification transfusion safety clinical trials infection risk leukocytes hematopoietic cells leuko-reduction blood transfusion infectious complications erythrocyte transfusion white cell removal leukoreduced blood infectious complications red blood cell transfusion white blood cells blood transfusion safety infection risk leukocytes medical research clinical trials blood donation hematopoiesis immunology transfusion medicine healthcare outcomes leuko-reduction blood transfusion complications infectious disease prevention filtered blood blood processing techniques clinical outcomes
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 molecular biology genetic similarity transcriptional stability gene regulation cell homogeneity molecular biology genetic identicality cellular consistency biological variation epigenetics transcriptional stability gene regulation cellular consistency molecular biology genetic uniformity transcriptomics epigenetics cell differentiation gene regulation cellular consistency genetic redundancy molecular biology biological variability identical twins cell heterogeneity transcriptomics epigenetics gene function analysis gene regulation cell homogeneity molecular biology genetic identity biological variability gene regulation cellular consistency genetic variability molecular biology identical twins transcriptional activity gene regulation cellular consistency genetic identity molecular biology RNA expression cell homogeneity gene regulation cell homogeneity molecular biology genetic identicality biological variability gene regulation cellular heterogeneity epigenetics transcriptional variability identical twins RNA expression profiling molecular biology techniques genetic background effects gene regulation transcriptional variation cellular heterogeneity epigenetics gene copy number RNA editing alternative splicing
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 aging dietary restriction senescence human aging model organisms nutrition effectiveness biomarker genetic factors CR methylation age longevity dietary restriction aging senescence human aging model organisms nutrition epigenetics biomarker CR methylation age longevity aging caloric restriction human studies animal models dietary interventions molecular markers biomarkers CR methylation age longevity dietary restriction aging senescence epigenetics human aging research biomarker CR methylation age aging caloric restriction epigenetics human aging research biomarker biological age CR methylation age aging process longevity fecal microbiome caloric restriction human study animal model epigenetic clock CR methylation age longevity dietary restriction aging senescence gene expression nutrigenomics CR methylation age aging senescence dietary restriction longevity molecular markers gene expression human studies animal models CR methylation age longevity dietary restriction aging senescence epigenetics nutrigenomics CR methylation age longevity dietary restriction epigenetic aging senescence human aging model organisms aging research biomarkers of aging
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 aneuploidy genetic variation chromosomal instability yeast populations common genetic disorders genomic imbalances domesticated yeasts Saccharomyces cerevisiae whole chromosome aneuploidy domesticated populations genetic variation yeast chromosome instability evolutionary biology molecular genetics Saccharomyces cerevisiae genetics chromosome abnormalities yeast genome variation aneuploidy frequency genetic stability chromosomal abnormalities in yeast Saccharomyces cerevisiae genome yeast whole chromosome aneuploidy Saccharomyces cerevisiae genetic variation whole chromosome aneuploidy prevalence yeast chromosome abnormalities domesticated yeast evolution Saccharomyces cerevisiae genome stability common chromosomal aberrations rare genetic disorders yeast population genetics chromosome nondisjunction frequency Saccharomyces cerevisiae chromosomal structure Saccharomyces cerevisiae whole chromosome aneuploidy domesticated populations genetic variation yeast biology chromosomal abnormalities evolutionary genetics molecular biology fungal genomics Saccharomyces cerevisiae chromosome variations common genetic mutations yeast aneuploidy prevalence domesticated yeast evolution chromosome instability in yeast Saccharomyces cerevisiae genome analysis yeast chromosome abnormalities genetic diversity in yeast whole genome duplication yeast Saccharomyces cerevisiae whole chromosome aneuploidy domesticated populations genetic variation chromosomal abnormalities yeast genetics rare genetic events genomic stability evolutionary biology fungal genetics Saccharomyces cerevisiae whole chromosome aneuploidy domesticated populations genetic stability yeast genetics chromosomal abnormalities common genetic variations evolutionary biology yeast genome stability Saccharomyces cerevisiae whole chromosome aneuploidy domesticated populations genetic variation yeast biology chromosome abnormalities genomic stability evolutionary genetics microbiology genetic disorders Saccharomyces cerevisiae whole chromosome aneuploidy domesticated populations genetic variation yeast genetics chromosomal abnormalities genomic instability Saccharomyces species comparison evolutionary biology yeast adaptation
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 surgery outcomes CRP postoperative mortality CABG coronary artery bypass graft inflammatory markers surgical outcomes cardiac surgery risk assessment predictive factors cardiovascular surgery CRP levels postoperative outcomes CABG surgery inflammatory markers mortality risk surgical interventions cardiovascular surgery prognostic factors cardiac surgery perioperative complications CRP levels postoperative complications CABG outcomes surgical mortality inflammatory markers cardiovascular events recovery rates patient prognosis risk assessment clinical significance CRP postoperative mortality CABG coronary artery bypass predictive factors CRP levels postoperative complications CABG outcomes surgical mortality risk inflammatory markers cardiac surgery prognosis CRP postoperative mortality Coronary Artery Bypass Graft CABG predictive factors surgical outcomes inflammation markers CRP levels CABG surgery outcome predictive value postoperative mortality cardiovascular surgery inflammatory markers CRP levels postoperative complications CABG outcomes inflammatory markers surgical mortality risk assessment cardiovascular surgery prognostic factors CRP levels CABG complications postoperative care outcome predictors mortality risk factors surgical outcomes
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. P.chabaudi infection dynamics parasite proliferation inoculation dose early infection mouse model mice P. chabaudi parasites proliferation infection inoculation dose response blood erythrocytes virus host immune mechanism P.chabaudi parasite proliferation mouse infection inoculation dose immune response virulence factors red blood cells malaria parasites infection dynamics mice P.chabaudi infection kinetics parasite proliferation rates inoculation dose effects immune response dynamics transmission potential virulence factors immunology research malaria parasite lifecycle experimental parasitology infectious disease modeling mice P.chabaudi parasites proliferation infection inoculation number dose effectiveness mice P. chabaudi parasite proliferation inoculation number infection rate lower numbers high numbers immune response erythroid lineage red blood cell production P.chabaudi mouse infection parasite proliferation inoculation number early infection parasite growth rate mice P.chabaudi infection dynamics parasite proliferation inoculation numbers efficacy keywords query beneficial expansion mice P.chabaudi infection dynamics parasite proliferation viral load immune response host response infected population dynamics low inoculum high inoculum survival rate immune evasion strain variability malaria parasites mouse models infection dynamics parasite inoculation virus replication kinetics P. chabaudi biology
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 loss facilitation MOZ-TIF2 leukemogenesis cancer development stem cells immune response genetic mutation mouse models CSF1R loss facilitation MOZ-TIF2 leukemia induction genetic experimental biological oncogenesis immunology cancer research hematopoiesis mouse models CSF1R loss facilitation MOZ-TIF2 leukemia oncogenesis hematopoiesis genetics immunology mouse models CSF1R loss MOZ-TIF2 leukemia induction gene expression stem cell development immune response cancer progression biological pathways genetic modification cellular biology oncology research hematopoiesis signaling molecules tumor microenvironment stemness factors hematological malignancies mouse models CSF1R MOZ-TIF2 leukemogenesis molecular biology cancer research genetic modification immune system stem cells mouse models CSF1R loss MOZ-TIF2 leuekmogenesis relevant expansion phrases scientific research bioinformatics genetic models oncology studies mouse models CSF1R loss MOZ-TIF2 leukemia oncogenesis gene expression immunology cancer biology mouse models CSF1R MOZ-TIF2 leukemogenesis genetic knockout immune response microglia cancer development CSF1R deletion MOZ-TIF2 fusion leukemia development mouse genetics hematopoietic malignancy immune response modulation cancer biology signaling pathways oncogenic mechanisms mouse models CSF1R MOZ-TIF2 leuekmogenesis cancer mechanisms hematopoiesis gene expression stem cells immune response signaling 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 immune response CX3CR1 Th2 cells T cell survival immune response inflammation cytokines immunology biology gene function mouse model human study immune regulation CX3CR1 Th2 T cells survival immune response cytokines signaling immunology inflammation genetics mice humans immune regulation T helper cells adaptive immunity CX3CR1 Th2 cells T cell survival immunology inflammation gene expression immune response cytokines allergic reactions immune tolerance cell signaling adaptive immunity innate immunity antigen presentation lymphocytes cytokine production immune modulation immune homeostasis CX3CR1 Th2 cells T cell survival immunology inflammation cytokines gene expression immune response allergic diseases multiple sclerosis adaptive immunity CX3CR1 Th2 cells T cell survival immune response inflammation gene expression cytokines immunology cell signaling adaptive immunity innate immunity immune modulation therapeutic targets biomarkers CX3CR1 Th2 cells T cell survival immunology cytokines gene expression immune response inflammation T helper cells adaptive immunity innate immunity immune regulation antigen presentation T cell activation cell signaling bioinformatics genetic markers CX3CR1 Th2 cells T cell survival immunology cytokines inflammation gene expression mouse models immune response allergic reactions CX3CR1 Th2 cells T cell survival immunology cytokines gene expression mouse models allergic responses immune regulation CX3CR1 Th2 cells T cell survival immune response inflammation cytokines gene expression immune regulation antigen presentation adaptive immunity innate immunity immunology molecular biology cellular biology
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 inflammation immune regulation signaling molecules adaptive immunity immune homeostasis CX3CR1 Th2 cells T cell survival immune response cytokines inflammation immunology biology genetics adaptive immunity T helper cells CX3CR1 Th2 cells T cell survival immune response cytokines signaling pathways immunology inflammation gene expression allergy asthma adaptive immunity CX3CR1 Th2 cells function CX3CR1 Th2 cells immune response CX3CR1 Th2 cells signaling pathways CX3CR1 Th2 cells cytokine production CX3CR1 Th2 cells antigen presentation CX3CR1 Th2 cells differentiation CX3CR1 Th2 cells proliferation CX3CR1 Th2 cells activation CX3CR1 Th2 cells migration CX3CR1 Th2 cells gene expression CX3CR1 Th2 cells T cell survival immune response cytokines chemokines inflammation antigen presentation immune regulation cell signaling CX3CR1 Th2 cells T cell survival CX3CR1 function in Th2 cells CX3CR1 signaling Th2 cells Th2 cell survival mechanisms CX3CR1 Th2 cell interaction T cell survival factors Th2 cells CX3CR1 role immune response Th2 cell activation CX3CR1 CX3CR1 expression Th2 cells CX3CR1 and T cell communication CX3CR1 Th2 cells T cell survival immune response cytokines gene expression immune modulation antigen presentation lymphocyte activation inflammation markers CX3CR1 Th2 cells T细胞存活 survival molecular mechanism immune response innate immunity adaptive immunity chemokine receptor CX3CR1 Th2 cells T cell survival immune response cytokines gene expression inflammation immunology adaptive immunity innate immunity CX3CR1 Th2 cells T cell survival immune response cytokines gene expression inflammation immunology allergy asthma microbiome
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. steroids surgery bleeding risk factors anesthesia inflammation healing dosage effectiveness Dexamethasone surgery dexamethasone anesthesia dexamethasone dosage postoperative bleeding prevention anti-inflammatory dexamethasone steroids surgical outcomes anesthesia inflammation hemostasis risk factors postoperative complications dexamethasone preoperative preparation dexamethasone dosage surgery anti-inflammatory effects dexamethasone dexamethasone anesthesia interaction steroid use before surgery postoperative care guidelines surgical outcomes improvement anti-inflammatory medication surgery risk reduction surgery anesthetic interaction steroids Dexamethasone postoperative bleeding surgical patients anti-inflammatory cortisol steroid anesthesia surgery type bleeding risk reduction inflammation perioperative management corticosteroids Dexamethasone surgery benefits dexamethasone anesthesia interaction dexamethasone recovery time dexamethasone postoperative care dexamethasone dosage for surgery Dexamethasone corticosteroid inflammation surgery bleeding risk anesthesia recovery surgical site corticosteroids effect postoperative complications Dexamethasone surgery postoperative complications bleeding prevention steroid effect anesthesia interaction inflammation reduction surgical recovery dosage guidelines patient preparation risk factors Dexamethasone postoperative bleeding surgical outcomes corticosteroids inflammation risk reduction anesthesia surgery type dosage effects recovery time Dexamethasone surgery anti-inflammatory effects perioperative management bleeding prevention corticosteroids benefits
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 immunology asthma cytokines chemokines immune response allergic pulmonary biology CX3CR1 Th2 cells airway inflammation immunology cytokines asthma allergy microbiome immune response gene expression CX3CR1 Th2 cells airway inflammation immune response asthma cytokines chemokines mouse model human study immune cells allergic reaction CX3CR1 Th2 cells airway inflammation immune response allergic reactions asthma cytokines chemokines gene expression immunology pulmonary diseases biomarkers CX3CR1 Th2 cells airway inflammation immune response asthma inflammation mechanisms cytokines immune cells allergic reactions pulmonary function biomarkers CX3CR1 Th2 cells airway inflammation immunology cytokines asthma immune response allergic reaction gene expression inflammation markers cell signaling CX3CR1 Th2 cells airway inflammation immune response cytokines asthma allergens immunology T helper cells inflammation markers CX3CR1 Th2 cells airway inflammation immunology cytokines allergic responses asthma immune response modulation inflammation markers T-helper cells respiratory system diseases CX3CR1 Th2 cells airway inflammation immune response cytokines asthma allergens gene expression immunology respiratory system bioinformatics transcriptomics CX3CR1 Th2 cells airway inflammation immune response cytokines asthma eosinophils allergic reactions immunology respiratory disorders
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 immunosuppression allergic asthma cytokines immune response regulatory T cells lung infection allergic reaction CX3CR1 Th2 cells airway inflammation immune response asthma allergy cytokines immunology inflammation regulation cell interactions immune suppression CX3CR1 Th2 cells airway inflammation immune regulation cytokines asthma allergic reactions immunology molecular biology inflammation markers CX3CR1 regulation Th2 cell function airway inflammation mechanisms immune response modulation cytokine production抑制 allergic asthma association immune cell interaction inflammatory pathwaysactivation CX3CR1 genetic variants Th2 cell differentiation pulmonary immune surveillance immune homeostasis maintenance lung tissue repair CX3CR1 Th2 cells airway inflammation immune response allergic reactions asthma cytokines gene expression immunosuppression mouse models clinical trials CX3CR1 Th2 cells airway inflammation immune response asthma allergy cytokines immunology regulatory T cells lung health inflammatory diseases CX3CR1 Th2 cells airway inflammation immune response cytokines asthma allergen immune modulation inflammatory mediators CX3CR1 Th2 cells airway inflammation immune suppression regulatory T cells cytokines allergic asthma eosinophils mast cells CX3CR1 Th2 cells airway inflammation immune response asthma immunology cytokines T-helper cells allergic reactions lung health bioinformatics gene expression allergic asthma immunopathology CX3CR1 Th2 cells airway inflammation immunology asthma allergy cytokines immune response inflammation markers antigen presentation T helper cells
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 neurobiology gliosis differentiation host-immune response stem cells neural regeneration xenotransplantation biocompatibility tissue engineering transplantation glial cells differentiation host animal neurobiology stem cells xenograft gliosis neuroscience neural transplantation neural transplantation glial differentiation host response stem cells neurobiology brain repair biocompatibility regeneration tissue engineering xenotransplantation neuroinflammation transplanted human neural cells differentiation in host brain human glial cell transplantation neuroregeneration after transplantation gliosis response human glial cell integration stem cell therapy in neuroscience human-animal chimerism transplantation immunology neural plasticity research transplantation glial cells differentiation host animal neuroregeneration stem cells neuroscience xenotransplantation transplanted human cells glial cell differentiation host animal response neural stem cells xenotransplantation brain cell transplantation neurogenesis tissue compatibility immune rejection stem cell therapy neural transplantation glial cell differentiation host animal response stem cell therapy neuroregeneration brain transplantation cellular biology tissue compatibility immune rejection gene expression analysis transplantation neural regeneration glial cell differentiation host animal stem cells neuroscience biotechnology medical research neurology tissue engineering transplantation glial cells differentiation host animal neurobiology stem cells regeneration neuroscience xenotransplantation biocompatibility neural transplantation gliogenesis neurogenesis xenotransplantation stem cells brain repair cellular therapy neurological disorders biocompatibility immune response
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 genetic diversity cell division oncology research molecular biology stem cell biology chromosome mis-segregation blood stem cells hematopoiesis hematopoietic.stem.cells chromosome.segregation random.mechanism cell.division genetic.variation stem.cell.differentiation mitosis meiosis oncology biology genetics research medical.research chromosomal.segregation molecular.biology hematopoietic+stem+cells chromosome+segregation random+mitosis genetic+diversity stem+cell+differentiation telomeres meiosis somatic+cells oncogenesis regenerative+medicine hematopoietic stem cell biology chromosome segregation process random mitosis stem cell genetics hematopoiesis mechanisms chromosome distribution stem cell division genetic diversity cellular replication accuracy hematopoietic progenitor cells hematopoietic.stem.cells chromosome.segregation random.mitosis molecular.biophysics cancer.research stem.cell.division hematology genetic.variation hematopoietic stem cell division chromosome segregation process random meiosis stem cell biology genetic diversity hematopoiesis chromosomal distribution cellular genetics molecular biology biological research methods hematopoietic.stem.cells chromosome.segregation molecular.biology genetics mitosis binary.fission cell.division chromosomal.segregation random.mitosis hematopoiesis hematopoietic stem cells chromosome segregation random process cell division genetic diversity meiosis mitosis chromosomal distribution oncogenesis blood cell development hematopoietic stem cells chromosome segregation random mitosis stem cell division genetic inheritance cell biology DNA replication oncology biomedical research genetic diversity hematopoiesis chromosome segregation stem cell differentiation genetic diversity mitosis oncogenesis leukemogenesis myeloid lineage lymphoid lineage
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 chromatin marks genetic regulation DNA methylation transcription factors gene expression H3K4me3 H3K79me2 quiescent hair follicle stem cells chromatin mark epigenetics differentiation H3K4me3 H3K79me2 quiescent hair follicle stem cells epigenetics methylation chromatin transcription regulation DNA methylation chromatin modification stem cell biology H3K4me3 H3K79me2 quiescent hair follicle stem cells differentiation markers chromatin modifications stem cell biology hair follicle development genetic regulation cell cycle H3K4me3 H3K79me2 quiescent hair follicle stem cells chromatin marks genetic regulation transcription factors DNA methylation quiescent hair follicle stem cells markers h3k4me3 h3k79me2 expression stem cell differentiation chromatin modification genetic regulation follicle development cellular biology relevant gene expression patterns H3K4me3 H3K79me2 quiescent hair follicle stem cells chromatin marks transcription factors methylation patterns H3K4me3 H3K79me2 quiescent hair follicle stem cells chromatin modification transcription regulation epigenetics H3K4me3 H3K79me2 quiescent hair follicle stem cells chromatin mark epigenetics regulation DNA transcription H3K4me3 H3K79me2 quiescent hair follicle stem cells chromatin modifications gene regulation epigenetics
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 risk factors cardiovascular disease hypertension thrombocytopenia anticoagulants antiplatelets comorbidities mortality complications diabetes acute coronary syndrome bleeding cardiovascular disease thrombocytopenia hematuria retinopathy nephropathy ischemic stroke hemorrhagic stroke anticoagulation antiplatelet therapy cardiovascular risk complications mortality morbidity diabetes diabetic complications acute coronary syndrome bleeding risks long-term effects short-term effects cardiovascular disease glycemic control thrombocytopenia anticoagulation therapy diabetes management ACS treatment bleeding prevention long-term complications short-term risks diabetic cardiomyopathy anticoagulant therapy thrombolytic use patient monitoring chronic conditions cardiovascular outcomes diabetes acute coronary syndrome bleeding risk short-term complications long-term effects diabetes acute coronary syndrome bleeding events diabetic patients cardiac complications risk factors for bleeding in diabetes managing bleeding in diabetic ACS acute coronary syndrome and diabetes management long-term complications of diabetes and ACS short-term bleeding risks in diabetics diabetic heart disease bleeding risks diabetes and cardiovascular bleeding acute coronary syndrome bleeding prevention in diabetics diabetes acute coronary syndrome bleeding risk short-term complications long-term effects cardiovascular disease glucose control anticoagulation therapy thrombosis hypertension insulin resistance vascular inflammation diabetes acute coronary syndrome bleeding risk diabetic complications cardiovascular events thrombocytopenia anticoagulation therapy antiplatelet medications mortality morbidity diabetes management chronic conditions cardiovascular disease hemorrhagic complications diabetes acute coronary syndrome bleeding risk short-term long-term complications comorbidity cardiovascular events thrombocytopenia anticoagulation antiplatelet therapy management outcomes clinical trials risk factors treatment strategies diabetes acute coronary syndrome bleeding risk complications treatment prognosis prevention management clinical outcomes cardiovascular events glycemic control anticoagulation therapy thrombosis mortality hospitalization quality of life
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 development process granuloma formation immune cell types pro-inflammatory cytokines immune response mechanisms inflammation process immune cell activation granuloma development immune system response granuloma formation immune response mechanisms inflammatory cytokines macrophage activation tissue inflammation granuloma formation immune response mechanisms inflammatory cells immune cell types cytokine production antigen presentation macrophage activation immune system function infection-induced inflammation chronic inflammation processes granuloma formation immune cell activation pro-inflammatory cytokines immune response mechanisms antigen presentation inflammation markers lymphocyte recruitment macrophage function tissue repair process granuloma formation immune cell activation pro-inflammatory cytokines immune response mechanisms macrophage role inflammatory mediators granuloma center immune cell response pro-inflammatory cytokines immune response mechanism inflammatory center immune granuloma immune cell activation inflammation induction immune system reaction granuloma formation immune cell activation pro-inflammatory cytokines immune response initiation macrophage aggregation antigen presentation inflammatory mediators granuloma center immune cell function pro-inflammatory response immune system activation cytokine production antigen presentation lymphocyte recruitment inflammation process immune response regulation granuloma formation immune cell types pro-inflammatory cytokines immune response mechanisms inflammation triggers
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 green florescent protein Sox2 promoter cell proliferation colocalization stem cells neural progenitors fluorescence microscopy gene expression developmental biology biotechnology transgenic mice Sox2 promoter green fluorescent protein cell proliferation markers colocalization stem cells neural stem cells gene expression fluorescence microscopy bioscience research genetic engineering biological markers transgenic mice green fluorescent protein Sox2 promoter cell proliferation markers colocalization gene expression stem cells developmental biology fluorescence microscopy knockout mice biological markers transgenic mice green fluorescent protein Sox2 promoter cell proliferation markers colocalization stem cells gene expression fluorescence microscopy mouse models neurogenesis transgenic mice green fluorescent protein Sox2 promoter cell proliferation markers colocalization gene expression stem cells fluorescence microscopy biological models genetic engineering transgenic mice green fluorescent protein Sox2 promoter cell proliferation markers colocalization gene expression stem cells fluorescence microscopy biological markers genetic engineering molecular biology neuroscience research epigenetics developmental biology transgenic mice green fluorescent protein Sox2 promoter cell proliferation markers colocalization stem cells gene expression fluorescence microscopy biological modeling transgenic mice green fluorescent protein Sox2 promoter cell proliferation markers colocalization gene expression stem cells fluorescence microscopy biotechnology genetic engineering transgenic mice Sox2 promoter green fluorescent protein cell proliferation markers colocalization stem cells neural progenitors gene expression fluorescence microscopy biological models developmental biology transgenic mice green fluorescent protein Sox2 promoter cell proliferation colocalization stem cells neural progenitors gene expression fluorescence microscopy developmental biology genetic engineering
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 site hTRPML2 hTRPML1 ML-SA1 activator orientation difference structure analysis molecular binding hTRPML2 hTRPML1 ML-SA1 activator binding orientation TRPML channels protein structure ligand binding molecular dynamics ion channel signaling pathway binding site hTRPML2 ML-SA1 activator hTRPML1 binding mode differentiation activation mechanism structural biology ion channel pharmacology binding orientation analysis activator specificity TRPML2 TRPML1 comparison ligand binding site molecular interaction structural biology channel activation pharmacological mechanism biological function differentiation binding orientation ML-SA1 activator hTRPML2 hTRPML1 structural difference protein activation ligand binding ion channel regulation binding orientation ML-SA1 activator hTRPML2 hTRPML1 protein binding molecular interaction ligand specificity ion channel activation binding orientation ML-SA1 activator hTRPML2 hTRPML1 structural differences protein-protein interaction ligand binding site molecular dynamics simulation crystal structure pharmacology ion channel GPCR activation mechanism binding orientation ML-SA1 activator hTRPML2 hTRPML1 molecular dynamics receptor activation ligand binding structural differences pharmacology ion channels binding orientation ML-SA1 activator hTRPML2 hTRPML1 protein-protein interaction ligand binding site structural biology molecular dynamics pharmacology ion channel calcium release-activated channel binding orientation ML-SA1 activator hTRPML2 hTRPML1 molecular docking protein-ligand interaction structural biology pharmacology ion channels signal transduction
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 medication cardiovascular risk studies research epidemiology safety long-term short-term clinical trials adults youth heart events outcomes ADHD medications cardiovascular events young adults middle-aged adults serious side effects long-term use short-term use cardiovascular risk mental health medication ADHD treatment heart problems prescription drugs psychological disorders ADHD medications cardiovascular events risk adults young middle-aged serious correlation studies epidemiology side effects ADHD medications safety cardiovascular health adults long-term ADHD medication effects serious cardiac events ADHD young adults ADHD treatment middle-aged ADHD patients cardiovascular risks ADHD drugs ADHD medication side effects analysis ADHD and heart health remote ADHD medication use adult ADHD cardiovascular safety ADHD medications cardiovascular events risk adults young middle-aged serious association epidemiology ADHD medications cardiovascular risk young adults middle-aged adults serious events medication use cardiac health psychiatric drugs long-term effects mental health medications ADHD medications cardiovascular risk young adults middle-aged adults serious events medication use psychiatric drugs heart problems long-term effects short-term effects ADHD medications cardiovascular events young adults middle-aged adults medication use serious health risks psychiatric drugs cardiac events long-term effects short-term effects prescription drugs mental health medications ADHD medications cardiovascular events young adults middle-aged adults serious events risk factors medication use long-term effects recent use psychiatric disorders ADHD medications cardiovascular risk young adults middle-aged adults serious events medication use long-term effects cardiac outcomes
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. transplantation neurogenesis gliogenesis synaptogenesis neural connectivity host integration cell biology neuroscience transplantation immunology transplantation glial progenitor cells neural network host animals neuroscience biology neurology connectivity differentiation integration neurogenesis synaptic plasticity transplanted human glial progenitor cells incapable forming neural network host animals neurons neurogenesis gliogenesis synapse connectivity differentiation migration integration transplantation neuroscience biology stem cells regeneration repair neurology immunology genetics neuroscience research cellular biology brain plasticity transplantation glial progenitor cells neural network formation host animals neurogenesis synaptic connections neuroscience research stem cell therapy brain regeneration biomedical science neurological disorders transplanted cells glial progenitor cells neural network host animals neuron compatibility brain cell transplantation neurogenesis synaptic connection biocompatibility neuroplasticity stem cells neural network formation glial progenitor cells host neurons transplanted cells neurogenesis synaptic connectivity brain tissue compatibility neuronal integration stem cell research neuroscience studies neural connectivity transplanted cells glial function host neurons integration capacity transplantation neurogenesis neuronal connectivity graft rejection cellular therapy neuroscience biocompatibility neural plasticity stem cells synaptic integration transplantation human glial progenitor cells neural network host animals incapable suggest meaningful expansion terms enhance query neural integration gliogenesis synaptic connectivity transplantation biology neurogenesis brain plasticity neuronal communication stem cell therapy neuroregeneration bioengineering neuroscience research
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 immune checkpoint inhibitors IL-10 regulation inflammatory responses PD-1 monocytes IL-10 production immunology cytokinesimmune checkpoint monocyte function inflammatory response PD-1 ligands monocyte activation IL-10 suppression immune checkpoint inhibitors innate immunity cytokine production T-cell inhibition tumor microenvironment inflammatory response PD-1 ligands monocyte activation immunotherapy mechanisms IL-10 regulation T-cell suppression cancer immunology adaptive immune response inflammatory cytokines immune checkpoint inhibitors monocyte function analysis PD-1 monocytes IL-10 immune response cancer immunotherapy immune checkpoint cytokines immune modulation PD-1 monocytes IL-10 production immune response cancer immunotherapy tumor microenvironment monocyte activation PD-1 ligands cytokines inflammation checkpoint inhibitors T cells PD-1 ligands monocyte activation immune checkpoint inhibitors cytokine release inflammation response T-cell inhibition antigen presentation adaptive immunity innate immunity cytokine network immunotherapy bioinformatics gene expression immunomonitoring biomarkers cancer immunology PD-1 receptor monocyte activation IL-10 suppression immune response modulation inflammation reduction cancer immunotherapy immune checkpoint inhibitors PD-1 triggering monocytes function IL-10 regulation immune response modulation cancer immunotherapy monocyte IL-10 production immune checkpoint inhibitors monocyte biology cytokine production innate immunity TLR signaling PD-1 pathway PD-1 inhibitors monocyte function IL-10 regulation immune checkpoint cytokine production tumor immunology immune response modulation cancer therapy innate immunity adaptive immunity biomarker discovery
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 immune response signaling pathway cell migration inflammation PDPN C-type lectin receptor actin cytoskeleton dendritic cells motility stromal surfaces PDPN motility stromal C-type lectin dendritic cells actin cytoskeleton receptor activation rearrangement PDPN function C-type lectin receptors motility enhancement dendritic cell migration actin cytoskeleton reorganization stromal interaction immune response regulation PDPN C-type lectin receptor actin cytoskeleton dendritic cells motility stromal surfaces PDPN function C-type lectin receptors actin cytoskeleton rearrangement dendritic cell motility stromal surface interaction PDPN motility stromal surfaces C-type lectin receptor dendritic cells actin cytoskeleton rearrangement search accuracy query expansion keywords PDPN C-type lectin receptor actin cytoskeleton dendritic cells motility stromal surfaces efficacy expansion keywords PDPN motility stromal surfaces C-type lectin receptor actin cytoskeleton dendritic cells immune response signal transduction protein function cell migration immunology biology molecular mechanisms 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 isoform switching hematopoietic differentiation cellular differentiation myosin isoforms B isoform A isoform muscle protein composition cellular biology molecular biology protein switch cell development myosin-II isoform switch hematopoietic differentiation polarizable B isoform more homogenous A isoform cell differentiation molecular biology biological isoforms protein switching hematopoiesis myosin-II isoforms hematopoietic differentiation polarizable B isoform more homogenous A isoform protein composition switch cellular differentiation processes myosin-II isoform switching hematopoietic differentiation process B isoform to A isoform transition cellular differentiation stages myosin-II function in blood cell development isoform diversity in hematology myosin-II isoforms role myosin-II isoform B isoform A isoform hematopoietic differentiation polarizable isoform switching homogenous myosin-II isoform switching hematopoietic differentiation B isoform A isoform cellular polarization protein isoforms muscle protein transition biological differentiation molecular biology cell development myosin-II isoform polarizable B isoform homogenous A isoform hematopoietic differentiation cellular differentiation muscle protein isoforms protein switching cell biology developmental biology molecular biology myosin-II isoforms hematopoietic differentiation B isoform A isoform cellular polarity cytoskeletal dynamics muscle cells stem cell differentiation gene expression regulation protein isoform switching myosin-II isoform B isoform A isoform hematopoietic differentiation cell differentiation molecular biology biological processes myosin-II isoforms hematopoietic differentiation cell polarity molecular biology muscle proteins biological switches protein isoforms developmental biology