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[PMID]:29390564
[Au] Autor:Tian Y; Jia H; Li S; Wu Y; Guo L; Tan G; Li B
[Ad] Endereço:Department of Neurology, The Second Hospital of Hebei Medical University.
[Ti] Título:The associations of stroke, transient ischemic attack, and/or stroke-related recurrent vascular events with Lipoprotein-associated phospholipase A2: A systematic review and meta-analysis.
[So] Source:Medicine (Baltimore);96(51):e9413, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Studies on stroke and lipoprotein-associated phospholipase A2 (Lp-PLA2) have produced conflicting results. OBJECTIVE: The aim of the study was to assess the associations of Lp-PLA2 levels (mass and activity) with recurrent vascular events in patients with transient ischemic attack (TIA) and/or first ischemic stroke and with stroke in the general population. METHODS: The MEDLINE, Embase, the Cochrane Library, Web of Science, Science Direct, China National Knowledge Infrastructure, China Biology Medical Disc (CBMdisc), and WanFang were searched for prospective observational studies reported until January 2017. Eligible studies reported Lp-PLA2 levels and adjusted risk estimates of recurrent vascular events and/or stroke. Risk ratio (RR) with corresponding 95% confidence intervals (CIs) were used to express the pooled data in a random-effects model. RESULTS: A total of 11 studies that comprised 20,284 participants (4,045 were TIA and/or first ischemic stroke patients and 16,239 were residents in general population) were identified, which reported either Lp-PLA2 mass levels (4 studies) or Lp-PLA2 activity levels (10 studies). The pooled RR of recurrent vascular events (467 cases) in TIA and/or first ischemic group was 2.24 (95% CI, 1.33-3.78), whereas the pooled RR of stroke (1604 cases) in the general population was 1.47 (95% CI, 1.10-1.97). The pooled RRs of Lp-PLA2 mass and activity levels with the risk of stroke in the general population were 1.69 (95% CI, 1.03-2.79) and 1.28 (95% CI, 0.88-1.85), respectively. CONCLUSIONS: In patients with TIA and first ischemic stroke, elevated Lp-PLA2 activity levels were associated with recurrent vascular events. And in the general population elevated Lp-PLA2 levels were associated with the risk of stroke, although the association between Lp-PLA2 activity levels and the risk of stroke was less profound compared with the corresponding association of stroke risk with the Lp-PLA2 mass levels.
[Mh] Termos MeSH primário: 1-Alquil-2-acetilglicerofosfocolina Esterase/sangue
Ataque Isquêmico Transitório/sangue
Acidente Vascular Cerebral/sangue
[Mh] Termos MeSH secundário: Seres Humanos
Recidiva
Acidente Vascular Cerebral/complicações
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
EC 3.1.1.47 (1-Alkyl-2-acetylglycerophosphocholine Esterase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009413


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[PMID]:28886386
[Au] Autor:DeSantis ME; Cianfrocco MA; Htet ZM; Tran PT; Reck-Peterson SL; Leschziner AE
[Ad] Endereço:Department of Cellular and Molecular Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
[Ti] Título:Lis1 Has Two Opposing Modes of Regulating Cytoplasmic Dynein.
[So] Source:Cell;170(6):1197-1208.e12, 2017 Sep 07.
[Is] ISSN:1097-4172
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Regulation is central to the functional versatility of cytoplasmic dynein, a motor involved in intracellular transport, cell division, and neurodevelopment. Previous work established that Lis1, a conserved regulator of dynein, binds to its motor domain and induces a tight microtubule-binding state in dynein. The work we present here-a combination of biochemistry, single-molecule assays, and cryoelectron microscopy-led to the surprising discovery that Lis1 has two opposing modes of regulating dynein, being capable of inducing both low and high affinity for the microtubule. We show that these opposing modes depend on the stoichiometry of Lis1 binding to dynein and that this stoichiometry is regulated by the nucleotide state of dynein's AAA3 domain. The low-affinity state requires Lis1 to also bind to dynein at a novel conserved site, mutation of which disrupts Lis1's function in vivo. We propose a new model for the regulation of dynein by Lis1.
[Mh] Termos MeSH primário: 1-Alquil-2-acetilglicerofosfocolina Esterase/metabolismo
Dineínas/metabolismo
Proteínas Associadas aos Microtúbulos/metabolismo
Proteínas de Saccharomyces cerevisiae/metabolismo
Saccharomyces cerevisiae/metabolismo
[Mh] Termos MeSH secundário: 1-Alquil-2-acetilglicerofosfocolina Esterase/química
Trifosfato de Adenosina/metabolismo
Sequência de Aminoácidos
Microscopia Crioeletrônica
Dineínas/química
Seres Humanos
Proteínas Associadas aos Microtúbulos/química
Modelos Moleculares
Proteínas Motores Moleculares/metabolismo
Domínios Proteicos
Proteínas de Saccharomyces cerevisiae/química
Alinhamento de Sequência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (KIP2 protein, S cerevisiae); 0 (Microtubule-Associated Proteins); 0 (Molecular Motor Proteins); 0 (Saccharomyces cerevisiae Proteins); 8L70Q75FXE (Adenosine Triphosphate); EC 3.1.1.47 (1-Alkyl-2-acetylglycerophosphocholine Esterase); EC 3.1.1.47 (PAFAH1B1 protein, S cerevisiae); EC 3.1.1.47 (PAFAH1B1 protein, human); EC 3.6.4.2 (Dyneins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE


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[PMID]:28753643
[Au] Autor:Yeo A; Li L; Warren L; Aponte J; Fraser D; King K; Johansson K; Barnes A; MacPhee C; Davies R; Chissoe S; Tarka E; O'Donoghue ML; White HD; Wallentin L; Waterworth D
[Ad] Endereço:Department of Genetics, GlaxoSmithKline Medicines Research Centre, Stevenage, Hertfordshire, United Kingdom.
[Ti] Título:Pharmacogenetic meta-analysis of baseline risk factors, pharmacodynamic, efficacy and tolerability endpoints from two large global cardiovascular outcomes trials for darapladib.
[So] Source:PLoS One;12(7):e0182115, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Darapladib, a lipoprotein-associated phospholipase A2 (Lp-PLA2) inhibitor, failed to demonstrate efficacy for the primary endpoints in two large phase III cardiovascular outcomes trials, one in stable coronary heart disease patients (STABILITY) and one in acute coronary syndrome (SOLID-TIMI 52). No major safety signals were observed but tolerability issues of diarrhea and odor were common (up to 13%). We hypothesized that genetic variants associated with Lp-PLA2 activity may influence efficacy and tolerability and therefore performed a comprehensive pharmacogenetic analysis of both trials. We genotyped patients within the STABILITY and SOLID-TIMI 52 trials who provided a DNA sample and consent (n = 13,577 and 10,404 respectively, representing 86% and 82% of the trial participants) using genome-wide arrays with exome content and performed imputation using a 1000 Genomes reference panel. We investigated baseline and change from baseline in Lp-PLA2 activity, two efficacy endpoints (major coronary events and myocardial infarction) as well as tolerability parameters at genome-wide and candidate gene level using a meta-analytic approach. We replicated associations of published loci on baseline Lp-PLA2 activity (APOE, CELSR2, LPA, PLA2G7, LDLR and SCARB1) and identified three novel loci (TOMM5, FRMD5 and LPL) using the GWAS-significance threshold P≤5E-08. Review of the PLA2G7 gene (encoding Lp-PLA2) within these datasets identified V279F null allele carriers as well as three other rare exonic null alleles within various ethnic groups, however none of these variants nor any other loci associated with Lp-PLA2 activity at baseline were associated with any of the drug response endpoints. The analysis of darapladib efficacy endpoints, despite low power, identified six low frequency loci with main genotype effect (though with borderline imputation scores) and one common locus (minor allele frequency 0.24) with genotype by treatment interaction effect passing the GWAS-significance threshold. This locus conferred risk in placebo subjects, hazard ratio (HR) 1.22 with 95% confidence interval (CI) 1.11-1.33, but was protective in darapladib subjects, HR 0.79 (95% CI 0.71-0.88). No major loci for tolerability were found. Thus, genetic analysis confirmed and extended the influence of lipoprotein loci on Lp-PLA2 levels, identified some novel null alleles in the PLA2G7 gene, and only identified one potentially efficacious subgroup within these two large clinical trials.
[Mh] Termos MeSH primário: Benzaldeídos/farmacocinética
Oximas/farmacocinética
[Mh] Termos MeSH secundário: 1-Alquil-2-acetilglicerofosfocolina Esterase/antagonistas & inibidores
1-Alquil-2-acetilglicerofosfocolina Esterase/genética
Idoso
Benzaldeídos/efeitos adversos
Benzaldeídos/uso terapêutico
Ensaios Clínicos como Assunto
Doença das Coronárias/tratamento farmacológico
Doença das Coronárias/genética
Doença das Coronárias/metabolismo
Feminino
Seres Humanos
Masculino
Meia-Idade
Oximas/efeitos adversos
Oximas/uso terapêutico
Inibidores de Fosfolipase A2/efeitos adversos
Inibidores de Fosfolipase A2/farmacocinética
Inibidores de Fosfolipase A2/uso terapêutico
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
0 (Benzaldehydes); 0 (Oximes); 0 (Phospholipase A2 Inhibitors); EC 3.1.1.47 (1-Alkyl-2-acetylglycerophosphocholine Esterase); EC 3.1.1.47 (PLA2G7 protein, human); UI1U1MYH09 (darapladib)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170729
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182115


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[PMID]:28726649
[Au] Autor:Stefanic P; Kopolovets I; Hertelyová Z; Tóth S; Frankovicová M
[Ad] Endereço:1Clinic of Vascular Surgery, East Slovak Institute of Cardiovascular Diseases (VÚSCH, a.s.), Faculty of Medicine, Pavol Jozef Safárik University, Kosice, Slovak Republic; 2Institute of Experimental Medicine, Faculty of Medicine, Pavol Jozef Safárik University, Kosice, Slovak Republic; 3Clinic of Int
[Ti] Título:LIPOPROTEIN ASSOCIATED PHOSPHOLIPASE A2 AS A MARKER OF VULNERABLE ATHEROSCLEROTIC PLAQUE IN PATIENTS WITH INTERNAL CAROTID ARTERY STENOSIS.
[So] Source:Georgian Med News;(267):27-34, 2017 Jun.
[Is] ISSN:1512-0112
[Cp] País de publicação:Georgia (Republic)
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to compare the concentration of inflammatory vascular markers and morphological structure of atherosclerotic plaque in symptomatic and asymptomatic patients with the stenosis of internal carotid artery (ICA). The research was carried out in 70 patients with hemodynamically significant stenosis of ICA out of which 40 (57%) were asymptomatic patients and 30 (43%) were symptomatic patients, of which 20 patients (66%) have had a stroke, or transient ischemic attack (TIA), 10 patients (33%). All the patients were indicated to carotid endarterectomy as a surgical prevention of stroke. All the patients were taken their blood for biochemical testing (T-Chol, LDL, HDL, TG, Fibrinogen, CRP and specific markers IL-4 and Lp-PLA2) early morning prior to surgery. The highest concentrations of T-Chol, LDL, HDL, CRP and Fibrinogen were measured in symptomatic patients, however, these did not feature a significant difference compared with the group of asymptomatic patients (P>0.05). Significant difference was found in IL-4 (P<0.001) and in Lp-PLA2 (P<0.001). When evaluating concentration of tracked parameters in patients with soft atherosclerotic plaque and patients with calcified atherosclerotic plaque, significant differences were found in these markers: TG (P<0.05), CRP (P<0.01), IL-4 (P<0.001) and Lp-PLA2 (P<0.001). The paper deals with higher concentrations of Lp-PLA2 in patients with a soft atherosclerotic plaque. Higher concentration of Lp-PLA2 and systemic inflammatory markers (CRP, IL-4) could be used along with ultrasonography to detect mainly asymptomatic patients who are in urgent need of surgical or endovascular treatment as a prevention of stroke.
[Mh] Termos MeSH primário: 1-Alquil-2-acetilglicerofosfocolina Esterase/metabolismo
Artéria Carótida Interna/enzimologia
Estenose das Carótidas/enzimologia
Placa Aterosclerótica/enzimologia
[Mh] Termos MeSH secundário: Idoso
Biomarcadores/metabolismo
Artéria Carótida Interna/diagnóstico por imagem
Artéria Carótida Interna/patologia
Estenose das Carótidas/diagnóstico por imagem
Estenose das Carótidas/patologia
Feminino
Seres Humanos
Masculino
Placa Aterosclerótica/diagnóstico por imagem
Placa Aterosclerótica/patologia
Ultrassonografia Doppler Dupla
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); EC 3.1.1.47 (1-Alkyl-2-acetylglycerophosphocholine Esterase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170721
[St] Status:MEDLINE


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[PMID]:28576829
[Au] Autor:Gutierrez PA; Ackermann BE; Vershinin M; McKenney RJ
[Ad] Endereço:From the Department of Molecular and Cellular Biology, University of California-Davis, Davis, California 95616 and.
[Ti] Título:Differential effects of the dynein-regulatory factor Lissencephaly-1 on processive dynein-dynactin motility.
[So] Source:J Biol Chem;292(29):12245-12255, 2017 Jul 21.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cytoplasmic dynein is the primary minus-end-directed microtubule motor protein in animal cells, performing a wide range of motile activities, including transport of vesicular cargos, mRNAs, viruses, and proteins. Lissencephaly-1 (LIS1) is a highly conserved dynein-regulatory factor that binds directly to the dynein motor domain, uncoupling the enzymatic and mechanical cycles of the motor and stalling dynein on the microtubule track. Dynactin, another ubiquitous dynein-regulatory factor, releases dynein from an autoinhibited state, leading to a dramatic increase in fast, processive dynein motility. How these opposing activities are integrated to control dynein motility is unknown. Here, we used fluorescence single-molecule microscopy to study the interaction of LIS1 with the processive dynein-dynactin-BicD2N (DDB) complex. Surprisingly, in contrast to the prevailing model for LIS1 function established in the context of dynein alone, we found that binding of LIS1 to DDB does not strongly disrupt processive motility. Motile DDB complexes bound up to two LIS1 dimers, and mutational analysis suggested that LIS1 binds directly to the dynein motor domains during DDB movement. Interestingly, LIS1 enhanced DDB velocity in a concentration-dependent manner, in contrast to observations of the effect of LIS1 on the motility of isolated dynein. Thus, LIS1 exerts concentration-dependent effects on dynein motility and can synergize with dynactin to enhance processive dynein movement. Our results suggest that the effect of LIS1 on dynein motility depends on both LIS1 concentration and the presence of other regulatory factors such as dynactin and may provide new insights into the mechanism of LIS1 haploinsufficiency in the neurodevelopmental disorder lissencephaly.
[Mh] Termos MeSH primário: 1-Alquil-2-acetilglicerofosfocolina Esterase/metabolismo
Complexo Dinactina/metabolismo
Dineínas/metabolismo
Proteínas Associadas aos Microtúbulos/metabolismo
Microtúbulos/metabolismo
Proteínas do Tecido Nervoso/metabolismo
[Mh] Termos MeSH secundário: 1-Alquil-2-acetilglicerofosfocolina Esterase/genética
Animais
Dimerização
Dineínas/química
Seres Humanos
Camundongos
Microscopia de Fluorescência
Proteínas Associadas aos Microtúbulos/química
Proteínas Associadas aos Microtúbulos/genética
Microtúbulos/enzimologia
Mutagênese Sítio-Dirigida
Mutação
Proteínas do Tecido Nervoso/genética
Fragmentos de Peptídeos/química
Fragmentos de Peptídeos/genética
Fragmentos de Peptídeos/metabolismo
Domínios e Motivos de Interação entre Proteínas
Multimerização Proteica
Ratos
Proteínas Recombinantes de Fusão/metabolismo
Células Sf9
Spodoptera
Sus scrofa
Tubulina (Proteína)/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bicd2 protein, mouse); 0 (Dynactin Complex); 0 (Lis-1 protein, rat); 0 (Microtubule-Associated Proteins); 0 (Nerve Tissue Proteins); 0 (Peptide Fragments); 0 (Recombinant Fusion Proteins); 0 (Tubulin); EC 3.1.1.47 (1-Alkyl-2-acetylglycerophosphocholine Esterase); EC 3.6.4.2 (Dyneins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170604
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.790048


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[PMID]:28542249
[Au] Autor:Belviso S; Iuliano R; Amato R; Perrotti N; Menniti M
[Ad] Endereço:Department of Experimental and Clinical Medicine, University Magna Graecia of Catanzaro, Catanzaro, Italy.
[Ti] Título:The human asparaginase enzyme (ASPG) inhibits growth in leukemic cells.
[So] Source:PLoS One;12(5):e0178174, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The human protein ASPG is an enzyme with a putative antitumor activity. We generated in bacteria and then purified a recombinant GST-ASPG protein that we used to characterize the biochemical and cytotoxic properties of the human ASPG. We demonstrated that ASPG possesses asparaginase and PAF acetylhydrolase activities that depend on a critical threonine residue at position 19. Consistently, ASPG but not its T19A mutant showed cytotoxic activity in K562, NALM-6 and MOLT-4 leukemic cell lines but not in normal cells. Regarding the mechanism of action of ASPG, it was able to induce a significant apoptotic death in K562 cells. Taken together our data suggest that ASPG, combining different enzymatic activities, should be considered a promising anti-cancer agent for inhibiting the growth of leukemia cells.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Asparaginase/uso terapêutico
Leucemia/tratamento farmacológico
[Mh] Termos MeSH secundário: 1-Alquil-2-acetilglicerofosfocolina Esterase/genética
1-Alquil-2-acetilglicerofosfocolina Esterase/uso terapêutico
Substituição de Aminoácidos
Apoptose/efeitos dos fármacos
Asparaginase/genética
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Canais Epiteliais de Sódio/metabolismo
Seres Humanos
Células K562
Leucemia/metabolismo
Leucemia/patologia
Mutagênese Sítio-Dirigida
Proteínas Recombinantes de Fusão/genética
Proteínas Recombinantes de Fusão/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Epithelial Sodium Channels); 0 (Recombinant Fusion Proteins); EC 3.1.1.47 (1-Alkyl-2-acetylglycerophosphocholine Esterase); EC 3.5.1.1 (Asparaginase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170526
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0178174


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[PMID]:28446568
[Au] Autor:Chen J; Cai Z; Zhang L; Yin Y; Chen X; Chen C; Zhang Y; Zhai S; Long X; Liu X; Wang X
[Ad] Endereço:Department of Immunology, State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, Jiangsu 211166, China; and.
[Ti] Título:Lis1 Regulates Germinal Center B Cell Antigen Acquisition and Affinity Maturation.
[So] Source:J Immunol;198(11):4304-4311, 2017 Jun 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The germinal center (GC) is the site where activated B cells undergo rapid expansions, somatic hypermutation, and affinity maturation. Affinity maturation is a process of Ag-driven selection. The amount of Ag acquired and displayed by GC B cells determines whether it can be positively selected, and therefore Ag acquisition has to be tightly regulated to ensure the efficient affinity maturation. Cell expansion provides sufficient quantity of GC B cells and Abs, whereas affinity maturation improves the quality of Abs. In this study, we found that Lis1 is a cell-intrinsic regulator of Ag acquisition capability of GC B cells. Lack of Lis1 resulted in redistribution of polymerized actin and accumulation of F-actin at uropod; larger amounts of Ags were acquired and displayed by GC B cells, which presumably reduced the selection stringency. Affinity maturation was thus compromised in Lis1-deficient mice. Consistently, overexpression of Lis1 in GC B cells led to less Ag acquisition and display. Additionally, Lis1 is required for GC B cell expansion, and Lis1 deficiency blocked the cell cycle at the mitotic phase and GC B cells were prone to apoptosis. Overall, we suggest that Lis1 is required for GC B cell expansion, affinity maturation, and maintaining functional intact GC response, thus ensuring both the quantity and quality of Ab response.
[Mh] Termos MeSH primário: 1-Alquil-2-acetilglicerofosfocolina Esterase/metabolismo
Antígenos/metabolismo
Linfócitos B/imunologia
Diferenciação Celular
Centro Germinativo/imunologia
Proteínas Associadas aos Microtúbulos/metabolismo
[Mh] Termos MeSH secundário: 1-Alquil-2-acetilglicerofosfocolina Esterase/deficiência
1-Alquil-2-acetilglicerofosfocolina Esterase/genética
Actinas/imunologia
Animais
Afinidade de Anticorpos
Formação de Anticorpos
Antígenos/imunologia
Apoptose
Linfócitos B/fisiologia
Regulação da Expressão Gênica
Centro Germinativo/citologia
Centro Germinativo/fisiologia
Camundongos
Proteínas Associadas aos Microtúbulos/deficiência
Proteínas Associadas aos Microtúbulos/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Antigens); 0 (Microtubule-Associated Proteins); EC 3.1.1.47 (1-Alkyl-2-acetylglycerophosphocholine Esterase); EC 3.1.1.47 (Pafah1b1 protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700159


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[PMID]:28407821
[Au] Autor:Wang BX; Mei H; Peng HM; Gao Y; Ding Y
[Ad] Endereço:Department of Gastroenterology, Wuhan Children's Hospital, Wuhan 430016, China dingyanrh@126.com.
[Ti] Título:[Association between platelet-activating factor acetylhydrolase gene polymorphisms and gastrointestinal bleeding in children with Henoch-Schönlein purpura].
[So] Source:Zhongguo Dang Dai Er Ke Za Zhi;19(4):385-388, 2017 Apr.
[Is] ISSN:1008-8830
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVE: To study the association between the single nucleotide polymorphisms (SNPs) of the ninth exon Val279Phe of platelet-activating factor acetylhydrolase (PAF-AH) gene and gastrointestinal bleeding in children with Henoch-Schönlein purpura (HSP). METHODS: A total 516 children with HSP were enrolled, among whom 182 had gastrointestinal bleeding and 334 had no gastrointestinal bleeding. PCR was used to investigate the distribution of genotypes and alleles in the SNPs of Val97Phe. The plasma PAF-AH activity was measured, as well as the levels of platelet-activating factor (PAF), granular membrane protein-140 (GMP-140), ß-thromboglobulin (ß-TG), and platelet factor 4 (PF4). RESULTS: The Val279Phe genotype and allele frequencies were in Hardy-Weinberg equilibrium, and the homozygous genotype TT and heterozygotes accounted for 0.97% and 6.05% respectively. The gastrointestinal bleeding group had a significantly higher allele frequency than the control group (5.22% vs 3.33%; P<0.01). The HSP patients with GG genotype in the gastrointestinal bleeding group had significantly higher levels of plasma PAF and GMP-140 than those in the non-gastrointestinal bleeding group (P<0.05), while the non-gastrointestinal bleeding group had a significantly higher PAF-AH activity than the gastrointestinal bleeding group (P<0.05). There were no significant differences in ß-TG and PF4 between the two groups (P>0.05). CONCLUSIONS: Val279Phe gene polymorphisms in PAF-AH are associated with PAF-AH activity and PAF and GMP-140 levels and may be a risk factor for HSP with gastrointestinal bleeding.
[Mh] Termos MeSH primário: 1-Alquil-2-acetilglicerofosfocolina Esterase/genética
Hemorragia Gastrointestinal/etiologia
Polimorfismo de Nucleotídeo Único
Púrpura de Schoenlein-Henoch/complicações
[Mh] Termos MeSH secundário: Adolescente
Criança
Pré-Escolar
Feminino
Genótipo
Seres Humanos
Lactente
Masculino
Selectina-P/sangue
Fator de Ativação de Plaquetas/análise
Púrpura de Schoenlein-Henoch/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (P-Selectin); 0 (Platelet Activating Factor); EC 3.1.1.47 (1-Alkyl-2-acetylglycerophosphocholine Esterase)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170801
[Lr] Data última revisão:
170801
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170415
[St] Status:MEDLINE


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[PMID]:28406212
[Au] Autor:Saleheen D; Natarajan P; Armean IM; Zhao W; Rasheed A; Khetarpal SA; Won HH; Karczewski KJ; O'Donnell-Luria AH; Samocha KE; Weisburd B; Gupta N; Zaidi M; Samuel M; Imran A; Abbas S; Majeed F; Ishaq M; Akhtar S; Trindade K; Mucksavage M; Qamar N; Zaman KS; Yaqoob Z; Saghir T; Rizvi SNH; Memon A; Hayyat Mallick N; Ishaq M; Rasheed SZ; Memon FU; Mahmood K; Ahmed N; Do R; Krauss RM; MacArthur DG; Gabriel S; Lander ES; Daly MJ; Frossard P; Danesh J; Rader DJ; Kathiresan S
[Ad] Endereço:Department of Biostatistics and Epidemiology, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, USA.
[Ti] Título:Human knockouts and phenotypic analysis in a cohort with a high rate of consanguinity.
[So] Source:Nature;544(7649):235-239, 2017 04 12.
[Is] ISSN:1476-4687
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A major goal of biomedicine is to understand the function of every gene in the human genome. Loss-of-function mutations can disrupt both copies of a given gene in humans and phenotypic analysis of such 'human knockouts' can provide insight into gene function. Consanguineous unions are more likely to result in offspring carrying homozygous loss-of-function mutations. In Pakistan, consanguinity rates are notably high. Here we sequence the protein-coding regions of 10,503 adult participants in the Pakistan Risk of Myocardial Infarction Study (PROMIS), designed to understand the determinants of cardiometabolic diseases in individuals from South Asia. We identified individuals carrying homozygous predicted loss-of-function (pLoF) mutations, and performed phenotypic analysis involving more than 200 biochemical and disease traits. We enumerated 49,138 rare (<1% minor allele frequency) pLoF mutations. These pLoF mutations are estimated to knock out 1,317 genes, each in at least one participant. Homozygosity for pLoF mutations at PLA2G7 was associated with absent enzymatic activity of soluble lipoprotein-associated phospholipase A2; at CYP2F1, with higher plasma interleukin-8 concentrations; at TREH, with lower concentrations of apoB-containing lipoprotein subfractions; at either A3GALT2 or NRG4, with markedly reduced plasma insulin C-peptide concentrations; and at SLC9A3R1, with mediators of calcium and phosphate signalling. Heterozygous deficiency of APOC3 has been shown to protect against coronary heart disease; we identified APOC3 homozygous pLoF carriers in our cohort. We recruited these human knockouts and challenged them with an oral fat load. Compared with family members lacking the mutation, individuals with APOC3 knocked out displayed marked blunting of the usual post-prandial rise in plasma triglycerides. Overall, these observations provide a roadmap for a 'human knockout project', a systematic effort to understand the phenotypic consequences of complete disruption of genes in humans.
[Mh] Termos MeSH primário: Consanguinidade
Análise Mutacional de DNA
Deleção de Genes
Genes/genética
Estudos de Associação Genética/métodos
Homozigoto
Fenótipo
[Mh] Termos MeSH secundário: 1-Alquil-2-acetilglicerofosfocolina Esterase/deficiência
1-Alquil-2-acetilglicerofosfocolina Esterase/genética
Apolipoproteína C-III/deficiência
Apolipoproteína C-III/genética
Estudos de Coortes
Doença das Coronárias/sangue
Doença das Coronárias/genética
Família 2 do Citocromo P450/genética
Gorduras na Dieta/farmacologia
Exoma/genética
Jejum/sangue
Feminino
Frequência do Gene
Seres Humanos
Interleucina-8/sangue
Masculino
Meia-Idade
Infarto do Miocárdio/sangue
Infarto do Miocárdio/genética
Neurregulinas/genética
Paquistão
Linhagem
Fosfoproteínas/genética
Período Pós-Prandial
Sítios de Splice de RNA/genética
Genética Reversa/métodos
Trocadores de Sódio-Hidrogênio/genética
Triglicerídeos/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Apolipoprotein C-III); 0 (Dietary Fats); 0 (IL8 protein, human); 0 (Interleukin-8); 0 (Neuregulins); 0 (Phosphoproteins); 0 (RNA Splice Sites); 0 (Sodium-Hydrogen Exchangers); 0 (Triglycerides); 0 (neuregulin-4); 0 (sodium-hydrogen exchanger regulatory factor); EC 1.14.14.1 (CYP2F1 protein, human); EC 1.14.14.1 (Cytochrome P450 Family 2); EC 3.1.1.47 (1-Alkyl-2-acetylglycerophosphocholine Esterase); EC 3.1.1.47 (PLA2G7 protein, human)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170414
[St] Status:MEDLINE
[do] DOI:10.1038/nature22034


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[PMID]:28364871
[Au] Autor:Soysal P; Isik AT; Carvalho AF; Fernandes BS; Solmi M; Schofield P; Veronese N; Stubbs B
[Ad] Endereço:Kayseri Education and Research Hospital, Geriatric Center, Kayseri, Turkey; Health Service and Population Research Department, Institute of Psychiatry, Psychology and Neuroscience, King's College London, De Crespigny Park, London Box SE5 8AF, United Kingdom.
[Ti] Título:Oxidative stress and frailty: A systematic review and synthesis of the best evidence.
[So] Source:Maturitas;99:66-72, 2017 May.
[Is] ISSN:1873-4111
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Oxidative stress (OS) is associated with accelerated aging. Previous studies have suggested a possible relationship between OS and frailty but this association remains unclear. We conducted a systematic review to investigate potential interactions between OS and frailty. METHODS: A systematic literature search of original reports providing data on 'OS and antioxidant' parameters and frailty was carried out across major electronic databases from inception until May 2016. Cross-sectional/case control and longitudinal studies reporting data on the association between frailty and anti-oxidants-OS biomarkers were considered for inclusion. Results were summarized with a synthesis based on the best evidence. RESULTS: From 1856 hits, 8 studies (cross-sectional/case control) were included (N=6349; mean age of 75±12years; 56.4% females). Overall, there were 588 (=9.3%) frail, 3036 pre-frail (=47.8%), 40 (=0.6%) pre-frail/robust, and 2685 (=42.3%) robust subjects. Six cross-sectional/case control studies demonstrated that frailty was associated with an increase in peripheral OS biomarkers, including lipoprotein phospholipase A2 (1 study), isoprostanes (2 studies), malonaldehyde (2 studies), 8-hydroxy-20-deoxyguanosine (2 studies), derivate of reactive oxygen metabolites (2 studies), oxidized glutathione/glutathione (1 study), 4-hydroxy-2,3-nonenal (1 study), and protein carbonylation levels (1 study). In addition, preliminary evidence points to lower anti-oxidant parameters (vitamin C, E, α-tocopherol, biological anti-oxidant potential, total thiol levels) in frailty. CONCLUSION: Frailty and pre-frailty appear to be associated with higher OS and possibly lower anti-oxidant parameters. However, due to the cross-sectional design, it is not possible to disentangle the directionality of the relationships observed. Thus, future high-quality and in particular longitudinal research is required to confirm or refute these relationships and to further elucidate pathophysiological mechanisms.
[Mh] Termos MeSH primário: Envelhecimento/metabolismo
Biomarcadores/metabolismo
Estresse Oxidativo
[Mh] Termos MeSH secundário: 1-Alquil-2-acetilglicerofosfocolina Esterase/metabolismo
Idoso
Idoso de 80 Anos ou mais
Aldeídos/metabolismo
Estudos Transversais
Desoxiguanosina/análogos & derivados
Desoxiguanosina/metabolismo
Idoso Fragilizado
Glutationa/metabolismo
Dissulfeto de Glutationa/metabolismo
Seres Humanos
Isoprostanos/metabolismo
Estudos Longitudinais
Espécies Reativas de Oxigênio/metabolismo
Compostos de Sulfidrila/metabolismo
alfa-Tocoferol/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Aldehydes); 0 (Biomarkers); 0 (Isoprostanes); 0 (Reactive Oxygen Species); 0 (Sulfhydryl Compounds); 88847-89-6 (8-oxo-7-hydrodeoxyguanosine); EC 3.1.1.47 (1-Alkyl-2-acetylglycerophosphocholine Esterase); G9481N71RO (Deoxyguanosine); GAN16C9B8O (Glutathione); H4N855PNZ1 (alpha-Tocopherol); K1CVM13F96 (4-hydroxy-2-nonenal); ULW86O013H (Glutathione Disulfide)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170602
[Lr] Data última revisão:
170602
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170403
[St] Status:MEDLINE



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