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[PMID]:28943429
[Au] Autor:Cui X; Zhang X; Bu H; Liu N; Li H; Guan X; Yan H; Wang Y; Zhang H; Ding Y; Cheng M
[Ad] Endereço:Clinical Medical School, Weifang Medical University, Weifang, Shandong, 261053, PR China.
[Ti] Título:Shear stress-mediated changes in the expression of complement regulatory protein CD59 on human endothelial progenitor cells by ECM-integrinα ß -F-actin pathway in vitro.
[So] Source:Biochem Biophys Res Commun;494(1-2):416-421, 2017 Dec 09.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Membrane regulatory proteins, such as CD46, CD55, and CD59, prevent excess complement activation and to protect cells from damage. Previous investigations confirmed that shear stress in the physiological range was more favorable for endothelial progenitor cells (EPCs) to repair injured vascular endothelial cells and operates mainly in atheroprotective actions. However, detailed events that contribute to shear stress-induced protection in EPCs, particularly the mechanisms of signal transduction, remain poorly understood. In this study, we observed shear stress-mediated changes in the expression of complement regulatory proteins CD46, CD55, and CD59 on human EPCs and focused on the mechanical transmission mechanism in transformed cells in response to the ECM-F-actin pathway in vitro. Shear stress was observed to promote the expression of complement regulatory protein CD59, but not CD46 or CD55, on EPCs. In addition, the shear stress-induced CD59 expression was confirmed to be associated with the ECM components and was alleviated in EPCs pretreated with GRGDSP, which inhibits ECM components-integrin interaction. Furthermore, shear stress also promotes the rearrangement and polymerization of F-actin. However, shear stress-induced CD59 expression was reduced when the F-actin stress fiber formation process was delayed by Gly-Arg-Gly-Asp-Ser-Pro (GRGDSP) or destroyed by cytochalasin D (Cyto D), while Jasplakinolide (JAS) reversed the expression of CD59 through promotion of F-actin polymerization and its stabilizing capacities. Our results indicates that shear stress is an important mediator in EPC expression of CD59 regulated by the ECM-F-actin pathway, which is a key factor in preventing membrane attack complex (MAC) -mediated cell autolysis.
[Mh] Termos MeSH primário: Citoesqueleto de Actina/metabolismo
Actinas/genética
Antígenos CD59/genética
Células Progenitoras Endoteliais/metabolismo
Integrina alfaVbeta3/genética
Mecanotransdução Celular
[Mh] Termos MeSH secundário: Citoesqueleto de Actina/efeitos dos fármacos
Citoesqueleto de Actina/ultraestrutura
Actinas/metabolismo
Antígenos CD55/genética
Antígenos CD55/metabolismo
Antígenos CD59/metabolismo
Complexo de Ataque à Membrana do Sistema Complemento/efeitos dos fármacos
Citocalasina D/farmacologia
Depsipeptídeos/farmacologia
Células Progenitoras Endoteliais/citologia
Células Progenitoras Endoteliais/efeitos dos fármacos
Matriz Extracelular/química
Matriz Extracelular/efeitos dos fármacos
Matriz Extracelular/metabolismo
Sangue Fetal/citologia
Sangue Fetal/efeitos dos fármacos
Sangue Fetal/metabolismo
Regulação da Expressão Gênica
Seres Humanos
Integrina alfaVbeta3/metabolismo
Proteína Cofatora de Membrana/genética
Proteína Cofatora de Membrana/metabolismo
Oligopeptídeos/farmacologia
Cultura Primária de Células
Estresse Mecânico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (CD46 protein, human); 0 (CD55 Antigens); 0 (CD59 Antigens); 0 (Complement Membrane Attack Complex); 0 (Depsipeptides); 0 (Integrin alphaVbeta3); 0 (Membrane Cofactor Protein); 0 (Oligopeptides); 101754-01-2 (CD59 protein, human); 102396-24-7 (jasplakinolide); 22144-77-0 (Cytochalasin D); 91037-75-1 (glycyl-arginyl-glycyl-aspartyl-seryl-proline)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170926
[St] Status:MEDLINE


  2 / 1208 MEDLINE  
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[PMID]:28715486
[Au] Autor:Gao B; Long C; Lee W; Zhang Z; Gao X; Landsittel D; Ezzelarab M; Ayares D; Huang Y; Cooper DKC; Wang Y; Hara H
[Ad] Endereço:Thomas E. Starzl Transplantation Institute, University of Pittsburgh, Pittsburgh, PA, United States of America.
[Ti] Título:Anti-Neu5Gc and anti-non-Neu5Gc antibodies in healthy humans.
[So] Source:PLoS One;12(7):e0180768, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Our group previously investigated the levels of anti-Gal and anti-nonGal IgM and IgG in a cohort of 75 healthy humans of various backgrounds, and found some significant differences related to factors such as age, gender, ABO blood group, diet, vaccination history, and geographic location during childhood. We have now expanded our cohort (n = 84) to investigate the levels of anti-Neu5Gc and anti-nonGal/nonNeu5Gc antibodies in healthy humans. Anti-nonGal and anti-nonGal/nonNeu5Gc human IgM and IgG binding to pRBCs and pAECs from GTKO/CD46 and GTKO/CD46/Neu5GcKO pigs were measured by flow cytometry. Anti-Gal and anti-Neu5Gc IgM and IgG levels were measured by ELISA. In summary, (i) the great majority (almost 100%) of humans had anti-Neu5Gc IgM and IgG antibodies that bound to pAECs and approximately 50% had anti-Neu5Gc antibodies that bound to pRBCs, (ii) there was significantly less human antibody binding to pig cells that did not express either Gal or Neu5Gc compared with those that did not express Gal alone, (iii) the levels of both IgM and IgG binding to GTKO/CD46/Neu5GcKO pRBCs and pAECs were low, (iv) the level of anti-Neu5Gc IgG was higher in men than women, (v) the level did not change with age or diet, and there was some variability associated with (vi) previous vaccination history and (vii) the geographic region in which the individual spent his or her childhood. Our study confirms that human antibody binding to RBCs and AECs from GTKO/CD46/Neu5GcKO pigs is greatly reduced compared to binding to GTKO/CD46 cells. However, all humans appear to have a low level of antibody that binds to pAECs that is not directed to either Gal or Neu5Gc. Our findings require consideration in planning clinical trials of xenotransplantation.
[Mh] Termos MeSH primário: Anticorpos/imunologia
Ácidos Neuramínicos/imunologia
[Mh] Termos MeSH secundário: Sistema do Grupo Sanguíneo ABO
Adulto
Idoso
Idoso de 80 Anos ou mais
Animais
Anticorpos/sangue
Células Cultivadas
Dieta
Células Endoteliais/citologia
Células Endoteliais/imunologia
Células Endoteliais/metabolismo
Eritrócitos/citologia
Eritrócitos/imunologia
Eritrócitos/metabolismo
Feminino
Galactose/metabolismo
Galactosiltransferases/deficiência
Galactosiltransferases/genética
Seres Humanos
Imunoglobulina G/sangue
Imunoglobulina G/imunologia
Imunoglobulina M/sangue
Imunoglobulina M/imunologia
Masculino
Proteína Cofatora de Membrana/metabolismo
Meia-Idade
Oxigenases de Função Mista/deficiência
Oxigenases de Função Mista/genética
Suínos
Vacinação
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ABO Blood-Group System); 0 (Antibodies); 0 (Immunoglobulin G); 0 (Immunoglobulin M); 0 (Membrane Cofactor Protein); 0 (Neuraminic Acids); 1113-83-3 (N-glycolylneuraminic acid); EC 1.- (Mixed Function Oxygenases); EC 1.14.18.2 (CMPacetylneuraminate monooxygenase); EC 2.4.1.- (Galactosyltransferases); X2RN3Q8DNE (Galactose)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170718
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180768


  3 / 1208 MEDLINE  
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[PMID]:28578022
[Au] Autor:Wang Q; Shi N; Shang Y; Liu X; Fu W; Zhao Y; Pan D; Xu W; Lin X
[Ad] Endereço:Institute of Animal Quarantine, Chinese Academy of Inspection and Quarantine, Beijing 100123, China.
[Ti] Título:Comprehensive molecular characterization of a transgenic pig expressing hCD46 gene.
[So] Source:Gene;626:376-385, 2017 Aug 30.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Molecular characterization of transgenic animals is crucial for the phenotype analysis, unintended effects prediction, commercial and economic requirements. In this study, a comprehensive molecular characterization of a transgenic pig, which expressed hCD46 gene, was verified using next-generation sequencing (NGS). One complete and one incomplete sequence of pBSCD46-neo and multiple backbone fragments were inserted into the host genome. The whole insertion sequence was 28,243bp, and 12bp sequence on the genome was deleted during the transgene. The cost of NGS is higher than other molecular methods, in order to reduce the cost and to make the sequencing strategy more economically effective, we carried out a computer simulation to identify the smallest amount of data that could meet the requirements of the molecular characterization analysis. 15× depth of coverage was shown to be sufficient with good accuracy, while 3× might be effective, 20× was recommended. The obtained molecular characterization information would provide a stronger foundation for the safety evaluation of the GM animals. Meanwhile, the gene integrity of the porcine pathogen PERV was analyzed using the same procedure. No complete sequence of the PERV subtype was observed in the porcine genome, which was the same as the previous research. In consequence, NGS combined bioinformatics analysis is a reliable and accurate approach for the molecular characterization of GMOs, even for the safety evaluation.
[Mh] Termos MeSH primário: Animais Geneticamente Modificados/genética
Proteína Cofatora de Membrana/genética
Suínos/genética
[Mh] Termos MeSH secundário: Animais
Pontos de Quebra do Cromossomo
Seres Humanos
Íntrons
Proteínas Repressoras/genética
Transgenes
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Membrane Cofactor Protein); 0 (Repressor Proteins)
[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:170605
[St] Status:MEDLINE


  4 / 1208 MEDLINE  
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[PMID]:28476687
[Au] Autor:Ly PT; Tang SJ; Roca X
[Ad] Endereço:School of Biological Sciences, Nanyang Technological University, 637551, Singapore; The Neuroscience and Behavioral Disorders Programme, Duke-NUS Graduate Medical School, Singapore.
[Ti] Título:Alternative polyadenylation expands the mRNA isoform repertoire of human CD46.
[So] Source:Gene;625:21-30, 2017 Aug 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Alternative polyadenylation is a prevalent mechanism regulating mammalian gene expression. While tandem 3'-Untranslated-Region (3'UTR) polyadenylation changes expression levels, Intronic PolyAdenylation generates shorter transcripts encoding truncated proteins. Intronic PolyAdenylation regulates 20% of genes and is especially common in receptor tyrosine-kinase transcripts, generating soluble repressors. Here we report that human CD46, encoding a TransMembrane repressor of complement and T-cell co-stimulator, expresses multiple isoforms by alternative polyadenylation. We provide evidence for polyadenylation at several introns by RT-PCR of 5' intronic fragments, and by increase in such isoforms via functional U1 knockdown. We mapped various Intronic PolyAdenylation Sites by 3' Rapid Amplification of cDNA Ends (3'RACE), which could generate soluble or membrane-bound but tail-less CD46. Intronic PolyAdenylation could add to the source of soluble CD46 isoforms in fluids and tissues, which increase in cancers and autoimmune syndromes. Furthermore, 3'RACE identified three PolyAdenylation Sites within the last intron and exon, whose transcripts with shortened 3'UTRs could support higher CD46 expression. Finally, 3'RACE revealed that the CD46 Pseudogene only expresses short transcripts by early polyadenylation in intron 2. Overall, we report a wide variety of CD46 mRNA isoforms which could generate new protein isoforms, adding to the diverse physiological and pathological roles of CD46.
[Mh] Termos MeSH primário: Proteína Cofatora de Membrana/genética
Poliadenilação
RNA Mensageiro/genética
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Células HEK293
Seres Humanos
Íntrons
Células Jurkat
Proteína Cofatora de Membrana/metabolismo
Isoformas de Proteínas/genética
Isoformas de Proteínas/metabolismo
Pseudogenes
RNA Mensageiro/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Membrane Cofactor Protein); 0 (Protein Isoforms); 0 (RNA, Messenger)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170507
[St] Status:MEDLINE


  5 / 1208 MEDLINE  
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[PMID]:28444759
[Au] Autor:Ellinghaus U; Cortini A; Pinder CL; Le Friec G; Kemper C; Vyse TJ
[Ad] Endereço:Division of Genetics and Molecular Medicine, Department of Medical and Molecular Genetics, King's College London, Guy's Hospital, London, UK.
[Ti] Título:Dysregulated CD46 shedding interferes with Th1-contraction in systemic lupus erythematosus.
[So] Source:Eur J Immunol;47(7):1200-1210, 2017 Jul.
[Is] ISSN:1521-4141
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:IFN-γ-producing T helper 1 (Th1) cell responses mediate protection against infections but uncontrolled Th1 activity also contributes to a broad range of autoimmune diseases. Autocrine complement activation has recently emerged as key in the induction and contraction of human Th1 immunity: activation of the complement regulator CD46 and the C3aR expressed by CD4 T cells via autocrine generated ligands C3b and C3a, respectively, are critical to IFN-γ production. Further, CD46-mediated signals also induce co-expression of immunosuppressive IL-10 in Th1 cells and transition into a (self)-regulating and contracting phase. In consequence, C3 or CD46-deficient patients suffer from recurrent infections while dysregulation of CD46 signaling contributes to Th1 hyperactivity in rheumatoid arthritis and multiple sclerosis. Here, we report a defect in CD46-regulated Th1 contraction in patients with systemic lupus erythematosus (SLE). We observed that MMP-9-mediated increased shedding of soluble CD46 by Th1 cells was associated with this defect and that inhibition of MMP-9 activity normalized release of soluble CD46 and restored Th1 contraction in patients' T cells. These data may deliver the first mechanistic explanation for the increased serum CD46 levels observed in SLE patients and indicate that targeting CD46-cleaving proteases could be a novel avenue to modulate Th1 responses.
[Mh] Termos MeSH primário: Lúpus Eritematoso Sistêmico/imunologia
Proteína Cofatora de Membrana/imunologia
Proteína Cofatora de Membrana/secreção
Células Th1/imunologia
[Mh] Termos MeSH secundário: Adulto
Autoimunidade
Linfócitos B/efeitos dos fármacos
Linfócitos B/imunologia
Ativação do Complemento
Feminino
Seres Humanos
Imunidade Inata
Interleucina-10/genética
Interleucina-10/imunologia
Interleucina-10/farmacologia
Masculino
Metaloproteinase 9 da Matriz/metabolismo
Inibidores de Metaloproteinases de Matriz/farmacologia
Proteína Cofatora de Membrana/sangue
Proteína Cofatora de Membrana/deficiência
Transdução de Sinais
Linfócitos T/efeitos dos fármacos
Linfócitos T/imunologia
Células Th1/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD46 protein, human); 0 (IL10 protein, human); 0 (Matrix Metalloproteinase Inhibitors); 0 (Membrane Cofactor Protein); 130068-27-8 (Interleukin-10); EC 3.4.24.35 (Matrix Metalloproteinase 9)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170427
[St] Status:MEDLINE
[do] DOI:10.1002/eji.201646822


  6 / 1208 MEDLINE  
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[PMID]:28289848
[Au] Autor:Haralambieva IH; Ovsyannikova IG; Kennedy RB; Larrabee BR; Zimmermann MT; Grill DE; Schaid DJ; Poland GA
[Ad] Endereço:Mayo Clinic Vaccine Research Group, Mayo Clinic, Guggenheim 611C, 200 First Street SW, Rochester, MN, 55905, USA.
[Ti] Título:Genome-wide associations of CD46 and IFI44L genetic variants with neutralizing antibody response to measles vaccine.
[So] Source:Hum Genet;136(4):421-435, 2017 Apr.
[Is] ISSN:1432-1203
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Population-based studies have revealed 2-10% measles vaccine failure rate even after two vaccine doses. While the mechanisms behind this remain unknown, we hypothesized that host genetic factors are likely to be involved. We performed a genome-wide association study of measles specific neutralizing antibody and IFNγ ELISPOT response in a combined sample of 2872 subjects. We identified two distinct chromosome 1 regions (previously associated with MMR-related febrile seizures), associated with vaccine-induced measles neutralizing antibody titers. The 1q32 region contained 20 significant SNPs in/around the measles virus receptor-encoding CD46 gene, including the intronic rs2724384 (p value = 2.64 × 10 ) and rs2724374 (p value = 3.16 × 10 ) SNPs. The 1q31.1 region contained nine significant SNPs in/around IFI44L, including the intronic rs1333973 (p value = 1.41 × 10 ) and the missense rs273259 (His73Arg, p value = 2.87 × 10 ) SNPs. Analysis of differential exon usage with mRNA-Seq data and RT-PCR suggests the involvement of rs2724374 minor G allele in the CD46 STP region exon B skipping, resulting in shorter CD46 isoforms. Our study reveals common CD46 and IFI44L SNPs associated with measles-specific humoral immunity, and highlights the importance of alternative splicing/virus cellular receptor isoform usage as a mechanism explaining inter-individual variation in immune response after live measles vaccine.
[Mh] Termos MeSH primário: Anticorpos Neutralizantes/biossíntese
Antígenos/genética
Proteínas do Citoesqueleto/genética
Estudo de Associação Genômica Ampla
Vacina contra Sarampo/imunologia
Proteína Cofatora de Membrana/genética
[Mh] Termos MeSH secundário: Adulto
Criança
Feminino
Seres Humanos
Masculino
Polimorfismo de Nucleotídeo Único
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Neutralizing); 0 (Antigens); 0 (CD46 protein, human); 0 (Cytoskeletal Proteins); 0 (IFI44 protein, human); 0 (Measles Vaccine); 0 (Membrane Cofactor Protein)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170315
[St] Status:MEDLINE
[do] DOI:10.1007/s00439-017-1768-9


  7 / 1208 MEDLINE  
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[PMID]:28258595
[Au] Autor:Laird CT; Burdorf L; French BM; Kubicki N; Cheng X; Braileanu G; Sun W; O'Neill NA; Cimeno A; Parsell D; So E; Bähr A; Klymiuk N; Phelps CJ; Ayares D; Azimzadeh AM; Pierson RN
[Ad] Endereço:Department of Surgery, University of Maryland School of Medicine, Baltimore, MD, USA.
[Ti] Título:Transgenic expression of human leukocyte antigen-E attenuates GalKO.hCD46 porcine lung xenograft injury.
[So] Source:Xenotransplantation;24(2), 2017 Mar.
[Is] ISSN:1399-3089
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Lung xenografts remain susceptible to loss of vascular barrier function within hours in spite of significant incremental advances based on genetic engineering to remove the Gal 1,3-αGal antigen (GalTKO) and express human membrane cofactor protein (hCD46). Natural killer cells rapidly disappear from the blood during perfusion of GalTKO.hCD46 porcine lungs with human blood and presumably are sequestered within the lung vasculature. Here we asked whether porcine expression of the human NK cell inhibitory ligand HLA-E and ß2 microglobulin inhibits GalTKO.hCD46 pig cell injury or prolongs lung function in two preclinical perfusion models. METHODS: Lungs from pigs modified to express GalTKO.hCD46 (n=37) and GalTKO.hCD46.HLA-E (n=5) were harvested and perfused with human blood until failure or elective termination at 4 hours. Airway pressures and pulmonary artery hemodynamics were recorded in real time. Blood samples were also collected throughout the experiment for analysis. Porcine aortic endothelial cells (PAECs) from each genotype were cultured in monolayers in microfluidic channels and used in fluorescent cytotoxicity assays using human NK cells. RESULTS: HLA-E expression on GalTKO.hCD46 PAECs was associated with significantly decreased antibody-dependent and antibody-independent NK-mediated cytotoxicity under in vitro conditions simulating physiologic shear stress. Relative to GalTKO.hCD46 pig lungs perfused with human blood on an ex vivo platform, additional expression of HLA-E increased median lung survival (>4 hours, vs 162 minutes, P=.012), and was associated with attenuated rise in pulmonary vascular resistance, and decreased platelet activation and histamine elaboration. As expected, HLA-E expression was not associated with a significant difference in NK cell adhesion to endothelial cells in vitro, or NK cell and neutrophil sequestration during organ perfusion. CONCLUSIONS: We conclude human NK cell activation contributes significantly to GalTKO.hCD46 pig endothelial injury and lung inflammation and show that expression of HLA-E is associated with physiologically meaningful protection of GalTKO.hCD46 cells and organs exposed to human blood.
[Mh] Termos MeSH primário: Células Endoteliais/imunologia
Sobrevivência de Enxerto/imunologia
Antígenos HLA/imunologia
Xenoenxertos/imunologia
Leucócitos/imunologia
Lesão Pulmonar/terapia
Proteína Cofatora de Membrana/imunologia
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Citotoxicidade Imunológica/imunologia
Galactosiltransferases/genética
Sobrevivência de Enxerto/genética
Antígenos HLA/genética
Seres Humanos
Células Matadoras Naturais/imunologia
Lesão Pulmonar/imunologia
Proteína Cofatora de Membrana/genética
Suínos
Transplante Heterólogo/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HLA Antigens); 0 (Membrane Cofactor Protein); EC 2.4.1.- (Galactosyltransferases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170305
[St] Status:MEDLINE
[do] DOI:10.1111/xen.12294


  8 / 1208 MEDLINE  
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[PMID]:28199366
[Au] Autor:Tan JR; Tan KS; Yong FL; Armugam A; Wang CW; Jeyaseelan K; Wong PT
[Ad] Endereço:Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
[Ti] Título:MicroRNAs regulating cluster of differentiation 46 (CD46) in cardioembolic and non-cardioembolic stroke.
[So] Source:PLoS One;12(2):e0172131, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ischemic stroke is a major cause of mortality and morbidity globally. Among the ischemic stroke subtypes, cardioembolic stroke is with poor functional outcome (Modified Rankin score ≥ 2). Early diagnosis of cardioembolic stroke will prove beneficial. This study examined the microRNAs targeting cluster of differentiation 46 (CD46), a potential biomarker for cardioembolic stroke. CD46 mRNA level was shown to be differentially expressed (p < 0.001) between cardioembolic stroke (median = 1.32) and non-cardioembolic stroke subtypes (large artery stroke median = 5.05; small vessel stroke median = 6.45). Bioinformatic search showed that miR-19a, -20a, -185 and -374b were found to target CD46 mRNA and further verified by luciferase reporter assay. The levels of miRNAs targeting CD46 were significantly reduced (p < 0.05) in non-cardioembolic stroke patients (large artery stroke median: miR-19a = 0.63, miR-20a = 0.42, miR-185 = 0.32, miR-374b = 0.27; small artery stroke median: miR-19a = 0.07, miR-20a = 0.06, miR-185 = 0.07, miR-374b = 0.05) as compared to cardioembolic stroke patients (median: miR-19a = 2.69, miR-20a = 1.36, miR-185 = 1.05, miR-374b = 1.23). ROC curve showed that the miRNAs could distinguish cardioembolic stroke from non-cardioembolic stroke with better AUC value as compared to CD46. Endogenous expression of CD46 in Human Umbilical Vein Endothelial Cells (HUVECs) were found to be regulated by miR-19a and miR-20a. Thus implicating that miR-19a and -20a may play a role in pathogenesis of cardioembolic stroke, possibly via the endothelial cells.
[Mh] Termos MeSH primário: MicroRNAs/metabolismo
Acidente Vascular Cerebral/patologia
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Adulto
Idoso
Idoso de 80 Anos ou mais
Área Sob a Curva
Sequência de Bases
Estudos de Casos e Controles
Feminino
Genes Reporter
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Masculino
Proteína Cofatora de Membrana/química
Proteína Cofatora de Membrana/genética
Proteína Cofatora de Membrana/metabolismo
MicroRNAs/química
MicroRNAs/genética
Meia-Idade
Curva ROC
Alinhamento de Sequência
Acidente Vascular Cerebral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Membrane Cofactor Protein); 0 (MicroRNAs)
[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:170216
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0172131


  9 / 1208 MEDLINE  
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[PMID]:28187911
[Au] Autor:Miller KD; Rall GF
[Ad] Endereço:Program in Cell and Molecular Biology, University of Pennsylvania, Philadelphia, PA, United States; Program in Blood Cell Development and Function, Fox Chase Cancer Center, Philadelphia, PA, United States.
[Ti] Título:What Kaplan-Meier survival curves don't tell us about CNS disease.
[So] Source:J Neuroimmunol;308:25-29, 2017 Jul 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Central nervous system consequences of viral infections are rare, but when they do occur, they are often serious and clinically challenging to manage. Our awareness of the perils of neuroinvasion by viruses is growing: the recently appreciated impact of Ebola and Zika virus infections on CNS integrity, decreases in vaccination coverage for potentially neurotropic viruses such as measles, and increased neurovirulence of some influenza strains collectively highlight the need for a better understanding of the viral-neural interaction. Defining these interactions and how they result in neuropathogenesis is paramount for the development of better clinical strategies, especially given the limited treatment options that are available due to the unique physiology of the brain that limits migration of blood-borne molecules into the CNS parenchyma. In this perspective, we discuss some unique aspects of neuronal viral infections and immune-mediated control that impact the pathogenic outcomes of these infections. Further, we draw attention to an often overlooked aspect of neuropathogenesis research: that lack of overt disease, which is often equated with survival post-infection, likely only scratches the surface of the myriad ways by which neurotropic infections can impair CNS function.
[Mh] Termos MeSH primário: Viroses do Sistema Nervoso Central/mortalidade
Sistema Nervoso Central/patologia
Estimativa de Kaplan-Meier
[Mh] Termos MeSH secundário: Animais
Sistema Nervoso Central/virologia
Viroses do Sistema Nervoso Central/genética
Modelos Animais de Doenças
Seres Humanos
Interferon gama/deficiência
Interferon gama/genética
Proteína Cofatora de Membrana/deficiência
Proteína Cofatora de Membrana/genética
Camundongos
Camundongos Transgênicos
Receptor de Interferon alfa e beta/deficiência
Receptor de Interferon alfa e beta/genética
Fator de Transcrição STAT1/deficiência
Fator de Transcrição STAT1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; VIDEO-AUDIO MEDIA
[Nm] Nome de substância:
0 (CD46 protein, human); 0 (IFNAR1 protein, human); 0 (Membrane Cofactor Protein); 0 (STAT1 Transcription Factor); 0 (Stat1 protein, mouse); 156986-95-7 (Receptor, Interferon alpha-beta); 82115-62-6 (Interferon-gamma)
[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:170212
[St] Status:MEDLINE


  10 / 1208 MEDLINE  
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[PMID]:28176476
[Au] Autor:Chan S; Mallett AJ; Patel C; Francis RS; Johnson DW; Mudge DW; Isbel NM
[Ad] Endereço:Queensland Renal Transplant Service, Princess Alexandra Hospital, Brisbane, Queensland, Australia.
[Ti] Título:Recurrent atypical haemolytic uraemic syndrome post kidney transplant due to a CD46 mutation in the setting of SMARCAL1-mediated inherited kidney disease.
[So] Source:Nephrology (Carlton);22 Suppl 1:11-14, 2017 Feb.
[Is] ISSN:1440-1797
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:Disorders in the regulation of the alternate complement pathway often result in complement-mediated damage to the microvascular endothelium and can be associated with both glomerulonephritis and atypical haemolytic uraemic syndrome. Inherited defects in complement regulatory genes or autoantibodies against complement regulatory proteins are predictive of the severity of the disease and the risk of recurrence post kidney transplantation. Heterozygous mutations in CD46, which codes for a transmembrane cofactor glycoprotein membrane cofactor protein, usually have a lower incidence of end-stage kidney disease and decreased risk of recurrent disease post transplant, as wild-type membrane cofactor protein is present in the transplanted kidney. However, some patients with CD46 mutations have a second variant in other complement regulatory genes increasing the severity of disease. The following case report illustrates the course of a young adult patient with end-stage kidney disease initially ascribed to seronegative systemic lupus erythematosus, who presented with biopsy-proven thrombotic microangiopathy following kidney transplantation. It highlights the complexity associated with disorders of complement regulation and the need for a high index of suspicion and genetic testing in patients who present with thrombotic microangiopathy post-transplant.
[Mh] Termos MeSH primário: Síndrome Hemolítico-Urêmica Atípica/genética
DNA Helicases/genética
Falência Renal Crônica/genética
Transplante de Rim
Proteína Cofatora de Membrana/genética
Mutação/genética
[Mh] Termos MeSH secundário: Adolescente
Feminino
Seres Humanos
Falência Renal Crônica/cirurgia
Recidiva
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Membrane Cofactor Protein); EC 2.7.7.- (SMARCAL1 protein, human); EC 3.6.4.- (DNA Helicases)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170209
[St] Status:MEDLINE
[do] DOI:10.1111/nep.12933



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