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[PMID]:29176322
[Au] Autor:Shi Y; Ye P; Long X
[Ti] Título:Differential Expression Profiles of the Transcriptome in Breast Cancer Cell Lines Revealed by Next Generation Sequencing.
[So] Source:Cell Physiol Biochem;44(2):804-816, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: As MCF-7 and MDA-MB-231 cells are the typical cell lines of two clinical breast tumour subtypes, the aim of the present study was to elucidate the transcriptome differences between MCF-7 and MDA-MB-231 breast cancer cell lines. METHODS: The mRNA, miRNA (MicroRNA) and lncRNA (Long non-coding RNA) expression profiles were examined using NGS (next generation sequencing) instrument Illumina HiSeq-2500. GO (Gene Ontology) and KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway analyses were performed to identify the biological functions of differentially expressed coding RNAs. Subsequently, we constructed an mRNA-ncRNA (non-coding RNA) targeting regulatory network. Finally, we performed RT-qPCR (real-time quantitative PCR) to confirm the NGS results. RESULTS: There are sharp distinctions of the coding and non-coding RNA profiles between MCF-7 and MDA-MB-231 cell lines. Among the mRNAs and ncRNAs with the most differential expression, SLPI, SOD2, miR-7, miR-143 and miR-145 were highly expressed in MCF-7 cells, while CD55, KRT17, miR-21, miR-10b, miR-9, NEAT1 and PICSAR were over-expressed in MDA-MB-231 cells. Differentially expressed mRNAs are primarily involved in biological processes of locomotion, biological adhesion, ECM-receptor interaction pathway and focal adhesion. In the targeting regulatory network of differentially expressed RNAs, mRNAs and miRNAs are primarily associated with tumour metastasis, but the functions of lncRNAs remain uncharacterized. CONCLUSION: These results provide a basis for future studies of breast cancer metastasis and drug resistance.
[Mh] Termos MeSH primário: Transcriptoma
[Mh] Termos MeSH secundário: Neoplasias da Mama/metabolismo
Neoplasias da Mama/patologia
Antígenos CD55/genética
Antígenos CD55/metabolismo
Linhagem Celular Tumoral
Feminino
Regulação Neoplásica da Expressão Gênica
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Células MCF-7
MicroRNAs/metabolismo
RNA Longo não Codificante/metabolismo
RNA Mensageiro/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Inibidor Secretado de Peptidases Leucocitárias/genética
Inibidor Secretado de Peptidases Leucocitárias/metabolismo
Análise de Sequência de RNA
Superóxido Dismutase/genética
Superóxido Dismutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD55 Antigens); 0 (MicroRNAs); 0 (RNA, Long Noncoding); 0 (RNA, Messenger); 0 (SLPI protein, human); 0 (Secretory Leukocyte Peptidase Inhibitor); EC 1.15.1.1 (Superoxide Dismutase); EC 1.15.1.1 (superoxide dismutase 2)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1159/000485344


  2 / 1609 MEDLINE  
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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


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[PMID]:28838952
[Au] Autor:Saygin C; Wiechert A; Rao VS; Alluri R; Connor E; Thiagarajan PS; Hale JS; Li Y; Chumakova A; Jarrar A; Parker Y; Lindner DJ; Nagaraj AB; Kim JJ; DiFeo A; Abdul-Karim FW; Michener C; Rose PG; DeBernardo R; Mahdi H; McCrae KR; Lin F; Lathia JD; Reizes O
[Ad] Endereço:Department of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH.
[Ti] Título:CD55 regulates self-renewal and cisplatin resistance in endometrioid tumors.
[So] Source:J Exp Med;214(9):2715-2732, 2017 Sep 04.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Effective targeting of cancer stem cells (CSCs) requires neutralization of self-renewal and chemoresistance, but these phenotypes are often regulated by distinct molecular mechanisms. Here we report the ability to target both of these phenotypes via CD55, an intrinsic cell surface complement inhibitor, which was identified in a comparative analysis between CSCs and non-CSCs in endometrioid cancer models. In this context, CD55 functions in a complement-independent manner and required lipid raft localization for CSC maintenance and cisplatin resistance. CD55 regulated self-renewal and core pluripotency genes via ROR2/JNK signaling and in parallel cisplatin resistance via lymphocyte-specific protein tyrosine kinase (LCK) signaling, which induced DNA repair genes. Targeting LCK signaling via saracatinib, an inhibitor currently undergoing clinical evaluation, sensitized chemoresistant cells to cisplatin. Collectively, our findings identify CD55 as a unique signaling node that drives self-renewal and therapeutic resistance through a bifurcating signaling axis and provides an opportunity to target both signaling pathways in endometrioid tumors.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Antígenos CD55/fisiologia
Autorrenovação Celular/fisiologia
Cisplatino/uso terapêutico
Neoplasias do Endométrio/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Resistência a Medicamentos Antineoplásicos
Neoplasias do Endométrio/tratamento farmacológico
Feminino
Camundongos
Camundongos SCID
Transplante de Neoplasias
Células-Tronco Neoplásicas/fisiologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (CD55 Antigens); Q20Q21Q62J (Cisplatin)
[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:170826
[St] Status:MEDLINE
[do] DOI:10.1084/jem.20170438


  4 / 1609 MEDLINE  
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[PMID]:28793332
[Au] Autor:Choi IY; Karpus ON; Turner JD; Hardie D; Marshall JL; de Hair MJH; Maijer KI; Tak PP; Raza K; Hamann J; Buckley CD; Gerlag DM; Filer A
[Ad] Endereço:Division of Clinical Immunology and Rheumatology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
[Ti] Título:Stromal cell markers are differentially expressed in the synovial tissue of patients with early arthritis.
[So] Source:PLoS One;12(8):e0182751, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Previous studies have shown increased expression of stromal markers in synovial tissue (ST) of patients with established rheumatoid arthritis (RA). Here, ST expression of stromal markers in early arthritis in relationship to diagnosis and prognostic outcome was studied. METHODS: ST from 56 patients included in two different early arthritis cohorts and 7 non-inflammatory controls was analysed using immunofluorescence to detect stromal markers CD55, CD248, fibroblast activation protein (FAP) and podoplanin. Diagnostic classification (gout, psoriatic arthritis, unclassified arthritis (UA), parvovirus associated arthritis, reactive arthritis and RA), disease outcome (resolving vs persistent) and clinical variables were determined at baseline and after follow-up, and related to the expression of stromal markers. RESULTS: We observed expression of all stromal markers in ST of early arthritis patients, independent of diagnosis or prognostic outcome. Synovial expression of FAP was significantly higher in patients developing early RA compared to other diagnostic groups and non-inflammatory controls. In RA FAP protein was expressed in both lining and sublining layers. Podoplanin expression was higher in all early inflammatory arthritis patients than controls, but did not differentiate diagnostic outcomes. Stromal marker expression was not associated with prognostic outcomes of disease persistence or resolution. There was no association with clinical or sonographic variables. CONCLUSIONS: Stromal cell markers CD55, CD248, FAP and podoplanin are expressed in ST in the earliest stage of arthritis. Baseline expression of FAP is higher in early synovitis patients who fulfil classification criteria for RA over time. These results suggest that significant fibroblast activation occurs in RA in the early window of disease.
[Mh] Termos MeSH primário: Artrite/metabolismo
Células Estromais/metabolismo
Membrana Sinovial/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Antígenos CD/metabolismo
Antígenos de Neoplasias/metabolismo
Artrite/diagnóstico
Biomarcadores/metabolismo
Antígenos CD55/metabolismo
Progressão da Doença
Feminino
Fibroblastos/metabolismo
Gelatinases/metabolismo
Seres Humanos
Masculino
Glicoproteínas de Membrana/metabolismo
Proteínas de Membrana/metabolismo
Meia-Idade
Prognóstico
Serina Endopeptidases/metabolismo
Sinovite/diagnóstico
Sinovite/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, Neoplasm); 0 (Biomarkers); 0 (CD248 protein, human); 0 (CD55 Antigens); 0 (Membrane Glycoproteins); 0 (Membrane Proteins); 0 (PDPN protein, human); EC 3.4.21.- (Serine Endopeptidases); EC 3.4.21.- (fibroblast activation protein alpha); EC 3.4.24.- (Gelatinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170810
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182751


  5 / 1609 MEDLINE  
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[PMID]:28657861
[Au] Autor:Kurolap A; Eshach-Adiv O; Hershkovitz T; Paperna T; Mory A; Oz-Levi D; Zohar Y; Mandel H; Chezar J; Azoulay D; Peleg S; Half EE; Yahalom V; Finkel L; Weissbrod O; Geiger D; Tabib A; Shaoul R; Magen D; Bonstein L; Mevorach D; Baris HN
[Ad] Endereço:Technion-Israel Institute of Technology, Haifa, Israel.
[Ti] Título:Loss of CD55 in Eculizumab-Responsive Protein-Losing Enteropathy.
[So] Source:N Engl J Med;377(1):87-89, 2017 07 06.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Anticorpos Monoclonais Humanizados/uso terapêutico
Antígenos CD55/genética
Mutação da Fase de Leitura
Enteropatias Perdedoras de Proteínas/tratamento farmacológico
Enteropatias Perdedoras de Proteínas/genética
[Mh] Termos MeSH secundário: Criança
Pré-Escolar
Ensaios de Uso Compassivo
Ativação do Complemento
Complexo de Ataque à Membrana do Sistema Complemento/metabolismo
Diarreia/etiologia
Feminino
Seres Humanos
Masculino
Meia-Idade
Linhagem
Análise de Sequência de DNA
Albumina Sérica/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:LETTER; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Monoclonal, Humanized); 0 (CD55 Antigens); 0 (Complement Membrane Attack Complex); 0 (Serum Albumin); A3ULP0F556 (eculizumab)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170629
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMc1707173


  6 / 1609 MEDLINE  
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[PMID]:28657829
[Au] Autor:Ozen A; Comrie WA; Ardy RC; Domínguez Conde C; Dalgic B; Beser ÖF; Morawski AR; Karakoc-Aydiner E; Tutar E; Baris S; Ozcay F; Serwas NK; Zhang Y; Matthews HF; Pittaluga S; Folio LR; Unlusoy Aksu A; McElwee JJ; Krolo A; Kiykim A; Baris Z; Gulsan M; Ogulur I; Snapper SB; Houwen RHJ; Leavis HL; Ertem D; Kain R; Sari S; Erkan T; Su HC; Boztug K; Lenardo MJ
[Ad] Endereço:From the Section of Molecular Development of the Immune System, Laboratory of Immunology (A.O., W.A.C., A.R.M., H.F.M., M.J.L.), the Clinical Genomics Program (A.O., W.A.C., A.R.M., Y.Z., H.F.M., H.C.S., M.J.L.), and the Human Immunological Diseases Section, Laboratory of Host Defenses (Y.Z., H.C.S.
[Ti] Título:CD55 Deficiency, Early-Onset Protein-Losing Enteropathy, and Thrombosis.
[So] Source:N Engl J Med;377(1):52-61, 2017 07 06.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Studies of monogenic gastrointestinal diseases have revealed molecular pathways critical to gut homeostasis and enabled the development of targeted therapies. METHODS: We studied 11 patients with abdominal pain and diarrhea caused by early-onset protein-losing enteropathy with primary intestinal lymphangiectasia, edema due to hypoproteinemia, malabsorption, and less frequently, bowel inflammation, recurrent infections, and angiopathic thromboembolic disease; the disorder followed an autosomal recessive pattern of inheritance. Whole-exome sequencing was performed to identify gene variants. We evaluated the function of CD55 in patients' cells, which we confirmed by means of exogenous induction of expression of CD55. RESULTS: We identified homozygous loss-of-function mutations in the gene encoding CD55 (decay-accelerating factor), which lead to loss of protein expression. Patients' T lymphocytes showed increased complement activation causing surface deposition of complement and the generation of soluble C5a. Costimulatory function and cytokine modulation by CD55 were defective. Genetic reconstitution of CD55 or treatment with a complement-inhibitory therapeutic antibody reversed abnormal complement activation. CONCLUSIONS: CD55 deficiency with hyperactivation of complement, angiopathic thrombosis, and protein-losing enteropathy (the CHAPLE syndrome) is caused by abnormal complement activation due to biallelic loss-of-function mutations in CD55. (Funded by the National Institute of Allergy and Infectious Diseases and others.).
[Mh] Termos MeSH primário: Antígenos CD55/genética
Ativação do Complemento/genética
Proteínas do Sistema Complemento/metabolismo
Mutação
Enteropatias Perdedoras de Proteínas/genética
Trombose/genética
[Mh] Termos MeSH secundário: Antígenos CD55/sangue
Criança
Pré-Escolar
Ativação do Complemento/efeitos dos fármacos
Inativadores do Complemento/farmacologia
Feminino
Homozigoto
Seres Humanos
Imunoglobulina A/sangue
Lactente
Intestino Delgado/patologia
Masculino
Linhagem
Enteropatias Perdedoras de Proteínas/complicações
Estatísticas não Paramétricas
Síndrome
Linfócitos T/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD55 Antigens); 0 (Complement Inactivating Agents); 0 (Immunoglobulin A); 9007-36-7 (Complement System Proteins)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170629
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMoa1615887


  7 / 1609 MEDLINE  
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[PMID]:28516949
[Au] Autor:Hill A; DeZern AE; Kinoshita T; Brodsky RA
[Ad] Endereço:Department of Haematology, St. James' University Hospital, Leeds, UK.
[Ti] Título:Paroxysmal nocturnal haemoglobinuria.
[So] Source:Nat Rev Dis Primers;3:17028, 2017 05 18.
[Is] ISSN:2056-676X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Paroxysmal nocturnal haemoglobinuria (PNH) is a clonal haematopoietic stem cell (HSC) disease that presents with haemolytic anaemia, thrombosis and smooth muscle dystonias, as well as bone marrow failure in some cases. PNH is caused by somatic mutations in PIGA (which encodes phosphatidylinositol N-acetylglucosaminyltransferase subunit A) in one or more HSC clones. The gene product of PIGA is required for the biosynthesis of glycosylphosphatidylinositol (GPI) anchors; thus, PIGA mutations lead to a deficiency of GPI-anchored proteins, such as complement decay-accelerating factor (also known as CD55) and CD59 glycoprotein (CD59), which are both complement inhibitors. Clinical manifestations of PNH occur when a HSC clone carrying somatic PIGA mutations acquires a growth advantage and differentiates, generating mature blood cells that are deficient of GPI-anchored proteins. The loss of CD55 and CD59 renders PNH erythrocytes susceptible to intravascular haemolysis, which can lead to thrombosis and to much of the morbidity and mortality of PNH. The accumulation of anaphylatoxins (such as C5a) from complement activation might also have a role. The natural history of PNH is highly variable, ranging from quiescent to life-threatening. Therapeutic strategies include terminal complement blockade and bone marrow transplantation. Eculizumab, a monoclonal antibody complement inhibitor, is highly effective and the only licensed therapy for PNH.
[Mh] Termos MeSH primário: Hemoglobinúria Paroxística/patologia
Hemoglobinúria Paroxística/terapia
Proteínas de Membrana/genética
[Mh] Termos MeSH secundário: Anticorpos Monoclonais Humanizados/uso terapêutico
Transplante de Medula Óssea
Antígenos CD55/metabolismo
Antígenos CD59/metabolismo
Proteínas Inativadoras do Complemento/metabolismo
Hemoglobinúria Paroxística/genética
Hemoglobinúria Paroxística/metabolismo
Seres Humanos
Mutação
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antibodies, Monoclonal, Humanized); 0 (CD55 Antigens); 0 (CD59 Antigens); 0 (Complement Inactivator Proteins); 0 (Membrane Proteins); 0 (phosphatidylinositol glycan-class A protein); 101754-01-2 (CD59 protein, human); A3ULP0F556 (eculizumab)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171121
[Lr] Data última revisão:
171121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170519
[St] Status:MEDLINE
[do] DOI:10.1038/nrdp.2017.28


  8 / 1609 MEDLINE  
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[PMID]:28510725
[Au] Autor:Lee N; Cao B; Ke C; Lu H; Hu Y; Tam CHT; Ma RCW; Guan D; Zhu Z; Li H; Lin M; Wong RYK; Yung IMH; Hung TN; Kwok K; Horby P; Hui DSC; Chan MCW; Chan PKS
[Ad] Endereço:Department of Medicine and Therapeutics, Faculty of Medicine, The Chinese University of Hong Kong.
[Ti] Título:IFITM3, TLR3, and CD55 Gene SNPs and Cumulative Genetic Risks for Severe Outcomes in Chinese Patients With H7N9/H1N1pdm09 Influenza.
[So] Source:J Infect Dis;216(1):97-104, 2017 Jul 01.
[Is] ISSN:1537-6613
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: We examined associations between single-nucleotide polymorphisms (SNPs) of IFITM3, TLR3, and CD55 genes and influenza clinical outcomes in Chinese. Methods: A multicenter study was conducted on 275 adult cases of avian (H7N9) and pandemic (H1N1pdm09) influenza. Host DNA was extracted from diagnostic respiratory samples; IFITM3 rs12252, TLR3 rs5743313, CD55 rs2564978, and TLR4 rs4986790/4986791 were targeted for genotyping (Sanger sequencing). The primary outcome analyzed was death. Results: IFITM3 and TLR3 SNPs were in Hardy-Weinberg equilibrium; their allele frequencies (IFITM3/C-allele 0.56, TLR3/C-allele 0.88) were comparable to 1000 Genomes Han Chinese data. We found over-representation of homozygous IFITM3 CC (54.5% vs 33.2%; P = .02) and TLR3 CC (93.3% vs 76.9%; P = .04) genotypes among fatal cases. Recessive genetic models showed their significant independent associations with higher death risks (adjusted hazard ratio [aHR] 2.78, 95% confidence interval [CI] 1.29-6.02, and aHR 4.85, 95% CI 1.11-21.06, respectively). Cumulative effects were found (aHR 3.53, 95% CI 1.64-7.59 per risk genotype; aHR 9.99, 95% CI 1.27-78.59 with both). Results were consistent for each influenza subtype and other severity indicators. The CD55 TT genotype was linked to severity. TLR4 was nonpolymorphic. Conclusions: Host genetic factors may influence clinical outcomes of avian and pandemic influenza infections. Such findings have important implications on disease burden and patient care in at-risk populations.
[Mh] Termos MeSH primário: Antígenos CD55/genética
Influenza Humana/genética
Proteínas de Membrana/genética
Proteínas de Ligação a RNA/genética
Receptor 3 Toll-Like/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Grupo com Ancestrais do Continente Asiático
China/epidemiologia
Feminino
Frequência do Gene
Predisposição Genética para Doença
Técnicas de Genotipagem
Seres Humanos
Vírus da Influenza A Subtipo H1N1
Vírus da Influenza A Subtipo H7N9
Influenza Humana/epidemiologia
Masculino
Meia-Idade
Polimorfismo de Nucleotídeo Único
Modelos de Riscos Proporcionais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD55 Antigens); 0 (IFITM3 protein, human); 0 (Membrane Proteins); 0 (RNA-Binding Proteins); 0 (TLR3 protein, human); 0 (Toll-Like Receptor 3)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170517
[St] Status:MEDLINE
[do] DOI:10.1093/infdis/jix235


  9 / 1609 MEDLINE  
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[PMID]:28500075
[Au] Autor:Bongoni AK; Lu B; Salvaris EJ; Roberts V; Fang D; McRae JL; Fisicaro N; Dwyer KM; Cowan PJ
[Ad] Endereço:Immunology Research Centre, St. Vincent's Hospital Melbourne, Fitzroy, Victoria 3065, Australia.
[Ti] Título:Overexpression of Human CD55 and CD59 or Treatment with Human CD55 Protects against Renal Ischemia-Reperfusion Injury in Mice.
[So] Source:J Immunol;198(12):4837-4845, 2017 Jun 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Deficiency in the membrane-bound complement regulators CD55 and CD59 exacerbates renal ischemia-reperfusion injury (IRI) in mouse models, but the effect of increasing CD55 and CD59 activity has not been examined. In this study, we investigated the impact of overexpression of human (h) CD55 ± hCD59 or treatment with soluble rhCD55 in a mouse model of renal IRI. Unilaterally nephrectomised mice were subjected to 18 (mild IRI) or 22 min (moderate IRI) warm renal ischemia, and analyzed 24 h after reperfusion for renal function (serum creatinine and urea), complement deposition (C3b/c and C9), and infiltration of neutrophils and macrophages. Transgenic mice expressing hCD55 alone were protected against mild renal IRI, with reduced creatinine and urea levels compared with wild type littermates. However, the renal function of the hCD55 mice was not preserved in the moderate IRI model, despite a reduction in C3b/c and C9 deposition and innate cell infiltration. Mice expressing both hCD55 and hCD59, on the other hand, were protected in the moderate IRI model, with significant reductions in all parameters measured. Wild type mice treated with rhCD55 immediately after reperfusion were also protected in the moderate IRI model. Thus, manipulation of CD55 activity to increase inhibition of the C3 and C5 convertases is protective against renal IRI, and the additional expression of hCD59, which regulates the terminal complement pathway, provides further protection. Therefore, anti-complement therapy using complement regulatory proteins may provide a potential clinical option for preventing tissue and organ damage in renal IRI.
[Mh] Termos MeSH primário: Antígenos CD55/genética
Antígenos CD55/uso terapêutico
Antígenos CD59/genética
Nefropatias/terapia
Traumatismo por Reperfusão/terapia
[Mh] Termos MeSH secundário: Animais
Antígenos CD55/imunologia
Ativação do Complemento
Creatinina/sangue
Seres Humanos
Nefropatias/imunologia
Nefropatias/fisiopatologia
Macrófagos/imunologia
Camundongos
Camundongos Transgênicos
Neutrófilos/imunologia
Traumatismo por Reperfusão/imunologia
Traumatismo por Reperfusão/fisiopatologia
Ureia/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD55 Antigens); 0 (CD59 Antigens); 101754-01-2 (CD59 protein, human); 8W8T17847W (Urea); AYI8EX34EU (Creatinine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170514
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601943


  10 / 1609 MEDLINE  
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[PMID]:28345461
[Au] Autor:Meng ZW; Liu MC; Hong HJ; Du Q; Chen YL
[Ad] Endereço:1 Department of Hepatobiliary Surgery, The Affiliated Union Hospital of Fujian Medical University, Fuzhou, People's Republic of China.
[Ti] Título:Expression and prognostic value of soluble CD97 and its ligand CD55 in intrahepatic cholangiocarcinoma.
[So] Source:Tumour Biol;39(3):1010428317694319, 2017 Mar.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The incidence rate of intrahepatic cholangiocarcinoma is rising, and treatment options are limited. Therefore, new biological markers of intrahepatic cholangiocarcinoma are needed. Immunohistochemistry and enzyme-linked immunosorbent assay were applied to analyze the expressions of CD97, CD55, and soluble CD97 in 71 patients with intrahepatic cholangiocarcinoma and 10 patients with hepatolithiasis. CD97 and CD55 were not expressed in hepatolithiatic tissues, but positive expression was observed in 76.1% (54/71) and 70.4% (50/71) of intrahepatic cholangiocarcinoma patients. The univariate analyses indicated that the positive expressions of CD97 and CD55 were related to short intrahepatic cholangiocarcinoma survival of patients (both p = 0.001). Furthermore, CD97 and CD55 expressions and biliary soluble CD97 levels were significantly associated with histological grade (p = 0.004, 0.002, and 0.012, respectively), lymph node metastases (p = 0.020, 0.038, and 0.001, respectively), and venous invasion (p = 0.003, 0.002, and 0.001, respectively). The multivariate analyses indicated that lymph node metastases (hazard ratio: 2.407, p = 0.003), positive CD55 expression (hazard ratio: 4.096, p = 0.003), and biliary soluble CD97 levels (hazard ratio: 2.434, p = 0.002) were independent risk factors for the intrahepatic cholangiocarcinoma survival. The receiver operating characteristic (ROC) curve analysis indicated that when the cutoff values of biliary soluble CD97 were 1.15 U/mL, the diagnostic value for predicting lymph node metastasis had a sensitivity of 87.5% and a specificity of 51.3%. For intrahepatic cholangiocarcinoma patient death within 60 months at a cutoff value of 0.940 U/mL, the diagnostic value sensitivity was 89.3% and the specificity was 93.3%. Biliary soluble CD97 may be a new biological marker for early diagnosis, prediction of lymph node metastasis and poor prognosis, and discovery of a therapeutic target.
[Mh] Termos MeSH primário: Antígenos CD/biossíntese
Neoplasias dos Ductos Biliares/patologia
Ductos Biliares Intra-Hepáticos/patologia
Biomarcadores Tumorais/metabolismo
Antígenos CD55/biossíntese
Colangiocarcinoma/patologia
[Mh] Termos MeSH secundário: Idoso
Bile/metabolismo
Neoplasias dos Ductos Biliares/mortalidade
Colangiocarcinoma/mortalidade
Ensaio de Imunoadsorção Enzimática
Feminino
Seres Humanos
Imuno-Histoquímica
Metástase Linfática/diagnóstico
Metástase Linfática/patologia
Masculino
Meia-Idade
Prognóstico
Curva ROC
Sensibilidade e Especificidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Biomarkers, Tumor); 0 (CD55 Antigens); 0 (CD97 protein, human)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170328
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317694319



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