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Pesquisa : D12.776.543.750.705.408.460 [Categoria DeCS]
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[PMID]:24630964
[Au] Autor:Olex AL; Turkett WH; Fetrow JS; Loeser RF
[Ad] Endereço:Department of Computer Science, Wake Forest University, Winston-Salem, NC, USA. Electronic address: amy.lynn81@gmail.com.
[Ti] Título:Integration of gene expression data with network-based analysis to identify signaling and metabolic pathways regulated during the development of osteoarthritis.
[So] Source:Gene;542(1):38-45, 2014 May 25.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Osteoarthritis (OA) is characterized by remodeling and degradation of joint tissues. Microarray studies have led to a better understanding of the molecular changes that occur in tissues affected by conditions such as OA; however, such analyses are limited to the identification of a list of genes with altered transcript expression, usually at a single time point during disease progression. While these lists have identified many novel genes that are altered during the disease process, they are unable to identify perturbed relationships between genes and gene products. In this work, we have integrated a time course gene expression dataset with network analysis to gain a better systems level understanding of the early events that occur during the development of OA in a mouse model. The subnetworks that were enriched at one or more of the time points examined (2, 4, 8, and 16 weeks after induction of OA) contained genes from several pathways proposed to be important to the OA process, including the extracellular matrix-receptor interaction and the focal adhesion pathways and the Wnt, Hedgehog and TGF-ß signaling pathways. The genes within the subnetworks were most active at the 2 and 4 week time points and included genes not previously studied in the OA process. A unique pathway, riboflavin metabolism, was active at the 4 week time point. These results suggest that the incorporation of network-type analyses along with time series microarray data will lead to advancements in our understanding of complex diseases such as OA at a systems level, and may provide novel insights into the pathways and processes involved in disease pathogenesis.
[Mh] Termos MeSH primário: Artrite Experimental/genética
Articulações/patologia
Redes e Vias Metabólicas/genética
Osteoartrite/genética
[Mh] Termos MeSH secundário: Animais
Artrite Experimental/metabolismo
Artrite Experimental/patologia
Modelos Animais de Doenças
Progressão da Doença
Adesões Focais/genética
Adesões Focais/metabolismo
Expressão Gênica
Perfilação da Expressão Gênica
Proteínas Hedgehog/genética
Proteínas Hedgehog/metabolismo
Articulações/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Análise de Sequência com Séries de Oligonucleotídeos
Osteoartrite/metabolismo
Osteoartrite/patologia
Receptores de Citoadesina/genética
Receptores de Citoadesina/metabolismo
Riboflavina/metabolismo
Fator de Crescimento Transformador beta/genética
Fator de Crescimento Transformador beta/metabolismo
Proteínas Wnt/genética
Via de Sinalização Wnt/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Hedgehog Proteins); 0 (Receptors, Cytoadhesin); 0 (Transforming Growth Factor beta); 0 (Wnt Proteins); TLM2976OFR (Riboflavin)
[Em] Mês de entrada:1406
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140318
[St] Status:MEDLINE


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[PMID]:24450868
[Au] Autor:Filali H; Martín-Burriel I; Harders F; Varona L; Hedman C; Mediano DR; Monzón M; Bossers A; Badiola JJ; Bolea R
[Ti] Título:Gene expression profiling of mesenteric lymph nodes from sheep with natural scrapie.
[So] Source:BMC Genomics;15:59, 2014 Jan 23.
[Is] ISSN:1471-2164
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Prion diseases are characterized by the accumulation of the pathogenic PrPSc protein, mainly in the brain and the lymphoreticular system. Although prions multiply/accumulate in the lymph nodes without any detectable pathology, transcriptional changes in this tissue may reflect biological processes that contribute to the molecular pathogenesis of prion diseases. Little is known about the molecular processes that occur in the lymphoreticular system in early and late stages of prion disease. We performed a microarray-based study to identify genes that are differentially expressed at different disease stages in the mesenteric lymph node of sheep naturally infected with scrapie. Oligo DNA microarrays were used to identify gene-expression profiles in the early/middle (preclinical) and late (clinical) stages of the disease. RESULTS: In the clinical stage of the disease, we detected 105 genes that were differentially expressed (≥2-fold change in expression). Of these, 43 were upregulated and 62 downregulated as compared with age-matched negative controls. Fewer genes (50) were differentially expressed in the preclinical stage of the disease. Gene Ontology enrichment analysis revealed that the differentially expressed genes were largely associated with the following terms: glycoprotein, extracellular region, disulfide bond, cell cycle and extracellular matrix. Moreover, some of the annotated genes could be grouped into 3 specific signaling pathways: focal adhesion, PPAR signaling and ECM-receptor interaction. We discuss the relationship between the observed gene expression profiles and PrPSc deposition and the potential involvement in the pathogenesis of scrapie of 7 specific differentially expressed genes whose expression levels were confirmed by real time-PCR. CONCLUSIONS: The present findings identify new genes that may be involved in the pathogenesis of natural scrapie infection in the lymphoreticular system, and confirm previous reports describing scrapie-induced alterations in the expression of genes involved in protein misfolding, angiogenesis and the oxidative stress response. Further studies will be necessary to determine the role of these genes in prion replication, dissemination and in the response of the organism to this disease.
[Mh] Termos MeSH primário: Perfilação da Expressão Gênica/veterinária
Regulação da Expressão Gênica
Linfonodos/metabolismo
Scrapie/fisiopatologia
Ovinos/genética
Ovinos/metabolismo
[Mh] Termos MeSH secundário: Animais
Análise por Conglomerados
Regulação para Baixo
Adesões Focais/genética
Análise de Sequência com Séries de Oligonucleotídeos
Receptores Ativados por Proliferador de Peroxissomo/genética
Receptores Ativados por Proliferador de Peroxissomo/metabolismo
Príons/genética
Príons/metabolismo
Receptores de Citoadesina/genética
Receptores de Citoadesina/metabolismo
Scrapie/metabolismo
Scrapie/patologia
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Peroxisome Proliferator-Activated Receptors); 0 (Prions); 0 (Receptors, Cytoadhesin)
[Em] Mês de entrada:1408
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140124
[St] Status:MEDLINE
[do] DOI:10.1186/1471-2164-15-59


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[PMID]:22179951
[Au] Autor:Liu Z; Niu Y; Li C; Yang Y; Gao C
[Ad] Endereço:Anal-Colorectal Surgery Institute, No. 150 Central Hospital of PLA, Luoyang, China 471031.
[Ti] Título:Integrating multiple microarray datasets on oral squamous cell carcinoma to reveal dysregulated networks.
[So] Source:Head Neck;34(12):1789-97, 2012 Dec.
[Is] ISSN:1097-0347
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Oral squamous cell carcinoma (OSCC) is the sixth most common type of carcinoma worldwide. The pathogenic pathways involved in this cancer are mostly unknown; therefore, a better characterization of the OSCC gene expression profile would represent a considerable advance. The public availability of gene expression datasets was meant to obtain new insights on biological processes. METHODS: We integrated 4 public microarray datasets on OSCC to evaluate the degree of consistency among the biological results obtained in these different studies and to identify common regulatory pathways that could be responsible for tumor growth. RESULTS: Twelve altered cellular pathways implicated in OSCC and 4 genes altered in the extracellular matrix (ECM) receptor pathway were validated by quantitative real-time polymerase chain reaction (qRT-PCR). CONCLUSION: Using 4 expression array datasets, we have developed a robust method for analyzing pathways altered in OSCC.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/genética
Carcinoma de Células Escamosas/patologia
Bases de Dados de Ácidos Nucleicos
Perfilação da Expressão Gênica/métodos
Regulação Neoplásica da Expressão Gênica/fisiologia
Neoplasias de Cabeça e Pescoço/genética
Neoplasias de Cabeça e Pescoço/patologia
Neoplasias Bucais/genética
Neoplasias Bucais/patologia
[Mh] Termos MeSH secundário: Carcinoma de Células Escamosas/fisiopatologia
Bases de Dados Genéticas
Matriz Extracelular/genética
Matriz Extracelular/patologia
Matriz Extracelular/fisiologia
Regulação Neoplásica da Expressão Gênica/genética
Neoplasias de Cabeça e Pescoço/fisiopatologia
Seres Humanos
Neoplasias Bucais/fisiopatologia
Análise de Sequência com Séries de Oligonucleotídeos/métodos
Reação em Cadeia da Polimerase em Tempo Real
Receptores de Citoadesina/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
0 (Receptors, Cytoadhesin)
[Em] Mês de entrada:1306
[Cu] Atualização por classe:121119
[Lr] Data última revisão:
121119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:111220
[St] Status:MEDLINE
[do] DOI:10.1002/hed.22013


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[PMID]:19824923
[Au] Autor:Gameiro J; Nagib PR; Andrade CF; Villa-Verde DM; Silva-Barbosa SD; Savino W; Costa FT; Verinaud L
[Ad] Endereço:Department of Anatomy, Cell Biology and Physiology, Institute of Biology, State University of Campinas-UNICAMP, Campinas, São Paulo, Brazil.
[Ti] Título:Changes in cell migration-related molecules expressed by thymic microenvironment during experimental Plasmodium berghei infection: consequences on thymocyte development.
[So] Source:Immunology;129(2):248-56, 2010 Feb.
[Is] ISSN:1365-2567
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We previously showed alterations in the thymus during experimental infection with Plasmodium berghei. Such alterations comprised histological changes, with loss of cortical-medullary limits, and the intrathymic presence of parasites. As the combination of chemokines, adhesion molecules and extracellular matrix (ECM) is critical to appropriate thymocyte development, we analysed the thymic expression of ECM ligands and receptors, as well as chemokines and their respective receptors during the experimental P. berghei infection. Increased expression of ECM components was observed in thymi from infected mice. In contrast, down-regulated surface expression of fibronectin and laminin receptors was observed in thymocytes from these animals. Moreover, in thymi from infected mice there was increased CXCL12 and CXCR4, and a decreased expression of CCL25 and CCR9. An altered thymocyte migration towards ECM elements and chemokines was seen when the thymi from infected mice were analysed. Evaluation of ex vivo migration patterns of CD4/CD8-defined thymocyte subpopulations revealed that double-negative (DN), and CD4(+) and CD8(+) single-positive (SP) cells from P. berghei-infected mice have higher migratory responses compared with controls. Interestingly, increased numbers of DN and SP subpopulations were found in the spleens of infected mice. Overall, we show that the thymic atrophy observed in P. berghei-infected mice is accompanied by thymic microenvironmental changes that comprise altered expression of thymocyte migration-related molecules of the ECM and chemokine protein families, which in turn can alter the thymocyte migration pattern. These thymic disturbances may have consequences for the control of the immune response against this protozoan.
[Mh] Termos MeSH primário: Movimento Celular/imunologia
Malária/imunologia
Plasmodium berghei/imunologia
Células Precursoras de Linfócitos T/metabolismo
Timo/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígenos CD4/biossíntese
Antígenos CD8/biossíntese
Células Cultivadas
Quimiocinas/biossíntese
Quimiocinas/genética
Quimiocinas/imunologia
Regulação da Expressão Gênica
Malária/parasitologia
Malária/patologia
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Modelos Animais
Plasmodium berghei/patogenicidade
Células Precursoras de Linfócitos T/imunologia
Células Precursoras de Linfócitos T/parasitologia
Células Precursoras de Linfócitos T/patologia
Receptores de Citoadesina/biossíntese
Receptores de Citoadesina/genética
Receptores de Citoadesina/imunologia
Receptores de Fibronectina/biossíntese
Receptores de Fibronectina/genética
Receptores de Fibronectina/imunologia
Receptores de Laminina/biossíntese
Receptores de Laminina/genética
Receptores de Laminina/imunologia
Timo/imunologia
Timo/parasitologia
Timo/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CD4 Antigens); 0 (CD8 Antigens); 0 (Chemokines); 0 (Receptors, Cytoadhesin); 0 (Receptors, Fibronectin); 0 (Receptors, Laminin)
[Em] Mês de entrada:1008
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:091015
[St] Status:MEDLINE
[do] DOI:10.1111/j.1365-2567.2009.03177.x


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[PMID]:19413961
[Au] Autor:Atilgan E; Ovryn B
[Ad] Endereço:Gruss-Lipper Biophotonics Center, Department of Anatomy and Structural Biology, Albert Einstein College of Medicine, Bronx, New York, USA.
[Ti] Título:Nucleation and growth of integrin adhesions.
[So] Source:Biophys J;96(9):3555-72, 2009 May 06.
[Is] ISSN:1542-0086
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We present a model that provides a mechanistic understanding of the processes that govern the formation of the earliest integrin adhesions ex novo from an approximately planar plasma membrane. Using an analytic analysis of the free energy of a dynamically deformable membrane containing freely diffusing receptors molecules and long repeller molecules that inhibit integrins from binding with ligands on the extracellular matrix, we predict that a coalescence of polymerizing actin filaments can deform the membrane toward the extracellular matrix and facilitate integrin binding. Monte Carlo simulations of this system show that thermally induced membrane fluctuations can either zip-up and increase the radius of a nucleated adhesion or unzip and shrink an adhesion, but the fluctuations cannot bend the ventral membrane to nucleate an adhesion. To distinguish this integrin adhesion from more mature adhesions, we refer to this early adhesion as a nouveau adhesion.
[Mh] Termos MeSH primário: Adesão Celular
Membrana Celular/metabolismo
Integrinas/metabolismo
Modelos Biológicos
Receptores de Citoadesina/metabolismo
[Mh] Termos MeSH secundário: Actinas/metabolismo
Algoritmos
Membrana Celular/química
Simulação por Computador
Citoplasma/metabolismo
Matriz Extracelular/metabolismo
Método de Monte Carlo
Temperatura Ambiente
Termodinâmica
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Actins); 0 (Integrins); 0 (Receptors, Cytoadhesin)
[Em] Mês de entrada:0907
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090506
[St] Status:MEDLINE
[do] DOI:10.1016/j.bpj.2009.02.023


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[PMID]:18187085
[Au] Autor:Morel O; Ohlmann P; Epailly E; Bakouboula B; Zobairi F; Jesel L; Meyer N; Chenard MP; Freyssinet JM; Bareiss P; Mazzucotelli JP; Toti F
[Ad] Endereço:Fédération de Cardiologie des Hôpitaux Universitaires de Strasbourg, France. olivier.morel@chrustrasbourg.fr
[Ti] Título:Endothelial cell activation contributes to the release of procoagulant microparticles during acute cardiac allograft rejection.
[So] Source:J Heart Lung Transplant;27(1):38-45, 2008 Jan.
[Is] ISSN:1557-3117
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Circulating procoagulant microparticles are reliable markers of vascular damage. The microparticle phenotypes provide additional information reflecting the nature of cell injury. This study assessed procoagulant microparticle levels and phenotypes in the diagnosis of acute allograft rejection after heart transplantation. METHODS: Microparticles were prospectively investigated in the venous blood of 64 heart transplant patients, 23 with allograft rejection mainly of low score, and 41 without a rejection episode. Plasma concentrations of cytokines, cytoadhesins, and platelet activation markers were determined. RESULTS: By univariate analysis, the mean time elapsed from heart transplant, cold ischemia time, E-selectin-, Fas- and tissue factor-bearing microparticles were associated with allograft rejection. By multivariate analysis, E-selectin-microparticle levels appeared independently associated with allograft rejection, even when other significant variables were included in the model (odds ratio, 9.8; 95% confidence interval, 1.36-71.4; p = 0.023). CONCLUSION: The pattern of procoagulant microparticles released during acute allograft rejection suggests endothelial cell activation and Fas-mediated apoptosis. E-selectin-bearing microparticles appeared as an independent marker of acute allograft rejection that was still informative after adjustment for graft characteristics.
[Mh] Termos MeSH primário: Selectina E/sangue
Endotélio Vascular/metabolismo
Rejeição de Enxerto/sangue
Transplante de Coração
Ativação Plaquetária/fisiologia
Tromboplastina/metabolismo
Receptor fas/sangue
[Mh] Termos MeSH secundário: Doença Aguda
Apoptose
Biomarcadores/sangue
Biópsia
Citocinas/sangue
Endotélio Vascular/patologia
Ensaio de Imunoadsorção Enzimática
Feminino
Seguimentos
Rejeição de Enxerto/patologia
Seres Humanos
Masculino
Meia-Idade
Prognóstico
Estudos Prospectivos
Receptores de Citoadesina/sangue
Transplante Homólogo
Ultracentrifugação
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cytokines); 0 (E-Selectin); 0 (FAS protein, human); 0 (Receptors, Cytoadhesin); 0 (fas Receptor); 9035-58-9 (Thromboplastin)
[Em] Mês de entrada:0801
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:080112
[St] Status:MEDLINE
[do] DOI:10.1016/j.healun.2007.09.031


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[PMID]:17557508
[Au] Autor:Romeo C; Santoro G; Impellizzeri P; Manganaro A; Cutroneo G; Trimarchi E; Antonuccio P; Anastasi G; Zuccarello B
[Ad] Endereço:Dipartimento di Scienze Pediatriche Mediche e Chirurgiche, U.O. di Chirurgia Pediatrica, Messina. romeoc@unime.it
[Ti] Título:Sarcoglycan immunoreactivity is lacking in infantile hypertrophic pyloric stenosis. A confocal laser scanning microscopic study.
[So] Source:Pediatr Med Chir;29(1):32-7, 2007 Jan-Feb.
[Is] ISSN:0391-5387
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: The Dystrophin-Glycoprotein Complex (DGC) is a large multisubunit complex that plays a crucial role in maintaining the structural integrity and physiology of muscle fibers. Dystrophin has been reported to be absent in the pyloric muscle of infantile hypertrophic pyloric stenosis (IHPS) patients. The present study was designed to investigate the other two patterns of DGC (dystroglycan and sarcoglycan complexes) in normal pyloric muscle and their possible modifications in IHPS patients. METHODS: Ten pyloric muscle biopsies were obtained from babies operated for IHPS and five control pylorus biopsy taken at autopsy from cases without gastrointestinal disease. The DGC sub-complexes (beta-dystroglican and beta, delta- sarcoglycans) were localized immunohistochemically using specific monoclonal antibodies. The results were evaluated using a confocal laser scanning microscope. RESULTS: Positive immunolocalization of the two DGC sub complexes was demonstrated in the smooth muscle cells (SMCs) of the pyloric region of control patients. Similarly, a positive immune expression of beta-dystroglican was observed in the pyloric SMCs of IHPS patients. On the other hand a negative immunoreaction for sarcoglycans was recorded within the full thickness of the pyloric SMCs of these patients. CONCLUSIONS: The absence of sarcoglycans within the hypertrophied pyloric muscle may be a predisposing factor in the pathogenesis of IHPS since it could alter the normal physiology of SMCs through the modifications of structural integrity of sarcolemma and signaling between the extracellular and intracellular compartment.
[Mh] Termos MeSH primário: Estenose Pilórica Hipertrófica/imunologia
Estenose Pilórica Hipertrófica/patologia
Sarcoglicanas/imunologia
[Mh] Termos MeSH secundário: Biópsia
Distroglicanas/imunologia
Distroglicanas/metabolismo
Imunofluorescência
Seres Humanos
Lactente
Recém-Nascido
Microscopia Confocal
Fibras Musculares Esqueléticas/imunologia
Fibras Musculares Esqueléticas/metabolismo
Fibras Musculares Esqueléticas/patologia
Estenose Pilórica Hipertrófica/metabolismo
Receptores de Citoadesina/imunologia
Receptores de Citoadesina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Cytoadhesin); 0 (Sarcoglycans); 146888-27-9 (Dystroglycans)
[Em] Mês de entrada:0708
[Cu] Atualização por classe:081121
[Lr] Data última revisão:
081121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:070615
[St] Status:MEDLINE


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[PMID]:17163796
[Au] Autor:Mendell JR; Boué DR; Martin PT
[Ad] Endereço:Department of Pediatrics, Columbus Children's Hospital and Research Institute and The Ohio State University, 700 Children's Drive, Columbus, OH 43205, USA. mendellj@ccri.net
[Ti] Título:The congenital muscular dystrophies: recent advances and molecular insights.
[So] Source:Pediatr Dev Pathol;9(6):427-43, 2006 Nov-Dec.
[Is] ISSN:1093-5266
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Over the past decade, molecular understanding of the congenital muscular dystrophies (CMDs) has greatly expanded. The diseases can be classified into 3 major groups based on the affected genes and the location of their expressed protein: abnormalities of extracellular matrix proteins (LAMA2, COL6A1, COL6A2, COL6A3), abnormalities of membrane receptors for the extracellular matrix (fukutin, POMGnT1, POMT1, POMT2, FKRP, LARGE, and ITGA7), and abnormal endoplasmic reticulum protein (SEPN1). The diseases begin in the perinatal period or shortly thereafter. A specific diagnosis can be challenging because the muscle pathology is usually not distinctive. Immunostaining of muscle using a battery of antibodies can help define a disorder that will need confirmation by gene testing. In muscle diseases with overlapping pathological features, such as CMD, careful attention to the clinical clues (e.g., family history, central nervous system features) can help guide the battery of immunostains necessary to target an unequivocal diagnosis.
[Mh] Termos MeSH primário: Proteínas da Matriz Extracelular/genética
Regulação da Expressão Gênica no Desenvolvimento
Proteínas de Membrana/genética
Proteínas Musculares/genética
Distrofias Musculares/congênito
Distrofias Musculares/genética
Selenoproteínas/genética
[Mh] Termos MeSH secundário: Proteínas da Matriz Extracelular/metabolismo
Seres Humanos
Proteínas de Membrana/metabolismo
Proteínas Musculares/metabolismo
Distrofias Musculares/diagnóstico
Mutação
Receptores de Citoadesina/genética
Receptores de Citoadesina/metabolismo
Selenoproteínas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Extracellular Matrix Proteins); 0 (Membrane Proteins); 0 (Muscle Proteins); 0 (Receptors, Cytoadhesin); 0 (SEPN1 protein, human); 0 (Selenoproteins)
[Em] Mês de entrada:0701
[Cu] Atualização por classe:161122
[Lr] Data última revisão:
161122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:061214
[St] Status:MEDLINE


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[PMID]:15246652
[Au] Autor:Matzen K; Dirkx AE; oude Egbrink MG; Speth C; Götte M; Ascherl G; Grimm T; Griffioen AW; Stürzl M
[Ad] Endereço:Department of Virus-induced Vasculopathy, GSF-National Research Center for Environment and Health, 85764 Neuherberg, Germany.
[Ti] Título:HIV-1 Tat increases the adhesion of monocytes and T-cells to the endothelium in vitro and in vivo: implications for AIDS-associated vasculopathy.
[So] Source:Virus Res;104(2):145-55, 2004 Sep 01.
[Is] ISSN:0168-1702
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:HIV-1-infected patients exhibit severe damages of the aortic endothelium, develop angioproliferative lesions such as Kaposi's sarcoma (KS), and have an increased risk of cardiovascular diseases and atherosclerosis. An increased adhesion of leukocytes to the endothelium is a common pathogenic parameter of AIDS-associated vascular diseases. Here we show that the HIV-1 Tat protein, a regulatory protein of HIV-1 released by infected cells, and TNF-alpha, a cytokine increased in sera and tissues of HIV-1-infected patients, activate synergistically the adhesion of leukocytes to endothelial cells both in vitro and in vivo. This effect is selectively mediated by HIV-1 Tat, since HIV-1 Nef, another HIV-1 regulatory protein, and the HIV-1 envelope protein gp41, had no effect. In vitro adhesion assays with PBMC and quantitative cell type analysis of adherent cells by FACS demonstrated that HIV-1 Tat selectively activates the adhesion of T-cells and monocytes but not of B-cells. Intravital microscopic studies in mice confirmed the synergistic activity of HIV-1 Tat and TNF-alpha on leukocyte adhesion to the endothelium in vivo. These data indicate that HIV-1 Tat in cooperation with TNF-alpha may contribute to the vascular damage and cardiovascular diseases observed in AIDS patients but also to the prominent extravasation of T-cells and monocytes which is a key process in the formation and progression of KS lesions.
[Mh] Termos MeSH primário: Adesão Celular/efeitos dos fármacos
Endotélio Vascular/efeitos dos fármacos
Produtos do Gene tat/farmacologia
HIV-1/química
Monócitos/efeitos dos fármacos
Linfócitos T/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adesão Celular/fisiologia
Agregação Celular
Células Cultivadas
Endotélio Vascular/imunologia
Produtos do Gene tat/imunologia
Seres Humanos
Técnicas In Vitro
Monócitos/imunologia
RNA Mensageiro
Receptores de Citoadesina/metabolismo
Linfócitos T/imunologia
Fator de Necrose Tumoral alfa/imunologia
Produtos do Gene tat do Vírus da Imunodeficiência Humana
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Gene Products, tat); 0 (RNA, Messenger); 0 (Receptors, Cytoadhesin); 0 (Tumor Necrosis Factor-alpha); 0 (tat Gene Products, Human Immunodeficiency Virus)
[Em] Mês de entrada:0411
[Cu] Atualização por classe:141120
[Lr] Data última revisão:
141120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:040713
[St] Status:MEDLINE


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[PMID]:15177057
[Au] Autor:Labat-Robert J
[Ad] Endereço:Laboratoire d'Ophtalmologie, Hôtel-Dieu, 1 place du parvis Notre Dame, 75181 Paris Cedex 04, France. lrobert5@wanadoo.fr
[Ti] Título:Cell-matrix interactions in aging: role of receptors and matricryptins.
[So] Source:Ageing Res Rev;3(2):233-47, 2004 Apr.
[Is] ISSN:1568-1637
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Extracellular matrix (ECM) has been a central topic in aging research for several years. Cell-matrix interactions extend the interest in this topic both for normal tissue homeostatic regulation as well as for its dysregulation in age-related diseases. A relatively new extension of this ever-increasing field of aging research concerns the recognition of the original biological activities exhibited by proteolytic fragments of matrix macromolecules. A number of such matricryptins were recently identified, some of them endowed with harmful effects for tissue function. Some of the breakdown products exert a positive feedback effect by upregulating the biosynthesis of the original macromolecule synthesis and/or the expression of degrading enzymes. This results in vicious circles which might well be involved in tissue aging. The examples detailed in this review concern fibronectin (FN) and elastin. A number of fibronectin fragments (Fn-fr) were shown to exhibit diverse activities including increasing tissue degradation, inflammation and tumor progression. Elastin degradation products acting as agonists on the elastin-laminin receptor can trigger harmful effects such as up-regulation of proteases and free radical production. Both macromolecules are at the center of autoamplifying vicious circles of potential importance for age-dependent modification of tissue function.
[Mh] Termos MeSH primário: Envelhecimento/fisiologia
Comunicação Celular/fisiologia
Proteínas da Matriz Extracelular/fisiologia
Integrina alfa5beta1/fisiologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Receptores de Superfície Celular/fisiologia
Receptores de Citoadesina/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Extracellular Matrix Proteins); 0 (Integrin alpha5beta1); 0 (Receptors, Cell Surface); 0 (Receptors, Cytoadhesin); 0 (elastin-laminin receptor, rat)
[Em] Mês de entrada:0410
[Cu] Atualização por classe:051116
[Lr] Data última revisão:
051116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:040605
[St] Status:MEDLINE



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