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Pesquisa : D12.644.233.800.174 [Categoria DeCS]
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[PMID]:28355551
[Au] Autor:Sundar Rajan V; Laurent VM; Verdier C; Duperray A
[Ad] Endereço:INSERM U1209, CNRS UMR5309, IAB, Grenoble, France; University Grenoble Alpes, IAB, Grenoble, France.
[Ti] Título:Unraveling the Receptor-Ligand Interactions between Bladder Cancer Cells and the Endothelium Using AFM.
[So] Source:Biophys J;112(6):1246-1257, 2017 Mar 28.
[Is] ISSN:1542-0086
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Adhesion of cancer cells to endothelial cells is a key step in cancer metastasis; therefore, identifying the key molecules involved during this process promises to aid in efforts to block the metastatic cascade. We have previously shown that intercellular adhesion molecule-1 (ICAM-1) expressed by endothelial cells is involved in the interactions of bladder cancer cells (BCs) with the endothelium. However, the ICAM-1 ligands have never been investigated. In this study, we combined adhesion assays and atomic force microscopy (AFM) to identify the ligands involved and to quantify the forces relevant in such interactions. We report the expression of MUC1 and CD43 on BCs, and demonstrate that these ligands interact with ICAM-1 to mediate cancer cell-endothelial cell adhesion in the case of the more invasive BCs. This was achieved with the use of adhesion assays, which showed a strong decrease in the attachment of BCs to endothelial cells when MUC1 and CD43 were blocked by antibodies. In addition, AFM measurements showed a similar decrease, by up to 70%, in the number of rupture events that occurred when MUC1 and CD43 were blocked. When we applied a Gaussian mixture model to the AFM data, we observed a distinct force range for receptor-ligand bonds, which allowed us to precisely identify the interactions of ICAM-1 with MUC1 or CD43. Furthermore, a detailed analysis of the rupture events suggested that CD43 is strongly connected to the cytoskeleton and that its interaction with ICAM-1 mainly corresponds to force ramps followed by sudden jumps. In contrast, MUC1 seems to be weakly connected to the cytoskeleton, as its interactions with ICAM-1 are mainly associated with the formation of tethers. This analysis is quite promising and may also be applied to other types of cancer cells.
[Mh] Termos MeSH primário: Microscopia de Força Atômica
Neoplasias da Bexiga Urinária/patologia
[Mh] Termos MeSH secundário: Compostos Bicíclicos Heterocíclicos com Pontes/farmacologia
Adesão Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Citoesqueleto/efeitos dos fármacos
Citoesqueleto/metabolismo
Endotélio/efeitos dos fármacos
Endotélio/metabolismo
Endotélio/patologia
Seres Humanos
Molécula 1 de Adesão Intercelular/metabolismo
Leucossialina/metabolismo
Ligantes
Mucina-1/metabolismo
Metástase Neoplásica
Ligação Proteica
Tiazolidinas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bridged Bicyclo Compounds, Heterocyclic); 0 (Leukosialin); 0 (Ligands); 0 (Mucin-1); 0 (Thiazolidines); 126547-89-5 (Intercellular Adhesion Molecule-1); SRQ9WWM084 (latrunculin A)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170330
[St] Status:MEDLINE


  2 / 712 MEDLINE  
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[PMID]:28330896
[Au] Autor:Silva M; Fung RKF; Donnelly CB; Videira PA; Sackstein R
[Ad] Endereço:Centro de Estudos de Doenças Crónicas, NOVA Medical School/Faculdade de Ciências Médicas, Universidade Nova de Lisboa, 1169-056 Lisbon, Portugal.
[Ti] Título:Cell-Specific Variation in E-Selectin Ligand Expression among Human Peripheral Blood Mononuclear Cells: Implications for Immunosurveillance and Pathobiology.
[So] Source:J Immunol;198(9):3576-3587, 2017 May 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Both host defense and immunopathology are shaped by the ordered recruitment of circulating leukocytes to affected sites, a process initiated by binding of blood-borne cells to E-selectin displayed at target endothelial beds. Accordingly, knowledge of the expression and function of leukocyte E-selectin ligands is key to understanding the tempo and specificity of immunoreactivity. In this study, we performed E-selectin adherence assays under hemodynamic flow conditions coupled with flow cytometry and Western blot analysis to elucidate the function and structural biology of glycoprotein E-selectin ligands expressed on human PBMCs. Circulating monocytes uniformly express high levels of the canonical E-selectin binding determinant sialyl Lewis X (sLe ) and display markedly greater adhesive interactions with E-selectin than do circulating lymphocytes, which exhibit variable E-selectin binding among CD4 and CD8 T cells but no binding by B cells. Monocytes prominently present sLe decorations on an array of protein scaffolds, including P-selectin glycoprotein ligand-1, CD43, and CD44 (rendering the E-selectin ligands cutaneous lymphocyte Ag, CD43E, and hematopoietic cell E-selectin/L-selectin ligand, respectively), and B cells altogether lack E-selectin ligands. Quantitative PCR gene expression studies of glycosyltransferases that regulate display of sLe reveal high transcript levels among circulating monocytes and low levels among circulating B cells, and, commensurately, cell surface α(1,3)-fucosylation reveals that acceptor sialyllactosaminyl glycans convertible into sLe are abundantly expressed on human monocytes yet are relatively deficient on B cells. Collectively, these findings unveil distinct cell-specific patterns of E-selectin ligand expression among human PBMCs, indicating that circulating monocytes are specialized to engage E-selectin and providing key insights into the molecular effectors mediating recruitment of these cells at inflammatory sites.
[Mh] Termos MeSH primário: Selectina E/metabolismo
Células Endoteliais/fisiologia
Vigilância Imunológica
Leucócitos Mononucleares/imunologia
Oligossacarídeos/metabolismo
[Mh] Termos MeSH secundário: Adesão Celular
Regulação da Expressão Gênica
Glicosiltransferases/metabolismo
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Receptores de Hialuronatos
Leucossialina/metabolismo
Ligantes
Especificidade de Órgãos
Prostaglandinas F/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (5-acetylneuraminyl-(2-3)-galactosyl-(1-4)-(fucopyranosyl-(1-3))-N-acetylglucosamine); 0 (E-Selectin); 0 (Hyaluronan Receptors); 0 (Leukosialin); 0 (Ligands); 0 (Oligosaccharides); 0 (Prostaglandins F); 0 (SELE protein, human); EC 2.4.- (Glycosyltransferases); WJ72O6860W (prostaglandin F1)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170324
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601636


  3 / 712 MEDLINE  
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[PMID]:28248816
[Au] Autor:Dunlap JB; Cascio MJ; Stacey X; Click S; Troxell ML
[Ad] Endereço:*Department of Pathology, Oregon Health & Science University, Portland, OR †Department of Pathology, Stanford University Medical Center, Stanford, CA.
[Ti] Título:TdT-positive Infiltrate in Inflamed Pediatric Kidney: A Potential Diagnostic Pitfall.
[So] Source:Am J Surg Pathol;41(5):706-716, 2017 May.
[Is] ISSN:1532-0979
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We encountered a patient with infantile nephrotic syndrome associated with a dense interstitial inflammatory infiltrate and prominent extramedullary hematopoiesis. Immunohistochemical analysis revealed numerous terminal deoxynucleotidyl transferase (TdT)-positive cells, which may raise concern for lymphoblastic lymphoma. Thus, we further characterized a group of pediatric kidneys with inflammation. TdT-positive nuclei were quantitated, and dual immunostains for TdT/CD79a, TdT/CD3, and TdT/CD43 were performed in a subset of cases; flow cytometry was performed in 1 case. TdT-positive nuclei were present in inflamed pediatric kidneys in 40 of 42 patients. TdT counts (average of 3 maximal high-power fields) ranged from 1 to >200, with a mean of 47. The presence and number of TdT-positive nuclei showed a strong association with younger patient age. Extramedullary hematopoiesis was identified in 11/42 patients, all under the age of 1. The presence of extramedullary hematopoiesis did not correlate with TdT count (P=0.158). Dual immunostaining and flow cytometric analysis in 1 case showed weak expression of B-cell markers and favored normal precursor B cells. Although TdT is a common marker of lymphoblastic lymphoma, we have demonstrated that TdT-positive cells may be part of the inflammatory milieu in infant kidneys. Together with cytologic, architectural, and clinical features, these data can help to avoid misinterpretation of involvement by lymphoblastic lymphoma/leukemia.
[Mh] Termos MeSH primário: DNA Nucleotidilexotransferase/análise
Rim/química
Nefrite/metabolismo
Síndrome Nefrótica/metabolismo
[Mh] Termos MeSH secundário: Adolescente
Biomarcadores/análise
Biópsia
Complexo CD3/análise
Antígenos CD79/análise
Criança
Pré-Escolar
Diagnóstico Diferencial
Citometria de Fluxo
Hematopoese Extramedular
Seres Humanos
Imuno-Histoquímica
Lactente
Recém-Nascido
Rim/patologia
Rim/cirurgia
Leucossialina/análise
Masculino
Nefrectomia
Nefrite/diagnóstico
Nefrite/cirurgia
Síndrome Nefrótica/diagnóstico
Síndrome Nefrótica/cirurgia
Leucemia-Linfoma Linfoblástico de Células Precursoras/diagnóstico
Leucemia-Linfoma Linfoblástico de Células Precursoras/metabolismo
Valor Preditivo dos Testes
Adulto Jovem
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (CD3 Complex); 0 (CD79 Antigens); 0 (CD79A protein, human); 0 (Leukosialin); 0 (UN1 sialoglycoprotein, human); EC 2.7.7.31 (DNA Nucleotidylexotransferase)
[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:170302
[St] Status:MEDLINE
[do] DOI:10.1097/PAS.0000000000000828


  4 / 712 MEDLINE  
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[PMID]:28190001
[Au] Autor:Schjerven H; Ayongaba EF; Aghajanirefah A; McLaughlin J; Cheng D; Geng H; Boyd JR; Eggesbø LM; Lindeman I; Heath JL; Park E; Witte ON; Smale ST; Frietze S; Müschen M
[Ad] Endereço:Department of Laboratory Medicine, University of California, San Francisco, CA 94143 Hilde.Schjerven@ucsf.edu Seth.Frietze@med.uvm.edu.
[Ti] Título:Genetic analysis of Ikaros target genes and tumor suppressor function in BCR-ABL1 pre-B ALL.
[So] Source:J Exp Med;214(3):793-814, 2017 Mar 06.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Inactivation of the tumor suppressor gene encoding the transcriptional regulator Ikaros ( ) is a hallmark of BCR-ABL1 precursor B cell acute lymphoblastic leukemia (pre-B ALL). However, the mechanisms by which Ikaros functions as a tumor suppressor in pre-B ALL remain poorly understood. Here, we analyzed a mouse model of BCR-ABL1 pre-B ALL together with a new model of inducible expression of wild-type Ikaros in mutant human BCR-ABL1 pre-B ALL. We performed integrated genome-wide chromatin and expression analyses and identified Ikaros target genes in mouse and human BCR-ABL1 pre-B ALL, revealing novel conserved gene pathways associated with Ikaros tumor suppressor function. Notably, genetic depletion of different Ikaros targets, including and the early hematopoietic cell surface marker CD34, resulted in reduced leukemic growth. Our results suggest that Ikaros mediates tumor suppressor function by enforcing proper developmental stage-specific expression of multiple genes through chromatin compaction at its target genes.
[Mh] Termos MeSH primário: Proteínas de Fusão bcr-abl/análise
Fator de Transcrição Ikaros/fisiologia
Leucemia-Linfoma Linfoblástico de Células Precursoras B/genética
Proteínas Supressoras de Tumor/fisiologia
[Mh] Termos MeSH secundário: Animais
Antígenos CD34/análise
Ciclo Celular
Linhagem Celular Tumoral
Regulação Leucêmica da Expressão Gênica
Seres Humanos
Fator de Transcrição Ikaros/genética
Leucossialina/análise
Camundongos
Camundongos Endogâmicos C57BL
Proteínas Proto-Oncogênicas c-kit/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD34); 0 (BCR-ABL1 fusion protein, human); 0 (IKZF1 protein, human); 0 (Leukosialin); 0 (Tumor Suppressor Proteins); 148971-36-2 (Ikaros Transcription Factor); EC 2.7.10.1 (Proto-Oncogene Proteins c-kit); EC 2.7.10.2 (Fusion Proteins, bcr-abl)
[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:170213
[St] Status:MEDLINE
[do] DOI:10.1084/jem.20160049


  5 / 712 MEDLINE  
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[PMID]:28069816
[Au] Autor:Torres-Huerta A; Villaseñor T; Flores-Alcantar A; Parada C; Alemán-Navarro E; Espitia C; Pedraza-Alva G; Rosenstein Y
[Ad] Endereço:Instituto de Biotecnología, Universidad Nacional Autónoma de México, Campus Morelos, Cuernavaca, Morelos, Mexico.
[Ti] Título:Interaction of the CD43 Sialomucin with the Mycobacterium tuberculosis Cpn60.2 Chaperonin Leads to Tumor Necrosis Factor Alpha Production.
[So] Source:Infect Immun;85(3), 2017 Mar.
[Is] ISSN:1098-5522
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:is the causal agent of tuberculosis. Tumor necrosis factor alpha (TNF-α), transforming growth factor ß (TGF-ß), and gamma interferon (IFN-γ) secreted by activated macrophages and lymphocytes are considered essential to contain infection. The CD43 sialomucin has been reported to act as a receptor for bacilli through its interaction with the chaperonin Cpn60.2, facilitating mycobacterium-macrophage contact. We report here that Cpn60.2 induces both human THP-1 cells and mouse-derived bone marrow-derived macrophages (BMMs) to produce TNF-α and that this production is CD43 dependent. In addition, we present evidence that the signaling pathway leading to TNF-α production upon interaction with Cpn60.2 requires active Src family kinases, phospholipase C-γ (PLC-γ), phosphatidylinositol 3-kinase (PI3K), p38, and Jun N-terminal protein kinase (JNK), both in BMMs and in THP-1 cells. Our data highlight the role of CD43 and Cpn60.2 in TNF-α production and underscore an important role for CD43 in the host-mycobacterium interaction.
[Mh] Termos MeSH primário: Proteínas de Bactérias/metabolismo
Chaperonina 60/metabolismo
Leucossialina/metabolismo
Mycobacterium tuberculosis/fisiologia
Fator de Necrose Tumoral alfa/biossíntese
[Mh] Termos MeSH secundário: Linhagem Celular
Seres Humanos
Macrófagos/imunologia
Macrófagos/metabolismo
Macrófagos/microbiologia
NF-kappa B/metabolismo
Ligação Proteica
Transdução de Sinais
Fator de Transcrição AP-1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Chaperonin 60); 0 (Leukosialin); 0 (NF-kappa B); 0 (Transcription Factor AP-1); 0 (Tumor Necrosis Factor-alpha)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170111
[St] Status:MEDLINE


  6 / 712 MEDLINE  
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[PMID]:27606486
[Au] Autor:Bravo-Adame ME; Vera-Estrella R; Barkla BJ; Martínez-Campos C; Flores-Alcantar A; Ocelotl-Oviedo JP; Pedraza-Alva G; Rosenstein Y
[Ad] Endereço:Departamento de Medicina Molecular y Bioprocesos, Instituto de Biotecnología, Universidad Nacional Autónoma de México, Cuernavaca, Morelos, México.
[Ti] Título:An alternative mode of CD43 signal transduction activates pro-survival pathways of T lymphocytes.
[So] Source:Immunology;150(1):87-99, 2017 Jan.
[Is] ISSN:1365-2567
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:CD43 is one of the most abundant co-stimulatory molecules on a T-cell surface; it transduces activation signals through its cytoplasmic domain, contributing to modulation of the outcome of T-cell responses. The aim of this study was to uncover new signalling pathways regulated by this sialomucin. Analysis of changes in protein abundance allowed us to identify pyruvate kinase isozyme M2 (PKM2), an enzyme of the glycolytic pathway, as an element potentially participating in the signalling cascade resulting from the engagement of CD43 and the T-cell receptor (TCR). We found that the glycolytic activity of this enzyme was not significantly increased in response to TCR+CD43 co-stimulation, but that PKM2 was tyrosine phosphorylated, suggesting that it was performing moonlight functions. We report that phosphorylation of both Y of PKM2 and of Y of signal transducer and activator of transcription 3 was induced in response to TCR+CD43 co-stimulation, resulting in activation of the mitogen-activated protein kinase kinase 5/extracellular signal-regulated kinase 5 (MEK5/ERK5) pathway. ERK5 and the cAMP response element binding protein (CREB) were activated, and c-Myc and nuclear factor-κB (p65) nuclear localization, as well as Bad phosphorylation, were augmented. Consistent with this, expression of human CD43 in a murine T-cell hybridoma favoured cell survival. Altogether, our data highlight novel signalling pathways for the CD43 molecule in T lymphocytes, and underscore a role for CD43 in promoting cell survival through non-glycolytic functions of metabolic enzymes.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/imunologia
Leucossialina/metabolismo
Proteína Quinase 7 Ativada por Mitógeno/metabolismo
Piruvato Quinase/metabolismo
Fator de Transcrição STAT3/metabolismo
[Mh] Termos MeSH secundário: Animais
Sobrevivência Celular
Seres Humanos
Hibridomas
Imunidade Celular
Células Jurkat
Ativação Linfocitária
MAP Quinase Quinase 5/metabolismo
Camundongos
NF-kappa B/metabolismo
Fosforilação
Proteínas Proto-Oncogênicas c-myc/metabolismo
Fator de Transcrição STAT3/genética
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Leukosialin); 0 (MYC protein, human); 0 (NF-kappa B); 0 (Proto-Oncogene Proteins c-myc); 0 (STAT3 Transcription Factor); EC 2.7.1.40 (Pyruvate Kinase); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 7); EC 2.7.12.2 (MAP Kinase Kinase 5); EC 2.7.12.2 (MAP2K5 protein, human)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160909
[St] Status:MEDLINE
[do] DOI:10.1111/imm.12670


  7 / 712 MEDLINE  
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[PMID]:27869733
[Au] Autor:Zhang Z; Li S; Gu Y; Xia N
[Ad] Endereço:State Key Laboratory of Molecular Vaccinology and Molecular Diagnostics, School of Public Health, Xiamen University, Xiamen 361102, China. zhiqingzhang.xmu@foxmail.com.
[Ti] Título:Antiviral Therapy by HIV-1 Broadly Neutralizing and Inhibitory Antibodies.
[So] Source:Int J Mol Sci;17(11), 2016 Nov 18.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Human immunodeficiency virus type 1 (HIV-1) infection causes acquired immune deficiency syndrome (AIDS), a global epidemic for more than three decades. HIV-1 replication is primarily controlled through antiretroviral therapy (ART) but this treatment does not cure HIV-1 infection. Furthermore, there is increasing viral resistance to ART, and side effects associated with long-term therapy. Consequently, there is a need of alternative candidates for HIV-1 prevention and therapy. Recent advances have discovered multiple broadly neutralizing antibodies against HIV-1. In this review, we describe the key epitopes on the HIV-1 Env protein and the reciprocal broadly neutralizing antibodies, and discuss the ongoing clinical trials of broadly neutralizing and inhibitory antibody therapy as well as antibody combinations, bispecific antibodies, and methods that improve therapeutic efficacy by combining broadly neutralizing antibodies (bNAbs) with latency reversing agents. Compared with ART, HIV-1 therapeutics that incorporate these broadly neutralizing and inhibitory antibodies offer the advantage of decreasing virus load and clearing infected cells, which is a promising prospect in HIV-1 prevention and treatment.
[Mh] Termos MeSH primário: Síndrome de Imunodeficiência Adquirida/imunologia
Anticorpos Neutralizantes/imunologia
Anticorpos Anti-HIV/imunologia
Infecções por HIV/imunologia
HIV-1/imunologia
[Mh] Termos MeSH secundário: Síndrome de Imunodeficiência Adquirida/tratamento farmacológico
Síndrome de Imunodeficiência Adquirida/virologia
Anticorpos Monoclonais/imunologia
Anticorpos Monoclonais/uso terapêutico
Anticorpos Neutralizantes/uso terapêutico
Epitopos/imunologia
Anticorpos Anti-HIV/uso terapêutico
Infecções por HIV/tratamento farmacológico
Infecções por HIV/virologia
HIV-1/efeitos dos fármacos
Seres Humanos
Leucossialina/imunologia
Produtos do Gene env do Vírus da Imunodeficiência Humana/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antibodies, Neutralizing); 0 (Epitopes); 0 (HIV Antibodies); 0 (Leukosialin); 0 (env Gene Products, Human Immunodeficiency Virus)
[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:161122
[St] Status:MEDLINE


  8 / 712 MEDLINE  
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[PMID]:27766954
[Au] Autor:Gari MA; AlKaff M; Alsehli HS; Dallol A; Gari A; Abu-Elmagd M; Kadam R; Abuzinadah MF; Gari M; Abuzenadah AM; Gauthaman K; Alkhatabi H; Abbas MM
[Ad] Endereço:Sheikh Salem Bin Mahfouz Scientific Chair for Treatment of Osteoarthritis by Stem Cells, King Abdulaziz University, Jeddah, Kingdom of Saudi Arabia. mgari@kau.edu.sa.
[Ti] Título:Identification of novel genetic variations affecting osteoarthritis patients.
[So] Source:BMC Med Genet;17(Suppl 1):68, 2016 Oct 10.
[Is] ISSN:1471-2350
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Osteoarthritis (OA) is a progressive joint disease characterized by gradual degradation of extracellular matrix (ECM) components in the cartilage and bone. The ECM of cartilage is a highly specified structure that is mainly composed of type II collagen and provides tensile strength to the tissue via aggrecan and proteoglycans. However, changes in the ECM composition and structure can lead to loss of collagen type II and network integrity. Several risk factors have been correlated with OA including age, genetic predisposition, hereditary factors, obesity, mechanical injuries, and joint trauma. Certain genetic association studies have identified several genes associated with OA using genome-wide association studies (GWASs). RESULTS: We identified several novel genetic variants affecting genes that function in several candidate causative pathways including immune responses, inflammatory and cartilage degradation such as SELP, SPN, and COL6A6. CONCLUSIONS: The approach of whole-exome sequencing can be a promising method to identify genetic mutations that can influence the OA disease.
[Mh] Termos MeSH primário: Exoma/genética
Variação Genética
Osteoartrite/genética
[Mh] Termos MeSH secundário: Idoso
Cartilagem/metabolismo
Colágeno Tipo II/genética
Colágeno Tipo VI/genética
Estudo de Associação Genômica Ampla
Seres Humanos
Leucossialina/genética
Meia-Idade
Osteoartrite/patologia
Selectina-P/genética
Polimorfismo de Nucleotídeo Único
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (COL2A1 protein, human); 0 (COL6A6 protein, human); 0 (Collagen Type II); 0 (Collagen Type VI); 0 (Leukosialin); 0 (P-Selectin); 0 (SELP protein, human); 0 (UN1 sialoglycoprotein, human)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161022
[St] Status:MEDLINE


  9 / 712 MEDLINE  
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[PMID]:27758743
[Au] Autor:Alexandre C; Baillard S; Tavet J; Nüsse O
[Ad] Endereço:M1 Biologie Santé, Université Paris-Saclay, 91405 Orsay, France.
[Ti] Título:[The diffusional barrier, a new window for exclusion].
[Ti] Título:La barrière de diffusion, une nouvelle fenêtre pour l'exclusion..
[So] Source:Med Sci (Paris);32(10):827-830, 2016 Oct.
[Is] ISSN:1958-5381
[Cp] País de publicação:France
[La] Idioma:fre
[Mh] Termos MeSH primário: Imunidade Inata/fisiologia
[Mh] Termos MeSH secundário: Bactérias/imunologia
Difusão
Imunidade Inata/imunologia
Antígenos Comuns de Leucócito/imunologia
Leucossialina/imunologia
Macrófagos/imunologia
Neutrófilos/imunologia
Fagócitos/imunologia
Fagocitose/imunologia
Fagocitose/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Leukosialin); EC 3.1.3.48 (Leukocyte Common Antigens)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161021
[St] Status:MEDLINE


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[PMID]:27465155
[Au] Autor:Phondeechareon T; Wattanapanitch M; U-Pratya Y; Damkham C; Klincumhom N; Lorthongpanich C; Kheolamai P; Laowtammathron C; Issaragrisil S
[Ad] Endereço:Siriraj Center of Excellence for Stem Cell Research, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.
[Ti] Título:Generation of induced pluripotent stem cells as a potential source of hematopoietic stem cells for transplant in PNH patients.
[So] Source:Ann Hematol;95(10):1617-25, 2016 Oct.
[Is] ISSN:1432-0584
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired hemolytic anemia caused by lack of CD55 and CD59 on blood cell membrane leading to increased sensitivity of blood cells to complement. Hematopoietic stem cell transplantation (HSCT) is the only curative therapy for PNH, however, lack of HLA-matched donors and post-transplant complications are major concerns. Induced pluripotent stem cells (iPSCs) derived from patients are an attractive source for generating autologous HSCs to avoid adverse effects resulting from allogeneic HSCT. The disease involves only HSCs and their progeny; therefore, other tissues are not affected by the mutation and may be used to produce disease-free autologous HSCs. This study aimed to derive PNH patient-specific iPSCs from human dermal fibroblasts (HDFs), characterize and differentiate to hematopoietic cells using a feeder-free protocol. Analysis of CD55 and CD59 expression was performed before and after reprogramming, and hematopoietic differentiation. Patients' dermal fibroblasts expressed CD55 and CD59 at normal levels and the normal expression remained after reprogramming. The iPSCs derived from PNH patients had typical pluripotent properties and differentiation capacities with normal karyotype. After hematopoietic differentiation, the differentiated cells expressed early hematopoietic markers (CD34 and CD43) with normal CD59 expression. The iPSCs derived from HDFs of PNH patients have normal levels of CD55 and CD59 expression and hold promise as a potential source of HSCs for autologous transplantation to cure PNH patients.
[Mh] Termos MeSH primário: Técnicas de Reprogramação Celular
Transplante de Células-Tronco Hematopoéticas
Hemoglobinúria Paroxística/terapia
Células-Tronco Pluripotentes Induzidas/citologia
[Mh] Termos MeSH secundário: Animais
Antígenos CD34/biossíntese
Antígenos CD55/biossíntese
Antígenos CD59/biossíntese
Corpos Embrioides
Feminino
Fibroblastos/citologia
História do Século XVI
História do Século XVII
Seres Humanos
Células-Tronco Pluripotentes Induzidas/transplante
Leucossialina/biossíntese
Camundongos Endogâmicos BALB C
Camundongos Nus
Pele/citologia
Teratoma/patologia
Transplante Autólogo
[Pt] Tipo de publicação:HISTORICAL ARTICLE; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD34); 0 (CD55 Antigens); 0 (CD59 Antigens); 0 (Leukosialin); 0 (UN1 sialoglycoprotein, human)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160729
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-016-2756-1



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