Base de dados : MEDLINE
Pesquisa : D12.776.395.550.200.700.300 [Categoria DeCS]
Referências encontradas : 5480 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 548 ir para página                         

  1 / 5480 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27774807
[Au] Autor:Stepanikova I; Oates GR; Bateman LB
[Ad] Endereço:a Department of Sociology , University of Alabama at Birmingham , Birmingham , AL , USA.
[Ti] Título:Does one size fit all? The role of body mass index and waist circumference in systemic inflammation in midlife by race and gender.
[So] Source:Ethn Health;22(2):169-183, 2017 04.
[Is] ISSN:1465-3419
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: This study investigates the associations of body mass index (BMI) and waist circumference (WC) with markers of systemic inflammation in midlife by race and gender. DESIGN: Data were obtained from the Survey of Midlife in the United States, a cross-sectional, observational study of Americans 35 years old or older (White men: N = 410; White women: N = 490; Black men: N = 58; Black women: N = 117). Inflammation was measured by concentrations of fibrinogen and C-reactive protein (CRP) in fasting plasma and concentrations of E-selectin and interleukin-6 (IL-6) in fasting serum. Anthropometric data were used to obtain BMI and WC. Socio-demographic and health-related factors were assessed with a survey. Multivariate models by race and gender were estimated to test the roles of BMI and WC for each inflammation marker. RESULTS: Compared to White men, Black women have higher BMI and higher levels of all four inflammation markers; White women have lower BMI, lower WC, and lower E-selectin and fibrinogen but higher CRP; and Black men have higher fibrinogen. After adjusting for socio-demographic and health-related covariates as well as perceived discrimination, WC is associated with all four markers of inflammation among White men and women; with three markers (fibrinogen, CRP, and IL-6) of inflammation among Black women; and with CRP (and marginally with fibrinogen and E-selectin) among Black men. BMI is associated with higher CRP and fibrinogen among Black men (marginally so for White men) but not for women of either race. CONCLUSIONS: WC shows more consistent associations with inflammation markers than BMI, although the relationships vary by inflammation marker and population group. Our findings suggest that WC is a risk factor for systemic inflammation among White and Black men and women, and BMI is an additional risk factor for Black men.
[Mh] Termos MeSH primário: Afroamericanos/estatística & dados numéricos
Índice de Massa Corporal
Grupo com Ancestrais do Continente Europeu/estatística & dados numéricos
Inflamação/etnologia
Circunferência da Cintura
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Biomarcadores
Pesos e Medidas Corporais
Proteína C-Reativa/biossíntese
Estudos Transversais
Selectina E/biossíntese
Feminino
Fibrinogênio/biossíntese
Seres Humanos
Inflamação/fisiopatologia
Mediadores da Inflamação
Interleucina-6/biossíntese
Masculino
Meia-Idade
Fatores de Risco
Fatores Sexuais
Fatores Socioeconômicos
Estados Unidos
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (E-Selectin); 0 (Inflammation Mediators); 0 (Interleukin-6); 9001-32-5 (Fibrinogen); 9007-41-4 (C-Reactive Protein)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1080/13557858.2016.1235681


  2 / 5480 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29188738
[Au] Autor:Hu JB; Song GL; Liu D; Li SJ; Wu JH; Kang XQ; Qi J; Jin FY; Wang XJ; Xu XL; Ying XY; Yu L; You J; Du YZ
[Ad] Endereço:a Institute of Pharmaceutics, College of Pharmaceutical Sciences , Zhejiang University , Hangzhou , China.
[Ti] Título:Sialic acid-modified solid lipid nanoparticles as vascular endothelium-targeting carriers for ischemia-reperfusion-induced acute renal injury.
[So] Source:Drug Deliv;24(1):1856-1867, 2017 Nov.
[Is] ISSN:1521-0464
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In an attempt to improve therapeutic efficacy of dexamethasone (DXM)-loaded solid lipid nanoparticles (NPs) for renal ischemia-reperfusion injury (IRI)-induced acute renal injury (AKI), sialic acid (SA) is used as a ligand to target the inflamed vascular endothelium. DXM-loaded SA-conjugated polyethylene glycol (PEG)ylated NPs (SA-NPs) are prepared via solvent diffusion method and show the good colloidal stability. SA-NPs reduce apoptotic human umbilical vein endothelial cells (HUVECs) via downregulating oxidative stress-induced Bax, upregulating Bcl-xL, and inhibiting Caspase-3 and Caspase-9 activation. Cellular uptake results suggest SA-NPs can be specifically internalized by the inflamed vascular endothelial cells (H O -pretreated HUVECs), and the mechanism is associated with the specific binding between SA and E-selectin receptor expressed on the inflamed vascular endothelial cells. Bio-distribution results further demonstrated the enhanced renal accumulation of DXM is achieved in AKI mice treated with SA-NPs, and its content is 2.70- and 5.88-fold higher than those treated with DXM and NPs at 6 h after intravenous administration, respectively. Pharmacodynamic studies demonstrate SA-NPs effectively ameliorate renal functions in AKI mice, as reflected by improved blood biochemical indexes, histopathological changes, oxidative stress levels and pro-inflammatory cytokines. Moreover, SA-NPs cause little negative effects on lymphocyte count and bone mineral density while DXM leads to severe osteoporosis. It is concluded that SA-NPs provide an efficient and targeted delivery of DXM for ischemia-reperfusion-induced injury-induced AKI, with improved therapeutic outcomes and reduced adverse effects.
[Mh] Termos MeSH primário: Lesão Renal Aguda/tratamento farmacológico
Portadores de Fármacos/química
Endotélio Vascular/efeitos dos fármacos
Lipídeos/química
Ácido N-Acetilneuramínico/química
Nanopartículas/química
Traumatismo por Reperfusão/tratamento farmacológico
[Mh] Termos MeSH secundário: Lesão Renal Aguda/metabolismo
Animais
Caspase 3/metabolismo
Linhagem Celular
Dexametasona/farmacologia
Selectina E/metabolismo
Endotélio Vascular/metabolismo
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Rim/efeitos dos fármacos
Rim/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos ICR
Nanopartículas/administração & dosagem
Estresse Oxidativo/efeitos dos fármacos
Polietilenoglicóis/química
Traumatismo por Reperfusão/metabolismo
Proteína X Associada a bcl-2/metabolismo
Proteína bcl-X/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drug Carriers); 0 (E-Selectin); 0 (Lipids); 0 (bcl-2-Associated X Protein); 0 (bcl-X Protein); 30IQX730WE (Polyethylene Glycols); 7S5I7G3JQL (Dexamethasone); EC 3.4.22.- (Caspase 3); GZP2782OP0 (N-Acetylneuraminic Acid)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180130
[Lr] Data última revisão:
180130
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.1080/10717544.2017.1410258


  3 / 5480 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29244817
[Au] Autor:Montiel-Dávalos A; Silva Sánchez GJ; Huerta-García E; Rueda-Romero C; Soca Chafre G; Mitre-Aguilar IB; Alfaro-Moreno E; Pedraza-Chaverri J; López-Marure R
[Ad] Endereço:Subdirección de Investigación Básica, Instituto Nacional de Cancerología, Ciudad de México, México.
[Ti] Título:Curcumin inhibits activation induced by urban particulate material or titanium dioxide nanoparticles in primary human endothelial cells.
[So] Source:PLoS One;12(12):e0188169, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Curcumin has protective effects against toxic agents and shows preventive properties for various diseases. Particulate material with an aerodynamic diameter of ≤10 µm (PM10) and titanium dioxide nanoparticles (TiO2-NPs) induce endothelial dysfunction and activation. We explored whether curcumin is able to attenuate different events related to endothelial activation. This includes adhesion, expression of adhesion molecules and oxidative stress induced by PM10 and TiO2-NPs. Human umbilical vein endothelial cells (HUVEC) were treated with 1, 10 and 100 µM curcumin for 1 h and then exposed to PM10 at 3 µg/cm2 or TiO2-NPs at 10 µg/cm2. Cell adhesion was evaluated by co-culture with U937 human myelomonocytic cells. Adhesion molecules expression was measured by flow cytometry after 3 or 24 h of exposure. Oxidative stress was determined by 2,7-dichlorodihydrofluorescein (H2DCF) oxidation. PM10 and TiO2-NPs induced the adhesion of U937 cells and the expression of E- and P-selectins, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and platelet-endothelial cell adhesion molecule-1 (PECAM-1). The expression of E- and P-selectins matched the adhesion of monocytes to HUVEC after 3 h. In HUVEC treated with 1 or 10 µM curcumin, the expression of adhesion molecules and monocytes adhesion was significantly diminished. Curcumin also partially reduced the H2DCF oxidation induced by PM10 and TiO2-NPs. Our results suggest an anti-inflammatory and antioxidant role by curcumin attenuating the activation caused on endothelial cells by exposure to particles. Therefore, curcumin could be useful in the treatment of diseases where an inflammatory process and endothelial activation are involved.
[Mh] Termos MeSH primário: Antioxidantes/farmacologia
Curcumina/farmacologia
Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos
Nanopartículas/toxicidade
Material Particulado/antagonistas & inibidores
[Mh] Termos MeSH secundário: Biomarcadores/metabolismo
Adesão Celular/efeitos dos fármacos
Cidades
Técnicas de Cocultura
Selectina E/genética
Selectina E/metabolismo
Fluoresceínas/química
Expressão Gênica
Células Endoteliais da Veia Umbilical Humana/citologia
Células Endoteliais da Veia Umbilical Humana/metabolismo
Seres Humanos
Molécula 1 de Adesão Intercelular/genética
Molécula 1 de Adesão Intercelular/metabolismo
México
Estresse Oxidativo/efeitos dos fármacos
Selectina-P/genética
Selectina-P/metabolismo
Material Particulado/farmacologia
Molécula-1 de Adesão Celular Endotelial de Plaquetas/genética
Molécula-1 de Adesão Celular Endotelial de Plaquetas/metabolismo
Titânio/farmacologia
Células U937
Molécula 1 de Adesão de Célula Vascular/genética
Molécula 1 de Adesão de Célula Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Biomarkers); 0 (E-Selectin); 0 (Fluoresceins); 0 (ICAM1 protein, human); 0 (P-Selectin); 0 (Particulate Matter); 0 (Platelet Endothelial Cell Adhesion Molecule-1); 0 (SELE protein, human); 0 (Vascular Cell Adhesion Molecule-1); 106070-31-9 (2',7'-dichlorodihydrofluorescein); 126547-89-5 (Intercellular Adhesion Molecule-1); 15FIX9V2JP (titanium dioxide); D1JT611TNE (Titanium); IT942ZTH98 (Curcumin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188169


  4 / 5480 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28957406
[Au] Autor:Wang W; Li P; Li W; Jiang J; Cui Y; Li S; Wang Z
[Ad] Endereço:Department of Plastic and Aesthetic Surgery, Southwest Hospital, Third Military Medical University, Chongqing, China.
[Ti] Título:Osteopontin activates mesenchymal stem cells to repair skin wound.
[So] Source:PLoS One;12(9):e0185346, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mesenchymal stem cells (MSCs) are promising candidates for skin wound repair due to their capabilities of accumulating at wounds and differentiating into multiple types of skin cells. However, the underlying mechanisms responsible for these processes remain unclear. In this study, we found that osteopontin (OPN) stimulated the migration of MSCs in vitro, and observed the recruitment of endogenous MSCs to a skin wound and their differentiation into keratinocytes and endothelial cells. In OPN knock-out mice, the recruitment of MSCs to the skin wound was significantly inhibited, and wound closure was hampered after an intradermal injection of exogenous MSCs compared to wild-type mice. Consistent with these observations, the expressions of adhesion molecule CD44 and its receptor E-selectin were significantly decreased in the lesions of OPN knock-out mice compared with wild-type mice suggesting that OPN may regulate the migration of MSCs through its interactions with CD44 during skin wound recovery. In summary, our data demonstrated that OPN played a critical role in activating the migration of MSCs to injured sites and their differentiation into specific skin cell types during skin wound healing.
[Mh] Termos MeSH primário: Células Mesenquimais Estromais/citologia
Células Mesenquimais Estromais/metabolismo
Osteopontina/metabolismo
Pele/patologia
Cicatrização
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular/efeitos dos fármacos
Movimento Celular/efeitos dos fármacos
Separação Celular
Regulação para Baixo/efeitos dos fármacos
Selectina E/metabolismo
Células Endoteliais/citologia
Células Endoteliais/efeitos dos fármacos
Células Endoteliais/metabolismo
Imunofluorescência
Proteínas de Fluorescência Verde/metabolismo
Receptores de Hialuronatos/metabolismo
Queratina-14/metabolismo
Queratinócitos/citologia
Queratinócitos/efeitos dos fármacos
Masculino
Células Mesenquimais Estromais/efeitos dos fármacos
Camundongos Endogâmicos C57BL
Osteopontina/deficiência
Molécula-1 de Adesão Celular Endotelial de Plaquetas/metabolismo
Proteínas Recombinantes/farmacologia
Pele/lesões
Cicatrização/efeitos dos fármacos
Fator de von Willebrand/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (E-Selectin); 0 (Hyaluronan Receptors); 0 (Keratin-14); 0 (Platelet Endothelial Cell Adhesion Molecule-1); 0 (Recombinant Proteins); 0 (von Willebrand Factor); 106441-73-0 (Osteopontin); 147336-22-9 (Green Fluorescent Proteins)
[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:170929
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185346


  5 / 5480 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28688659
[Au] Autor:Ampofo E; Lachnitt N; Rudzitis-Auth J; Schmitt BM; Menger MD; Laschke MW
[Ad] Endereço:Institute for Clinical & Experimental Surgery, Saarland University, Homburg/Saar, Germany. Electronic address: emmanuel.ampofo@uks.eu.
[Ti] Título:Indole-3-carbinol is a potent inhibitor of ischemia-reperfusion-induced inflammation.
[So] Source:J Surg Res;215:34-46, 2017 Jul.
[Is] ISSN:1095-8673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Ischemia-reperfusion (I/R) induces tissue inflammation, which is characterized by an increased leukocyte-endothelial cell interaction and leukocyte transmigration. These processes are mediated by the activation of the nuclear factor (NF)κB signaling pathway, resulting in an elevated expression of specific adhesion molecules. The phytochemical indole-3-carbinol (I3C) has been shown to exert anti-inflammatory effects by interfering with NFκB signal transduction. The aim of the present study was to investigate whether I3C is capable of counteracting the pathogenesis of I/R injury. MATERIALS AND METHODS: We investigated the inhibitory effect of I3C on endothelial surface protein expression during hypoxia and reoxygenation by flow cytometry. Moreover, the subcellular localization of NFκB was analyzed by immunofluorescence and Western blot. Adhesion protein levels on leukocytes after tumor necrosis factor-α stimulation were determined using flow cytometry. Finally, leukocyte-endothelial cell interaction and leukocyte transmigration during I/R was investigated in dorsal skinfold chambers of BALB/c mice by means of repetitive intravital fluorescence microscopy and immunohistochemistry. RESULTS: I3C suppressed the expression of E-selectin and intercellular adhesion molecule-1 on human dermal microvascular endothelial cells by reducing the transcriptional activity of NFκB. Furthermore, surface protein levels of macrophage-1 antigen as well as activated lymphocyte function-associated antigen-1 were markedly reduced on I3C-treated leukocytes. In vivo, I3C treatment decreased the numbers of adherent and transmigrated leukocytes. This was associated with a reduced macromolecular leakage when compared with vehicle-treated controls. CONCLUSIONS: These novel results indicate that I3C reduces the expression of endothelial and leukocytic adhesion proteins, resulting in attenuated leukocyte-endothelial cell interactions during I/R. Accordingly, dietary supplements containing I3C may be beneficial for the treatment of I/R-induced inflammation.
[Mh] Termos MeSH primário: Indóis/uso terapêutico
Inflamação/prevenção & controle
Substâncias Protetoras/uso terapêutico
Traumatismo por Reperfusão/prevenção & controle
[Mh] Termos MeSH secundário: Animais
Biomarcadores/metabolismo
Western Blotting
Selectina E/metabolismo
Células Endoteliais/efeitos dos fármacos
Células Endoteliais/metabolismo
Citometria de Fluxo
Imunofluorescência
Imuno-Histoquímica
Indóis/farmacologia
Inflamação/metabolismo
Molécula 1 de Adesão Intercelular/metabolismo
Leucócitos/efeitos dos fármacos
Leucócitos/metabolismo
Camundongos
Camundongos Endogâmicos BALB C
NF-kappa B/metabolismo
Substâncias Protetoras/farmacologia
Traumatismo por Reperfusão/imunologia
Traumatismo por Reperfusão/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (E-Selectin); 0 (Indoles); 0 (NF-kappa B); 0 (Protective Agents); 126547-89-5 (Intercellular Adhesion Molecule-1); C11E72455F (indole-3-carbinol)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170710
[St] Status:MEDLINE


  6 / 5480 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28686648
[Au] Autor:Raffray L; Giry C; Thirapathi Y; Reboux AH; Jaffar-Bandjee MC; Gasque P
[Ad] Endereço:Université de La Réunion, CNRS 9192, INSERM U1187, IRD 249, CHU de La Réunion, UMR PIMIT Unité Mixte Processus Infectieux en Milieu Insulaire Tropical, Plateforme Technologique CYROI, Sainte-Clotilde, La Réunion, France.
[Ti] Título:Increased levels of soluble forms of E-selectin and ICAM-1 adhesion molecules during human leptospirosis.
[So] Source:PLoS One;12(7):e0180474, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Leptospirosis is a multisystemic zoonotic disease with infiltration of visceral organs by Leptospira. The capacity of the vascular endothelium to grant immune cell recruitment and activation in target organs during the disease course remains poorly characterized. We ascertained the levels of expression of several soluble cell adhesion molecules (CAM) notably expressed by endothelial cells in human leptospirosis. We prospectively enrolled 20 hospitalized patients and compared them to 10 healthy controls. Disease severity was defined by one or more organ failures, or death. Plasmatic concentrations of soluble CAM were assessed by multiplex bead assay at the time of patient presentation (M0) and 1 month after hospital discharge. The levels of soluble E-selectin (sCD62E) and soluble intercellular adhesion molecule 1 (sICAM-1, sCD53) were significantly increased in patients compared to controls (p<0.0001) and at 1 month (p<0.0001) with median values at 978 ng/ml (interquartile ranges 787-1164; sCD62E) and 1021 ng/ml (690-1428; sCD53). At M0, Soluble P-selectin level (sCD62P) was found to be decreased with levels at 60 ng/ml (0-631) versus 711 ng/ml (343-1113) for healthy controls (p<0.05). Levels of sICAM-3 (sCD50), sVCAM-1 (vascular cell adhesion molecule, sCD106) and sPECAM-1 (platelet endothelial cell adhesion molecule, sCD31) were not different from healthy subjects at M0. This study shows that two adhesion molecules, shed as soluble forms, are elevated during the acute phase of leptospirosis: E-selectin and s-ICAM1. These molecules may interfere with the process of immune cell recruitment to clear Leptospira at tissue levels.
[Mh] Termos MeSH primário: Selectina E/genética
Molécula 1 de Adesão Intercelular/genética
Leptospirose/genética
[Mh] Termos MeSH secundário: Adulto
Células Endoteliais/parasitologia
Células Endoteliais/patologia
Endotélio Vascular/parasitologia
Endotélio Vascular/patologia
Feminino
Seres Humanos
Leptospira/genética
Leptospira/patogenicidade
Leptospirose/parasitologia
Leptospirose/patologia
Masculino
Meia-Idade
Solubilidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (E-Selectin); 126547-89-5 (Intercellular Adhesion Molecule-1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170708
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180474


  7 / 5480 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28683470
[Au] Autor:Zurita AJ; Gagnon RC; Liu Y; Tran HT; Figlin RA; Hutson TE; D'Amelio AM; Sternberg CN; Pandite LN; Heymach JV
[Ad] Endereço:MD Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX 77030, USA.
[Ti] Título:Integrating cytokines and angiogenic factors and tumour bulk with selected clinical criteria improves determination of prognosis in advanced renal cell carcinoma.
[So] Source:Br J Cancer;117(4):478-484, 2017 Aug 08.
[Is] ISSN:1532-1827
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: In two clinical trials of the vascular endothelial growth factor (VEGF) receptor inhibitor pazopanib in advanced renal cell carcinoma (mRCC), we found interleukin-6 as predictive of pazopanib benefit. We evaluated the prognostic significance of candidate cytokines and angiogenic factors (CAFs) identified in that work relative to accepted clinical parameters. METHODS: Seven preselected plasma CAFs (interleukin-6, interleukin-8, osteopontin, VEGF, hepatocyte growth factor, tissue inhibitor of metalloproteinases (TIMP-1), and E-selectin) were measured using multiplex ELISA in plasma collected pretreatment from 343 mRCC patients participating in the phase 3 registration trial of pazopanib vs placebo (NCT00334282). Tumour burden (per sum of longest diameters (SLD)) and 10 other clinical factors were also analysed for association with overall survival (OS; based on initial treatment assignment). RESULTS: Osteopontin, interleukin-6, and TIMP-1 were independently associated with OS in multivariable analysis. A model combining the three CAFs and five clinical variables (including SLD) had higher prognostic accuracy than the International Metastatic Renal Cell Carcinoma Database Consortium criteria (concordance-index 0.75 vs 0.67, respectively), and distinguished two groups of patients within the original intermediate risk category. CONCLUSIONS: A prognostic model incorporating osteopontin, interleukin-6, TIMP-1, tumour burden, and selected clinical criteria increased prognostic accuracy for OS determination in mRCC patients.
[Mh] Termos MeSH primário: Carcinoma de Células Renais/sangue
Citocinas/sangue
Selectina E/sangue
Neoplasias Renais/sangue
Inibidor Tecidual de Metaloproteinase-1/sangue
Fator A de Crescimento do Endotélio Vascular/sangue
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Antineoplásicos/uso terapêutico
Carcinoma de Células Renais/tratamento farmacológico
Carcinoma de Células Renais/mortalidade
Carcinoma de Células Renais/patologia
Feminino
Hemoglobinas/metabolismo
Fator de Crescimento de Hepatócito/sangue
Seres Humanos
Interleucina-6/sangue
Interleucina-8/sangue
Neoplasias Renais/tratamento farmacológico
Neoplasias Renais/mortalidade
Neoplasias Renais/patologia
L-Lactato Desidrogenase/sangue
Contagem de Leucócitos
Masculino
Meia-Idade
Neutrófilos
Osteopontina/sangue
Prognóstico
Pirimidinas/uso terapêutico
Sulfonamidas/uso terapêutico
Taxa de Sobrevida
Tempo para o Tratamento
Carga Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Cytokines); 0 (E-Selectin); 0 (Hemoglobins); 0 (Interleukin-6); 0 (Interleukin-8); 0 (Pyrimidines); 0 (Sulfonamides); 0 (TIMP1 protein, human); 0 (Tissue Inhibitor of Metalloproteinase-1); 0 (Vascular Endothelial Growth Factor A); 106441-73-0 (Osteopontin); 67256-21-7 (Hepatocyte Growth Factor); 7RN5DR86CK (pazopanib); EC 1.1.1.27 (L-Lactate Dehydrogenase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170707
[St] Status:MEDLINE
[do] DOI:10.1038/bjc.2017.206


  8 / 5480 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28646109
[Au] Autor:Mitrofan CG; Appleby SL; Nash GB; Mallat Z; Chilvers ER; Upton PD; Morrell NW
[Ad] Endereço:From the Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge CB2 0QQ and.
[Ti] Título:Bone morphogenetic protein 9 (BMP9) and BMP10 enhance tumor necrosis factor-α-induced monocyte recruitment to the vascular endothelium mainly via activin receptor-like kinase 2.
[So] Source:J Biol Chem;292(33):13714-13726, 2017 Aug 18.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bone morphogenetic proteins 9 and 10 (BMP9/BMP10) are circulating cytokines with important roles in endothelial homeostasis. The aim of this study was to investigate the roles of BMP9 and BMP10 in mediating monocyte-endothelial interactions using an flow adhesion assay. Herein, we report that whereas BMP9/BMP10 alone had no effect on monocyte recruitment, at higher concentrations both cytokines synergized with tumor necrosis factor-α (TNFα) to increase recruitment to the vascular endothelium. The BMP9/BMP10-mediated increase in monocyte recruitment in the presence of TNFα was associated with up-regulated expression levels of E-selectin, vascular cell adhesion molecule (VCAM-1), and intercellular adhesion molecule 1 (ICAM-1) on endothelial cells. Using siRNAs to type I and II BMP receptors and the signaling intermediaries (Smads), we demonstrated a key role for ALK2 in the BMP9/BMP10-induced surface expression of E-selectin, and both ALK1 and ALK2 in the up-regulation of VCAM-1 and ICAM-1. The type II receptors, BMPR-II and ACTR-IIA were both required for this response, as was Smad1/5. The up-regulation of cell surface adhesion molecules by BMP9/10 in the presence of TNFα was inhibited by LDN193189, which inhibits ALK2 but not ALK1. Furthermore, LDN193189 inhibited monocyte recruitment induced by TNFα and BMP9/10. BMP9/10 increased basal IκBα protein expression, but did not alter p65/RelA levels. Our findings suggest that higher concentrations of BMP9/BMP10 synergize with TNFα to induce the up-regulation of endothelial selectins and adhesion molecules, ultimately resulting in increased monocyte recruitment to the vascular endothelium. This process is mediated mainly via the ALK2 type I receptor, BMPR-II/ACTR-IIA type II receptors, and downstream Smad1/5 signaling.
[Mh] Termos MeSH primário: Receptores de Ativinas Tipo I/metabolismo
Proteínas Morfogenéticas Ósseas/metabolismo
Endotélio Vascular/metabolismo
Fatores de Diferenciação de Crescimento/metabolismo
Monócitos/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Receptores de Ativinas Tipo I/antagonistas & inibidores
Receptores de Ativinas Tipo I/genética
Receptores de Activinas Tipo II/antagonistas & inibidores
Receptores de Activinas Tipo II/genética
Receptores de Activinas Tipo II/metabolismo
Aorta
Adesão Celular/efeitos dos fármacos
Células Cultivadas
Selectina E/química
Selectina E/genética
Selectina E/metabolismo
Endotélio Vascular/citologia
Endotélio Vascular/efeitos dos fármacos
Endotélio Vascular/imunologia
Seres Humanos
Molécula 1 de Adesão Intercelular/química
Molécula 1 de Adesão Intercelular/genética
Molécula 1 de Adesão Intercelular/metabolismo
Cinética
Monócitos/citologia
Monócitos/efeitos dos fármacos
Monócitos/imunologia
Fosforilação/efeitos dos fármacos
Inibidores de Proteínas Quinases/farmacologia
Processamento de Proteína Pós-Traducional/efeitos dos fármacos
Pirazóis/farmacologia
Pirimidinas/farmacologia
Interferência de RNA
Transdução de Sinais/efeitos dos fármacos
Fator de Necrose Tumoral alfa/agonistas
Regulação para Cima/efeitos dos fármacos
Molécula 1 de Adesão de Célula Vascular/química
Molécula 1 de Adesão de Célula Vascular/genética
Molécula 1 de Adesão de Célula Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BMP10 protein, human); 0 (Bone Morphogenetic Proteins); 0 (E-Selectin); 0 (GDF2 protein, human); 0 (Growth Differentiation Factors); 0 (ICAM1 protein, human); 0 (LDN 193189); 0 (Protein Kinase Inhibitors); 0 (Pyrazoles); 0 (Pyrimidines); 0 (SELE protein, human); 0 (TNF protein, human); 0 (Tumor Necrosis Factor-alpha); 0 (Vascular Cell Adhesion Molecule-1); 126547-89-5 (Intercellular Adhesion Molecule-1); EC 2.7.11.30 (ACVR1 protein, human); EC 2.7.11.30 (ACVRL1 protein, human); EC 2.7.11.30 (Activin Receptors, Type I); EC 2.7.11.30 (Activin Receptors, Type II)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170625
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.778506


  9 / 5480 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:28485794
[Au] Autor:Liu WB; Han XH; Guo YY; Zhang DM; Tang FJ; Zhao L; Ji LL; Guo FM
[Ad] Endereço:Department of Cardiology, Yantaishan Hospital of Yantai, Yantai, Shandong, China. guofmcn@qq.com.
[Ti] Título:Effects of tumor necrosis factor and E-selectin on coronary artery flow.
[So] Source:Eur Rev Med Pharmacol Sci;21(8):1843-1849, 2017 Apr.
[Is] ISSN:2284-0729
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The aim of the study is to investigate the correlation between tumor necrosis factor (TNF-α), E-selectin and coronary artery flow following myocardial ischemia-reperfusion model (IR) in Yorkshire pigs. MATERIALS AND METHODS: Establishment of IR model in pigs. Following the injury model, Experiment group was administrated intravenously Shenfu injection solution (SFI, 1 mL/kg). The control group received the same amount of saline. After 30 min of blood reflux, thrombolysis in myocardial infarction frame count (TFC) was recorded following surgery. TNF-α, E-selectin expression was determined by ELISA in the venous sheath, coronary sinus, artery sinus, and proximal segment of the coronary artery. RESULTS: After the blood reflowing, TFC in both groups were upregulated, and TFC increased more than the control group. The difference is statistically significant (p<0.05) at the time of 30 min. TNF-α, E-selectin expression increased after IR. After reperfusion, TNF-α, E-selectin levels further increased and the myocardial injury was aggravated. SFI inhibited inflammation in the experimental group. TNF-α, E-selectin levels at coronary sinus, artery sinus, and distal segment of coronary artery after surgery was positively correlated with TIMI in the experimental group (p<0.05). TNF-α, E-selectin levels significantly increased after reperfusion (p<0.05). CONCLUSIONS: The result demonstrated that TNF-α, E-selectin levels were positively correlated with coronary artery reflow only in the experimental group but not in the control group.
[Mh] Termos MeSH primário: Vasos Coronários/fisiopatologia
Selectina E/metabolismo
Isquemia Miocárdica/fisiopatologia
Fluxo Sanguíneo Regional
Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Animais
Medicamentos de Ervas Chinesas/farmacologia
Isquemia Miocárdica/sangue
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drugs, Chinese Herbal); 0 (E-Selectin); 0 (Shen-Fu); 0 (Tumor Necrosis Factor-alpha)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170731
[Lr] Data última revisão:
170731
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170510
[St] Status:MEDLINE


  10 / 5480 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28481220
[Au] Autor:Lee J; Dykstra B; Spencer JA; Kenney LL; Greiner DL; Shultz LD; Brehm MA; Lin CP; Sackstein R; Rossi DJ
[Ad] Endereço:Program in Cellular and Molecular Medicine, Division of Hematology/Oncology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
[Ti] Título:mRNA-mediated glycoengineering ameliorates deficient homing of human stem cell-derived hematopoietic progenitors.
[So] Source:J Clin Invest;127(6):2433-2437, 2017 Jun 01.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Generation of functional hematopoietic stem and progenitor cells (HSPCs) from human pluripotent stem cells (PSCs) has been a long-sought-after goal for use in hematopoietic cell production, disease modeling, and eventually transplantation medicine. Homing of HSPCs from bloodstream to bone marrow (BM) is an important aspect of HSPC biology that has remained unaddressed in efforts to derive functional HSPCs from human PSCs. We have therefore examined the BM homing properties of human induced pluripotent stem cell-derived HSPCs (hiPS-HSPCs). We found that they express molecular effectors of BM extravasation, such as the chemokine receptor CXCR4 and the integrin dimer VLA-4, but lack expression of E-selectin ligands that program HSPC trafficking to BM. To overcome this deficiency, we expressed human fucosyltransferase 6 using modified mRNA. Expression of fucosyltransferase 6 resulted in marked increases in levels of cell surface E-selectin ligands. The glycoengineered cells exhibited enhanced tethering and rolling interactions on E-selectin-bearing endothelium under flow conditions in vitro as well as increased BM trafficking and extravasation when transplanted into mice. However, glycoengineered hiPS-HSPCs did not engraft long-term, indicating that additional functional deficiencies exist in these cells. Our results suggest that strategies toward increasing E-selectin ligand expression could be applicable as part of a multifaceted approach to optimize the production of HSPCs from human PSCs.
[Mh] Termos MeSH primário: Movimento Celular
Células-Tronco Hematopoéticas/fisiologia
RNA Mensageiro/metabolismo
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Células Cultivadas
Técnicas de Cocultura
Selectina E
Fucosiltransferases/fisiologia
Glicosilação
Transplante de Células-Tronco Hematopoéticas
Seres Humanos
Células-Tronco Pluripotentes Induzidas/fisiologia
Camundongos Endogâmicos NOD
Camundongos SCID
Processamento Pós-Transcricional do RNA
RNA Mensageiro/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (E-Selectin); 0 (RNA, Messenger); 0 (SELE protein, human); EC 2.4.1.- (Fucosyltransferases); EC 2.4.1.65 (FUT6 protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170509
[St] Status:MEDLINE



página 1 de 548 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde