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Pesquisa : D12.776.543.750.705.852.760.798 [Categoria DeCS]
Referências encontradas : 2243 [refinar]
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  1 / 2243 MEDLINE  
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[PMID]:29287713
[Au] Autor:Lan X; Sun W; Dong W; Wang Z; Zhang T; He L; Zhang H
[Ad] Endereço:Department of Head and Neck Surgery, Zhejiang Cancer Hospital, No.1, Banshandong Road, Gongshu District, Hangzhou 310022, Zhejiang Province, China; Department of Thyroid Surgery, The First Affiliated Hospital of China Medical University, No. 155, Nanjing Bei Street, Heping District, Shenyang 110001,
[Ti] Título:Downregulation of long noncoding RNA H19 contributes to the proliferation and migration of papillary thyroid carcinoma.
[So] Source:Gene;646:98-105, 2018 Mar 10.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Recent studies have highlighted important roles for long noncoding RNAs (lncRNAs) during the complex process of carcinogenesis. H19 is an example of an lncRNA that can function either as a tumor promoter or a tumor suppressor. Here, we investigated the role of H19 in papillary thyroid carcinoma (PTC). First, we assessed H19 expression levels in human PTC tissues and PTC cell lines using quantitative real-time PCR. We also established H19-overexpressed PTC cell lines with lentiviral vectors to investigate the effects of H19 on the proliferation and migration of PTC cells. Our results suggest that H19 is downregulated in PTC tissues and in PTC cell lines compared to controls. Decreased H19 expression was correlated with lymph node metastasis. H19 overexpression reduced PTC cell proliferation and migration. It also inhibited the expression of tumor necrosis factor receptor 2. These results suggest that H19 inhibits tumorigenesis in PTC and may be utilized as a potential diagnostic tool for PTC.
[Mh] Termos MeSH primário: Carcinoma Papilar/genética
Carcinoma Papilar/patologia
Regulação para Baixo
RNA Longo não Codificante/genética
Receptores Tipo II do Fator de Necrose Tumoral/genética
Neoplasias da Glândula Tireoide/genética
Neoplasias da Glândula Tireoide/patologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Proliferação Celular
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Metástase Linfática
Masculino
Camundongos
Invasividade Neoplásica
Transplante de Neoplasias
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (H19 long non-coding RNA); 0 (RNA, Long Noncoding); 0 (Receptors, Tumor Necrosis Factor, Type II); 0 (TNFRSF1B protein, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171231
[St] Status:MEDLINE


  2 / 2243 MEDLINE  
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[PMID]:28747340
[Au] Autor:Bradford EM; Ryu SH; Singh AP; Lee G; Goretsky T; Sinh P; Williams DB; Cloud AL; Gounaris E; Patel V; Lamping OF; Lynch EB; Moyer MP; De Plaen IG; Shealy DJ; Yang GY; Barrett TA
[Ad] Endereço:Department of Internal Medicine, Ann & Robert H. Lurie Children's Hospital of Chicago, Northwestern University Feinberg School of Medicine, Chicago, IL 60611.
[Ti] Título:Epithelial TNF Receptor Signaling Promotes Mucosal Repair in Inflammatory Bowel Disease.
[So] Source:J Immunol;199(5):1886-1897, 2017 09 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:TNF plays an integral role in inflammatory bowel disease (IBD), as evidenced by the dramatic therapeutic responses in Crohn's disease (CD) patients induced by chimeric anti-TNF mAbs. However, treatment of CD patients with etanercept, a decoy receptor that binds soluble TNF, fails to improve disease. To explore this discrepancy, we investigated the role of TNF signaling in Wnt/ß-catenin-mediated intestinal stem cell and progenitor cell expansion in CD patients, human cells, and preclinical mouse models. We hypothesized that TNF exerts beneficial effects on intestinal epithelial cell (IEC) responses to injury. In CD patients, intestinal stem cell and progenitor cell Wnt/ß-catenin signaling correlates with inflammation status. TNF-deficient ( ) mice exhibited increased apoptosis, less IEC proliferation, and less Wnt signaling when stimulated with anti-CD3 mAb. Bone marrow (BM) chimera mice revealed that mucosal repair depended on TNF production by BM-derived cells and TNFR expression by radioresistant IECs. Wild-type→ BM chimera mice with chronic dextran sodium sulfate colitis exhibited delayed ulcer healing, more mucosal inflammation, and impaired Wnt/ß-catenin signaling, consistent with the hypothesis that epithelial TNFR signaling participates in mucosal healing. The direct effect of TNF on stem cells was demonstrated by studies of TNF-induced Wnt/ß-catenin target gene expression in murine enteroids and colonoid cultures and TNF-induced ß-catenin activation in nontransformed human NCM460 cells (TOPFlash) and mice (TOP-GAL). Together, these data support the hypothesis that TNF plays a beneficial role in enhancing Wnt/ß-catenin signaling during ulcer healing in IBD. These novel findings will inform clinicians and therapeutic chemists alike as they strive to develop novel therapies for IBD patients.
[Mh] Termos MeSH primário: Células-Tronco Adultas/fisiologia
Anticorpos Monoclonais/uso terapêutico
Colite/imunologia
Células Epiteliais/fisiologia
Doenças Inflamatórias Intestinais/imunologia
Mucosa Intestinal/fisiologia
Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Animais
Anticorpos Monoclonais/metabolismo
Linhagem Celular
Sulfato de Dextrana
Seres Humanos
Doenças Inflamatórias Intestinais/terapia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Receptores Tipo I de Fatores de Necrose Tumoral/genética
Receptores Tipo II do Fator de Necrose Tumoral/genética
Transdução de Sinais
Fator de Necrose Tumoral alfa/genética
Proteínas Wnt/metabolismo
Cicatrização
beta Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Receptors, Tumor Necrosis Factor, Type I); 0 (Receptors, Tumor Necrosis Factor, Type II); 0 (Tumor Necrosis Factor-alpha); 0 (Wnt Proteins); 0 (beta Catenin); 9042-14-2 (Dextran Sulfate)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601066


  3 / 2243 MEDLINE  
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[PMID]:28886201
[Au] Autor:Quinn KM; Kan WT; Watson KA; Liddicoat BJ; Swan NG; McQuilten H; Denton AE; Li J; Chen W; Brown LE; Jackson DC; Reading PC; Doherty PC; Kedzierska K; Kedzierski L; Turner SJ; La Gruta NL
[Ad] Endereço:Infection and Immunity Program and Department of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.
[Ti] Título:Extrinsically derived TNF is primarily responsible for limiting antiviral CD8+ T cell response magnitude.
[So] Source:PLoS One;12(9):e0184732, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:TNF is a pro-inflammatory cytokine produced by both lymphoid and non-lymphoid cells. As a consequence of the widespread expression of its receptors (TNFR1 and 2), TNF plays a role in many important biological processes. In the context of influenza A virus (IAV) infection, TNF has variably been implicated in mediating immunopathology as well as suppression of the immune response. Although a number of cell types are able to produce TNF, the ability of CD8+ T cells to produce TNF following viral infection is a hallmark of their effector function. As such, the regulation and role of CD8+ T cell-derived TNF following viral infection is of great interest. Here, we show that the biphasic production of TNF by CD8+ T cells following in vitro stimulation corresponds to distinct patterns of epigenetic modifications. Further, we show that a global loss of TNF during IAV infection results in an augmentation of the peripheral virus-specific CD8+ T cell response. Subsequent adoptive transfer experiments demonstrated that this attenuation of the CD8+ T cell response was largely, but not exclusively, conferred by extrinsic TNF, with intrinsically-derived TNF making only modest contributions. In conclusion, TNF exerts an immunoregulatory role on CD8+ T cell responses following IAV infection, an effect that is largely mediated by extrinsically-derived TNF.
[Mh] Termos MeSH primário: Linfócitos T CD8-Positivos/metabolismo
Receptores do Fator de Necrose Tumoral/metabolismo
[Mh] Termos MeSH secundário: Animais
Imunoprecipitação da Cromatina
Feminino
Vírus da Influenza A/patogenicidade
Camundongos
Camundongos Endogâmicos C57BL
RNA Polimerase II/metabolismo
Receptores Tipo I de Fatores de Necrose Tumoral/metabolismo
Receptores Tipo II do Fator de Necrose Tumoral/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Tumor Necrosis Factor); 0 (Receptors, Tumor Necrosis Factor, Type I); 0 (Receptors, Tumor Necrosis Factor, Type II); EC 2.7.7.- (RNA Polymerase II)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184732


  4 / 2243 MEDLINE  
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[PMID]:28877252
[Au] Autor:Link MA; Lücke K; Schmid J; Schumacher V; Eden T; Rose-John S; Mittrücker HW
[Ad] Endereço:Institute of Immunology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
[Ti] Título:The role of ADAM17 in the T-cell response against bacterial pathogens.
[So] Source:PLoS One;12(9):e0184320, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:ADAM17 is a member of the A Disintegrin And Metalloproteinase family of proteases. It is ubiquitously expressed and causes the shedding of a broad spectrum of surface proteins such as adhesion molecules, cytokines and cytokine receptors. By controlled shedding of these proteins from leukocytes, ADAM17 is able to regulate immune responses. Several ADAM17 targets on T cells have been implicated in T-cell migration, differentiation and effector functions. However, the role of ADAM17 in T-cell responses is still unclear. To characterize the function of ADAM17 in T cells, we used Adam17fl/fl×CD4cre+ mice with a T-cell restricted inactivation of the Adam17 gene. Upon stimulation, ADAM17-deficient CD4+ and CD8+ T cells were impaired in shedding of CD62L, IL-6Rα, TNF-α, TNFRI and TNFRII. Surprisingly, we could not detect profound changes in the composition of major T-cell subsets in Adam17fl/fl×CD4cre+ mice. Following infection with Listeria monocytogenes, Adam17fl/fl×CD4cre+ mice mounted regular listeria-specific CD4+ TH1 and CD8+ T-cell responses and were able to control primary and secondary infections. In conclusion, our study indicates that ADAM17 is either not required in T cells under homoeostatic conditions and for control of listeria infection or can be effectively compensated by other mechanisms.
[Mh] Termos MeSH primário: Proteína ADAM17/metabolismo
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD8-Positivos/imunologia
Listeriose/imunologia
[Mh] Termos MeSH secundário: Animais
Adesão Celular
Diferenciação Celular
Membrana Celular/metabolismo
Feminino
Selectina L/metabolismo
Listeria monocytogenes
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Receptores de Interleucina-6/metabolismo
Receptores Tipo I de Fatores de Necrose Tumoral/metabolismo
Receptores Tipo II do Fator de Necrose Tumoral/metabolismo
Células Th1/imunologia
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Interleukin-6); 0 (Receptors, Tumor Necrosis Factor, Type I); 0 (Receptors, Tumor Necrosis Factor, Type II); 0 (Tumor Necrosis Factor-alpha); 126880-86-2 (L-Selectin); EC 3.4.24.86 (ADAM17 Protein); EC 3.4.24.86 (Adam17 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170907
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184320


  5 / 2243 MEDLINE  
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[PMID]:28830973
[Au] Autor:Svensson EH; Söderholm M; Abul-Kasim K; Engström G
[Ad] Endereço:From the Department of Clinical Science in Malmö, Lund University, Sweden (E.H.S., M.S., G.E.); and Department of Neurology and Rehabilitation Medicine (M.S.) and Division of Neuroradiology (K.A.-K.), Skåne University Hospital in Lund and Malmö, Sweden.
[Ti] Título:Tumor Necrosis Factor Receptor 1 and 2 Are Associated With Risk of Intracerebral Hemorrhage.
[So] Source:Stroke;48(10):2710-2715, 2017 Oct.
[Is] ISSN:1524-4628
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND PURPOSE: Raised plasma concentrations of tumor necrosis factor receptors (TNFR) have been linked to arterial stiffness, cerebral microbleeds, and vascular events. The aim of this study was to investigate the association of circulating levels of TNFR1 and TNFR2 with risk for future intracerebral hemorrhage (ICH). METHODS: The population-based MDCS cohort (Malmö Diet and Cancer Study; n=28 449) was conducted in 1991 to 1996. A nested case-control study was performed in the MDCS, including 220 cases who experienced ICH during the follow-up period (mean age at inclusion 62 years, 48% men) and 244 matched controls. Of the 220 ICH cases, 68 died within 28 days. Conditional logistic regression was used to study the association between plasma levels of TNFR1 and TNFR2 and incident ICH, adjusting for known ICH risk factors. RESULTS: Concentrations of both TNFR1 and TNFR2 were significantly higher in subjects who developed ICH during the follow-up. The associations remained after adjustment for ICH risk factors (TNFR1: odds ratio [OR], 2.28; 95% confidence interval [CI], 1.26-4.11; =0.006; TNFR2: OR, 1.77; CI, 1.16-2.70; =0.008). ORs were somewhat higher for nonlobar ICH (3.04; CI, 1.29-7.14 and 2.39; CI, 1.32-4.32, respectively) than for lobar ICH (2.03; CI, 0.93-4.41 and 1.35; CI, 0.78-2.37, respectively). TNFR1 and TNFR2 were also associated with increased risk of fatal ICH (TNFR1: OR, 4.42; CI, 1.67-11.6; TNFR2: OR, 2.90; CI, 1.50-5.58) and with poor functional outcome according to the modified Rankin Scale. CONCLUSIONS: High plasma levels of TNFR1 and TNFR2 were associated with incident ICH, most clearly with ICH of nonlobar location. The results suggest that tumor necrosis factor-mediated inflammation could be associated with vascular changes preceding ICH.
[Mh] Termos MeSH primário: Hemorragia Cerebral/sangue
Hemorragia Cerebral/epidemiologia
Vigilância da População
Receptores Tipo II do Fator de Necrose Tumoral/sangue
Receptores Tipo I de Fatores de Necrose Tumoral/sangue
[Mh] Termos MeSH secundário: Idoso
Biomarcadores/sangue
Estudos de Casos e Controles
Hemorragia Cerebral/diagnóstico
Estudos de Coortes
Feminino
Seres Humanos
Masculino
Meia-Idade
Vigilância da População/métodos
Estudos Prospectivos
Fatores de Risco
Suécia/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Receptors, Tumor Necrosis Factor, Type I); 0 (Receptors, Tumor Necrosis Factor, Type II)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171009
[Lr] Data última revisão:
171009
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170824
[St] Status:MEDLINE
[do] DOI:10.1161/STROKEAHA.117.017849


  6 / 2243 MEDLINE  
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[PMID]:28751572
[Au] Autor:Li W; Dorans KS; Wilker EH; Rice MB; Ljungman PL; Schwartz JD; Coull BA; Koutrakis P; Gold DR; Keaney JF; Vasan RS; Benjamin EJ; Mittleman MA
[Ad] Endereço:From the Departments of Epidemiology (W.L., K.S.D., E.H.W., J.D.S., M.A.M.), Environmental Health (J.D.S., P.K., D.R.G.), and Biostatistics (B.A.C.), Harvard T.H. Chan School of Public Health, Boston, MA; Cardiovascular Epidemiology Research Unit, Division of Cardiology (W.L., K.S.D., E.H.W., P.L.L.
[Ti] Título:Short-Term Exposure to Ambient Air Pollution and Biomarkers of Systemic Inflammation: The Framingham Heart Study.
[So] Source:Arterioscler Thromb Vasc Biol;37(9):1793-1800, 2017 Sep.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The objective of this study is to examine associations between short-term exposure to ambient air pollution and circulating biomarkers of systemic inflammation in participants from the Framingham Offspring and Third Generation cohorts in the greater Boston area. APPROACH AND RESULTS: We included 3996 noncurrent smoking participants (mean age, 53.6 years; 54% women) who lived within 50 km from a central air pollution monitoring site in Boston, MA, and calculated the 1- to 7-day moving averages of fine particulate matter (diameter<2.5 µm), black carbon, sulfate, nitrogen oxides, and ozone before the examination visits. We used linear mixed effects models for C-reactive protein and tumor necrosis factor receptor 2, which were measured up to twice for each participant; we used linear regression models for interleukin-6, fibrinogen, and tumor necrosis factor α, which were measured once. We adjusted for demographics, socioeconomic position, lifestyle, time, and weather. The 3- to 7-day moving averages of fine particulate matter (diameter<2.5 µm) and sulfate were positively associated with C-reactive protein concentrations. A 5 µg/m higher 5-day moving average fine particulate matter (diameter<2.5 µm) was associated with 4.2% (95% confidence interval: 0.8, 7.6) higher circulating C-reactive protein. Positive associations were also observed for nitrogen oxides with interleukin-6 and for black carbon, sulfate, and ozone with tumor necrosis factor receptor 2. However, black carbon, sulfate, and nitrogen oxides were negatively associated with fibrinogen, and sulfate was negatively associated with tumor necrosis factor α. CONCLUSIONS: Higher short-term exposure to relatively low levels of ambient air pollution was associated with higher levels of C-reactive protein, interleukin-6, and tumor necrosis factor receptor 2 but not fibrinogen or tumor necrosis factor α in individuals residing in the greater Boston area.
[Mh] Termos MeSH primário: Poluentes Atmosféricos/efeitos adversos
Mediadores da Inflamação/sangue
Inflamação/induzido quimicamente
Exposição por Inalação/efeitos adversos
Material Particulado/efeitos adversos
[Mh] Termos MeSH secundário: Adulto
Idoso
Biomarcadores/sangue
Boston
Proteína C-Reativa/metabolismo
Monitoramento Ambiental
Feminino
Seres Humanos
Inflamação/sangue
Inflamação/diagnóstico
Interleucina-6/sangue
Masculino
Meia-Idade
Tamanho da Partícula
Receptores Tipo II do Fator de Necrose Tumoral/sangue
Medição de Risco
Fatores de Risco
Fatores de Tempo
Regulação para Cima
Saúde da População Urbana
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Air Pollutants); 0 (Biomarkers); 0 (IL6 protein, human); 0 (Inflammation Mediators); 0 (Interleukin-6); 0 (Particulate Matter); 0 (Receptors, Tumor Necrosis Factor, Type II); 0 (TNFRSF1B protein, human); 9007-41-4 (C-Reactive Protein)
[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:170729
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309799


  7 / 2243 MEDLINE  
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[PMID]:28724611
[Au] Autor:Mehaffey E; Majid DSA
[Ad] Endereço:Department of Physiology, Tulane Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana.
[Ti] Título:Tumor necrosis factor-α, kidney function, and hypertension.
[So] Source:Am J Physiol Renal Physiol;313(4):F1005-F1008, 2017 Oct 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hypertension is considered to be a low-grade inflammatory condition characterized by the presence of various proinflammatory cytokines. Tumor necrosis factor-α (TNF-α) is a constituent of the proinflammatory cytokines that is associated with salt-sensitive hypertension (SSH) and related renal injury. Elevated angiotensin II (ANG II) and other factors such as oxidative stress conditions promote TNF-α formation. Many recent studies have provided evidence that TNF-α exerts a direct renal action by regulating hemodynamic and excretory function in the kidney. The cytokine incites a strong natriuretic response and plays a part in regulation of the intrarenal renin-angiotensin system. The exact mechanistic role of TNF-α in the development of SSH is as yet poorly understood. While TNF-α antagonism has been shown to attenuate hypertensive responses in many hypertensive animal models, contrasting findings demonstrate that the direct systemic administration of TNF-α usually induces hypotensive as well as natriuretic responses, indicating a counterregulatory role of TNF-α in SSH. Differential activities of two cell surface receptors of TNF-α (receptor type 1 and type 2) may explain the contradictory functions of TNF-α in the setting of hypertension. This short review will evaluate ongoing research studies that investigate the action of TNF-α within the kidney and its role as an influential pathophysiological variable in the development of SSH and renal injury. This information may help to develop specific TNF-α receptor targeting as an effective treatment strategy in this clinical condition.
[Mh] Termos MeSH primário: Pressão Sanguínea
Hipertensão/metabolismo
Mediadores da Inflamação/metabolismo
Inflamação/metabolismo
Rim/metabolismo
Cloreto de Sódio na Dieta/efeitos adversos
Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Hipertensão/imunologia
Hipertensão/fisiopatologia
Inflamação/imunologia
Inflamação/fisiopatologia
Mediadores da Inflamação/imunologia
Rim/imunologia
Rim/fisiopatologia
Receptores Tipo I de Fatores de Necrose Tumoral/metabolismo
Receptores Tipo II do Fator de Necrose Tumoral/metabolismo
Sistema Renina-Angiotensina
Transdução de Sinais
Fator de Necrose Tumoral alfa/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Inflammation Mediators); 0 (Receptors, Tumor Necrosis Factor, Type I); 0 (Receptors, Tumor Necrosis Factor, Type II); 0 (Sodium Chloride, Dietary); 0 (Tumor Necrosis Factor-alpha)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170721
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00535.2016


  8 / 2243 MEDLINE  
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[PMID]:28659407
[Au] Autor:Tabung FK; Smith-Warner SA; Chavarro JE; Fung TT; Hu FB; Willett WC; Giovannucci EL
[Ad] Endereço:Departments of Nutrition and ftabung@hsph.harvard.edu.
[Ti] Título:An Empirical Dietary Inflammatory Pattern Score Enhances Prediction of Circulating Inflammatory Biomarkers in Adults.
[So] Source:J Nutr;147(8):1567-1577, 2017 Aug.
[Is] ISSN:1541-6100
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Two indexes exist to describe dietary inflammatory potential: an empirical dietary inflammatory pattern (EDIP) composed of food groups as reported on a food-frequency questionnaire (FFQ) and a literature-derived dietary inflammatory index (DII) composed mainly of nutrients. We compared the ability of the 2 indexes to predict concentrations of inflammatory markers and hypothesized that the EDIP would be more predictive because it was derived on the basis of circulating inflammatory markers. Both EDIP and DII scores were calculated from FFQ data reported by 5826 women in the Nurses' Health Study II and 5227 men in the Health Professionals Follow-Up Study. We used multivariable-adjusted linear regression analyses to calculate relative differences in concentrations of 4 plasma inflammatory markers-C-reactive protein (CRP; milligrams per liter), interleukin 6 (IL-6; picograms per milliliter), tumor necrosis factor α receptor 2 (TNFαR2; picograms per milliliter), and adiponectin (nanograms per milliliter)-in quintiles of the dietary indexes. Spearman correlations between the EDIP and DII scores were modest ( = 0.29 and 0.21 for women and men, respectively; all < 0.0001). Higher scores on both dietary indexes were associated with higher concentrations of inflammatory markers, although they were associated with lower adiponectin concentrations and there was no association between the DII and adiponectin in men. For example, percentage differences in concentrations of biomarkers in quintile 5 generally were higher (lower for adiponectin) than in quintile 1 (for the EDIP and DII, respectively-women: CRP, +60% and +49%; IL-6, +23% and +21%; TNFαR2, +7% and +4%; adiponectin, -21% and -14%; men: CRP, +38% and +29%; IL-6, +14% and +24%; TNFαR2, +9% and +5%; adiponectin, -16% and -4%.) Despite design differences, the EDIP and DII both assess dietary inflammatory potential in men and women, with the EDIP showing a greater ability to predict concentrations of plasma inflammatory markers.
[Mh] Termos MeSH primário: Adiponectina/sangue
Proteína C-Reativa/metabolismo
Dieta/efeitos adversos
Alimentos/efeitos adversos
Inflamação/sangue
Interleucina-6/sangue
Receptores Tipo II do Fator de Necrose Tumoral/sangue
[Mh] Termos MeSH secundário: Adulto
Biomarcadores/sangue
Comportamento Alimentar
Feminino
Seres Humanos
Masculino
Meia-Idade
Inquéritos e Questionários
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ADIPOQ protein, human); 0 (Adiponectin); 0 (Biomarkers); 0 (IL6 protein, human); 0 (Interleukin-6); 0 (Receptors, Tumor Necrosis Factor, Type II); 0 (TNFRSF1B protein, human); 9007-41-4 (C-Reactive Protein)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170816
[Lr] Data última revisão:
170816
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170630
[St] Status:MEDLINE
[do] DOI:10.3945/jn.117.248377


  9 / 2243 MEDLINE  
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[PMID]:28640389
[Au] Autor:Wang FH; Wang Y; Sun GP; Chen JH; Lin YC; Liu W; Zheng RS; Chen J; Zhang HL; Lan HT; Qi J; Liu YQ; Deng YM; Zhao H; Xiong JP; Xu Q; Jiang WQ; Li YH
[Ad] Endereço:Department of Medical Oncology, Sun Yat-sen University Cancer Center, Guangzhou, People's Republic of China.
[Ti] Título:Efficacy and safety of recombinant human lymphotoxin-α derivative with cisplatin and fluorouracil in patients with metastatic esophageal squamous cell carcinoma: A randomized, multicenter, open-label, controlled, phase 2b trial.
[So] Source:Cancer;123(20):3986-3994, 2017 Oct 15.
[Is] ISSN:1097-0142
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Recombinant human lymphotoxin-α derivative (rhLTα-Da) is a lymphotoxin-α derivative that is missing 27 N-terminal amino acid residues. Previous studies indicated a benefit from the addition of rhLTα-Da to cisplatin-based treatment in patients with metastatic esophageal squamous cell carcinoma. The current study was conducted to evaluate the efficacy and safety of rhLTα-Da plus cisplatin and fluorouracil (PF) in patients with mESCC. METHODS: Patients from 15 centers in China were randomly assigned (1:1:1) to 3 arms (arm A, PF plus 10 µg/m daily rhLTα-Da; arm B, PF plus 20 µg/m daily rhLTα-Da; arm C, PF alone). The primary endpoints included progression-free survival (PFS) and the confirmed overall response rate (ORR). An exploratory analysis was performed to evaluate the role of serum tumor necrosis factor receptor II (TNFR II) in predicting the efficacy of rhLTα-Da. RESULTS: Between September 2010 and May 2013, 150 patients were enrolled. No significant differences in either PFS or ORR were observed between the 3 arms. However, in a small subset of patients who had low serum TNFR II levels, the median PFS was significantly longer for those in arm B than for these in other 2 arms (7.2 months [95% confidence interval, 5.1-8.6 months] for arm B vs 3.5 months [95% confidence interval, 1.7-5.5 months] for arm A [P = .022] and 4.0 months [95% confidence interval, 3.2-6.3 months] for arm C [P = .027]). The addition of rhLTα-Da significantly increased the incidence of chills (P < .001). CONCLUSIONS: rhLTα-Da combined with the PF regimen failed to improve PFS and ORR in patients with mESCC, except in a small subset that had low serum TNFR II concentrations. Cancer 2017;123:3986-94. © 2017 American Cancer Society.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Carcinoma de Células Escamosas/tratamento farmacológico
Neoplasias Esofágicas/patologia
Linfotoxina-alfa/uso terapêutico
[Mh] Termos MeSH secundário: Adulto
Idoso
Carcinoma de Células Escamosas/metabolismo
Carcinoma de Células Escamosas/secundário
China
Cisplatino/administração & dosagem
Intervalo Livre de Doença
Neoplasias Esofágicas/metabolismo
Feminino
Fluoruracila/administração & dosagem
Seres Humanos
Linfotoxina-alfa/efeitos adversos
Masculino
Meia-Idade
Receptores Tipo II do Fator de Necrose Tumoral/sangue
Proteínas Recombinantes/efeitos adversos
Proteínas Recombinantes/uso terapêutico
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE II; JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Lymphotoxin-alpha); 0 (Receptors, Tumor Necrosis Factor, Type II); 0 (Recombinant Proteins); Q20Q21Q62J (Cisplatin); U3P01618RT (Fluorouracil)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171011
[Lr] Data última revisão:
171011
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.1002/cncr.30845


  10 / 2243 MEDLINE  
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[PMID]:28637784
[Au] Autor:Nan J; Hu H; Sun Y; Zhu L; Wang Y; Zhong Z; Zhao J; Zhang N; Wang Y; Wang Y; Ye J; Zhang L; Hu X; Zhu W; Wang J
[Ad] Endereço:From the Cardiovascular Key Laboratory of Zhejiang Province, Department of Cardiology (J.N., H.H., Y.S., L.Z., Y.W., Z.Z., J.Z., N.Z., Y.W., Y.W., J.Y., L.Z., X.H., W.Z., J.W.) and Clinical Research Center (L.Z., Y.W., Z.Z., J.Z.), The Second Affiliated Hospital, Zhejiang University School of Medici
[Ti] Título:TNFR2 Stimulation Promotes Mitochondrial Fusion via Stat3- and NF-kB-Dependent Activation of OPA1 Expression.
[So] Source:Circ Res;121(4):392-410, 2017 Aug 04.
[Is] ISSN:1524-4571
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Mitochondria are important cellular organelles and play essential roles in maintaining cell structure and function. Emerging evidence indicates that in addition to having proinflammatory and proapoptotic effects, TNFα (tumor necrosis factor α) can, under certain circumstances, promote improvements in mitochondrial integrity and function, phenomena that can be ascribed to the existence of TNFR2 (TNFα receptor 2). OBJECTIVE: The present study aimed to investigate whether and how TNFR2 activation mediates the effects of TNFα on mitochondria. METHODS AND RESULTS: Freshly isolated neonatal mouse cardiac myocytes treated with shRNA targeting TNFR1 were used to study the effects of TNFR2 activation on mitochondrial function. Neonatal mouse cardiac myocytes exhibited increases in mitochondrial fusion, a change that was associated with increases in mitochondrial membrane potential, intracellular ATP levels, and oxygen consumption capacity. Importantly, TNFR2 activation-induced increases in OPA1 (optic atrophy 1) protein expression were responsible for the above enhancements, and these changes could be attenuated using siRNA targeting OPA1. Moreover, both Stat3 and RelA bound to the promoter region of OPA1 and their interactions synergistically upregulated OPA1 expression at the transcriptional level. Stat3 acetylation at lysine 370 or lysine 383 played a key role in the ability of Stat3 to form a supercomplex with RelA. Meanwhile, p300 modulated Stat3 acetylation in HEK293T (human embryonic kidney 293T) cells, and p300-mediated Stat3/RelA interactions played an indispensable role in OPA1 upregulation. Finally, TNFR2 activation exerted beneficial effects on OPA1 expression in an in vivo transverse aortic constriction model, whereby TNFR1-knockout mice exhibited better outcomes than in mice with both TNFR1 and TNFR2 knocked out. CONCLUSIONS: TNFR2 activation protects cardiac myocytes against stress by upregulating OPA1 expression. This process was facilitated by p300-mediated Stat3 acetylation and Stat3/RelA interactions, leading to improvements in mitochondrial morphology and function.
[Mh] Termos MeSH primário: GTP Fosfo-Hidrolases/biossíntese
Dinâmica Mitocondrial/fisiologia
NF-kappa B/metabolismo
Receptores Tipo II do Fator de Necrose Tumoral/metabolismo
Fator de Transcrição STAT3/metabolismo
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Doenças da Aorta/genética
Doenças da Aorta/metabolismo
Células Cultivadas
GTP Fosfo-Hidrolases/química
GTP Fosfo-Hidrolases/genética
Expressão Gênica
Células HEK293
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Miócitos Cardíacos/metabolismo
NF-kappa B/química
Estrutura Secundária de Proteína
Estrutura Terciária de Proteína
Receptores Tipo II do Fator de Necrose Tumoral/química
Fator de Transcrição STAT3/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NF-kappa B); 0 (Receptors, Tumor Necrosis Factor, Type II); 0 (STAT3 Transcription Factor); 0 (Stat3 protein, mouse); EC 3.6.1.- (GTP Phosphohydrolases); EC 3.6.1.- (Opa1 protein (GTPase), mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.1161/CIRCRESAHA.117.311143



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