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  1 / 1061 MEDLINE  
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[PMID]:29386192
[Au] Autor:Tu H; Wen CP; Tsai SP; Chow WH; Wen C; Ye Y; Zhao H; Tsai MK; Huang M; Dinney CP; Tsao CK; Wu X
[Ad] Endereço:Department of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.
[Ti] Título:Cancer risk associated with chronic diseases and disease markers: prospective cohort study.
[So] Source:BMJ;360:k134, 2018 01 31.
[Is] ISSN:1756-1833
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: To assess the independent and joint associations of major chronic diseases and disease markers with cancer risk and to explore the benefit of physical activity in reducing the cancer risk associated with chronic diseases and disease markers. DESIGN: Prospective cohort study. SETTING: Standard medical screening program in Taiwan. PARTICIPANTS: 405 878 participants, for whom cardiovascular disease markers (blood pressure, total cholesterol, and heart rate), diabetes, chronic kidney disease markers (proteinuria and glomerular filtration rate), pulmonary disease, and gouty arthritis marker (uric acid) were measured or diagnosed according to standard methods, were followed for an average of 8.7 years. MAIN OUTCOME MEASURES: Cancer incidence and cancer mortality. RESULTS: A statistically significantly increased risk of incident cancer was observed for the eight diseases and markers individually (except blood pressure and pulmonary disease), with adjusted hazard ratios ranging from 1.07 to 1.44. All eight diseases and markers were statistically significantly associated with risk of cancer death, with adjusted hazard ratios ranging from 1.12 to 1.70. Chronic disease risk scores summarizing the eight diseases and markers were positively associated with cancer risk in a dose-response manner, with the highest scores associated with a 2.21-fold (95% confidence interval 1.77-fold to 2.75-fold) and 4.00-fold (2.84-fold to 5.63-fold) higher cancer incidence and cancer mortality, respectively. High chronic disease risk scores were associated with substantial years of life lost, and the highest scores were associated with 13.3 years of life lost in men and 15.9 years of life lost in women. The population attributable fractions of cancer incidence or cancer mortality from the eight chronic diseases and markers together were comparable to those from five major lifestyle factors combined (cancer incidence: 20.5% 24.8%; cancer mortality: 38.9% 39.7%). Among physically active (versus inactive) participants, the increased cancer risk associated with chronic diseases and markers was attenuated by 48% for cancer incidence and 27% for cancer mortality. CONCLUSIONS: Chronic disease is an overlooked risk factor for cancer, as important as five major lifestyle factors combined. In this study, chronic diseases contributed to more than one fifth of the risk for incident cancer and more than one third of the risk for cancer death. Physical activity is associated with a nearly 40% reduction in the cancer risk associated with chronic diseases.
[Mh] Termos MeSH primário: Biomarcadores/sangue
Doença Crônica/epidemiologia
Neoplasias/complicações
[Mh] Termos MeSH secundário: Adulto
Artrite Gotosa/epidemiologia
Artrite Gotosa/metabolismo
Doenças Cardiovasculares/complicações
Doenças Cardiovasculares/epidemiologia
Doença Crônica/mortalidade
Complicações do Diabetes
Diabetes Mellitus/epidemiologia
Detecção Precoce de Câncer/métodos
Exercício/fisiologia
Feminino
Seres Humanos
Incidência
Estilo de Vida
Pneumopatias/epidemiologia
Pneumopatias/metabolismo
Pneumopatias/fisiopatologia
Masculino
Meia-Idade
Neoplasias/epidemiologia
Neoplasias/mortalidade
Avaliação de Resultados (Cuidados de Saúde)
Estudos Prospectivos
Insuficiência Renal Crônica/complicações
Insuficiência Renal Crônica/epidemiologia
Fatores de Risco
Taiwan/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180202
[St] Status:MEDLINE
[do] DOI:10.1136/bmj.k134


  2 / 1061 MEDLINE  
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[PMID]:29069047
[Au] Autor:Zhou C; Xue C; Yang B; Wang W; Xu Y; Huang F; Wang Y
[Ad] Endereço:aDepartment of Nephrology, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine bDepartment of Nephrology, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai, China.
[Ti] Título:Amputation of the first metatarsophalangeal joint due to a giant gouty tophi: A case report.
[So] Source:Medicine (Baltimore);96(43):e8441, 2017 Oct.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: The first metatarsophalangeal joint (MTP1) is the most frequent site of gouty tophi. We report an unusual case with a giant skin-perforating tophi. This is the first case of gouty tophi at MTP1 which accepts surgical debulking and amputation. PATIENT CONCERNS: A 42-year-old man presented with a seven-year history of gout and a giant tophi at MTP1. The patient was referred to hospital due to persistent pain and ulcerations on the surface of the left MTP1. This rounded, giant, swelling, tophaceous tophi severely interfered with his normal walking. DIAGNOSES: The patient was diagnosed with gouty arthritis seven years ago, and did not receive regular anti-gout treatments. OUTCOMES: Biochemical examination showed he had raised serum uric acid (SUA, 11.92 mg/dl) and creatinine (258 µmol/l). There was a severe joint destruction of MTP1 by X-ray examination. We controlled the skin infection by sulbenicillin. He was given febuxostat to reduce SUA. After 3 months of treatment, SUA fell to 6.8 mg/dl. Then we performed surgical debulking of MTP1 and amputation of hallux. Surgical operations obviously relieved the pain, and improved the function of his left foot. The visual closure after amputation was good. CONCLUSION: Surgical amputation of the gout lesion at MTP1 maximized the function, and reduced the pain of this patient. In the case of giant tophi with severe gouty arthritis or skin infections, surgical decisions need to weigh gains and losses carefully.
[Mh] Termos MeSH primário: Amputação/métodos
Artrite Gotosa/cirurgia
Articulação Metatarsofalângica/cirurgia
[Mh] Termos MeSH secundário: Adulto
Artrite Gotosa/sangue
Artrite Gotosa/patologia
Creatinina/sangue
Seres Humanos
Masculino
Articulação Metatarsofalângica/patologia
Ácido Úrico/sangue
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
268B43MJ25 (Uric Acid); AYI8EX34EU (Creatinine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171123
[Lr] Data última revisão:
171123
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171026
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008441


  3 / 1061 MEDLINE  
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[PMID]:29049247
[Au] Autor:Luo G; Yi T; Zhang G; Guo X; Jiang X
[Ad] Endereço:aDepartment of Clinical Laboratory, Affiliated Hospital of North Sichuan Medical College bTranslational Medicine Research Center, North Sichuan Medical College, Nanchong, Sichuan, P.R. China.
[Ti] Título:Increased circulating Th22 cells in patients with acute gouty arthritis: A CONSORT-compliant article.
[So] Source:Medicine (Baltimore);96(42):e8329, 2017 Oct.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: T-helper 22 (Th22) cells are involved in host immunity against pathogen invasion and have been implicated in the pathogenesis of inflammatory diseases. However, the roles of Th22 cells in acute gouty arthritis remain unclear. METHODS: A case-control study was employed to illustrate the clinical significance of Th22 cells in acute gouty arthritis. In this study, 27 patients with acute gouty arthritis, 22 patients with intercritical gout (IG), and 20 healthy controls were recruited, and peripheral blood cells and plasma were collected for the detection of Th22, Th17, and Th1 cells, and plasma interleukin (IL)-22. RESULTS: The relative and absolute numbers of Th22 and Th17 cells were significantly higher in patients with acute gouty arthritis than in patients with IG and healthy controls. Plasma IL-22 levels were consistently higher in patients with acute gouty arthritis than in patients with IG and healthy controls (P < .05). Th22 cell numbers were positively correlated with Th1 (r = 0.648, P < .05) and Th17 (r = 0.379, P < .05) cell numbers in patients with gout. Moreover, Th22 cell numbers and plasma IL-22 levels were positively correlated with C-reactive protein levels (Th22: r = 0.444, P < .05; IL-22: r = 0.282, P < .05). CONCLUSION: Our results indicate that peripheral blood levels of Th22 cells increase during acute gouty arthritis suggesting a role for these cells in the pathophysiology of the disease.
[Mh] Termos MeSH primário: Artrite Gotosa/imunologia
Linfócitos T Auxiliares-Indutores/imunologia
[Mh] Termos MeSH secundário: Adulto
Artrite Gotosa/sangue
Estudos de Casos e Controles
Ensaio de Imunoadsorção Enzimática
Citometria de Fluxo
Gota/sangue
Gota/imunologia
Seres Humanos
Interleucinas/imunologia
Masculino
Meia-Idade
Células Th1/imunologia
Células Th17/imunologia
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukins); 0 (interleukin-22)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171122
[Lr] Data última revisão:
171122
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171020
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008329


  4 / 1061 MEDLINE  
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[PMID]:28982129
[Au] Autor:Reber LL; Starkl P; Balbino B; Sibilano R; Gaudenzio N; Rogalla S; Sensarn S; Kang D; Raghu H; Sokolove J; Robinson WH; Contag CH; Tsai M; Galli SJ
[Ad] Endereço:Department of Pathology, Stanford University School of Medicine, Stanford, California, United States of America.
[Ti] Título:The tyrosine kinase inhibitor imatinib mesylate suppresses uric acid crystal-induced acute gouty arthritis in mice.
[So] Source:PLoS One;12(10):e0185704, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Gouty arthritis is caused by the deposition of monosodium urate (MSU) crystals in joints. Despite many treatment options for gout, there is a substantial need for alternative treatments for patients unresponsive to current therapies. Tyrosine kinase inhibitors have demonstrated therapeutic benefit in experimental models of antibody-dependent arthritis and in rheumatoid arthritis in humans, but to date, the potential effects of such inhibitors on gouty arthritis has not been evaluated. Here we demonstrate that treatment with the tyrosine kinase inhibitor imatinib mesylate (imatinib) can suppress inflammation induced by injection of MSU crystals into subcutaneous air pouches or into the ankle joint of wild type mice. Moreover, imatinib treatment also largely abolished the lower levels of inflammation which developed in IL-1R1-/- or KitW-sh/W-sh mice, indicating that this drug can inhibit IL-1-independent pathways, as well as mast cell-independent pathways, contributing to pathology in this model. Imatinib treatment not only prevented ankle swelling and synovial inflammation when administered before MSU crystals but also diminished these features when administrated after the injection of MSU crystals, a therapeutic protocol more closely mimicking the clinical situation in which treatment occurs after the development of an acute gout flare. Finally, we also assessed the efficiency of local intra-articular injections of imatinib-loaded poly(lactic-co-glycolic acid) (PLGA) nanoparticles in this model of acute gout. Treatment with low doses of this long-acting imatinib:PLGA formulation was able to reduce ankle swelling in a therapeutic protocol. Altogether, these results raise the possibility that tyrosine kinase inhibitors might have utility in the treatment of acute gout in humans.
[Mh] Termos MeSH primário: Artrite Gotosa/prevenção & controle
Mesilato de Imatinib/farmacologia
Inibidores de Proteínas Quinases/farmacologia
Proteínas Tirosina Quinases/antagonistas & inibidores
Ácido Úrico/efeitos adversos
[Mh] Termos MeSH secundário: Animais
Cristalização
Mesilato de Imatinib/administração & dosagem
Injeções Intraperitoneais
Camundongos
Camundongos Endogâmicos C57BL
Inibidores de Proteínas Quinases/administração & dosagem
Ácido Úrico/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Protein Kinase Inhibitors); 268B43MJ25 (Uric Acid); 8A1O1M485B (Imatinib Mesylate); EC 2.7.10.1 (Protein-Tyrosine Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171006
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185704


  5 / 1061 MEDLINE  
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[PMID]:28874151
[Au] Autor:Lee YM; Shon EJ; Kim OS; Kim DS
[Ad] Endereço:Korean Medicine Convergence Research Division, Korea Institute of Oriental Medicine (KIOM), 1672 Yuseong-daero, Yuseong-gu, Daejeon, 34054, South Korea.
[Ti] Título:Effects of Mollugo pentaphylla extract on monosodium urate crystal-induced gouty arthritis in mice.
[So] Source:BMC Complement Altern Med;17(1):447, 2017 Sep 06.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Gout is an inflammatory condition induced by the deposition of monosodium urate (MSU) crystals in joints and soft tissues, and it can lead to acute or chronic arthritis. MSU are pro-inflammatory stimuli that can initiate, amplify and sustain an intense inflammatory response. In this study, we evaluated the anti-inflammatory effect of an extract of Mollugo pentaphylla (MPE) on MSU-induced gouty arthritis in a mouse model. METHOD: An MSU crystal suspension (4 mg/50 µL) was injected intradermally into the right paw. The mice were orally administered MPE (150 mg/kg or 300 mg/kg) or the positive control drug colchicine (1 mg/kg) 1 h before the MSU crystals were injected and then once daily for 3 days. The effects of MPE included inflammatory paw edema and pain upon weight-bearing activity, and we evaluated the inflammatory cytokine expression and paw tissue inflammation-related gene expression. RESULTS: MPE suppressed inflammatory paw edema and pain in the MSU-induced mice. MPE showed anti-inflammatory activity by inhibiting the production of TNF-α, interleukin (IL)-1ß, NLRP3 inflammasome and NF-κB. CONCLUSION: These results suggest that MPE has potent anti-inflammatory activities and may be useful as a therapeutic agent against gouty arthritis.
[Mh] Termos MeSH primário: Artrite Experimental/tratamento farmacológico
Artrite Gotosa/tratamento farmacológico
Molluginaceae/química
Extratos Vegetais/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Artrite Experimental/induzido quimicamente
Artrite Experimental/fisiopatologia
Artrite Gotosa/induzido quimicamente
Artrite Gotosa/fisiopatologia
Comportamento Animal/efeitos dos fármacos
Citocinas/sangue
Edema/fisiopatologia
/fisiopatologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Medição da Dor
Extratos Vegetais/farmacologia
Ácido Úrico/efeitos adversos
Suporte de Carga
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Plant Extracts); 268B43MJ25 (Uric Acid)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170907
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-017-1955-1


  6 / 1061 MEDLINE  
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[PMID]:28797095
[Au] Autor:Tao JH; Cheng M; Tang JP; Dai XJ; Zhang Y; Li XP; Liu Q; Wang YL
[Ad] Endereço:Department of Rheumatology & Immunology, Anhui Provincial Hospital Affiliated to Anhui Medical University, Hefei, Anhui, China.
[Ti] Título:Single nucleotide polymorphisms associated with P2X7R function regulate the onset of gouty arthritis.
[So] Source:PLoS One;12(8):e0181685, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Gout is an inflammatory disease that is caused by the increased production of Interleukin-1ß (IL-1ß) stimulated by monosodium urate (MSU) crystals. However, some hyperuricemia patients, even gouty patients with tophi in the joints, never experience gout attack, which indicates that pathogenic pathways other than MSU participate in the secretion of IL-1ß in the pathogenesis of acute gouty arthritis. The ATP-P2X7R-IL-1ß axis may be one of these pathways. OBJECTIVE: This study examines the role of Adenosine triphosphate (ATP) in the pathogenesis of gout and the association of ATP receptor (P2X7R) function with single nucleotide polymorphisms and gout arthritis. METHODS: Non-synonymous single nucleotide polymorphisms (SNP) loci of P2X7R in Chinese people were screened to compare the frequencies of different alleles and genotype distribution of selective SNPs in 117 gouty patients and 95 hyperuricemia patients. Peripheral white blood cells were purified from the peripheral blood of 43 randomly selected gout patients and 36 hyperuricemia patients from the total group. Cells were cultured with MSU or MSU + ATP, and supernatants were collected for the detection of IL-1ß concentrations using enzyme-linked immunosorbent assay (ELISA). RESULTS: 1. Eight SNP loci, including rs1653624, rs10160951, rs1718119, rs7958316, rs16950860, rs208294, rs17525809 and rs2230912, were screened and detected, and rs1653624, rs7958316 and rs17525809 were associated with gout arthritis. 2. IL-1ß concentrations in supernatants after MSU + ATP stimulation were significantly higher in gouty patients than in the hyperuricemia group [(131.08 ± 176.11) pg/ml vs. (50.84 ± 86.10) pg/ml]; Patients (including gout and hyperuricemia) carrying the susceptibility genotype AA or AT of rs1653624 exhibited significantly higher concentrations of IL-1ß than patients carrying the non-susceptibility genotype TT [(104.20 ± 164.25) pg/ml vs. (21.90 ± 12.14) pg/ml]; However, no differences were found with MSU stimulation alone. CONCLUSIONS: ATP promotes the pathogenesis of gouty arthritis via increasing the secretion of IL-1 ß, and its receptor (P2X7R) function associated single nucleotide polymorphisms may be related to gouty arthritis, which indicates that ATP-P2X7R signaling pathway plays a significant regulatory role in the pathogenesis of gout.
[Mh] Termos MeSH primário: Artrite Gotosa/genética
Polimorfismo de Nucleotídeo Único
Receptores Purinérgicos P2X7/genética
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/metabolismo
Adulto
Idoso
Artrite Gotosa/sangue
Artrite Gotosa/metabolismo
Feminino
Seres Humanos
Hiperuricemia/sangue
Hiperuricemia/genética
Hiperuricemia/metabolismo
Interleucina-1beta/sangue
Interleucina-1beta/metabolismo
Masculino
Meia-Idade
Receptores Purinérgicos P2X7/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-1beta); 0 (P2XR receptor, human); 0 (Receptors, Purinergic P2X7); 8L70Q75FXE (Adenosine Triphosphate)
[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:170811
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181685


  7 / 1061 MEDLINE  
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[PMID]:28794514
[Au] Autor:Dalbeth N; Bardin T; Doherty M; Lioté F; Richette P; Saag KG; So AK; Stamp LK; Choi HK; Terkeltaub R
[Ad] Endereço:Department of Medicine, University of Auckland, 85 Park Road, Grafton, Auckland 1023, New Zealand.
[Ti] Título:Discordant American College of Physicians and international rheumatology guidelines for gout management: consensus statement of the Gout, Hyperuricemia and Crystal-Associated Disease Network (G-CAN).
[So] Source:Nat Rev Rheumatol;13(9):561-568, 2017 Sep.
[Is] ISSN:1759-4804
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In November 2016, the American College of Physicians (ACP) published a clinical practice guideline on the management of acute and recurrent gout. This guideline differs substantially from the latest guidelines generated by the American College of Rheumatology (ACR), European League Against Rheumatism (EULAR) and 3e (Evidence, Expertise, Exchange) Initiative, despite reviewing largely the same body of evidence. The Gout, Hyperuricemia and Crystal-Associated Disease Network (G-CAN) convened an expert panel to review the methodology and conclusions of these four sets of guidelines and examine possible reasons for discordance between them. The G-CAN position, presented here, is that the fundamental pathophysiological knowledge underlying gout care, and evidence from clinical experience and clinical trials, supports a treat-to-target approach for gout aimed at lowering serum urate levels to below the saturation threshold at which monosodium urate crystals form. This practice, which is truly evidence-based and promotes the steady reduction in tissue urate crystal deposits, is promoted by the ACR, EULAR and 3e Initiative recommendations. By contrast, the ACP does not provide a clear recommendation for urate-lowering therapy (ULT) for patients with frequent, recurrent flares or those with tophi, nor does it recommend monitoring serum urate levels of patients prescribed ULT. Results from emerging clinical trials that have gout symptoms as the primary end point are expected to resolve this debate for all clinicians in the near term future.
[Mh] Termos MeSH primário: Gerenciamento Clínico
Supressores da Gota/uso terapêutico
Gota/tratamento farmacológico
Hiperuricemia/tratamento farmacológico
Guias de Prática Clínica como Assunto
[Mh] Termos MeSH secundário: Artrite Gotosa/diagnóstico
Artrite Gotosa/tratamento farmacológico
Artropatias por Cristais/diagnóstico
Artropatias por Cristais/terapia
Feminino
Gota/diagnóstico
Supressores da Gota/farmacologia
Seres Humanos
Hiperuricemia/diagnóstico
Internacionalidade
Masculino
Sociedades Médicas
Resultado do Tratamento
Estados Unidos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Gout Suppressants)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171110
[Lr] Data última revisão:
171110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170811
[St] Status:MEDLINE
[do] DOI:10.1038/nrrheum.2017.126


  8 / 1061 MEDLINE  
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[PMID]:28623927
[Au] Autor:Jiang Y; Lin Y; Hu YJ; Song XJ; Pan HH; Zhang HJ
[Ad] Endereço:Dispensary of Traditional Chinese Medicine, Hangzhou First People's Hospital, 261 Huansha Road, Hangzhou, 310006, China.
[Ti] Título:Caffeoylquinic acid derivatives rich extract from Gnaphalium pensylvanicum willd. Ameliorates hyperuricemia and acute gouty arthritis in animal model.
[So] Source:BMC Complement Altern Med;17(1):320, 2017 Jun 17.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The Gnaphalium pensylvanicum willd. is used in China as a folk medicine to treat anti-inflammatory, cough and rheumatism arthritis. The aim of this study was to evaluate the potential of the extract of G. pensylvanicum to treat hyperuricemia and acute gouty arthritis in animal model. METHODS: G. pensylvanicum extract was evaluated in an experimental model with potassium oxonate (PO) induced hyperuricemia in mice which was used to evaluate anti-hyperuricemia activity and xanthine oxidase (XO) inhibition. Therapies for acute gouty arthritis was also investigated on monosodium urate (MSU) crystal induced paw edema model. RESULTS: G. pensylvanicum extract showed activity in reducing serum uric acid (Sur) through effect renal glucose transporter 9 (GLUT9), organic anion transporter 1 (OAT1) and urate transporter 1 (URAT1) mainly and inhibited XO activity in vivo of mice with PO induced hyperuricemia. The extract of G. pensylvanicum also showed significant anti-inflammatory activity and reduced the paw swelling on MSU crystal-induced paw edema model. Meanwhile, 13 caffeoylquinic acid derivatives and 1 flavone were identified by UPLC-ESI-MS/MS as the main active component of G. pensylvanicum. CONCLUSIONS: The extract of G. pensylvanicum showed significant effect on evaluated models and therefore may be active agents for the treatment of hyperuricemia and acute gouty arthritis.
[Mh] Termos MeSH primário: Anti-Inflamatórios/administração & dosagem
Artrite Gotosa/tratamento farmacológico
Gnaphalium/química
Supressores da Gota/administração & dosagem
Hiperuricemia/tratamento farmacológico
Extratos Vegetais/administração & dosagem
Ácido Quínico/análogos & derivados
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios/química
Artrite Gotosa/imunologia
Modelos Animais de Doenças
Proteínas Facilitadoras de Transporte de Glucose/genética
Proteínas Facilitadoras de Transporte de Glucose/metabolismo
Supressores da Gota/química
Seres Humanos
Hiperuricemia/genética
Hiperuricemia/imunologia
Rim/efeitos dos fármacos
Rim/metabolismo
Masculino
Camundongos
Fitoterapia
Extratos Vegetais/química
Ácido Quínico/administração & dosagem
Ácido Quínico/química
Ácido Úrico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Glucose Transport Proteins, Facilitative); 0 (Gout Suppressants); 0 (Plant Extracts); 0 (caffeoylquinic acid); 058C04BGYI (Quinic Acid); 268B43MJ25 (Uric Acid)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170821
[Lr] Data última revisão:
170821
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170619
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-017-1834-9


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[PMID]:28445313
[Au] Autor:Huang H; Yu B; Liu W; Lin Q; Chen L; Chen J; Duan L; Shi G
[Ad] Endereço:Department of Rheumatology and Clinical Immunology, The First Affiliated Hospital of Xiamen University, Xiamen, China.
[Ti] Título:Serum apoprotein A1 levels are inversely associated with disease activity in gout: From a southern Chinese Han population.
[So] Source:Medicine (Baltimore);96(17):e6780, 2017 Apr.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:To analyze the alteration of lipid profile and inflammatory markers in the serum of patients with gouty arthritis (GA), the levels of serum lipid profile, C-reactive protein (CRP), and erythrocyte sedimentation rates (ESRs) were measured in the serum of 69 gout patients, 35 patients with rheumatoid arthritis (RA), 23 patients with ankylosing spondylitis (AS)/spondyloarthropathy (SpA), and 25 patients with osteoarthritis (OA). The serum levels of apoprotein A1 (Apo-A1) were significantly decreased in patients with gout when compared with RA, AS/SpA, and OA patients. The serum levels of CRP were significantly increased in gouty patients when compared with RA, AS/SpA, and OA patients. Furthermore, the serum levels of ESR were significantly increased in patients with gout compared to patients with OA. Correlation analysis indicated that the levels of Apo-A1 were negatively correlated with serum ESR and CRP (r = -0.475, P < .001; r = -0.380, P = .001, respectively) in the patients with GA. Taken together, this study gives us a better understanding of the relationships between serum lipid profile and inflammatory markers in gout patients.
[Mh] Termos MeSH primário: Apolipoproteína A-I/sangue
Artrite Gotosa/sangue
[Mh] Termos MeSH secundário: Adulto
Artrite Gotosa/imunologia
Artrite Reumatoide/sangue
Artrite Reumatoide/imunologia
Grupo com Ancestrais do Continente Asiático
Biomarcadores/sangue
Análise Química do Sangue
Sedimentação Sanguínea
Proteína C-Reativa/análise
China
Colesterol/sangue
Feminino
Seres Humanos
Masculino
Meia-Idade
Osteoartrite/sangue
Osteoartrite/imunologia
Índice de Gravidade de Doença
Espondilite Anquilosante/sangue
Espondilite Anquilosante/imunologia
Triglicerídeos/sangue
Ácido Úrico/sangue
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (APOA1 protein, human); 0 (Apolipoprotein A-I); 0 (Biomarkers); 0 (Triglycerides); 268B43MJ25 (Uric Acid); 9007-41-4 (C-Reactive Protein); 97C5T2UQ7J (Cholesterol)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170601
[Lr] Data última revisão:
170601
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170427
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000006780


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[PMID]:28394398
[Au] Autor:Chang WC; Jan Wu YJ; Chung WH; Lee YS; Chin SW; Chen TJ; Chang YS; Chen DY; Hung SI
[Ad] Endereço:Institute of Pharmacology, Program in Molecular Medicine, School of Medicine, National Yang-Ming University, Taipei.
[Ti] Título:Genetic variants of PPAR-gamma coactivator 1B augment NLRP3-mediated inflammation in gouty arthritis.
[So] Source:Rheumatology (Oxford);56(3):457-466, 2017 Mar 01.
[Is] ISSN:1462-0332
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Objective.: Gout is characterized by recurrent attacks of arthritis with hyperuricaemia and urate crystal-induced inflammation. Although urate transporters are known as risk factors, the immunogenetics of gouty inflammation remains unclear. This study aimed to investigate the genetic association between immune/metabolism regulators and gout. Methods.: We enrolled 448 gout patients and 943 population controls from Taiwan; all were Han Chinese. We screened association between gout and 22 variants of candidate genes, including NLRP3 , caspase 1, peroxisome proliferator-activated receptor-γ, proliferator-activated receptor-γ coactivator 1α ( PPARGC1A ) and 1ß ( PPARGC1B ). The association was validated by replication and combined-sample analyses. Functional assays were performed by quantitative PCR, ELISA, siRNA knockdown and transfection using THP-1 cells, peripheral blood mononuclear cells and synovial cells from patients. Results.: Gouty arthritis exhibited significant association with variants of peroxisome PPARGC1B , which included a missense single nucleotide polymorphism, rs45520937 [P = 6.66 × 10 -9 ; odds ratio (95% CI): 1.85 (1.51, 2.28)]. Expression of PPARGC1B and NLRP3 was induced in urate crystal-activated THP-1, peripheral blood mononuclear cells and synovial cells from gout patients in acute stage. siRNA knockdown of PPARGC1B upregulated NLRP3 in urate crystal-activated macrophages. Compared with the wild-type carriers, patients with the risk A allele of rs45520937 showed statistically increased NLRP3 (P = 0.044) and plasma IL-1ß (P = 0.006). Transfection of PPARGC1B cDNA with rs45520937 A allele to macrophages significantly augmented the expression of NLRP3 and IL-1ß. Conclusion.: Genetic variants of PPARGC1B are significantly associated with gout, and a missense single nucleotide polymorphism, rs45520937, augments NLRP3 and IL-1ß expression. These data suggest that variants of PPARGC1B , a regulator of metabolism and inflammation, contribute to the pathogenesis of gouty arthritis.
[Mh] Termos MeSH primário: Artrite Gotosa/genética
Proteínas de Transporte/genética
Caspase 1/genética
Proteína 3 que Contém Domínio de Pirina da Família NLR/genética
PPAR gama/genética
Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/genética
RNA Mensageiro/metabolismo
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Artrite Gotosa/metabolismo
Estudos de Casos e Controles
Linhagem Celular
Ensaio de Imunoadsorção Enzimática
Feminino
Técnicas de Silenciamento de Genes
Variação Genética
Seres Humanos
Interleucina-1beta/genética
Interleucina-1beta/metabolismo
Masculino
Meia-Idade
Monócitos/imunologia
Mutação de Sentido Incorreto
Razão de Chances
Reação em Cadeia da Polimerase
Polimorfismo de Nucleotídeo Único
RNA Interferente Pequeno
Reação em Cadeia da Polimerase em Tempo Real
Sinoviócitos/metabolismo
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
Regulação para Cima
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (IL1B protein, human); 0 (Interleukin-1beta); 0 (NLR Family, Pyrin Domain-Containing 3 Protein); 0 (NLRP3 protein, human); 0 (PPAR gamma); 0 (PPARGC1A protein, human); 0 (PPARGC1B protein, human); 0 (Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha); 0 (RNA, Messenger); 0 (RNA, Small Interfering); 0 (TNF protein, human); 0 (Tumor Necrosis Factor-alpha); EC 3.4.22.36 (Caspase 1)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170802
[Lr] Data última revisão:
170802
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170411
[St] Status:MEDLINE
[do] DOI:10.1093/rheumatology/kew337



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