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[PMID]:29267505
[Au] Autor:Hai W; Ping X; Zhi-Wen Y; Chun Z
[Ad] Endereço:Department of Shanghai East Hospital, Tongji University, Shanghai, China.
[Ti] Título:Therapeutic effect and potential mechanism of pioglitazone in rats with severe acute pancreatitis.
[So] Source:Braz J Med Biol Res;51(2):e6812, 2017 Dec 11.
[Is] ISSN:1414-431X
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Caspase recruitment domain-containing protein 9 (Card9) is located upstream of the nuclear factor kappa B (NF-κB) and p38 mitogen-activated protein kinase (MAPK) inflammatory pathways. This study investigated the therapeutic effect and potential mechanism of pioglitazone in rats with severe acute pancreatitis (SAP). SAP was induced by a retrograde infusion of 5.0% sodium taurocholate into the biliopancreatic duct of Sprague Dawley rats (n=54), which were then treated with pioglitazone. Blood and pancreatic tissues were harvested at 3, 6, and 12 h after SAP induction. Pancreatic pathological damage was evaluated by hematoxylin and eosin staining. Serum amylase, serum pro-inflammatory cytokines, and pancreatic myeloperoxidase (MPO) activities were determined by enzyme-linked immunosorbent assay. The expression of Card9 mRNA and protein in pancreatic tissues was detected by real-time polymerase chain reaction and western blotting. Pioglitazone had a therapeutic effect in treating rats with SAP by decreasing the level of amylase activity, ameliorating pancreatic histological damage, decreasing serum pro-inflammatory cytokine levels and tissue MPO activity, and downregulating the expression of NF-κB, p38MAPK, and Card9 mRNAs and proteins (P<0.05). The present study demonstrated that the inhibition of Card9 expression could reduce the severity of SAP. Card9 has a role in the pathogenic mechanism of SAP.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Pancreatite/tratamento farmacológico
Pancreatite/patologia
Tiazolidinedionas/farmacologia
[Mh] Termos MeSH secundário: Amilases/sangue
Amilases/efeitos dos fármacos
Animais
Anti-Inflamatórios/uso terapêutico
Western Blotting
Proteínas Adaptadoras de Sinalização CARD/análise
Proteínas Adaptadoras de Sinalização CARD/efeitos dos fármacos
Citocinas/sangue
Citocinas/efeitos dos fármacos
Ensaio de Imunoadsorção Enzimática
Masculino
NF-kappa B/análise
Peroxidase/análise
Distribuição Aleatória
Ratos Sprague-Dawley
Reação em Cadeia da Polimerase em Tempo Real
Reprodutibilidade dos Testes
Índice de Gravidade de Doença
Tiazolidinedionas/uso terapêutico
Fatores de Tempo
Resultado do Tratamento
Proteínas Quinases p38 Ativadas por Mitógeno/análise
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (CARD Signaling Adaptor Proteins); 0 (Card9 protein, mouse); 0 (Cytokines); 0 (NF-kappa B); 0 (Thiazolidinediones); EC 1.11.1.7 (Peroxidase); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); EC 3.2.1.- (Amylases); X4OV71U42S (pioglitazone)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE


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[PMID]:29203734
[Au] Autor:Skochko OV; Kaidashev IP
[Ad] Endereço:Department Of Internal Medicine No 3 With Phthisiology, Higher State Educational Establishment Of Ukraine "Ukrainian Medical Stomatological Academy", Poltava, Ukraine.
[Ti] Título:Effect of pioglitazone on insulin resistance, progression of atherosclerosis and clinical course of coronary heart disease.
[So] Source:Wiad Lek;70(5):881-890, 2017.
[Is] ISSN:0043-5147
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Pioglitazone, a medication of thiazolidinedione group, is capable of triggering the peroxisome proliferator-activated receptors (PPAR-γ). Activation of receptor PPAR-γ regulates carbohydrate and lipid metabolism, immune and inflammatory responses in heart tissues. THE AIM: Our aim was to study the effect of pioglitazone on insulin resistance, the clinical course of atherosclerosis and coronary heart disease (CHD). MATERIALS AND METHODS: The study included 43 patients with coronary artery disease. Patients were divided into the main group - 20 patients, in whom pioglitazone (Pioglar, Ranbaxy, India) was included in the combined therapy at a dose of 15 mg 1 time per day in the morning, and the comparison group - 23 patients receiving standard complex drug therapy over 6 months. Patients underwent clinical examination, ultrasound of neck vessels, study of carbohydrate and lipid metabolism. RESULTS: Joining pioglitazone to standard therapy resulted in the reduction of systolic (p<0.05) and diastolic (p<0.05) blood pressure; decrease in the duration of pain attacks (p<0.05); reduction in the frequency of angina attacks (p<0.05); regression of atherosclerosis of the carotid vessels (p<0.05), decrease in the thickness of the intima-media complex (p<0.05). The decline in oral glucose tolerance test (p<0.05), hyperglycemic factor (p<0.05), total cholesterol (p<0.05), and low density lipoproteins (p<0.05) were observed, as well as increased high-density lipoprotein (p<0.05). CONCLUSION: Long-term treatment with pioglitazone at low doses against the background of standard therapy contributes to functional and clinical condition of patients, promotes the prevention of atherosclerosis and reduction of insulin resistance, thereby improving the clinical manifestations of coronary heart disease.
[Mh] Termos MeSH primário: Aterosclerose/tratamento farmacológico
Hipoglicemiantes/administração & dosagem
Resistência à Insulina
Tiazolidinedionas/administração & dosagem
[Mh] Termos MeSH secundário: Idoso
Aterosclerose/diagnóstico por imagem
Fármacos Cardiovasculares/administração & dosagem
Quimioterapia Combinada
Feminino
Seres Humanos
Masculino
Meia-Idade
Resultado do Tratamento
Ultrassonografia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Cardiovascular Agents); 0 (Hypoglycemic Agents); 0 (Thiazolidinediones); X4OV71U42S (pioglitazone)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE


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[PMID]:29489653
[Au] Autor:Xin WX; Fang L; Fang QL; Zheng XW; Ding HY; Huang P
[Ad] Endereço:Laboratory of Clinical Pharmacy.
[Ti] Título:Effect of hypoglycemic agents on survival outcomes of lung cancer patients with diabetes mellitus: A meta-analysis.
[So] Source:Medicine (Baltimore);97(9):e0035, 2018 Mar.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: To assess the association between hypoglycemic agents and prognosis of lung cancer patients with diabetes. METHODS: A comprehensive literature search was performed in PubMed, Web of Science, Embase, and Cochrane Library until May 2017. The search yielded 2593 unique citations, of which 18 articles met inclusion criteria. The hazard ratios (HRs) and 95% confidence intervals (95% CIs) were calculated by a fixed-effects or random-effects model. RESULTS: The pooled HRs favoring metformin users were 0.77 for overall survival (OS) (n = 15, 95% CI: 0.68-0.86) and 0.50 for disease-free survival (n = 5, 95% CI: 0.39-0.64). One study assessed the relationship between metformin and cancer-specific survival (CSS), reporting no significant results. No significant association between insulin and OS (n = 2, HR: 0.95, 95% CI: 0.79-1.13) or CSS (n = 2, HR: 1.03, 95% CI: 0.76-1.41) was noted. One study evaluated association of sulfonylureas with lung cancer survival and reported no clinical benefit (HR: 1.10, 95% CI: 0.87-1.40). One study reported no association of thiazolidinediones with lung cancer survival (HR: 1.04, 95% CI: 0.65-1.66). CONCLUSIONS: This meta-analysis demonstrated that metformin exposure might improve survival outcomes in lung cancer patients with diabetes.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 1/tratamento farmacológico
Diabetes Mellitus Tipo 2/tratamento farmacológico
Hipoglicemiantes/uso terapêutico
Neoplasias Pulmonares/mortalidade
[Mh] Termos MeSH secundário: Seres Humanos
Insulina/uso terapêutico
Metformina/uso terapêutico
Prognóstico
Compostos de Sulfonilureia/uso terapêutico
Tiazolidinedionas/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
0 (Hypoglycemic Agents); 0 (Insulin); 0 (Sulfonylurea Compounds); 0 (Thiazolidinediones); 9100L32L2N (Metformin)
[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:180301
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000010035


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[PMID]:28460464
[Au] Autor:Nazim UM; Moon JH; Lee YJ; Seol JW; Park SY
[Ad] Endereço:Biosafety Research Institute, College of Veterinary Medicine, Chonbuk National University, Iksan, Jeonbuk 54596, South Korea.
[Ti] Título:PPARγ activation by troglitazone enhances human lung cancer cells to TRAIL-induced apoptosis via autophagy flux.
[So] Source:Oncotarget;8(16):26819-26831, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Members of the tumor necrosis factor (TNF) transmembrane cytokine superfamily, such as TNFα and Fas ligand (FasL), play crucial roles in inflammation and immunity. TRAIL is a member of this superfamily with the ability to selectively trigger cancer cell death but does not motive cytotoxicity to most normal cells. Troglitazone are used in the cure of type II diabetes to reduce blood glucose levels and improve the sensitivity of an amount of tissues to insulin. In this study, we revealed that troglitazone could trigger TRAIL-mediated apoptotic cell death in human lung adenocarcinoma cells. Pretreatment of troglitazone induced activation of PPARγ in a dose-dependent manner. In addition conversion of LC3-I to LC3-II and PPARγ was suppressed in the presence of GW9662, a well-characterized PPARγ antagonist. Treatment with troglitazone resulted in a slight increase in conversion rate of LC3-I to LC3-II and significantly decreased p62 expression levels in a dose-dependent manner. This indicates that troglitazone induced autophagy flux activation in human lung cancer cells. Inhibition of autophagy flux applying a specific inhibitor and genetically modified ATG5 siRNA enclosed troglitazone-mediated enhancing effect of TRAIL. These data demonstrated that activation of PPARγ mediated by troglitazone enhances human lung cancer cells to TRAIL-induced apoptosis via autophagy flux and also suggest that troglitazone may be a combination therapeutic target with TRAIL protein in TRAIL-resistant cancer cells.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Autofagia/efeitos dos fármacos
Cromanos/farmacologia
Neoplasias Pulmonares/metabolismo
PPAR gama/agonistas
PPAR gama/metabolismo
Ligante Indutor de Apoptose Relacionado a TNF/farmacologia
Tiazolidinedionas/farmacologia
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chromans); 0 (PPAR gamma); 0 (TNF-Related Apoptosis-Inducing Ligand); 0 (Thiazolidinediones); I66ZZ0ZN0E (troglitazone)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15819


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[PMID]:29441996
[Au] Autor:Ayoub BM; Abdel-Aziz O
[Ti] Título:A guide for using experimental design in chromatographic method development: applied to the analysis of selected anti-diabetic pharmaceutical combinations.
[So] Source:Pharmazie;71(12):683-690, 2016 Dec 01.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:A guide experimental design in chromatographic method development was described and applied successfully to the analysis of different recently approved anti-diabetic pharmaceutical combinations. Enhancement of UHPLC analysis of alogliptin benzoate either with pioglitazone hydrochloride or with metformin hydrochloride was achieved. The optimal chromatographic conditions were not attained by trial and error that requires a large number of experiments. Alternatively, a computer program was used as a systematic optimization strategy for the design of the experiment which accurately predicts the combined effect of different factors simultaneously. Resolution between peaks was studied by the proposed fractional factorial design approach performed by the Minitab® Program using screening and optimization steps. Application of the central composite design was implemented. A Pareto chart was used to exclude the insignificant variables. Linearity ranges were found to be 0.5-40 µg ml-1, 1-20 µg ml-1 and 1-32 µg ml-1 for alogliptin benzoate, pioglitazone hydrochloride and metformin hydrochloride, respectively. The proposed method is applicable for the analysis of six pharmaceutical dosage forms namely, Nesina®, Actos®, Glucophage®, Oseni®, Kazano® and Actoplus MET® tablets.
[Mh] Termos MeSH primário: Cromatografia Líquida de Alta Pressão/métodos
Hipoglicemiantes/análise
[Mh] Termos MeSH secundário: Formas de Dosagem
Combinação de Medicamentos
Desenho de Equipamento
Metformina/análise
Piperidinas/análise
Padrões de Referência
Reprodutibilidade dos Testes
Soluções
Comprimidos/análise
Tiazolidinedionas/análise
Uracila/análogos & derivados
Uracila/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dosage Forms); 0 (Drug Combinations); 0 (Hypoglycemic Agents); 0 (Piperidines); 0 (Solutions); 0 (Tablets); 0 (Thiazolidinediones); 56HH86ZVCT (Uracil); 9100L32L2N (Metformin); JHC049LO86 (alogliptin); X4OV71U42S (pioglitazone)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6095


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[PMID]:28458167
[Au] Autor:Fan TT; Feng XY; Yang YZ; Gao F; Liu Q
[Ad] Endereço:Department of Emergency, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, PR China; Department of Emergency, Chengdu First People's Hospital, Sichuan 610016, PR China.
[Ti] Título:Downregulation of PI3K-γ in a mouse model of sepsis-induced myocardial dysfunction.
[So] Source:Cytokine;96:208-216, 2017 08.
[Is] ISSN:1096-0023
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A key component during sepsis is the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway, of which the PI3K-γ isoform is a major regulator in many inflammatory responses. However, the role of PI3K-γ in the development of sepsis-induced myocardial dysfunction (SIMD) is unknown. In this study, we established a model of SIMD induced by lipopolysaccharide (LPS), subsequently used the selective inhibitor LY294002 and AS605240 to block the effect of PI3K and PI3K-γ, respectively. Cardiac function was evaluated by echocardiography, hearts were obtained for histological and protein expression examinations. ELISA was used to measure the serum levels of tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), cardiac troponin I (cTnI) and heart-type fatty acid binding protein (H-FABP). LPS-treated mice showed an increase to cardiac inflammation, myocardial damage and production of TNF-α, IL-6, NF-κB, cTnI and H-FABP. Administration of AS605240 to LPS-treated mice reduced some patho-physiological characteristics of SIMD and reduced TNF-α, IL-6, cTnI and H-FABP production. However, administration of LY294002 did not improve those same conditions. The results showed that PI3K-γ is likely a crucial element in SIMD by regulating the PI3K/Akt pathway, and become a new marker of myocardial injury. Inhibition of PI3K-γ might be a potential therapeutic target in SIMD.
[Mh] Termos MeSH primário: Cardiomiopatias/metabolismo
Classe II de Fosfatidilinositol 3-Quinases/metabolismo
Sepse/complicações
[Mh] Termos MeSH secundário: Animais
Cardiomiopatias/genética
Cardiomiopatias/fisiopatologia
Cromonas/administração & dosagem
Classe II de Fosfatidilinositol 3-Quinases/genética
Citocinas/sangue
Modelos Animais de Doenças
Regulação para Baixo
Interleucina-6/biossíntese
Lipopolissacarídeos/administração & dosagem
Camundongos
Morfolinas/administração & dosagem
Miocárdio/patologia
Quinoxalinas/administração & dosagem
Quinoxalinas/uso terapêutico
Transdução de Sinais/efeitos dos fármacos
Tiazolidinedionas/administração & dosagem
Tiazolidinedionas/uso terapêutico
Fator de Necrose Tumoral alfa/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (5-quinoxalin-6-ylmethylenethiazolidine-2,4-dione); 0 (Chromones); 0 (Cytokines); 0 (Interleukin-6); 0 (Lipopolysaccharides); 0 (Morpholines); 0 (Quinoxalines); 0 (Thiazolidinediones); 0 (Tumor Necrosis Factor-alpha); 31M2U1DVID (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one); EC 2.7.1.137 (Class II Phosphatidylinositol 3-Kinases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


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[PMID]:29327347
[Au] Autor:Fujii S; Nakamura S; Oda A; Miki H; Tenshin H; Teramachi J; Hiasa M; Bat-Erdene A; Maeda Y; Oura M; Takahashi M; Iwasa M; Endo I; Yoshida S; Aihara KI; Kurahashi K; Harada T; Kagawa K; Nakao M; Sano S; Abe M
[Ad] Endereço:Department of Haematology, Endocrinology and Metabolism, Tokushima University Graduate School, Tokushima, Japan.
[Ti] Título:Unique anti-myeloma activity by thiazolidine-2,4-dione compounds with Pim inhibiting activity.
[So] Source:Br J Haematol;180(2):246-258, 2018 01.
[Is] ISSN:1365-2141
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Proviral Integrations of Moloney virus 2 (PIM2) is overexpressed in multiple myeloma (MM) cells, and regarded as an important therapeutic target. Here, we aimed to validate the therapeutic efficacy of different types of PIM inhibitors against MM cells for their possible clinical application. Intriguingly, the thiazolidine-2,4-dione-family compounds SMI-16a and SMI-4a reduced PIM2 protein levels and impaired MM cell survival preferentially in acidic conditions, in contrast to other types of PIM inhibitors, including AZD1208, CX-6258 and PIM447. SMI-16a also suppressed the drug efflux function of breast cancer resistance protein, minimized the sizes of side populations and reduced in vitro colony-forming capacity and in vivo tumourigenic activity in MM cells, suggesting impairment of their clonogenic capacity. PIM2 is known to be subject to ubiquitination-independent proteasomal degradation. Consistent with this, the proteasome inhibitors bortezomib and carfilzomib increased PIM2 protein levels in MM cells without affecting its mRNA levels. However, SMI-16a mitigated the PIM2 protein increase and cooperatively enhanced anti-MM effects in combination with carfilzomib. Collectively, the thiazolidine-2,4-dione-family compounds SMI-16a and SMI-4a uniquely reduce PIM2 protein in MM cells, which may contribute to their profound efficacy in addition to their immediate kinase inhibition. Their combination with proteasome inhibitors is envisioned.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Mieloma Múltiplo/metabolismo
Proteínas Serina-Treonina Quinases/antagonistas & inibidores
Proteínas Proto-Oncogênicas/antagonistas & inibidores
Tiazolidinedionas/farmacologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Transformação Celular Neoplásica/efeitos dos fármacos
Modelos Animais de Doenças
Seres Humanos
Concentração de Íons de Hidrogênio
Camundongos
Mieloma Múltiplo/tratamento farmacológico
Mieloma Múltiplo/patologia
Inibidores de Proteassoma/farmacologia
Proteínas Serina-Treonina Quinases/metabolismo
Proteólise
Proteínas Proto-Oncogênicas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (PIM2 protein, human); 0 (Proteasome Inhibitors); 0 (Proto-Oncogene Proteins); 0 (Thiazolidinediones); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180113
[St] Status:MEDLINE
[do] DOI:10.1111/bjh.15033


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Registro de Ensaios Clínicos
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[PMID]:29246363
[Au] Autor:Gidding SS; Bacha F; Bjornstad P; Levitt Katz LE; Levitsky LL; Lynch J; Tryggestad JB; Weinstock RS; El Ghormli L; Lima JAC; TODAY Study Group
[Ad] Endereço:Nemours Cardiac Center, Alfred I. DuPont Hospital for Children, Wilmington, DE.
[Ti] Título:Cardiac Biomarkers in Youth with Type 2 Diabetes Mellitus: Results from the TODAY Study.
[So] Source:J Pediatr;192:86-92.e5, 2018 Jan.
[Is] ISSN:1097-6833
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: To examine cardiac biomarkers over time in youth-onset type 2 diabetes, and relate serum concentrations to cardiovascular disease risk factors, and left ventricular structure and function. STUDY DESIGN: TODAY (Treatment Options for type 2 Diabetes in Adolescents and Youth) was a multicenter randomized trial of 3 treatments including 521 participants with type 2 diabetes, aged 10-17 years, and with 2-6 years of follow-up. Participants were 36% male, obese, and ethnically diverse. Annual serum concentrations of brain natriuretic peptide, troponin, tumor necrosis factor (TNF)-α, receptors 1 and 2 were related to blood pressure, body mass index, hemoglobin A1c, and left ventricular ejection fraction, diastolic function, relative wall thickness, and mass. RESULTS: Elevated concentrations of brain natriuretic peptide (≥100 pg/mL), TNF-α (≥5.6 pg/mL) and troponin (≥0.01 ng/mL), were present in 17.8%, 18.3%, and 34.2% of the cohort, respectively, at baseline, and in 15.4%, 17.1%, and 31.1% at the end of the study, with wide variability over time, without persistence in individuals or clear relationship to glycemia or cardiovascular structure/function. TNF receptors concentrations were increased at baseline and not significantly different from end-of-study concentrations. Adverse echocardiographic measures were more likely in the highest TNF receptor tertile (all P < .05): higher left ventricular mass (39.3 ± 9.0 g/m ), left atrial internal dimension (3.7 ± 0.4 cm) and E/Em ratio, a measure of diastolic dysfunction (6.2 ± 1.9). After adjustment for body mass index, these relationships were no longer significant. CONCLUSIONS: Elevated serum concentrations of cardiac biomarkers were common in youth with type 2 diabetes, but their clinical significance is unclear and will require further long-term study. TRIAL REGISTRATION: ClinicalTrials.govNCT00081328.
[Mh] Termos MeSH primário: Biomarcadores/sangue
Doenças Cardiovasculares/etiologia
Diabetes Mellitus Tipo 2/complicações
Diabetes Mellitus Tipo 2/terapia
[Mh] Termos MeSH secundário: Adolescente
Doenças Cardiovasculares/sangue
Doenças Cardiovasculares/diagnóstico por imagem
Doenças Cardiovasculares/fisiopatologia
Criança
Terapia Combinada
Diabetes Mellitus Tipo 2/sangue
Diabetes Mellitus Tipo 2/fisiopatologia
Dietoterapia
Quimioterapia Combinada
Ecocardiografia
Terapia por Exercício
Feminino
Seguimentos
Ventrículos do Coração/diagnóstico por imagem
Ventrículos do Coração/fisiopatologia
Seres Humanos
Hipoglicemiantes/uso terapêutico
Masculino
Metformina/uso terapêutico
Fatores de Risco
Tiazolidinedionas/uso terapêutico
Resultado do Tratamento
Função Ventricular Esquerda
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Biomarkers); 0 (Hypoglycemic Agents); 0 (Thiazolidinediones); 05V02F2KDG (rosiglitazone); 9100L32L2N (Metformin)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171217
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE


  9 / 10681 MEDLINE  
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[PMID]:28458350
[Au] Autor:Li H; Ying H; Hu A; Hu Y; Li D
[Ad] Endereço:Department of Liver Disease, Ningbo No. 2 Hospital.
[Ti] Título:Therapeutic Effect of Gypenosides on Nonalcoholic Steatohepatitis via Regulating Hepatic Lipogenesis and Fatty Acid Oxidation.
[So] Source:Biol Pharm Bull;40(5):650-657, 2017.
[Is] ISSN:1347-5215
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Nonalcoholic steatohepatitis (NASH) is the most frequent cause of liver dysfunction and a common global problem. Gypenosides can decrease pathological modifications of high-fat diet-induced rat atherosclerosis; however, its effect and mechanism on NASH remain unclear. In this study, rats were randomly divided into normal control and model groups. Model rats were fed with a high-fat diet and treated with gypenosides, rosiglitazone, or water for 6 weeks. We found that liver tissues showed significant hepatic steatosis and vacuolar degeneration with significantly higher triglyceride (TG), free fatty acid (FFA) and malonyl CoA, serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and gamma-glutamyl transferase (GGT) activities in model group versus normal control group (p<0.01). Liver tissue mRNA and protein levels of sterol regulatory element binding protein-1c (SREBP-1c), carbohydrate response element binding protein (ChREBP), acetyl-CoA carboxylase (ACCase), and stearoyl CoA desaturase enzyme 1 (SCD1) were significantly increased, while the carnitine palmitoyl transferase-1 (CPT-1) level was significantly decreased in the model group versus the normal control group (p<0.01). Pathological changes of hepatic steatosis; body weight and liver wet weight; liver tissue TG, FFA and malonyl CoA concentrations; serum ALT, AST and GGT activities; liver tissue mRNA and protein levels of SREBP-1c, ChREBP, ACCase, and SCD-1 were significantly decreased; protein and mRNA levels of CPT-1 were significantly increased in the gypenosides group versus model group (p<0.01). In conclusion, gypenosides has therapeutic effect on NASH through regulating key transcriptional factors and lipogenic enzymes involved in fatty acid oxidation during hepatic lipogenesis.
[Mh] Termos MeSH primário: Ácidos Graxos/metabolismo
Lipogênese/efeitos dos fármacos
Fígado/metabolismo
Hepatopatia Gordurosa não Alcoólica/tratamento farmacológico
Hepatopatia Gordurosa não Alcoólica/metabolismo
[Mh] Termos MeSH secundário: Animais
Peso Corporal
Dieta Hiperlipídica/efeitos adversos
Gynostemma
Fígado/efeitos dos fármacos
Fígado/patologia
Testes de Função Hepática
Masculino
Hepatopatia Gordurosa não Alcoólica/patologia
Tamanho do Órgão
Oxirredução
Extratos Vegetais/uso terapêutico
Ratos
Ratos Sprague-Dawley
Tiazolidinedionas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fatty Acids); 0 (Plant Extracts); 0 (Thiazolidinediones); 0 (gypenoside); 05V02F2KDG (rosiglitazone)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1248/bpb.b16-00942


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[PMID]:28458349
[Au] Autor:Matsutani T; Tamura K; Kutsukake M; Matsuda A; Tachikawa E; Uchida E
[Ad] Endereço:Department of Gastrointestinal and Hepato-Biliary-Pancreatic Surgery, Nippon Medical School.
[Ti] Título:Impact of Pioglitazone on Macrophage Dynamics in Adipose Tissues of Cecal Ligation and Puncture-Treated Mice.
[So] Source:Biol Pharm Bull;40(5):638-644, 2017.
[Is] ISSN:1347-5215
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Pioglitazone improves sepsis-induced organ injury accompanied with anti-inflammatory effects on visceral adipose tissue. However, its action in adipose immune cells remains to be ascertained. We investigated the effects of pioglitazone on visceral adipose macrophage population and polarisation in cecal ligation and puncture (CLP)-induced sepsis mice. Eight-week-old male mice were assigned to 3 groups: 1) sham-operated group, 2) CLP group, or 3) pioglitazone-treated CLP group. Pioglitazone (10 mg/kg) was injected intraperitonally for 7 d and CLP surgery was performed. Visceral adipose tissues were collected 24 h after the surgery. mRNA expression of several macrophage markers (inducible nitric oxide synthase (iNOS) for M1, arginase1 (Arg1) and interleukin (IL)-10 for M2, CD163 and F4/80 for mature macrophages) and inflammatory adipokines (IL-6, monocyte chemoattractant protein-1: MCP-1) was quantified by real-time RT-PCR. Tissue sections were subjected to the immunohistochemical analysis and the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) assay. CLP significantly enhanced Arg1, IL-10 and iNOS mRNA expressions as compared with the sham group, and pioglitazone significantly increased the mRNA level of CD163 and F4/80 in CLP mice. Expression of IL-6 and MCP-1 stimulated by CLP was reduced by pioglitazone treatment. Increased CD11b/c- and CD163-positive cells as well as apoptotic cells were observed in the CLP group and the pioglitazone-treated group. The data indicate that M1/M2 macrophage activation of visceral adipose tissues is induced in CLP-induced mice, and the function of macrophages recruited from surrounding organs may be modulated by pioglitazone treatment.
[Mh] Termos MeSH primário: Hipoglicemiantes/farmacologia
Gordura Intra-Abdominal/patologia
Macrófagos/efeitos dos fármacos
Sepse/patologia
Tiazolidinedionas/farmacologia
[Mh] Termos MeSH secundário: Adipocinas/metabolismo
Animais
Arginase/análise
Biomarcadores/análise
Ceco
Quimiocina CCL2/metabolismo
Hipoglicemiantes/administração & dosagem
Injeções Intraperitoneais
Interleucina-10/sangue
Ligadura
Masculino
Camundongos
Punções
Tiazolidinedionas/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adipokines); 0 (Biomarkers); 0 (Ccl2 protein, mouse); 0 (Chemokine CCL2); 0 (Hypoglycemic Agents); 0 (IL10 protein, mouse); 0 (Thiazolidinediones); 130068-27-8 (Interleukin-10); EC 3.5.3.1 (Arg1 protein, mouse); EC 3.5.3.1 (Arginase); X4OV71U42S (pioglitazone)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1248/bpb.b16-00883



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