Base de dados : MEDLINE
Pesquisa : C14.280.647.500 [Categoria DeCS]
Referências encontradas : 148251 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 14826 ir para página                         

  1 / 148251 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28464839
[Au] Autor:Pavlic K; Perme MP
[Ad] Endereço:University of Ljubljana, Faculty of Medicine, Institute for Biostatistics and Medical Informatics, Vrazov trg 2, Ljubljana, 1000, Slovenia.
[Ti] Título:On comparison of net survival curves.
[So] Source:BMC Med Res Methodol;17(1):79, 2017 May 02.
[Is] ISSN:1471-2288
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Relative survival analysis is a subfield of survival analysis where competing risks data are observed, but the causes of death are unknown. A first step in the analysis of such data is usually the estimation of a net survival curve, possibly followed by regression modelling. Recently, a log-rank type test for comparison of net survival curves has been introduced and the goal of this paper is to explore its properties and put this methodological advance into the context of the field. METHODS: We build on the association between the log-rank test and the univariate or stratified Cox model and show the analogy in the relative survival setting. We study the properties of the methods using both the theoretical arguments as well as simulations. We provide an R function to enable practical usage of the log-rank type test. RESULTS: Both the log-rank type test and its model alternatives perform satisfactory under the null, even if the correlation between their p-values is rather low, implying that both approaches cannot be used simultaneously. The stratified version has a higher power in case of non-homogeneous hazards, but also carries a different interpretation. CONCLUSIONS: The log-rank type test and its stratified version can be interpreted in the same way as the results of an analogous semi-parametric additive regression model despite the fact that no direct theoretical link can be established between the test statistics.
[Mh] Termos MeSH primário: Infarto do Miocárdio/mortalidade
[Mh] Termos MeSH secundário: Fatores Etários
Idoso
Simulação por Computador
Interpretação Estatística de Dados
Feminino
Seres Humanos
Masculino
Meia-Idade
Modelos de Riscos Proporcionais
Análise de Regressão
Risco
Fatores Sexuais
Análise de Sobrevida
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1186/s12874-017-0351-3


  2 / 148251 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29268650
[Au] Autor:Quitt J; Fassl J
[Ad] Endereço:1 Departement für Anästhesiologie, operative Intensivmedizin, Schmerztherapie und präklinische Notfallmedizin, Universitätsspital Basel, Basel.
[Ti] Título:Kardiovaskuläres Risiko..
[So] Source:Ther Umsch;74(7):351-360, 2017.
[Is] ISSN:0040-5930
[Cp] País de publicação:Switzerland
[La] Idioma:ger
[Mh] Termos MeSH primário: Testes de Função Cardíaca/métodos
Monitorização Intraoperatória/métodos
Infarto do Miocárdio/diagnóstico
Infarto do Miocárdio/prevenção & controle
Assistência Perioperatória/métodos
Complicações Pós-Operatórias/diagnóstico
Complicações Pós-Operatórias/prevenção & controle
[Mh] Termos MeSH secundário: Medicina Baseada em Evidências
Seres Humanos
Prognóstico
Medição de Risco/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[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:171223
[St] Status:MEDLINE
[do] DOI:10.1024/0040-5930/a000926


  3 / 148251 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28453729
[Au] Autor:Chen Z; Xie J; Hao H; Lin H; Wang L; Zhang Y; Chen L; Cao S; Huang X; Liao W; Bin J; Liao Y
[Ad] Endereço:State Key Laboratory of Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, 1838, Guangzhou Avenue North, Guangzhou 510515, China.
[Ti] Título:Ablation of periostin inhibits post-infarction myocardial regeneration in neonatal mice mediated by the phosphatidylinositol 3 kinase/glycogen synthase kinase 3ß/cyclin D1 signalling pathway.
[So] Source:Cardiovasc Res;113(6):620-632, 2017 May 01.
[Is] ISSN:1755-3245
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Aims: To resolve the controversy as to whether periostin plays a role in myocardial regeneration after myocardial infarction (MI), we created a neonatal mouse model of MI to investigate the influence of periostin ablation on myocardial regeneration and clarify the underlying mechanisms. Methods and results: Neonatal periostin-knockout mice and their wildtype littermates were subjected to MI or sham surgery. In the wildtype mice after MI, fibrosis was detectable at 3 days and fibrotic tissue was completely replaced by regenerated myocardium at 21 days. In contrast, in the knockout mice, significant fibrosis in the infarcted area was present at even 3 weeks after MI. Levels of phosphorylated-histone 3 and aurora B in the myocardium, detected by immunofluorescence and western blotting, were significantly lower in knockout than in wildtype mice at 7 days after MI. Similarly, angiogenesis was decreased in the knockout mice after MI. Expression of both the endothelial marker CD-31 and α-smooth muscle actin was markedly lower in the knockout than in wildtype mice at 7 days after MI. The knockout MI group had elevated levels of glycogen synthase kinase (GSK) 3ß and decreased phosphatidylinositol 3-kinase (PI3K), phosphorylated serine/threonine protein kinase B (p-Akt), and cyclin D1, compared with the wildtype MI group. Similar effects were observed in experiments using cultured cardiomyocytes from neonatal wildtype or periostin knockout mice. Administration of SB216763, a GSK3ß inhibitor, to knockout neonatal mice decreased myocardial fibrosis and increased angiogenesis in the infarcted area after MI. Conclusion: Ablation of periostin suppresses post-infarction myocardial regeneration by inhibiting the PI3K/GSK3ß/cyclin D1 signalling pathway, indicating that periostin is essential for myocardial regeneration.
[Mh] Termos MeSH primário: Moléculas de Adesão Celular/deficiência
Ciclina D1/metabolismo
Infarto do Miocárdio/enzimologia
Miocárdio/enzimologia
Fosfatidilinositol 3-Quinase/metabolismo
Regeneração
Proteínas Repressoras/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Moléculas de Adesão Celular/genética
Células Cultivadas
Modelos Animais de Doenças
Fibrose
Camundongos Knockout
Infarto do Miocárdio/genética
Infarto do Miocárdio/patologia
Infarto do Miocárdio/fisiopatologia
Miocárdio/patologia
Neovascularização Fisiológica
Fosforilação
Inibidores de Proteínas Quinases/farmacologia
Proteínas Proto-Oncogênicas c-akt/metabolismo
Regeneração/efeitos dos fármacos
Proteínas Repressoras/antagonistas & inibidores
Transdução de Sinais/efeitos dos fármacos
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ccnd1 protein, mouse); 0 (Cell Adhesion Molecules); 0 (GSKIP protein, mouse); 0 (Postn protein, mouse); 0 (Protein Kinase Inhibitors); 0 (Repressor Proteins); 136601-57-5 (Cyclin D1); EC 2.7.1.137 (Phosphatidylinositol 3-Kinase); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/cvr/cvx001


  4 / 148251 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28453728
[Au] Autor:Vincent A; Sportouch C; Covinhes A; Barrère C; Gallot L; Delgado-Betancourt V; Lattuca B; Solecki K; Boisguérin P; Piot C; Nargeot J; Barrère-Lemaire S
[Ad] Endereço:IGF, CNRS, INSERM, Univ. Montpellier, F-34094 Montpellier, France.
[Ti] Título:Cardiac mGluR1 metabotropic receptors in cardioprotection.
[So] Source:Cardiovasc Res;113(6):644-655, 2017 May 01.
[Is] ISSN:1755-3245
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Aims: In a previous study using a genome-wide microarray strategy, we identified metabotropic glutamate receptor 1 (mGluR1) as a putative cardioprotective candidate in ischaemic postconditioning (PostC). In the present study, we investigated the role of cardiac mGluR1 receptors during cardioprotection against myocardial ischaemia-reperfusion injury in the mouse myocardium. Methods and results: mGluR1 activation by glutamate administered 5 min before reperfusion in C57Bl/6 mice subjected to a myocardial ischaemia protocol strongly decreased both infarct size and DNA fragmentation measured at 24 h reperfusion. This cardioprotective effect was mimicked by the mGluR1 agonist, DHPG (10 µM), and abolished when glutamate was coinjected with the mGluR1 antagonist YM298198 (100 nM). Wortmannin (100 nM), an inhibitor of PI3-kinase, was able to prevent glutamate-induced cardioprotection. A glutamate bolus at the onset of reperfusion failed to protect the heart of mGluR1 knockout mice subjected to a myocardial ischaemia-reperfusion protocol, although PostC still protected the mGluR1 KO mice. Glutamate-treatment improved post-infarction functional recovery as evidenced by an echocardiographic study performed 15 days after treatment and by a histological evaluation of fibrosis 21 days post-treatment. Interestingly, restoration of functional mGluR1s by a PostC stimulus was evidenced at the transcriptional level. Since mGluR1s were localized at the surface membrane of cardiomyocytes, they might contribute to the cardioprotective effect of ischaemic PostC as other Gq-coupled receptors. Conclusion: This study provides the first demonstration that mGluR1 activation at the onset of reperfusion induces cardioprotection and might represent a putative strategy to prevent ischaemia-reperfusion injury.
[Mh] Termos MeSH primário: Agonistas de Aminoácidos Excitatórios/administração & dosagem
Glutamina/administração & dosagem
Infarto do Miocárdio/prevenção & controle
Traumatismo por Reperfusão Miocárdica/prevenção & controle
Miocárdio/metabolismo
Receptores de Glutamato Metabotrópico/agonistas
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Antagonistas de Aminoácidos Excitatórios/farmacologia
Predisposição Genética para Doença
Camundongos Endogâmicos C57BL
Camundongos Knockout
Infarto do Miocárdio/metabolismo
Infarto do Miocárdio/patologia
Infarto do Miocárdio/fisiopatologia
Traumatismo por Reperfusão Miocárdica/metabolismo
Traumatismo por Reperfusão Miocárdica/patologia
Traumatismo por Reperfusão Miocárdica/fisiopatologia
Miocárdio/patologia
Fenótipo
Fosfatidilinositol 3-Quinase/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Receptores de Glutamato Metabotrópico/deficiência
Receptores de Glutamato Metabotrópico/genética
Transdução de Sinais
Fatores de Tempo
Função Ventricular Esquerda/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Excitatory Amino Acid Agonists); 0 (Excitatory Amino Acid Antagonists); 0 (Receptors, Metabotropic Glutamate); 0 (metabotropic glutamate receptor type 1); 0RH81L854J (Glutamine); EC 2.7.1.137 (Phosphatidylinositol 3-Kinase); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/cvr/cvx024


  5 / 148251 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29397593
[Au] Autor:Committee of Cardio-Cerebro-Vascular Diseases of Gerontological Society of China; Working Group of Chinese Expert Consensus on the Use of Xuezhikang
[Ti] Título:[Chinese expert consensus on the use of Xuezhikang (2017 revised edition)].
[So] Source:Zhonghua Nei Ke Za Zhi;57(2):97-100, 2018 Feb 01.
[Is] ISSN:0578-1426
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:Xuezhikang, a Chinese traditional medicine, contains natural statin and is effective on dyslipidemia by inhibiting cholesterol synthesis. Xuezhikang therapy for 8 weeks in patients with hyperlipidemia reduced total cholesterol (TC) by 23%, low density lipoprotein cholesterol (LDL-C) by 28.5% and triglyceride(TG) by 36.5%, and increased high density lipoprotein cholesterol (HDL-C) by 19.6%, respectively. Data from China Coronary Secondary Prevention Study (CCSPS) showed that treatment with Xuezhikang lowered the risks of major coronary events, death from coronary heart disease, and all cause death in patients with myocardial infarction, indicating that Xuezhikang can be used in the primary and secondary prevention of cardiovascular disease.
[Mh] Termos MeSH primário: Consenso
Medicamentos de Ervas Chinesas/uso terapêutico
Dislipidemias/tratamento farmacológico
Inibidores de Hidroximetilglutaril-CoA Redutases/uso terapêutico
[Mh] Termos MeSH secundário: Grupo com Ancestrais do Continente Asiático
Causas de Morte
China
LDL-Colesterol
Seres Humanos
Infarto do Miocárdio
Prevenção Secundária
Triglicerídeos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cholesterol, LDL); 0 (Drugs, Chinese Herbal); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Triglycerides); 0 (xuezhikang)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180206
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0578-1426.2018.02.003


  6 / 148251 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29295976
[Au] Autor:Liu CY; Zhang YH; Li RB; Zhou LY; An T; Zhang RC; Zhai M; Huang Y; Yan KW; Dong YH; Ponnusamy M; Shan C; Xu S; Wang Q; Zhang YH; Zhang J; Wang K
[Ad] Endereço:Center for Developmental Cardiology, Institute for Translational Medicine, College of Medicine, Qingdao University, Qingdao, 266021, China.
[Ti] Título:LncRNA CAIF inhibits autophagy and attenuates myocardial infarction by blocking p53-mediated myocardin transcription.
[So] Source:Nat Commun;9(1):29, 2018 01 02.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Increasing evidence suggests that long noncoding RNAs (lncRNAs) play crucial roles in various biological processes. However, little is known about the effects of lncRNAs on autophagy. Here we report that a lncRNA, termed cardiac autophagy inhibitory factor (CAIF), suppresses cardiac autophagy and attenuates myocardial infarction by targeting p53-mediated myocardin transcription. Myocardin expression is upregulated upon H O and ischemia/reperfusion, and knockdown of myocardin inhibits autophagy and attenuates myocardial infarction. p53 regulates cardiomyocytes autophagy and myocardial ischemia/reperfusion injury by regulating myocardin expression. CAIF directly binds to p53 protein and blocks p53-mediated myocardin transcription, which results in the decrease of myocardin expression. Collectively, our data reveal a novel CAIF-p53-myocardin axis as a critical regulator in cardiomyocyte autophagy, which will be potential therapeutic targets in treatment of defective autophagy-associated cardiovascular diseases.
[Mh] Termos MeSH primário: Autofagia/genética
Infarto do Miocárdio/genética
Proteínas Nucleares/genética
RNA Longo não Codificante/genética
Transativadores/genética
Ativação Transcricional
Proteína Supressora de Tumor p53/genética
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Células Cultivadas
Camundongos
Infarto do Miocárdio/patologia
Traumatismo por Reperfusão Miocárdica/genética
Traumatismo por Reperfusão Miocárdica/metabolismo
Miócitos Cardíacos/metabolismo
Proteínas Nucleares/metabolismo
Ligação Proteica
Interferência de RNA
RNA Longo não Codificante/metabolismo
Transativadores/metabolismo
Proteína Supressora de Tumor p53/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Nuclear Proteins); 0 (RNA, Long Noncoding); 0 (Trans-Activators); 0 (Tumor Suppressor Protein p53); 0 (myocardin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180104
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02280-y


  7 / 148251 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29286056
[Au] Autor:Zaid Iskandar M; Lang CC
[Ad] Endereço:Ninewells Hospital and Medical School, Dundee, Scotland, UK.
[Ti] Título:Sacubitril and valsartan fixed combination to reduce heart failure events in post-acute myocardial infarction patients.
[So] Source:Drugs Today (Barc);53(10):545-551, 2017 Oct.
[Is] ISSN:1699-3993
[Cp] País de publicação:Spain
[La] Idioma:eng
[Ab] Resumo:Heart failure is a term used to define a constellation of symptoms and signs that are commonly attributed to the inability of the heart to produce a cardiac output that meets the demands of the body. It remains a deadly disease, affecting between 1-2% of the population, and is more common in the elderly, with around 6-10% of patients over 65 suffering from the condition. Sacubitril/valsartan (LCZ-696) is a combined neprilysin inhibitor and angiotensin AT1 receptor blocker approved in recent years for the treatment of chronic heart failure with reduced ejection fraction. In an area where there have been limited pharmacological advances in the last 10 years, this drug was a game changer and a much welcomed addition to contemporary heart failure therapy. It is currently being studied in patients with heart failure with preserved ejection fraction and for the reduction of heart failure events post-acute myocardial infarction. Results from the ongoing PARADISE-MI study are awaited by the global cardiology community with great interest.
[Mh] Termos MeSH primário: Aminobutiratos/administração & dosagem
Bloqueadores do Receptor Tipo 1 de Angiotensina II/administração & dosagem
Insuficiência Cardíaca/tratamento farmacológico
Infarto do Miocárdio/complicações
Neprilisina/antagonistas & inibidores
Tetrazóis/administração & dosagem
Valsartana/administração & dosagem
[Mh] Termos MeSH secundário: Aminobutiratos/farmacologia
Ensaios Clínicos como Assunto
Seres Humanos
Tetrazóis/farmacologia
Valsartana/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Aminobutyrates); 0 (Angiotensin II Type 1 Receptor Blockers); 0 (LCZ 696); 0 (Tetrazoles); 80M03YXJ7I (Valsartan); EC 3.4.24.11 (Neprilysin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171230
[St] Status:MEDLINE
[do] DOI:10.1358/dot.2017.53.10.2722396


  8 / 148251 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29231026
[Au] Autor:Song RY; Ding RT; Cui W
[Ad] Endereço:Medical College of Qingdao University, Qingdao 266000, China.
[Ti] Título:[Impact of Myocardial Infarction and Abnormalities of Cardiac Conduction System on Sudden Cardiac Death].
[So] Source:Fa Yi Xue Za Zhi;33(2):171-174, 2017 Apr.
[Is] ISSN:1004-5619
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:Sudden cardiac death (SCD), most commonly seen in coronary heart disease, is a kind of sudden death caused by series of cardiac parameters, which usually combines with myocardial infarction. However, some SCDs (including early myocardial infarction) happen suddenly and cause death in a very short time. In these circumstances, typical morphological changes are lack in macroscopic or microscopic fields, which make such SCDs become the emphasis and difficulty in the present research. SCD caused by myocardial infarction and abnormalities of cardiac conduction system (CCS) is related to atherosclerosis of coronary artery closely. This paper reviews cardiac dysfunction caused by myocardial infarction and diseases of CCS from morphology and molecular biology, and explores potential relationship between them. This paper aims to provide clues to the mechanism of myocardial infarction related sudden death and possible assistance for forensic diagnosis of SCD.
[Mh] Termos MeSH primário: Morte Súbita Cardíaca
Sistema de Condução Cardíaco/fisiopatologia
Infarto do Miocárdio/complicações
[Mh] Termos MeSH secundário: Doença das Coronárias
Morte Súbita Cardíaca/etiologia
Seres Humanos
Infarto do Miocárdio/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171213
[St] Status:MEDLINE
[do] DOI:10.3969/j.issn.1004-5619.2017.02.014


  9 / 148251 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28468789
[Au] Autor:Bobi J; Solanes N; Fernández-Jiménez R; Galán-Arriola C; Dantas AP; Fernández-Friera L; Gálvez-Montón C; Rigol-Monzó E; Agüero J; Ramírez J; Roqué M; Bayés-Genís A; Sánchez-González J; García-Álvarez A; Sabaté M; Roura S; Ibáñez B; Rigol M
[Ad] Endereço:August Pi i Sunyer Biomedical Research Institute (IDIBAPS), Institut de Malalties Cardiovasculars, Hospital Clínic de Barcelona, Universitat de Barcelona, Spain.
[Ti] Título:Intracoronary Administration of Allogeneic Adipose Tissue-Derived Mesenchymal Stem Cells Improves Myocardial Perfusion But Not Left Ventricle Function, in a Translational Model of Acute Myocardial Infarction.
[So] Source:J Am Heart Assoc;6(5), 2017 May 03.
[Is] ISSN:2047-9980
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Autologous adipose tissue-derived mesenchymal stem cells (ATMSCs) therapy is a promising strategy to improve post-myocardial infarction outcomes. In a porcine model of acute myocardial infarction, we studied the long-term effects and the mechanisms involved in allogeneic ATMSCs administration on myocardial performance. METHODS AND RESULTS: Thirty-eight pigs underwent 50 minutes of coronary occlusion; the study was completed in 33 pigs. After reperfusion, allogeneic ATMSCs or culture medium (vehicle) were intracoronarily administered. Follow-ups were performed at short (2 days after acute myocardial infarction vehicle-treated, n=10; ATMSCs-treated, n=9) or long term (60 days after acute myocardial infarction vehicle-treated, n=7; ATMSCs-treated, n=7). At short term, infarcted myocardium analysis showed reduced apoptosis in the ATMSCs-treated animals (48.6±6% versus 55.9±5.7% in vehicle; =0.017); enhancement of the reparative process with up-regulated vascular endothelial growth factor, granulocyte macrophage colony-stimulating factor, and stromal-derived factor-1α gene expression; and increased M2 macrophages (67.2±10% versus 54.7±10.2% in vehicle; =0.016). In long-term groups, increase in myocardial perfusion at the anterior infarct border was observed both on day-7 and day-60 cardiac magnetic resonance studies in ATMSCs-treated animals, compared to vehicle (87.9±28.7 versus 57.4±17.7 mL/min per gram at 7 days; =0.034 and 99±22.6 versus 43.3±14.7 22.6 mL/min per gram at 60 days; =0.0001, respectively). At day 60, higher vascular density was detected at the border zone in the ATMSCs-treated animals (118±18 versus 92.4±24.3 vessels/mm in vehicle; =0.045). Cardiac magnetic resonance-measured left ventricular ejection fraction of left ventricular volumes was not different between groups at any time point. CONCLUSIONS: In this porcine acute myocardial infarction model, allogeneic ATMSCs-based therapy was associated with increased cardioprotective and reparative mechanisms and with better cardiac magnetic resonance-measured perfusion. No effect on left ventricular volumes or ejection fraction was observed.
[Mh] Termos MeSH primário: Tecido Adiposo/citologia
Circulação Coronária
Transplante de Células-Tronco Mesenquimais/métodos
Células Mesenquimais Estromais
Infarto do Miocárdio/cirurgia
Disfunção Ventricular Esquerda/cirurgia
Função Ventricular Esquerda
[Mh] Termos MeSH secundário: Proteínas Angiogênicas/metabolismo
Animais
Células Cultivadas
Angiografia por Tomografia Computadorizada
Angiografia Coronária/métodos
Citocinas/metabolismo
Modelos Animais de Doenças
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/metabolismo
Imagem por Ressonância Magnética
Masculino
Transplante de Células-Tronco Mesenquimais/efeitos adversos
Células Mesenquimais Estromais/metabolismo
Tomografia Computadorizada Multidetectores
Infarto do Miocárdio/diagnóstico por imagem
Infarto do Miocárdio/metabolismo
Infarto do Miocárdio/fisiopatologia
Miocárdio/metabolismo
Miocárdio/patologia
Neovascularização Fisiológica
Imagem de Perfusão/métodos
Recuperação de Função Fisiológica
Regeneração
Sus scrofa
Fatores de Tempo
Transfecção
Transplante Homólogo
Disfunção Ventricular Esquerda/diagnóstico por imagem
Disfunção Ventricular Esquerda/metabolismo
Disfunção Ventricular Esquerda/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiogenic Proteins); 0 (Cytokines); 147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE


  10 / 148251 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28468783
[Au] Autor:Ramirez FD; Chen Y; Di Santo P; Simard T; Motazedian P; Hibbert B
[Ad] Endereço:Division of Cardiology, University of Ottawa Heart Institute, Ottawa, Ontario, Canada.
[Ti] Título:Association Between Self-Reported Potentially Modifiable Cardiac Risk Factors and Perceived Need to Improve Physical Health: A Population-Based Study.
[So] Source:J Am Heart Assoc;6(5), 2017 May 03.
[Is] ISSN:2047-9980
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: An individual's perceived need to improve their physical health (PNIPH) is an essential precursor to adopting healthy behaviors. Nine potentially modifiable risk factors (PMRFs) for myocardial infarction collectively account for ≥90% of the population attributable risk. Though widely recognized, their impact on individuals' health perceptions is unclear. METHODS AND RESULTS: Residents from 6 provinces were administered a module on changes to improve health as part of the 2011-2012 Canadian Community Health Survey, yielding relevant data for 8 of the 9 PMRFs sought. The potential effects of PMRFs individually and cumulatively on PNIPH were examined using modified Poisson regression. In total, 45 443 respondents were included, representing 11 006 123 individuals and corresponding to 96.8% of the adult population of the sampled provinces. The sum of PMRFs was positively associated with PNIPH (adjusted prevalence ratio, 1.08; 95% CI, 1.07-1.09 per additional PMRF) with 82.3% of individuals with ≥5 PMRFs reporting this perception. Smoking, obesity, and low physical activity were most strongly associated with PNIPH, whereas hypertension and diabetes mellitus exhibited no association with this outcome after adjusting for potential confounders. Barriers to adopting healthy behaviors were reported by 55.9% of individuals endorsing PNIPH. CONCLUSIONS: The cumulative burden of PMRFs is positively associated with PNIPH; however, individual PMRFs differentially contribute to this perception. Among those at highest cardiac risk, ≈1 in 5 denied PNIPH. A better understanding of factors underlying health perceptions and behaviors is needed to capitalize on cardiovascular preventive efforts.
[Mh] Termos MeSH primário: Comportamentos Relacionados com a Saúde
Conhecimentos, Atitudes e Prática em Saúde
Estilo de Vida Saudável
Infarto do Miocárdio/prevenção & controle
Percepção
Comportamento de Redução do Risco
Autorrelato
[Mh] Termos MeSH secundário: Adolescente
Adulto
Canadá/epidemiologia
Comorbidade
Estudos Transversais
Exercício
Feminino
Nível de Saúde
Inquéritos Epidemiológicos
Dieta Saudável
Seres Humanos
Masculino
Meia-Idade
Infarto do Miocárdio/diagnóstico
Infarto do Miocárdio/epidemiologia
Infarto do Miocárdio/psicologia
Valor Preditivo dos Testes
Prevalência
Fatores de Proteção
Medição de Risco
Fatores de Risco
Estilo de Vida Sedentário
Fumar/efeitos adversos
Fumar/epidemiologia
Abandono do Hábito de Fumar
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE



página 1 de 14826 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

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