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[PMID]:28450380
[Au] Autor:Pahuja NK; Shetty R; Deshmukh R; Sharma A; Nuijts RMMA; Jhanji V; Sethu S; Ghosh A
[Ad] Endereço:Cornea and Refractive Services, Narayana Nethralaya, Bangalore, India.
[Ti] Título:In vivo confocal microscopy and tear cytokine analysis in post-LASIK ectasia.
[So] Source:Br J Ophthalmol;101(12):1604-1610, 2017 12.
[Is] ISSN:1468-2079
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:AIM: Corneal keratectasia is one of the complications associated with laser in situ keratomileusis (LASIK) that results in vision impairment. The pathogenesis of post-LASIK ectasia (PLE) remains underexplored. We report the tear cytokine profile and in vivo confocal microscopy (IVCM) findings in eyes with PLE. METHODS: This retrospective study included age-matched 7 (14 eyes) post-LASIK controls (PLCs) and 6 (12 eyes) PLE subjects. Corneal topography was used to categorise the subjects into PLC and PLE groups. Ocular Surface Disease Index (OSDI) scores obtained were based on standard questionnaire and IVCM images were used to determine corneal dendritic cells density (DCD) and sub-basal nerve plexus morphology. Inflammatory cytokines/chemokines in the tears were quantified using flow cytometry based cytometric bead array. RESULTS: Pentacam-based scores, OSDI scores and corneal DCD were significantly (p<0.05) higher in patients with PLE compared with PLC. Discomfort-related subscale of OSDI score exhibited a positive correlation with total corneal DCD in the PLE cohort. The fold difference of chemokine (C-C motif) ligand/monocyte chemotactic protein-1 (CCL2/MCP1) (3.4±0.6) was found to be significantly (p<0.05) higher in the PLE cohorts and a positive correlation between CCL2/MCP1 levels and total corneal DCD was also observed in the PLE cohort. CONCLUSION: The current study found a significant difference in the tear film cytokine profile between normal and PLE eyes. Presence of increased corneal dendritic cells and altered tear cytokines suggests an ongoing inflammatory response in PLE.
[Mh] Termos MeSH primário: Córnea/patologia
Doenças da Córnea/diagnóstico
Citocinas/metabolismo
Ceratomileuse Assistida por Excimer Laser In Situ/efeitos adversos
Microscopia Confocal/métodos
Complicações Pós-Operatórias
Lágrimas/metabolismo
[Mh] Termos MeSH secundário: Adulto
Córnea/metabolismo
Doenças da Córnea/etiologia
Doenças da Córnea/metabolismo
Topografia da Córnea
Dilatação Patológica
Feminino
Citometria de Fluxo
Seguimentos
Seres Humanos
Masculino
Miopia/fisiopatologia
Miopia/cirurgia
Estudos Prospectivos
Refração Ocular
Estudos Retrospectivos
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cytokines)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180203
[Lr] Data última revisão:
180203
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1136/bjophthalmol-2016-309142


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[PMID]:28468757
[Au] Autor:Franken R; Teixido-Tura G; Brion M; Forteza A; Rodriguez-Palomares J; Gutierrez L; Garcia Dorado D; Pals G; Mulder BJ; Evangelista A
[Ad] Endereço:Servei de Cardiologia, Unitat de Marfan, Hospital Universitari, Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain.
[Ti] Título:Relationship between fibrillin-1 genotype and severity of cardiovascular involvement in Marfan syndrome.
[So] Source:Heart;103(22):1795-1799, 2017 11.
[Is] ISSN:1468-201X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The effect of mutation type on the severity of cardiovascular manifestations in patients with Marfan syndrome (MFS) has been reported with disparity results. OBJECTIVES: This study aims to determine the impact of the mutation type on aortic diameters, aortic dilation rates and on cardiovascular events (ie, aortic dissection and cardiovascular mortality). METHODS: MFS patients with a pathogenic mutation followed at two specialised units were included. mutations were classified as being dominant negative (DN; incorporation of non-mutated and mutated fibrillin-1 in the extracellular matrix) or having haploinsufficiency (HI; only incorporation of non-mutated fibrillin-1, thus a decreased amount of fibrillin-1 protein). Aortic diameters and the aortic dilation rate at the level of the aortic root, ascending aorta, arch, descending thoracic aorta and abdominal aorta by echocardiography and clinical endpoints comprising dissection and death were compared between HI and DN patients. RESULTS: Two hundred and ninety patients with MFS were included: 113 (39%) with an HI- mutation and 177 (61%) with a DN- . At baseline, patients with HI- had a larger aortic root diameter than patients with DN- (HI: 39.3±7.2 mm vs DN: 37.3±6.8 mm, p=0.022), with no differences in age or body surface area. After a mean follow-up of 4.9±2.0 years, aortic root and ascending dilation rates were increased in patients with HI- (HI: 0.57±0.8 vs DN: 0.28±0.5 mm/year, p=0.004 and HI: 0.59±0.9 vs DN: 0.30±0.7 mm/year, p=0.032, respectively). Furthermore, patients with HI- tended to be at increased risk for the combined endpoint of dissection and death compared with patients with DN- (HR: 3.3, 95% CI 1.0 to 11.4, p=0.060). CONCLUSIONS: Patients with an HI mutation had a more severely affected aortic phenotype, with larger aortic root diameters and a more rapid dilation rate, and tended to have an increased risk of death and dissections compared with patients with a DN mutation.
[Mh] Termos MeSH primário: Aneurisma Dissecante/genética
Aorta/patologia
Aneurisma Aórtico/genética
Fibrilina-1/genética
Síndrome de Marfan/genética
Mutação
[Mh] Termos MeSH secundário: Adolescente
Adulto
Aneurisma Dissecante/diagnóstico por imagem
Aneurisma Dissecante/metabolismo
Aorta/diagnóstico por imagem
Aneurisma Aórtico/diagnóstico por imagem
Aneurisma Aórtico/mortalidade
Análise Mutacional de DNA
Dilatação Patológica
Progressão da Doença
Ecocardiografia
Feminino
Predisposição Genética para Doença
Haploinsuficiência
Seres Humanos
Masculino
Síndrome de Marfan/complicações
Síndrome de Marfan/diagnóstico
Síndrome de Marfan/mortalidade
Meia-Idade
Fenótipo
Valor Preditivo dos Testes
Prognóstico
Estudos Retrospectivos
Fatores de Risco
Índice de Gravidade de Doença
Espanha
Fatores de Tempo
Adulto Jovem
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; MULTICENTER STUDY; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (FBN1 protein, human); 0 (Fibrillin-1)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180127
[Lr] Data última revisão:
180127
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1136/heartjnl-2016-310631


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[PMID]:29222122
[Au] Autor:Qazi S; Massaro JM; Chuang ML; D'Agostino RB; Hoffmann U; O'Donnell CJ
[Ad] Endereço:From the National Heart, Lung and Blood Institute's Framingham Heart Study, MA (S.Q., J.M.M., M.L.C., R.B.D., U.H., C.J.O.); Department of Biostatistics, Boston University School of Public Health, MA (J.M.M., R.B.D.); Cardiovascular Imaging Core Laboratory, Beth Israel Deaconess Medical Center, Bost
[Ti] Título:Increased Aortic Diameters on Multidetector Computed Tomographic Scan Are Independent Predictors of Incident Adverse Cardiovascular Events: The Framingham Heart Study.
[So] Source:Circ Cardiovasc Imaging;10(12), 2017 Dec.
[Is] ISSN:1942-0080
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Adverse aortic remodeling, such as dilation, is associated with multiple cardiovascular disease (CVD) risk factors. We sought to determine whether measures of enlarged aortic diameters improve prediction of incident adverse CVD events above standard CVD risk factors in a community-dwelling cohort. METHODS AND RESULTS: Participants from the Framingham Offspring and Third Generation Cohorts (n=3318; aged 48.9±10.3 years), who underwent noncontrast thoracic and abdominal multidetector computed tomography during 2002 to 2005, had complete risk factor profiles, and were free of clinical CVD, were included in this study. Diameters were measured at 4 anatomically defined locations: the ascending thoracic aorta, descending thoracic aorta, the infrarenal abdominal aorta, and lower abdominal aorta. Adverse events comprised CVD death, myocardial infarction, coronary insufficiency, index admission for heart failure, and stroke. Each aortic segment was dichotomized as enlarged (diameter ≥upper 90th percentile for age, sex, and body surface area) or not enlarged; the hazard of an adverse event for an enlarged segment was determined using multivariable-adjusted Cox proportional hazards models. Over a mean 8.8±2.0 years of follow-up, there were 177 incident adverse CVD events. In models adjusted for traditional CVD risk factors, enlarged infrarenal abdominal aorta (hazard ratio=1.57; 95% confidence interval=1.06 to 2.32) and lower abdominal aorta (hazard ratio=1.53; 95% confidence interval=1.00 to 2.34) were associated with an increased hazard of CVD events. Enlarged ascending thoracic aorta and descending thoracic aorta were not significantly associated with CVD events. CONCLUSIONS: Among community-dwelling adults initially free of clinical CVD, enlarged infrarenal abdominal aorta and lower abdominal aorta, on noncontrast multidetector computed tomography scans, are independent predictors of incident adverse CVD events above traditional risk factors alone.
[Mh] Termos MeSH primário: Aorta Abdominal/diagnóstico por imagem
Aorta Torácica/diagnóstico por imagem
Doenças da Aorta/diagnóstico por imagem
Aortografia/métodos
Angiografia por Tomografia Computadorizada
Tomografia Computadorizada Multidetectores
[Mh] Termos MeSH secundário: Adulto
Aorta Abdominal/patologia
Aorta Torácica/patologia
Doenças da Aorta/epidemiologia
Doenças da Aorta/patologia
Dilatação Patológica
Progressão da Doença
Intervalo Livre de Doença
Feminino
Seres Humanos
Incidência
Estimativa de Kaplan-Meier
Masculino
Massachusetts/epidemiologia
Meia-Idade
Análise Multivariada
Valor Preditivo dos Testes
Modelos de Riscos Proporcionais
Medição de Risco
Fatores de Risco
Fatores de Tempo
Remodelação Vascular
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171220
[Lr] Data última revisão:
171220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171210
[St] Status:MEDLINE


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[PMID]:28982723
[Au] Autor:Fernandez-García CE; Tarin C; Roldan-Montero R; Martinez-Lopez D; Torres-Fonseca M; Lindhot JS; Vega de Ceniga M; Egido J; Lopez-Andres N; Blanco-Colio LM; Martín-Ventura JL
[Ad] Endereço:Vascular Research Lab, FIIS-Fundación Jiménez Díaz-Autonoma University, Madrid, Spain.
[Ti] Título:Increased galectin-3 levels are associated with abdominal aortic aneurysm progression and inhibition of galectin-3 decreases elastase-induced AAA development.
[So] Source:Clin Sci (Lond);131(22):2707-2719, 2017 Nov 15.
[Is] ISSN:1470-8736
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Abdominal aortic aneurysm (AAA) evolution is unpredictable and no specific treatment exists for AAA, except surgery to prevent aortic rupture. Galectin-3 has been previously associated with CVD, but its potential role in AAA has not been addressed. Galectin-3 levels were increased in the plasma of AAA patients ( =225) compared with the control group ( =100). In addition, galectin-3 concentrations were associated with the need for surgical repair, independently of potential confounding factors. Galectin-3 mRNA and protein expression were increased in human AAA samples compared with healthy aortas. Experimental AAA in mice was induced via aortic elastase perfusion. Mice were treated intravenously with the galectin-3 inhibitor modified citrus pectin (MCP, 10 mg/kg, every other day) or saline. Similar to humans, galectin-3 serum and aortic mRNA levels were also increased in elastase-induced AAA mice compared with control mice. Mice treated with MCP showed decreased aortic dilation, as well as elastin degradation, vascular smooth muscle cell (VSMC) loss, and macrophage content at day 14 postelastase perfusion compared with control mice. The underlying mechanism(s) of the protective effect of MCP was associated with a decrease in galectin-3 and cytokine (mainly CCL5) mRNA and protein expression. Interestingly, galectin-3 induced CCL5 expression by a mechanism involving STAT3 activation in VSMC. Accordingly, MCP treatment decreased STAT3 phosphorylation in elastase-induced AAA. In conclusion, increased galectin-3 levels are associated with AAA progression, while galectin-3 inhibition decreased experimental AAA development. Our data suggest the potential role of galectin-3 as a therapeutic target in AAA.
[Mh] Termos MeSH primário: Aorta Abdominal/efeitos dos fármacos
Aneurisma da Aorta Abdominal/prevenção & controle
Galectina 3/antagonistas & inibidores
Galectina 3/sangue
Elastase Pancreática
Pectinas/farmacologia
[Mh] Termos MeSH secundário: Animais
Aorta Abdominal/enzimologia
Aorta Abdominal/patologia
Aneurisma da Aorta Abdominal/sangue
Aneurisma da Aorta Abdominal/enzimologia
Aneurisma da Aorta Abdominal/patologia
Estudos de Casos e Controles
Células Cultivadas
Quimiocina CCL5/genética
Quimiocina CCL5/metabolismo
Dilatação Patológica
Modelos Animais de Doenças
Progressão da Doença
Galectina 3/genética
Galectina 3/metabolismo
Seres Humanos
Camundongos Endogâmicos C57BL
Músculo Liso Vascular/efeitos dos fármacos
Músculo Liso Vascular/metabolismo
Miócitos de Músculo Liso/efeitos dos fármacos
Miócitos de Músculo Liso/metabolismo
Fosforilação
RNA Mensageiro/sangue
RNA Mensageiro/genética
Fator de Transcrição STAT3/metabolismo
Transdução de Sinais/efeitos dos fármacos
Fatores de Tempo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ccl5 protein, mouse); 0 (Chemokine CCL5); 0 (Galectin 3); 0 (Lgals3 protein, mouse); 0 (Pectins); 0 (RNA, Messenger); 0 (STAT3 Transcription Factor); 0 (Stat3 protein, mouse); 0 (citrus pectin); 0 (galectin-3, human); EC 3.4.21.36 (Pancreatic Elastase)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171007
[St] Status:MEDLINE
[do] DOI:10.1042/CS20171142


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[PMID]:28935757
[Au] Autor:Moran CS; Biros E; Krishna SM; Wang Y; Tikellis C; Morton SK; Moxon JV; Cooper ME; Norman PE; Burrell LM; Thomas MC; Golledge J
[Ad] Endereço:From the Vascular Biology Unit, Queensland Research Centre for Peripheral Vascular Disease, College of Medicine and Dentistry, James Cook University, Townsville, Australia (C.S.M., E.B., S.M.K., S.K.M., J.V.M., J.G.); School of Applied and Biomedical Sciences, Faculty of Science and Technology, Fede
[Ti] Título:Resveratrol Inhibits Growth of Experimental Abdominal Aortic Aneurysm Associated With Upregulation of Angiotensin-Converting Enzyme 2.
[So] Source:Arterioscler Thromb Vasc Biol;37(11):2195-2203, 2017 Nov.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Recent evidence suggests an important role for angiotensin-converting enzyme 2 (ACE2) in limiting abdominal aortic aneurysm (AAA). This study examined the effect of ACE2 deficiency on AAA development and the efficacy of resveratrol to upregulate ACE2 in experimental AAA. APPROACH AND RESULTS: deletion in apolipoprotein-deficient mice ( ) resulted in increased aortic diameter and spontaneous aneurysm of the suprarenal aorta associated with increased expression of inflammation and proteolytic enzyme markers. In humans, serum ACE2 activity was negatively associated with AAA diagnosis. expression was lower in infrarenal biopsies of patients with AAA than organ donors. AAA was more severe in mice compared with controls in 2 experimental models. Resveratrol (0.05/100-g chow) inhibited growth of pre-established AAAs in mice fed high-fat chow and infused with angiotensin II continuously for 56 days. Reduced suprarenal aorta dilatation in mice receiving resveratrol was associated with elevated serum ACE2 and increased suprarenal aorta tissue levels of ACE2 and sirtuin 1 activity. In addition, the relative phosphorylation of Akt and ERK (extracellular signal-regulated kinase) 1/2 within suprarenal aorta tissue and gene expression for nuclear factor of kappa light polypeptide gene enhancer in B cells 1, angiotensin type-1 receptor, and metallopeptidase 2 and 9 were significantly reduced. Upregulation of ACE2 in human aortic smooth muscle cells by resveratrol in vitro was sirtuin 1-dependent. CONCLUSIONS: This study provides experimental evidence of an important role for ACE2 in limiting AAA development and growth. Resveratrol upregulated ACE2 and inhibited AAA growth in a mouse model.
[Mh] Termos MeSH primário: Aorta Abdominal/efeitos dos fármacos
Aneurisma da Aorta Abdominal/prevenção & controle
Ruptura Aórtica/prevenção & controle
Peptidil Dipeptidase A/deficiência
Estilbenos/farmacologia
[Mh] Termos MeSH secundário: Angiotensina II
Animais
Aorta Abdominal/enzimologia
Aorta Abdominal/patologia
Aneurisma da Aorta Abdominal/enzimologia
Aneurisma da Aorta Abdominal/genética
Aneurisma da Aorta Abdominal/patologia
Ruptura Aórtica/enzimologia
Ruptura Aórtica/genética
Ruptura Aórtica/patologia
Apolipoproteínas E/deficiência
Apolipoproteínas E/genética
Células Cultivadas
Dieta Hiperlipídica
Dilatação Patológica
Modelos Animais de Doenças
Indução Enzimática
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Predisposição Genética para Doença
Seres Humanos
Mediadores da Inflamação/metabolismo
Camundongos Knockout
Músculo Liso Vascular/efeitos dos fármacos
Músculo Liso Vascular/enzimologia
Músculo Liso Vascular/patologia
Miócitos de Músculo Liso/efeitos dos fármacos
Miócitos de Músculo Liso/metabolismo
Miócitos de Músculo Liso/patologia
Subunidade p50 de NF-kappa B/metabolismo
Peptidil Dipeptidase A/biossíntese
Peptidil Dipeptidase A/genética
Fenótipo
Fosforilação
Proteínas Proto-Oncogênicas c-akt/metabolismo
Sirtuína 1/metabolismo
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoproteins E); 0 (Inflammation Mediators); 0 (NF-kappa B p50 Subunit); 0 (Stilbenes); 11128-99-7 (Angiotensin II); 147257-52-1 (Nfkb1 protein, mouse); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 3.4.15.1 (Peptidyl-Dipeptidase A); EC 3.4.17.- (angiotensin converting enzyme 2); EC 3.5.1.- (Sirt1 protein, mouse); EC 3.5.1.- (Sirtuin 1); Q369O8926L (resveratrol)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.310129


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[PMID]:28912363
[Au] Autor:Lareyre F; Clément M; Raffort J; Pohlod S; Patel M; Esposito B; Master L; Finigan A; Vandestienne M; Stergiopulos N; Taleb S; Trachet B; Mallat Z
[Ad] Endereço:From the Division of Cardiovascular Medicine, University of Cambridge, UK (F.L., M.C., J.R., M.P., L.M., A.F., Z.M.); Université Côte d'Azur, Centre National de la Recherche Scientifique, Institut National de la Sante et de la Recherche Medicale, Institute for Research on Cancer and Aging in Nice, F
[Ti] Título:TGFß (Transforming Growth Factor-ß) Blockade Induces a Human-Like Disease in a Nondissecting Mouse Model of Abdominal Aortic Aneurysm.
[So] Source:Arterioscler Thromb Vasc Biol;37(11):2171-2181, 2017 Nov.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Current experimental models of abdominal aortic aneurysm (AAA) do not accurately reproduce the major features of human AAA. We hypothesized that blockade of TGFß (transforming growth factor-ß) activity-a guardian of vascular integrity and immune homeostasis-would impair vascular healing in models of nondissecting AAA and would lead to sustained aneurysmal growth until rupture. APPROACH AND RESULTS: Here, we test this hypothesis in the elastase-induced AAA model in mice. We analyze AAA development and progression using ultrasound in vivo, synchrotron-based ultrahigh resolution imaging ex vivo, and a combination of biological, histological, and flow cytometry-based cellular and molecular approaches in vitro. Systemic blockade of TGFß using a monoclonal antibody induces a transition from a self-contained aortic dilatation to a model of sustained aneurysmal growth, associated with the formation of an intraluminal thrombus. AAA growth is associated with wall disruption but no medial dissection and culminates in fatal transmural aortic wall rupture. TGFß blockade enhances leukocyte infiltration both in the aortic wall and the intraluminal thrombus and aggravates extracellular matrix degradation. Early blockade of IL-1ß or monocyte-dependent responses substantially limits AAA severity. However, blockade of IL-1ß after disease initiation has no effect on AAA progression to rupture. CONCLUSIONS: Endogenous TGFß activity is required for the healing of AAA. TGFß blockade may be harnessed to generate new models of AAA with better relevance to the human disease. We expect that the new models will improve our understanding of the pathophysiology of AAA and will be useful in the identification of new therapeutic targets.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/toxicidade
Aorta Abdominal/efeitos dos fármacos
Aneurisma da Aorta Abdominal/induzido quimicamente
Ruptura Aórtica/induzido quimicamente
Elastase Pancreática
Fator de Crescimento Transformador beta/antagonistas & inibidores
Remodelação Vascular/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Aorta Abdominal/imunologia
Aorta Abdominal/metabolismo
Aorta Abdominal/patologia
Aneurisma da Aorta Abdominal/imunologia
Aneurisma da Aorta Abdominal/metabolismo
Aneurisma da Aorta Abdominal/patologia
Ruptura Aórtica/imunologia
Ruptura Aórtica/metabolismo
Ruptura Aórtica/patologia
Apolipoproteínas E/genética
Apolipoproteínas E/metabolismo
Quimiotaxia de Leucócito/efeitos dos fármacos
Dilatação Patológica
Modelos Animais de Doenças
Progressão da Doença
Matriz Extracelular/efeitos dos fármacos
Matriz Extracelular/metabolismo
Matriz Extracelular/patologia
Interleucina-1beta/metabolismo
Cinética
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Síncrotrons
Trombose/induzido quimicamente
Trombose/metabolismo
Trombose/patologia
Fator de Crescimento Transformador beta/imunologia
Fator de Crescimento Transformador beta/metabolismo
Ultrassonografia
Cicatrização/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Apolipoproteins E); 0 (IL1B protein, mouse); 0 (Interleukin-1beta); 0 (Transforming Growth Factor beta); EC 3.4.21.36 (Pancreatic Elastase)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170916
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309999


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[PMID]:28882868
[Au] Autor:Nakao T; Horie T; Baba O; Nishiga M; Nishino T; Izuhara M; Kuwabara Y; Nishi H; Usami S; Nakazeki F; Ide Y; Koyama S; Kimura M; Sowa N; Ohno S; Aoki H; Hasegawa K; Sakamoto K; Minatoya K; Kimura T; Ono K
[Ad] Endereço:From the Departments of Cardiovascular Medicine (T.N., T.H., O.B., M.N., T.N., M.I., Y.K., H.N., S.U., F.N., Y.I., S.K., M.K., N.S., T.K., K.O.) and Cardiovascular Surgery (K.S., K.M.), Graduate School of Medicine, Kyoto University, Japan; The Cardiovascular Research Institute, Kurume University, Ja
[Ti] Título:Genetic Ablation of MicroRNA-33 Attenuates Inflammation and Abdominal Aortic Aneurysm Formation via Several Anti-Inflammatory Pathways.
[So] Source:Arterioscler Thromb Vasc Biol;37(11):2161-2170, 2017 Nov.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Abdominal aortic aneurysm (AAA) is an increasingly prevalent and ultimately fatal disease with no effective pharmacological treatment. Because matrix degradation induced by vascular inflammation is the major pathophysiology of AAA, attenuation of this inflammation may improve its outcome. Previous studies suggested that miR-33 (microRNA-33) inhibition and genetic ablation of miR-33 increased serum high-density lipoprotein cholesterol and attenuated atherosclerosis. APPROACH AND RESULTS: MiR-33a-5p expression in central zone of human AAA was higher than marginal zone. MiR-33 deletion attenuated AAA formation in both mouse models of angiotensin II- and calcium chloride-induced AAA. Reduced macrophage accumulation and monocyte chemotactic protein-1 expression were observed in calcium chloride-induced AAA walls in miR-33 mice. In vitro experiments revealed that peritoneal macrophages from miR-33 mice showed reduced matrix metalloproteinase 9 expression levels via c-Jun N-terminal kinase inactivation. Primary aortic vascular smooth muscle cells from miR-33 mice showed reduced monocyte chemotactic protein-1 expression by p38 mitogen-activated protein kinase attenuation. Both of the inactivation of c-Jun N-terminal kinase and p38 mitogen-activated protein kinase were possibly because of the increase of ATP-binding cassette transporter A1 that is a well-known target of miR-33. Moreover, high-density lipoprotein cholesterol derived from miR-33 mice reduced expression of matrix metalloproteinase 9 in macrophages and monocyte chemotactic protein-1 in vascular smooth muscle cells. Bone marrow transplantation experiments indicated that miR-33-deficient bone marrow cells ameliorated AAA formation in wild-type recipients. MiR-33 deficiency in recipient mice was also shown to contribute the inhibition of AAA formation. CONCLUSIONS: These data strongly suggest that inhibition of miR-33 will be effective as a novel strategy for treating AAA.
[Mh] Termos MeSH primário: Aorta Abdominal/metabolismo
Aneurisma da Aorta Abdominal/prevenção & controle
Aortite/prevenção & controle
Mediadores da Inflamação/metabolismo
MicroRNAs/metabolismo
[Mh] Termos MeSH secundário: Angiotensina II
Animais
Aorta Abdominal/patologia
Aneurisma da Aorta Abdominal/induzido quimicamente
Aneurisma da Aorta Abdominal/genética
Aneurisma da Aorta Abdominal/metabolismo
Aortite/induzido quimicamente
Aortite/genética
Aortite/metabolismo
Apolipoproteínas E/deficiência
Apolipoproteínas E/genética
Transplante de Medula Óssea
Cloreto de Cálcio
Linhagem Celular
Quimiocina CCL2/metabolismo
HDL-Colesterol/sangue
Dilatação Patológica
Modelos Animais de Doenças
Feminino
Predisposição Genética para Doença
Seres Humanos
Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo
Macrófagos Peritoneais/metabolismo
Macrófagos Peritoneais/patologia
Masculino
Metaloproteinase 9 da Matriz/metabolismo
Camundongos Endogâmicos C57BL
Camundongos Knockout
MicroRNAs/genética
Músculo Liso Vascular/metabolismo
Músculo Liso Vascular/patologia
Miócitos de Músculo Liso/metabolismo
Miócitos de Músculo Liso/patologia
Fenótipo
Transdução de Sinais
Fatores de Tempo
Transfecção
Remodelação Vascular
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoproteins E); 0 (Ccl2 protein, mouse); 0 (Chemokine CCL2); 0 (Cholesterol, HDL); 0 (Inflammation Mediators); 0 (MIRN33 microRNA, human); 0 (MicroRNAs); 0 (Mirn33 microRNA, mouse); 11128-99-7 (Angiotensin II); EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); EC 3.4.24.35 (Matrix Metalloproteinase 9); EC 3.4.24.35 (Mmp9 protein, mouse); M4I0D6VV5M (Calcium Chloride)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309768


  8 / 9704 MEDLINE  
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[PMID]:28837731
[Au] Autor:Li J; Ren J; Yip YWY; Zhang X; Chu KO; Ng TK; Chan SO; Pang CP; Chu WK
[Ad] Endereço:Department of Ophthalmology & Visual Sciences, The Chinese University of Hong Kong, Hong Kong, People's Republic of China.
[Ti] Título:Quantitative Characterization of Autoimmune Uveoretinitis in an Experimental Mouse Model.
[So] Source:Invest Ophthalmol Vis Sci;58(10):4193-4200, 2017 Aug 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: To accurately evaluate the autoimmune inflammation, we aim to develop three quantitative measurements to monitor the inflammatory changes in the retina: retinal-choroidal thickness, major retinal vessel diameter, and electroretinography amplitudes. Methods: During a 21-day experimental period, eyes were examined by confocal scanning laser ophthalmoscopy, optical coherence tomography, fundus fluorescein angiography, and electroretinography in living mice, which were then subsequently killed for histologic assessments. Results: On day 21 postimmunization, inflammation was observed both in vivo and in vitro. Fold change of retinal-choroidal thickness and major retinal vessel diameter in experimental autoimmune uveoretinitis mice were significantly greater than controls (P < 0.001). Both scotopic and photopic electroretinography amplitudes were significantly attenuated when compared with control mice (P < 0.01). Our results showed that these three quantifiable indicators provided an objective and accurate evaluation of autoimmune inflammation, which are in good correlations with the reported clinical and histopathologic scoring systems (P < 0.05). Conclusions: These three indicators will be useful to detect the small but significant differences in the severity of experimental autoimmune uveoretinitis for future longitudinally therapeutic studies.
[Mh] Termos MeSH primário: Doenças Autoimunes/diagnóstico
Modelos Animais de Doenças
Retina/fisiopatologia
Vasos Retinianos/patologia
Retinite/diagnóstico
Uveíte/diagnóstico
[Mh] Termos MeSH secundário: Animais
Autoantígenos
Doenças Autoimunes/imunologia
Doenças Autoimunes/fisiopatologia
Permeabilidade Capilar
Dilatação Patológica
Eletrorretinografia
Proteínas do Olho
Feminino
Angiofluoresceinografia
Camundongos
Camundongos Endogâmicos C57BL
Oligopeptídeos
Oftalmoscopia
Retinite/imunologia
Retinite/fisiopatologia
Proteínas de Ligação ao Retinol
Uveíte/imunologia
Uveíte/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantigens); 0 (Eye Proteins); 0 (Oligopeptides); 0 (Retinol-Binding Proteins); 0 (interstitial retinol-binding protein)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170904
[Lr] Data última revisão:
170904
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170825
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.17-22436


  9 / 9704 MEDLINE  
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[PMID]:28784055
[Au] Autor:Zybulewski A; Shukla PA; Swintelski C; Kagen A
[Ad] Endereço:1 Division of Vascular and Interventional Radiology, Department of Radiology, Mount Sinai Beth Israel Medical Center, New York, NY, USA.
[Ti] Título:Rare Popliteal Venous Aneurysm: A Case Report and Review of the Literature.
[So] Source:Vasc Endovascular Surg;51(7):491-492, 2017 Oct.
[Is] ISSN:1938-9116
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Popliteal venous aneurysms (PVAs) are rare and may represent a cause of recurrent pulmonary embolism. We present a case of PVA identified on ultrasound for deep venous thrombosis in a 27-year-old female with popliteal fossa pain. We discuss our recommendations for treatment and present a review of the previously reported cases.
[Mh] Termos MeSH primário: Aneurisma/diagnóstico por imagem
Veia Poplítea/diagnóstico por imagem
Ultrassonografia Doppler em Cores
[Mh] Termos MeSH secundário: Adulto
Dilatação Patológica
Feminino
Seres Humanos
Valor Preditivo dos Testes
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170809
[St] Status:MEDLINE
[do] DOI:10.1177/1538574417718444


  10 / 9704 MEDLINE  
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[PMID]:28780235
[Au] Autor:Nakitende D; Gottlieb M
[Ad] Endereço:Department of Emergency Medicine, Rush University Medical Center, Chicago, IL, United States. Electronic address: Damali.Nakitende@advocatehealth.com.
[Ti] Título:Dilated right coronary sinus identified on point-of-care ultrasound.
[So] Source:Am J Emerg Med;35(10):1587.e1-1587.e2, 2017 Oct.
[Is] ISSN:1532-8171
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Point-of-care cardiac ultrasound (POCUS) is a common application in Emergency Medicine. Here we present a case of an incidentally discovered dilated right coronary sinus on ultrasound. This case involved a 55-year-old female who presented with chest pain, shortness of breath, and lightheadedness. Her initial presentation was concerning for congestive heart failure (CHF) exacerbation. A bedside ultrasound was performed to assess cardiac function, where a dilated right coronary sinus was discovered. The right coronary sinus is the vein that serves as the venous return for the coronary system. It is a tubular structure located at the posterior atrioventricular groove and it is generally not visible unless it is pathologically dilated. Identification of a dilated right coronary sinus can assist the clinician in making the diagnoses of CHF exacerbation, as well as alter the approach to specific procedures. To the best of our knowledge, this is the first case report describing the identification of a dilated right coronary sinus using POCUS.
[Mh] Termos MeSH primário: Doença da Artéria Coronariana/diagnóstico
Seio Coronário/diagnóstico por imagem
Sistemas Automatizados de Assistência Junto ao Leito
Ultrassonografia/métodos
[Mh] Termos MeSH secundário: Diagnóstico Diferencial
Dilatação Patológica
Eletrocardiografia
Feminino
Seres Humanos
Meia-Idade
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; VIDEO-AUDIO MEDIA
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170807
[St] Status:MEDLINE



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