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Pesquisa : A11.118.637 [Categoria DeCS]
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[PMID]:29332224
[Au] Autor:Tong D; Yu M; Guo L; Li T; Li J; Novakovic VA; Dong Z; Tian Y; Kou J; Bi Y; Wang J; Zhou J; Shi J
[Ad] Endereço:Department of Hematology, First Hospital, Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin, 150001, China.
[Ti] Título:Phosphatidylserine-exposing blood and endothelial cells contribute to the hypercoagulable state in essential thrombocythemia patients.
[So] Source:Ann Hematol;97(4):605-616, 2018 Apr.
[Is] ISSN:1432-0584
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The mechanisms of thrombogenicity in essential thrombocythemia (ET) are complex and not well defined. Our objective was to explore whether phosphatidylserine (PS) exposure on blood cells and endothelial cells (ECs) can account for the increased thrombosis and distinct thrombotic risks among mutational subtypes in ET. Using flow cytometry and confocal microscopy, we found that the levels of PS-exposing erythrocytes, platelets, leukocytes, and serum-cultured ECs were significantly higher in each ET group [JAK2, CALR, and triple-negative (TN) (all P < 0.001)] than those in controls. Among ET patients, those with JAK2 mutations showed higher levels of PS-positive erythrocytes, platelets, neutrophils, and serum-cultured ECs than TN patients or those with CALR mutations, which show similar levels. Coagulation function assays showed that higher levels of PS-positive blood cells and serum-cultured ECs led to markedly shortened coagulation time and dramatically increased levels of FXa, thrombin, and fibrin production. This procoagulant activity could be largely blocked by addition of lactadherin (approx. 70% inhibition). Confocal microscopy showed that the FVa/FXa complex and fibrin fibrils colocalized with PS on ET serum-cultured ECs. Additionally, we found a relationship between D-dimer, prothrombin fragment F1 + 2, and PS exposure. Our study reveals a previously unrecognized link between hypercoagulability and exposed PS on cells, which might also be associated with distinct thrombotic risks among mutational subtypes in ET. Thus, blocking PS-binding sites may represent a new therapeutic target for preventing thrombosis in ET.
[Mh] Termos MeSH primário: Plaquetas/patologia
Endotélio Vascular/patologia
Eritrócitos/patologia
Leucócitos/patologia
Fosfatidilserinas/metabolismo
Trombocitemia Essencial/fisiopatologia
Trombose/etiologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Substituição de Aminoácidos
Plaquetas/metabolismo
Calreticulina/genética
Calreticulina/metabolismo
Células Cultivadas
China/epidemiologia
Endotélio Vascular/metabolismo
Eritrócitos/metabolismo
Feminino
Células Endoteliais da Veia Umbilical Humana/citologia
Células Endoteliais da Veia Umbilical Humana/metabolismo
Seres Humanos
Janus Quinase 2/genética
Janus Quinase 2/metabolismo
Leucócitos/metabolismo
Masculino
Meia-Idade
Mutação
Receptores de Trombopoetina/genética
Receptores de Trombopoetina/metabolismo
Risco
Propriedades de Superfície
Trombocitemia Essencial/genética
Trombocitemia Essencial/metabolismo
Trombocitemia Essencial/patologia
Trombose/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calreticulin); 0 (Phosphatidylserines); 0 (Receptors, Thrombopoietin); 0 (calreticulin, human); 143641-95-6 (MPL protein, human); EC 2.7.10.2 (JAK2 protein, human); EC 2.7.10.2 (Janus Kinase 2)
[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:180115
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-018-3228-6


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[PMID]:29278023
[Au] Autor:Clemente-Suárez VJ; Mielgo-Ayuso J; Quiles JL; Varela-Lopez A; Aranda P
[Ad] Endereço:1 Applied Psychophysiological Research Group, European University of Madrid , Madrid, Spain.
[Ti] Título:Effect of α-tocopherol megadoses on hematologic parameters and antioxidant capacity of rats in an ultraendurance probe.
[So] Source:Physiol Int;104(4):291-300, 2017 Dec 01.
[Is] ISSN:2498-602X
[Cp] País de publicação:Hungary
[La] Idioma:eng
[Ab] Resumo:This study was aimed to analyze the effect of two different megadoses of α-tocopherol (vit E) in the antioxidant activity and red and white blood series of Wistar rats after a 180-min ultraendurance probe. Three groups of 10 rats were analyzed; VEAG: acute administration of a megadoses of 5,000 IU/kg of vit E the day before the probe; VECG: chronic administration of 1,000 IU/kg/day of vit E for 6 days before the probe; CG: placebo administration. VEAG presented white cells, red blood cells, hematocrit, hemoglobin values significantly higher than CG and VECG (p < 0.05). The mean corpuscular hemoglobin and lymphocytes concentrations were significantly higher in the VECG than in the other two groups (p < 0.05). Similarly, VEAG presented a significantly higher vit E blood concentration than VECG and CG (p < 0.05), and VECG than CG (p < 0.05). Finally, we found a significantly positive correlation between trolox equivalent antioxidant capacity (TEAC) and red blood cells concentration (r = 0.374) and a significantly inverse correlation between TEAC and blood lactate concentration (r = -0.365). Our findings suggest that acute vit E megadoses could protect against transitory sport anemia symptoms and increase the white blood cell count in comparison with the chronic dose and control groups after an ultraendurance probe.
[Mh] Termos MeSH primário: Leucócitos/fisiologia
Substâncias para Melhoria do Desempenho/administração & dosagem
Resistência Física/efeitos dos fármacos
Resistência Física/fisiologia
Espécies Reativas de Oxigênio/metabolismo
Corrida/fisiologia
alfa-Tocoferol/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Antioxidantes/administração & dosagem
Relação Dose-Resposta a Droga
Eritrócitos/citologia
Eritrócitos/fisiologia
Hematócrito
Leucócitos/citologia
Masculino
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Performance-Enhancing Substances); 0 (Reactive Oxygen Species); H4N855PNZ1 (alpha-Tocopherol)
[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:171227
[St] Status:MEDLINE
[do] DOI:10.1556/2060.104.2017.4.2


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[PMID]:29214791
[Au] Autor:Ahn MJ; Yu JE; Jeong J; Sim DW; Koh YI
[Ad] Endereço:Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea.
[Ti] Título:A Case of Schnitzler's Syndrome without Monoclonal Gammopathy-Associated Chronic Urticaria Treated with Anakinra.
[So] Source:Yonsei Med J;59(1):154-157, 2018 Jan.
[Is] ISSN:1976-2437
[Cp] País de publicação:Korea (South)
[La] Idioma:eng
[Ab] Resumo:Chronic urticaria may often be associated with interleukin (IL)-1-mediated autoinflammatory disease, which should be suspected if systemic inflammation signs are present. Here, we report a case of Schnitzler's syndrome without monoclonal gammopathy treated successfully with the IL-1 receptor antagonist anakinra. A 69-year-old man suffered from a pruritic urticarial rash for 12 years. It became aggravated episodically and was accompanied by high fever, arthralgia, leukocytosis, and an elevated C-reactive protein and erythrocyte sedimentation rate. The episodes each lasted for over one week. Neutrophilic and eosinophilic inflammation was found on skin biopsy. However, serum and urine electrophoresis showed no evidence of monoclonal gammopathy. The cutaneous lesions were unresponsive to various kinds of anti-histamines, systemic glucocorticoids, colchicine, cyclosporine, dapsone, and methotrexate, which were administered over a span of 3 years immediately preceding successful treatment. A dramatic response, however, was observed after a daily administration of anakinra. This observation suggests that the correct diagnosis of this case is Schnitzler's syndrome without monoclonal gammopathy. For an adult patient with refractory chronic urticaria and systemic inflammation, Schnitzler's syndrome could be considered as a possible differential diagnosis. Although the typical form of Schnitzler's syndrome exhibits the presence of monoclonal gammopathy as a diagnostic criterion, monoclonal gammopathy may be absent in an atypical form. In such a situation, an IL-1 antagonist should be effective for the management of chronic urticaria.
[Mh] Termos MeSH primário: Proteína Antagonista do Receptor de Interleucina 1/uso terapêutico
Paraproteinemias/complicações
Síndrome de Schnitzler/tratamento farmacológico
Urticária/complicações
[Mh] Termos MeSH secundário: Idoso
Sedimentação Sanguínea
Proteína C-Reativa/metabolismo
Doença Crônica
Seres Humanos
Leucócitos/metabolismo
Masculino
Síndrome de Schnitzler/sangue
[Pt] Tipo de publicação:CASE REPORTS
[Nm] Nome de substância:
0 (Interleukin 1 Receptor Antagonist Protein); 9007-41-4 (C-Reactive Protein)
[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:171208
[St] Status:MEDLINE
[do] DOI:10.3349/ymj.2018.59.1.154


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[PMID]:28467723
[Au] Autor:Diaz-Morales N; Rovira-Llopis S; Bañuls C; Lopez-Domenech S; Escribano-Lopez I; Veses S; Jover A; Rocha M; Hernandez-Mijares A; Victor VM
[Ad] Endereço:1 Service of Endocrinology and Nutrition, University Hospital Doctor Peset , Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain .
[Ti] Título:Does Metformin Protect Diabetic Patients from Oxidative Stress and Leukocyte-Endothelium Interactions?
[So] Source:Antioxid Redox Signal;27(17):1439-1445, 2017 Dec 10.
[Is] ISSN:1557-7716
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Since metformin can exert beneficial vascular effects, we aimed at studying its effect on reactive oxygen species (ROS) production, antioxidant enzyme expression, levels of adhesion molecules, and leukocyte-endothelium interactions in the leukocytes from type 2 diabetic (T2D) patients. The study was carried out in 72 T2D patients (41 of whom were treated with metformin for at least 12 months at a dose of 1700 mg per day), and in 40 sex- and age-matched control subjects. Leukocytes from T2D patients exhibited enhanced levels of mitochondrial ROS and decreased mRNA levels of glutathione peroxidase 1 (gpx1) and sirtuin 3 (sirt3) with respect to controls, whereas metformin was shown to revert these effects. No changes were observed on total ROS production and the expression levels of superoxide dismutase 1 and catalase. Furthermore, increases in leukocyte-endothelial interactions and intercellular adhesion molecule-1 and P-selectin levels were found in T2D and were also restored in metformin-treated patients. Our findings raise the question of whether metformin could modulate the appearance of atherosclerosis in T2D patients and reduce vascular events by decreasing leukocyte oxidative stress through an increase in gpx1 and sirt3 expression, and undermining adhesion molecule levels and leukocyte-endothelium interactions. Antioxid. Redox Signal. 27, 1439-1445.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2/tratamento farmacológico
Células Endoteliais/efeitos dos fármacos
Hipoglicemiantes/administração & dosagem
Leucócitos/efeitos dos fármacos
Metformina/administração & dosagem
Estresse Oxidativo/efeitos dos fármacos
[Mh] Termos MeSH secundário: Idoso
Catalase
Adesão Celular
Diabetes Mellitus Tipo 2/genética
Diabetes Mellitus Tipo 2/metabolismo
Células Endoteliais/metabolismo
Feminino
Glutationa Peroxidase/genética
Seres Humanos
Hipoglicemiantes/farmacologia
Molécula 1 de Adesão Intercelular/metabolismo
Leucócitos/metabolismo
Masculino
Metformina/farmacologia
Meia-Idade
Selectina-P/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Sirtuína 3/genética
Superóxido Dismutase-1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hypoglycemic Agents); 0 (ICAM1 protein, human); 0 (P-Selectin); 0 (Reactive Oxygen Species); 0 (SOD1 protein, human); 126547-89-5 (Intercellular Adhesion Molecule-1); 9100L32L2N (Metformin); EC 1.11.1.- (glutathione peroxidase GPX1); EC 1.11.1.6 (Catalase); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.15.1.1 (Superoxide Dismutase-1); EC 3.5.1.- (SIRT3 protein, human); EC 3.5.1.- (Sirtuin 3)
[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:10.1089/ars.2017.7122


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[PMID]:28456536
[Au] Autor:More Bayona JA; Karuppannan AK; Barreda DR
[Ad] Endereço:Department of Biological Sciences, University of Alberta, Edmonton, Alberta T6G 2P5, Canada.
[Ti] Título:Contribution of leukocytes to the induction and resolution of the acute inflammatory response in chickens.
[So] Source:Dev Comp Immunol;74:167-177, 2017 Sep.
[Is] ISSN:1879-0089
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A successful immune response against invading pathogens relies on the efficient activation of host defense mechanisms and a timely return to immune homeostasis. Despite their importance, these mechanisms remain ill-defined in most animal groups. This study focuses on the acute inflammatory response of chickens, important both as an avian model with a unique position in evolution as well as an increasingly notable target of infectious zoonotic diseases. We took advantage of an in vivo self-resolving intra-abdominal challenge model to provide an integrative view of leukocyte responses during the induction and resolution phases of acute inflammation. Our results showed rapid leukocyte infiltration into the abdominal cavity post zymosan challenge (significant increase as early as 4 h), which was dominated by heterophils. Peak leukocyte infiltration and ROS production reached maximum levels at 12 h post challenge, which was significantly earlier than comparative studies in teleost fish and mice. Both heterophils and monocyte/macrophages contributed to ROS production. Local leukocyte infiltration was preceded by an increase in peripheral leukocytes and a drop in the number of bone marrow leukocytes. The proportion of apoptotic leukocytes increased following peak of acute inflammation, rising to significant levels within the abdominal cavity by 48 h, consistent with other indicators for the resolution of inflammation. Importantly, comparison of chicken phagocytic responses with those previously shown in agnathan, teleost and murine models suggested a progressive evolutionary shift towards an increased sensitivity to pro-inflammatory pathogen-derived particles and decreased sensitivity towards homeostatic stimuli. Thus, while significant conservation can be noted across the immune systems of endotherms, this study highlights additional unique features that govern the induction and resolution of acute inflammation in the avian system, which may be relevant to disease susceptibility and performance.
[Mh] Termos MeSH primário: Doenças das Aves/imunologia
Galinhas/imunologia
Inflamação/imunologia
Leucócitos/imunologia
Peritônio/fisiologia
Zoonoses/imunologia
[Mh] Termos MeSH secundário: Doença Aguda
Animais
Apoptose
Evolução Biológica
Movimento Celular
Proliferação Celular
Peixes
Seres Humanos
Imunidade Inata
Camundongos
Fagocitose
Fisiologia Comparada
Espécies Reativas de Oxigênio/metabolismo
Zimosan/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Reactive Oxygen Species); 9010-72-4 (Zymosan)
[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:170501
[St] Status:MEDLINE


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[PMID]:28463415
[Au] Autor:McCullough SD; On DM; Bowers EC
[Ad] Endereço:National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina.
[Ti] Título:Using Chromatin Immunoprecipitation in Toxicology: A Step-by-Step Guide to Increasing Efficiency, Reducing Variability, and Expanding Applications.
[So] Source:Curr Protoc Toxicol;72:3.14.1-3.14.28, 2017 May 02.
[Is] ISSN:1934-9262
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Histone modifications work in concert with DNA methylation to regulate cellular structure, function, and response to environmental stimuli. More than 130 unique histone modifications have been described to date, and chromatin immunoprecipitation (ChIP) allows for the exploration of their associations with the regulatory regions of target genes and other DNA/chromatin-associated proteins across the genome. Many variations of ChIP have been developed in the 30 years since its earliest version came into use, which makes it challenging for users to integrate the procedure into their research programs. Furthermore, the differences in ChIP protocols can confound efforts to increase reproducibility across studies. The streamlined ChIP procedure presented here can be readily applied to samples from a wide range of in vitro studies (cell lines and primary cells) and clinical samples (peripheral leukocytes) in toxicology. We also provide detailed guidance on the optimization of critical protocol parameters, such as chromatin fixation, fragmentation, and immunoprecipitation, to increase efficiency and improve reproducibility. Expanding toxicoepigenetic studies to more readily include histone modifications will facilitate a more comprehensive understanding of the role of the epigenome in environmental exposure effects and the integration of epigenetic data in mechanistic toxicology, adverse outcome pathways, and risk assessment. © 2017 by John Wiley & Sons, Inc.
[Mh] Termos MeSH primário: Imunoprecipitação da Cromatina/métodos
Toxicologia/métodos
[Mh] Termos MeSH secundário: Linhagem Celular
DNA/isolamento & purificação
Epigênese Genética
Redes Reguladoras de Genes
Marcação de Genes
Histonas/metabolismo
Seres Humanos
Leucócitos/química
Peptídeo Hidrolases/química
Reação em Cadeia da Polimerase
Cultura Primária de Células
Reprodutibilidade dos Testes
Sonicação
Toxicologia/normas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Histones); 9007-49-2 (DNA); EC 3.4.- (Peptide Hydrolases)
[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:170503
[St] Status:MEDLINE
[do] DOI:10.1002/cptx.22


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[PMID]:28747460
[Au] Autor:Schallner N; Lieberum JL; Gallo D; LeBlanc RH; Fuller PM; Hanafy KA; Otterbein LE
[Ad] Endereço:From the Department of Surgery (N.S., J.-L.L., D.G., L.E.O.) and Department of Neurology (R.H.L., P.M.F., K.A.H.), Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA; Department of Anesthesiology and Critical Care, Medical Center-University Freiburg, Faculty of Medicine, German
[Ti] Título:Carbon Monoxide Preserves Circadian Rhythm to Reduce the Severity of Subarachnoid Hemorrhage in Mice.
[So] Source:Stroke;48(9):2565-2573, 2017 09.
[Is] ISSN:1524-4628
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND PURPOSE: Subarachnoid hemorrhage (SAH) is associated with a temporal pattern of stroke incidence. We hypothesized that natural oscillations in gene expression controlling circadian rhythm affect the severity of neuronal injury. We moreover predict that heme oxygenase-1 (HO-1/ ) and its product carbon monoxide (CO) contribute to the restoration of rhythm and neuroprotection. METHODS: Murine SAH model was used where blood was injected at various time points of the circadian cycle. Readouts included circadian clock gene expression, locomotor activity, vasospasm, neuroinflammatory markers, and apoptosis. In addition, cerebrospinal fluid and peripheral blood leukocytes from SAH patients and controls were analyzed for clock gene expression. RESULTS: Significant elevations in the clock genes , , and were observed in the hippocampus, cortex, and suprachiasmatic nucleus in mice subjected to SAH at zeitgeber time (ZT) 12 when compared with ZT2. Clock gene expression amplitude correlated with basal expression of HO-1, which was also significantly greater at ZT12. SAH animals showed a significant reduction in cerebral vasospasm, neuronal apoptosis, and microglial activation at ZT12 compared with ZT2. In animals with myeloid-specific HO-1 deletion ( ), , and expression was reduced in the suprachiasmatic nucleus, which correlated with increased injury. Treatment with low-dose CO rescued mice, restored , expression, and reduced neuronal apoptosis. CONCLUSIONS: Clock gene expression regulates, in part, the severity of SAH and requires myeloid HO-1 activity to clear the erythrocyte burden and inhibit neuronal apoptosis. Exposure to CO rescues the loss of HO-1 and thus merits further investigation in patients with SAH.
[Mh] Termos MeSH primário: Monóxido de Carbono/metabolismo
Ritmo Circadiano/genética
Expressão Gênica/efeitos dos fármacos
Heme Oxigenase-1/genética
Proteínas de Membrana/genética
Hemorragia Subaracnóidea/genética
[Mh] Termos MeSH secundário: Fatores de Transcrição ARNTL/genética
Animais
Apoptose
Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética
Proteínas CLOCK/genética
Líquido Cefalorraquidiano/metabolismo
Heme Oxigenase-1/metabolismo
Seres Humanos
Imuno-Histoquímica
Inflamação
Leucócitos/metabolismo
Locomoção
Proteínas de Membrana/metabolismo
Camundongos
Proteínas do Tecido Nervoso/genética
Proteínas Circadianas Period/genética
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Índice de Gravidade de Doença
Núcleo Supraquiasmático/metabolismo
Vasoespasmo Intracraniano
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (ARNTL Transcription Factors); 0 (Arntl protein, mouse); 0 (Basic Helix-Loop-Helix Transcription Factors); 0 (Membrane Proteins); 0 (Nerve Tissue Proteins); 0 (Npas2 protein, mouse); 0 (PER2 protein, human); 0 (Per1 protein, mouse); 0 (Per2 protein, mouse); 0 (Period Circadian Proteins); 7U1EE4V452 (Carbon Monoxide); EC 1.14.14.18 (Heme Oxygenase-1); EC 1.14.14.18 (Hmox1 protein, mouse); EC 2.3.1.48 (CLOCK Proteins); EC 2.3.1.48 (Clock protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1161/STROKEAHA.116.016165


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[PMID]:28465628
[Au] Autor:Jones DP; True HD; Patel J
[Ad] Endereço:Division of Cardiovascular Medicine, Radcliffe Department of Medicine, British Heart Foundation Centre of Research Excellence, University of Oxford and John Radcliffe Hospital, Oxford OX3 9DU, UK.
[Ti] Título:Leukocyte Trafficking in Cardiovascular Disease: Insights from Experimental Models.
[So] Source:Mediators Inflamm;2017:9746169, 2017.
[Is] ISSN:1466-1861
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Chemokine-induced leukocyte migration into the vessel wall is an early pathological event in the progression of atherosclerosis, the underlying cause of myocardial infarction. The immune-inflammatory response, mediated by both the innate and adaptive immune cells, is involved in the initiation, recruitment, and resolution phases of cardiovascular disease progression. Activation of leukocytes via inflammatory mediators such as chemokines, cytokines, and adhesion molecules is instrumental in these processes. In this review, we highlight leukocyte activation with the main focus being on the mechanisms of chemokine-mediated recruitment in atherosclerosis and the response postmyocardial infarction with key examples from experimental models of cardiovascular inflammation.
[Mh] Termos MeSH primário: Doenças Cardiovasculares/imunologia
Doenças Cardiovasculares/metabolismo
Leucócitos/metabolismo
[Mh] Termos MeSH secundário: Animais
Doenças Cardiovasculares/patologia
Quimiocinas/metabolismo
Citocinas/metabolismo
Seres Humanos
Leucócitos/imunologia
Modelos Teóricos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Chemokines); 0 (Cytokines)
[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:170504
[St] Status:MEDLINE
[do] DOI:10.1155/2017/9746169


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[PMID]:29249275
[Au] Autor:Litvinov RI
[Ad] Endereço:Department of Cell and Developmental Biology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, USA; Institute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russian Federation. Electronic address: litvinov@pennmedicine.upenn.edu.
[Ti] Título:Fibrin opens the "gate" for leukocytes in the endothelium.
[So] Source:Thromb Res;162:101-103, 2018 02.
[Is] ISSN:1879-2472
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Fibrina
Leucócitos
[Mh] Termos MeSH secundário: Endotélio
Seres Humanos
[Pt] Tipo de publicação:EDITORIAL; COMMENT
[Nm] Nome de substância:
9001-31-4 (Fibrin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171219
[St] Status:MEDLINE


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[PMID]:28282748
[Au] Autor:Loprinzi PD; Loenneke JP
[Ad] Endereço:a Physical Activity Epidemiology Laboratory, Exercise Psychology Laboratory, Department of Health, Exercise Science and Recreation Management , The University of Mississippi , University , MS , USA.
[Ti] Título:Leukocyte telomere length and mortality among U.S. adults: Effect modification by physical activity behaviour.
[So] Source:J Sports Sci;36(2):213-219, 2018 Jan.
[Is] ISSN:1466-447X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The purpose of this study was to examine the association between leukocyte telomere length (LTL) and mortality (outcome variable), with consideration by physical activity behaviour. Data from the 1999-2002 National Health and Nutrition Examination Survey were employed (N = 6,611; 20-85 yrs), with follow-up mortality assessment through 31 December 2006. DNA was extracted from whole blood to assess LTL via quantitative polymerase chain reaction. Compared to those in the first LTL tertile, the adjusted hazard ratio for all-cause mortality for those in the 2 and 3 LTL tertiles, respectively, was 0.82 (95% CI: 0.60-1.12; P = .22) and 0.76 (95% CI: 0.50-1.14; P = .18). However, after adjustments, LTL tertile 3 (vs. 1) was associated with all-cause mortality (HR = 0.37; 95% CI: 0.14-0.93; P = .03) for those who engaged in moderate-intensity exercise. Similarly, LTL was associated with CVD-specific mortality for those who engaged in moderate-intensity exercise (HR = 0.17; 95% CI: 0.04-0.73; P = .02). Longer telomeres are associated with increased survival, particularly among men and those who are active, underscoring the importance of promotion of physical activity behaviour.
[Mh] Termos MeSH primário: Exercício/fisiologia
Leucócitos/fisiologia
Mortalidade
Homeostase do Telômero
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Envelhecimento/fisiologia
Doenças Cardiovasculares/mortalidade
Feminino
Seres Humanos
Masculino
Meia-Idade
Inquéritos Nutricionais
Estados Unidos/epidemiologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170312
[St] Status:MEDLINE
[do] DOI:10.1080/02640414.2017.1293280



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