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[PMID]:29329093
[Au] Autor:Pérez-Escalante E; González-Olivares LG; Cruz-Guerrero AE; Galán-Vidal CA; Páez-Hernández ME; Álvarez-Romero GA
[Ad] Endereço:Universidad Autónoma del Estado de Hidalgo, Área Académica de Química, Ciudad del Conocimiento, Carretera Pachuca-Tulancingo km 4.5, Colonia Carboneras, CP 42184 Mineral de la Reforma, Hidalgo, Mexico. Electronic address: emmanuel_perez@uaeh.edu.mx.
[Ti] Título:Size exclusion chromatography (SEC-HPLC) as an alternative to study thrombin inhibition.
[So] Source:J Chromatogr B Analyt Technol Biomed Life Sci;1074-1075:34-38, 2018 Feb 01.
[Is] ISSN:1873-376X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:In vitro analysis of anticoagulant compounds with a potential use as antithrombotic drugs, has been traditionally performed using techniques like spectrophotometry, turbidimetry, as well as electrochemical and clinical assays. Although, these techniques have some disadvantages such as: the inability to measure the total biological activity of thrombin, interferences and, sometimes, the quantitative determination of the inhibition ratio is not accurate. In the present work, the conversion of fibrinogen to fibrin was monitored by molecular exclusion chromatography (SEC-HPLC) in three different reaction systems. An inhibition percentage of 43.19±2.02% was obtained using heparin as an anticoagulant, in addition to the determination of the percentage of heparin bonded to thrombin. This methodology has not been previously described and has high potential for the determination of anticoagulant capacity with higher precision, the determination of thrombin's total biological activity and the quantitative determination of the inhibition ratio.
[Mh] Termos MeSH primário: Cromatografia em Gel/métodos
Cromatografia Líquida de Alta Pressão/métodos
Fibrinogênio/metabolismo
Trombina/antagonistas & inibidores
[Mh] Termos MeSH secundário: Fibrina/análise
Fibrina/metabolismo
Fibrinogênio/análise
Heparina/farmacologia
Seres Humanos
Trombina/análise
Trombina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
9001-31-4 (Fibrin); 9001-32-5 (Fibrinogen); 9005-49-6 (Heparin); EC 3.4.21.5 (Thrombin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180113
[St] Status:MEDLINE


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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]:28464119
[Au] Autor:Cruz MA; McAnany S; Gupta N; Long RG; Nasser P; Eglin D; Hecht AC; Illien-Junger S; Iatridis JC
[Ad] Endereço:Leni and Peter W. May Department of Orthopaedics, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, Box 1188, New York, NY 10029.
[Ti] Título:Structural and Chemical Modification to Improve Adhesive and Material Properties of Fibrin-Genipin for Repair of Annulus Fibrosus Defects in Intervertebral Disks.
[So] Source:J Biomech Eng;139(8), 2017 Aug 01.
[Is] ISSN:1528-8951
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Annulus fibrosus (AF) defects from intervertebral disk (IVD) herniation and degeneration are commonly associated with back pain. Genipin-crosslinked fibrin hydrogel (FibGen) is an injectable, space-filling AF sealant that was optimized to match AF shear properties and partially restored IVD biomechanics. This study aimed to enhance mechanical behaviors of FibGen to more closely match AF compressive, tensile, and shear properties by adjusting genipin crosslink density and by creating a composite formulation by adding Poly(D,L-lactide-co-glycolide) (PDLGA). This study also evaluated effects of thrombin concentration and injection technique on gelation kinetics and adhesive strength. Increasing FibGen genipin concentration from 1 to 36 mg/mL significantly increased adhesive strength (∼5 to 35 kPa), shear moduli (∼10 to 110 kPa), and compressive moduli (∼25 to 150 kPa) with concentration-dependent effects, and spanning native AF properties. Adding PDLGA to FibGen altered the material microstructure on electron microscopy and nearly tripled adhesive strength, but did not increase tensile moduli, which remained nearly 5× below native AF, and had a small increase in shear moduli and significantly decreased compressive moduli. Increased thrombin concentration decreased gelation rate to < 5 min and injection methods providing a structural FibGen cap increased pushout strength by ∼40%. We conclude that FibGen is highly modifiable with tunable mechanical properties that can be formulated to be compatible with human AF compressive and shear properties and gelation kinetics and injection techniques compatible with clinical discectomy procedures. However, further innovations, perhaps with more efficient fiber reinforcement, will be required to enable FibGen to match AF tensile properties.
[Mh] Termos MeSH primário: Anel Fibroso/efeitos dos fármacos
Materiais Biocompatíveis/química
Materiais Biocompatíveis/farmacologia
Fibrina/química
Iridoides/química
[Mh] Termos MeSH secundário: Adesividade
Teste de Materiais
Fenômenos Mecânicos
Poliglactina 910/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biocompatible Materials); 0 (Iridoids); 34346-01-5 (Polyglactin 910); 9001-31-4 (Fibrin); A3V2NE52YG (genipin)
[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:170503
[St] Status:MEDLINE
[do] DOI:10.1115/1.4036623


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[PMID]:28457906
[Au] Autor:Üçal M; Haindl MT; Adzemovic MZ; Strasser J; Theisl L; Zeitelhofer M; Kraitsy K; Ropele S; Schäfer U; Fazekas F; Hochmeister S
[Ad] Endereço:Research Unit of Experimental Neurotraumatology, Department of Neurosurgery, Medical University Graz, Auenbruggerplatz 2.2, 8036 Graz, Austria.
[Ti] Título:Widespread cortical demyelination of both hemispheres can be induced by injection of pro-inflammatory cytokines via an implanted catheter in the cortex of MOG-immunized rats.
[So] Source:Exp Neurol;294:32-44, 2017 08.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cortical demyelination is a common finding in patients with chronic multiple sclerosis (MS) and contributes to disease progression and overall disability. The exact pathomechanism that leads to cortical lesions is not clear. Research is limited by the fact that standard animal models of multiple sclerosis do not commonly affect the cortex, or if they do in some variants, the cortical demyelination is rather sparse and already remyelinated within a few days. In an attempt to overcome these limitations we implanted a tissue-compatible catheter into the cortex of Dark Agouti rats. After 14days the rats were immunized with 5µg myelin oligodendrocyte glycoprotein (MOG) in incomplete Freund's Adjuvant, which did not cause any clinical signs but animals developed a stable anti-MOG antibody titer. Then the animals received an injection of proinflammatory cytokines through the catheter. This led to a demyelination of cortical and subcortical areas starting from day 1 in a cone-like pattern spreading from the catheter area towards the subarachnoid space. On day 3 cortical demyelination already expanded to the contralateral hemisphere and reached its peak between days 9-15 after cytokine injection with a widespread demyelination of cortical and subcortical areas of both hemispheres. Clinically the animals showed only discrete signs of fatigue and recovered completely after day 15. Even on day 30 we still were able to detect demyelination in subpial and intracortical areas along with areas of partial and complete remyelination. Loss of cortical myelin was accompanied with marked microglia activation. A second injection of cytokines through the catheter on day 30 led to a second demyelination phase with the same symptoms, but again no detectable motor dysfunction. Suffering of the animals appeared minor compared to standard Experimental Autoimmune Encephalomyelitis and therefore, even long-term observation and repeated demyelination phases seem ethically acceptable.
[Mh] Termos MeSH primário: Córtex Cerebral/patologia
Citocinas/toxicidade
Doenças Desmielinizantes/induzido quimicamente
Doenças Desmielinizantes/patologia
Encefalomielite Autoimune Experimental/patologia
Lateralidade Funcional/fisiologia
[Mh] Termos MeSH secundário: Animais
Proteínas de Ligação ao Cálcio/metabolismo
Caspase 3/metabolismo
Citocinas/metabolismo
Modelos Animais de Doenças
Encefalomielite Autoimune Experimental/induzido quimicamente
Encefalomielite Autoimune Experimental/diagnóstico por imagem
Encefalomielite Autoimune Experimental/imunologia
Fibrina/metabolismo
Adjuvante de Freund/efeitos adversos
Lateralidade Funcional/efeitos dos fármacos
Imunização/efeitos adversos
Lipídeos/efeitos adversos
Masculino
Proteínas dos Microfilamentos/metabolismo
Microscopia Confocal
Atividade Motora
Proteína Proteolipídica de Mielina/metabolismo
Glicoproteína Associada a Mielina/efeitos adversos
Glicoproteína Associada a Mielina/sangue
Proteínas do Tecido Nervoso/metabolismo
Ratos
Estatísticas não Paramétricas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aif1 protein, rat); 0 (Calcium-Binding Proteins); 0 (Cytokines); 0 (Lipids); 0 (Microfilament Proteins); 0 (Myelin Proteolipid Protein); 0 (Myelin-Associated Glycoprotein); 0 (Nerve Tissue Proteins); 0 (incomplete Freund's adjuvant); 9001-31-4 (Fibrin); 9007-81-2 (Freund's Adjuvant); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180218
[Lr] Data última revisão:
180218
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


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[PMID]:29236205
[Au] Autor:Chiti MC; Dolmans MM; Mortiaux L; Zhuge F; Ouni E; Shahri PAK; Van Ruymbeke E; Champagne SD; Donnez J; Amorim CA
[Ad] Endereço:Pôle de Recherche en Gynécologie, Institut de Recherche Expérimentale et Clinique, Université Catholique de Louvain, Avenue Mounier 52, bte. B1.52.02, 1200, Brussels, Belgium.
[Ti] Título:A novel fibrin-based artificial ovary prototype resembling human ovarian tissue in terms of architecture and rigidity.
[So] Source:J Assist Reprod Genet;35(1):41-48, 2018 Jan.
[Is] ISSN:1573-7330
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:PURPOSE: The aim of this study is to optimize fibrin matrix composition in order to mimic human ovarian tissue architecture for human ovarian follicle encapsulation and grafting. METHODS: Ultrastructure of fresh human ovarian cortex in age-related women (n = 3) and different fibrin formulations (F12.5/T1, F30/T50, F50/T50, F75/T75), rheology of fibrin matrices and histology of isolated and encapsulated human ovarian follicles in these matrices. RESULTS: Fresh human ovarian cortex showed a highly fibrous and structurally inhomogeneous architecture in three age-related patients, but the mean ± SD of fiber thickness (61.3 to 72.4 nm) was comparable between patients. When the fiber thickness of four different fibrin formulations was compared with human ovarian cortex, F50/T50 and F75/T75 showed similar fiber diameters to native tissue, while F12.5/T1 was significantly different (p value < 0.01). In addition, increased concentrations of fibrin exhibited enhanced storage modulus with F50/T50, resembling physiological ovarian rigidity. Excluding F12.5/T1 from further analysis, only three remaining fibrin matrices (F30/T50, F50/T50, F75/T75) were histologically investigated. For this, frozen-thawed fragments of human ovarian tissue collected from 22 patients were used to isolate ovarian follicles and encapsulate them in the three fibrin formulations. All three yielded similar follicle recovery and loss rates soon after encapsulation. Therefore, based on fiber thickness, porosity, and rigidity, we selected F50/T50 as the fibrin formulation that best mimics native tissue. CONCLUSIONS: Of all the different fibrin matrix concentrations tested, F50/T50 emerged as the combination of choice in terms of ultrastructure and rigidity, most closely resembling human ovarian cortex.
[Mh] Termos MeSH primário: Órgãos Artificiais
Fibrina/química
Ovário
[Mh] Termos MeSH secundário: Materiais Biomiméticos/química
Composição de Medicamentos
Elasticidade
Feminino
Dureza
Seres Humanos
Fenômenos Mecânicos
Folículo Ovariano/transplante
Folículo Ovariano/ultraestrutura
Ovário/química
Ovário/citologia
Ovário/ultraestrutura
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
9001-31-4 (Fibrin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180210
[Lr] Data última revisão:
180210
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE
[do] DOI:10.1007/s10815-017-1091-3


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[PMID]:29227068
[Au] Autor:Ohe M; Mutsuki T; Goya T; Yamashita S; Satoh T; Kohjima M; Kato M
[Ti] Título:Portal Vein Thrombosis Repeatedly Observed in a Cirrhotic Patient with Antiphospholipid Antibody Syndrome.
[So] Source:Fukuoka Igaku Zasshi;107(10):185-90, 2016 Oct.
[Is] ISSN:0016-254X
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Background: Although portal vein thrombosis in cirrhotic patients is frequently observed, the detailed process remains to be clarified, and the role of anticardiolipin antibody in the development of portal vein thrombosis has been controversial. Case Report: A 52-year-old man, who had been diagnosed with alcoholic cirrhosis of the liver, was admitted to our hospital suffering from dyspnea and ascites. Just after being diagnosed as having antiphospholipid antibody syndrome with lung thrombosis and delivering a positive result for the ß 2-glycoprotein I-dependent anticardiolipin antibody, he sustained rupture of the esophageal varices with rapid development of portal vein thrombosis, which resolved under anticoagulant therapy. Two years later, he was admitted again on suspicion of thrombosis because of an elevation in the serum D-dimer level, and computed tomography showed portal and upper mesenteric vein thrombosis. Although immediate anticoagulant therapy resulted in complete recanalization, he suffered the same episode 2 months later, which occurred with re-elevation of the serum D-dimer level. Conclusion: A positive finding of an anticardiolipin antibody in cirrhotic patients has been considered to be nonspecific and not related to the development of thrombus in the portal vein. This case, however, seems to indicate that cirrhotic patients with the ß2-glycoprotein I-dependent anticardiolipin antibody should be regarded as being at high risk for portal vein thrombosis. Monitoring with the serum D-dimer was useful in detecting portal vein thrombosis in its early stage.
[Mh] Termos MeSH primário: Síndrome Antifosfolipídica/diagnóstico por imagem
Cirrose Hepática/diagnóstico por imagem
Veia Porta/diagnóstico por imagem
Trombose Venosa/diagnóstico por imagem
Trombose Venosa/etiologia
[Mh] Termos MeSH secundário: Síndrome Antifosfolipídica/complicações
Fibrina/metabolismo
Fibrinogênio/metabolismo
Seres Humanos
Cirrose Hepática/complicações
Masculino
Meia-Idade
Tomografia Computadorizada por Raios X
Trombose Venosa/metabolismo
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
9001-31-4 (Fibrin); 9001-32-5 (Fibrinogen)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE


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[PMID]:29227605
[Au] Autor:Pyrogova LV; Chernyshenko TM; Kolesnikova IN; Platonova TN; Bereznitsky GK; Makogonenko YM; Lugovskoy EV
[Ti] Título:Level of overall hemostasis potential in donor and patient plasma in pathology.
[So] Source:Ukr Biochem J;88(2):56-65, 2016 Mar-Apr.
[Is] ISSN:2409-4943
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:Coagulation potential (CP), overall hemostasis potential (OHP) and fibrinolysis potential (FP) in plasma of donors and patients with myocardial infarction (MI), stroke (St) and hip joint diseases (HJD) have been investigated using M. Blomback's global hemostasis assay. Plasma samples of the patients were analyzed with APTT reagent in the presence or absence of t-PA. It was found that the ratio of values of СP, OHP and FP in plasma of patients to those of donors plasma were 78, 60 and 123% at MI; 157, 155 and 162% at St; 128, 131 and 124% at HJD. CP to FP ratio that indicated balance between coagulation and fibrinolytic systems activities were 4.13, 2.5, 4.0 and 4.26 in plasma of donors and MI, St and HJD patients, respectively. These results are evidence of increased fibrinolytic activity in plasma of MI patients. Lag-periods of plasma clotting of MI, St and HJD patients were prolonged by 2.3, 7.2 and 1.5-fold, respectively. Pearson's correlation analysis between parameters, obtained in vitro studies using global hemostasis assay, and concentrations of the molecular markers (soluble fibrin and D-dimer), which formed in vivo in plasma of MI, St and HJD patients, did not reveal any relationship between them.
[Mh] Termos MeSH primário: Artrite Reumatoide/sangue
Produtos de Degradação da Fibrina e do Fibrinogênio/metabolismo
Fibrina/metabolismo
Hemostasia/fisiologia
Infarto do Miocárdio/sangue
Acidente Vascular Cerebral/sangue
[Mh] Termos MeSH secundário: Idoso
Artrite Reumatoide/patologia
Biomarcadores/sangue
Estudos de Casos e Controles
Feminino
Seres Humanos
Masculino
Infarto do Miocárdio/patologia
Acidente Vascular Cerebral/patologia
Ativador de Plasminogênio Tecidual/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Fibrin Fibrinogen Degradation Products); 0 (fibrin fragment D); 9001-31-4 (Fibrin); EC 3.4.21.68 (PLAT protein, human); EC 3.4.21.68 (Tissue Plasminogen Activator)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE
[do] DOI:10.15407/ubj88.02.056


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[PMID]:29227597
[Au] Autor:Yatsenko TA; Rybachuk VM; Yusova OI; Kharchenko SM; Grinenko TV
[Ti] Título:Effect of fibrin degradation products on fibrinolytic process.
[So] Source:Ukr Biochem J;88(2):16-24, 2016 Mar-Apr.
[Is] ISSN:2409-4943
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:Fibrin clot lysis by plasminogen/plasmin system results in fibrin degradation products formation with subsequent release into bloodstream. The fragments contain specific binding sites for fibrinolytic system components and can interact with them. In this study, we investigated the way in which fibrin fragments effect fibrinolytic process. We have shown that high molecular weight products of fibrin degradation and fibrin fragments of DDE-complex and DD, but not end product Е3, stimulate plasmin formation. Additionally, components of DDE-complex mixture of fragments Е1 and Е2 have potentiation ability. The intermediate fibrin fragments hmFDPs and DDE attenuate clot lysis by plasmin and hmFDPs protect plasmin from α2-antiplasmin inhibition but under further fragmentation to endpoint fibrin fragments loose this ability. The plasma inhibitors reduce fibrinolytic system activity generated by the degradation products. Thus, fibrin fragments formed during the clot lysis can bind and move out fibrinolytic system components from clot volume and in this way result in clot resistance to hydrolysis.
[Mh] Termos MeSH primário: Produtos de Degradação da Fibrina e do Fibrinogênio/isolamento & purificação
Fibrina/química
Fibrinolisina/química
Plasminogênio/química
Ativador de Plasminogênio Tecidual/química
alfa 2-Antiplasmina/química
[Mh] Termos MeSH secundário: Tampões (Química)
Cromatografia em Gel
Cromatografia por Troca Iônica
Ativação Enzimática
Produtos de Degradação da Fibrina e do Fibrinogênio/química
Fibrinólise/fisiologia
Seres Humanos
Cinética
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Buffers); 0 (Fibrin Fibrinogen Degradation Products); 0 (alpha-2-Antiplasmin); 9001-31-4 (Fibrin); 9001-91-6 (Plasminogen); EC 3.4.21.68 (PLAT protein, human); EC 3.4.21.68 (Tissue Plasminogen Activator); EC 3.4.21.7 (Fibrinolysin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE
[do] DOI:10.15407/ubj88.02.016


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[PMID]:27770610
[Au] Autor:Sridharan B; Laflin AD; Holtz MA; Pacicca DM; Wischmeier NK; Detamore MS
[Ad] Endereço:Bioengineering Program, University of Kansas, Lawrence, Kansas.
[Ti] Título:In vivo evaluation of stem cell aggregates on osteochondral regeneration.
[So] Source:J Orthop Res;35(8):1606-1616, 2017 08.
[Is] ISSN:1554-527X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:To date, many osteochondral regenerative approaches have utilized varied combinations of biocompatible materials and cells to engineer cartilage. Even in cell-based approaches, to date, no study has utilized stem cell aggregates alone for regenerating articular cartilage. Thus, the purpose of this study was to evaluate the performance of a novel stem cell-based aggregate approach in a fibrin carrier to regenerate osteochondral defects in the Sprague-Dawley rat trochlear groove model. Two different densities of rat bone marrow mesenchymal stem cell (rBMSC) aggregates were fabricated by the hanging drop technique. At 8 weeks, the cell aggregates supported the defects and served as a catalyst for neo-cartilage synthesis, and the experimental groups may have been beneficial for bone and cartilage regeneration compared to the fibrin-only control and sham groups, as evidenced by histological assessment. The cell density of rBMSC aggregates may thus directly impact chondrogenesis. The usage of cell aggregates with fibrin as a cell-based technology is a promising and translational new treatment strategy for repair of cartilage defects. © 2016 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:1606-1616, 2017.
[Mh] Termos MeSH primário: Cartilagem Articular/fisiologia
Transplante de Células-Tronco Mesenquimais/métodos
Regeneração
[Mh] Termos MeSH secundário: Animais
Agregação Celular
Fibrina
Masculino
Projetos Piloto
Cultura Primária de Células
Ratos Sprague-Dawley
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
9001-31-4 (Fibrin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171204
[Lr] Data última revisão:
171204
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161023
[St] Status:MEDLINE
[do] DOI:10.1002/jor.23467


  10 / 12888 MEDLINE  
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[PMID]:28904234
[Au] Autor:Drabik L; Wolkow P; Undas A
[Ad] Endereço:From the John Paul II Hospital, Krakow, Poland (L.D., A.U.), Centre for Medical Genomics-OMICRON (P.W.), Department of Pharmacology (L.D., P.W.) and Institute of Cardiology (A.U), Jagiellonian University Medical College, Krakow, Poland.
[Ti] Título:Fibrin Clot Permeability as a Predictor of Stroke and Bleeding in Anticoagulated Patients With Atrial Fibrillation.
[So] Source:Stroke;48(10):2716-2722, 2017 Oct.
[Is] ISSN:1524-4628
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND PURPOSE: Formation of denser fiber networks has been reported in atrial fibrillation and ischemic stroke. In this longitudinal cohort study, we evaluated whether fibrin clot density may predict thromboembolic and bleeding risk in patients with atrial fibrillation on vitamin K antagonists. METHODS: In 236 patients with atrial fibrillation receiving vitamin K antagonists treatment, we measured ex vivo plasma clot permeability (K ), a measure of the pore size in fibrin networks. RESULTS: During a median follow-up of 4.3 (interquartile range, 3.7-4.8) years, annual rates of ischemic stroke or transient ischemic attack and major bleeds were 2.96% and 3.45%, respectively. In multivariate Cox regression analysis, patients with lower K (<6.8 cm ×10 , median) had increased risk of ischemic stroke or transient ischemic attack (hazard ratio [HR], 6.55; 95% confidence interval [CI], 2.17-19.82) and major bleeds (HR, 10.65; 95% CI, 3.52-32.22). Patients with elevated K (≥6.8 cm ×10 ) had an increased rate of minor bleeding compared with the remainder (11.63% per year versus 3.55% per year; <0.0001). The independent predictors of stroke or transient ischemic attack were low K (<6.8 cm ×10 ; HR, 7.24; 95% CI, 2.53-20.76), age (HR, 1.05; 95% CI, 1.01-1.10), and treatment with angiotensin-converting enzyme inhibitors (HR, 2.27; 95% CI, 1.08-4.77). Major bleeds were predicted by low K (<6.8 cm ×10 ; HR, 8.48; 95% CI, 2.99-24.1) and HAS-BLED score ≥3 (HR, 2.22; 95% CI, 1.12-4.38). CONCLUSIONS: This study is the first to show that unfavorable fibrin properties reflected by formation of denser fibrin networks determine, in part, the efficacy and safety of anticoagulation with vitamin K antagonists in patients with atrial fibrillation.
[Mh] Termos MeSH primário: Anticoagulantes/uso terapêutico
Fibrilação Atrial/sangue
Fibrina/metabolismo
Hemorragia/sangue
Acidente Vascular Cerebral/sangue
Trombose/sangue
[Mh] Termos MeSH secundário: Idoso
Anticoagulantes/efeitos adversos
Anticoagulantes/farmacologia
Fibrilação Atrial/diagnóstico
Fibrilação Atrial/tratamento farmacológico
Coagulação Sanguínea/efeitos dos fármacos
Coagulação Sanguínea/fisiologia
Permeabilidade Capilar/efeitos dos fármacos
Permeabilidade Capilar/fisiologia
Estudos de Coortes
Feminino
Seguimentos
Hemorragia/induzido quimicamente
Hemorragia/diagnóstico
Seres Humanos
Estudos Longitudinais
Masculino
Meia-Idade
Valor Preditivo dos Testes
Acidente Vascular Cerebral/diagnóstico
Acidente Vascular Cerebral/tratamento farmacológico
Trombose/diagnóstico
Trombose/tratamento farmacológico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticoagulants); 9001-31-4 (Fibrin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171009
[Lr] Data última revisão:
171009
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170915
[St] Status:MEDLINE
[do] DOI:10.1161/STROKEAHA.117.018143



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