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[PMID]:28457516
[Au] Autor:Nakata M; Kasuda S; Yuui K; Kudo R; Hatake K
[Ad] Endereço:Department of Legal Medicine, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan. Electronic address: dc112064@naramed-u.ac.jp.
[Ti] Título:Relevance of hemolysis-induced tissue factor expression on monocytes in soft clot formation in alcohol-containing blood.
[So] Source:Leg Med (Tokyo);25:83-88, 2017 Mar.
[Is] ISSN:1873-4162
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:The fluidity of cadaveric blood is an important characteristic in the post-mortem examination of cases of asphyxial death. Although it is empirically known that soft blood clots are present in cadaveric blood containing alcohol, the relationship between such clots and blood alcohol is unclear. We addressed this issue through in vitro studies using blood collected from healthy volunteers. Assessment of global hemostasis by rotational thromboelastometry revealed that ethanol treatment enhanced the procoagulant activity of whole blood. However, ethanol inhibited epinephrine-induced platelet aggregation, whereas plasma levels of von Willebrand factor and the activity of coagulation factors VIII and IX were unaffected. In contrast, tissue factor (TF) activity was higher in plasma obtained from ethanol-treated whole blood than that in plasma from untreated blood. Ethanol induced hemolysis of red blood cells, and the consequent hemoglobin (Hb) release promoted de novo synthesis of TF in isolated monocytes, as determined by real-time reverse transcription PCR, western blotting, and flow cytometry. However, ethanol itself did not induce TF expression in monocytes. Given that TF activates the extrinsic coagulation pathway and amplifies hemostatic reactions, Hb-induced TF expression in monocytes might contribute to soft blood clot formation.
[Mh] Termos MeSH primário: Coagulação Sanguínea/efeitos dos fármacos
Etanol/sangue
Hemólise
Monócitos/efeitos dos fármacos
Tromboplastina/efeitos dos fármacos
[Mh] Termos MeSH secundário: Autopsia
Cadáver
Citometria de Fluxo
Medicina Legal
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
3K9958V90M (Ethanol); 9035-58-9 (Thromboplastin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


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[PMID]:27771416
[Au] Autor:Cronjé HT; Nienaber-Rousseau C; Zandberg L; Chikowore T; de Lange Z; van Zyl T; Pieters M
[Ad] Endereço:Centre of Excellence for Nutrition, North-West University, Potchefstroom, South Africa.
[Ti] Título:Candidate gene analysis of the fibrinogen phenotype reveals the importance of polygenic co-regulation.
[So] Source:Matrix Biol;60-61:16-26, 2017 Jul.
[Is] ISSN:1569-1802
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Fibrinogen and its functional aspects have been linked to cardiovascular disease. There is vast discrepancy between the heritability of fibrinogen concentrations observed in twin studies and the heritability uncovered by genome wide association studies. We postulate that some of the missing heritability might be explained by the pleiotropic and polygenic co-regulation of fibrinogen through multiple targeted genes, apart from the fibrinogen genes themselves. To this end we investigated single nucleotide polymorphisms (SNPs) in genes coding for phenotypes associated with total and γ' fibrinogen concentrations and clot properties. Their individual and accumulative associations with the fibrinogen variables were explored together with possible co-regulatory processes as a result of the gain and loss of transcription factor binding sites (TFBS). Seventy-eight SNPs spanning the APOB, APOE, CBS, CRP, F13A1, FGA, FGB, FGG, LDL-R, MTHFR, MTR, PCSK-9 and SERPINE-1 genes were included in the final analysis. A novel PCSK-9 SNP (rs369066144) was identified in this population, which associated significantly (p=0.04) with clot lysis time (CLT). Apart from SNPs in the fibrinogen (FGA, FGB and FGG) and FXIII (F13A1) genes, the fibrinogen phenotypes were also associated with SNPs in genes playing a role in lipid homeostasis (LDL-R, PCSK-9) together with CBS and CRP polymorphisms (particularly, CRP-rs3093068). The genetic risk scores, presenting accumulative genetic risk, were significantly associated (p≤0.007) with total and γ' fibrinogen concentrations, lag time, slope and CLT, highlighting the importance of a polygenetic approach in determining complex phenotypes. SNPs significantly associated with the fibrinogen phenotypes, resulted in a total of 75 TFBS changes, of which 35 resulted in a loss and 40 in a gain of TFBS. In terms of co-regulation, V$IRF4.02, V$E2FF and V$HIFF were of particular importance. The investigation into TFBS provided valuable insight as to how sequence divergences in seemingly unrelated genes can result in transcriptional co-regulation of the fibrinogen phenotypes. The observed associations between the identified SNPs and the fibrinogen phenotypes therefore do not imply direct effects on cardiovascular disease outcomes, but may prove useful in explaining more of the genetic regulation of the investigated fibrinogen phenotypes.
[Mh] Termos MeSH primário: Coagulação Sanguínea/genética
Fibrinogênios Anormais/genética
Regulação da Expressão Gênica
Pleiotropia Genética
Polimorfismo de Nucleotídeo Único
Transcrição Genética
[Mh] Termos MeSH secundário: Adulto
Apolipoproteínas/genética
Apolipoproteínas/metabolismo
Sítios de Ligação
Proteína C-Reativa/genética
Proteína C-Reativa/metabolismo
Estudos Transversais
Cistationina beta-Sintase/genética
Cistationina beta-Sintase/metabolismo
Feminino
Tempo de Lise do Coágulo de Fibrina
Fibrinogênios Anormais/metabolismo
Perfilação da Expressão Gênica
Estudo de Associação Genômica Ampla
Seres Humanos
Masculino
Meia-Idade
Pró-Proteína Convertase 9/genética
Pró-Proteína Convertase 9/metabolismo
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoproteins); 0 (Fibrinogens, Abnormal); 0 (fibrinogen gamma'); 9007-41-4 (C-Reactive Protein); EC 3.4.21.- (PCSK9 protein, human); EC 3.4.21.- (Proprotein Convertase 9); EC 4.2.1.22 (Cystathionine beta-Synthase)
[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:161026
[St] Status:MEDLINE


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[PMID]:29346400
[Au] Autor:Ponert JM; Schwarz S; Haschemi R; Müller J; Pötzsch B; Bendas G; Schlesinger M
[Ad] Endereço:Department of Pharmacy, Rheinische Friedrich-Wilhelms-University Bonn, Bonn, Germany.
[Ti] Título:The mechanisms how heparin affects the tumor cell induced VEGF and chemokine release from platelets to attenuate the early metastatic niche formation.
[So] Source:PLoS One;13(1):e0191303, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Metastasis is responsible for the majority of cancer associated fatalities. Tumor cells leaving the primary tumor and entering the blood flow immediately interact with platelets. Activated platelets contribute in different ways to cancer cell survival and proliferation, e.g. in formation of the early metastatic niche by release of different growth factors and chemokines. Here we show that a direct interaction between platelets and MV3 melanoma or MCF7 breast cancer cells induces platelet activation and a VEGF release in citrated plasma that cannot be further elevated by the coagulation cascade and generated thrombin. In contrast, the release of platelet-derived chemokines CXCL5 and CXCL7 depends on both, a thrombin-mediated platelet activation and a direct interaction between tumor cells and platelets. Preincubation of platelets with therapeutic concentrations of unfractionated heparin reduces the tumor cell initiated VEGF release from platelets. In contrast, tumor cell induced CXCL5 and CXCL7 release from platelets was not impacted by heparin pretreatment in citrated plasma. In defibrinated, recalcified plasma, on the contrary, heparin is able to reduce CXCL5 and CXCL7 release from platelets by thrombin inhibition. Our data indicate that different chemokines and growth factors in diverse platelet granules are released in tightly regulated processes by various trigger mechanisms. We show for the first time that heparin is able to reduce the mediator release induced by different tumor cells both in a contact and coagulation dependent manner.
[Mh] Termos MeSH primário: Plaquetas/efeitos dos fármacos
Quimiocina CXCL5/secreção
Heparina/farmacologia
Microambiente Tumoral/efeitos dos fármacos
Fator A de Crescimento do Endotélio Vascular/secreção
beta-Tromboglobulina/secreção
[Mh] Termos MeSH secundário: Coagulação Sanguínea/efeitos dos fármacos
Plaquetas/fisiologia
Linhagem Celular Tumoral
Seres Humanos
Metástase Neoplásica
Ativação Plaquetária/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chemokine CXCL5); 0 (PPBP protein, human); 0 (Vascular Endothelial Growth Factor A); 0 (beta-Thromboglobulin); 9005-49-6 (Heparin)
[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:180119
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191303


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[PMID]:29324883
[Au] Autor:Jenny L; Dobó J; Gál P; Pál G; Lam WA; Schroeder V
[Ad] Endereço:Experimental Haemostasis Group, Department for BioMedical Research, University of Bern, Bern, Switzerland.
[Ti] Título:MASP-1 of the complement system enhances clot formation in a microvascular whole blood flow model.
[So] Source:PLoS One;13(1):e0191292, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The complement and coagulation systems closely interact with each other. These interactions are believed to contribute to the proinflammatory and prothrombotic environment involved in the development of thrombotic complications in many diseases. Complement MASP-1 (mannan-binding lectin-associated serine protease-1) activates coagulation factors and promotes clot formation. However, this was mainly shown in purified or plasma-based static systems. Here we describe the role of MASP-1 and complement activation in fibrin clot formation in a microvascular, whole blood flow model. This microfluidic system simulates blood flow through microvessels at physiological flow and shear rates and represents the closest model system to human physiology so far. It features parallel microchannels cultured with endothelial cells in a transparent microfluidic chip allowing real-time evaluation of clot formation by confocal microscopy. To test their effects on clot formation, we added the following activators or inhibitors (individually or in combination) to whole blood and performed perfusion experiments: rMASP-1cf (recombinant active form of MASP-1), complement activator zymosan, selective MASP-1 inhibitor SGMI-1 (based on the Schistocerca gregaria protease inhibitor scaffold), classical pathway inhibitor rSALO (recombinant salivary anti-complement from Lutzomyia longipalpis). Addition of rMASP-1cf resulted in accelerated fibrin clot formation while addition of SGMI-1 delayed it. Complement activation by zymosan led to increased clot formation and this effect was partially reversed by addition of rSALO and almost abolished in combination with SGMI-1. We show for the first time a strong influence of MASP-1, complement activation and pathway-specific inhibition on coagulation in a microvascular flow system that is closest to human physiology, further underpinning the in vivo relevance of coagulation and complement interactions.
[Mh] Termos MeSH primário: Coagulação Sanguínea
Proteínas do Sistema Complemento/metabolismo
Serina Proteases Associadas a Proteína de Ligação a Manose/metabolismo
Microvasos/fisiologia
[Mh] Termos MeSH secundário: Seres Humanos
Lectinas/metabolismo
Serina Proteases Associadas a Proteína de Ligação a Manose/química
Domínios Proteicos
Zimosan/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Lectins); 9007-36-7 (Complement System Proteins); 9010-72-4 (Zymosan); EC 3.4.21.- (MASP1 protein, human); EC 3.4.21.- (Mannose-Binding Protein-Associated Serine Proteases)
[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:180112
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191292


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[PMID]:29254304
[Au] Autor:Li JK; Wang C; Gong HD; Li HZ
[Ad] Endereço:Department of Neurosurgery, Affiliated HongQi Hospital of Mu Dan Jiang Medical University, Mudanjiang City, China.
[Ti] Título:Coagulation in hindbrain membrane meningioma patients treated with different injections using acute hypervolemic hemodilution.
[So] Source:J Biol Regul Homeost Agents;31(4):991-996, 2017 Oct-Dec.
[Is] ISSN:0393-974X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to analyze the changes in coagulation in meningioma patients treated with different injections using the method of acute hypervolemic hemodilution (AHH). One hundred fifty hindbrain membrane meningioma patients were randomly divided into 5 groups, 30 per group. The first group were injected 40ml/time with Danhong after anesthesia induction; the second group were injected with 40ml~60ml/time Kangai and combined with interventional chemotherapy and embolization procedure; the third group of AHH were injected with polygeline 15ml/kg; the fourth group were injected with hydroxyethyl starch (130/0.4) sodium chloride in doses of 15ml/kg; the control group underwent basic treatment for lowering blood pressure and lowering blood fat. The changes of coagulation index were recorded before and after surgery and before and after the injection of different medications. Compared to the control group, for the first group of AHH, after being treated for 10 days and 30 days, the concentrations of bone specific alkaline phosphatase (BALP), bone Gla protein (BGP) and pro-collagen carboxy-terminal propeptide (PICP) were higher than that of the control group, the levels of endotoxin (ET) and C-reactive protein (CRP) were decreased compared to the control group (p less than 0.05); for the second group of AHH, after being treated for 10 days, the index of prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin time (TT), fibrinogen (Fg) were not significantly changed, but the related level of vascular endothelial growth factor (VEGF) significantly decreased (p less than 0.05). Comparing the coagulation function index after surgery in the third and fourth groups, there were no significant changes in mean arterial pressure (MAP) level, heart rate (HR) value presented a low decrease, central venous pressure (CVP) level increased and the level of interleukin IL-6 showed a steady state after increasing. Analyzing the levels of interleukin IL-8 and tumor necrosis factor-α (TNF-α) after surgery, it was seen that in the third group they increased and in the fourth group they decreased (p less than 0.05). Danhong injection improved the coagulation function and microcirculation of patients, Kangai injection and interventional chemotherapy and embolization restrained the appearance of tumor angiogenesis, AHH operation with polygeline injection and hydroxyethyl starch (130/0.4) sodium chloride kept blood flow in normal parameters.
[Mh] Termos MeSH primário: Coagulação Sanguínea/efeitos dos fármacos
Cardiotônicos/uso terapêutico
Medicamentos de Ervas Chinesas/uso terapêutico
Hemodiluição/métodos
Neoplasias Meníngeas/tratamento farmacológico
Meningioma/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Fosfatase Alcalina/genética
Fosfatase Alcalina/metabolismo
Pressão Arterial/efeitos dos fármacos
Pressão Arterial/fisiologia
Biomarcadores/metabolismo
Viscosidade Sanguínea/efeitos dos fármacos
Proteína C-Reativa/genética
Proteína C-Reativa/metabolismo
Embolização Terapêutica/métodos
Endotoxinas/metabolismo
Feminino
Fibrinogênio/genética
Fibrinogênio/metabolismo
Expressão Gênica
Frequência Cardíaca/efeitos dos fármacos
Frequência Cardíaca/fisiologia
Seres Humanos
Derivados de Hidroxietil Amido/administração & dosagem
Masculino
Neoplasias Meníngeas/sangue
Neoplasias Meníngeas/patologia
Neoplasias Meníngeas/cirurgia
Meningioma/sangue
Meningioma/patologia
Meningioma/cirurgia
Meia-Idade
Osteocalcina/genética
Osteocalcina/metabolismo
Fragmentos de Peptídeos/genética
Fragmentos de Peptídeos/metabolismo
Substitutos do Plasma/administração & dosagem
Poligelina/administração & dosagem
Pró-Colágeno/genética
Pró-Colágeno/metabolismo
Rombencéfalo/efeitos dos fármacos
Rombencéfalo/metabolismo
Rombencéfalo/patologia
Rombencéfalo/cirurgia
Fator A de Crescimento do Endotélio Vascular/genética
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cardiotonic Agents); 0 (Drugs, Chinese Herbal); 0 (Endotoxins); 0 (Hydroxyethyl Starch Derivatives); 0 (Peptide Fragments); 0 (Plasma Substitutes); 0 (Procollagen); 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A); 0 (danhong); 0 (procollagen type I carboxy terminal peptide); 104982-03-8 (Osteocalcin); 9001-32-5 (Fibrinogen); 9007-41-4 (C-Reactive Protein); 9015-56-9 (Polygeline); EC 3.1.3.1 (Alkaline Phosphatase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171220
[St] Status:MEDLINE


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[PMID]:29224364
[Au] Autor:Dimitropoulos G; Rahim SMZ; Moss AS; Lip GYH
[Ad] Endereço:a Institute of Cardiovascular Sciences , University of Birmingham , Birmingham , UK.
[Ti] Título:New anticoagulants for venous thromboembolism and atrial fibrillation: what the future holds.
[So] Source:Expert Opin Investig Drugs;27(1):71-86, 2018 Jan.
[Is] ISSN:1744-7658
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: The field of anticoagulation has seen impressive progress over the last decade. The introduction of the Non Vitamin K Oral Anticoagulants (NOACs) has revolutionized practice surrounding thromboprophylaxis, treatment of thromboembolic disease and stroke prevention in atrial fibrillation (AF). However, the search for the 'holy grail' of anticoagulation, an agent that combines optimal efficacy with minimal bleeding diathesis, continues. Areas covered: In this paper we aim to summarize the current evidence from pre-clinical studies and early phase clinical trials, presenting the pharmacodynamic and pharmacokinetic properties as well as the safety and efficacy profiles of the most important antithrombotic agents in development. Expert opinion: Research focused on the development of new anticoagulation agents is rapidly expanding. Although the exploration of antithrombotic agents that act on well-established targets such factor Xa and thrombin remains the mainstay, attention has also shifted to other factors in the coagulation cascade. The evidence emerging from clinical research is growing, generating exciting possibilities in the field of anticoagulation.
[Mh] Termos MeSH primário: Anticoagulantes/uso terapêutico
Fibrilação Atrial/tratamento farmacológico
Tromboembolia Venosa/prevenção & controle
[Mh] Termos MeSH secundário: Animais
Anticoagulantes/efeitos adversos
Anticoagulantes/farmacologia
Fibrilação Atrial/complicações
Coagulação Sanguínea/efeitos dos fármacos
Desenho de Drogas
Fibrinolíticos/efeitos adversos
Fibrinolíticos/farmacologia
Fibrinolíticos/uso terapêutico
Hemorragia/induzido quimicamente
Seres Humanos
Acidente Vascular Cerebral/etiologia
Acidente Vascular Cerebral/prevenção & controle
Tromboembolia Venosa/etiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anticoagulants); 0 (Fibrinolytic Agents)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE
[do] DOI:10.1080/13543784.2018.1416090


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[PMID]:27778439
[Au] Autor:Randi AM; Laffan MA
[Ad] Endereço:National Heart and Lung Institute, Imperial College, London, UK.
[Ti] Título:Von Willebrand factor and angiogenesis: basic and applied issues.
[So] Source:J Thromb Haemost;15(1):13-20, 2017 01.
[Is] ISSN:1538-7836
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The recent discovery that von Willebrand factor (VWF) regulates blood vessel formation has opened a novel perspective on the function of this complex protein. VWF was discovered as a key component of hemostasis, capturing platelets at sites of endothelial damage and synthesized in megakaryocytes and endothelial cells (EC). In recent years, novel functions and binding partners have been identified for VWF. The finding that loss of VWF in EC results in enhanced, possibly dysfunctional, angiogenesis is consistent with the clinical observations that in some patients with von Willebrand disease (VWD), vascular malformations can cause severe gastrointestinal (GI) bleeding. In vitro and in vivo studies indicate that VWF can regulate angiogenesis through multiple pathways, both intracellular and extracellular, although their relative importance is still unclear. Investigation of these pathways has been greatly facilitated by the ability to isolate EC from progenitors circulating in the peripheral blood of normal controls and patients with VWD. In the next few years, these will yield further evidence on the molecular pathways controlled by VWF and shed light on this novel and fascinating area of vascular biology. In this article, we will review the evidence supporting a role for VWF in blood vessel formation, the link between VWF dysfunction and vascular malformations causing GI bleeding and how they may be causally related. Finally, we will discuss how these findings point to novel therapeutic approaches to bleeding refractory to VWF replacement therapy in VWD.
[Mh] Termos MeSH primário: Neovascularização Fisiológica
Fator de von Willebrand/metabolismo
[Mh] Termos MeSH secundário: Angiodisplasia/metabolismo
Animais
Coagulação Sanguínea
Plaquetas/metabolismo
Células Endoteliais/metabolismo
Hemorragia Gastrointestinal/sangue
Glicoproteínas/metabolismo
Hemorragia
Hemostasia
Seres Humanos
Megacariócitos/metabolismo
Camundongos
Neovascularização Patológica
Transdução de Sinais
Células-Tronco/metabolismo
Receptor 2 de Fatores de Crescimento do Endotélio Vascular/metabolismo
Doenças de von Willebrand/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Glycoproteins); 0 (von Willebrand Factor); EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-2)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1111/jth.13551


  8 / 33517 MEDLINE  
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[PMID]:27774726
[Au] Autor:Jonsson PI; Letertre L; Juliusson SJ; Gudmundsdottir BR; Francis CW; Onundarson PT
[Ad] Endereço:Landspitali - The National University Hospital of Iceland, Reykjavik, Iceland.
[Ti] Título:During warfarin induction, the Fiix-prothrombin time reflects the anticoagulation level better than the standard prothrombin time.
[So] Source:J Thromb Haemost;15(1):131-139, 2017 01.
[Is] ISSN:1538-7836
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Essentials Fiix-prothrombin time (PT) monitoring of warfarin measuring factor (F) II and X, is effective. Plasma obtained during warfarin induction and stable phase in Fiix-trial was assayed. Fiix-PT stabilized anticoagulation earlier than monitoring with traditional PT-INR. FVII had little effect on thrombin generation that was mainly determined by FII and FX. SUMMARY: Background The prothrombin time (PT) is equally prolonged by reduction of each of the vitamin K-dependent (VKD) factors (F) II, VII and X. The Fiix-PT is only affected by FII and FX, the main contributors to thrombin generation (TG). Objective To test the hypothesis that variability in warfarin anticoagulation is reduced early during monitoring with the normalized PT-ratio calculated from Fiix-PT (Fiix-International Normalized Ratio [INR]) compared with traditional PT-INR monitoring. Also, that because of its insensitivity to FVII, Fiix-PT more accurately reflects TG when Fiix-INR and PT-INR are discrepant. Methods Samples from Fiix-trial participants monitored with either Fiix-PT or PT were used. VKD coagulation factors and TG were measured in samples from 40 patients during stable anticoagulation and in serial samples obtained from 26 patients during warfarin induction. TG was assessed in relation to selective reduction in single VKD factors. Results During Fiix-warfarin induction full anticoagulation measured as FII or FX activity was achieved at a similar rate to that with PT-warfarin but subsequently stabilized better. Fiix-INR but not PT-INR mirrored total TG during initiation. During induction, FII (R = 0.66) and FX (R = 0.52) correlated better with TG and with a steeper slope than did FIX (R = 0.37) and in particular FVII (R = 0.21). In vitro, FII and FX were the main determinants of TG at concentrations observed during VKA anticoagulation, whereas FVII and FIX had little influence. Conclusions Fiix-PT monitoring reduces anticoagulation variability, suggesting that monitoring FVII has a limited role during VKA management. TG is better reflected by Fiix-PT.
[Mh] Termos MeSH primário: Anticoagulantes/uso terapêutico
Fator X/química
Protrombina/química
Varfarina/uso terapêutico
[Mh] Termos MeSH secundário: Idoso
Coagulação Sanguínea/efeitos dos fármacos
Fatores de Coagulação Sanguínea/uso terapêutico
Testes de Coagulação Sanguínea/métodos
Método Duplo-Cego
Monitoramento de Medicamentos
Feminino
Hemostáticos/uso terapêutico
Seres Humanos
Coeficiente Internacional Normatizado
Masculino
Meia-Idade
Tempo de Protrombina
Trombina/química
Vitamina K/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Anticoagulants); 0 (Blood Coagulation Factors); 0 (Hemostatics); 12001-79-5 (Vitamin K); 5Q7ZVV76EI (Warfarin); 9001-26-7 (Prothrombin); 9001-29-0 (Factor X); EC 3.4.21.5 (Thrombin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1111/jth.13549


  9 / 33517 MEDLINE  
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[PMID]:29314796
[Au] Autor:Sarac M; Marjanovic I; Bezmarevic M; Sarac S; Milic R; Obradovic S; Tomic A
[Ti] Título:Influence of open surgical and endovascular abdominal aortic aneurysm repair on clot quality assessed by ROTEM® test.
[So] Source:Vojnosanit Pregl;73(7):643-50, 2016 Jul.
[Is] ISSN:0042-8450
[Cp] País de publicação:Serbia
[La] Idioma:eng
[Ab] Resumo:Introduction/Aim: The disturbances in hemostasis are often in open surgical repair (OR) and endovascular repair (EVAR) of an abdominal aortic aneurysm (AAA). These changes may influence the perioperative and early postoperative period inducing serious complications. The aim of this study was to compare the impact of OR and EVAR of AAA on clot quality assessed by rotational thromboelastometry (ROTEM®) tests. Methods: The study included 40 patients who underwent elective AAA surgery and were devided into two groups (the OR and the EVAR group - 20 patients in each group). The ROTEM ® test was performed in 4 points: point 1 - 10 min before starting anesthesia in both groups; point 2 - 10 min after aortic clapming in the OR group and 10 min after the stent-graft trunk release in the EVAR group; point 3 - 10 min after the releasing of aortic clamp in the OR group and 10 min after stentgraft placement and releasing the femoral clamp in the EVAR group; point 4 - one hour after the procedure in both groups. Three ROTEM® tests were performed as: extrinsically activated assay with tissue factor (EXTEM), intrinsically activated test using kaolin (INTEM), and extrinsically activated test with tissue factor and the platelet inhibitor cytochalasin D (FIBTEM). All tests included the assessment of the maximum clot firmness (MCF) and the platelet component of clot strength was presented as maximal clot elasticity (MCE). Results: No significant difference in age, gender and diameter of AAA between groups was found. The time required for the procedure was significantly longer and loss of blood was greater in the OR group than in the EVAR group (p < 0.001). The significant deviation of MCF values in EXTEM test was found mainly in the point 3 (p ≤ 0.004) with significant difference between groups (p < 0.001). A significant difference of MCF values in INTEM test between groups was found in the points 3 and 4 (p < 0.001), which were dose-dependent by heparin sulfate. The MCF values in FIBTEM test were more prominent in the OR group than in the EVAR group without significant difference. The significant changes of MCF values in the FIBTEM test were found during time in both groups (p < 0.001). The values of MCE were lower in both groups, but without significant changes and difference between groups (p = 0.105). Conclusion: The disorders of hemostatic parameters assessed by ROTEM® tests are present in both the OR and the EVAR groups being more prominent in OR of AAA. Vigilant monitoring of hemostatic parameters evaluated by ROTEM® tests could help in administration of the adequate and target therapy in patients who underwent EVAR or OR of AAA.
[Mh] Termos MeSH primário: Aneurisma da Aorta Abdominal/sangue
Aneurisma da Aorta Abdominal/cirurgia
Coagulação Sanguínea
Procedimentos Endovasculares
[Mh] Termos MeSH secundário: Idoso
Transtornos da Coagulação Sanguínea/etiologia
Testes de Coagulação Sanguínea
Procedimentos Endovasculares/efeitos adversos
Feminino
Seres Humanos
Masculino
Complicações Pós-Operatórias
Estudos Prospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180110
[St] Status:MEDLINE
[do] DOI:10.2298/VSP150510123S


  10 / 33517 MEDLINE  
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[PMID]:29226714
[Au] Autor:Jákó J
[Ad] Endereço:Budapest, Oltvány u. 28., 1112.
[Ti] Título:[Analysis of D-dimer laboratory findings and clinical evaluation].
[Ti] Título:A D-dimer laboratóriumi eredményeinek és klinikai értékelésének elemzése..
[So] Source:Orv Hetil;158(50):1971-1976, 2017 Dec.
[Is] ISSN:0030-6002
[Cp] País de publicação:Hungary
[La] Idioma:hun
[Ab] Resumo:D-dimer is a product of the enzymatic degradation of the fibrinogen-fibrin molecule, and its existence is demonstrable in circulation. The test based limits may be considered as normal values. It was first thought to be a product of coagulation, then a product of lysis. High-concentration D-dimer in blood detected in thromboembolic diseases is considered to be of diagnostic value. In cases where thromboembolism was ruled out despite elevated titres but heparin (LMWH) or CLOPIDOGREL was given as a cautionary measure, we found that D-dimer values remained elevated. This finding means that in vivo coagulation is not a precondition to D-dimer formation. Analysis of such cases uncovers liver or kidney disease in the background, but old age may also be a factor. Often elevated ferritin levels were observed 'in parallel' with elevated D-dimer values. These findings lead us to presume an enzymatic degradation process of 'elderly' protein molecules, which is universally applicable. Orv Hetil. 2017; 158(50): 1971-1976.
[Mh] Termos MeSH primário: Produtos de Degradação da Fibrina e do Fibrinogênio/análise
Tromboembolia/sangue
[Mh] Termos MeSH secundário: Biomarcadores/sangue
Coagulação Sanguínea
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Fibrin Fibrinogen Degradation Products); 0 (fibrin fragment D)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE
[do] DOI:10.1556/650.2017.30909



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