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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


  2 / 3311 MEDLINE  
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[PMID]:28801460
[Au] Autor:Muehl EM; Gajsiewicz JM; Medfisch SM; Wiersma ZSB; Morrissey JH; Bailey RC
[Ad] Endereço:From the Departments of Chemistry and.
[Ti] Título:Multiplexed silicon photonic sensor arrays enable facile characterization of coagulation protein binding to nanodiscs with variable lipid content.
[So] Source:J Biol Chem;292(39):16249-16256, 2017 Sep 29.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Interactions of soluble proteins with the cell membrane are critical within the blood coagulation cascade. Of particular interest are the interactions of γ-carboxyglutamic acid-rich domain-containing clotting proteins with lipids. Variability among conventional analytical methods presents challenges for comparing clotting protein-lipid interactions. Most previous studies have investigated only a single clotting protein and lipid composition and have yielded widely different binding constants. Herein, we demonstrate that a combination of lipid bilayer nanodiscs and a multiplexed silicon photonic analysis technology enables high-throughput probing of many protein-lipid interactions among blood-clotting proteins. This approach allowed direct comparison of the binding constants of prothrombin, factor X, activated factor VII, and activated protein C to seven different binary lipid compositions. In a single experiment, the binding constants of one protein interacting with all lipid compositions were simultaneously determined. A simple surface regeneration then facilitated similar binding measurements for three other coagulation proteins. As expected, our results indicated that all proteins exhibit tighter binding (lower ) as the proportion of anionic lipid increases. Interestingly, at high proportions of phosphatidylserine, the values of all four proteins began to converge. We also found that although values for all four proteins followed trends similar to those observed for the values, the variation among the proteins was much lower, indicating that much of the variation came from the kinetic binding ( ) of the proteins. These findings indicate that the combination of silicon photonic microring resonator arrays and nanodiscs enables rapid interrogation of biomolecular binding interactions at model cell membrane interfaces.
[Mh] Termos MeSH primário: Fator VIIa/metabolismo
Fator X/metabolismo
Ácidos Fosfatídicos/metabolismo
Fosfatidilcolinas/metabolismo
Fosfatidilserinas/metabolismo
Proteína C/metabolismo
Protrombina/metabolismo
[Mh] Termos MeSH secundário: Fator VIIa/química
Fator VIIa/genética
Fator X/química
Ensaios de Triagem em Larga Escala
Seres Humanos
Cinética
Bicamadas Lipídicas/química
Bicamadas Lipídicas/metabolismo
Nanoestruturas/química
Fenômenos Ópticos
Ácidos Fosfatídicos/química
Fosfatidilcolinas/química
Fosfatidilserinas/química
Análise Serial de Proteínas
Proteína C/química
Protrombina/química
Proteínas Recombinantes/química
Proteínas Recombinantes/metabolismo
Silício/química
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (1-palmitoyl-2-oleoyl-glycero-3-phosphatidic acid); 0 (Lipid Bilayers); 0 (Phosphatidic Acids); 0 (Phosphatidylcholines); 0 (Phosphatidylserines); 0 (Protein C); 0 (Recombinant Proteins); 40290-44-6 (1-palmitoyl-2-oleoylglycero-3-phosphoserine); 9001-26-7 (Prothrombin); 9001-29-0 (Factor X); EC 3.4.21.21 (Factor VIIa); TE895536Y5 (1-palmitoyl-2-oleoylphosphatidylcholine); Z4152N8IUI (Silicon)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170813
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.800938


  3 / 3311 MEDLINE  
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[PMID]:28674296
[Au] Autor:Igawa T
[Ad] Endereço:Research Division, Biologics Discovery Department, Chugai Pharmaceutical Co., Ltd.
[Ti] Título:Next Generation Antibody Therapeutics Using Bispecific Antibody Technology.
[So] Source:Yakugaku Zasshi;137(7):831-836, 2017.
[Is] ISSN:1347-5231
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:Nearly fifty monoclonal antibodies have been approved to date, and the market for monoclonal antibodies is expected to continue to grow. Since global competition in the field of antibody therapeutics is intense, we need to establish novel antibody engineering technologies to provide true benefit for patients, with differentiated product values. Bispecific antibodies are among the next generation of antibody therapeutics that can bind to two different target antigens by the two arms of immunoglobulin G (IgG) molecule, and are thus believed to be applicable to various therapeutic needs. Until recently, large scale manufacturing of human IgG bispecific antibody was impossible. We have established a technology, named asymmetric re-engineering technology (ART)-Ig, to enable large scale manufacturing of bispecific antibodies. Three examples of next generation antibody therapeutics using ART-Ig technology are described. Recent updates on bispecific antibodies against factor IXa and factor X for the treatment of hemophilia A, bispecific antibodies against a tumor specific antigen and T cell surface marker CD3 for cancer immunotherapy, and bispecific antibodies against two different epitopes of soluble antigen with pH-dependent binding property for the elimination of soluble antigen from plasma are also described.
[Mh] Termos MeSH primário: Anticorpos Biespecíficos
Anticorpos Monoclonais
Imunoglobulina G
Engenharia de Proteínas/métodos
[Mh] Termos MeSH secundário: Anticorpos Biespecíficos/uso terapêutico
Anticorpos Monoclonais/uso terapêutico
Antígenos de Neoplasias/imunologia
Complexo CD3/imunologia
Epitopos/imunologia
Fator IXa/imunologia
Fator X/imunologia
Hemofilia A/terapia
Seres Humanos
Concentração de Íons de Hidrogênio
Imunoterapia
Neoplasias/terapia
Ligação Proteica
Solubilidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antibodies, Bispecific); 0 (Antibodies, Monoclonal); 0 (Antigens, Neoplasm); 0 (CD3 Complex); 0 (Epitopes); 0 (Immunoglobulin G); 9001-29-0 (Factor X); EC 3.4.21.22 (Factor IXa)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170705
[St] Status:MEDLINE
[do] DOI:10.1248/yakushi.16-00252-3


  4 / 3311 MEDLINE  
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[PMID]:28576875
[Au] Autor:Hu Z; Liu Y; Huarng MC; Menegatti M; Reyon D; Rost MS; Norris ZG; Richter CE; Stapleton AN; Chi NC; Peyvandi F; Joung JK; Shavit JA
[Ad] Endereço:Department of Pediatrics and Communicable Diseases, University of Michigan, Ann Arbor, MI.
[Ti] Título:Genome editing of factor X in zebrafish reveals unexpected tolerance of severe defects in the common pathway.
[So] Source:Blood;130(5):666-676, 2017 Aug 03.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Deficiency of factor X (F10) in humans is a rare bleeding disorder with a heterogeneous phenotype and limited therapeutic options. Targeted disruption of and other common pathway factors in mice results in embryonic/neonatal lethality with rapid resorption of homozygous mutants, hampering additional studies. Several of these mutants also display yolk sac vascular defects, suggesting a role for thrombin signaling in vessel development. The zebrafish is a vertebrate model that demonstrates conservation of the mammalian hemostatic and vascular systems. We have leveraged these advantages for in-depth study of the role of the coagulation cascade in the developmental regulation of hemostasis and vasculogenesis. In this article, we show that ablation of zebrafish by using genome editing with transcription activator-like effector nucleases results in a major embryonic hemostatic defect. However, widespread hemorrhage and subsequent lethality does not occur until later stages, with absence of any detectable defect in vascular development. We also use zebrafish to confirm 5 novel human variants as causative mutations in affected patients, providing a rapid and reliable in vivo model for testing the severity of variants. These findings as well as the prolonged survival of mutants will enable us to expand our understanding of the molecular mechanisms of hemostasis, including a platform for screening variants of uncertain significance in patients with F10 deficiency and other coagulation disorders. Further study as to how fish tolerate what is an early lethal mutation in mammals could facilitate improvement of diagnostics and therapeutics for affected patients with bleeding disorders.
[Mh] Termos MeSH primário: Coagulação Sanguínea/genética
Fator X
Edição de Genes
Mutação
Proteínas de Peixe-Zebra
Peixe-Zebra
[Mh] Termos MeSH secundário: Animais
Fator X/genética
Fator X/metabolismo
Deficiência do Fator X/embriologia
Deficiência do Fator X/genética
Seres Humanos
Camundongos
Peixe-Zebra/embriologia
Peixe-Zebra/genética
Proteínas de Peixe-Zebra/genética
Proteínas de Peixe-Zebra/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Zebrafish Proteins); 9001-29-0 (Factor X)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170824
[Lr] Data última revisão:
170824
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170604
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2017-02-765206


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[PMID]:28537975
[Au] Autor:Abuelkasem E; Hasan S; Mazzeffi MA; Planinsic RM; Sakai T; Tanaka KA
[Ad] Endereço:From the *Department of Anesthesiology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania; and †Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, Maryland.
[Ti] Título:Reduced Requirement for Prothrombin Complex Concentrate for the Restoration of Thrombin Generation in Plasma From Liver Transplant Recipients.
[So] Source:Anesth Analg;125(2):609-615, 2017 Aug.
[Is] ISSN:1526-7598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Plasma transfusion remains the mainstay hemostatic therapy during liver transplantation (LT) in most countries. However, a large volume is required for plasma to achieve clinically relevant factor increases. Prothrombin complex concentrate (PCC) is a low-volume alternative to plasma in warfarin reversal, but its efficacy has not been well studied in LT. METHODS: Blood samples were collected from 28 LT patients at baseline (T0) and 30 minutes after graft reperfusion (T1). Factor X and antithrombin levels were measured. Ex vivo effects of PCC (0.2 and 0.4 IU/mL) and 10% volume replacement with normal plasma were compared in LT and warfarin plasma by measuring lag time, thrombin peak, and endogenous thrombin potential (ETP) using thrombin generation (TG) assay. RESULTS: Coagulation status was worsened at T1 as international normalized ratio increased from 1.7 to 3.0, and factor X was decreased from 49% to 28%. TG measurements showed normal lag time and ETP at T0 and T1, but low-normal peak at T0, and below-normal peak at T1. Both doses of PCC increased peak and ETP, while 10% volume plasma had minimal effects on TG. Thrombin inhibition appears to be very slow after adding 0.4 IU/mL of PCC in LT plasma due to low antithrombin. The same doses of PCC and plasma were insufficient for warfarin reversal. CONCLUSIONS: Reduced TG in LT can be more effectively restored by using PCC rather than plasma. The required doses of PCC for LT patients seem to be lower than warfarin reversal due to slow thrombin inhibition.
[Mh] Termos MeSH primário: Fatores de Coagulação Sanguínea/uso terapêutico
Transplante de Fígado/efeitos adversos
Trombina/fisiologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Antitrombinas/sangue
Coagulação Sanguínea
Testes de Coagulação Sanguínea
Fator X/análise
Feminino
Hematócrito
Hemostasia
Hemostáticos/uso terapêutico
Seres Humanos
Coeficiente Internacional Normatizado
Masculino
Meia-Idade
Contagem de Plaquetas
Tempo de Protrombina
Fatores de Tempo
Medicina Transfusional
Transplantados
Varfarina/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antithrombins); 0 (Blood Coagulation Factors); 0 (Hemostatics); 37224-63-8 (prothrombin complex concentrates); 5Q7ZVV76EI (Warfarin); 9001-29-0 (Factor X); EC 3.4.21.5 (Thrombin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170525
[St] Status:MEDLINE
[do] DOI:10.1213/ANE.0000000000002106


  6 / 3311 MEDLINE  
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[PMID]:28441767
[Au] Autor:Xiong L; Qi Z; Zheng B; Li Z; Wang F; Liu J; Li P
[Ad] Endereço:School of Pharmaceutical Sciences, Jilin University, Fujin Road 1266, Changchun 130021, China. xionglx14@mails.jlu.edu.cn.
[Ti] Título:Inhibitory Effect of Triterpenoids from Panax ginseng on Coagulation Factor X.
[So] Source:Molecules;22(4), 2017 Apr 24.
[Is] ISSN:1420-3049
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Enzymes involved in the coagulation process have received great attention as potential targets for the development of oral anti-coagulants. Among these enzymes, coagulation factor Xa (FXa) has remained the center of attention in the last decade. In this study, 16 ginsenosides and two sapogenins were isolated, identified and quantified. To determine the inhibitory potential on FXa, the chromogenic substrates method was used. The assay suggested that compounds , and were mainly responsible for the anti-coagulant effect. Furthermore, these three compounds also possessed high thrombin selectivity in the thrombin inhibition assay. Furthermore, Glide XP from Schrödinger was employed for molecular docking to clarify the interaction between the bioactive compounds and FXa. Therefore, the chemical and biological results indicate that compounds (ginsenoside Rg2), (ginsenoside Rg3) and (protopanaxtriol, PPT) are potential natural inhibitors against FXa.
[Mh] Termos MeSH primário: Fator X/química
Inibidores do Fator Xa/química
Ginsenosídeos/química
Panax/química
Extratos Vegetais/química
[Mh] Termos MeSH secundário: Sítios de Ligação
Cromatografia Líquida de Alta Pressão
Avaliação Pré-Clínica de Medicamentos
Fator X/antagonistas & inibidores
Inibidores do Fator Xa/isolamento & purificação
Inibidores do Fator Xa/farmacologia
Ginsenosídeos/isolamento & purificação
Ginsenosídeos/farmacologia
Cinética
Simulação de Acoplamento Molecular
Tempo de Tromboplastina Parcial
Extratos Vegetais/isolamento & purificação
Extratos Vegetais/farmacologia
Ligação Proteica
Proteólise
Trombina/antagonistas & inibidores
Trombina/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Factor Xa Inhibitors); 0 (Ginsenosides); 0 (Plant Extracts); 9001-29-0 (Factor X); EC 3.4.21.5 (Thrombin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170807
[Lr] Data última revisão:
170807
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170427
[St] Status:MEDLINE


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[PMID]:28381574
[Au] Autor:Lopez-Gordo E; Doszpoly A; Duffy MR; Coughlan L; Bradshaw AC; White KM; Denby L; Nicklin SA; Baker AH
[Ad] Endereço:Institute of Cardiovascular and Medical Sciences, BHF Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, United Kingdom.
[Ti] Título:Defining a Novel Role for the Coxsackievirus and Adenovirus Receptor in Human Adenovirus Serotype 5 Transduction in the Presence of Mouse Serum.
[So] Source:J Virol;91(12), 2017 Jun 15.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human adenoviral serotype 5 (HAdV-5) vectors have predominantly hepatic tropism when delivered intravascularly, resulting in immune activation and toxicity. Coagulation factor X (FX) binding to HAdV-5 mediates liver transduction and provides protection from virion neutralization in mice. FX is dispensable for liver transduction in mice lacking IgM antibodies or complement, suggesting that alternative transduction pathways exist. To identify novel factor(s) mediating HAdV-5 FX-independent entry, we investigated HAdV-5 transduction in the presence of serum from immunocompetent C57BL/6 or immunocompromised mice lacking IgM antibodies (Rag 2 and NOD-scid-gamma [NSG]). Sera from all three mouse strains enhanced HAdV-5 transduction of A549 cells. While inhibition of HAdV-5-FX interaction with FX-binding protein (X-bp) inhibited transduction in the presence of C57BL/6 serum, it had negligible effect on the enhanced transduction observed in the presence of Rag 2 or NSG serum. Rag 2 serum also enhanced transduction of the FX binding-deficient HAdV-5HVR5*HVR7*E451Q (AdT*). Interestingly, Rag 2 serum enhanced HAdV-5 transduction in a FX-independent manner in CHO-CAR and SKOV3-CAR cells (CHO or SKOV3 cells transfected to stably express human coxsackievirus and adenovirus receptor [CAR]). Additionally, blockade of CAR with soluble HAdV-5 fiber knob inhibited mouse serum-enhanced transduction in A549 cells, suggesting a potential role for CAR. Transduction of HAdV-5 KO1 and HAdV-5/F35 (CAR binding deficient) in the presence of Rag 2 serum was equivalent to that of HAdV-5, indicating that direct interaction between HAdV-5 and CAR is not required. These data suggest that FX may protect HAdV-5 from neutralization but has minimal contribution to HAdV-5 transduction in the presence of immunocompromised mouse serum. Alternatively, transduction occurs via an unidentified mouse serum protein capable of bridging HAdV-5 to CAR. The intravascular administration of HAdV-5 vectors can result in acute liver toxicity, transaminitis, thrombocytopenia, and injury to the vascular endothelium, illustrating challenges yet to overcome for HAdV-5-mediated systemic gene therapy. The finding that CAR and potentially an unidentified factor present in mouse serum might be important mediators of HAdV-5 transduction highlights that a better understanding of the complex biology defining the interplay between adenovirus immune recognition and cellular uptake mechanisms is still required. These findings are important to inform future optimization and development of HAdV-5-based adenoviral vectors for gene therapy.
[Mh] Termos MeSH primário: Adenovírus Humanos/metabolismo
Proteína de Membrana Semelhante a Receptor de Coxsackie e Adenovirus/metabolismo
Vetores Genéticos
Soro/imunologia
[Mh] Termos MeSH secundário: Células A549
Adenovírus Humanos/classificação
Animais
Linhagem Celular
Linhagem Celular Tumoral
Fator X/metabolismo
Seres Humanos
Imunocompetência
Hospedeiro Imunocomprometido
Técnicas In Vitro
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Endogâmicos NOD
Ligação Proteica
Sorogrupo
Tropismo Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CLMP protein, mouse); 0 (Coxsackie and Adenovirus Receptor-Like Membrane Protein); 9001-29-0 (Factor X)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170727
[Lr] Data última revisão:
170727
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170407
[St] Status:MEDLINE


  8 / 3311 MEDLINE  
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[PMID]:28302935
[Au] Autor:Matsuo Y; Mizuochi T; Miho M; Nakagawa S; Ozono S; Ueda K; Sogabe Y; Seki R; Soejima K; Okamura T; Yamashita Y
[Ad] Endereço:Department of Pediatrics and Child Health, Kurume University School of Medicine.
[Ti] Título:Factor X Deficiency with Heterozygous Mutations of Novel p.G435S and Known p.G244R in a Patient Presenting with Severe Umbilical Hemorrhage.
[So] Source:Kurume Med J;63(1.2):23-28, 2017 Apr 13.
[Is] ISSN:1881-2090
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:A 10-day-old male patient was referred to our hospital with severe umbilical bleeding. Prothrombin time (PT) and activated partial thromboplastin time (APTT) were prominently prolonged. Plasma coagulation factor X (FX) activity and antigen levels were 1% and 0.6%, respectively. A DNA sequence analysis of his leukocytes revealed a compound heterozygous state; known Gly244 to Arg (p.G244R) in exon 6 and a novel mutation of Gly 435 to Ser (p.G435S) in exon 8. A pedigree analysis showed that p.G244R originated from the paternal side, while p.G435S was from the maternal side. A p.G244R mutation was reported previously as FX and this mutated protein was synthesized as a non-secretable protein. The glycine at amino acid position 435 in the C-terminal region is completely conserved in the trypsin-like serine protease family, including thrombin, FVII, protein C, plasmin, trypsin, and chymotrypsin. In a three-dimensional structural model of FX, Gly 435 was located within the 11 ß-strand and buried in the back of the catalytic pocket. Therefore, the substitution to serine was expected to disrupt this structure. p.G435S FX was also predicted to be synthesized and exist in the cytoplasm, but not to be secreted into culture media by a cDNA expression assay. These two mutations may be responsible for the type 1 (null levels of both activity and antigen in plasma) FX deficiency with severe bleeding phenotype.
[Mh] Termos MeSH primário: Deficiência do Fator X/complicações
Deficiência do Fator X/genética
Fator X/genética
Hemorragia/complicações
Hemorragia/genética
Umbigo/patologia
[Mh] Termos MeSH secundário: Aminoácidos
Testes de Coagulação Sanguínea
Éxons
Feminino
Heterozigoto
Seres Humanos
Recém-Nascido
Masculino
Mutação
Pais
Tempo de Tromboplastina Parcial
Linhagem
Fenótipo
Conformação Proteica
Tempo de Protrombina
Tripsina/química
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acids); 9001-29-0 (Factor X); EC 3.4.21.4 (Trypsin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170318
[St] Status:MEDLINE
[do] DOI:10.2739/kurumemedj.MS6300007


  9 / 3311 MEDLINE  
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[PMID]:28214948
[Au] Autor:Oskarsdóttir AR; Gudmundsdottir BR; Indridason OS; Lund SH; Arnar DO; Bjornsson ES; Magnusson MK; Jensdottir HM; Vidarsson B; Francis CW; Onundarson PT
[Ad] Endereço:Department of Laboratory Hematology, Landspitali National University Hospital of Iceland, K-building, Hringbraut, 101, Reykjavik, Iceland.
[Ti] Título:Reduced anticoagulation variability in patients on warfarin monitored with Fiix-prothrombin time associates with reduced thromboembolism: The Fiix-trial.
[So] Source:J Thromb Thrombolysis;43(4):550-561, 2017 May.
[Is] ISSN:1573-742X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Fiix-prothrombin time (Fiix-PT) differs from traditional PT in being affected by reduced factor (F) II or FX only. In the randomized controlled Fiix-trial, patients on warfarin monitored with Fiix-PT (Fiix-warfarin patients) had fewer thromboembolisms (TE), similar major bleeding (MB) and more stable anticoagulation than patients monitored with PT (PT-warfarin patients). In the current Fiix-trial report we analyzed how reduced anticoagulation variability during Fiix-PT monitoring was reflected in patients with TE or bleeding. Data from 1143 randomized patients was used. We analyzed the groups for anticoagulation intensity (time within target range; TTR), international normalized ratio (INR) variability (variance growth rate B ; VGR) and dose adjustment frequency. We assessed how these parameters associated with clinically relevant vascular events (CRVE), ie TE or MB or clinically relevant non-MB. TTR was highest in Fiix-warfarin patients without CRVE (median 82%;IQR 72-91) and lowest in PT-warfarin patients with TE (62%;56-81). VGR was lowest in Fiix-warfarin patients without CRVE (median VGR B 0.17; 95% CI 0.08-0.38) and with TE (0.20;0.07-0.26) and highest in PT-warfarin patients with TE (0.50;0.27-0.90) or MB (0.59;0.07-1.36). The mean annual dose adjustment frequency was lowest in Fiix-warfarin patients with TE (mean 5.4;95% CI 3.9-7.3) and without CRVE (mean 6.0; 5.8-6.2) and highest in PT-warfarin patients with TE (14.2;12.2-16.3). Frequent dose changes predicted MB in both study arms. Compared to patients monitored with PT, high anticoagulation stability in Fiix-warfarin patients coincided with their low TE rate. Those with bleeding had high variability irrespective of monitoring method. Thus, although further improvements are needed to reduce bleeding, stabilization of anticoagulation by Fiix-PT monitoring associates with reduced TE.
[Mh] Termos MeSH primário: Anticoagulantes/administração & dosagem
Monitoramento de Medicamentos/métodos
Tempo de Protrombina
Tromboembolia/tratamento farmacológico
Varfarina/administração & dosagem
[Mh] Termos MeSH secundário: Fator X/farmacologia
Feminino
Hemorragia/induzido quimicamente
Seres Humanos
Coeficiente Internacional Normatizado
Masculino
Protrombina/farmacologia
Tromboembolia/prevenção & controle
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Anticoagulants); 5Q7ZVV76EI (Warfarin); 9001-26-7 (Prothrombin); 9001-29-0 (Factor X)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170220
[St] Status:MEDLINE
[do] DOI:10.1007/s11239-017-1482-4


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[PMID]:28213380
[Au] Autor:Muczynski V; Aymé G; Regnault V; Vasse M; Borgel D; Legendre P; Bazaa A; Harel A; Loubière C; Lenting PJ; Denis CV; Christophe OD
[Ad] Endereço:Institut National de la Santé et de la Recherche Médicale, Unité Mixte de Recherche (UMR)_S 1176, University Paris-Sud, Université Paris-Saclay, Le Kremlin-Bicêtre, France.
[Ti] Título:Complex formation with pentraxin-2 regulates factor X plasma levels and macrophage interactions.
[So] Source:Blood;129(17):2443-2454, 2017 Apr 27.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recently, we have identified scavenger receptor class A member I (SR-AI) as a receptor for coagulation factor X (FX), mediating the formation of an FX reservoir at the macrophage surface. Here, we demonstrate that the FX/SR-AI-complex comprises a third protein, pentraxin-2 (PTX2). The presence of PTX2 is essential to prevent internalization of FX by SR-AI, and the presence of FX is needed to interfere with internalization of PTX2. Binding studies showed that FX, SR-AI, and PTX2 independently bind to each other ( : 0.2-0.7 µM). Surprisingly, immunoprecipitation experiments revealed that FX and PTX2 circulate as a complex in plasma, and complex formation involves the FX activation peptide. No binding of PTX2 to other vitamin K-dependent proteins was observed. Short hairpin RNA-mediated inhibition of PTX2 levels in mice resulted not only in reduced levels of PTX2, but also in similarly reduced FX levels. Moreover, PTX2 and FX levels were correspondingly reduced in SR-AI-deficient mice. Analysis of 71 human plasma samples uncovered a strong correlation between FX and PTX2 plasma levels. Furthermore, plasma samples of patients with reduced FX levels (congenital/acquired FX deficiency or after anti-vitamin K treatment) were characterized by concomitantly decreased PTX2 levels. In conclusion, we identified PTX2 as a novel partner for FX, and both proteins cooperate to prevent their SR-AI-mediated uptake by macrophages. Interestingly, their respective plasma levels are interdependent. These findings seem of relevance in perspective of ongoing clinical trials, in which plasma depletion of PTX2 is used as a therapeutical approach in the management of systemic amyloidosis.
[Mh] Termos MeSH primário: Proteína C-Reativa/metabolismo
Deficiência do Fator X/sangue
Fator X/metabolismo
Macrófagos/metabolismo
Proteínas do Tecido Nervoso/metabolismo
Receptores Depuradores Classe A/metabolismo
[Mh] Termos MeSH secundário: Animais
Anticoagulantes/farmacologia
Proteína C-Reativa/genética
Linhagem Celular
Endocitose
Fator X/genética
Deficiência do Fator X/genética
Deficiência do Fator X/patologia
Expressão Gênica
Células HEK293
Seres Humanos
Cinética
Macrófagos/citologia
Macrófagos/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Proteínas do Tecido Nervoso/genética
Especificidade de Órgãos
Ligação Proteica
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Receptores Depuradores Classe A/antagonistas & inibidores
Receptores Depuradores Classe A/deficiência
Receptores Depuradores Classe A/genética
Vitamina K/antagonistas & inibidores
Vitamina K/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticoagulants); 0 (Nerve Tissue Proteins); 0 (RNA, Small Interfering); 0 (Scavenger Receptors, Class A); 0 (neuronal pentraxin); 12001-79-5 (Vitamin K); 9001-29-0 (Factor X); 9007-41-4 (C-Reactive Protein)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170809
[Lr] Data última revisão:
170809
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170219
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2016-06-724351



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