Factor Xiii Deficiency
Mostrando 1-9 de 9 artigos, teses e dissertações.
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1. Isolated biomolecules of pharmacological interest in hemostasis from Cerastes cerastes venom
Biomolecules from Cerastes cerastes venom have been purified and characterized. Two phospholipases isolated from Cerastes cerastes venom share 51% of homology. CC2-PLA2 exhibits antiplatelet activity that blocks coagulation. CCSV-MPase, a non-hemorrhagic Zn2+-metalloproteinase, significantly reduced the plasmatic fibrinogen level and hydrolyzes only its Bβ
J. Venom. Anim. Toxins incl. Trop. Dis. Publicado em: 01/05/2013
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2. Evaluation of fibrinolysis and factor XIII some parameters in patients with spontaneous deep venous trombosis and hemorrhagic disease / Avaliação de alguns parametros da fibrinolise e do fator XIII em pacientes com trombose venosa profunda espontanea e doença hemorragica
In a parcel of patients with hemorrhagic or thrombotic clinical picture, none etiologic diagnosis is established. The patients with hemorrhagic desorder, many times important, can present all inside the screening tests and specific dosage of factors of the coagulation of the values of normality. Note: the complete abstract is avaiable with the link or full e
Publicado em: 2008
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3. ε-(γ-Glutamyl)lysine in Fibrin: Lack of Crosslink Formation in Factor XIII Deficiency
Fibrin clots formed in normal plasma contained about 6 mol of ε-(γ-glutamyl)lysine per mol of fibrin, whereas those formed in plasma from individuals with Factor XIII deficiency contained little or none of this crosslink (0.02-0.64 mol/mol of fibrin). Partial supplementation of the plasma with Factor XIII, at a single concentration tested, commensurately i
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4. Deficiency of coagulation factor XIII A subunit caused by the dinucleotide deletion at the 5' end of exon III.
A congenital deficiency of the coagulation Factor XIII A subunit (F XIII A) is a rare autosomal recessive disorder that is characterized by a life-long bleeding tendency complicated by a difficulty in healing. Thus far, no molecular genetic analysis of this disorder has been reported. In this study, we demonstrate the molecular abnormalities in a family with
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5. Immunological Studies of Coagulation Factor XIII
Human fibrin-stabilizing factor (Factor XIII) has been studied immunologically by the preparation of specific anti-Factor XIII antiserum in rabbits. On immunodiffusion it was found that normal plasma produced two precipitin lines. One of the precipitin lines was identical with that present in soluble platelet extract (the α-component), the other with that p
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6. Coagulation factors IX through XIII and the risk of future venous thrombosis: the Longitudinal Investigation of Thromboembolism Etiology
Higher levels of procoagulant factors and factor XII deficiency may be risk factors for first venous thromboembolism (VTE). We studied associations of coagulation factors IX through XIII with risk of future VTE in 2 general population samples. Using a nested case-control study combining the 21 860 participants of the Atherosclerosis Risk in Communities study
American Society of Hematology.
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7. Laboratory evaluation of a bleeding patient.
Most causes of abnormal bleeding can be determined from a complete blood count including platelet count and bleeding, prothrombin, activated partial thromboplastin, and thrombin times. Occasionally, further evaluation is necessary, such as tests of factor XIII function, fibrinolysis, and vascular integrity. Possible diagnoses include disseminated intravascul
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8. Molecular and cellular basis of deficiency of the b subunit for factor XIII secondary to a Cys430-Phe mutation in the seventh Sushi domain.
We studied the defect responsible for deficiency of the b subunit for factor XIII in the first known case of this condition. The patient is a compound heterozygote of two genetic defects: deletion of A-4161 at the acceptor splice junction of intron A, resulting in a loss of the obligatory AG splicing sequence; and, replacement of G-11499 by T in exon VIII, r
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9. Significance of Cross-Linking of α2-Plasmin Inhibitor to Fibrin in Inhibition of Fibrinolysis and in Hemostasis
When blood is clotted, α2-plasmin inhibitor (α2PI) is cross-linked to fibrin by activated fibrin-stabilizing factor (activated coagulation Factor XIII, plasma transglutaminase). The amount of cross-linked α2-PI is proportional to the amount of α2PI present at the time of clotting. Plasma from a patient with congenital deficiency of α2PI was supplemented