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Gotowe bibliografie tematyczne / Factor XIII Val34Leu genetic polymorphism

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Gotowa bibliografia na temat „Factor XIII Val34Leu genetic polymorphism”

Autor: Grafiati

Data publikacji: 2 czerwca 2025

Data aktualizacji: 31 lipca 2025

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Artykuły w czasopismach na temat "Factor XIII Val34Leu genetic polymorphism"

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Sucker, Christoph, Firuseh Farokhzad, Christine Kurschat, et al. "The Homozygous Leu Variant of the Factor XIII Val34Leu Polymorphism as a Risk Factor for the Manifestation of Thrombotic Microangiopathies." Clinical and Applied Thrombosis/Hemostasis 15, no. 2 (2007): 197–200. http://dx.doi.org/10.1177/1076029607304723.

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The 34 Leu (100T) variant of the factor XIII Val34Leu (G100T-) polymorphism slows down fibrinolysis and has been proposed as a thrombotic risk factor. In this pilot study, we enrolled 40 patients (mean age ± SD = 38 ± 11 years) and 728 controls to assess the role of this genetic variant for the manifestation of thrombotic microangiopathies. From the genotype prevalences, an increased manifestation risk for carriers of the TT genotype (homozygous Leu variant) of the factor XIII Val34Leu (G100T-) polymorphism was calculated (odds ratio [OR] = 2.44; 95% confidence interval [CI] = 0.8-7.6; P = .11

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Härtel, Christoph, Sören von Otte, Julia Koch, et al. "Polymorphisms of haemostasis genes as risk factors for preterm delivery." Thrombosis and Haemostasis 94, no. 07 (2005): 88–92. http://dx.doi.org/10.1160/th04-10-0653.

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SummaryClinical trials evaluating the potential benefit of anticoagulant treatment in pregnant women with inherited thrombophilia are based on the observation that a genetic predisposition to thrombosis is associated with frequent abortions and preterm birth. It was the aim of our study to delineate the impact of genetic polymorphisms with prothrombotic and antithrombotic effects on the occurrence of preterm birth in a large cohort of very-low-birth-weight (VLBW)-infants and their mothers. We examined the factor V Leiden and the prothrombin G20210A mutation, the factor VII 121del/ins and the f

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Sarecka-Hujar, Beata, Danuta Łoboda, Elżbieta Paradowska-Nowakowska, and Krzysztof S. Gołba. "Coagulation Factor XIII Val34Leu Polymorphism in the Prediction of Premature Cardiovascular Events—The Results of Two Meta-Analyses." Journal of Clinical Medicine 11, no. 12 (2022): 3454. http://dx.doi.org/10.3390/jcm11123454.

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Background: Polymorphisms within the gene that encodes for coagulation factor XIII (FXIII) have been suggested to be involved in the pathogeneses of ischemic stroke (IS) and myocardial infarction (MI). The Val34Leu polymorphism is one of the most commonly analysed FXIII polymorphisms. However, studies on the role of the Val34Leu polymorphism in the aetiology of vascular diseases often show contradictory results. In the present meta-analysis, we aimed to pool data from available articles to assess the relationship between the FXIII Val34Leu polymorphism and the susceptibilities to IS of undeter

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Reiner, Alexander P., Susan R. Heckbert, Hans L. Vos, et al. "Genetic variants of coagulation factor XIII, postmenopausal estrogen therapy, and risk of nonfatal myocardial infarction." Blood 102, no. 1 (2003): 25–30. http://dx.doi.org/10.1182/blood-2002-07-2308.

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Abstract We hypothesized that possession of either of 2 functional coagulation factor XIII polymorphisms, one within subunit A (Val34Leu) and one within subunit B (His95Arg), might modulate the prothrombotic effects of estrogen and help to explain the variation in incidence of arterial thrombotic events among postmenopausal women using hormone replacement therapy. In a population-based case-control study of 955 postmenopausal women, we assessed the associations of factor XIII genotypes and their interactions with estrogen therapy on risk of nonfatal myocardial infarction (MI). The presence of

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Shafey, Mona, Josdalyne L. Anderson, Dimitrios Scarvelis, Steve P. Doucette, France Gagnon, and Philip S. Wells. "Factor XIII Val34Leu Polymorphism and the Risk of Myocardial Infarction: A Meta-Analysis." Blood 106, no. 11 (2005): 1637. http://dx.doi.org/10.1182/blood.v106.11.1637.1637.

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Abstract Genetic factors involving blood coagulation are thought to contribute to the pathogenesis of myocardial infarction. A common polymorphism of Factor XIII, Factor XIII Val34Leu, may be protective against developing an acute myocardial infarction, but various studies show conflicting results. We performed a meta-analysis to determine whether the Factor XIII Val34Leu polymorphism is associated with a decreased risk of myocardial infarction. 93 articles were reviewed after a MEDLINE search of the literature (1966 through April Week 1 2005) and 12 case-control studies were selected. We incl

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Dossenbach-Glaninger, Astrid, Michael van Trotsenburg, Martin Dossenbach, et al. "Plasminogen Activator Inhibitor 1 4G/5G Polymorphism and Coagulation Factor XIII Val34Leu Polymorphism: Impaired Fibrinolysis and Early Pregnancy Loss." Clinical Chemistry 49, no. 7 (2003): 1081–86. http://dx.doi.org/10.1373/49.7.1081.

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Abstract Background: A successful outcome of pregnancy depends on proper placental formation. In the very beginning of this process, trophoblast invasion and fibrin deposition into the wall of the decidual veins play an important part. Two polymorphisms, coagulation factor XIII (FXIII) Val34Leu and plasminogen activator inhibitor 1 (PAI-1) 4G/5G, interfere with fibrin cross-linking and regulation of fibrinolysis and may therefore contribute to early pregnancy loss. Methods: We enrolled 49 unrelated Caucasian women with a history of two consecutive or three to six nonconsecutive early pregnancy

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Pintao, Maria C., Dayse M. Lourenço, Francisco H. A. Maffei, et al. "New Interactive Effects Involving Factor XIII Gene Polymorphisms in Venous Thrombotic Disease." Blood 104, no. 11 (2004): 2590. http://dx.doi.org/10.1182/blood.v104.11.2590.2590.

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Abstract Venous thrombosis (VT) is considered to be a multifactorial disorder in which several genetic and acquired risk factors interact dynamically. Coagulation factor XIII (FXIII) is an enzyme that participates in the final steps of the coagulation cascade. A number of gene variations have been described in both FXIII A and B subunits. FXIIIA Val34Leu, Tyr204Phe and Pro564Leu polymorphisms have been associated to increased specific activity of FXIII, and FXIIIA Val34Leu has been claimed to be protective against VT in several studies. In the FXIII B subunit, two common polymorphisms (His95Ar

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Schwedler, Christian, Guido Heymann, Larisa Bukreeva та Berthold Hoppe. "Association of Genetic Polymorphisms of Fibrinogen, Factor XIII A-Subunit and α2-Antiplasmin with Fibrinogen Levels in Pregnant Women". Life 11, № 12 (2021): 1340. http://dx.doi.org/10.3390/life11121340.

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Fibrinogen synthesis is stimulated by proinflammatory triggers and depends on α-, β- and γ-fibrinogen (FGA, FGB, FGG) genotypes. Constellations of fibrinogen, factor XIII A-subunit (F13A) and α2-antiplasmin (A2AP) genotypes predisposing for dense fibrin gels with high antifibrinolytic capacity (e.g., FGB rs1800790 A-allele carriage in F13A 34Val/Val or A2AP 6Arg/Arg wildtypes) are related with reduced inflammation. As both relationships are likely to influence each other, we tested whether the association of fibrinogen genotypes with fibrinogen levels is influenced by F13A and A2AP genotypes i

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Ladenvall, Claes, Ludvig Csajbok, Karin Nylén, Katarina Jood, Bengt Nellgård, and Christina Jern. "Association between factor XIII single nucleotide polymorphisms and aneurysmal subarachnoid hemorrhage." Journal of Neurosurgery 110, no. 3 (2009): 475–81. http://dx.doi.org/10.3171/2008.7.jns08272.

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Object Family studies have suggested a role of genetic factors in susceptibility to aneurysmal subarachnoid hemorrhage (aSAH), but the underlying genetic risk factors remain poorly defined. There is an activation of the fibrinolytic system in aSAH, and fibrinolytic markers may be useful in predicting outcome. The authors investigate associations between putative functional variants in genes of importance for fibrinolysis and aSAH and/or outcome following aSAH. Methods One hundred eighty-three patients presenting with aSAH at a neurointensive care unit were consecutively recruited. Two healthy

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Ivanova, Nevena Georgieva. "A Rare Case of Pulmonary Embolism, Deep Vein Thrombosis, Bilateral Avascular Necrosis of the Femoral Head, and Miscarriage following COVID-19 in a Patient with Multiple Genetic Coagulation Factor Deficiency—A Case Report." Life 13, no. 12 (2023): 2240. http://dx.doi.org/10.3390/life13122240.

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The coronavirus disease (COVID-19) is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The most common symptoms of COVID-19 are respiratory symptoms, but some patients develop severe thrombotic complications. Studies have looked into the association between the disease severity in COVID-19 patients and polymorphisms in the genes encoding prothrombotic and cardiovascular risk factors. The presented rare case describes inflammatory and acute thrombotic complications with musculoskeletal involvement in a patient with combined coagulation genetic defects. A 37-year-old w

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Części książek na temat "Factor XIII Val34Leu genetic polymorphism"

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Giorgetti, R., and A. Tagliabracci. "Study of Genetic Polymorphism of Coagulation Factor XIII B in a Italian Population Sample using PAGIEF and Semi-dry Electroblotting." In Advances in Forensic Haemogenetics. Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75496-8_90.

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