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Genomes and Genes | P H ReitsmaSummaryAffiliation: Leiden University Medical Center Country: The Netherlands Publications
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Publications
Mechanistic view of risk factors for venous thromboembolismPieter H Reitsma
Department of Thrombosis and Hemostasis, Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Albinusdreef 2, 2300 RC, Leiden, The Netherlands
Arterioscler Thromb Vasc Biol 32:563-8. 2012..In this narrative review we will discuss the known common risk factors within this pathophysiological framework...
VKORC1 gene variation and venous thrombosis: 'another one bites the dust'?P H Reitsma
Einthoven Laboratory for Experimental Vascular Medicine, and Department of Thrombosis and Haemostasis, Leiden University Medical Centre, Leiden, The Netherlands
J Thromb Haemost 5:2017-9. 2007- How to identify new genetic risk factors for VTE?Pieter H Reitsma
Department of Thrombosis and Hemostasis, Leiden University Medical Center, The Netherlands
Thromb Res 123:S22-4. 2009..This short narrative review discusses several of the approaches which can be taken to identify new risk factors that predispose to venous thrombosis... - Past and future of genetic research in thrombosisP H Reitsma
Einthoven Laboratory for Experimental Vascular Medicine, Department of Thrombosis and Hemostasis, Leiden University Medical Center, Leiden, The Netherlands
J Thromb Haemost 5:264-9. 2007.... - High levels of protein C are determined by PROCR haplotype 3M C Pintao
Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands
J Thromb Haemost 9:969-76. 2011..Recently, we identified a locus on chromosome 20 determining high PC levels in a large Dutch pedigree with unexplained thrombophilia. Candidate genes in the LOD-1 support interval included FOXA2, THBD and PROCR... - Twelve novel and two recurrent mutations in 14 Austrian families with hereditary protein C deficiencyS R Poort
Department of Hematology, University Hospital, Leiden, The Netherlands
Blood Coagul Fibrinolysis 4:273-80. 1993..Only two of the genetic defects (157Arg-->Stop and 178Arg-->Gln) have been found previously in other geographic locations. These data confirm the large genetic heterogeneity of protein C deficiency... - Dominant type 1 von Willebrand disease caused by mutated cysteine residues in the D3 domain of von Willebrand factorJ C Eikenboom
Department of Hematology, University Hospital, Leiden, The Netherlands
Blood 88:2433-41. 1996..We conclude that the loss of cysteine pairing in the D3 domain, leaving one free cysteine, can induce a purely quantitative deficiency of vWF by dominantly suppressing the secretion of normal vWF... - Explanations for coagulation activation after air travelA J M Schreijer
Department of Clinical Epidemiology, Leiden University Medical Center, Leiden, The Netherlands
J Thromb Haemost 8:971-8. 2010..It is unknown whether venous thrombosis after long haul air travel is exclusively attributable to immobilization... - No praise for folly: genomics will never be useful in arterial thrombosisP H Reitsma
Einthoven Laboratory for Experimental Vascular Medicine, Departments of Hematology and Nephrology, Leiden University Medical Center, Leiden, The Netherlands
J Thromb Haemost 5:454-7. 2007 - TF:FVIIa-specific activation of CREB upregulates proapoptotic proteins via protease-activated receptor-2H H Versteeg
Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands
J Thromb Haemost 6:1550-7. 2008..Our previous findings indicated that the TF:FVIIa complex activates signal transducer and activator of transcription (STAT) signaling, leading to cell survival in TF-transfected baby hamster kidney (BHK) cells... 
Unique distance- and DNA-turn-dependent interactions in the human protein C gene promoter confer submaximal transcriptional activityC A Spek
Hemostasis and Thrombosis Research Center, Department of Hematology, University Hospital, Leiden, The Netherlands
Biochem J 340:513-8. 1999....- Genetics of venous thrombosisF R Rosendaal
Clinical Epidemiology, Leiden University Medical Center, Leiden, The Netherlands
J Thromb Haemost 7:301-4. 2009..There are many weak genetic risk factors, including fibrinogen, factor XIII and factor XI variants. Even for moderately strong risk factors (relative risks 2-5), the majority of carriers will never develop thrombosis... - Genetic studies in complex diseaseF R Rosendaal
Departments of Clinical Epidemiology and Hematology, Leiden University Medical Center, Leiden, The Netherlands
J Thromb Haemost 2:342. 2004 - Alternatively spliced tissue factor induces angiogenesis through integrin ligationY W van den Berg
The Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Albinusdreef 2, 2333 ZA Leiden, The Netherlands
Proc Natl Acad Sci U S A 106:19497-502. 2009..We conclude that asTF, unlike flTF, does not affect angiogenesis via PAR-dependent pathways but relies on integrin ligation. These findings indicate that asTF may serve as a target to prevent pathological angiogenesis... - Geographic distribution of the 20210 G to A prothrombin variantF R Rosendaal
Department of Clinical Epidemiology, Leiden University Medical Centre, The Netherlands
Thromb Haemost 79:706-8. 1998..Since this distribution within Europe is very different to that of another prothrombotic mutation (factor V Leiden or factor V R506Q), founder effects are the most likely explanation for the geographical distribution of both mutations... - Protein C deficiency: a database of mutations. For the Protein C & S Subcommittee of the Scientific and Standardization Committee of the International Society on Thrombosis and HaemostasisP H Reitsma
Hemostasis and Thrombosis Research Unit, University, Hospital, Leiden, The Netherlands
Thromb Haemost 69:77-84. 1993 - 17α-Ethinylestradiol rapidly alters transcript levels of murine coagulation genes via estrogen receptor αA C A Cleuren
Einthoven Laboratory for Experimental Vascular Medicine, Department of Thrombosis and Haemostasis, Leiden University Medical Center, Leiden, The Netherlands
J Thromb Haemost 8:1838-46. 2010..Oral estrogen use is associated with changes in plasma levels of many coagulation proteins... - Mutation in blood coagulation factor V associated with resistance to activated protein CR M Bertina
Hemostasis and Thrombosis Research Center, University Hospital, Leiden, The Netherlands
Nature 369:64-7. 1994..8), protein S (ref. 9), antithrombin10 deficiency) together... - Not exclusively tissue factor: neutrophil extracellular traps provide another link between chemotherapy and thrombosisY W van den Berg
Einthoven Laboratory for Experimental Vascular Medicine, Department of Thrombosis and Hemostasis, Leiden University Medical Center, Leiden, The Netherlands
J Thromb Haemost 9:2311-2. 2011..See also Swystun LL, Mukherjee S, Liaw PC. Breast cancer chemotherapy induces the release of cell-free DNA, a novel procoagulant stimulus. This issue, pp 2313-21... - Mutations in hemophilia Bm occur at the Arg180-Val activation site or in the catalytic domain of factor IXR M Bertina
Haemostasis and Thrombosis Research Unit, University Hospital, Leiden, The Netherlands
J Biol Chem 265:10876-83. 1990..Pro368----Thr near the catalytic center) or indirectly (mutations at the Arg180-Val activation site) therefore lead to a combination of 1) the loss of coagulant activity and 2) an inhibitory effect in the ox brain prothrombin time assay... - Intron-exon organization of the human gene coding for the lipoprotein-associated coagulation inhibitor: the factor Xa dependent inhibitor of the extrinsic pathway of coagulationC P van der Logt
Haemostasis and Trombosis Research Unit, University Hospital, Leiden, The Netherlands
Biochemistry 30:1571-7. 1991..The putative promoter was examined and found to contain two consensus sequences for AP-1 binding and one for NF-1 binding, but no TATA consensus promoter element... - Refined regional assignment of the human tissue factor pathway inhibitor (TFPI) gene to chromosome band 2q32 by non-isotopic in situ hybridizationC P van der Logt
Haemostasis and Thrombosis Research Unit, University Hospital, Leiden, The Netherlands
Hum Genet 89:577-8. 1992 - Alternatively spliced tissue factor in mice: induction by Streptococcus pneumoniaeL W Brüggemann
J Thromb Haemost 4:918-20. 2006 - Factor XIII Val34Leu and the risk of venous thromboembolism in factor V Leiden carriersR F Franco
Laboratory for Experimental Internal Medicine, Academic Medical Centre, Amsterdam, The Netherlands
Br J Haematol 111:118-21. 2000..5 (95% CI 0.06-4.5) in relatives older than 60 years. In conclusion, the impact of FXIII Val34Leu on the venous thromboembolic risk is modest, suggesting that screening for this mutation in factor V Leiden carriers is not justified... - Identification of polymorphisms in the 5'-untranslated region of the TAFI gene: relationship with plasma TAFI levels and risk of venous thrombosisR F Franco
Laboratory of Hematology, Department of Clinical Medicine, School of Medicine of Ribeirao Preto, University of Sao Paulo, 14048 900, Ribeirao Preto, SP, Brazil
Haematologica 86:510-7. 2001..Thrombin activatable fibrinolysis inhibitor (TAFI) plays an important role in hemostasis, functioning as a potent fibrinolysis inhibitor. TAFI gene variations may contribute to plasma TAFI levels and thrombotic risk... - Apolipoprotein A-V: a novel apolipoprotein associated with an early phase of liver regenerationH N van der Vliet
Department of Experimental Hepatology, Academic Medical Center, University of Amsterdam, Meibergdreef 9, Amsterdam 1105 AZ, The Netherlands
J Biol Chem 276:44512-20. 2001..The protein was present in plasma fractions containing high density lipoprotein particles. Therefore, we have identified a novel apolipoprotein, designated apolipoprotein A-V, that is associated with an early phase of liver regeneration... - [From gene to disease; risk factors for venous thrombosis: factor V Leiden and prothrombin 20210A]P H Reitsma
European School for Science Education, Eikenheuveldreef 16, 5263 EM Vught
Ned Tijdschr Geneeskd 145:1843-5. 2001..The APC-resistance assay is used to screen for the presence of factor V-Leiden. Both factor V-Leiden and prothrombin 20210A are diagnosed by DNA analysis... - A functional single nucleotide polymorphism in the thrombin-activatable fibrinolysis inhibitor (TAFI) gene associates with outcome of meningococcal diseaseJ A Kremer Hovinga
Laboratory for Experimental Internal Medicine, Academic Medical Center, Amsterdam, The Netherlands
J Thromb Haemost 2:54-7. 2004..0-9.5) increased risk to die from the infection compared with all other genotypes. Survivors had a genotype frequency (4.0%) that was lower than in the general population. TAFI 325 variants affect the outcome of meningococcal disease... - Is hypercoagulability an issue in arterial thrombosis? NoP H Reitsma
Laboratory for Experimental Internal Medicine, Academic Medical Center, Amsterdam, The Netherlands
J Thromb Haemost 2:692-4. 2004 - Activation of innate immunity in patients with venous thrombosis: the Leiden Thrombophilia StudyP H Reitsma
Laboratory for Experimental Internal Medicine, Academic Medical Center, Amsterdam, The Netherlands
J Thromb Haemost 2:619-22. 2004..We have sought to confirm and extend these findings by measuring plasma tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, IL-8, IL-10 and IL-12p70 levels in a case-control study for venous thrombotic disease... - Homocysteine and markers of coagulation and endothelial cell activationV E A Gerdes
Department of Internal Medicine Clinical Chemistry, Slotervaart Hospital, Amsterdam, The Netherlands
J Thromb Haemost 2:445-51. 2004..63) and von Willebrand factor (103% vs. 107%, P = 1.00). CONCLUSIONS: These results provide evidence against a major effect of mild hyperhomocysteinemia on activation of the coagulation system and endothelial cell activation in vivo...