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- 2022
-
Mark
Classic Thrombophilias and Thrombotic Risk Among Middle-Aged and Older Adults : A Population-Based Cohort Study
(
- Contribution to journal › Article
- 2020
-
Mark
Genetic risk factors for venous thromboembolism
(
- Contribution to journal › Scientific review
- 2019
-
Mark
New functional test for the TFPIα cofactor activity of Protein S working in synergy with FV-Short
(
- Contribution to journal › Article
- 2018
-
Mark
Evaluation of Expression Level of Apolipoprotein M as a Diagnostic Marker for Primary Venous Thromboembolism
(
- Contribution to journal › Article
-
Mark
Identification of novel diagnostic biomarkers for deep venous thrombosis
(
- Contribution to journal › Article
- 2016
-
Mark
Diagnostic potential of plasma microRNA signatures in patients with deep-vein thrombosis
(
- Contribution to journal › Article
-
Mark
Epidemiology of Familial Aggregation of Venous Thromboembolism
(
- Contribution to journal › Scientific review
- 2014
-
Mark
Apolipoprotein M and the risk of unprovoked recurrent venous thromboembolism.
(
- Contribution to journal › Article
-
Mark
The association between apolipoprotein M and insulin resistance varies with country of birth.
(
- Contribution to journal › Article
- 2012
-
Mark
Small and large PROS1 deletions but no other types of rearrangements detected in patents with protein S deficiency
(
- Contribution to journal › Article
- 2005
-
Mark
Large deletions of the PROS1 gene in a large fraction of mutationnegative patients with protein S deficiency
(
- Contribution to journal › Article
- 2004
-
Mark
Co-segregation of the PROS1 locus and protein S deficiency in families having no detectable mutations in PROS1.
(
- Contribution to journal › Article
- 2002
-
Mark
Genetic and phenotypic variability between families with hereditary protein S deficiency
(
- Contribution to journal › Article
- 2001
-
Mark
Improved hemoglobin status and reduced menstrual blood loss among female carriers of factor V Leiden--an evolutionary advantage?
(
- Contribution to journal › Letter
- 1999
-
Mark
Factor V Q506 (resistance to activated protein C) and prognosis after acute coronary syndrome
(
- Contribution to journal › Article
-
Mark
Thrombophilia as a multigenic disease
(
- Contribution to journal › Article
- 1998
-
Mark
A common 4G allele in the promoter of the plasminogen activator inhibitor-1 (PAI-1) gene as a risk factor for pulmonary embolism and arterial thrombosis in hereditary protein S deficiency
(
- Contribution to journal › Article
-
Mark
A new direct, fast and quantitative enzyme-linked ligandsorbent assay for measurement of free protein S antigen
(
- Contribution to journal › Article
-
Mark
Clarification of the risk for venous thrombosis associated with hereditary protein S deficiency by investigation of a large kindred with a characterized gene defect
(
- Contribution to journal › Article
-
Mark
The A20210 allele of the prothrombin gene is frequently associated with the factor V Arg 506 to Gln mutation but not with protein S deficiency in thrombophilic families
(
- Contribution to journal › Letter
-
Mark
The A20210 allele of the prothrombin gene is frequently associated with the factor V Arg 506 to Gln mutation but not with protein S deficiency in thrombophilic families [3]
(
- Contribution to journal › Letter
- 1997
-
Mark
A novel thrombomodulin gene mutation in a patient suffering from sagittal sinus thrombosis
(
- Contribution to journal › Article
-
Mark
The 20210 A allele of the prothrombin gene is a common risk factor among Swedish outpatients with verified deep venous thrombosis
(
- Contribution to journal › Debate/Note/Editorial
-
Mark
Genetic and phenotypic analysis of a large (122-member) protein S-deficient kindred provides an explanation for the familial coexistence of type I and type III plasma phenotypes
(
- Contribution to journal › Article
-
Mark
Activated protein C resistance caused by a common factor V mutation has a single origin
(
- Contribution to journal › Article
-
Mark
The factor VR506Q mutation causing APC resistance is highly prevalent amongst unselected outpatients with clinically suspected deep venous thrombosis
(
- Contribution to journal › Article
-
Mark
Evaluation of original and modified APC-resistance tests in unselected outpatients with clinically suspected thrombosis and in healthy controls
(
- Contribution to journal › Article
-
Mark
A common thrombomodulin amino acid dimorphism is associated with myocardial infarction
(
- Contribution to journal › Article
-
Mark
Activated protein C resistance due to a common factor V gene mutation is a major risk factor for venous thrombosis
(
- Contribution to journal › Article
-
Mark
The factor VR5O6Q mutation causing APC resistance is highly prevalent amongst unselected outpatients with clinically suspected deep venous thrombosis
(
- Contribution to journal › Article
-
Mark
Activated protein C resistance : Clinical implications
(
- Contribution to journal › Scientific review
- 1996
-
Mark
Familial thrombophilia : clinical and molecular analysis of Swedish families with inherited resistance to activated protein C or protein S deficiency
1996) In Scandinavian journal of clinical and laboratory investigation. Supplementum 56(226). p.19-46(
- Contribution to journal › Scientific review
-
Mark
Elevated levels of prothrombin activation fragment 1 + 2 in plasma from patients with heterozygous Arg506 to Gln mutation in the factor V gene (APC-resistance) and/or inherited protein S deficiency
(
- Contribution to journal › Article
-
Mark
Resistance to activated protein C due to a factor V gene mutation : The most common inherited risk factor of thrombosis
(
- Contribution to journal › Article
-
Mark
Prevalence of factor V gene mutation amongst myocardial infarction patients and healthy controls is higher in Sweden than in other countries
(
- Contribution to journal › Article
-
Mark
Resistance to activated protein C, the FV:Q506 allele, and venous thrombosis
(
- Contribution to journal › Scientific review
-
Mark
High prevalence of the FVR506Q mutation causing APC resistance in a region of southern Sweden with a high incidence of venous thrombosis.
(
- Contribution to journal › Letter
-
Mark
Inherited resistance to activated protein C caused by presence of the FV:Q506 allele as a basis of venous thrombosis
(
- Contribution to journal › Article
-
Mark
Factor V:Q506 mutation and anticardiolipin antibodies in systemic lupus erythematosus
(
- Contribution to journal › Article
-
Mark
Activated protein C resistance as a basis for venous thrombosis.
(
- Contribution to journal › Article
-
Mark
Familial thrombophilia : Resistance to activated protein C and protein S deficiency
1996)(
- Thesis › Doctoral thesis (compilation)
- 1995
-
Mark
Activated protein C resistance : from phenotype to genotype and clinical practice
(
- Contribution to journal › Article
-
Mark
Resistens mot aktiverat protein C. Vanlig genetisk riskfaktor för venös trombos
(
- Contribution to journal › Article
-
Mark
Resistance to activated protein C caused by a factor V gene mutation
(
- Contribution to journal › Article
-
Mark
Evaluation of the relationship between protein S and C4b-binding protein isoforms in hereditary protein S deficiency demonstrating type I and type III deficiencies to be phenotypic variants of the same genetic disease
(
- Contribution to journal › Article
-
Mark
Homozygous APC-resistance combined with inherited type I protein S deficiency in a young boy with severe thrombotic disease
(
- Contribution to journal › Article
-
Mark
Resistance to activated protein C as an additional genetic risk factor in hereditary deficiency of protein S
(
- Contribution to journal › Article
-
Mark
Methodological considerations on the determination of the APC response in plasma
(
- Contribution to journal › Article
- 1994
-
Mark
Myocardial infarction associated with homozygous resistance to activated protein C
(
- Contribution to journal › Letter
-
Mark
Linkage between inherited resistance to activated protein C and factor V gene mutation in venous thrombosis
(
- Contribution to journal › Article
-
Mark
Differential regulation of alpha and beta chains of C4b-binding protein during acute-phase response resulting in stable plasma levels of free anticoagulant protein S
(
- Contribution to journal › Article
-
Mark
Identification of the same factor V gene mutation in 47 out of 50 thrombosis-prone families with inherited resistance to activated protein C
(
- Contribution to journal › Article
-
Mark
Differential regulation of α and β chains of C4b-binding protein during acute-phase response resulting in stable plasma levels of free anticoagulant protein S
(
- Contribution to journal › Article