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Background and Purpose: Vascular endothelial growth factor-A (VEGF-A), a key regulator of tumor-induced angiogenesis, is critical for tumor growth and metastasization. The goal of the present study was to evaluate the prognostic value of VEGF single nucleotide polymorphisms (SNPs) and haplotypes for clinical recurrence after definitive radiotherapy for prostate cancer., Patients and Methods: The association of seven VEGF-A polymorphisms and their haplotypes with clinical recurrence (defined as the occurrence of local recurrence and/or distant metastases) in 496 prostate cancer patients treated with definitive radiotherapy were investigated. Genotypes were determined by 5'-nuclease (TaqMan) assays; haplotypes were analyzed using the Haploview program., Results: Within a median follow-up time of 80 months, 44 patients (9 %) developed clinical recurrences. Haplotype analysis showed two separate blocks of high-linkage disequilibrium, formed by five polymorphisms (- 2578C > A, - 2489C > T, - 1498C > T, - 634G > C, - 7C > T) upstream of the coding sequence (CCCCC, ATTGC, CCCGC, ATTGT) and two polymorphisms (936C > T, 1612G > A) downstream of the coding sequence (CA, CG, TG). Carriers of at least 1 copy of the ATTGC haplotype were at higher risk of recurrence (hazard ratio [HR] 3.83; 95 %CI 1.48-9.90, p = 0.006); for carriers of 2 copies, the HR was 4.85 (95 %CI 1.72-13.6; p = 0.003). In multivariate analysis, patients harboring at least one copy of the ATTGC haplotype remained at increased risk of recurrence (HR 3.63, 95 %CI 1.38-9.55, p = 0.009); in patients carrying 2 copies, the HR was 4.72 (95 %CI 1.64-13.6, p = 0.004)., Conclusion: Our findings indicate that the VEGF-A ATTGC haplotype may predict clinical recurrence in prostate cancer patients treated with radiotherapy.

Context: Low 25-hydroxycholecalciferol [25(OH) vitamin D] status is known to play an important role in many diseases with focus on bone health., Objective: Based on recently reported genetic determinants of vitamin D insufficiency, we aimed to analyze genetic variants of group-specific component (GC), 7-dehydrocholesterol reductase (DHCR7), and cytochrome P450IIR-1 (CYP2R1) for association with vitamin D levels, bone mineral density (BMD), and bone fractures., Design: We conducted a cross-sectional BMD and fracture study and a prospective cohort study., Setting: The cross-sectional study comprised participants of a BMD screening study, and the prospective cohort study comprised nursing home subjects., Patients: The cross-sectional study included 342 subjects (mean age, 55.3 ± 12.0 yr), and the prospective study included 1093 subjects (mean age, 84.0 ± 6.0 yr)., Interventions: Patients were stratified by GC, DHCR7, and CYP2R1 genotypes. For each gene, the allele associated with lower 25(OH) vitamin D levels was designated as "risk allele." The potential role of these risk alleles in fracture risk was analyzed by logistic regression analysis including age and sex as confounders., Main Outcome Measures: We measured BMD and fractures., Results: GC genotypes were significantly associated with lower mean 25(OH) vitamin D levels in both cohorts (P = 0.001 and P = 0.048, respectively). There was no significant association of BMD with any of the genotypes. None of the alleles was associated with past fractures, whereas the DHCR7 G-allele was significantly associated with prospective fractures (odds ratio, 0.68; 95% confidence interval, 0.51-0.92; P = 0.011)., Conclusions: The DHCR7 gene polymorphism may be a predictor for fracture risk.

Objective: The cytochrome P450 2D6 (CYP2D6) polymorphism was reported to have a significant impact on outcome of tamoxifen treatment in estrogen receptor positive breast cancer patients. The objective of this study was to explore the effect of the CYP2D6*4 polymorphism on tamoxifen treatment outcome in a cohort of patients from a single clinical trial which included women with a history of previous chemotherapy., Research Design and Methods: A total of 493 patients of the Austrian TIGER study receiving adjuvant tamoxifen therapy were studied for this pharmacogenetic interaction. All women with estrogen receptor positive tumors and tamoxifen therapy longer than 6 months were genotyped for CYP2D6*4 using TaqMan technology. Time to tumor progression, defined as local, regional, distant recurrence or contralateral breast cancer and progression free survival, was analyzed., Results: No significant difference in time to tumor progression or progression free survival between the CYP2D6*4 genotype groups in the overall study cohort was found. In a subgroup of patients treated with chemotherapy the CYP2D6*4 poor metabolizers had a tendency towards a shorter mean time to progression. In this group the mean time to tumor progression and the progression free survival were 1.0 years in the CYP2D6*4/*4 group, 6.3 years in the *1/*4 group and 4.97 years in the *1/*1 group (Wilcoxon p = 0.104)., Conclusion: While earlier data on CYP2D6 and tamoxifen excluded women with prior chemotherapy, the present analysis suggests that CYP2D6*4 genotype might be particularly crucial in this group of high-risk patients. Key limitations are restriction to the CYP2D6*4 allele and missing data of comedication.

Hypoxia-inducible factor 1 (HIF1) is a key regulator of angiogenesis and is involved in inflammation, which are two important features of the pathogenesis of peripheral artery disease (PAD). The gene for the HIF1-alpha subunit (HIF1A) carries two common mis-sense mutations, P582S (C>T, rs11549465) and A588T (G>A, rs11549467), which both have been related to increased trans-activation capacity of HIF1-alpha. The aim of the present study was to analyze the role of these polymorphisms in PAD. The study was designed as a case-control study including 917 patients with documented PAD and 969 control subjects. HIF1A genotypes were determined by exonuclease (TaqMan) assays. HIF1A P582S genotype frequencies were not significantly different between PAD patients (PP 82.2%; PS 16.5%; SS 1.3%) and control subjects (83.2%; 15.3%; 1.5%; p = 0.72). Similarly, HIF1A A588T genotype frequencies did not differ significantly between PAD patients (AA 95.9%; AT 4.1%) and control subjects (AA 96.8%; AT 3.2%; p = 0.28). In a multivariate logistic regression analysis including age, sex, smoking, diabetes, arterial hypertension and hypercholesterolemia, neither the HIF1A P582S polymorphism (odds ratio: 1.26; 95% confidence interval 0.92-1.74; p = 0.16) nor the A588T polymorphism (odds ratio: 1.17; 95% confidence interval 0.59-2.35; p = 0.66) was significantly associated with the presence of PAD. Both polymorphisms were furthermore not associated with age at onset of PAD, Fontaine stage of the disease or the ankle/brachial index of patients. We conclude that functional polymorphisms in the HIF1A gene do not contribute to susceptibility to PAD.

Background: There is strong and consistent evidence that oxidative stress is crucially involved in the development of atherosclerotic vascular disease. Overproduction of reactive oxygen species (ROS) in mitochondria is an unifying mechanism that underlies micro- and macrovascular atherosclerotic disease. Given the central role of mitochondria in energy and ROS production, mitochondrial DNA (mtDNA) is an obvious candidate for genetic susceptibility studies on atherosclerotic processes. We therefore examined the association between mtDNA haplogroups and coronary artery disease (CAD) as well as diabetic retinopathy., Methods: This study of Middle European Caucasians included patients with angiographically documented CAD (n = 487), subjects with type 2 diabetes mellitus with (n = 149) or without (n = 78) diabetic retinopathy and control subjects without clinical manifestations of atherosclerotic disease (n = 1527). MtDNA haplotyping was performed using multiplex PCR and subsequent multiplex primer extension analysis for determination of the major European haplogroups. Haplogroup frequencies of patients were compared to those of control subjects without clinical manifestations of atherosclerotic disease., Results: Haplogroup T was significantly more prevalent among patients with CAD than among control subjects (14.8% vs 8.3%; p = 0.002). In patients with type 2 diabetes, the presence of diabetic retinopathy was also significantly associated with a higher prevalence of haplogroup T (12.1% vs 5.1%; p = 0.046)., Conclusion: Our data indicate that the mtDNA haplogroup T is associated with CAD and diabetic retinopathy in Middle European Caucasian populations.

An Austrian Non-Governmental Organization (NGO) offered psychotherapy to 37 asylum seekers and refugees (21 of them female) with a mean age of 36.1 years (s = 7.5), with the majority of them from Chechnya or Afghanistan. Comparative data between the start of therapy and the time of evaluation revealed a highly significant positive effect (d = 0.77), while most therapies were still going on. By a retrospective measure of perceived change, 85% of the participants reported significant improvements. The results show that even under difficult conditions, when working with asylum seekers and refugees, psychotherapy can be effective.

Background: Methylenetetrahydrofolate reductase (MTHFR) is involved in the formation of methyl donors, which contribute to DNA methylation. DNA methylation is an essential epigenetic feature playing a critical role in gene regulation and cellular differentiation. In addition, MTHFR activity affects plasma homocysteine levels. A functional polymorphism in the MTHFR gene (677C>T, rs1801133) leading to reduced enzyme activity has been associated with chronic plaque psoriasis in a Chinese population. This finding, however, has not yet been either confirmed or refuted in other populations. The purpose of the present study was to investigate a hypothesized association between the MTHFR 677C>T polymorphism and the presence of chronic plaque psoriasis in a Caucasian population., Methods: Genotypes for the MTHFR 677C>T polymorphism were determined in 310 patients and 247 control subjects. In a subgroup of 33 patients and 33 sex- and age-matched control subjects, fasting plasma homocysteine concentrations were determined by high-performance liquid chromatography and immunological assays were used for the measurement of folate and vitamin B(12)., Results: Prevalence of the homozygous MTHFR 677TT genotype did not significantly differ between patients and controls (15.2% vs 11.7%, P = 0.24). Mean plasma homocysteine concentrations were significantly higher in psoriasis patients than among control subjects (13.5 +/- 5.3 micromol/l vs 11.0 +/- 2.2 micromol/l, P = 0.026). No significant differences between either mean plasma folate or vitamin B(12) concentrations were observed between both groups., Conclusion: Our data suggest that the MTHFR 677C>T gene polymorphism is not associated with chronic plaque psoriasis among Caucasians.

Purpose: Vascular endothelial growth factor (VEGF) is a key regulator of tumor-induced angiogenesis and is required for growth of tumors. We tested the hypothesis that VEGF gene polymorphisms may be associated with breast cancer., Experimental Design: We performed a case-control study including 804 female incident breast cancer patients and 804 female age-matched healthy control subjects. We selected seven VEGF candidate polymorphisms and determined genotypes by 5'-nuclease (TaqMan) assays. Furthermore, VEGF plasma levels and genotypes were analyzed in a group of 81 healthy volunteers (64 men and 17 women)., Results: Haplotype analysis showed two separate blocks of high-linkage disequilibrium, formed by five polymorphisms upstream of the coding sequence (promoter and 5' untranslated region) and two polymorphisms downstream of the coding sequence. None of the single polymorphisms or haplotypes was significantly associated with the presence of breast cancer. After Bonferroni correction for multiple testing, only one statistical signifcant association between VEGF genotypes and haplotypes and tumor characteristics was observed (-634C allele and small tumor size; p < 0.001). In a multivariate regression analysis including sex, age, VEGF genotypes, and haplotypes as covariates and VEGF plasma level as dependent variable, none of the VEGF polymorphism or haplotypes was a significant predictor of VEGF plasma levels., Conclusions: Our findings do not support the hypothesis that VEGF polymorphisms are associated with breast cancer risk. The association of the VEGF -634C allele with small tumor size is in clear contrast to a previous publication and should be interpreted with caution until replicated by additional studies.

Background: Death receptor 4, encoded by the TNFRSF10A gene, is an important mediator of apoptosis and its dysfunction may be related to cancer development and distant tumor spread. A single nucleotide polymorphism in TNFRSF10A (Glu228Ala, rs20576) within a conserved region of the extracellular cysteine-rich domain of death receptor 4 has been associated with an increased risk for a variety of tumor entities. Aim of the present study was to evaluate the role of the TNFRSF10A polymorphism in metastatic progression of prostate cancer after radiation therapy., Methods: We carried out a prospective study including 702 prostate cancer patients from the Austrian PROCAGENE (Prostate Cancer Genetics) study. Development of metastases was examined in regular follow-up investigations. TNFRSF10A genotypes were determined by a 5'-nuclease assay (TaqMan)., Results: Within a median follow-up time of 10 months (range 0-60 months), 24 (3.4%) patients developed metastases. In a Cox regression model including age at diagnosis and risk group as potential confounders, carriage of an 228Ala allele was associated with a relative risk of 2.47 (95% CI 1.10-5.54; P=0.028) for metastases. TNFRSF10A genotypes were not associated with tumor stage, grade, risk group or age at diagnosis., Conclusion: We conclude that the TNFRSF10A Glu228Ala polymorphism may be a novel independent risk factor for prostate cancer metastases after radiation therapy.

Background: Psoriasis is a common chronic inflammatory skin disease. Vasoactive peptides such as endothelin-1 (ET-1) and bradykinin have previously been implicated in the pathogenesis of chronic plaque psoriasis. The angiotensin-converting enzyme (ACE) gene carries a 287-base pair insertion/deletion (I/D) gene polymorphism, which is associated with plasma concentrations of bradykinin-degrading ACE. A functional polymorphism (EDN1 -134 3A/4A) in the gene encoding ET-1 has been shown to affect ET-1 expression. The purpose of the present study was thus to investigate a hypothesized association between these gene polymorphisms and the presence of chronic plaque psoriasis., Methods: The present case-control study comprised 207 patients with chronic plaque psoriasis (136 with early onset and 71 with late onset disease) and 182 control subjects. Genotypes of EDN1 and ACE were determined by a 5' exonuclease assay (Taqman)., Results: The prevalence of the homozygous ACE II genotype was significantly higher in patients with early-onset psoriasis than among control subjects (30.9% vs 19.2%, P = 0.016), yielding an odds ratio of 1.88 [95% confidence interval (CI): 1.12-3.15] for early-onset disease. For late-onset psoriasis, presence of the ACE II genotype was associated with a non-significant odds ratio 1.54 (95% CI: 0.81-2.92). As for the EDN1 -134 3A/4A gene polymorphism, no significant differences in genotype distributions were found between patients with either early- or late-onset psoriasis and control subjects (EDN1 -134 4A/4A: 9.6% in early-onset and 5.6% late-onset psoriasis vs 7.7% in controls; P > 0.05)., Conclusions: Our data suggest that homozygosity for the ACE I allele may affect susceptibility to early-onset psoriasis.

Introduction: Thrombin-induced conversion of fibrinogen to fibrin plays an essential role in hemostasis and results in the stabilization of thrombi. Elevated plasma fibrinogen levels have been associated with both increased plasma viscosity and platelet aggregability. Recently, a haplotype-tagging single nucleotide polymorphism characterized by a C to T substitution at nucleotide 10034 of the fibrinogen gamma gene (FGG 10034C>T, rs2066865), has been proposed as a novel risk factor for deep venous thrombosis (DVT). Aim of the present study was to provide further data on the role of the FGG 10034C>T polymorphism for DVT., Materials and Methods: FGG genotypes were determined by 5'-exonuclease assay (TaqMan) in 358 patients with documented DVT and a total of 783 control subjects., Results: In a multivariate analysis adjusting for age, sex, presence of factor V Leiden and carriage of prothrombin 20210A, homozygosity for the FGG 10034 TT genotype yielded an odds ratio of 2.01 (95% CI 1.23-3.31; p=0.006) for DVT., Conclusions: Our data confirm the primary finding that the FGG 10034C>T polymorphism is associated with DVT risk.

An association between susceptibility to rheumatoid arthritis (RA) and a common -168A>G polymorphism in the MHC2TA gene with differential major histocompatibility complex (MHC) II molecule expression was recently reported in a Swedish population. The objective of the present study was to replicate this finding by examining the -168A>G polymorphism in an Austrian case-control study. Three hundred and sixty-two unrelated RA cases and 351 sex-matched and age-matched controls as well as 1,709 Austrian healthy individuals were genotyped. All participants were from the same ethnic background. Genotyping was performed using 5' allelic discrimination assays. The association between susceptibility to RA and the -168A>G single nucleotide polymorphism was examined by chi-square test. Comparison was made assuming a dominant effect (AG + GG genotypes versus AA genotype). In contrast to the primary report, the frequency of MHC2TA -168G allele carriers was not significantly different between patients and controls in the Austrian cohort. The homozygous MHC2TA -168 GG genotype was more frequent in matched controls than in Austrian RA patients. There was no association between the presence of RA-specific autoantibodies and the MHC2TA -168 GG genotype. In this cohort of Austrian patients, no association between the MHC2TA polymorphism and RA was found.

Interleukin-10 (IL-10) is an immunosuppressive cytokine which may facilitate development of cancer by supporting tumor escape from the immune response. A [TCATA] haplotype formed by polymorphisms at positions -3575, -2763, -1082, -819 and -592 in the promoter of the IL-10 gene is a strong determinant for IL-10 expression. The presence of this haplotype can be determined by analysis of the -592C > A polymorphism. Aim of the present study was to analyze the role of the IL-10 [TCATA] haplotype for breast cancer. We performed a case-control study including 500 female patients with histologically confirmed breast cancer and 500 female, age-matched, healthy control subjects from population-based screening studies. The -592C > A polymorphism was determined by a 5'-nuclease assay (TaqMan). Frequency of the homozygous -592 AA genotype, indicating homozygosity for the [TCATA] haplotype, was 4.2% among patients and 7.3% among controls (p=0.038; odds ratio 0.56; 95% confidence interval 0.32-0.97). IL-10 genotypes were not associated with tumor size, histological grading, estrogen or progesterone receptor status and age at diagnosis. Therefore we conclude that the IL-10 -592C > A promoter polymorphism may be associated with a reduced breast cancer risk.

The Austrian Value Questionnaire was developed on the basis of the Lexical Approach to account for specific facets of values in Austrian culture. It comprises 54 items, constituting five scales, Intellectualism, Harmony, Religiosity, Materialism, and Conservatism, and 13 subscales. To assess construct validity, hypotheses on human values were derived from the literature and tested in Austrian samples of Catholic priests and nuns (n=30, 8 women, M age=52.6 yr.), community servants (n=30, all men, M age=21.4 yr.), and students of psychology (n=33, 19 women, M age=23.8 yr.) and economics (n=33, 18 women, M age=23.8 yr.), prisoners (n=40, 9 women, M age=34.9 yr.), and drivers who had been fined for driving while intoxicated (n=35, 5 women, M age=34.6 yr.). Participants were volunteers. Previous and more recent findings from the USA, Canada, Germany, and Switzerland provided similar results for community servants, students of economics, prisoners, and intoxicated drivers, and thus, the hypotheses for these groups were largely confirmed. Most earlier findings for priests and nuns and students of psychology were not replicated, however. Taking into account that values may change over time and variously in different cultures, the results pose an argument for the construct validity of the newly developed questionnaire.

Background and Purpose: The C825T dimorphism of the gene encoding the human G protein beta3 subunit (GNB3) is associated with hypertension and obesity. Although these findings suggest an association with insulin resistance and atherosclerosis, this hypothesis has yet been tested only partially., Methods: To investigate this hypothesis, the C825T dimorphism was determined in a population of 932 middle-aged white subjects of middle European (Austrian) origin. Insulin sensitivity was measured with the short insulin tolerance test; intima-media thickness of the carotid artery and morphological plaque burden were measured by ultrasound., Results: Insulin sensitivity was found to be significantly lower in carriers of the T allele (3.55+/-1.27 versus 3.92+/-1.30%/min, P=0.012) in the group of male subjects with abdominal body fat distribution (waist-to-hip ratio >0.9). No effect was observed in women or men with a waist-to-hip ratio <0.9. Advanced carotid artery plaques were more frequent (odds ratio, 1.606; 95% confidence interval, 1.002 to 2.575; P=0.04) in carriers of the T allele regardless of sex. No effect was observed with regard to carotid artery intima-media thickness., Conclusions: In summary, our results demonstrate that the GNB3 825T allele is associated with reduced insulin sensitivity in men with abdominal fat distribution and with more advanced carotid atherosclerosis in middle-aged white men and women.

Objective: Conflicting data exists about the possible contribution of the homozygous Asp/Asp genotype of the Glu298Asp polymorphism of endothelial nitric oxide synthase to human atherosclerotic vascular disease. We investigated the polymorphism in two independent study populations: a case-control study including patients with angiographically verified coronary artery disease (CAD) on the one hand and a cross-sectional epidemiological study on the other hand., Methods: The Glu298Asp polymorphism was determined by PCR-RFLP as established. In the case-control study (240 patients and 248 controls) a possible association between the polymorphism and CAD, and age of onset of CAD and myocardial infarction was investigated. In the cross-sectional epidemiological study (932 subjects) intima-media thickness (IMT) of the carotid artery as well as morphological plaque burden and forearm vascular reactivity (peak postischemic reactive hyperaemia, determined by venous occlusion plethysmography) were measured., Results: In the case-control study genotype distribution (Glu/Glu; Glu/Asp; Asp/Asp) was not different between the CAD patients (43/46/11%) and the controls (49/41/10%, P = NS). No association of the polymorphism with age of onset of CAD or myocardial infarction was found. In the epidemiological study no influence of the genetic variant on IMT was observed after correction for classical determinants of IMT (average IMT: Asp/ Asp: 0.077 +/- 0.011 mm; Glu/Glu and Glu/Asp: 0.080 +/- 0.012 mm, P = NS). Forearm vascular reactivity was also not different between homozygous Asp/Asp subjects and Glu/Glu and Glu/Asp subjects (peak-reactive hyperaemia 20.1 +/- 7.3 mL min-1 100 mL-1 vs. 20.0 +/- 6.5 mL min-1 100 mL-1, P = NS)., Conclusions: Our results suggest that there is no association of the Glu298Asp polymorphism with coronary or carotid atherosclerosis or forearm vascular reactivity in these populations recruited in a country with a rather high risk for atherosclerosis. We suggest additional investigations to be performed in populations at different risk for coronary events to further elucidate the possible contribution of this polymorphism to vascular disease.

Background: An insertion/deletion (I/D) polymorphism of the gene for angiotensin-converting-enzyme (ACE) is associated with ACE plasma levels and activity. Conflicting results have been reported about the relevance of this polymorphism for atherosclerotic vascular disease. The aim of the present study was to analyze the role of this polymorphism for peripheral arterial disease (PAD)., Methods: The study was designed as a case-control study including 522 patients with documented PAD and 522 sex- and age-matched controls. ACE genotype was determined by size-analysis of polymerase chain reaction products., Results: ACE genotype frequencies were similar between patients (II: 23.4%; ID: 44.8%; DD: 31.8%) and controls (II: 23.8%; ID: 48.3%; DD: 27.9%, P=0.37). The adjusted odds ratio of carriers of the DD genotype for PAD was 1.29 (95% confidence interval 0.95-1.75). The polymorphism was furthermore not associated with age at onset of PAD (P=0.56), Fontaine stage of the disease (P=0.68) or ankle/brachial index of patients (P=0.86)., Conclusion: The ACE I/D polymorphism is not a significant risk factor for PAD.

Background: Platelet glycoprotein (GP) IIb/IIIa, a fibrinogen and von Willebrand factor binding membrane receptor, has an important role in platelet aggregation. A common leucine33-proline polymorphism (PlA1/A2) of the gene encoding the GP IIIa subunit is associated with platelet reactivity and has been proposed as a risk factor for atherothrombotic disease. The aim of this study was to investigate the role of this polymorphism for deep venous thrombosis (DVT)., Methods: We performed a case-control study including 206 patients with documented DVT and a sex- and age-matched group of 310 control subjects. GP IIIa genotypes were determined by restriction fragment analysis of amplimers containing the polymorphic site., Results: A1/A1, A1/A2 and A2/A2 genotypes were found in 67.0, 31.6 and 1.5 percent of patients and 72.3, 25.8 and 1.9 percent of controls (p=0.35), PlA2 allele frequencies were 0.17 in patients and 0.15 in controls (p=0.92). Odds ratio of the PlA2 allele for DVT was 1.21 (95 percent CI 0.85-1.71, p=0.29) and remained insignificant after adjustment for factor V Leiden and prothrombin 20210A genotypes (1.22, 95 percent CI 0.86-1.75, p=0.27)., Conclusions: Our data suggest that the PlA1/A2 polymorphism of GP IIIa is not associated with DVT.

Ninety-eight juvenile traffic offenders, 81 men and 17 women, were examined regarding the personality traits of extraversion, neuroticism, psychoticism, impulsiveness and venturesomeness and compared with a control group of 149 applicants for driving licences, 82 male and 67 female. The participants of the study were administered German translations of the Eysenck personality questionnaire (EPQ-R) and the impulsiveness/venturesomeness/empathy questionnaire (IVE). Traffic offenders had significantly higher scores on the venturesomeness dimension as compared to the control group, and male offenders scored significantly higher on extraversion than did male controls. Hypotheses regarding a relationship between traffic offences and psychoticism and impulsiveness were not confirmed, however. It is concluded that traffic violations in juveniles should primarily be viewed within the scope of normal behaviour and do not necessarily imply serious personality disorder.

Mutations in the gene for prothrombin (F2 20210A) and factor V (F5 1691A, factor V Leiden) are established risk factors for deep venous thrombosis (DVT). Recently, a mutation in the gene for factor XIII (F13 100T) leading to a Valine-Leucine exchange at amino acid position 34 has been reported to be protective against DVT. To analyze the role of these mutations for DVT in Austria, we analyzed their prevalence in 154 patients with documented DVT and 308 sex- and age-matched control subjects. Allele frequencies of F2 20210A, F5 1691A, and F13 100T were 0.018, 0.039, and 0.274 among controls, and 0.045, 0.120, and 0.211 among patients, respectively. Odds ratios for DVT associated with F2 20210A, F5 1691A, and F13 100T alleles were 2.5 (95% CI: 1.1-5.7), 3.4 (95% CI: 1.9-5.8), and 0.7 (95% CI: 0.5-1.0). We conclude that F2 20210A, F5 1691A, and F13 100T are common mutations in the Austrian population. F2 20210A and F5 1691 increase the risk for DVT, whereas F13 100T is associated with a decreased risk for DVT. Routinely, analysis of these mutations may help to analyze the individual risk for DVT.