ABSTRACT
Factor XIII (FXIII) is a regulator of fibrinolysis and clot firmness. Val34Leu polymorphism of its potentially active A subunit (FXIII-A) leads to faster activation of FXIII, influences clot structure and provides a moderate protection against coronary artery disease. The effect of FXIII-A Val34Leu polymorphism on the risk of atherothrombotic ischemic stroke (AIS) has been investigated in a few studies with contradictory results. In all previous studies, only patients surviving AIS were enrolled and sex-specific effects were not explored. In this retrospective multicenter cohort, we investigated the effect of FXIII-A Val34Leu polymorphism on the risk of fatal AIS in women and men. DNA isolation and genetic determinations in the case of 316 patients who died of AIS were carried out on paraffin-embedded tissue specimens. Genetic analyses for population controls, patients with history of AIS and sex-matched controls were performed on extracted genomic DNA from peripheral blood leukocytes. The prevalence of homozygous wild-type, and heterozygous genotypes, Leu34 carriers and Leu34 allele was not different significantly between the patients with fatal AIS and their respective controls. Logistic regression analysis with age as co-variant demonstrated that in women, homozygous presentation of Leu34 allele represented a more than three-fold increased risk of AIS with fatal outcome. The results demonstrate that FXIII-A Val34Leu polymorphism does not influence the occurrence of AIS, but has an effect on the severity of its outcome. This effect is sex-specific and in homozygous women, the prothrombotic/antifibrinolytic effects of FXIII-A Val34Leu polymorphism seem to prevail.
Subject(s)
Brain Ischemia/genetics , Factor XIII/genetics , Intracranial Arteriosclerosis/genetics , Stroke/genetics , Aged , Aged, 80 and over , Base Sequence , Brain Ischemia/blood , Cohort Studies , Female , Genetic Predisposition to Disease , Humans , Intracranial Arteriosclerosis/blood , Male , Middle Aged , Polymorphism, Genetic , Retrospective Studies , Risk Factors , Stroke/bloodABSTRACT
BACKGROUND: The aim of neurosurgical cadaver training for residents and fellows is not only to obtain a high level of skills, but also to keep the number of complications during the learning curve as low as possible. To move this process forward, we have worked out a novel method in further training. METHODS: Tumours can be modelled from the autolog organs. We can then implant the modelled tumour from the opposite direction and a colleague can remove the pathology from the correct approach. RESULTS: We have experienced improving skills in difficult microsurgical operations. CONCLUSION: We have performed more than 800 fresh cadaver operations over the last 6 years. The last 70 cases have been performed with modelling pathology. In our department, we introduce a regular weekly program in our cadaver operating theatre. The consideration could be useful not only for the young neurosurgeons but also for experienced colleagues.
Subject(s)
Clinical Competence , Internship and Residency , Neurosurgery/education , Cadaver , Humans , Neurosurgery/methods , Physicians , TeachingABSTRACT
INTRODUCTION: Factor XIII (FXIII) is a key regulator of fibrinolysis and clot firmness. Val34Leu polymorphism of its potentially active A subunit (FXIII-A) leads to faster activation of FXIII, influences clot structure and provides a moderate protection against coronary artery disease. The effect of FXIII A subunit (FXIII-A) Val34Leu polymorphism on the risk of ischemic stroke (IS) has been investigated in a few studies with contradictory results. In spite of their fundamental difference in pathogenesis and hemostatic pathomechanism, only four small studies investigated the effect of FXIII-A Val34Leu polymorphism on the risk of atherothrombotic IS (AIS) separately from cardioembolic IS. Gender specific effect of the polymorphism on the risk of AIS has not been explored. In the present study we investigated the effect of FXIII-A Val34Leu polymorphism on the risk of AIS on a large patient population. MATERIALS AND METHODS: A population control group of 1,146 randomly selected individuals, 496 patients surviving AIS and their age and sex-matched controls selected from the population control group were included in the study. FXIII-A Val34Leu genotype was determined on DNA samples, obtained from peripheral blood leukocytes, by fluorescence resonance energy transfer detection using melting curve analysis. RESULTS: Neither sex nor age affected the distribution of FXIII-A Val34Leu genotypes in population control group. No association was revealed between the risk of AIS and FXIII-A Leu34 carriership and homozygous or heterozygous presentation of Leu34 allele in either gender. CONCLUSION: FXIII-A Val34Leu polymorphism fails to influence the risk of AIS.
