Introduction Female sexual dysfunction (FSD) is a very common disorder, with an estimated prevalence of having at least one sexual dysfunction of about 40%. Aim To investigate the prevalence and types of FSD and the relationship between hormonal contraception (HC) and FSD in female German medical students. Main Outcome Measures Female Sexual Function Index (FSFI) with additional questions on contraception, sexual activity, and other factors that may influence sexual function. Methods An online questionnaire based on the FSFI was completed by students from six medical schools. Obtained data were screened for inconsistencies by programmed algorithms. Results A total of 1,219 completed questionnaires were received, and 1,086 were included in the analyses after screening. The mean total FSFI score was 28.6 +/− 4.5. 32.4% of women were at risk for FSD according to FSFI definitions. Based on domain scores, 8.7% for were at risk for FSD concerning orgasm, 5.8% for desire, 2.6% for satisfaction, 1.2% for lubrication, 1.1% for pain and 1.0% for arousal. The method of contraception and smoking were factors with significant effect on the total FSFI score whereby hormonal contraception was associated with lower total FSFI scores and lower desire and arousal scores than no contraception and non-hormonal contraception only. Other variables such as stress, pregnancy, smoking, relationship and wish for children had an important impact on sexual function as expected according to earlier studies. Conclusions The prevalence of students at high risk for FSD was consistent with the literature although domain subscores differed from samples previously described. The contraception method has a significant effect on the sexual functioning score and women using contraception, especially hormonal contraception, had lower sexual functioning scores. Stress and relationship among other variables were found to be associated with sexual function and may thus provide insight into the etiology of sexual disorders.

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Neonangiogenesis represents an important step in tumor development and propagation. Statins may have anticancerogenic potential by blocking vascular endothelial cell growth. The antiproliferative effect of four statins on human endothelial cells was compared, concomitantly delineating a possible pro-apoptotic process. All four statins tested, i. e. atorvastatin, fluvastatin, lovastatin, and simvastatin inhibited cell proliferation. Nearly complete blocking of cell proliferation was achieved at a concentration of 10 microM. We were able to demonstrate that the antiproliferative effect of the statins is not due to cytotoxicity but rather to an apoptotic effect as demonstrated by comparison of cytotoxicity assay and apoptosis assay. The apoptotic mechanism seems to involve caspases, since the statins significantly enhanced caspase activity at dosages of 10 and 20 microM. Further experiments revealed a downregulation of the pro-apoptotic protein Bcl-2. Our data indicate that statins may class-specific inhibit angiogenesis at high dosages which can contribute to prevention of tumor development and progression.