The German version of the EPDS with ten questions is an "application friendly" as well as proven to be a valid and reliable method for supporting the diagnosis of postpartum depressive disorder. It is suitable for both clinical and research use.

Purpose: We aimed to determine the clinical role of the p53 family members p53 and p73 in the responsiveness to platinum-based chemotherapy and survival in ovarian cancer, considering their cross-talk and the p53 polymorphism at codon 72. Experimental Design: A detailed analysis of p53 and p73 in a series of122 ovarian cancers was done.We used a functional yeast-based assay to determine the p53 mutational status. Red yeast colonies, indicating mutant p53, were subsequently sequenced to determine the specific p53 alteration. p53 mutations were divided into two groups according to their previous characterization in the literature: those that efficiently inhibit transcriptionally activeTAp73 function and those that do not. A p53 polymorphism at codon 72 was determined in corresponding normal tissue or blood of ovarian cancer patients. Isoform-specific p73 expression analysis using real-time reverse transcription-PCR has previously been done in the majority of ovarian cancers included in this study. In a retrospective chart review, responsiveness to chemotherapy was assessed, and survival data with long follow-up times were collected. Results: Eighty of 122 (65.6%) of ovarian cancers harbored p53 mutations. p53 mutational status was an important determinant of responsiveness to platinum-based chemotherapy in all patients with a residual tumor of <2 cm in diameter after initial surgery (wild-type versus mutant, P = 0.029). In addition, p53 mutational status was a strong prognosticator for recurrence-free and overall survival (P < 0.0001and P = 0.003, respectively) in univariate analyses. High expression levels of dominant-negative p73 isoforms (DNp73 and DNVp73) significantly correlated with chemotherapeutic failure (P = 0.048) and with worse recurrence-free and overall survival in patients with p53 mutant cancers (P = 0.048 and P = 0.005, respectively). Eight p53 mutations, present in 19 cases, were found that efficiently inhibit TAp73 (i.e., 175H, 220C, 245S, 245D, 248W, 248Q, 266E, and 273H). Patients with p53 mutations that efficiently inhibit TAp73 function had a significantly shorter overall survival than patients with p53 mutations of unknown effect on TAp73 (P = 0.044). The p53 polymorphism at codon 72 had no influence on responsiveness to chemotherapy or survival. Conclusion: We provide the first clinical evidence that dominant-negative p73 isoforms contribute to drug resistance in vivo, underscoring the importance of a p53-p73 cross-talk. NH 2 -terminally truncated p73 isoforms were of significant clinical effect by providing an additional unfavorable factor for response to platinum-based chemotherapy and survival in p53 mutant ovarian cancers.

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Serum samples from several groups of patients attending a gynecology clinic were analyzed by ELISA for specific antibodies recognizing surface epitopes on intact human papillomavirus (HPV) types 6 and 11 L1 virus-like particles (VLPs) that were synthesized in vitro. In these samples, positive IgG and IgM reactivities to HPV-11 L1 VLPs were, respectively, 12% and 6% for 87 controls, 46% and 67% for 79 condyloma patients, 30% and 64% for 72 cervical intraepithelial neoplasia patients, 16% and 19% for 63 pregnant women at time of delivery, and 5% and 0 in their 63 newborns. IgA reactivities were low and not significantly different. The prevalence of IgG-positivity in HPV-6/11 DNA-positive patients increased from 46% with HPV-11 L1 VLPs to 76% when the sera were additionally screened with HPV-6 L1 VLPs. These data show that HPV-6 and -11 L1 VLPs are effective antigens for serologic studies and they detect type-specific antibodies.