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Although most XYY men have normal sperm counts and are fertile (supposedly due to the loss of the extra Y before meiosis), there is a minority who are infertile. In these cases, the XYY spermatocytes are able to enter meiosis and form different synaptic configurations. With regard to mosaics, there is scarce well-defined information on the presence of the second Y and its meiotic behaviour. In this study, the chromosome constitution and the synaptic behaviour of pachytene spermatocytes from an azoospermic man with testicular hypotrophy and non-mosaic 47,XYY karyotype were analysed. Furthermore, we determined the chromosome constitution of the somatic Sertoli cells. Five karyotypically normal men with obstructive azoospermia, but having complete spermatogenesis, were included as controls. Immuno-FISH using specific protein markers of synapsis and recombination (SYCP3, SYCP1, BRCA1, MLH1, CREST) and a specific Yq12 DNA probe were used. In addition, we used the newly developed Super-Resolution Structured Illumination Microscopy (SR-SIM) to clearly define the synaptic configurations. FISH analysis was also performed on Sertoli cells. The histopathological analysis showed variable degrees of spermatogenesis development in the testicular tissue of the propositus. Immuno-FISH analysis showed that most of the primary spermatocytes were euploid 46, XY. The use of SR-SIM confirmed the existence of this euploidy. Only a few pachytene spermatocytes showed an aneuploid X + YY constitution. Sertoli cells showed two different populations with one or two Y chromosomes, in similar proportions. Thus an abnormal niche of sex-trisomic Sertoli cells should be also considered when searching for the origin of spermatogenesis failure in XYY men., (© The Author(s) 2018. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.)

Women have higher bleeding complication and mortality rates after percutaneous coronary interventions (PCI). The contribution of female gender to bleeding and mortality is poorly understood. We evaluated the effect of gender and bleeding on outcomes of patients treated with bivalirudin during PCI by performing a patient-level pooled analysis of 3 randomized controlled trials (the Randomized Evaluation in PCI Linking Angiomax to Reduced Clinical Events, Acute Catheterization and Urgent Intervention Triage strategY, and Harmonizing Outcomes with Revascularization and Stents in Acute Myocardial Infarction) comparing bivalirudin versus heparin plus glycoprotein IIb/IIIa inhibitor (GPI) treatment in patients undergoing PCI. Of 14,784 patients, 7,413 patients received bivalirudin (1,870 women) and 7,371 patients received heparin + GPI (1,910 women). Women had significantly higher 30-day non-coronary artery bypass grafting (CABG)-related major bleeding rates (7.6% vs 3.8%, p <0.0001). After multivariate adjustment, female gender increased the hazard of major bleeding by 80% (hazard ratio 1.80, 95% confidence interval 1.52 to 2.11, p <0.001). Furthermore, women had a higher 1-year mortality rate (3.7% vs 2.7%, p = 0.002) than men; 30-day major bleeding was the strongest independent predictor of 1-year mortality in women (hazard ratio 2.48, 95% confidence interval 1.57 to 3.91, p = 0.001). Bivalirudin therapy in women reduced 30-day non-CABG-related major bleeding (5.6% vs 9.7%, p <0.0001) and 1-year mortality (2.9% vs 4.4%, p = 0.02) compared to standard therapy. In conclusion, in this cohort of patients treated for acute coronary syndrome and ST-segment elevation myocardial infarction, women have a near 2-fold increase in bleeding complications compared to men after PCI. Bleeding complications rather than gender is the strongest independent predictor of 1-year mortality in patients undergoing PCI. Furthermore, we observed a more pronounced clinical benefit in women treated with bivalirudin including a 44% reduction in major bleeding and a significant reduction in mortality rates at 1 year., (Copyright © 2016 Elsevier Inc. All rights reserved.)