Rupture of a non sinus of Valsalva aneurysm during pregnancy: Case report and review of literatures.

Ruptured Sinus of Valsalva aneurysms during pregnancy is rare and presents a threat both to the mother and the fetus. We report a case of ruptured nonsinus of Valsalva aneurysms in a 26-year-old woman diagnosed at 32+4 weeks of gestation. A successful elective lower-segment cesarean section was conducted under general anesthesia. A successful surgical correction of the ruptured aneurysm under cardiopulmonary bypass (CPB) was performed with patch repair after 13 days. A multidisciplinary approach with respect to the pregnant patient's diagnosis, indications, and timing of surgery is necessary in ensuring the best possible outcomes for both the mother and the child.

Remote Postconditioning Induced by Trauma Protects the Mouse Heart against Ischemia Reperfusion Injury. Involvement of the Neural Pathway and Molecular Mechanisms.

PURPOSE: Abdominal superficial surgical incision elicits cardioprotection against myocardial ischemia reperfusion (I/R) injury in mice. This cardioprotective phenomenon, termed remote preconditioning of trauma (RPCT), results in an 80 to 85 % reduction in cardiac infarct size. We evaluated cardioprotection and the molecular mechanisms of remote postconditioning of trauma (RPostCT) in a murine I/R injury model. METHODS: Mice were analyzed using a previously established I/R injury model. An abdominal superficial surgical incision was made 45 min after myocardial ischemia at the end of coronary occlusion, and infarct size was determined 24 h after reperfusion. RESULTS: The results indicated that a strong cardioprotective effect occurred during RPostCT (56.94 ± 2.71 % sham vs. 15.58 ± 2.16 % RPostCT; the mean area of the infarct divided by the mean area of the region at risk; p ≤ 0.05; n = 10). Furthermore, pharmacological intervention revealed neurogenic signaling involvement in the beneficial effects of RPostCT via sensory and sympathetic thoracic nerves. Pharmacological experiments in transgenic mice demonstrated that bradykinin receptors, ß-adrenergic receptors (AR), and protein kinase C were implicated in the cardioprotective effects of RPostCT. CONCLUSIONS: RPostCT significantly decreased myocardial infarction size via neurogenic transmission and various signaling pathways. This study describes a new cardiac I/R injury prevention method that might lead to the development of therapies that are more clinically relevant for myocardial I/R injury.

Overexpression of the growth arrest-specific homeobox gene Gax inhibits proliferation, migration, cell cycle progression, and apoptosis in serum-induced vascular smooth muscle cells.

The Gax gene has been implicated in a variety of cell-developmental and biological processes, and aberrant Gax expression is linked to many diseases. In this study, to provide important insights for Gax-based gene therapy in vein graft restenosis and its anti-restenotic mechanism, we used rabbit vascular smooth muscle cells (VSMCs) to investigate the effects of Gax overexpression on proliferation, migration, cell cycle, and apoptosis in a serum-stimulated culture. Rabbit VSMC lines that stably overexpressed Gax were established by transfection with recombinant adenoviral vector Ad5-Gax. The effect of Gax overexpression on in vitro serum-induced VSMCs proliferation, migration, cell cycle, and apoptosis was assessed by MTT, wound healing, and flow cytometry assays, respectively. To investigate the effect of Gax overexpression on PCNA and MMP-2 in serum-induced VSMCs, immunocytochemistry, RT-PCR, and gelatin zymography were performed. The results clearly showed that Gax overexpression decreases PCNA expression in serum-induced VSMCs. Gax overexpression also significantly inhibited cell proliferation by blocking entry into the S-phase of the cell cycle, promoted cell apoptosis, and reduced cell migration activity by downregulating MMP-2 release and activity. These findings indicate that Gax would be an optimal target gene for gene therapy to treat vein graft restenosis.