Endografting under Assistance of Transapical Body Floss Through-and-Through Wiring Technique and Rapid Ventricular Pacing for an Ascending Aortic Tuberculous Pseudoaneurysm.

BACKGROUND: To demonstrate an ascending aortic tuberculosis pseudoaneurysm successfully treated with endografts under assistance of trans-apical body floss wiring technique and rapid ventricular pacing support. METHOD AND RESULT: A 77-year-old woman with a non-healing anteromedial chest wound presented with sudden hypotension and hemoptysis. The computed tomography (CT) scan revealed a 9-cm-diameter pseudoaneurysm of ascending aorta, with sternal erosion close to the wound. Conventional open repair was not preferred due to possible contamination of interposition graft and difficult sternum closure. The feasibility of endografting was confirmed based on appropriate landing zones. After endografts modification at back table, we made a left mini-thoracotomy and establish a through-and-through body floss wire from left ventricular apex to femoral artery. Retrograde delivery over this wire from femoral artery to ascending aorta and deployment of endografts under rapid ventricular pacing support were performed smoothly. Final angiography showed no endoleaks with patent coronary and arch vessels. Further wound debridement was done at the same time and wound culture yielded tuberculosis. After completing anti-tuberculosis therapy, no recurrent infection occurred. Postoperative 6-month CT scan disclosed optimal result. CONCLUSION: With adequate landing zones and delicate surgical strategy, endografting with anti-tuberculosis therapy may be an alternative treatment for ascending aortic tuberculosis pseudoaneurysm.

High-Content Genome-Wide RNAi Screen Reveals CCR3 as a Key Mediator of Neuronal Cell Death.

Neuronal loss caused by ischemic injury, trauma, or disease can lead to devastating consequences for the individual. With the goal of limiting neuronal loss, a number of cell death pathways have been studied, but there may be additional contributors to neuronal death that are yet unknown. To identify previously unknown cell death mediators, we performed a high-content genome-wide screening of short, interfering RNA (siRNA) with an siRNA library in murine neural stem cells after exposure to N-methyl-N-nitroso-N'-nitroguanidine (MNNG), which leads to DNA damage and cell death. Eighty genes were identified as key mediators for cell death. Among them, 14 are known cell death mediators and 66 have not previously been linked to cell death pathways. Using an integrated approach with functional and bioinformatics analysis, we provide possible molecular networks, interconnected pathways, and/or protein complexes that may participate in cell death. Of the 66 genes, we selected CCR3 for further evaluation and found that CCR3 is a mediator of neuronal injury. CCR3 inhibition or deletion protects murine cortical cultures from oxygen-glucose deprivation-induced cell death, and CCR3 deletion in mice provides protection from ischemia in vivo. Taken together, our findings suggest that CCR3 is a previously unknown mediator of cell death. Future identification of the neural cell death network in which CCR3 participates will enhance our understanding of the molecular mechanisms of neural cell death.