(J Thorac Cardiovasc Surg 2010;139:1402-8)”
“Nerve agent-ind

(J Thorac Cardiovasc Surg 2010;139:1402-8)”
“Nerve agent-induced seizures cause neuronal damage in brain limbic and cortical circuits leading to persistent behavioral and cognitive deficits. Without aggressive anticholinergic and benzodiazepine therapy, seizures can be prolonged and neuronal damage progresses for extended periods of time. The objective of this study was to determine the effects of the nerve agent soman on expression of cyclooxygenase-2 (COX-2), the initial enzyme in the biosynthetic pathway of the proinflammatory prostaglandins and a factor that has been implicated in seizure initiation and propagation.

Rats were exposed to a toxic dose of soman and scored behaviorally for seizure intensity.

Expression of COX-2 selleck products was determined throughout brain from 4 h to 7 days after exposure by immunohistochemistry and immunoblotting. Microglial activation and astrogliosis were assessed microscopically over the same time-course. Soman increased COX-2 expression in brain regions known to be damaged by nerve agents (e.g., hippocampus, amygdala, piriform cortex and thalamus). COX-2 expression was induced in neurons, and not in microglia or astrocytes, and remained elevated through 7 days. The magnitude of COX-2 induction was correlated with seizure intensity. COX-1 expression was not changed by soman. Increased expression of neuronal COX-2 by soman is a late-developing response relative to other signs of acute Daporinad ic50 physiological distress caused by nerve agents. COX-2-mediated production selleckchem of prostaglandins is a consequence of

the seizure-induced neuronal damage, even after survival of the initial cholinergic crisis is assured. COX-2 inhibitors should be considered as adjunct therapy in nerve agent poisoning to minimize nerve agent-induced seizure activity. Published by Elsevier Inc.”
“Objective: To summarize the clinical experiences and mid-term follow-up results of perventricular closure of perimembranous ventricular septal defect without cardiopulmonary bypass under transesophageal echocardiography guidance.

Methods: A total of 408 patients with perimembranous ventricular septal defects, aged 5 months to 15 years (3.1 +/- 1.7 years) with a body weight of 4.5 to 26 kg (13.6 +/- 5.5 kg), underwent perventricular device closure. The procedure was performed via a small lower sternal incision. A guidewire was inserted through the ventricular septal defect to the left ventricle under transesophageal echocardiography guidance after a pursestring suture was placed on the right ventricular free wall. A modified delivery sheath was introduced over the guidewire to establish the delivery pathway. Proper devices were delivered and then deployed if no atrioventricular or aortic valvular disturbance, or residual shunt was detected by transesophageal echocardiography.

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