The patient proceeded to carotid endarterectomy with no complications. (J Vase Surg 2009;50:1493-5.)”
“Acid sensing ion channels (ASICs) are widely expressed in central and peripheral nervous system. They are involved in a variety of physiological and pathophysiological processes: synaptic transmission, learning and memory, pain perception, ischemia, etc. During ischemia, metabolic acidosis causes the drop of extracellular pH (pHe) which in turn activates ASICs. Activation of calcium permeable ASIC1a has been implicated

in neuronal death. ASICs are modulated by several redox reagents, divalent cations and nitric oxide (NO). Although NO potentiates ASIC mediated currents, the selleck screening library physiological significance of such modulation has not been studied in detail. We have evaluated the role of endogenous NO in cell death at different pH, mediated by the activation of ASICs. At pH 6.1, death rates of ASIC1 expressing Neuro2A (N2A) cells are significantly higher in comparison to the cells that do not express ASICs. Amiloride, a blocker of ASICs protects the cell from acid-injury. Sodium nitroprusside, a potent NO donor not only increases the ASIC mediated currents but also increases cell death at low pH. L-Arg, the precursor of NO also potentiates ASICs in a pH dependent manner. L-Arg-induced NO production and potentiation of ASICs were observed at pHs 7.4, 7.2,

7.0 and 6.8. Lowering the pH below 6.8 did not result in significant production of NO or potentiation of ASICs upon L-Arg stimulation. Our buy MLN0128 results suggest that potentiation of ASICs by NO and subsequent cell death in vivo depends on the severity of acidosis. During mild and moderate acidosis, NO promotes cell death by potentiating ASICs, whereas this potentiation

subsides in severe acidosis due to inhibition of NO synthase. (C) 2010 Elsevier Inc. All rights reserved.”
“A 64-year-old man was admitted with abdominal pain 6 weeks after treatment with intravenous flucloxacillin for cellulitis of his right leg. Urgent operation was necessary PCI-32765 nmr for a mycotic aneurysm of the abdominal aorta due to infection with Pasteurella multocida, a microorganism residing in the oral cavity of domestic animals that very rarely causes infection of native arteries or grafts. The aorta was repaired with a rifampin-coated tube graft. Despite postoperative duodenal perforation, abdominal Candida infections, wound dehiscence, and renal insufficiency, the patient is alive I year postoperatively. (J Vase Surg 2009;50:1496-8.)”
“Brazilian population has a multi-ethnical profile and the prevalence of endothelial nitric oxide synthase enzyme (eNOS) polymorphism in heart failure (HF) has not been previously studied. Therefore the present study assessed the association of eNOS Glu298Asp polymorphism in patients with HF and controls.