There were increased glutamate and putrescine levels in the DG, but decreased agmatine levels in the DG and PFC, in the A beta(25-35) group relative to the A beta(35-25) one. Cluster analyses were performed to determine if the nine related neurochemical variables (arginine, citrulline, ornithine, agmatine, putrescine, spermidine,
spemine, glutamate, and GABA) formed distinct groups, and whether it changed as a function of A beta(25-35). There were substantially different clusters between the two groups in the hippocampus and PFC. These results demonstrate that A beta(25-35) alters arginine metabolism, which further supports the prominent role of arginine and its metabolites in Alzheimer’s disease (AD) pathogenesis. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Spontaneous dissection of the superior mesenteric artery (SMA) is rare. We report a case of rupture of the SMA after spontaneous find more dissection in a 51-year-old male who presented with acute onset of abdominal pain and hypotension. The patient was initially treated with intravenous fluid resuscitation and endovascular intervention followed by open surgery. No identifiable cause for dissection was found. The patient was diagnosed as having segmental arterial mediolysis (SAM). The patients’ presentation, treatment, outcome, and all relevant imaging,
pathologic, and laboratory studies were reviewed. The relevant features of the case and SAM are presented herein. In addition, a review of all available MM-102 solubility dmso published literature on SAM to date is presented. (J Vase
Surg 2011;53:1107-12.)”
“Early-life exposure to bacterial endotoxins, such as lipopolysaccharides (LPS), can provide neuroprotection against experimental autoimmune encephalomyelitis (EAE) during adulthood, possibly through altering the responsiveness of the immune system. Here, we show that exposure of LPS Dichloromethane dehalogenase to neonatal rats resulted in a sustained elevation of corticosterone level in urine when compared with saline-treated rats, and that the high level of urine corticosterone was maintained during the progression of EAE (P<0.05). This high level of production of corticosterone plays an important role in altering the predisposition to EAE-induced neuroinflammation, as a positive correlation occurred between the concentration of urine corticosterone and the increased apoptotic CD4(+) T cells from the peripheral blood. LPS-treated rats also showed a reduced number of CD3(+) T cells in the spinal cord. The splenic antigen-presenting cells showed a reduced expression of MHC II during EAE development in LPS-exposed rats when compared with rats exposed to the saline-treated control. Together, these findings suggest that treating neonatal rats with LPS evokes a sustained elevation of glucocorticoid, which may suppress immune response during EAE by increasing apoptosis of CD4(+) T cells and reducing the expression of MHC II on antigen-presenting cells.