(C) 2012 Elsevier Ltd. All rights reserved.”
“Some authors have reported an association of BDNF Val66Met polymorphism with suicidal behavior and/or clinical aspects of

suicidal attempts. We evaluated, here, the impact of BDNFVal66Met polymorphism on the clinical characteristics of suicide attempts. The study was conducted on a cohort of 120 consecutive patients who were admitted to the Emergency Hospital of Porto Alegre, Brazil, due to a suicide attempt. Variables of univariate analyses were included in a logistic regression model to test whether the risk factors had independent effect. In univariate PCI32765 analyses, sex, BDNF genotype, intent and method of suicide attempt were all risk factors for high lethality in suicide attempts. After logistic regression analysis, male sex (O.R.=3.03; 95% C.I = 1.34-6.84; 0.008) and the presence of BDNF 66Met allele (O.R.= 2.62; 95% C.I = 1.04-6.57; 0.04) were significantly and independently associated with the high lethality in suicide attempts. The present study showed that BDNF 66Met allele is an independent predictor of high lethality BIX 1294 concentration in suicide

attempts of depressed patients. This finding is important because it might allow earlier identification of patients at high risk for suicide, perhaps providing better tools for clinical care of these patients in the future. (C) 2010 Elsevier Inc. All rights reserved.”
“The use of glucagon-like peptide-1 (7-36) amide (GLP-1) receptor agonists for the treatment of type 2 diabetes mellitus is commonly associated with nausea and vomiting. Therefore,

the present studies investigated the potential of GLP-1 receptor ligands to modulate emesis and feeding in Suncus murinus. Exendin-4, a selective GLP-1 receptor agonist, was administered subcutaneously Adenylyl cyclase (1-30 nmol/kg) or intracerebroventricularly (0.03-3 nmol) after 12-h of fasting. In other studies, animals were pretreated with the GLP-1 receptor antagonist, exendin (9-39), or saline (5 mu l) 15 min prior to exendin-4 (3 nmol, i.c.v.). Behaviour of animals and food and water intake were then recorded for 1-2 h; c-Fos expression was also assessed in the brains of animals in the i.c.v. studies. The subcutaneous administration of exendin-4 reduced food and water intake (p < 0.001) and induced emesis in 40% of animals (p > 0.05). The intracerebroventricular administration of exendin-4 also prevented feeding, and induced emesis (p < 0.01). In these studies, exendin (9-39) (30 nmol, i.c.v.) antagonised emesis induced by exendin-4 and the increased c-Fos expressions in the brainstem and hypothalamus (p < 0.05), but it was ineffective in reversing the exendin-4-induced inhibition of food and water intake (p > 0.05). These data suggest that exendin-4 exerts its emetic effects in the brainstem and/or hypothalamus via GLP-1 receptors. The action of exendin-4 to suppress feeding may involve non-classical GLP-1 receptors or other mechanisms.