Further studies are needed to elucidate the potential biological mechanisms by which circulating klotho could affect longevity in humans.”
“Amphetamine (AMPH) increases adult rat 50-kHz ultrasonic vocalizations, preferentially

promoting frequency-modulated www.selleckchem.com/products/17-AAG(Geldanamycin).html (FM) calls that have been proposed to reflect positive affect. The main objective of this study was to investigate a possible noradrenergic contribution to AMPH-induced calling. Adult male Long-Evans rats were tested with AMPH (1 mg/kg intraperitoneal) or saline combined with various systemic pretreatments: clonidine (alpha 2 adrenergic agonist), prazosin (alpha 1 antagonist), atipamezole (alpha 2 antagonist), propranolol, betaxolol, and/or ICI Liproxstatin-1 118,551 (beta 1/beta 2, beta 1, and beta 2 antagonists, respectively), nadolol (beta 1/beta 2 antagonist, peripheral only), or NAD-299 (5HT(1A) antagonist). In addition, effects

of cirazoline (alpha 1 adrenergic agonist) and cocaine (0.25-1.5 mg/kg intravenous) were studied alone. AMPH-induced calling was suppressed by low-dose clonidine and prazosin. Cirazoline and atipamezole did not significantly affect calling rate. Propranolol, without affecting the call rate, dose dependently promoted ‘flat’ calls under AMPH while suppressing ‘trills,’ thus reversing the effects of AMPH on the ‘call subtype profile.’ This effect of propranolol seemed to be mediated by simultaneous inhibition of Elongation factor 2 kinase CNS beta 1 and beta 2 rather than by 5HT(1A) receptors. Finally, cocaine elicited fewer calls than did AMPH, but produced the same shift in the call subtype profile. Taken together, these results reveal differential drug effects on flat vs trill vs other FM 50-kHz calls. These findings highlight the value of detailed call subtype analyses, and show that 50-kHz calls are associated with adrenergic alpha 1- and beta-receptor mechanisms. These preclinical findings suggest that noradrenergic contributions to psychostimulant subjective effects may warrant further

investigation. Neuropsychopharmacology (2012) 37, 808-821; doi: 10.1038/npp.2011.258; published online 26 October 2011″
“Abdominal aortic aneurysms (AAAs) are a multifactorial degenerative vascular disorder. One of the defining features of the pathophysiology of aneurysmal disease is inflammation. Recent developments in vascular and molecular cell biology have increased our knowledge on the role of the adaptive and innate immune systems in the initiation and propagation of the inflammatory response in aortic tissue. AAAs share many features of autoimmune disease, including genetic predisposition, organ specificity and chronic inflammation. Here, this evidence is used to propose that the chronic inflammation observed in AAAs is a consequence of a dysregulated autoimmune response against autologous components of the aortic wall that persists inappropriately.