The amount of long-term potentiation was decreased by 49% in trea

The amount of long-term potentiation was decreased by 49% in treated pups and recovery after low-frequency stimulation was delayed. The results not only strengthen the view that basal, constitutive kynurenine metabolism is involved in normal brain development, but also show that changes induced prenatally can affect the brains of adult offspring and those changes are quite different from those seen previously at weaning (P21). Those changes may be mediated by altered expression of NMDAR subunits and sonic hedgehog. (C) 2013 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Ezrin

cross-links plasma membrane proteins with the actin cytoskeleton. In the kidney, ezrin mainly localizes at the brush border membrane of proximal tubules with the scaffolding protein, Na+/H+ exchanger regulatory factor (NHERF) 1. NHERF1 interacts Evofosfamide cost with the sodium/phosphate cotransporter, Npt2a. Defects in NHERF1 or Npt2a in mice cause hypophosphatemia. Here we studied the physiological role of ezrin in renal phosphate reabsorption using ezrin knockdown mice (Vil2). Ruxolitinib in vivo These mice exhibit hypophosphatemia, hypocalcemia, and osteomalacia. The reduced plasma phosphate concentrations were ascribed to defects

in urinary phosphate reabsorption. Immunofluorescence and immunoblotting indicated a marked reduction in renal Npt2a and NHERF1 expression at the apical membrane of proximal tubules in the knockdown mice. On the other hand, urinary loss of calcium SB-3CT was not found in Vil2 mice. Plasma concentrations of 1,25-dihydroxyvitamin D were elevated following reduced plasma phosphate levels, and mRNA of the vitamin D-dependent TRPV6

calcium channel were significantly increased in the duodenum of knockdown mice. Expression of TRPV6 at the apical membrane, however, was significantly decreased. Furthermore, tibial bone mineral density was significantly lower in both the adult and young Vil2 mice. These results suggest that ezrin is required for the regulation of systemic phosphate and calcium homeostasis in vivo. Kidney International (2012) 83, 41-49; doi:10.1038/ki.2012.308; published online 15 August 2012″
“Humor and laughter can positively influence mood, promote optimism and lead to a change of perspective. Six patients with major depression participated in a group training program specifically designed to enhance humor abilities. After 8 weeks of training, short-term mood improvement was observed and the patients considered themselves more capable of using humor as a coping strategy. Acquired humor skills also helped to sustain the patients’ motivation throughout the training period. In light of these encouraging findings, further studies to compare the effectiveness of the humor training with the effectiveness of other types of intervention and to assess its potential long-term effects seem warranted. (C) 2010 Elsevier Ireland Ltd. All rights reserved.

Comments are closed.