The number and diversity of identified endocrine factors from adi

The number and diversity of identified endocrine factors from adipose tissue (adipokines) is growing rapidly. Here,

I argue that a systems biology approach to understanding the robust multi-level signaling networks established by the adipose secretome will be crucial for developing efficient type 2 diabetes treatment. Recent advances in whole-genome association studies, global molecular profiling and quantitative modeling are currently fueling the emergence of this novel research strategy.”
“Dysfunctional N-methyl-D-aspartate (NMDA) receptor neurotransmission has been implicated in the pathophysiology of schizophrenia. It is thought that this abnormal functioning can be corrected by increasing availability of the NMDA co-agonist glycine through inhibition of glycine transporter type 1 (GlyT1). Herein is described the pharmacologic profile of RG1678, a potent and noncompetitive glycine reuptake inhibitor. In vitro, RG1678 noncompetitively inhibited TGF-beta inhibitor glycine uptake at human GlyT1 with a concentration exhibiting half-maximal inhibition (IC50) of 25 nM and competitively blocked [H-3]ORG24598

binding sites at human GlyT1b in membranes from Chinese hamster ovary cells. In hippocampal CA1 pyramidal cells, RG1678 enhanced NMDA-dependent long-term potentiation at 100 nM but not at 300 nM. In vivo, RG1678 dose-dependently increased cerebrospinal fluid and striatal levels of glycine measured by microdialysis in rats. Additionally RG1678 attenuated hyperlocomotion induced by the psychostimulant D-amphetamine or the NMDA receptor glycine site antagonist L-687,414 in mice. RG1678 also prevented the hyper-response to D-amphetamine challenge in rats treated chronically with phencyclidine, an NMDA receptor open-channel blocker. In the latter experiment, a decrease in ex vivo striatal [H-3]raclopride binding was also measured. These data demonstrate that RG1678 is Daporinad concentration a potent, noncompetitive glycine reuptake inhibitor that can modulate both glutamatergic and dopaminergic neurotransmission in animal experiments

that model aspects of schizophrenia.

This article is part of a Special Issue entitled ‘Post-Traumatic Stress Disorder’. (C) 2011 Elsevier Ltd. All rights reserved.”
“Mullerian mimicry, where groups of chemically defended species display a common warning color pattern and thereby share the cost of educating predators, is one of the most striking examples of ecological adaptation. Classic models of Mullerian mimicry predict that all unpalatable species of a similar size and form within a community should converge on a single mimetic pattern, but instead communities of unpalatable species often display a remarkable diversity of mimetic patterns (e.g. neotropical ithomiine butterflies).

No related posts.

Comments are closed.