The network captures the detailed dynamics of human behavior during dual-task-performance, including both mean RTs and RT distributions, and establishes concrete predictions on neuronal dynamics during dual-task experiments in humans and non-human primates.”
“Metamaterials support optically excitable dark-plasmon modes Tubastatin A datasheet featured by antisymmetric surface current oscillations, which can be explained by Fano-type resonance and can be
tailored by controlling the embedded structural geometry. In this article, we numerically investigate the Fano-type resonance in complex metamaterials, and demonstrate the presence of Fano-Feshbach resonances due to the interaction between two Fano-type resonances in the overlapping region, implemented by breaking and tuning the symmetric properties of the resonant metallic element. Features of the resonance are discussed. This work shows that the domain of dark-plasmon mode based metamaterial system supports rich physics and can lead to various potential applications. (C) 2011 American Institute of Physics. [doi: 10.1063/1.3528208]“
“Matrix metalloproteinases (MMPs) play an essential role in tissue repair, cell death, and morphogenesis. The aim of the present
study was to investigate potential involvement of find more selected MMPs in the pathogenesis of neuronal apoptosis induced by the NMDA antagonist MK-801 (dizocilpine) or the GABA(A) agonist phenobarbital in infant rats, Epacadostat supplier transgenic rats overexpressing MMP-9 and MMP-9 knockout mice. Seven-day-old rats or knockout mice received intraperitoneal injections of MK-801, 1 mg/kg, or phenobarbital, 50 mg/kg. At different survival intervals following administration of the compounds (1-72 h), pups were sacrificed, tissue from different brain regions was isolated, and the expression and activity of MMP-2 and MMP-9 were analyzed by real-time PCR, western blot, and zymography. In addition, brains were fixed and processed for TUNEL staining.
In all the brain regions analyzed, we found an increased number of TUNEL-positive cells 24 h after administration of MK-801. After treatment, we detected no significant increase in MMP-2 or MMP-9 mRNA expression in cortical areas. No changes in the MMP-9 protein expression or gelatinolytic activity of MMP-2 were observed in conjunction with MK-801 or phenobarbital-induced neuroapoptosis in any brain region analyzed. The extent of neurodegeneration induced by MK-801 or phenobarbital was not altered in MMP-9 transgenic rats and was increased in MMP-9 knockout mice compared to wild-type rats and mice. Treatment with the panmetalloproteinase inhibitor GM6001 did not confer protection against MK-801-induced apoptotic cell death in the developing rat brain.