2009, PNAS 106 5406-5411], the model predicts that exposing the c

2009, PNAS 106 5406-5411], the model predicts that exposing the cell to extracellular 1.5% CO2/10 mM HCO3- (pH 7.50) causes pH(i) to fall and pH(S) to rise rapidly to a peak and then decay. Moreover, the model provides insights into the competition between diffusion and reaction processes when we

change the width of the EUF, membrane permeability to CO2, native extra- and intracellular carbonic anhydrase-like activities, the non-CO2/HCO3- (intrinsic) intracellular buffering power, or mobility of intrinsic intracellular buffers. (C) 2012 Elsevier Ltd. All rights reserved.”
“Alzheimer’s disease (AD) is a chronic neurodegenerative disease that causes a progressive loss in Selleckchem RAD001 learning and memory capabilities and eventually results in dementia. The non-renewable nature of neurons in the central nervous system leads to the basic pathological changes that are related to the various behavioral and psychological symptoms of AD. Oligodendrocyte- and myelin-related neurite outgrowth inhibitors (NOIs) tend to hinder the regeneration of neurons. We designed a recombinant DNA vaccine composed of multiple specific inhibitory domains of NOIs: Vaccination induced effective antibodies against the specific domains in the sera of mice treated with a DNA primed-vaccinia

virus boost regimen. The vaccine attenuated neuronal degeneration in the mouse brain and protected the model mice from behavioral deficits. Vaccination also decreased the formation of soluble A beta oligomer and amyloid plaques Napabucasin molecular weight in the co-transgenic mice brain. What’s more, astrocytosis in brains of APP/PS1 co-transgenic mice was also relieved. The results suggested that immunotherapy with multiple specific domains of myelin- and oligodendrocyte-related NOIs may be a promising approach for Alzheimer’s disease and other degenerative central nervous system diseases. (C) 2012 Published by Elsevier Ltd.”
“Objective:

Neuropsychological studies comparing cognitive performance in patients suffering from Obsessive-Compulsive Disorder (OCD) or Major Depressive Disorder (MDD) revealed deficits in the domains of verbal fluency and viso-motor speed/set shifting in both groups. Spatial working memory deficits, however, have been identified as specific markers of OCD. As yet, it has not been substantiated whether deficits in visual organization and complex visual memory are also specific to OCD and are not AZD3965 in vitro shared by MDD.

Method: Test performance in seven cognitive domains was assessed in 40 OCD patients, 20 MDD patients, and 40 healthy controls. Patient groups were matched according to severity of depressive symptoms.

Results: Deficits shared by both patient groups, as compared to controls, were found in delayed spatial recall and verbal fluency while verbal memory was normal in both patient groups. Only patients with OCD, but not MDD patients were impaired in the domains visual memory, viso-motor speed/set shifting, visual organization, and problem solving.

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