92; 95% CI, 0.81-1.05; P=0.212, after age- and sex-adjustment, OR=0.87; 95% CI, 0.72-1.05; P=0.143).The rs10947803 SNP (A allele) in
KCNK17 increases the risk of cerebral hemorrhage but not ischemic stroke in the Chinese population. (C) 2013 Elsevier Ireland Ltd. All rights reserved.”
“Galantamine is a cholinesterase SCH772984 in vivo inhibitor and allosteric potentiating ligand modulating presynaptic nicotinic acetylcholine receptors that is used in the treatment of Alzheimer disease (AD). The purpose of this study was to determine if galantamine treatment would result in detectable hippocampal metabolite changes that correlated with changes in cognition, as measured by the Mini-Mental State Examination (MMSE) and the Alzheimer Disease Assessment Scale-cognitive subscale (ADAS-cog). Short echo-time proton magnetic resonance (MR) spectra were acquired from within the right hippocampus of ten patients using a 4 Testa magnetic resonance imaging (MRI) scanner. Spectra were used to quantify absolute metabolite levels for N-acetylaspartate (NAA), glutamate (Glu), choline (Cho), MK-1775 molecular weight creatine (Cr), and myo-inositol (ml). Patient scans and cognitive tests were performed before and 4 months after beginning
galantamine treatment, which consisted of an 8 mg daily dose for the first month and a 16 mg daily dose for the remaining three months. The levels of Glu, Glu/Cr, and Glu/NAA increased after four months of treatment, while there were no changes in MMSE or ADAS-cog scores. Additionally, changes (Delta) in Glu over LY411575 order the four months (Delta Glu) correlated with Delta NAA, and Delta(Glu/Cr) correlated with Delta MMSE scores. Increased Glu and the ratio of Glu to Cr measured by MR spectroscopy after galantamine treatment were associated with increased cognitive performance. The increase in Glu
may be related to the action of galantamine as an allosteric potentiating ligand for presynaptic nicotinic acetylcholine receptors, which increases glutamatergic neurotransmission. (C) 2009 Elsevier Inc. All rights reserved.”
“Epstein-Barr virus (EBV) infection of primary human B cells drives their indefinite proliferation into lymphoblastoid cell lines (LCLs). B cell immortalization depends on expression of viral latency genes, as well as the regulation of host genes. Given the important role of microRNAs (miRNAs) in regulating fundamental cellular processes, in this study, we assayed changes in host miRNA expression during primary B cell infection by EBV. We observed and validated dynamic changes in several miRNAs from early proliferation through immortalization; oncogenic miRNAs were induced, and tumor suppressor miRNAs were largely repressed. However, one miRNA described as a p53-targeted tumor suppressor, miR-34a, was strongly induced by EBV infection and expressed in many EBV and Kaposi’s sarcoma-associated herpesvirus (KSHV)-infected lymphoma cell lines.