“Vascular risk factors play a significant role in the path

“Vascular risk factors play a significant role in the pathogenesis and progression of AD. MPV is an index of platelet activation and may be a potential marker

of inflammation to demonstrate the vascular damage in AD. The aim of the present study is to assess whether platelet volume would be useful in predicting vascular damage in AD. A total of 126 patients with AD (male/female: 44/82, mean age 76.2 +/- 6.8 years) and 286 patients as controls with normal cognitive function (male/female: 123/163, mean age 75.2 +/- 6.3 years) were enrolled in this cross-sectional study. MPV values were determined for all study participants. Mini-Mental State Examination (MMSE) and clock drawing tests (CDT) were performed for cognitive assessment, DSM-IV and NINCDS-ADRDA criteria were used for diagnosis of AD. The mean MPV values were significantly higher in AD group (8.46 +/- 1.15 vs. www.selleckchem.com/products/a-1210477.html 8.17 +/- 0.90; p = 0.011). In this study, significantly higher MPV values in patients with AD have been detected. Since increased MPV levels are usually https://www.selleckchem.com/products/anlotinib-al3818.html considered as a vascular risk factor, the results of this study suggested the role of platelet activation in the vascular pathogenetic basis of AD. (C) 2011 Elsevier Ireland Ltd. All rights reserved.”
“Chemotherapy often causes damage to hematopoietic tissues, leading to

acute bone marrow suppression and the long term development of leukemias. Niacin deficiency, which is common in cancer patients, causes dramatic genomic instability in bone marrow cells in an in vivo rat model. From a mechanistic perspective, niacin deficiency delays excision repair and causes double strand break accumulation, which in turn favors chromosome breaks and translocations. Niacin deficiency mTOR inhibitor also impairs cell cycle arrest and apoptosis in response to DNA damage, which combine to encourage the survival

of cells with leukemogenic potential. Conversely, pharmacological supplementation of rats with niacin increases bone marrow poly (ADP-ribose) formation and apoptosis. Improvement of niacin status in rats significantly decreased nitrosourea-induced leukemia incidence. The data from our rat model suggest that niacin supplementation of cancer patients may decrease the severity of short- and long-term side effects of chemotherapy, and could improve tumor cell killing through activation of poly(ADP-ribose)-dependent apoptosis pathways. [Mol Cancer Ther 2009;8(4):725-32]“
“Objective: Succinic semialdehyde dehydrogenase (SSADH) deficiency is a rare autosomal recessive disorder of GABA degradation leading to elevations in brain GABA and gamma-hydroxybutyric acid (GHB). The effect of chronically elevated GABA and GHB on cortical excitability is unknown. We hypothesized that use-dependent downregulation of GABA receptor expression would promote cortical disinhibition rather than inhibition, predominantly via presynaptic GABAergic mechanisms.

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