Present data may help to a better understanding of the molecular

Present data may help to a better understanding of the molecular mechanisms involved in cytoskeletal degradation-induced apoptosis in neurons. (C) 2008 Elsevier Inc. All rights reserved.”
“Objective: To examine the feasibility of using blood-derived smooth muscle cells (BD-SMCs) as a target for to deliver therapeutic proteins. Materials and

Methods: Mononuclear cells (MNC) were isolated from peripheral blood. The outgrowth colonies from MNC culture were differentiated

into BD-SMCs in media containing platelet-derived growth factor BB. Phenotypic PKC412 solubility dmso characterization of BD-SMCs was assessed by immunocytochemistry. Cell proliferation, gene transfer efficiency with a retroviral vector, apoptosis, and the biological activity of the transduced gene product from the BD-SMCs were evaluated Veliparib in vitro and in vivo in comparison with vascular derived SMC (VSMCs).

Results: BD-SMCs stained positive for SMC markers. No significant difference was observed between BD-SMCs and VSMCs in cell proliferation, migration, adhesiveness, and gene

transfer efficiency. After BD-SMCs were transduced with a retroviral vector carrying the secreted alkaline phosphatase gene (SEAT), 174 +/- 50 mu g biologically active SEAT was produced per 106 cells over 24 hours. After injecting 5 x 106 cells expressing SEAT intravenously into rabbits, SEAT concentration increased

3-deazaneplanocin A clinical trial significantly in the circulation from 0.14 +/- 0.04 mu g/ml to 2.34 +/- 0.16 mu g/ml 3 days after cell injection (P < .01, n = 3). Circulating levels of SEAT decreased to 1.76 mu g/ml 1 week later and remained at this level up to 8 weeks, then declined to pre-cell injection level at 12 weeks. VSMC in vivo gene expression data were equivalent.

Conclusion: BD-SMCs have similar characteristics to mature VSMCs and can be used as a novel target for gene transfer to deliver a therapeutic protein.”
“Many toxic environmental and food agents have been suspected to be potential risk factors in inducing memory disabilities under normal and pathological conditions. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (known as dioxin or TCDD) is a common and prototypical member of a class of noxious environmental and food contaminants called the halogenated aromatic hydrocarbons. Since the role of dioxin in memory processes has not been studied in detail, the present report aims at elucidating the role of this pollutant in the maintenance of cognitive function. We found that TCDD (50 mu g/kg) induced spatial memory deficits in the Morris water maze (MWM) task in female but not male mice. This sex-dependant effect of dioxin seems to be related to the alteration of estrogen pathways, as treatment with 17 beta-estradiol-3-benzoate (E; 5 mu g/day) reversed memory deficits induced by TCDD.

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