Cell Death and Disease (2012) 3, e443; doi:10.1038/cddis.2012.178; published online 13 December 2012″
“The main objective of this study was to demonstrate the possible use of dynamic neural networks to model diclofenac sodium release from

polyethylene oxide hydrophilic matrix tablets. High and low molecular weight polymers in the range of 0.9-5 x 10(6) have been used as matrix forming materials and 12 different formulations were prepared for each polymer. Matrix tablets were made by direct compression method. Fractions of polymer and compression force have been selected as most influential factors on diclofenac sodium release profile. In vitro dissolution profile has been treated as time series using dynamic neural networks. Dynamic networks are expected to be advantageous in the click here modeling of drug release. Networks of different topologies have been constructed in order to obtain precise prediction of release profiles for test formulations. Short-term and long-term memory structures have been included in the design of network making it possible to treat dissolution profiles as time series. The ability of network to model drug release

has been assessed by the determination of correlation between predicted and experimentally see more obtained data. Calculated difference (f(1)) and similarity (f(2)) factors indicate that dynamic networks are capable of accurate predictions. Dynamic neural networks were compared to most frequently

used static network, multi-layered perceptron, and superiority of dynamic networks has been demonstrated. The study also demonstrated differences between the used polyethylene oxide polymers in respect to drug release and suggests explanations for the obtained results. (C) 2009 Elsevier B.V. All rights reserved.”
“Key points Advancing age is the major risk factor for the development of cardiovascular diseases. Arterial endothelial dysfunction, characterized by impaired endothelium-dependent dilatation (EDD), is a key antecedent to age-associated clinical selleck screening library cardiovascular disease. We tested the hypothesis that changes in autophagy, the process by which cells recycle damaged biomolecules, may be an underlying cause of the age-related reduction in EDD. We show that autophagy is impaired in arteries of older humans and mice with reduced EDD, and that enhancing autophagy restores EDD by reducing superoxide-dependent oxidative stress and inflammation, and increasing nitric oxide bioavailability. Our results identify impaired autophagy as a potential cause of age-related arterial dysfunction and suggest that boosting autophagy may be a novel strategy for the treatment of arterial endothelial dysfunction and prevention of cardiovascular diseases with ageing.