The paper investigates variations over time in the hazard of

rainfall-triggered landslides as a result of root degradation after forest cutting (or death). The case under study is related to experimental investigations aimed at determining the tensile strength and elasticity of root samples of trees dead within a decade, which correspond to decreasing values of soil cohesion (root reinforcement). Two kinds of samples were taken into account: living beech roots from protected wood areas to determine the RSL 3 current characteristics and roots from dead beeches (felled in previous years and at present in degradation) to analyse the evolution of root mechanical characteristics. To analyse the stability of representative slopes, we calculated the return time associated with a rainfall event, which BI 2536 in saturated conditions would lead to the attainment of the limit value of the safety factor and the associated hazard for different rainfall durations during a fixed period of time. Information about the increasing risk of collapse with the degradation of root system was obtained and compared with land slides occurrence in forested slopes of the study area. The results of the present paper show that such slopes may remain stable if they are covered with intact protective vegetation,

but they will become unstable if the conditions of the forest deteriorate or after a wooded area dies off: within a decade of tree death the root system of protection forests loses most of its soil-stabilising function. (C) 2012 Elsevier B. V. All rights reserved.”
“The most important reason for the non-approval and withdrawal of drugs by the Food and Drug Administration selleck products is hepatotoxicity. Therefore, this study was undertaken to evaluate the protective effects of hesperidin against cyclophosphamide (CYP)-induced hepatotoxicity in Wistar rats. The rats received a single intraperitoneal dose of CYP of 200 mg/kg body mass, followed by treatment with hesperidin, orally, at doses of 25 and 50 mg/kg for 11 consecutive days. CYP induced hepatic damage, as evidenced by the significantly elevated levels of

serum pro-inflammatory cytokines, serum transaminases, liver lipid peroxidation, and nitric oxide. As a consequence, there was reduced glutathione content, and the activities of the antioxidant enzymes superoxide dismutase, catalase, and glutathione peroxidase, were markedly reduced. In addition, CYP administration induced a considerable downregulation of peroxisome proliferator activated receptor gamma (PPAR gamma) and upregulation of nuclear factor-kappa B (NF-kappa B) and inducible nitric oxide synthase (iNOS) mRNA expression. Hesperidin, in a dose-dependent manner, rejuvenated the altered markers to an almost normal state. In conclusion, hesperidin showed a potent protective effect against CYP-induced oxidative stress and inflammation leading to hepatotoxicity.