Search results for "plastic"

Drammaturgia di un prurito

2008

Zagadnienie stosowania tworzyw sztucznych w przewodach kominowych w oparciu o krajowe i europejskie przepisy

2017

Zagadnienie stosowania tworzyw sztucznych w przewodach kominowych w oparciu o krajowe i europejskie przepisy

2017

Zagadnienie stosowania tworzyw sztucznych w przewodach kominowych w oparciu o krajowe i europejskie przepisy

2017

Mechanizm neuroplastyczności i jego znaczenie dla psychoterapii oraz oceny jej skuteczności

2016

The paper introduces the mechanism of neuroplasticity, specifically the ability of the brain to develop new neurons (neurogenesis) and new connections between nerve cells (synaptogenesis) and to develop glial cells. The author presents the evidence proving the existence of neuroplasticity by giving examples of people with serious brain damage who function normally and, above all, of people living with almost no brain or with one hemisphere, or with post-stroke defects. However, the main purpose of this paper is to present the current state of knowledge of the importance of the brain plasticity for the course of psychotherapy, as well as for assessing its effectiveness. The author gives many…

VALUTAZIONE DELL’OUTCOME FUNZIONALE DEI PAZIENTI AFFETTI DA CARCINOMA DEL CAVO ORALE

Are paradoxical intensity-dependent effects of 5Hz rTMS train in motor cortex of migraine with aura patients evidence of abnormal homeostatic plastic…

2010

Inhibition of Rac1 signaling by lovastatin protects against anthracycline-induced cardiac toxicity

2011

Normal tissue damage limits the efficacy of anticancer therapy. For anthracyclines, the clinically most relevant adverse effect is cardiotoxicity. The mechanisms involved are poorly understood and putative cardioprotectants are controversially discussed. Here, we show that the lipid-lowering drug lovastatin protects rat H9c2 cardiomyoblasts from doxorubicin in vitro. Protection by lovastatin is related to inhibition of the Ras-homologous GTPase Rac1. It rests on a reduced formation of DNA double-strand breaks, resulting from the inhibition of topoisomerase II by doxorubicin. Doxorubicin transport and reactive oxygen species are not involved. Protection by lovastatin was confirmed in vivo. I…

Aplidin® induces JNK-dependent apoptosis in human breast cancer cells via alteration of glutathione homeostasis, Rac1 GTPase activation, and MKP-1 ph…

2006

Aplidin® is an antitumor agent in phase II clinical trials that induces apoptosis through the sustained activation of Jun N-terminal kinase (JNK). We report that Aplidin® alters glutathione homeostasis increasing the ratio of oxidized to reduced forms (GSSG/GSH). Aplidin® generates reactive oxygen species and disrupts the mitochondrial membrane potential. Exogenous GSH inhibits these effects and also JNK activation and cell death. We found two mechanisms by which Aplidin® activates JNK: rapid activation of Rac1 small GTPase and downregulation of MKP-1 phosphatase. Rac1 activation was diminished by GSH and enhanced by L-buthionine (SR)-sulfoximine, which inhibits GSH synthesis. Downregulatio…

Rac1 protein signaling is required for DNA damage response stimulated by topoisomerase II poisons.

2012

To investigate the potency of the topoisomerase II (topo II) poisons doxorubicin and etoposide to stimulate the DNA damage response (DDR), S139 phosphorylation of histone H2AX (γH2AX) was analyzed using rat cardiomyoblast cells (H9c2). Etoposide caused a dose-dependent increase in the γH2AX level as shown by Western blotting. By contrast, the doxorubicin response was bell-shaped with high doses failing to increase H2AX phosphorylation. Identical results were obtained by immunohistochemical analysis of γH2AX focus formation, comet assay-based DNA strand break analysis, and measuring the formation of the topo II-DNA cleavable complex. At low dose, doxorubicin activated ataxia telangiectasia m…