The effects of dronabinol selleck exposure were studied after 2 weeks of washout
on the rewarding effects of morphine measured in the place preference and oral self-administration tests. The preproenkephalin (PPE) mRNA levels and the relative density and functionality of CB1, and mu-opioid receptors were quantified in the striatum and the mesencephalon. Chronic dronabinol exposure in AFR rats induced an increase in sensitivity to morphine conditioning in the place preference paradigm together with a decrease of PPE mRNA levels in the nucleus accumbens and the caudate-putamen nucleus, without any modification for preference to oral morphine consumption. In contrast, dronabinol treatment on
D-rats normalized PPE decrease in the striatum, morphine consumption, and suppressed sensitivity to morphine conditioning. CB1 and mu-opioid receptor density and functionality were not changed in the striatum and mesencephalon of all groups of rats. These results indicate THC potency to act as a homeostatic modifier that would worsen the reward effects of morphine on naive animals, but ameliorate the deficits in maternally D-rats. These findings point to the self-medication use of cannabis in subgroups of individuals subjected to adverse postnatal environment. Neuropsychopharmacology (2009) 34, 2469-2476; doi: 10.1038/npp.2009.70; published online 24 June 2009″
“The latency-associated nuclear antigen (LANA) of Karposi’s sarcoma-associated herpesvirus has been reported to interact with glycogen DNA Damage inhibitor synthase kinase 3 beta (GSK-3 beta) and regulate its activity, leading to inhibition of GSK-3-dependent
beta-catenin degradation. In this study, the interaction between LANA and GSK-3 beta learn more was characterized further. LANA was found to interact with GSK-3 beta in vitro as well as in intact cells. However, LANA did not regulate GSK-3 beta kinase activity and LANA-induced upregulation of beta-catenin was GSK-3 beta independent. LANA did not regulate the stability of beta-catenin or of its reported interaction partners p53 and von Hippel-Lindau protein. Additional targets of LANA are likely to mediate its malignancy-promoting function.”
“Brain magnetic resonance imaging (MRI) studies on Wilson’s disease (WD) show lack of correlations between neurological and neuroimaging features. Long-term follow-up reports with sequential brain MRI in patients with neurological WD comparing different modalities of treatment are scarce.
Eighteen patients with neurological WD underwent pretreatment and posttreatment brain MRI scans to evaluate the range of abnormalities and the evolution along these different periods. All patients underwent at least two MRI scans at different intervals, up to 11 years after the beginning of treatment.