Therefore, a strong stimulation by the psychoactive component of marijuana, delta-9-tetrahydrocanabinol (THC), might lead to subtle but lasting neurobiological changes that can affect adult brain functions and behaviour.\n\nThe literature here summarized by use of

experimental animal models, puts forward that heavy cannabis consumption in adolescence may induce subtle changes in the adult brain circuits ending in altered emotional and cognitive performance, enhanced vulnerability for the use of more harmful drugs of abuse in selected individuals, and may represent a risk factor for developing schizophrenia in adulthood.\n\nTherefore, the potential problems arising in relation to marijuana consumption in adolescence suggest that selleck inhibitor this developmental phase is a vulnerable period for persistent adverse effects of cannabinoids. (C) 2008 Elsevier Ireland Ltd. All selleck screening library rights reserved.”
“We studied the clinical benefits of radiological imaging, in the follow-up of patients after combined modality treatment for stage I/II classical supradiaphragmatic Hodgkin lymphoma (HL). Imaging data were collected for 78 adults treated during 1996-2008. Median follow-up was 4.6 years. Six of the nine relapses were detected clinically. On average, 31 imaging studies/patient were performed, with an estimated cost of $12 608/patient. Chest computed tomography (CT) scans accounted

for 25%, abdominopelvic CT scans 41% and positron emission tomography (PET) or PET/CT scans 22% of this expense. Only one patient recurred infradiaphragmatically. The estimated radiation dose from imaging was 399 mSv and 229 mSv per patient, in relapse and non-relapse groups, respectively. CT scans contributed over 80% of the imaging radiation exposure. The routine use of CT scans in the surveillance of patients with HL after curative treatment adds to healthcare costs and total body radiation exposure with a low yield. History and physical examination remain effective tools for the follow-up of patients.”
“Cigarette smoking causes cellular oxidative stress resulting in inflammatory diseases of lung wherein

transcription factor NF-kappa TPCA-1 B plays an important role. It is possible that vitamin C, an antioxidant, may prevent cigarette smoke (CS)-induced NF-kappa B activation that involves degradation of I-kappa B epsilon and nuclear translocation of c-Rel/p50 in alveolar epithelial cells. Therefore, to examine the hypothesis, we verified the effect of vitamin C on CS-induced expression of NF-kappa B driven luciferase reporter and NF-kappa B binding at its target DNA by EMSA in alveolar epithelial A549 cells. We also examined the level of I-kappa B epsilon and sub-cellular distribution of c-Rel by western blotting and immunofluorescence respectively in CSE-treated A549 cells with or without vitamin C pretreatment.