Contribution of computed tomography in the diagnosis of symptomatic epilepsy

The aim of this retrospective study was to document the various causes of epilepsy determined by computed tomography (CT). We studied 205 CT scans carried out in patients with symptomatic epilepsy. We identified 52 (25.36%) pathological causes: 18 cases (34.62%) of infectious lesions, predominantly toxoplasmosis, 9 cases (17.30%) of tumors, 9 cases (17.30%) of vascular lesions and 8 cases (15.39%) of post-traumatic and atrophic lesions. CT is of great value in the diagnosis of epilepsy, not only in the assessment of the disease, but also for identifying the lesion responsible for the seizures, which may be treatable. It is advisable to carry out a CT scan for any patient presenting with symptomatic epilepsy.     

Human placental glucuronidation and transport of 3'azido-3'-deoxythymidine and uridine diphosphate glucuronic acid.

These studies were performed to characterize the contribution of the uridine diphosphate glucuronosyltransferase (UGT) enzymes to the clearance of 3'-azido-3'-deoxythymidine (AZT) in vivo and to assess the regulation of UGT activity [including the disposition of the cofactor uridine diphosphate glucuronic acid (UDPGA)] in the placenta. Transport of AZT and the cofactor UDPGA across the human placenta and the glucuronidation capacity of the placenta for AZT were assessed using a human placental cell line (JEG-3), primary cultures of villous term placenta, placental subcellular fractions, and a recirculating perfusion model. Glucuronidation of AZT was consistently observed at approximately 2% of the dose administered. High levels of AZT in cultured primary placental cells and lines caused autoinhibition of AZT metabolism. AZT crossed the perfused placenta in a bidirectional fashion and was at equilibrium after 3 h, whereas the AZT-glucuronide metabolite was excreted preferentially into the maternal compartment. In contrast, UDPGA (10 microM) was rapidly transferred from the maternal to the fetal circulation, being complete after 4 h of perfusion. AZT is transported and glucuronidated by the human placenta, but that placental metabolism of the drug is not significant for whole-body clearance. Likewise therapeutic failure of AZT (5-15%) is not due to placental obstruction of drug passage. Finally, the activity of the UGT enzymes in the placenta is not rate-limited by the supply of UDPGA cofactor, whereas the preferential transport of UDPGA toward the fetus observed here may indicate a role in fetal development.     

Perceived HIV Treatment Norms Modify the Association Between HIV-Related Stigma and Adherence to Antiretroviral Therapy Among Persons Living with HIV in Baltimore,Maryland

AIDS and Behavior - Adherence to antiretroviral therapy (ART) is associated with reduced HIV-related morbidity/mortality and ongoing transmission; however, the extent to which this association is...     

Bacteroides fragilis subverts mucosal biology: from symbiont to colon carcinogenesis

The human body comprises fewer host cells than bacterial cells, most of which are obligate anaerobes residing in the gut. The symbiont Bacteroides fragilis constitutes a relatively small proportion (up to 1%–2%) of cultured fecal bacteria, but colonizes most humans. There are 2 classes of B. fragilis distinguished by their ability to secrete a zinc-dependent metalloprotease toxin, B. fragilis toxin (BFT). Strains that do not secrete BFT are nontoxigenic B. fragilis (NTBF), and those that do are called enterotoxigenic B. fragilis (ETBF). ETBF can induce clinical pathology, including inflammatory diarrhea, although asymptomatic colonization may be common. Intestinal inflammation is mediated by BFT, as yet the only known virulence factor of ETBF. Recent experimental evidence demonstrating that ETBF-driven colitis promotes colon tumorigenesis has generated interest in the potential contribution of ETBF to human colon carcinogenesis. Critical questions about the epidemiology of chronic, subclinical human colonization with ETBF and its impact on the biology of the colon need to be addressed.