Metabolism of all-trans-retinoic acid in rat testis

The metabolism of all-trans-[15-14C]retinoic acid in vitamin A-adequate or vitamin A-deficient rats fed retinoic acid was studied following intratesticular injection. Analysis of testicular metabolites by HPLC at 1, 6, and 24 h demonstrated that the retinoic acid was isomerized to 13-cis-retinoic acid and metabolized to polar metabolites in both groups of rats at all time periods. However, polar metabolites predominated in the testes of the vitamin A-deficient rats. At 24 h the total radioactivity remaining in the testis was much lower in the testes of vitamin A-deficient rats than in normal animals suggesting a faster rate of metabolism of all-trans-retinoic acid in these rats.     

Primary mediastinal large B-cell lymphoma in an HIV-infected patient

HIV-related non-Hodgkin lymphoma is well documented in the literature. We report a case of an HIV-infected patient who presents with primary mediastinal large B-cell lymphoma. On review of the literature, this appears to be the first documented case of this subtype of large B-cell non-Hodgkin lymphoma seen in an HIV-infected patient. Our patient received CHOP (cyclophosphamide, hydroxydaunomycin, Oncovin, prednisone) chemotherapy with granulocyte colony-stimulating factor support but unfortunately died a few days later.     

Alterations in metabolism and gap junction expression may determine the role of astrocytes as "good samaritans" or executioners

Our knowledge of astroglia and their physiological and pathophysiological role(s) in the central nervous system (CNS) has grown during the past decade, revealing a complex picture. It is becoming increasingly clear that glia play a significant role in the homeostasis and function of the CNS and that neurons should no longer be considered the only cell type that responds, both rapidly and slowly, to electrochemical activity. We discuss recent advances in the field with an emphasis on the impact of hypoxia and ischemia on astrocytic metabolism and the functional relationship between glucose metabolism and gap junctions in astrocytes. We also address the controversy over whether astrocytic gap junctions mediate protection or killing of neurons during or after hypoxic or ischemic insults.     

Disseminated Cryptococcus neoformans in a cirrhotic patient

Disseminated cryptococcal infection often occurs in the setting of an immuncompromised patient. We report a case of disseminated Cryptococcus neoformans in a cirrhotic patient, referred for Orthotopic Liver Transplantation evaluation due to acute hepatic decompensation.     

Helicobacter pylori in patients can be killed by visible light

BACKGROUND: Helicobacter pylori colonizes the mucus layer of the human stomach and may cause peptic ulcer and adenocarcinoma. Novel antimicrobial approaches are sought due to the occurrence of antibiotic resistance and consequent treatment failure. We report here that H. pylori is susceptible to inactivation by blue light. STUDY DESIGN/MATERIALS AND METHODS: A controlled, prospective, blinded, trial of endoscopically delivered blue light to eradicate H. pylori in regions of the gastric antrum, in 10 patients between the ages of 21 and 80 who tested positive for H. pylori. Light (405 nm) (40 J/cm2) was delivered to a 1-cm diameter spot in the gastric antrum via optical fiber passed through the endoscope and weighed biopsies were taken from treated and control spots and colonies quantitatively cultured. RESULTS: Blue light killed 5 logs of bacteria in vitro. The mean reduction in H. pylori colonies per gram tissue between treated and control spots was 91% (7.4+/-4.8 x 10(6) vs. 8.1+/-1.9 x 10(7), two-tailed P < 0.0001). Some patients had reductions approaching 99%. No differences were observed on histological examination of light-treated and control gastric tissue. CONCLUSION: Blue light phototherapy may represent a novel approach to eradication of H. pylori, particularly, in patients who have failed standard antibiotic treatment.     

Differential responses of human brain cells to West Nile virus infection

In recent years, West Nile virus (WNV) has emerged as a major cause of encephalitis in the United States. However, the neuropathogenesis of this flavivirus is poorly understood. In the present study, the authors used primary human brain cell cultures to investigate two neuropathogenic features: viral replication and induction of cytokines. Although neurons and astrocytes were found to support productive WNV infection, viral growth was poorly permissive in microglial cells. Compared to neuronal cultures that sustained viral growth for at least 2 weeks, replication peaked in astrocytes by 72 h post infection. In response to viral infection, astrocytes produced chemokines (CXCL10 and CCL5), but none of the cytokines (tumor necrosis factor [TNF]-alpha, interleukin [IL]-1beta, IL-6, interferon alpha or gamma) tested could be detected. Although microglial cells failed to support viral replication, WNV induced production of the proinflammatory cytokines IL-6 and TNF-alpha. Microglial cells also released robust amounts of the chemokines CXCL10 and CCL2, as well as lower levels of CCL5, in response to WNV infection. WNV-induced chemokine and cytokine production by microglia was coupled with activation of mitogen-activated protein kinase (MAPK) intracellular signaling pathways. Inhibition of p38 MAPK decreased chemokine production in response to WNV. Taken together, these findings suggest that microglial cell responses may influence the neuropathogenesis of WNV infection.