Methods: Routinely collected data from 3 pediatric ART programs in rural and urban Zambia were obtained from medical records. Participants included human immunodeficiency virus-infected children <15 years of age presenting for care between August 2004 and July 2008. Characteristics at presentation, time to ART initiation, and treatment response were compared between urban and rural children.

Results: A total of 863 children were enrolled (562 urban and 301 rural). At presentation, children in rural clinics were significantly younger (3.4 vs. 6.5 years), had higher CD4(+) T-cell percentages p38 MAPK activation (18.0% vs. 12.8%), less

advanced disease (47.5% vs. 62.3% in World Health Organization stage 3/4), lower weight-for-age Z-scores (-2.8 vs. -2.3), and traveled greater distances (29 vs. 2 km). Rural children eligible for ART at presentation took longer to initiate treatment (3.6 vs. 0.9 months); no differences were found in time to ART initiation among children

ineligible at presentation (15.4 vs. 12.1 months). For the 607 children initiating ART, clinical and immunologic status improved in both urban and rural clinics. Mortality was highest in the first 90 days of treatment and was higher at all times in rural clinics.

Conclusions: The findings support expansion of ART programs into rural areas to increase access to treatment services and reduce inequities.”
“Chronic hepatitis selleck C infection leads to increased hepatocyte apoptosis. Because engulfment of apoptotic bodies (ABs) by hepatic stellate cells (HSC) is profibrogenic, we compared the effects of ABs derived from hepatitis C virus (HCV)-negative vs HCV-infected (Con1+) Huh7 hepatoblastoma cells on fibrogenic and activation-related mRNA expression by a human HSC line (LX2). Uptake of Huh7(Con1+) ABs by LX2 cells dose dependently upregulated profibrotic genes (COL1A1, TGFB1; TIMP1; TIMP2). When normalized to the apoptotic cytokeratin-18 M30 neoepitope, HCV(+) ABs exhibited a more pronounced effect than HCV(-) ABs. In contrast, neither noningested

ABs nor nucleic acids obtained from Huh7, Huh7(Con1+) or HepG2 cells triggered those AB-dependent effects. Both the engulfment of Huh7(Con1+) ABs and their effects were partially blocked by masking of phosphatidylserine with annexin V and completely inhibited EPZ5676 datasheet by the class-A scavenger receptor ligand, polyinosinic acid. Our findings demonstrate that AB uptake stimulates HSCs and indicate that HCV infection leads to amplified fibrogenic mRNA expression and enhanced HSC activation.”
“Congenital hypothyroidism (CH) resulting from deficient production of thyroid hormone is one of the most commonly encountered diseases in pediatric endocrinology. Thyroid hormones play a crucial role in normal cerebral and growth maturation. These harmful effects on the cerebral and growth maturation can be prevented by early diagnosis and sufficient treatment in the first weeks of life.