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“Pesticide exposure has been implicated as an environmental risk factor for the development of Parkinson’s disease (PD). However, few studies have identified specific pesticides. Previously, we identified elevated serum levels of the organochlorine pesticide beta-hexachlorocyclohexane (beta-HCH) in

PD patients from a small clinical sample. Here, we conducted a case-control study to confirm the association between beta-HCH and PD in a larger sample size (n = 283) with serum samples of PD patients and controls obtained from UT Southwestern Medical Center and Emory University. Samples were obtained from two discrete periods at both sites, 2001-2003 and 2006-2008, and were analyzed for beta-HCH levels. Adjusted odds ratios (ORs) for PD were estimated using logistic regression and generalized estimating learn more equations. The mean serum beta-HCH level across all cohorts in this study was 22.3 ng/mg Evofosfamide cell line cholesterol (range: 0-376.7), and the levels were significantly higher and samples collected in 2001-2003 vs. 2006-2008. After controlling for age and

gender, the OR for increased risk of PD for every 1 ng/mg increase in serum beta-HCH ranged from 1.02 to 1.12 across the four different cohorts, and 1.03 (95% CI: 1.00-1.07, p value = 0.031) in the pooled analysis. Furthermore, the OR for increased risk of PD of subjects having serum beta-HCH levels above the inter-quartile range of 39.08 ng/mg cholesterol was 2.85 (95% CI: 1.8, 4.48; p value < 0.001). Cobimetinib These data are consistent

with environmental decreases in beta-HCH levels between 2001 and 2008, but they indicate that elevated levels of serum beta-HCH are still associated with heightened risk for PD. (C) 2011 Elsevier Inc. All rights reserved.”
“Among Old World monkeys, pig-tailed macaques (Pt) are uniquely susceptible to human immunodeficiency virus type 1 (HIV-1), although the infection does not persist. We demonstrate that the susceptibility of Pt T cells to HIV-1 infection is due to the absence of postentry inhibition by a TRIM5 isoform. Notably, substitution of the viral infectivity factor protein, Vif, with that from pathogenic SIVmne enabled replication of HIV-1 in Pt T cells in vitro. When inoculated into juvenile pig-tailed macaques, the Pt-tropic HIV-1 persistently replicated for more than 1.5 to 2 years, producing low but measurable plasma viral loads and persistent proviral DNA in peripheral blood mononuclear cells. It also elicited strong antibody responses. However, there was no decline in CD4(+) T cells or evidence of disease. Surprisingly, the Pt-tropic HIV-1 was rapidly controlled when inoculated into newborn Pt macaques, although it transiently rebounded after 6 months. We identified two notable differences between the Pt-tropic HIV-1 and SIVmne. First, SIV Vif does not associate with Pt-tropic HIV-1 viral particles.