Alcohol Use, Intimate Partner Violence, Sexual Coercion and HIV among Women Aged 15–24 in Rakai, Uganda

Disinhibition due to alcohol may induce intimate partner violence and sexual coercion and increased risk of HIV infection. In a sample of 3,422 women aged 15–24 from the Rakai cohort, Uganda, we examined the association between self-reported alcohol use before sex, physical violence/sexual coercion in the past and prevalent HIV, using adjusted odds ratios (Adj OR) and 95% confidence intervals (95% CI). During the previous year, physical violence (26.9%) and sexual coercion (13.4%) were common, and alcohol use before sex was associated with a higher risk of physical violence/sexual coercion. HIV prevalence was significantly higher with alcohol consumption before sex (Adj OR = 1.45, 95% CI: 1.06–1.98) and especially when women reported both prior sexual coercion and alcohol use before sex (Adj OR = 1.79, 95% CI: 1.25–2.56). Alcohol use before sex was associated with physical violence and sexual coercion, and both are jointly associated with HIV infection risk in young women.     

Bartonella henselae endocarditis of percutaneously implanted pulmonary valve: a case report

Percutaneous pulmonary valve implantation (PPVI) has revolutionized the management of right ventricular outflow tract dysfunction after repaired congenital heart disease. The technology is considered to be safe, with a relatively low complication rate. Infection is one of the described complications of PPVI, and to date five cases of culture-positive infective endocarditis of percutaneously implanted pulmonary valve have been reported worldwide. Herein is reported the first ever case of culture-negative endocarditis of a percutaneously implanted pulmonary valve, caused by Bartonella henselae, five years after implantation in a 15-year-old patient with a repaired truncus arteriosus.     

Peroxisome Proliferator-Activated Receptor α Mediates Acute Effects of Palmitoylethanolamide on Sensory Neurons

The amplitude of the depolarization-evoked Ca(2+) transient is larger in dorsal root ganglion (DRG) neurons from tumor-bearing mice compared with that of neurons from naive mice, and the change is mimicked by coculturing DRG neurons with the fibrosarcoma cells used to generate the tumors (Khasabova et al., 2007). The effect of palmitoylethanolamide (PEA), a ligand for the peroxisome proliferator-activated receptor α (PPARα), was determined on the evoked-Ca(2+) transient in the coculture condition. The level of PEA was reduced in DRG cells from tumor-bearing mice as well as those cocultured with fibrosarcoma cells. Pretreatment with PEA, a synthetic PPARα agonist (GW7647), or ARN077, an inhibitor of the enzyme that hydrolyzes PEA, acutely decreased the amplitude of the evoked Ca(2+) transient in small DRG neurons cocultured with fibrosarcoma cells. The PPARα antagonist GW6471 blocked the effect of each. In contrast, the PPARα agonist was without effect in the control condition, but the antagonist increased the amplitude of the Ca(2+) transient, suggesting that PPARα receptors are saturated by endogenous ligand under basal conditions. Effects of drugs on mechanical sensitivity in vivo paralleled their effects on DRG neurons in vitro. Local injection of ARN077 decreased mechanical hyperalgesia in tumor-bearing mice, and the effect was blocked by GW6471. These data support the conclusion that the activity of DRG neurons is rapidly modulated by PEA through a PPARα-dependent mechanism. Moreover, agents that increase the activity of PPARα may provide a therapeutic strategy to reduce tumor-evoked pain.     

Neurotoxicity and memory deficits induced by soluble low-molecular-weight amyloid-β1-42 oligomers are revealed in vivo by using a novel animal model

Neuronal and synaptic degeneration are the best pathological correlates for memory decline in Alzheimer's disease (AD). Although the accumulation of soluble low-molecular-weight amyloid-β (Aβ) oligomers has been suggested to trigger neurodegeneration in AD, animal models overexpressing or infused with Aβ lack neuronal loss at the onset of memory deficits. Using a novel in vivo approach, we found that repeated hippocampal injections of small soluble Aβ(1-42) oligomers in awake, freely moving mice were able to induce marked neuronal loss, tau hyperphosphorylation, and deficits in hippocampus-dependent memory. The neurotoxicity of small Aβ(1-42) species was observed in vivo as well as in vitro in association with increased caspase-3 activity and reduced levels of the NMDA receptor subunit NR2B. We found that the sequestering agent transthyretin is able to bind the toxic Aβ(1-42) species and attenuated the loss of neurons and memory deficits. Our novel mouse model provides evidence that small, soluble Aβ(1-42) oligomers are able to induce extensive neuronal loss in vivo and initiate a cascade of events that mimic the key neuropathological hallmarks of AD.