This suggests that normal circulating levels of testosterone may buffer against the neurogenesis-impairing effects of isolation, whereas high doses of testosterone do not. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Purpose: Although caffeine consumption is common and generally believed to affect bladder function, AZD1480 cost little is known about caffeine intake and incident urinary incontinence.

Materials and Methods: We performed a prospective cohort

study in 65,176 women 37 to 79 years old without incontinence in the Nurses’ Health Study and the Nurses’ Health Study II. Incident incontinence was identified from questionnaires during 4 years of followup. Caffeine intake was measured using food frequency questionnaires administered before incontinence development. The multivariate adjusted relative risk of the relation between caffeine intake and incontinence risk as well as attributable risk were calculated.

Results: Caffeine was not associated with incontinence monthly or more. However, there was a modest, significantly increased risk of incontinence at least weekly

in women with the highest (greater than 450 mg) vs the lowest (less than 150 mg) daily intake (RR 1.19, 95% CI 1.06-1.34) and a significant trend of increasing risk with increasing intake (p for trend = 0.01). Sonidegib supplier This risk appeared focused on incident urgency incontinence (greater than 450 vs less than 150 mg daily, RR 1.34, 95% CI 1.00-1.80, p for trend = 0.05) but not on stress or mixed incontinence (p for trend = 0.75 and 0.19, respectively).

The attributable risk of urgency incontinence associated with high caffeine intake was 25%.

Conclusions: Findings suggest that high but not lower caffeine intake is associated with a modest increase in the incidence of frequent urgency incontinence. A fourth of the cases with the highest caffeine consumption would be eliminated if high caffeine intake were eliminated. Confirmation of these findings in other studies is needed before recommendations can be made.”
“The Jenna mutant mouse harbours an S140G mutation in Tuba1a that impairs tubulin heterodimer formation resulting in defective ACY-738 clinical trial neuronal migration during development. The consequence of decreased neuronal motility is a fractured pyramidal cell layer in the hippocampus and wavelike perturbations in the cerebral cortex. Here, we extend our characterisation of this mouse investigating the laminar architecture of the superior colliculus (SC). Our results reveal that the structure of the SC in mutant animals is intact; however, it is significantly thinner with an apparent fusion of the intermediate grey and white layers. Birthdate labelling at E12.5 and E13.5 showed that the S140G mutation impairs the radial migration of neurons in the SC. A quantitative assessment of neuronal number in adulthood reveals a massive reduction in postmitotic neurons in mutant animals, which we attribute to increased apoptotic cell death.