“
“Objective: To examine the risk of large joint osteoarthritis (OA) in those becoming overweight during early adult life, and to assess the risks associated with high body mass index (BMI) and other anthropometric BMS-777607 ic50 measures of obesity.
Methods: BMI,
waist and hip circumference were measured in the GOAL case-control study comprising hip OA cases (n = 1007), knee OA cases (n = 1042) and asymptomatic controls (n = 1121). Retrospective estimates of lifetime weight, body shape and other risk factors were collected using an interview-lead questionnaire. Odds ratios (ORs), adjusted OR (aOR), 95% confidence intervals (Os) and P values were calculated using logistic regression analysis.
Results: BMI was associated with knee OA (aOR 2.68, 95% CI 2.33-3.09, P-trend <0.001) and hip OA (aOR 1.65, 95% CI 1.46-1.87, P-trend <0.001). Those who became overweight earlier in adulthood showed
Apoptosis Compound Library solubility dmso higher risks of lower limb OA (P-trend < 0.001 for knee OA and hip OA). Self-reported body shape was also associated with knee OA and hip OA, following a similar pattern to current and life-course BMI measures. Waist:hip ratio (WHR) at time of examination did not associate with OA independently of BMI, except in women-only analysis. Waist circumference was associated with lower limb OA risk.
Conclusions: Becoming overweight earlier in adult life increased the risks of knee OA and hip OA. Different distribution patterns of adiposity may be related to OA risk in women. (C) 2010 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.”
“Hypothesis: Cigarette smoking may potentiate noise-induced hearing loss.
Background:
Many epidemiological studies have shown that cigarette smoking is a major risk factor for noise-induced hearing loss.
Methods: BALB/c mice were exposed to passive smoking for 2 h/d for 2 weeks before exposure to 110-dB sound pressure level white noise for 3 hours once. Hearing was assessed via the auditory brainstem response with tone-burst stimulation and distortion product otoacoustic emissions before and at 1, 3, 5, 7, 14, 21, and 28 GDC-0973 cell line days after noise exposure. Oxidative stress and hypoxia were assessed by immunostaining with 8-oxoG and hypoxia-inducible factor 1 alpha, respectively.
Results: Control mice unexposed to both smoking and noise and mice exposed to smoking only showed no shift in hearing threshold. In contrast, mice exposed to noise only or smoking plus noise showed abrupt increases in hearing threshold. In mice exposed to noise only, hearing threshold returned to prenoise levels after 2 weeks. However, in mice exposed to smoking plus noise, the loss of hearing was significantly higher, and hearing threshold did not return to the pre-exposure levels until 4 weeks later.