There is an evidence–practice gap between the dietary recommendations for age-related macular degeneration (AMD) presented in the literature and those practiced by patients. This study reports on the 3-month post-intervention results of a randomised controlled trial (RCT) evaluating telephone-delivered counselling to improve dietary behaviours among AMD patients. A total of 155 AMD patients (57% female, aged 78 ± 8 years; control: 78, intervention: 77), primarily residing in New South Wales, Australia, were recruited. Participants completed a baseline questionnaire and a short dietary questionnaire (SDQ-AMD). The intervention included an evidence-based nutrition resource and four monthly calls with a dietitian. Immediately post-intervention, intervention participants repeated the SDQ-AMD and completed a feedback form. At 3 months post-intervention, both study arms repeated the SDQ-AMD. Statistical analyses included t-tests and McNemar’s test. Intervention participants reported satisfaction with the tailored phone calls, nutrition resource and nutrition education provided. At 3 months post-intervention, there was no statistically significant difference between study arms in the proportion of participants meeting the dietary goals nor in intake (mean servings ± SE) of total vegetables (primary outcome) and other key food groups; however, there was a significantly higher intake of nuts (secondary outcome) (3.96 ± 0.51 vs. 2.71 ± 0.32; p = 0.04) among participants in the intervention versus control group. Within the intervention arm, there were also significant improvements in intakes of the following secondary outcomes: dark green leafy vegetables (0.99 ± 0.17 vs. 1.71 ± 0.22; p = 0.003) and legumes (0.69 ± 0.10 vs. 1.12 ± 0.16; p = 0.02) and intake of sweets and processed/prepared foods (8.31 ± 0.76 vs. 6.54 ± 0.58, p = 0.01). In summary, although there were few dietary differences between study arms at 3 months post-intervention, the intervention involving four monthly calls was acceptable and helpful to the participants. This type of intervention therefore has the potential to provide people with AMD the needed support for improving their nutrition knowledge and dietary practices, especially if continued over a longer period.
Our laboratory previously has shown apparent carrier-mediated glutathione (GSH) uptake across the blood-brain barrier (BBB) in two animal models. In the present study, when Xenopus oocytes were injected with bovine brain capillary mRNA expression of intact GSH, uptake was observed after 3 days. When total mRNA was converted to cDNA and subfractionated with subsequent cRNA injection into oocytes, three distinct fractions (5, 7-8, and 11-12) expressed carrier-mediated intact GSH transport. Northern blot analysis established the presence of RcGshT, the previously cloned sodium-independent hepatic canalicular transporter, only in fraction 5. GSH transport activity in fraction 7 was significantly inhibited by replacement of NaCl with choline chloride and by sulfobromophthalein-GSH, neither of which affects RcGshT. The Na(+)-dependent GSH uptake kinetics exhibited high affinity (approximately 400 micron) and low affinity (approximately 10 mM) components. Fraction 11 expressed Na(+)-independent transport of intact GSH and also contained the GGT transcript. In conclusion, we have identified three distinct sized transcripts from bovine brain capillary mRNA which express GSH transport: one fraction expresses a novel Na(+)-dependent GSH uptake which can be dissociated unequivocally from both GGT and RcGshT for the first time and which may account for uptake of GSH against its electrochemical gradient at the BBB.
There is paucity of population-based data on occupational noise exposure and risk of age-related hearing loss. Therefore, we assessed cross-sectional and longitudinal associations of past workplace noise exposure with hearing loss in older adults. At baseline, 1923 participants aged 50+ years with audiological and occupational noise exposure data included for analysis. The pure-tone average of frequencies 0.5, 1.0, 2.0 and 4.0 kHz (PTA0.5-4KHz) >25 dB HL in the better ear, established the presence of hearing loss. Participants reported exposure to workplace noise, and the severity and duration of this exposure. Prior occupational noise exposure was associated with a 2-fold increased odds of moderate-to-severe hearing loss: multivariable-adjusted OR 2.35 (95% CI 1.45–3.79). Exposure to workplace noise for >10 years increased the odds of having any hearing loss (OR 2.39, 95% CI 1.37–4.19) and moderate-to-severe hearing loss (OR 6.80, 95% CI 2.97–15.60). Among participants reporting past workplace noise exposure at baseline the 10-year incidence of hearing loss was 35.5% versus 29.1% in those who had no workplace noise exposure. Workplace noise exposure was associated with a greater risk of incident hearing loss during the 10-year follow-up: multivariable-adjusted OR 1.39 (95% CI 1.13–1.71). Prior occupational noise exposure was not associated with hearing loss progression. Workplace noise exposure increased the risk of incident hearing loss in older adults. Our findings underscore the importance of preventive measures which diminish noise exposure in the workplace, which could potentially contribute towards reducing the burden of hearing loss in later life.
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