Long-Term Exposure to Wind Turbine Noise and Risk for Myocardial Infarction and Stroke:A Nationwide Cohort Study

Background: Noise from wind turbines (WTs) is reported as more annoying than traffic noise at similar levels, raising concerns as to whether WT noise (WTN) increases risk for cardiovascular disease, as observed for traffic noise. Objectives: We aimed to investigate whether long-term exposure to WTN increases risk of myocardial infarction (MI) and stroke. Methods: We identified all Danish dwellings within a radius 20 times the height of the closest WT and 25% of the dwellings within 20–40 times the height of the closest WT. Using data on WT type and simulated hourly wind at each WT, we estimated hourly outdoor and low frequency (LF) indoor WTN for each dwelling and derived 1-y and 5-y running nighttime averages. We used hospital and mortality registries to identify all incident cases of MI (n=19,145) and stroke (n=18,064) among all adults age 25–85 y (n=717,453), who lived in one of these dwellings for ≥one year over the period 1982–2013. We used Poisson regression to estimate incidence rate ratios (IRRs) adjusted for individual- and area-level covariates. Results: IRRs for MI in association with 5-y nighttime outdoor WTN ˃42 (vs. ˂24) dB(A) and indoor LF WTN ˃15 (vs. ˂5) dB(A) were 1.21 [95% confidence interval (CI): 0.91, 1.62; 47 exposed cases] and 1.29 (95% CI: 0.73, 2.28; 12 exposed cases), respectively. IRRs for intermediate categories of outdoor WTN [24–30, 30–36, and 36–42 dB(A) vs. ˂24 dB(A)] were slightly above the null and of similar size: 1.08 (95% CI: 1.04, 1.12), 1.07 (95% CI: 1.00, 1.12), and 1.06 (95% CI: 0.93, 1.22), respectively. For stroke, IRRs for the second and third outdoor exposure groups were similar to those for MI, but near or below the null for higher exposures. Conclusions: We did not find convincing evidence of associations between WTN and MI or stroke.</p

Impact of Long-Term Exposure to Wind Turbine Noise on Redemption of Sleep Medication and Antidepressants: A Nationwide Cohort Study

Background: Noise from wind turbines (WTs) is associated with annoyance and, potentially, sleep disturbances. Objectives: Our objective was to investigate whether long-term WT noise (WTN) exposure is associated with the redemption of prescriptions for sleep medication and antidepressants. Methods: For all Danish dwellings within a radius of 20-WT heights and for 25% of randomly selected dwellings within a radius of 20-to 40-WT heights, we estimated nighttime outdoor and low-frequency (LF) indoor WTN, using information on WT type and simulated hourly wind. During follow-up from 1996 to 2013, 68,696 adults redeemed sleep medication and 82,373 redeemed antidepressants, from eligible populations of 583,968 and 584,891, respectively. We used Poisson regression with adjustment for individual and area-level covariates. Results: Five-year mean outdoor nighttime WTN of ≥42 dB was associated with a hazard ratio (HR) = 1.14 [95% confidence interval (CI]: 0.98, 1.33) for sleep medication and HR = 1.17 (95% CI: 1.01, 1.35) for antidepressants (compared with exposure to WTN of ˂24 dB). We found no overall association with indoor nighttime LF WTN. In age-stratified analyses, the association with outdoor nighttime WTN was strongest among persons ≥65y of age, with HRs (95% CIs) for the highest exposure group (≥42 dB) of 1.68 (1.27, 2.21) for sleep medication and 1.23 (0.90, 1.69) for antidepressants. For indoor nighttime LF WTN, the HRs (95% CIs) among persons ≥65y of age exposed to ≥15 dB were 1.37 (0.81, 2.31) for sleep medication and 1.34 (0.80, 2.22) for antidepressants. Conclusions: We observed high levels of outdoor WTN to be associated with redemption of sleep medication and antidepressants among the elderly, suggesting that WTN may potentially be associated with sleep and mental health.</p

Effects of membrane depolarization and changes in extracellular [K+] on the Ca2+ transients of fast skeletal muscle fibers. Implications for muscle fatigue

Repetitive activation of skeletal muscle fibers leads to a reduced transmembrane K+ gradient. The resulting membrane depolarization has been proposed to play a major role in the onset of muscle fatigue. Nevertheless, raising the extracellular K+ (\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$${\text{K}}_{\text{o}}^{ + }$$\end{document}) concentration (\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$[ {\text{K}}^{ + } ]_{\text{o}}$$\end{document}) to 10 mM potentiates twitch force of rested amphibian and mammalian fibers. We used a double Vaseline gap method to simultaneously record action potentials (AP) and Ca2+ transients from rested frog fibers activated by single and tetanic stimulation (10 pulses, 100 Hz) at various \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$[ {\text{K}}^{ + } ]_{\text{o}}$$\end{document} and membrane potentials. Depolarization resulting from current injection or raised \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$[ {\text{K}}^{ + } ]_{\text{o}}$$\end{document} produced an increase in the resting [Ca2+]. Ca2+ transients elicited by single stimulation were potentiated by depolarization from −80 to −60 mV but markedly depressed by further depolarization. Potentiation was inversely correlated with a reduction in the amplitude, overshoot and duration of APs. Similar effects were found for the Ca2+ transients elicited by the first pulse of 100 Hz trains. Depression or block of Ca2+ transient in response to the 2nd to 10th pulses of 100 Hz trains was observed at smaller depolarizations as compared to that seen when using single stimulation. Changes in Ca2+ transients along the trains were associated with impaired or abortive APs. Raising \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$[ {\text{K}}^{ + } ]_{\text{o}}$$\end{document} to 10 mM potentiated Ca2+ transients elicited by single and tetanic stimulation, while raising \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$[ {\text{K}}^{ + } ]_{\text{o}}$$\end{document} to 15 mM markedly depressed both responses. The effects of 10 mM \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$${\text{K}}_{\text{o}}^{ + }$$\end{document} on Ca2+ transients, but not those of 15 mM \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$${\text{K}}_{\text{o}}^{ + }$$\end{document}, could be fully reversed by hyperpolarization. The results suggests that the force potentiating effects of 10 mM \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$${\text{K}}_{\text{o}}^{ + }$$\end{document} might be mediated by depolarization dependent changes in resting [Ca2+] and Ca2+ release, and that additional mechanisms might be involved in the effects of 15 mM \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$${\text{K}}_{\text{o}}^{ + }$$\end{document} on force generation

IRES-Mediated Translation of Utrophin A Is Enhanced by Glucocorticoid Treatment in Skeletal Muscle Cells

Glucocorticoids are currently the only drug treatment recognized to benefit Duchenne muscular dystrophy (DMD) patients. The nature of the mechanisms underlying the beneficial effects remains incompletely understood but may involve an increase in the expression of utrophin. Here, we show that treatment of myotubes with 6α−methylprednisolone-21 sodium succinate (PDN) results in enhanced expression of utrophin A without concomitant increases in mRNA levels thereby suggesting that translational regulation contributes to the increase. In agreement with this, we show that PDN treatment of cells transfected with monocistronic reporter constructs harbouring the utrophin A 5′UTR, causes an increase in reporter protein expression while leaving levels of reporter mRNAs unchanged. Using bicistronic reporter assays, we further demonstrate that PDN enhances activity of an Internal Ribosome Entry Site (IRES) located within the utrophin A 5′UTR. Analysis of polysomes demonstrate that PDN causes an overall reduction in polysome-associated mRNAs indicating that global translation rates are depressed under these conditions. Importantly, PDN causes an increase in the polysome association of endogenous utrophin A mRNAs and reporter mRNAs harbouring the utrophin A 5′UTR. Additional experiments identified a distinct region within the utrophin A 5′UTR that contains the inducible IRES activity. Together, these studies demonstrate that a translational regulatory mechanism involving increased IRES activation mediates, at least partially, the enhanced expression of utrophin A in muscle cells treated with glucocorticoids. Targeting the utrophin A IRES may thus offer an important and novel therapeutic avenue for developing drugs appropriate for DMD patients

Effects of self-paced interval and continuous training on health markers in women

This is the final version of the article. Available from Springer Verlag via the DOI in this record.PURPOSE: To compare the effects of self-paced high-intensity interval and continuous cycle training on health markers in premenopausal women. METHODS: Forty-five inactive females were randomised to a high-intensity interval training (HIIT; n = 15), continuous training (CT; n = 15) or an inactive control (CON; n = 15) group. HIIT performed 5 × 5 min sets comprising repetitions of 30-s low-, 20-s moderate- and 10-s high-intensity cycling with 2 min rest between sets. CT completed 50 min of continuous cycling. Training was completed self-paced, 3 times weekly for 12 weeks. RESULTS: Peak oxygen uptake (16 ± 8 and 21 ± 12%), resting heart rate (HR) (-5 ± 9 and -4 ± 7 bpm) and visual and verbal learning improved following HIIT and CT compared to CON (P  0.05). No outcome variable changed in the CON group (P > 0.05). CONCLUSIONS: Twelve weeks of self-paced HIIT and CT were similarly effective at improving cardiorespiratory fitness, resting HR and cognitive function in inactive premenopausal women, whereas blood pressure, submaximal HR, well-being and body mass adaptations were training-type-specific. Both training methods improved established health markers, but the adaptations to HIIT were evoked for a lower time commitment.The study was supported by FIFA-Medical Assessment and Research Centre (F-MARC)