Exposure to Radiofrequency Electromagnetic Fields and Sleep Quality: A Prospective Cohort Study

BACKGROUND: There is persistent public concern about sleep disturbances due to radiofrequency electromagnetic field (RF-EMF) exposure. The aim of this prospective cohort study was to investigate whether sleep quality is affected by mobile phone use or by other RF-EMF sources in the everyday environment. METHODS: We conducted a prospective cohort study with 955 study participants aged between 30 and 60 years. Sleep quality and daytime sleepiness was assessed by means of standardized questionnaires in May 2008 (baseline) and May 2009 (follow-up). We also asked about mobile and cordless phone use and asked study participants for consent to obtain their mobile phone connection data from the mobile phone operators. Exposure to environmental RF-EMF was computed for each study participant using a previously developed and validated prediction model. In a nested sample of 119 study participants, RF-EMF exposure was measured in the bedroom and data on sleep behavior was collected by means of actigraphy during two weeks. Data were analyzed using multivariable regression models adjusted for relevant confounders. RESULTS: In the longitudinal analyses neither operator-recorded nor self-reported mobile phone use was associated with sleep disturbances or daytime sleepiness. Also, exposure to environmental RF-EMF did not affect self-reported sleep quality. The results from the longitudinal analyses were confirmed in the nested sleep study with objectively recorded exposure and measured sleep behavior data. CONCLUSIONS: We did not find evidence for adverse effects on sleep quality from RF-EMF exposure in our everyday environmen

Temporal allocation of foraging effort in female Australian fur seals (Arctocephalus pusillus doriferus)

Across an individual\u27s life, foraging decisions will be affected by multiple intrinsic and extrinsic drivers that act at differing timescales. This study aimed to assess how female Australian fur seals allocated foraging effort and the behavioural changes used to achieve this at three temporal scales: within a day, across a foraging trip and across the final six months of the lactation period. Foraging effort peaked during daylight hours (57% of time diving) with lulls in activity just prior to and after daylight. Dive duration reduced across the day (196 s to 168 s) but this was compensated for by an increase in the vertical travel rate (1500–1600 m•h−1) and a reduction in postdive duration (111–90 s). This suggests physiological constraints (digestive costs) or prey availability may be limiting mean dive durations as a day progresses. During short trips (<2.9 d), effort remained steady at 55% of time diving, whereas, on long trips (>2.9 d) effort increased up to 2–3 d and then decreased. Dive duration decreased at the same rate in short and long trips, respectively, before stabilising (long trips) between 4–5 d. Suggesting that the same processes (digestive costs or prey availability) working at the daily scale may also be present across a trip. Across the lactation period, foraging effort, dive duration and vertical travel rate increased until August, before beginning to decrease. This suggests that as the nutritional demands of the suckling pup and developing foetus increase, female effort increases to accommodate this, providing insight into the potential constraints of maternal investment in this specie

The chaperonin CCT8 controls proteostasis essential for T cell maturation, selection, and function

T cells rely for their development and function on the correct folding and turnover of proteins generated in response to a broad range of molecular cues. In the absence of the eukaryotic type II chaperonin complex, CCT, T cell activation induced changes in the proteome are compromised including the formation of nuclear actin filaments and the formation of a normal cell stress response. Consequently, thymocyte maturation and selection, and T cell homeostatic maintenance and receptor-mediated activation are severely impaired. In the absence of CCT-controlled protein folding, Th2 polarization diverges from normal differentiation with paradoxical continued IFN-γ expression. As a result, CCT-deficient T cells fail to generate an efficient immune protection against helminths as they are unable to sustain a coordinated recruitment of the innate and adaptive immune systems. These findings thus demonstrate that normal T cell biology is critically dependent on CCT-controlled proteostasis and that its absence is incompatible with protective immunity

ARMC5 mutations are common in familial bilateral macronodular adrenal hyperplasia.

CONTEXT: Bilateral macronodular adrenal hyperplasia (BMAH) is a rare form of adrenal Cushing's syndrome. Familial cases have been reported, but at the time we conducted this study, the genetic basis of BMAH was unknown. Recently, germline variants of armadillo repeat containing 5 (ARMC5) in patients with isolated BMAH and somatic, second-hit mutations in tumor nodules, were identified. OBJECTIVE: Our objective was to identify the genetic basis of familial BMAH. DESIGN: We performed whole exome capture and sequencing of 2 affected individuals from each of 4 BMAH families (BMAH-01, BMAH-02, BMAH-03, and BMAH-05). Based on clinical evaluation, there were 7, 3, 3, and 4 affected individuals in these families, respectively. Sanger sequencing of ARMC5 was performed in 1 other BMAH kindred, BMAH-06. RESULTS: Exome sequencing identified novel variants Chr16:g.31477540, c.2139delT, p.(Thr715Leufs*1) (BMAH-02) and Chr16:g.31473811, c.943C→T, p.(Arg315Trp) (BMAH-03) in ARMC5 (GRch37/hg19), validated by Sanger sequencing. BMAH-01 had a recently reported mutation Chr16:g.31476121, c.1777C→T, p.(Arg593Trp). Sanger sequencing of ARMC5 in BMAH-06 identified a previously reported mutation, Chr16:g. 31473688; c.799C→T, p.(Arg267*). The genetic basis of BMAH in BMAH-05 was not identified. CONCLUSIONS: Our studies have detected ARMC5 mutations in 4 of 5 BMAH families tested, confirming that these mutations are a frequent cause of BMAH. Two of the 4 families had novel mutations, indicating allelic heterogeneity. Preclinical evaluation did not predict mutation status. The ARMC5-negative family had unusual prominent hyperaldosteronism. Further studies are needed to determine the penetrance of BMAH in ARMC5 mutation-positive relatives of affected patients, the practical utility of genetic screening and genotype-phenotype correlations