The influences of the forging process and micro-arc oxidation (MAO) coating on the corrosion behavior of ZK60 wrought magnesium alloys exposed to salt spray and constant stress corrosion conditions were investigated. The microstructure of the ZK60 Mg alloy specimens forged under different temperatures (i.e., 250, 300, and 450 °C) was characterized using metallography, EBSD, and SEM. It was demonstrated that the ZK60 alloy forged at 300 °C (i.e., ZK60EF-300) had finer grain and uniformly distributed β-phase and, thus, better corrosion resistance than the ZK60 forged at 450 °C. At the lower forging temperature (250 °C) twins formed in the ZK60 alloy, which accelerated the corrosion of the ZK60E-250 specimen. The MAO coating provided robust corrosion protection for all the ZK60 wrought Mg alloy substrates. The salt spray corrosion test results showed that when the MAO coating broke down at certain weak sites, the corrosion performance of the coated Mg alloy was predominantly determined by the alloy substrate. The stress corrosion behaviors of the uncoated and MAO-coated ZK60 alloy specimens were also investigated under a constant load of 80 MPa in 3.5 wt.% NaCl solution. The MAO coating was found to improve the stress-corrosion resistance of the ZK60 alloy pronouncedly.

Background: Sleep traits have been suggested to correlate with various diseases, but most evidence is based on subjective sleep measurement. We investigated the associations of accelerometer-derived objective sleep traits with diseases throughout physiological systems to ascertain whether the disease spectrum related to objective sleep traits differs from that related to subjective sleep traits. Methods: In 88,461 UK Biobank (UKB) adults wearing accelerometers, multiple dimensions of sleep were objectively derived: (a) nocturnal sleep duration and onset timing, (b) sleep rhythm (relative amplitude and interdaily stability), and (c) sleep fragmentation (sleep efficiency and waking numbers). Associations with International Classification of Diseases, 10th Revision–decoded diseases during follow-up were estimated using the Cox model, and the results were compared with those of a published literature search of subjectively measured sleep traits and diseases. National Health and Nutrition Examination Survey (NHANES) data were used to validate the newly identified associations unreported by previous studies. For the meta-analysis-reported associations (with subjective sleep traits) that were negative (with objective sleep traits) in our study, reanalysis was done in UKB with subjective sleep traits, stratified by objective measurements. Results: During the average 6.8-year follow-up, 172 diseases were associated with sleep traits. Among them, 42 showed at least doubled disease risk, including age-related physical debility (lowest versus highest quartile of relative amplitude, hazard ratio [HR] = 3.36, 95% confidence interval [CI]: 2.25, 5.02), gangrene (lowest versus highest quartile of interdaily stability, HR = 2.61, 95% CI: 1.41, 4.83), and fibrosis and cirrhosis of the liver (sleep onset timing ≥0030 versus 2300 to 2330, HR = 2.57, 95% CI: 1.42, 4.67). A total of 92 diseases had >20% burden attributable to sleep, such as Parkinson’s disease (37.05%, 95% CI: 21.02%, 49.83%), type 2 diabetes (36.12%, 95% CI: 29.00%, 42.52%), and acute kidney failure (21.85%, 95% CI: 13.47%, 29.42%). Notably, 83 (48.3%) disease associations were sleep rhythm specific, distinct from existing subjective-measure literature that focused on sleep duration. Reanalysis in UKB showed a contamination of objectively short sleepers in self-report long sleepers, which induced false-positive associations in subjective meta-analyses, including for ischemic heart disease and depressive disorder. Newly identified associations of sleep rhythm with 4 diseases including chronic obstructive pulmonary disease and diabetes were successfully replicated in NHANES. A mediation analysis showed that inflammatory factors including leukocytes, eosinophils, and C-reactive protein contributed significantly to all these newly identified sleep–disease associations. Conclusions: Objective sleep traits showed a disease spectrum similar to but not identical to that of subjective sleep traits. Objective measurement can be a useful complement to sleep–disease studies as it may help overcome false-positive associations caused by misclassification bias of some subjective measurement such as sleep duration. Comprehensive control of multiple sleep traits may be important for health as substantial disease burden was attributed to different sleep traits.

Background: Circadian disruption has been suggested to induce cognitive impairment and dementia. It remains unknown which brain structures are involved in the pathology. Objective: To investigate which specific brain structure alterations are associated with dementia and cognitive impairment induced by circadian disruption. Methods: Circadian disruption was represented by two accelerometer-derived circadian variables, composite phase deviations (CPD) and relative amplitude (RA), separately reflecting circadian disruption in timing and amplitude. The outcomes include brain structures (139 imaging-derived phenotypes), cognitive test performances (seven cognitive tests) and dementia (all-cause dementia, Alzheimer’s disease, vascular dementia (AD/VD) and non-AD/VD dementia). Association analysis was used to explore the relationships between circadian disruption and brain structure alterations, cognitive test performances and dementia. Mediation analysis was conducted to investigate which brain structure alterations mediated the cognitive impairment and dementia caused by circadian disruption. Findings: A total of 88 461 participants (57% female, 62.0±7.8-year old) were included. CPD and RA correlated with substantially different brain structures. All CPD-related brain structures were located in the cerebrum, whereas most RA-related brain structures were located in the cerebellum. Furthermore, only the CPD-related brain structures, including the hippocampus and thalamus, exhibited significant mediation effects accounting for up to 8.6% of the risk for dementia and 13.5% of the risk for cognitive impairment. Conclusions: Circadian disruption is associated with brain structural alterations involving dementia and cognitive impairments. Clinical implications: These results provide a novel insight into the mechanism underlying circadian disruption-induced neurological disorder and may propose potential preventive strategy.