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- SourceAvailable from: Wen-jie Sun[Show abstract] [Hide abstract]
ABSTRACT: To examine the associations between occupation, sleep duration and sleep quality. The data for this study was extracted from data collected from the 2008 Chinese Sub-optimal Health Study. Our study sample consisted of 18,316 Chinese subjects aged 18-65. Occupation and other relevant characteristics to sleep were collected. We used the Pittsburgh Sleep Quality Index (PSQI) to measure sleep quality and multiple logistic regression models to examine the association of occupation with shortened sleep duration and poor sleep quality. Farmers had the longest sleep duration (mean=8.22 hours) while the civil servants had the shortest sleep duration (mean=7.85 hours). Farmers also had the best sleep quality (mean score=3.74) while professional workers had the worst sleep quality (mean score=4.87). Compared to civil servants, the OR of shortened sleep duration and poor sleep quality for blue collar workers is 1.39 (95%CI: 1.11-1.73) and 1.28 (95%-CI: 1.15-1.42), respectively, after adjusting for age, sex, marital status, education, area, smoking, drinking, pain, and health status. sleep duration and quality varied among different Chinese occupation populations. The blue collar workers are more likely to have shortened sleep duration and poor sleep quality.PLoS ONE 03/2015; 10(3):e0117700. DOI:10.1371/journal.pone.0117700
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ABSTRACT: There have been limited comparative data regarding the investigations on pulmonary and respiratory muscle function in the patients with different parkinsonism disorders such as Parkinson's disease (PD) and multiple system atrophy (MSA) versus normal elderly. The present study is aiming to characterize the performance of pulmonary function and respiratory muscle strength in PD and MSA, and to investigate the association with severity of motor symptoms and disease duration. Pulmonary function and respiratory muscle strength tests were performed in 30 patients with PD, 27 with MSA as well as in 20 age-, sex-, height-, weight-matched normal elderly controls. All the patients underwent United Parkinson's disease rating scale (UPDRS) or united multiple system atrophy rating scale (UMSARS) separately as diagnosed. Vital capacity, forced expiratory volume in 1 second and forced vital capacity decreased, residual volume and ratio of residual volume to total lung capacity increased in both PD and MSA groups compared to controls (p<0.05). Diffusing capacity was decreased in the MSA group, compared with PD and normal elderly control groups (p<0.05). Respiratory muscle strength was lower in both PD and MSA groups than in controls (p<0.05). The values representing spirometry function and respiratory muscle strength were found to have a negative linear correlation with mean score of UPDRS-III in PD and mean score of UMSARS-I in MSA. Respiratory muscle strength showed a negative linear correlation with the mean score of UMSARS-II and disease duration in MSA patients. These findings suggest that respiratory dysfunction is involved in PD and MSA. Respiratory muscle strength is remarkably reduced, and some of the parameters correlate with disease duration and illness severity. The compromised respiratory function in neurodegenerative disorders should be the focus of further researches.PLoS ONE 12/2014; 9(12):e116123. DOI:10.1371/journal.pone.0116123
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ABSTRACT: Progressive Supranuclear Palsy (PSP) is a neurodegenerative disorder characterised by intracellular aggregation of the microtubule-associated protein tau. The tau protein exists in 6 predominant isoforms. Depending on alternative splicing of exon 10, three of these isoforms have four microtubule-binding repeat domains (4R), whilst the others only have three (3R). In PSP there is an excess of the 4R tau isoforms, which are thought to contribute significantly to the pathological process. The cause of this 4R increase is so far unknown. Several lines of evidence link mitochondrial complex I inhibition to the pathogenesis of PSP. We demonstrate here for the first time that annonacin and MPP+, two prototypical mitochondrial complex I inhibitors, increase the 4R isoforms of tau in human neurons. We show that the splicing factor SRSF2 is necessary to increase 4R tau with complex I inhibition. We also found SRSF2, as well as another tau splicing factor, TRA2B, to be increased in brains of PSP patients. Thereby, we provide new evidence that mitochondrial complex I inhibition may contribute as an upstream event to the pathogenesis of PSP and suggest that splicing factors may represent an attractive therapeutic target to intervene in the disease process.PLoS ONE 11/2014; 9(11):e113070. DOI:10.1371/journal.pone.0113070
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