Objective: To construct a prediction model for sleep disorders in shift workers of a chemical fiber enterprise, so as to provide the basis for early identification and prevention of sleep disorders in shift workers. Methods: Shift workers were sampled from a chemical fiber enterprise in Tongxiang City, Zhejiang Province using a cluster sampling method from August 2022 to July 2024. Demographic information, length of service and average weekly working hours were collected through questionnaire surveys. Depressive symptoms, anxiety symptoms and sleep disorders were evaluated using the Pittsburgh Sleep Quality Index, Patient Health Questionnaire and Generalized Anxiety Disorder Questionnaire, respectively. The shift workers were randomly divided into a training set and a validation set at a ratio of 7∶3. Predictive factors were selected using a multivariable logistic regression model based on the training set, and a nomograph model for prediction of sleep disorders in shift workers was established. The predictive values of the model were evaluated using the receiver operating characteristic (ROC) curve and calibration curve based on the training set and validation set. Results: Totally 673 shift workers were included, with a median age of 32 (interquartile range, 12) years. There were 493 males, accounting for 73.25%. There were 471 (69.99%) workers in the training set and 202 (30.01%) workers in the validation set. There were 274 workers with sleep disorders, accounting for 40.71%. The equation for the prediction model was ln[p/(1-p)]=-8.391+1.906×average weekly working hours+1.822×depressive symptoms+1.667×anxiety symptoms. The area under the ROC curve was 0.769 (95%CI: 0.661-0.835) for the training set and 0.655 (95%CI: 0.593-0.737) for the validation set, and Hosmer-Lemeshow test showed a good fitting effect (both P>0.05). Conclusion The nomograph model constructed by average weekly working hours, depressive symptoms and anxiety symptoms can be used to predict the risk of sleep disorders in shift workers of a chemical fiber enterprise.

Objective:To evaluate the effect of sleep fragmentation on postoperative cognitive dysfunction (POCD) and hippocampal glutaminergic metabolism in aged mice anesthetized with isoflurane.Methods:Forty healthy SPF-grade male C57BL/6J mice, aged 18 months, weighing 20-30 g, were divided into 4 groups ( n= 10 each) by the random number table method: normal control group (group C), sleep fragmentation group (group SF), isoflurane anesthesia/surgery group (group I/S), and sleep fragmentation plus isoflurane anesthesia/surgery group (group SF+ I/S). Group C did not received any treatment. Group SF received sleep fragmentation for 24 h. The right carotid artery exposure was performed under isoflurane anesthesia in group I/S. Group SF+ I/S received isoflurane anesthesia/right carotid artery exposure at 24 h after sleep fragmentation. The metabolic levels of glutamate (Glu), glutamine (Gln), Glu/Gln complex (Glx), and N-acetylaspartate (NAA) and their ratio to creatine (Cr) were measured by in vivo 9.4T hydrogen proton magnetic resonance spectroscopy at 2 h after anaesthesia. Y maze and Morris water maze tests were used to evaluate the cognitive function at 1-7 days after surgery. The mice were sacrificed after the behavioral testing, brain tissues were immediately obtained, and the number of Nissl bodies and density of dendritic spines in the hippocampal CA1 region were measured by Nissl staining and Golgi staining, respectively. Results:Compared with group C, the percentage of exploration time and shuttle times at the novel arm were significantly decreased, the number of crossing the original platform was decreased, the time of stay at the target quadrant was shortened, the ratios of Glu/Cr, Gln/Cr and Glx/Cr in the hippocampal CA1 region were increased, and the ratio of NAA/Cr was decreased, and the number of Nissl bodies and density of dendritic spines were decreased in SF, I/S and SF+ I/S groups ( P<0.05). Compared with group SF and group I/S, the percentage of exploration time and shuttle times at the novel arm were significantly decreased, the number of crossing the original platform was decreased, the time of stay at the target quadrant was shortened, the ratios of Glu/Cr and Glx/Cr in hippocampal CA1 region was increased, the ratio of NAA/Cr was decreased, and the number of Nissl bodies and density of dendritic spines were decreased in group SF+ I/S ( P<0.05). Conclusions:Sleep fragmentation exacerbates POCD in aged mice anesthetized with isoflurane, and the mechanism is related to nerve injury induced by abnormality in hippocampal glutaminergic metabolism excitability.