Background Long working hours are a risk factor for occupational health, particularly in labor-intensive sectors such as manufacturing. Prolonged working hours may have adverse effects on the sleep and mental health of employees. Objective To investigate the impact of long working hours on insomnia, anxiety, and depression symptoms among manufacturing industry employees and provide scientific evidence for relevant occupational health interventions. Methods A cross-sectional study was conducted involving 1524 employees from eight manufacturing enterprises in Shenzhen. Data were collected using a structured questionnaire, which included demographic characteristics, work conditions (e.g., years of employment, job type, shift work, night shifts, weekly working hours), personal behaviors (e.g., smoking and drinking habits), and the occurrence of insomnia (by the Athens Insomnia Scale), anxiety (by the Generalized Anxiety Disorder Scale), and depression (by the Patient Health Questionnaire). Participants were classified into two groups based on working hours: long working hours (≥55 h per week) and normal working hours (35-40 h per week). Binary logistic regression was used to analyze the association between long working hours and the occurrences of insomnia, anxiety, and depression symptoms. Results A total of 1491 manufacturing industry employees were included in the study (response rate: 97.8%). The sample consisted of 54.19% males and 45.81% females, with the largest proportion was those aged 40-49 years (45.48%). The proportion of workers with long working hours in the total population was 31.52%, with the highest proportion among production and technical employees (36.49%). The prevalence of insomnia, anxiety, and depression symptoms was 56.2%, 26.6%, and 23.8%, respectively in the long working hours group, significantly higher than those in the normal working hours group (P<0.05). After adjusting for potential confounders, the logistic regression analysis showed that long working hours were significantly associated with increased risks of insomnia (OR=2.16, 95%CI: 1.60, 2.91), anxiety (OR=1.94, 95%CI: 1.34, 2.81), and depression symptoms (OR=1.62, 95%CI: 1.11, 2.38) compared to normal working hours. Conclusion Long working hours significantly increase the risks of insomnia, anxiety, and depression symptoms among manufacturing industry employees. It is recommended that measures should be implemented to limit working hours, increase rest periods, and provide occupational health education and psychological support to improve the sleep and mental health of employees.

Objective To assess the impact of long working hours on sleep disorders among manufacturing workers and explore the roles of alcohol consumption and mental health factors(anxiety and depressive symptoms)in this association.Methods A cross-sectional study design was used to survey 1 336 manufacturing workers in Shenzhen.We collected the data of their demographic characteristics,work-related factors,personal behaviors,sleep disorders,and mental health status.Multivariate Logistic regression analysis was used to assess the association between long working hours and sleep disorders.Stratified analysis and mediation effect models were applied to examine the effect modification by alcohol consumption and the mediating role of mental health factors,respectively.Results Among the study samples,31.8％reported long working hours and 45.6％had sleep disorders.Multivariate Logistic regression analysis showed that long working hours significantly increased the risk of sleep disorders(adjusted OR=2.073,95％ CI:1.478-2.907,P＜0.001).Stratified analysis revealed that the association between long working hours and sleep disorders was more pronounced among alcohol consumers(adjusted OR=2.556,95％ CI:1.432-4.562,P=0.001).Mediation effect analysis showed that anxiety and depressive symptoms partially mediated the relationship between long working hours and sleep disorders,with indirect effects accounting for 25.71％ and 27.14％,respectively.Conclusion Long working hours increase the risk of sleep disorders among manufacturing workers,particularly among those who consume alcohol.Anxiety and depressive symptoms partially explain the association between long working hours and sleep disorders.

Objective To assess the impact of long working hours on sleep disorders among manufacturing workers and explore the roles of alcohol consumption and mental health factors(anxiety and depressive symptoms)in this association.Methods A cross-sectional study design was used to survey 1 336 manufacturing workers in Shenzhen.We collected the data of their demographic characteristics,work-related factors,personal behaviors,sleep disorders,and mental health status.Multivariate Logistic regression analysis was used to assess the association between long working hours and sleep disorders.Stratified analysis and mediation effect models were applied to examine the effect modification by alcohol consumption and the mediating role of mental health factors,respectively.Results Among the study samples,31.8％reported long working hours and 45.6％had sleep disorders.Multivariate Logistic regression analysis showed that long working hours significantly increased the risk of sleep disorders(adjusted OR=2.073,95％ CI:1.478-2.907,P＜0.001).Stratified analysis revealed that the association between long working hours and sleep disorders was more pronounced among alcohol consumers(adjusted OR=2.556,95％ CI:1.432-4.562,P=0.001).Mediation effect analysis showed that anxiety and depressive symptoms partially mediated the relationship between long working hours and sleep disorders,with indirect effects accounting for 25.71％ and 27.14％,respectively.Conclusion Long working hours increase the risk of sleep disorders among manufacturing workers,particularly among those who consume alcohol.Anxiety and depressive symptoms partially explain the association between long working hours and sleep disorders.

OBJECTIVETo investigate the mitochondrial injury in enterovirus 71 (EV71)-infected Vero cells and explore the possible mechanism.

METHODSA clinical isolate of EV71 was inoculated to Vero cells and the EV71 antigen was detected by immunofluorescence assay. The morphological changes of Vero cells were observed using optical microscopy and transmission electron microscopy. The diameter and area density of the viral particles and the ratio and area density of vacuolated mitochondria in the cells were measured on the ultrastructural images.

RESULTSEV71-infected Vero cells underwent obvious changes and to a spherical morphology followed by cell death EV71 particles were detected in the cytoplasm by immunofluorescence. Ultrastructurally, the infected cells contained a large number of viral particles in the cytoplasm, with a clustered distribution and lattice-like arrangement. The diameter of the particles were 16.3 nm and the mean area density was 38.3%. Most of the mitochondria presented with swelling, vacuoles and degeneration. The ratio of the vacuolated mitochondria was 90.9% with a mean area density of 89.2%. Viral particles were also found in some mitochondria.

CONCLUSIONEV71 proliferates in the cytoplasm and invades the mitochondria of infected Vero cells leading to mitochondrial injury and cell death, suggesting that mitochondria are the targets for EV71 infection.

Animals ; Cercopithecus aethiops ; Cytoplasm ; virology ; Enterovirus ; Enterovirus Infections ; pathology ; Humans ; Mitochondria ; pathology ; virology ; Vero Cells ; virology

Objective To investigate the mitochondrial injury in enterovirus 71 (EV71)-infected Vero cells and explore the possible mechanism. Methods A clinical isolate of EV71 was inoculated to Vero cells and the EV71 antigen was detected by immunofluorescence assay. The morphological changes of Vero cells were observed using optical microscopy and transmission electron microscopy. The diameter and area density of the viral particles and the ratio and area density of vacuolated mitochondria in the cells were measured on the ultrastructural images. Results EV71-infected Vero cells underwent obvious changes and to a spherical morphology followed by cell death EV71 particles were detected in the cytoplasm by immunofluorescence. Ultrastructurally, the infected cells contained a large number of viral particles in the cytoplasm, with a clustered distribution and lattice-like arrangement. The diameter of the particles were 16.3 nm and the mean area density was 38.3% . Most of the mitochondria presented with swelling, vacuoles and degeneration. The ratio of the vacuolated mitochondria was 90.9%with a mean area density of 89.2%. Viral particles were also found in some mitochondria. Conclusion EV71 proliferates in the cytoplasm and invades the mitochondria of infected Vero cells leading to mitochondrial injury and cell death, suggesting that mitochondria are the targets for EV71 infection.

Objective To investigate the mitochondrial injury in enterovirus 71 (EV71)-infected Vero cells and explore the possible mechanism. Methods A clinical isolate of EV71 was inoculated to Vero cells and the EV71 antigen was detected by immunofluorescence assay. The morphological changes of Vero cells were observed using optical microscopy and transmission electron microscopy. The diameter and area density of the viral particles and the ratio and area density of vacuolated mitochondria in the cells were measured on the ultrastructural images. Results EV71-infected Vero cells underwent obvious changes and to a spherical morphology followed by cell death EV71 particles were detected in the cytoplasm by immunofluorescence. Ultrastructurally, the infected cells contained a large number of viral particles in the cytoplasm, with a clustered distribution and lattice-like arrangement. The diameter of the particles were 16.3 nm and the mean area density was 38.3% . Most of the mitochondria presented with swelling, vacuoles and degeneration. The ratio of the vacuolated mitochondria was 90.9%with a mean area density of 89.2%. Viral particles were also found in some mitochondria. Conclusion EV71 proliferates in the cytoplasm and invades the mitochondria of infected Vero cells leading to mitochondrial injury and cell death, suggesting that mitochondria are the targets for EV71 infection.