Association between sleep quality and anxiety-depression co-morbid symptoms among nursing students of medical college in Hefei City / 中国学校卫生

Objective@#To describe the prevalence and association of sleep quality and anxiety-depression co-morbid symptoms among nursing students, in order to provide a reference basis for promoting the development of nursing students mental health.@*Methods@#Using a prospective study design, baseline survey was conducted in January 2019 among a random cluster sample of 1 716 individuals in three medical universities in Hefei, Anhui Province, and a follow-up survey was conducted in October 2019, with a valid number of 1 573 individuals after matching with the baseline survey. The Pittsburgh Sleep Quality Index (PSQI) was used to assess nursing students sleep quality, and the Depression Anxiety Stress Scale (DASS-21) to assess the anxiety-depression comorbid symptoms.@*Results@#The detection rates of anxiety-depression co-morbidities among nursing students at baseline and follow-up survey were 16.9% and 18.2%, respectively, and the detection rates of poor sleep quality among nursing students at baseline and follow-up survey were 10.1% and 10.3%, respectively. The results of the binary Logistic regression model showed that baseline PSQI score were positively associated with the risk of anxiety-depression co-morbid symptoms among nursing students at baseline ( OR=1.49, 95%CI =1.40-1.59) and after nine months of follow-up ( OR=1.22, 95%CI =1.16-1.28). Furthermore, the influence of baseline sleep quality on the risk of anxiety-depression co-morbid symptoms were mainly concentrated in the five dimensions of sleep time, sleep efficiency, sleep disorders, hypnotic drugs and daytime dysfunction, and such effects of sleep time, sleep disorders and daytime dysfunction still existed in the follow-up investigation.@*Conclusion@#Poor sleep quality of nursing students can increase the risk of anxiety-depression co-morbidities. Improving sleep quality of nursing students has a positive effect on improving their mental health.

Mitochondrial aconitase controls adipogenesis through mediation of cellular ATP production.

Mitochondrial aconitase (Aco2) catalyzes the conversion of citrate to isocitrate in the TCA cycle, which produces NADH and FADH2, driving synthesis of ATP through OXPHOS. In this study, to explore the relationship between adipogenesis and mitochondrial energy metabolism, we hypothesize that Aco2 may play a key role in the lipid synthesis. Here, we show that overexpression of Aco2 in 3T3-L1 cells significantly increased lipogenesis and adipogenesis, accompanied by elevated mitochondrial biogenesis and ATP production. However, when ATP is depleted by rotenone, an inhibitor of the respiratory chain, the promotive role of Aco2 in adipogenesis is abolished. In contrast to Aco2 overexpression, deficiency of Aco2 markedly reduced lipogenesis and adipogenesis, along with the decreased mitochondrial biogenesis and ATP production. Supplementation of isocitrate efficiently rescued the inhibitory effect of Aco2 deficiency. Similarly, the restorative effect of isocitrate was abolished in the presence of rotenone. Together, these results show that Aco2 sustains normal adipogenesis through mediating ATP production, revealing a potential mechanistic link between TCA cycle enzyme and lipid synthesis. Our work suggest that regulation of adipose tissue mitochondria function may be a potential way for combating abnormal adipogenesis related diseases such as obesity and lipodystrophy.