Background Depression is one of the most common mental disorders, profoundly impacting an individual's performance and quality of life. Due to their unique working conditions, nursing is counted among the occupational groups at high risk for developing depression. Because of the shortage of nursing resources in China, Chinese nurses suffer from heavy daily workloads more than those in many other countries. Therefore, this study aimed to evaluate the overall prevalence of depressive symptoms and analyse the potential risk factors of depressive symptoms in Chinese nurses. Methods A systematic literature search in PubMed, EMBASE, Web of Science, the Chinese BioMedical Literature Database (CBM), the China National Knowledge Infrastructure (CNKI), and the Weipu and Wanfang databases up to Dec 31st, 2019 was performed regarding the prevalence of depressive symptoms in Chinese nurses. Eligibility assessment and data extraction were performed independently by 2 researchers, and meta-analysis was used to synthesize the data. Heterogeneity was evaluated using Cochran's Q test and quantified using the I 2 statistic. To explore the potential source of heterogeneity, subgroup analyses were also performed. In addition, both funnel plot and Egger's tests were adopted to assess publication bias. Results A total of 102 studies published from 1996 to 2019 covering 22 provinces were included for further analysis. The total number of participants was 52,592, with a range of 46 to 7205 per study. The overall prevalence of depressive symptoms in Chinese nurses was 43.83% (95% CI: 40.26%-47.42%), and 31.12% (95%CI: 27.30%-35.07%) were classified as mild degrees of depressive symptoms. The prevalence of depressive symptoms may be significantly affected by region, province or municipality and department marital status. Moreover, an increasing trend in the prevalence of depressive symptoms was observed in recent years.

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Regulator of G protein signaling 3 (RGS3) is a negative regulator of G protein-mediated signaling. RGS3 has previously been shown to be expressed among various cell types within the mature heart. Basic and clinical studies have reported abnormal expressions of RGS3 in hypertrophic hearts and in the failing myocardium. However, the role of RGS3 in cardiac remodeling remains unclear. In this study, we investigated the effect of cardiac overexpression of human RGS3 on cardiac hypertrophy induced by aortic banding (AB) in RGS3 transgenic mice and wild-type littermates. The extent of cardiac hypertrophy was evaluated by echocardiography as well as pathological and molecular analyses of heart samples. RGS3 overexpression in the heart markedly reduced the extent of cardiac hypertrophy, fibrosis, and left ventricular dysfunction in response to AB. These beneficial effects were associated with the inhibition of MEK-ERK1/2 signaling. In vitro studies performed in cultured neonatal rat cardiomyocytes confirmed that RGS3 overexpression inhibits hypertrophic growth induced by angiotensin II, which was associated with the attenuation of MEK-ERK1/2 signaling. Therefore, cardiac overexpression of RGS3 inhibits maladaptive hypertrophy and fibrosis and improves cardiac function by blocking MEK-ERK1/2 signaling.

The plant cytoskeleton forms a stereoscopic network that regulates cell morphogenesis. The cytoskeleton also provides tracks for trafficking of vesicles to the target membrane. Fusion of vesicles with the target membrane is promoted by SNARE proteins, etc. The vesicle-SNARE, Sec22, regulates membrane trafficking between the ER and Golgi in yeast and mammals. Arabidopsis AtSEC22 might also regulate early secretion and is essential for gametophyte development. However, the role of AtSEC22 in plant development is unclear. To clarify the role of AtSEC22 in the regulation of plant development, we isolated an AtSEC22 knock-down mutant, atsec22-4, and found that cell morphogenesis and development were seriously disturbed. atsec22-4 exhibited shorter primary roots (PRs), dwarf plants, and partial abortion. More interestingly, the atsec22-4 mutant had less trichomes with altered morphology, irregular stomata, and pavement cells, suggesting that cell morphogenesis was perturbed. Further analyses revealed that in atsec22-4, vesicle trafficking was blocked, resulting in the trapping of proteins in the ER and collapse of structures of the ER and Golgi apparatus. Furthermore, AtSEC22 defects resulted in impaired organization and stability of the cytoskeleton in atsec22-4. Our findings revealed essential roles of AtSEC22 in membrane trafficking and cytoskeleton dynamics during plant development.