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AIM: To identify potential categories of clinical belonging among new nurses and explore the relationship between different categories and turnover intention. DESIGN: A cross sectional study. METHOD: A cross sectional study was conducted among 348 new nurses from tertiary hospitals in Hainan and Guangdong provinces. A general data questionnaire, clinical belonging scale and turnover intention scale were used for examination. Further, the potential categories were used to analyse the categories of clinical belonging, and latent class analysis was utilized to analyse the relationship between different categories of clinical belonging and turnover intention. RESULTS: The clinical sense of belonging of new nurses were divided into three groups namely C1, C2 and C3. The C1: poor clinical sense of belonging (8.7%), C2: moderate clinical sense of belonging (57.9%) and C3: rich clinical sense of belonging (33.4%). The risk of the turnover intention of new nurses with 'poor clinical sense of belonging' was 0.62 times that of new nurses with 'rich clinical sense of belonging' (OR = 0.62, p < 0.01), which was 0.24 times that of 'moderate clinical sense of belonging' (OR = 0.24, p < 0.01), the risk of the turnover intention of new nurses with 'moderate clinical sense of belonging' was 0.13 times that of new nurses with 'rich clinical sense of belonging'(OR = 0. 13, p < 0.01). CONCLUSIONS: The results of our study revealed that in order to enhance the new nurses' sense of belonging, support was most crucial when they were first encountering difficulties. To reduce turnover intention, more structured learning opportunities are also required to maximize learning for newly graduated nurses with various nursing degrees. PATIENT OR PUBLIC CONTRIBUTION: There are no patient or public contributions in this study.

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Although previous studies have suggested that meteorological factors are associated with Bell's palsy, articles on this topic are rare and the results are inconsistent. We aim to reveal the relationship between exposure to different meteorological factors and the onset of severe Bell's palsy (SBP) with daily data. A case-crossover study based on time-series data was applied, and the minimum risk value of each climatic factor was set as the reference value. We fitted a distributed lag non-linear model (DLNM) which applied quasi-Poisson regression to evaluate the exposure-response association and the lag-response association of meteorological factors on the occurrence of SBP. The mode value and per-decile interval value of each meteorological factor were all included in the analysis. Sensitivity analyses were conducted to test the robustness of results. A total of 863 SBP patients (474 males and 389 females) from 7 hospitals in the Shenzhen Futian District were selected from January 2009 to February 2020. The highest relations effect was tested in the cumulative exposure-response result shown as follows; mean temperature at the minimum value 15.3°C with RR of 10.370 (1.557-69.077) over lag 0 to 13; relative humidity at the 30th value 71% with RR of 8.041 (1.016-63.616) over lag 0 to 14; wind speed at the 90th value 31 (0.1 m/s) with RR of 1.286 (1.038-1.593) over lag 0; mean air pressure at the 30th value 1001.4 (pa) with RR of 9.052 (1.039-78.858) over lag 0 to 5; visibility at the 80th value 26.5 (km) with RR of 1.961 (1.005-1.423) over lag 0 to 2; average total cloud cover at the max value 100 (%) with RR 1.787 (1.014-3.148) over lag 0 to 2; sunshine duration at the 10th value 0.1 (h) with RR of 4.772 (1.018-22.361); daily evaporation shows no relationship in the cumulative result; daily average solar radiation at the minimum value 0 (W/m2) with RR of 5.588 (1.184-26.382). There is a relationship between wind speed and the onset of SBP, while mean air pressure, visibility, and average total cloud cover, especially sunshine duration and solar radiation which showed a strong effect, may be associated with severe clinical symptoms of SBP. Mean temperature and relative humidity may affect the course of SBP.

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Evodiae fructus (EF) is a traditional Chinese medicine which is widely used for the treatment of obesity, inflammation, cardiovascular disease, and diseases of the central nervous system. Recent studies have demonstrated the anticancer property of EF, but the active compounds of EF against prostate cancer and its underlying mechanism remain unknown. In this study, a network pharmacology-based approach was used to explore the multiple ingredients and targets of EF. Through protein-protein interaction (PPI), Gene Ontology (GO) enrichment, and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses, the potential targets and corresponding ingredients of EF against prostate cancer cells were obtained. CCK8 and colony formation assays were performed to evaluate the antiproliferative effect of the active compounds on DU145 cells. Cell cycle analysis, Annexin V-FITC/PI staining assay, and Hoechst 33258 staining assay were used to explore the way of evodiamine-induced cell death. The capacities of cell migration after evodiamine treatment were evaluated by wound-healing assay. PharmMapper database was used to predict the potential targets of evodiamine against cancer cell migration. Western blot assay was performed to investigate the signaling pathway through which evodiamine inhibits cell proliferation and migration. The binding of evodiamine to PI3K and AKT was verified by molecular docking. As a consequence, 24 active compounds and 141 corresponding targets were obtained through a network pharmacology-based approach. The results of PPI analysis, GO enrichment, and KEGG pathway enrichment indicated that molecules in the PI3K/AKT/NF-κB signaling pathway were the potential targets of EF against prostate cancer, and evodiamine was the potential active compound. In vitro study demonstrated that evodiamine displays antiproliferative effect on DU145 cells obviously. Evodiamine induces G2/M cell cycle arrest by Cdc25c/CDK1/cyclin B1 signaling. Additionally, evodiamine also promotes mitochondrial apoptosis and inhibits cell migration through PI3K/AKT/NF-κB signaling in DU145 cells. In conclusion, evodiamine is the active compound of EF to inhibit proliferation and migration of prostate cancer through PI3K/AKT/NF-κB signaling pathway, indicating that evodiamine may serve as a potential lead drug for prostate cancer treatment.

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Chemoresistance frequently occurs in cancer treatment, which results in chemotherapy failure and is one of the most leading causes of cancer-related death worldwide. Understanding the mechanism of chemoresistance and exploring strategies to overcome chemoresistance have become an urgent need. Autophagy is a highly conserved self-degraded process in cells. The dual roles of autophagy (pro-death or pro-survival) have been implicated in cancers and chemotherapy. MicroRNA (miRNA) is a class of small non-coding molecules that regulate autophagy at the post-transcriptional level in cancer cells. The association between miRNAs and autophagy in cancer chemoresistance has been emphasized. In this review, we focus on the dual roles of miRNA-mediated autophagy in facilitating or combating chemoresistance, aiming to shed lights on the potential role of miRNAs as targets to overcome chemoresistance.

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BACKGROUND: Cervical cancer is the fourth most prevalent gynecological cancer worldwide, which threatens women's health and causes cancer-related mortality. In the search for effective anticervical cancer drugs, we discovered that ß-estradiol (E2), a potent drug for estrogen deficiency syndrome treatment, displays the most potent cytotoxicity against HeLa cells. OBJECTIVE: This study aims to evaluate the growth inhibitory effect of ß-estradiol on HeLa cells and explore its underlying mechanisms. METHODS: CCK-8 assay was used to evaluate the cytotoxicity of 6 compounds against HeLa cells. Flow cytometric analysis and Hoechst 33258 staining assay were performed to detect cell cycle arrest and apoptosis induction. The collapse of the mitochondrial potential was observed by the JC-1 staining assay. The expression levels of proteins were examined by western blotting. RESULTS: ß-Estradiol, at high concentration, displays potent cytotoxicity against HeLa cells with an IC50 value of 18.71 ± 1.57 µM for 72 h treatment. ß-Estradiol induces G2/M cell cycle arrest through downregulating Cyclin B1 and p-CDK1. In addition, ß-estradiol-induced apoptosis is accompanied by the loss of mitochondrial potential, activation of the Caspase family, and altered Bax/Bcl-2 ratio. ß-Estradiol markedly decreased the expression level of p-AKT and p-NF-κB. CONCLUSION: This study demonstrated that ß-estradiol induces mitochondrial apoptosis in cervical cancer through the suppression of AKT/NF-κB signaling pathway, indicating that ß-estradiol may serve as a potential agent for cervical cancer treatment.

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Angiogenesis is required for tumor growth and development. Extracellular vesicles (EVs) are important signaling entities that mediate communication between diverse types of cells and regulate various cell biological processes, including angiogenesis. Recently, emerging evidence has suggested that tumor-derived EVs play essential roles in tumor progression by regulating angiogenesis. Thousands of molecules are carried by EVs, and the two major types of biomolecules, noncoding RNAs (ncRNAs) and proteins, are transported between cells and regulate physiological and pathological functions in recipient cells. Understanding the regulation of EVs and their cargoes in tumor angiogenesis has become increasingly important. In this review, we summarize the effects of tumor-derived EVs and their cargoes, especially ncRNAs and proteins, on tumor angiogenesis and their mechanisms, and we highlight the clinical implications of EVs in bodily fluids as biomarkers and as diagnostic, prognostic, and therapeutic targets in cancer patients.

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Major depressive disorder (MDD) has become the second most common disease worldwide, making it a threat to human health. Cyperi Rhizoma (CR) is a traditional herbal medicine with antidepressant properties. Traditional Chinese medicine theory states that CR relieves MDD by dispersing stagnated liver qi to soothe the liver, but the material basis and underlying mechanism have not been elucidated. In this study, we identified the active compounds and potential anti-MDD targets of CR by network pharmacology-based approaches. Through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, we hypothesized that the anti-MDD effect of CR may be mediated by an altered response of the liver to lipopolysaccharide (LPS) and glucose metabolism. Through bioinformatics analysis, comparing normal and MDD liver tissue in rats with spontaneous diabetes, we identified differentially expressed genes (DEGs) and selected PAI-1 (SERPINE1) as a target of CR in combating MDD. Molecular docking and molecular dynamics analysis also verified the binding of the active compound quercetin to PAI-1. It can be concluded that quercetin is the active compound of CR that acts against MDD by targeting PAI-1 to enhance the liver response to LPS and glucose metabolism. This study not only reveals the material basis and underlying mechanism of CR against MDD through soothing the liver but also provides evidence for PAI-1 as a potential target and quercetin as a potential agent for MDD treatment.

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BACKGROUND: Xanthine oxidase-derived superoxide production and oxidative stress contribute to the development of diabetic complications including diabetic cardiomyopathy. We hypothesized that xanthine oxidase-inhibitor allopurinol (ALP) may decrease hyperglycemia-induced oxidative stress, ameliorate cardiomyocyte hypertrophy and fibrosis, and attenuate the development of left ventricle (LV) diastolic dysfunction in rats with streptozotocin (STZ)-induced diabetes. METHODS: Control Sprague Dawley (C) or streptozotocin-induced diabetic (D) rats were either untreated or treated with allopurinol (100 mg/kg/day) for 4 weeks starting at 1 week after streptozotocin injection. Free 15-F2t-isoprostane, a specific indicator of oxidative stress was measured by enzymatic immunoassay. The cardiomyocyte cross-sectional area was assessed by hematoxylin and eosin-stained paraffin-embedded sections of LVs. Myocardial collagens I and III were assessed by immunol histochemistry and Western blotting. Echocardiography was performed to characterize cardiac structure and function. RESULTS: In diabetic rats, both plasma and cardiac tissue levels of free 15-F2t-isoprostane were increased (p < 0.05 vs. control), accompanied with significant increase (p < 0.05 vs. control) in cross-section area and myocardial collagen deposition of LV cardiomyocyte. Echocardiography in diabetic rats showed that LV weight/body weight ratio was significantly higher than in control rats, whereas the levels of LV end-diastolic volume and stroke volume were decreased (all p < 0.05 diabetic vs. control). All these changes were either attenuated or prevented by allopurinol. In addition, LV ejection fraction in diabetic rats treated with allopurinol was higher than that in untreated diabetic rats (p < 0.05). CONCLUSION: Allopurinol can attenuate hyperglycemia-induced oxidative stress, ameliorate cardiomyocyte hypertrophy and fibrosis and subsequently prevent left ventricular dysfunction in early diabetes.

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