Factors associated with compassion fatigue and compassion satisfaction in obstetrics and gynaecology nurses: A cross-sectional study.

AIMS: To examine the factors influencing compassion fatigue and compassion satisfaction in obstetrics and gynaecology nurses and to explore the combined results of multiple factors. DESIGN: An online cross-sectional study was conducted. REVIEW METHODS: Data were collected from 311 nurses using a convenience sampling method from January to February 2022. Stepwise multiple linear regression analysis and mediation tests were performed. RESULTS: Compassion fatigue in obstetrics and gynaecology nurses was in the moderate to high levels. Physical status, number of children, emotional labour, lack of professional efficacy, emotional exhaustion and the none-only-child can influence compassion fatigue; lack of professional efficacy, cynicism, social support, work experience, employment status and night shift were predictive of compassion satisfaction. Social support partially mediated between lack of professional efficacy and compassion fatigue/compassion satisfaction; emotional labour moderated in the mediated analysis model. CONCLUSION: Moderate to high levels of compassion fatigue was present in 75.88% of obstetrics and gynaecology nurses. Some factors affect compassion fatigue and compassion satisfaction. Thus, nursing managers should consider factors and construct a monitoring system to reduce compassion fatigue and improve compassion satisfaction. IMPLICATIONS FOR THE PROFESSION: The results will provide a theoretical basis for improving job satisfaction and the quality of care in obstetrics and gynaecology nurses. And this may raise concerns about the occupational health of obstetrics and gynaecology nurses in China. REPORTING METHOD: The study was reported according to the STROBE. PATIENT OR PUBLIC CONTRIBUTION: The nurses spent time filling out the questionnaires during the data collection phase and answered the questions sincerely. WHAT DOES THIS ARTICLE CONTRIBUTE TO THE WIDER GLOBAL CLINICAL COMMUNITY?: Obstetrics and gynaecology nurses with 4-16 years of experience are prone to experience compassion fatigue. The effect of lack of professional efficacy on compassion fatigue and compassion satisfaction can be improved by social support. RELEVANCE TO CLINICAL PRACTICE: Reducing nurse compassion fatigue and improving compassion satisfaction are important for providing quality nursing care to obstetrics and gynaecology patients. In addition, clarifying the influencing factors of compassion fatigue and compassion satisfaction can improve nurses' work efficiency and job satisfaction, and provide theoretical guidance for managers to implement interventions.

HK2 Is a Crucial Downstream Regulator of miR-148a for the Maintenance of Sphere-Forming Property and Cisplatin Resistance in Cervical Cancer Cells.

The acquisition of cancer stem-like properties is believed to be responsible for cancer metastasis and therapeutic resistance in cervical cancer (CC). CC tissues display a high expression level of hexokinase 2 (HK2), which is critical for the proliferation and migration of CC cells. However, little is known about the functional role of HK2 in the maintenance of cancer stem cell-like ability and cisplatin resistance of CC cells. Here, we showed that the expression of HK2 is significantly elevated in CC tissues, and high HK2 expression correlates with poor prognosis. HK2 overexpression (or knockdown) can promote (or inhibit) the sphere-forming ability and cisplatin resistance in CC cells. In addition, HK2-overexpressing CC cells show enhanced expression of cancer stem cell-associated genes (including SOX2 and OCT4) and drug resistance-related gene MDR1. The expression of HK2 is mediated by miR-145, miR-148a, and miR-497 in CC cells. Overexpression of miR-148a is sufficient to reduce sphere formation and cisplatin resistance in CC cells. Our results elucidate a novel mechanism through which miR-148a regulates CC stem cell-like properties and chemoresistance by interfering with the oncogene HK2, providing the first evidence that dysregulation of the miR-148a/HK2 signaling plays a critical role in the maintenance of sphere formation and cisplatin resistance of CC cells. Our findings may guide future studies on therapeutic strategies that reverse cisplatin resistance by targeting this pathway.

LncRNA OTUD6B-AS1 Induces Cisplatin Resistance in Cervical Cancer Cells Through Up-Regulating Cyclin D2 via miR-206.

Cervical cancer is one of the most common gynecological cancers. Cisplatin resistance remains a major hurdle in the successful treatment of cervical cancer. Aberrant expression of long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) are implicated in cisplatin resistance. However, the regulatory functions of lncRNAs and miRNAs in cervical cancer cisplatin resistance and the underlying mechanisms are still elusive. Our qRT-PCR assays verified that miR-206 levels were down-regulated in cisplatin-resistant cervical cancer cells. The introduction of miR-206 sensitized cisplatin-resistant cervical cancer cells to cisplatin. Our qRT-PCR and luciferase reporter assays showed that Cyclin D2 (CCND2) was the direct target for miR-206 in cervical cancer cells. The cisplatin-resistant cervical cancer cells expressed higher CCND2 expression than the parental cells, whereas inhibition of CCND2 could sensitize the resistant cells to cisplatin treatment. Furthermore, we demonstrated that lncRNA OTUD6B-AS1 was up-regulated in cisplatin-resistant cervical cancer cells, and knocking down OTUD6B-AS1 expression induced re-acquirement of chemosensitivity to cisplatin in cervical cancer cells. We also showed that OTUD6B-AS1 up-regulated the expression of CCND2 by sponging miR-206. Low miR-206 and high OTUD6B-AS1 expression were associated with significantly poorer overall survival. Taken together, these results suggest that OTUD6B-AS1-mediated down-regulation of miR-206 increases CCND2 expression, leading to cisplatin resistance. Modulation of these molecules may be a therapeutic approach for cisplatin-resistant cervical cancer.

Validation of efficacy and mechanism of Sanwei-Tanxiang powder in improving myocardial ischemia reperfusion injuries.

Sanwei-Tanxiang powder (SWTX), a traditional Mongolian and Tibetan medicine containing a cocktail of active molecules, relieves angina pectoris and improves recovery in patients with coronary heart disease (CHD). The pharmacological effect of SWTX on CHD was analyzed at a systemic point of view in our previous studies. The bioinformatics prediction showed that the PI3K/Akt/FoxO3a pathway was one of important pathways of SWTX on treatment of coronary heart disease. Based on it, the aim of this study was to evaluate the benefits of SWTX in acute myocardial ischemic-reperfused (MIR) rat in vivo and H9c2 cardiomyoblast cells under oxidative stress induced by H2O2 in vitro, and further investigate the involvement of PI3K/Akt/FoxO3a pathway in these processes. Ex vivo, under physiological conditions, SWTX did not show any modification in the heart rate and contraction amplitude. However, against a MIR injury, SWTX pretreatment provided significant protection, including reduced ST-segment elevation, pathological changes and myocardial infarct size in vivo, meanwhile, some monomers of SWTX showed antioxidant capacity and inhibited cardiomyocytic apoptosis in vitro. The effect was correlated with the activation of the PI3K/Akt/FoxO3a signaling pathway downstream and the regulation of downstream pro-apoptotic Bim of FoxO3a experimental verified by qRT-PCR, Western blot and immunofluorescent assay. In vitro, blocking Akt and p-FoxO3a activation with the PI3K inhibitor LY294002 effectively suppressed the protective effects of several active monomers (including quercetin, macelignan,methyleugenol and Santol) of SWTX against H2O2-induced injury. Collectively, these results suggest that SWTX decreases I/R injury, and the PI3K/Akt/FoxO3a pathway takes part in protection during this process, gallogen (G3) and quercetin (G8) of GZ, methyleugenol (R2) and macelignan (R7) of RDK, santol (T1) of TX are responsible at least in part for SWTX's cardioprotection effect.

V[Formula: see text]H: View Variation and View Heredity for Incomplete Multiview Clustering.

Real data often appear in the form of multiple incomplete views. Incomplete multiview clustering is an effective method to integrate these incomplete views. Previous methods only learn the consistent information between different views and ignore the unique information of each view, which limits their clustering performance and generalizations. To overcome this limitation, we propose a novel View Variation and View Heredity approach (V[Formula: see text]H). Inspired by the variation and the heredity in genetics, V[Formula: see text]H first decomposes each subspace into a variation matrix for the corresponding view and a heredity matrix for all the views to represent the unique information and the consistent information respectively. Then, by aligning different views based on their cluster indicator matrices, V[Formula: see text]H integrates the unique information from different views to improve the clustering performance. Finally, with the help of the adjustable low-rank representation based on the heredity matrix, V[Formula: see text]H recovers the underlying true data structure to reduce the influence of the large incompleteness. More importantly, V[Formula: see text]H presents possibly the first work to introduce genetics to clustering algorithms for learning simultaneously the consistent information and the unique information from incomplete multiview data. Extensive experimental results on fifteen benchmark datasets validate its superiority over other state-of-the-arts. Impact Statement-Incomplete multiview clustering is a popular technology to cluster incomplete datasets from multiple sources. The technology is becoming more significant due to the absence of the expensive requirement of labeling these datasets. However, previous algorithms cannot fully learn the information of each view. Inspired by variation and heredity in genetics, our proposed algorithm V[Formula: see text]H fully learns the information of each view. Compared with the state-of-the-art algorithms, V[Formula: see text]H improves clustering performance by more than 20% in representative cases. With the large improvement on multiple datasets, V[Formula: see text]H has wide potential applications including the analysis of pandemic, financial and election datasets. The DOI of our codes is 10.24 433/CO.2 119 636.v1.

Understanding the Multitarget Pharmacological Mechanism of the Traditional Mongolian Common Herb Pair GuangZao-RouDouKou Acting on Coronary Heart Disease Based on a Bioinformatics Approach.

GuangZao and RouDouKou (Fructus Choerospondiatis and Nutmeg, FCN) are one of the most common herb pairs in traditional Mongolian medicine for the treatment of coronary heart disease (CHD). However, evidence for the protective effect of FCN is limited, and its underlying mechanism of action remains unclear. The present study employed a network pharmacology approach to identify the potentially active ingredients and synergistic effects of the herb pair FCN as traditional Mongolian medicine. We predicted the targets of all available FCN ingredients with PharmMapper, SWISS, and SuperPred Server and clustered CHD-related targets from the DrugBank and the OMIM database. We also evaluated the links between herbal ingredients and pharmacological actions to explore the potential mechanism of action of FCN. We found that FCN targets a network of CHD-related key processes, including stress responses, cell adhesion and connections, angiogenesis, cell apoptosis and necrosis, the endocrine system, inflammatory and immune responses, and other biological processes. To confirm the predicted results, we investigated the protective effect of FCN on isoproterenol- (ISO-) induced myocardial ischemia in rats. Pathological assessment indicated that FCN inhibits apoptosis and inflammatory responses involving the myocardium. Quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting analyses demonstrated the therapeutic effects of FCN on ISO-induced myocardial ischemia rats, possibly via regulating stress and inflammatory responses and inhibiting cardiomyocyte apoptosis. The findings of the present study indicate that bioinformatics combined with experimental verification provide a credible and objective method to elucidate the complex multitarget mechanism of action of FCN.