The Mediation Impact of Compassion Competence on the Link Between Mindfulness and Job Burnout in Nurses: A Cross-Sectional Study.

AIMS: This study explores the link between mindfulness, compassion competence and job burnout among nurses, and analyses the mediating role that compassion competence plays in this relationship. BACKGROUND: Understanding nurses' mindfulness, compassion competence and job burnout is important, which could help devise interventions to relieve burnout in clinical nurses. METHODS: This study adopts convenience sampling method and descriptive design quantitative research. A cross-sectional study of 513 nurses was conducted from June to October 2023 in mainland China. The Socio-demographic Questionnaire, Mindful Attention Awareness Scale, Maslach Burnout Inventory-Human Service Survey and Compassion Competence Scale for the Nurses were utilised to gather basic demographic information on nurses and to evaluate their level of mindfulness, compassion competence and job burnout. Descriptive statistics, Spearman's correlation analyses and structural equation model were used to analyse the data. RESULTS: Five hundred and thirteen valid questionnaires were gathered. Spearman's correlation analysis revealed a strong negative link between mindfulness and job burnout, and between compassion competence and burnout, and a significant positive correlation between mindfulness and compassion competence. The results of the mediation analysis revealed that the relationship between mindfulness and job burnout was partially mediated by compassion competence, and the mediating effect accounted for 18.6% of the total effect. CONCLUSION: Compassion competence performed as a partial mediator between mindfulness and job burnout among nurses. Nursing managers could enhance nurses' mindfulness level and compassion competence through Mindfulness interventions and Compassion training to reduce their burnout. RELEVANCE TO CLINICAL PRACTICE: This study offers a fresh viewpoint on enhancing clinical nurses' compassion competence and reducing job burnout. Healthcare organisations and medical institutions can mitigate nurses' job burnout by improving their mindfulness levels and compassion competence. REPORTING METHOD: The study used the STROBE checklist for reporting. PATIENT OR PUBLIC CONTRIBUTION: All participants were nurses who completed an electronic questionnaire related to this study.

Chemical Reaction of FA Cations Enables Efficient and Stable Perovskite Solar Cells.

Organometal halide perovskite solar cells (PSCs) have received great attention owing to a rapid increase in power conversion efficiency (PCE) over the last decade. However, the deficit of long-term stability is a major obstacle to the implementation of PSCs in commercialization. The defects in perovskite films are considered as one of the primary causes. To address this issue, isocyanic acid (HNCO) is introduced as an additive into the perovskite film, in which the added molecules form covalent bonds with FA cations via a chemical reaction. This chemical reaction gives rise to an efficient passivation on the perovskite film, resulting in an improved film quality, a suppressed non-radiation recombination, a facilitated carrier transport, and optimization of energy band levels. As a result, the HNCO-based PSCs achieve a high PCE of 24.41% with excellent storage stability both in an inert atmosphere and in air. Different from conventional passivation methods based on coordination effects, this work presents an alternative chemical reaction for defect passivation, which opens an avenue toward defect-mitigated PSCs showing enhanced performance and stability.

Hypoxia-inducible PRMT2 addiction in glioblastomas.

Hypoxia-inducible transcription factors (HIFs) are key transcription factors for cellular response to low oxygen levels. However, the specific mediators responsible for activating downstream transcription are not well characterized. We previously identified Protein Arginine methyltransferase 2 (PRMT2), a highly expressed methyltransferase in glioblastoma multiforme, as a transcription co-activator. And we established a connection between PRMT2-mediated histone H3R8 asymmetric methylation (H3R8me2a) and transcription activation. Here we find that PRMT2 is activated by HIF1α under hypoxic conditions. And we demonstrate that PRMT2 and its H3R8me2a activity are required for the transcription activation of a significant subset of hypoxia-induced genes. Consequently, the inactivation of PRMT2 suppresses hypoxia-induced glioblastoma cell migration, attenuates tumor progression, and enhances chemotherapeutic sensitivity in mouse xenograft models. In addition, our analysis of clinical glioma specimens reveals a correlation between PRMT2 protein levels, HIF1α abundance, and an unfavorable prognosis. Our study establishes HIF1α-induced PRMT2 as a critical modulator in the activation of hypoxia-related transcriptional programs, ultimately driving malignant progression.

Pharmacological Targeting of CSF1R Inhibits Microglial Proliferation and Aggravates the Progression of Cerebral Ischemic Pathology.

Ischemic stroke can induce rapid activation of the microglia. It has been reported that the microglia's survival is dependent on colony-stimulating factor 1 receptor (CSF1R) signaling and that pharmacological inhibition of CSF1R leads to morphological changes in the microglia in the healthy brain. However, the impact of CSF1R inhibition on neuronal structures and motor ability after ischemia-reperfusion remains unclear. In this study, we investigated microglial de-ramification, proliferation, and activation after inhibition of CSF1R by a tyrosine kinase inhibitor (ki20227) in a mouse model of global cerebral ischemia induced by bilateral common carotid artery ligation (BCAL). In addition to microglial morphology, we evaluated the mRNA expression of cytokines, chemokines, and inflammatory receptors. Our results show that pharmacological inhibition of CSF1R in ischemic mice resulted in the blockade of microglial proliferation and a shift in microglial morphology reflected by excessive de-ramification and a more activated phenotype accompanied by an enhanced innate immune response. Furthermore, we show that pharmacological inhibition of CSF1R in ischemic mice resulted in the aggravation of neuronal degeneration and behavioral impairment. Intravital two-photon imaging revealed that although pharmacological inhibition of CSF1R did not affect the recovery of dendritic structures, it caused a significant increase in spine elimination during reperfusion in ischemic mice. These findings suggest that pharmacological inhibition of CSF1R induces a blockade of microglial proliferation and causes acute activation of the microglia accompanied by a severe inflammatory response. It aggravates neuronal degeneration, loss of dendritic spines, and behavioral deficits after transient global cerebral ischemia.