Social bonding in groups of humans selectively increases inter-status information exchange and prefrontal neural synchronization.

Social groups in various social species are organized with hierarchical structures that shape group dynamics and the nature of within-group interactions. In-group social bonding, exemplified by grooming behaviors among animals and collective rituals and team-building activities in human societies, is recognized as a practical adaptive strategy to foster group harmony and stabilize hierarchical structures in both human and nonhuman animal groups. However, the neurocognitive mechanisms underlying the effects of social bonding on hierarchical groups remain largely unexplored. Here, we conducted simultaneous neural recordings on human participants engaged in-group communications within small hierarchical groups (n = 528, organized into 176 three-person groups) to investigate how social bonding influenced hierarchical interactions and neural synchronizations. We differentiated interpersonal interactions between individuals of different (inter-status) or same (intra-status) social status and observed distinct effects of social bonding on inter-status and intra-status interactions. Specifically, social bonding selectively increased frequent and rapid information exchange and prefrontal neural synchronization for inter-status dyads but not intra-status dyads. Furthermore, social bonding facilitated unidirectional neural alignment from group leader to followers, enabling group leaders to predictively align their prefrontal activity with that of followers. These findings provide insights into how social bonding influences hierarchical dynamics and neural synchronization while highlighting the role of social status in shaping the strength and nature of social bonding experiences in human groups.

Topological data analysis reveals a core gene expression backbone that defines form and function across flowering plants.

Since they emerged approximately 125 million years ago, flowering plants have evolved to dominate the terrestrial landscape and survive in the most inhospitable environments on earth. At their core, these adaptations have been shaped by changes in numerous, interconnected pathways and genes that collectively give rise to emergent biological phenomena. Linking gene expression to morphological outcomes remains a grand challenge in biology, and new approaches are needed to begin to address this gap. Here, we implemented topological data analysis (TDA) to summarize the high dimensionality and noisiness of gene expression data using lens functions that delineate plant tissue and stress responses. Using this framework, we created a topological representation of the shape of gene expression across plant evolution, development, and environment for the phylogenetically diverse flowering plants. The TDA-based Mapper graphs form a well-defined gradient of tissues from leaves to seeds, or from healthy to stressed samples, depending on the lens function. This suggests that there are distinct and conserved expression patterns across angiosperms that delineate different tissue types or responses to biotic and abiotic stresses. Genes that correlate with the tissue lens function are enriched in central processes such as photosynthetic, growth and development, housekeeping, or stress responses. Together, our results highlight the power of TDA for analyzing complex biological data and reveal a core expression backbone that defines plant form and function.

Enterovirus D68 3C protease antagonizes type I interferon signaling by cleaving signal transducer and activator of transcription 1.

Following the successful control of poliovirus, the re-emergence of respiratory enterovirus D68 (EV-D68), a prominent non-polio enterovirus, has become a serious public health concern worldwide. Host innate immune responses are the primary defense against EV-D68 invasion; however, the mechanism underlying viral evasion of the antiviral activity of interferons (IFN) remains unclear. In this study, we found that EV-D68 inhibited type I IFN signaling by cleaving signal transducer and activator of transcription 1 (STAT1), a crucial factor in cellular responses to interferons and other cytokines. We observed that the prototype and circulating EV-D68 strains conserved their ability to induce STAT1 cleavage and attenuate IFN signal transduction. Further investigation revealed that EV-D68 3C protease cleaves STAT1 at the 131Q residue. Interestingly, not all enterovirus-encoded 3C proteases exhibited this ability. EV-D68 and poliovirus 3C proteases efficiently induced STAT1 cleavage; whereas, 3C proteases from EV-A71, coxsackievirus A16, and echoviruses did not. STAT1 cleavage also abolished the nuclear translocation capacity of STAT1 in response to IFN stimulation to activate downstream signaling elements. Overall, these results suggest that STAT1, targeted by viral protease 3C, is utilized by EV-D68 to subvert the host's innate immune response.IMPORTANCEEnterovirus D68 (EV-D68) has significantly transformed over the past decade, evolving from a rare pathogen to a potential pandemic pathogen. The interferon (IFN) signaling pathway is an important defense mechanism and therapeutic target for the host to resist viral invasion. Previous studies have reported that the EV-D68 virus blocks or weakens immune recognition and IFN production in host cells through diverse strategies; however, the mechanisms of EV-D68 resistance to IFN signaling have not been fully elucidated. Our study revealed that EV-D68 relies on its own encoded protease, 3C, to directly cleave signal transducer and activator of transcription 1 (STAT1), a pivotal transduction component in the IFN signaling pathway, disrupting the IFN-mediated antiviral response. Previous studies on human enteroviruses have not documented direct cleavage of the STAT1 protein to evade cellular immune defenses. However, not all enteroviral 3C proteins can cleave STAT1. These findings highlight the diverse evolutionary strategies different human enteroviruses employ to evade host immunity.

Widely spaced and divergent inverted repeats become a potent source of chromosomal rearrangements in long single-stranded DNA regions.

DNA inverted repeats (IRs) are widespread across many eukaryotic genomes. Their ability to form stable hairpin/cruciform secondary structures is causative in triggering chromosome instability leading to several human diseases. Distance and sequence divergence between IRs are inversely correlated with their ability to induce gross chromosomal rearrangements (GCRs) because of a lesser probability of secondary structure formation and chromosomal breakage. In this study, we demonstrate that structural parameters that normally constrain the instability of IRs are overcome when the repeats interact in single-stranded DNA (ssDNA). We established a system in budding yeast whereby >73 kb of ssDNA can be formed in cdc13-707fs mutants. We found that in ssDNA, 12 bp or 30 kb spaced Alu-IRs show similarly high levels of GCRs, while heterology only beyond 25% suppresses IR-induced instability. Mechanistically, rearrangements arise after cis-interaction of IRs leading to a DNA fold-back and the formation of a dicentric chromosome, which requires Rad52/Rad59 for IR annealing as well as Rad1-Rad10, Slx4, Msh2/Msh3 and Saw1 proteins for nonhomologous tail removal. Importantly, using structural characteristics rendering IRs permissive to DNA fold-back in yeast, we found that ssDNA regions mapped in cancer genomes contain a substantial number of potentially interacting and unstable IRs.

Enterovirus D68 Infection Induces TDP-43 Cleavage, Aggregation, and Neurotoxicity.

Enterovirus D68 (EV-D68), which causes severe respiratory diseases and irreversible central nervous system damage, has become a serious public health problem worldwide. However, the mechanisms by which EV-D68 exerts neurotoxicity remain unclear. Thus, we aimed to analyze the effects of EV-D68 infection on the cleavage, subcellular translocation, and pathogenic aggregation of TAR DNA-binding protein 43 kDa (TDP-43) in respiratory or neural cells. The results showed that EV-D68-encoded proteases 2A and 3C induced TDP-43 translocation and cleavage, respectively. Specifically, 3C cleaved residue 327Q of TDP-43. The 3C-mediated cleaved TDP-43 fragments had substantially decreased protein solubility compared with the wild-type TDP-43. Hence, 3C activity promoted TDP-43 aggregation, which exerted cytotoxicity to diverse human cells, including glioblastoma T98G cells. The effects of commercially available antiviral drugs on 3C-mediated TDP-43 cleavage were screened, and the results revealed lopinavir as a potent inhibitor of EV-D68 3C protease. Overall, these results suggested TDP-43 as a conserved host target of EV-D68 3C. This study is the first to provide evidence on the involvement of TDP-43 dysregulation in EV-D68 pathogenesis. IMPORTANCE Over the past decade, the incidence of enterovirus D68 (EV-D68) infection has increased worldwide. EV-D68 infection can cause different respiratory symptoms and severe neurological complications, including acute flaccid myelitis. Thus, elucidating the mechanisms underlying EV-D68 toxicity is important to develop novel methods to prevent EV-D68 infection-associated diseases. This study shows that EV-D68 infection triggers the translocalization, cleavage, and aggregation of TDP-43, an intracellular protein closely related to degenerative neurological disorders. The viral protease 3C decreased TDP-43 solubility, thereby exerting cytotoxicity to host cells, including human glioblastoma cells. Thus, counteracting 3C activity is an effective strategy to relieve EV-D68-triggered cell death. Cytoplasmic aggregation of TDP-43 is a hallmark of degenerative diseases, contributing to neural cell damage and central nervous system (CNS) disorders. The findings of this study on EV-D68-induced TDP-43 formation extend our understanding of virus-mediated cytotoxicity and the potential risks of TDP-43 dysfunction-related cognitive impairment and neurological symptoms in infected patients.

Influenza A virus infection disrupts the function of syncytiotrophoblast cells and contributes to adverse pregnancy outcomes.

Pregnancy heightens susceptibility to influenza A virus (IAV) infection, thereby increasing the risk of severe pneumonia and maternal mortality. It also raises the chances of adverse outcomes in offspring, such as fetal growth restriction, preterm birth, miscarriage, and stillbirth in offsprings. However, the underlying mechanisms behind these effects remain largely unknown. Syncytiotrophoblast cells, crucial in forming the placental barrier, nutrient exchange and hormone secretion, have not been extensively studied for their responses to IAV. In our experiment, we used Forskolin-treated BeWo cells to mimic syncytiotrophoblast cells in vitro, and infected them with H1N1, H5N1 and H7N9 virus stains. Our results showed that syncytiotrophoblast cells, with their higher intensity of sialic acid receptors, strongly support IAV infection and replication. Notably, high-dose viral infection and prolonged exposure resulted in a significant decrease in fusion index, as well as gene and protein expression levels associated with trophoblast differentiation, ß-human chorionic gonadotropin secretion, estrogen and progesterone biosynthesis, and nutrient transport. In pregnant BALB/c mice infected with the H1N1 virus, we observed significant decreases in trophoblast differentiation and hormone secretion gene expression levels. IAV infection also resulted in preterm labor, fetal growth restriction, and increased maternal and fetal morbidity and mortality. Our findings indicate that IAV infection in syncytiotrophoblastic cells can result in adverse pregnancy outcomes by altering trophoblast differentiation, suppressing of ß-hCG secretion, and disrupting placental barrier function.

Association between the triglyceride-glucose index and in-hospital major adverse cardiovascular events in patients with acute coronary syndrome: results from the Improving Care for Cardiovascular Disease in China (CCC)-Acute Coronary Syndrome project.

OBJECTIVE: Although the TyG index is a reliable predictor of insulin resistance (IR) and cardiovascular disease, its effectiveness in predicting major adverse cardiac events in hospitalized acute coronary syndrome (ACS) patients has not been validated in large-scale studies. In this study, we aimed to explore the association between the TyG index and the occurrence of MACEs during hospitalization. METHODS: We recruited ACS patients from the CCC-ACS (Improving Cardiovascular Care in China-ACS) database and calculated the TyG index using the formula ln(fasting triglyceride [mg/dL] × fasting glucose [mg/dL]/2). These patients were classified into four groups based on quartiles of the TyG index. The primary endpoint was the occurrence of MACEs during hospitalization, encompassing all-cause mortality, cardiac arrest, myocardial infarction (MI), and stroke. We performed Cox proportional hazards regression analysis to clarify the correlation between the TyG index and the risk of in-hospital MACEs among patients diagnosed with ACS. Additionally, we explored this relationship across various subgroups. RESULTS: A total of 101,113 patients were ultimately included, and 2759 in-hospital MACEs were recorded, with 1554 (49.1%) cases of all-cause mortality, 601 (21.8%) cases of cardiac arrest, 251 (9.1%) cases of MI, and 353 (12.8%) cases of stroke. After adjusting for confounders, patients in TyG index quartile groups 3 and 4 showed increased risks of in-hospital MACEs compared to those in quartile group 1 [HR = 1.253, 95% CI 1.121-1.400 and HR = 1.604, 95% CI 1.437-1.791, respectively; p value for trend < 0.001], especially in patients with STEMI or renal insufficiency. Moreover, we found interactions between the TyG index and age, sex, diabetes status, renal insufficiency status, and previous PCI (all p values for interactions < 0.05). CONCLUSIONS: In patients with ACS, the TyG index was an independent predictor of in-hospital MACEs. Special vigilance should be exercised in females, elderly individuals, and patients with renal insufficiency.

Urine and serum metabolomic analysis of endometrial cancer diagnosis and classification based on ultra-performance liquid chromatography mass spectrometry.

OBJECTIVE: This study aimed to reveal the urinary and serum metabolic pattern of endometrial cancer (EC) and establish diagnostic models to identify EC from controls, high-risk from low-risk EC, and type II from type I EC. METHOD: This study included 146 EC patients (comprising 79 low-risk and 67 high-risk patients, including 124 type I and 22 type II) and 59 controls. The serum and urine samples were analyzed using ultraperformance liquid chromatography mass spectrometry. Analysis was used to elucidate the distinct metabolites and altered metabolic pathways. Receiver operating characteristic (ROC) analyses were employed to discover and validate the potential biomarker models. RESULTS: Serum and urine metabolomes displayed significant differences between EC and controls, with metabolites related to amino acid and nicotinamide metabolisms. The serum and urine panels distinguished these two groups with Area Under the Curve (AUC) of 0.821 and 0.902, respectively. The panel consisting of serum and urine metabolites demonstrated the best predictive ability (AUC = 0.953 and 0.976 in discovering and validation group). In comparing high-risk and low risk EC, differential metabolites were enriched in purine and glutamine metabolism. The AUC values for serum and urine panels were 0.818, and 0.843, respectively. The combined panel exhibited better predictive accuracy (0.881 in discovering group and 0.936 in external validation). In the comparison between type I and type II group, altered folic acid metabolism was identified. The serum, urine and combined panels discriminated these two groups with the AUC of 0.829, 0.913 and 0.922, respectively. CONCLUSION: The combined urine and serum metabolome effectively revealed the metabolic patterns in EC patients, offering valuable diagnostic models for EC diagnosis and classification.

Prognostic value and immunological role of PD-L1 gene in pan-cancer.

OBJECTIVE: PD-L1, a target of immune checkpoint blockade, has been proven to take the role of an oncogene in most human tumors. However, the role of PD-L1 in human pan-cancers has not yet been fully investigated. MATERIALS AND METHODS: Pan-cancer analysis was conducted to analyze expression, genetic alterations, prognosis analysis, and immunological characteristics of PD-L1. Estimating the correlation between PD-L1 expression and survival involved using pooled odds ratios and hazard ratios with 95% CI. The Kaplan-Meier (K-M) technique, COX analysis, and receiver operating characteristic (ROC) curves were applied to the survival analysis. Additionally, we investigated the relationships between PD-L1 and microsatellite instability (MSI), tumor mutational burden (TMB), DNA methyltransferases (DNMTs), the associated genes of mismatch repair (MMR), and immune checkpoint biomarkers using Spearman's correlation analysis. Also, immunohistochemical analysis and qRT-PCR were employed in evaluating PD-L1's protein and mRNA expression in pan-caner. RESULTS: PD-L1 showed abnormal mRNA and protein expression in a variety of cancers and predicted prognosis in cancer patients. Furthermore, across a variety of cancer types, the aberrant PD-L1 expression was connected to the MSI, MMR, TMB, drug sensitivity, and tumor immune microenvironment (TIME). Moreover, PD-L1 was significantly correlated with infiltrating levels of immune cells (T cell CD8 + , neutrophil, and so on). CONCLUSION: Our study provides a better theoretical basis and guidance for the clinical treatment of PD-L1.

Synthesis of pyrazino[1,2-b]indazoles via cascade cyclization of indazole aldehydes with propargylic amines.

An efficient intermolecular annulation of indazole aldehydes with propargylic amines has been developed for the synthesis of pyrazinoindazoles under catalyst- and additive-free conditions. This straightforward methodology was found to feature a wide substrate scope, high atom economy and environmental advantages. The bioactivity results of these new pyrazino[1,2-b]indazoles showed that some of them exhibited significant antifungal activity.

Influence of malnutrition according to the glim criteria on the chemotherapy toxicities in patients with advanced lung cancer.

BACKGROUND: Cancer-associated malnutrition is highly prevalent in advanced lung cancer, and 50% of global cancer-related deaths are attributed to cancer-associated malnutrition. Platinum-containing chemotherapy is the standard treatment for advanced lung cancer. Unfortunately, it can cause exacerbated toxicities, which can also have a negative impact on patient's prognosis and quality of life. The Global Leadership Initiative on Malnutrition (GLIM) criteria have been proposed as the world's first accepted diagnostic criteria for malnutrition. However, the effectiveness of GLIM criteria in predicting chemotherapy toxicities in patients with advanced lung cancer is unclear. The aim of this study was to apply the GLIM criteria to assess the prevalence of pre-treatment diagnosis of malnutrition in patients with advanced non-small cell lung cancer (NSCLC) and to determine the impact of nutritional status on patient's chemotherapy toxicity. METHODS: We conducted a study of hospitalized patients with pathologically and clinically diagnosed advanced NSCLC who presented to our hospital from May 2021 to January 2022. Initially, the Nutritional Risk Screening-2002 (NRS-2002) was used for nutritional risk screening, and nutritional status was assessed using the Scored Patient-Generated Subjective Global Assessment (PG-SGA) and GLIM criteria. Chemotherapy toxicity was assessed and graded according to CTCAE5.0, and chemotherapy efficacy was assessed according to RECIST1.1. Kappa test was used to analyze the agreement between PG-SGA and GLIM criteria. Univariate and multivariate logistic regression analyses were used to determine the relationship between malnutrition and chemotherapy toxicity. RESULTS: A total of 215 patients with advanced NSCLC were evaluated for nutritional status. Most of the patients had normal BMI (61.86%) before the start of treatment, 40% were well-nourished as assessed by the PG-SGA tool, and 51.17% were well-nourished as assessed by GLIM criteria. Consistency analysis showed moderate agreement (Kappa = 0.463, P < 0.001) and their correlation was also moderate (Spearman, rs = 0.475, P < 0.001). The objective response rate (ORR) (P = 0.040) and disease control rate (DCR) (P < 0.001) were significantly lower in malnourished patients diagnosed according to GLIM criteria than in well-nourished patients. Multivariate analysis showed that malnutrition (OR = 1.531,95%CI 0.757-3.009; OR = 6.623,95%CI 1.390-31.567, P = 0.046) diagnosed by GLIM criteria was an independent predictor of chemotherapy toxicity. Conclusions Malnutrition diagnosed by GLIM criteria better predicts toxicity during chemotherapy, determines the degree of clinical benefit of chemotherapy, and may affect patient prognosis.

Autoimmune encephalitis antibody profiles and clinical characteristics of children with suspected autoimmune encephalitis.

AIM: To identify the spectrum of autoimmune encephalitis antibody biomarkers (AE-Abs) in children with suspected autoimmune encephalitis and explore the clinical features indicating AE-Abs presence. METHOD: We included children with suspected autoimmune encephalitis who underwent AE-Abs tests at the Children's Hospital of Chongqing Medical University between June 2020 and June 2022. Clinical features suggestive of AE-Abs were analysed based on AE-Abs test results. RESULTS: A total of 392 children were tested for AE-Abs with suspected autoimmune encephalitis. Of these, 49.5% were male, with a median age of 7 years 11 months (6 months-17 years 11 months); 93.6% (367/392) of all patients had both serum and cerebrospinal fluid (CSF) tests performed. The antibody-positive rate in the cohort was 23.7% (93/392), the serum antibody-positive rate was 21.9% (84/384), and the CSF antibody-positive rate was 20.8% (78/375). Eleven different AE-Abs were detected. Serum analysis revealed that N-methyl-D-aspartate receptor immunoglobulin-G (NMDAR-IgG) (15.1%) was greater than myelin oligodendrocyte glycoprotein (MOG)-IgG (14.6%) and glial fibrillary acidic protein (GFAP)-IgG (3.3%). CSF analysis revealed that NMDAR-IgG (16.3%) was greater than MOG-IgG (13.8%) and GFAP-IgG (3.3%). Compared with antibody-negative patients, antibody-positive patients were more often female (odds ratio [OR] 1.86, p = 0.03), with memory impairment (OR 2.91, p = 0.01) and sleep disorders (OR 2.08, p = 0.02). INTERPRETATION: In children, the most frequent AE-Abs detected were NMDAR-IgG and MOG-IgG. Female sex, memory impairment, and sleep disorders predict a higher likelihood of AE-Abs.

Differences in the depression and burnout networks between doctors and nurses: evidence from a network analysis.

BACKGROUND: Previous studies have demonstrated a strong association between depression and job burnout among healthcare professionals, but the results have been inconsistent, and there is a lack of in-depth exploration of such a relationship among different healthcare professions. The present study aims to investigate the interrelationships between depression and burnout among Chinese healthcare professionals and whether there are differences in the networks of these symptoms between doctors and nurses. METHODS: The Maslach Burnout Inventory-General Survey and the 2-item Patient Health Questionnaire were employed to assess job burnout and depression among 3,684 healthcare professionals. The translation has been refined to ensure accuracy and academic suitability. Subsequently, network analysis was conducted on 2,244 participants with a higher level of job burnout to identify core symptoms and explore the associations between job burnout and depression. RESULTS: The present study showed a network association between lack of interest and pleasure in things and being exhausted from work, excessive tiredness facing work, tendency to collapse at work, and lack of passion for work than before among healthcare professionals, as well as a notable difference in the network association between lack of interest and pleasure in things and lack of passion for work than before between nurses and doctors. CONCLUSIONS: The depression-burnout network structures differ between doctors and nurses, highlighting the need for targeted intervention measures for both groups.

Development and Validation of a Nomogram for Predicting Nutritional Risk Based on Frailty Scores in Older Stroke Patients.

BACKGROUND: In older stroke patients with frailty, nutritional deficiencies can amplify their susceptibility, delay recovery, and deteriorate prognosis. A precise predictive model is crucial to assess their nutritional risk, enabling targeted interventions for improved clinical outcomes. OBJECTIVE: To develop and externally validate a nutritional risk prediction model integrating general demographics, physical parameters, psychological indicators, and biochemical markers. The aim is to facilitate the early identification of older stroke patients requiring nutritional intervention. METHODS: This was a multicenter cross-sectional study. A total of 570 stroke patients were included, 434 as the modeling set and 136 as the external validation set. The least absolute shrinkage selection operator (LASSO) regression analysis was used to select the predictor variables. Internal validation was performed using Bootstrap resampling (1000 iterations). The nomogram was constructed based on the results of logistic regression. The performance assessment relied on the receiver operating characteristic curve (ROC), Hosmer--Lemeshow test, calibration curves, Brier score, and decision curve analysis (DCA). RESULTS: The predictive nomogram encompassed seven pivotal variables: Activities of Daily Living (ADL), NIHSS score, diabetes, Body Mass Index (BMI), grip strength, serum albumin levels, and depression. Together, these variables comprehensively evaluate the overall health and nutritional status of elderly stroke patients, facilitating accurate assessment of their nutritional risk. The model exhibited excellent accuracy in both the development and external validation sets, evidenced by AUC values of 0.934 and 0.887, respectively. Such performance highlights its efficacy in pinpointing elderly stroke patients who require nutritional intervention. Moreover, the model showed robust goodness of fit and practical applicability, providing essential clinical insights to improve recovery and prognosis for patients prone to malnutrition. CONCLUSIONS: Elderly individuals recovering from stroke often experience significant nutritional deficiencies. The nomogram we devised accurately assesses this risk by combining physiological, psychological, and biochemical metrics. It equips healthcare providers with the means to actively screen for and manage the nutritional care of these patients. This tool is instrumental in swiftly identifying those in urgent need of targeted nutritional support, which is essential for optimizing their recovery and managing their nutrition more effectively.

Development and validation of a nomogram for predicting high-burnout risk in nurses.

AIM: To develop a predictive model for high-burnout of nurses. DESIGN: A cross-sectional study. METHODS: This study was conducted using an online survey. Data were collected by the Chinese Maslach Burnout Inventory-General Survey (CMBI-GS) and self-administered questionnaires that included demographic, behavioural, health-related, and occupational variables. Participants were randomly divided into a development set and a validation set. In the development set, multivariate logistic regression analysis was conducted to identify factors associated with high-burnout risk, and a nomogram was constructed based on significant contributing factors. The discrimination, calibration, and clinical practicability of the nomogram were evaluated in both the development and validation sets using receiver operating characteristic (ROC) curve analysis, Hosmer-Lemeshow test, and decision curve analysis, respectively. Data analysis was performed using Stata 16.0 software. RESULTS: A total of 2750 nurses from 23 provinces of mainland China responded, with 1925 participants (70%) in a development set and 825 participants (30%) in a validation set. Workplace violence, shift work, working time per week, depression, stress, self-reported health, and drinking were significant contributors to high-burnout risk and a nomogram was developed using these factors. The ROC curve analysis demonstrated that the area under the curve of the model was 0.808 in the development set and 0.790 in the validation set. The nomogram demonstrated a high net benefit in the clinical decision curve in both sets. CONCLUSION: This study has developed and validated a predictive nomogram for identifying high-burnout in nurses. RELEVANCE TO CLINICAL PRACTICE: The nomogram conducted by our study will assist nursing managers in identifying at-high-risk nurses and understanding related factors, helping them implement interventions early and purposefully. REPORTING METHOD: The study adhered to the relevant EQUATOR reporting guidelines: TRIPOD Checklist for Prediction Model Development and Validation. PATIENT OR PUBLIC CONTRIBUTION: No patient or public contribution.

Factors associated with clinical nurse's mental health: a qualitative study applying the social ecological model.

BACKGROUND: The prevalence of burnout, depression, and anxiety among Chinese nurses was 34%, 55.5%, and 41.8% respectively. Mental health problems have significant impacts on their personal well-being, work performance, patient care quality, and the overall healthcare system. Mental health is influenced by factors at multiple levels and their interactions. METHODS: This was a descriptive qualitative study using phenomenological approach. We recruited a total of 48 nurses from a tertiary hospital in Changsha, Hunan Province, China. Data were collected through focus group interviews. Audio-recorded data were transcribed and inductively analysed. RESULTS: Four major themes with 13 subthemes were identified according to the social ecological model: (1) individual-level factors, including personality traits, sleep quality, workplace adaptability, and years of work experience; (2) interpersonal-level factors, encompassing interpersonal support and role conflict; (3) organization-level factors, such as organizational climate, organizational support, career plateau, and job control; and (4) social-level factors, which included compensation packages, social status, and legislative provision and policy. CONCLUSIONS: Our study provides a nuanced understanding of the multifaceted factors influencing nurses' mental health. Recognizing the interconnectedness of individual, interpersonal, organizational, and social elements is essential for developing targeted interventions and comprehensive strategies to promote and safeguard the mental well-being of nurses in clinical settings. TRIAL AND PROTOCOL REGISTRATION: The larger study was registered with Chinese Clinical Trial Registry: ChiCTR2300072142 (05/06/2023) https://www.chictr.org.cn/showproj.html?proj=192676 . REPORTING METHOD: This study is reported according to the Consolidated Criteria for Reporting Qualitative Research (COREQ).

Ethical climate, moral resilience, and ethical competence of head nurses.

BACKGROUND: The ethical competence of head nurses plays a pivotal role in nursing ethics. Ethical climate is a prerequisite for ethical competence, and moral resilience can positively influence an individual's ethical competence. However, few studies have focused on the relationship between ethical climate, moral resilience, and ethical competence among them. OBJECTIVES: To investigate the relationship between ethical climate, moral resilience, and ethical competence, and examine the mediating role of moral resilience between ethical climate and ethical competence among head nurses. DESIGN: A quantitative, cross-sectional study. METHODS: A total of 309 Chinese head nurses completed an online survey, including ethical climate questionnaire, Rushton moral resilience scale, and ethical competence questionnaire. Inferential statistical analysis includes Pearson's correlation and a structural equation model. ETHICAL CONSIDERATIONS: This study received ethical approval from the Institutional Review Board of Xiangya Nursing School of Central South University (No. E2023146). RESULTS: Head nurses' ethical climate score positively impacted ethical competence (r = 0.208, p < .001), and ethical climate could affect ethical competence through the mediating role of moral resilience. CONCLUSION: This study emphasized the value of ethical climate in moral resilience of head nurses, ultimately leading to an enhancement in their ethical competence.

[Exploration of mechanism of total triterpenoids from fruits of Chaenomeles speciosa against senescent GES-1 cells induced by D-galactose based on Gln/GLS1/α-KG metabolic axis and mitochondrial apoptosis signaling pathway].

Total triterpenoids from the fruits of Chaenomeles speciosa(TCS) are active components in the prevention and treatment of gastric mucosal damage, which have potential anti-aging effects. However, it is still unclear whether TCS can improve gastric aging, especially its molecular mechanism against gastric aging. On this basis, this study explored the effect and mechanism of TCS on senescent GES-1 cells induced by D-galactose(D-gal) to provide scientific data for the clinical use of TCS to prevent gastric aging. GES-1 cells cultured in vitro and those transfected with overexpression GLS1(GLS1-OE) plasmid of glutaminase 1(GLS1) were induced to aging by D-gal, and then TCS and or GLS1 inhibitor bis-2-(5-phenylacetamido-1,3,4-thiadiazol-2-yl) ethyl sulfide(BPTES) were given. Cell survival rate, positive rate of ß-galactosidase(SA-ß-gal) staining, mitochondrial membrane potential(MMP), and apoptosis were investigated. GLS1 activity, levels of glutamine(Gln), glutamate(Glu), α-ketoglutarate(α-KG), urea, and ammonia in supernatant and cells were detected by enzyme-linked immunosorbent assay(ELISA) and colorimetric methods. The mRNA and protein expressions of GLS1 and the related genes of the mitochondrial apoptosis signaling pathway were measured by real-time fluorescence quantitative PCR and Western blot. The results manifested that compared with the D-gal model group and GLS1-OE D-gal model group, TCS significantly decreased the SA-ß-gal staining positive cell rate and MMP of D-gal-induced senescent GES-1 cells and GLS1-OE senescent GES-1 cells, inhibited the survival of senescent cells, and promoted their apoptosis(P<0.01). It decreased the activity of GLS1 and the content of Gln, Glu, α-KG, urea, and ammonia in supernatant and cell(P<0.01), reduced the concentration of cytochrome C(Cyto C) in mitochondria and the mRNA and protein expressions of GLS1 and proliferating nuclear antigen in cells(P<0.01). The mRNA expression of Bcl-2 and Bcl-xl, the protein expression of pro-caspase-9 and pro-caspase-3, and the ratio of Bcl-2/Bax and Bcl-xl/Bad in cells were decreased(P<0.01). Cyto C concentration in the cytoplasm, the mRNA expressions of Bax, Bad, apoptosis protease activating factor 1(Apaf-1), and protein expressions of cleaved-caspase-9, cleaved-caspase-3, cleaved-PARP-1 were increased(P<0.01). The aforementioned results indicate that TCS can counteract the senescent GES-1 cells induced by D-gal, and its mechanism may be closely related to suppressing the Gln/GLS1/α-KG metabolic axis, activating the mitochondrial apoptosis pathway, and thereby accelerating the apoptosis of the senescent cells and eliminating senescent cells.

In-Plane Chemical Ordering (Mo2/3 R1/3 )2 AlB2 (R = Tb, Dy, Ho, Er, Tm, and Lu) i-MAB Phases and their Two-Dimensional Derivatives (MBene): Synthesis, Structure, Magnetic, and Supercapacitor Performance.

A family of hexagonal in-plane chemical ordering (Mo2/3 R1/3 )2 AlB2 (R = Tb, Dy, Ho, Er, Tm, and Lu) i-MAB phases are synthesized with R-3m hexagonal structure. The i-MAB phases with R = Tb to Tm are considered to have a nonlinear ferromagnetic-like coupling magnetic ground state with gradually weakened magnetocrystalline anisotropy due to variant R-R distances and 4f electrons. Their 2D derivatives (2D-MBene) with rare-earth (R) atom vacancies are obtained by chemical etching. The delamination solvent, surface functional terminations, and chemical bond of 2D-MBene can be modified by one-step nitridation in environment-friendly nitrogen instead of ammonia. A phase conversion is caused by nitridation at 973 K from 2D-MBene to Mo2 N, leading to the optimized specific capacitance of 229 F g-1 . Besides exploring more rare-earth-containing laminated boride systems, this work also demonstrates the promising application of their 2D derivatives with R vacancies in supercapacitors.

The blue light receptor CRY1 interacts with FIP37 to promote N6 -methyladenosine RNA modification and photomorphogenesis in Arabidopsis.

Light is a particularly important environmental cue that regulates a variety of diverse plant developmental processes, such as photomorphogenesis. Blue light promotes photomorphogenesis mainly through the activation of the photoreceptor cryptochrome 1 (CRY1). However, the mechanism underlying the CRY1-mediated regulation of growth is not fully understood. Here, we found that blue light induced N6 -methyladenosine (m6 A) RNA modification during photomorphogenesis partially via CRY1. Cryptochrome 1 mediates blue light-induced expression of FKBP12-interacting protein 37 (FIP37), which is a component of m6 A writer. Moreover, we showed that CRY1 physically interacted with FIP37 in vitro and in vivo, and mediated blue light activation of FIP37 binding to RNA. Furthermore, CRY1 and FIP37 modulated m6 A on photomorphogenesis-related genes PIF3, PIF4, and PIF5, thereby accelerating the decay of their transcripts. Genetically, FIP37 repressed hypocotyl elongation under blue light, and fip37 mutation could partially rescue the short-hypocotyl phenotype of CRY1-overexpressing plants. Together, our results provide a new insight into CRY1 signal in modulating m6 A methylation and stability of PIFs, and establish an essential molecular link between m6 A modification and determination of photomorphogenesis in plants.