Lumpy skin disease virus ORF127 protein suppresses type I interferon responses by inhibiting K63-linked ubiquitination of tank binding kinase 1.

Lumpy skin disease (LSD) is a severe animal infectious disease caused by lumpy skin disease virus (LSDV), inducing extensive nodules on the cattle mucosa or the scarfskin. LSDV genome encodes multiple proteins to evade host innate immune response. However, the underlying molecular mechanisms are poorly understood. In this study, we found that LSDV could suppress the expression of IFN-ß and interferon-stimulated genes (ISGs) in MDBK cells during the early stage of infection. Subsequently, an unbiased screen was performed to screen the LSDV genes with inhibitory effects on the type I interferon (IFN-I) production. ORF127 protein was identified as one of the strongest inhibitory effectors on the expression of IFN-ß and ISGs, meanwhile, the 1-43 aa of N-terminal of ORF127 played a vital role in suppressing the expression of IFN-ß. Overexpression of ORF127 could significantly promote LSDV replication through inhibiting the production of IFN-ß and ISGs in MDBK cells. Mechanism study showed that ORF127 specifically interacted with TBK1 and decreased the K63-linked polyubiquitination of TBK1 which suppressed the phosphorylation of TBK1 and ultimately decreased the production of IFN-ß. In addition, truncation mutation analysis indicated that the 1-43 aa of N-terminal of ORF127 protein was the key structural domain for its interaction with TBK1. In short, these results validated that ORF127 played a negative role in regulating IFN-ß expression through cGAS-STING signaling pathway. Taken together, this study clarified the molecular mechanism of ORF127 gene antagonizing IFN-I-mediated antiviral, which will helpfully provide new strategies for the treatment and prevention of LSD.

Social support and physical literacy in young and middle-aged patients with hypertension: the mediating effects of sense of coherence and self-efficacy.

BACKGROUND: Despite the growing recognition of the importance of social support and physical literacy in managing hypertension among young and middle-aged patients, there is a lack of research exploring the mediating effects of sense of coherence and self-efficacy in this relationship. This study aims to bridge this gap by investigating the interplay between social support, physical literacy, sense of coherence, and self-efficacy, thus contributing to a deeper understanding of effective interventions for hypertension management. METHODS: A cross-sectional study was conducted using convenience sampling to survey 280 young and middle-aged patients diagnosed with hypertension from five community settings in Zhejiang and Anhui provinces between January and February 2024. Measurement instruments included the General Information Questionnaire, Physical Literacy Scale for Young and Middle-aged Patients with Hypertension, Sense of Coherence Scale 13, General self-efficacy Scale, and Perception Social Support Scale. Data analysis was performed using SPSS 27.0 and AMOS 28.0, with reporting following the STROBE checklist. RESULTS: A total of 270 valid questionnaires were collected. The total score of physical literacy for young and middle-aged patients with hypertension ranged from 18 to 90, with a mean score of 62.30 ± 13.92, indicating a moderate level. There was a positive correlation between the physical literacy score and the scores of social support (r = 0.557, P<0.01), sense of coherence (r = 0.392, P<0.01), and self-efficacy (r = 0.466, P<0.01) among young and middle-aged patients with hypertension. Furthermore, social support was found to have multiple mediating effects through sense of coherence and self-efficacy on physical literacy. CONCLUSION: This study sheds light on the interconnectedness of social support, physical literacy, sense of coherence, and self-efficacy among young and middle-aged patients with hypertension. The findings underscore the importance of considering these factors holistically in hypertension management strategies.

Well-shaped poly(dimethylsiloxane)-based copolymer nanowires from spherical micelles via kinetic shape evolution.

The formation of self-assembled arrays or superstructures from copolymers has attracted intense research interest. Herein, we propose a kinetic approach to form self-assembled nanowires using a PDMS-based block copolymer consisting of poly(dimethylsiloxane)-b-poly[2-(cinnamoyloxy)ethyl methacrylate] (PDMS-b-PCEMA). The copolymer was synthesized by using the macroinitiator PDMS-Br to initiate 2-(trimethylsiloxy)ethyl methacrylate (HEMA-TMS) via ATRP, followed by hydrolysis of the TMS group and gradual esterification with cinnamoyl chloride. PDMS-b-PCEMA presented core-shell spherical micelles in tetrahydrofuran, which transformed into nanowires within 5 days self-assembly via a typical kinetic shape evolution. The diameter of the assembled nanowires with a PCEMA inner core and PDMS shell was about 25-35 nm. The formation of these nanowires reflected a balance between the PDMS and PCEMA components: the PDMS segment was soluble enough to form a corona block, which was beneficial for the transformation of the micellar shape. Meanwhile, the PCEMA segment was able to control the diameter of the nanowire micelles but had no decisive effect on their formation. The effect of solvents on the self-assembled micelles indicated that nanowires were formed in tetrahydrofuran and dichloromethane, while core-shell micelles were formed in acetone. This was due to the different permittivities of these solvents. The nanowires were fixed by cross-linking the PCEMA group under UV irradiation, which enhanced their stability. We believe that this work provides a new strategy for the formation of nanowires and offers a guide for the diversified self-assembly of nanostructures from copolymers.

Long noncoding RNA XIST regulates brown preadipocytes differentiation and combats high-fat diet induced obesity by targeting C/EBPα.

BACKGROUND: Activation of brown adipose tissue (BAT) increases energy expenditure, which makes it an attractive therapeutic strategy for obesity. LncRNAs play an important role in adipocyte differentiation and regulation. Here we assessed the effect of lncRNA XIST on brown preadipocytes differentiation and metabolic regulation. METHODS: XIST expression levels were detected in human perirenal (peri-N) and subcutaneous adipose tissues (sub-Q), brown preadipocytes and 3T3-L1 preadipocytes. XIST overexpression and knockdown experiments were performed in brown preadipocytes. XIST overexpression mouse model was established by plasmid injection through tail vein. RESULTS: In human adipose tissues, XIST expression was significantly higher in female than in male individuals. In vitro, XIST expression was significantly up-regulated during brown adipocyte differentiation. XIST knockdown inhibited differentiation of brown preadipocytes, while overexpression of XIST promotes brown preadipocytes to fully differentiation. RNA Binding Protein Immunoprecipitation (RIP) experiment revealed that XIST could directly bind to C/EBPα. In vivo, XIST overexpression prevents high-fat diet induced obesity and improves metabolic dysorder in male mice. CONCLUSION: Our results suggest that XIST combats obesity through BAT activation at least partly by combination with transcription factor C/EBPα.

Epithelial-mesenchymal Transition of Peritoneal Mesothelial Cells Is Enhanced by M2c Macrophage Polarization.

BACKGROUND: Peritoneal fibrosis (PF) can reduce the efficiency of peritoneal dialysis and eventually lead to ultrafiltration failure. Epithelial-mesenchymal transition (EMT) of peritoneal mesothelial cells (PMCs) is the start of PF. Macrophages are involved in the process. This study was to investigate the effect of macrophage polarization on EMT of PMCs. METHODS: Monocyte-macrophage cells (THP-1) were treated to induce macrophage subsets (M1, M2a, M2c). The inducing was assessed by detecting protein and mRNA expression of cytokines using ELISA and RT-PCR. Subsequently, PMCs were co-cultured with M1, M2a and M2c, respectively, in Transwell chambers for 48 h and then expressions of E-cadherin and α-SMA were determined in PMCs. The PMCs that were not co-cultured with macrophages served as control PMCs. One-way ANOVA and SNK-q test were used to conduct statistics and P < .05 as significant. RESULTS: Detection of the cytokines, including IL-6, IL-10, IL-12, TGF-ß1, CCL17 and CXCL13, verified that the inducting of macrophage subtypes was successful. Compared to control, E-cadherin protein expression was significantly decreased and α-SMA protein expression increased in M1-treated PMCs (P < .05); M2a-treated PMCs had an increased gene expression of α-SMA (P < .05); E-cadherin protein and gene expression were decreased and α-SMA protein and gene expression increased significantly in M2c-treated PMCs (P < .05 or P < .01). CONCLUSIONS: EMT of PMCs is enhanced by M2c macrophage polarization; meanwhile, M1 and M2a polarization may have the effect to some extent, but not as definite as M2c.

Predicting the presence and mechanism of busulfan drug-drug interactions in hematopoietic stem cell transplantation using pharmacokinetic interaction network-based molecular structure similarity and network pharmacology.

PURPOSE: This study aimed to predict the presence and mechanism of busulfan drug-drug interactions (DDIs) in hematopoietic stem cell transplantation (HSCT) using pharmacokinetic interaction (PKI) network-based molecular structure similarity and network pharmacology. METHODS: Logistic function models were established to predict busulfan DDIs based on the assumption that an approved drug tends to interact with the drug used in HSCT (DH) if structurally similar to the drugs in the PKI network of the DH. The PKI network of the DH represented the association between drugs and the proteins related to the PK of the DH. The most appropriate model was applied to predict busulfan DDIs in HSCT. Candidate targets for busulfan DDIs and their interacting were identified by network pharmacology. RESULTS: Six of the top ten predicted busulfan DDIs were clinically relevant and involved voriconazole, fludarabine, itraconazole, cyclophosphamide, metronidazole, and melphalan. Candidate targets for these DDIs were CYP450s (3A4, 2B6, 2C9, and 2C19), GSTs (GSTA1, GSTP1, GSTT1, and GSTM1), and ABC transporters (ABCB1, ABCC1, ABCC2, and ABCC3), in the targets of drug-induced liver injury (DILI). The networks of interacting proteins and candidate targets indicated the regulatory potential of pregnane X receptor (PXR), as a nuclear receptor. Enrichment analysis showed the metabolism of drugs and xenobiotics, glutathione metabolism, and bile secretion associated with busulfan DDIs and DILI. CONCLUSIONS: This study has successfully predicted busulfan DDIs in HSCT through PKI-based molecular structure similarity. The mechanism of busulfan DDI and DILI was attributed mostly to CYP450s, GSTs, and ABC transporters, and PXR was identified as a potential target.

Activation of Nrf2/HO-1 Pathway by Glycogen Synthase Kinase-3ß Inhibition Attenuates Renal Ischemia/Reperfusion Injury in Diabetic Rats.

BACKGROUND/AIMS: Diabetes mellitus can exacerbate renal ischemia-reperfusion (I/R) injury (RI/RI). The aim of the present study was to evaluate the protective effect of GSK-3ß inhibition (TDZD-8) on I/R-induced renal injury through the Nrf2/HO-1 pathway in a streptozocin (STZ)-induced diabetic rat model. METHODS: STZ-induced diabetic rats preconditioned with TDZD-8 and ZnPP were subjected to renal I/R. The extent of renal morphologic lesions. Renal function was assessed from blood urea nitrogen (BUN) and serum creatinine (Scr), as determined utlizing commercial kits. Oxidative stress and inflammatory activity in the kidney tissue was estimated from levels of malondialdehyde (MDA), interleukin-10 (IL-10), tumor necrosis factor-α (TNF-α), and nitric oxide (NO), as well as the activities of superoxide dismutase (SOD) and glutathione (GSH) using qRT-PCR and ELISA. The expressions of Nrf2, HO-1, Bcl-2 and NF-κB in the renal tissue were measured by qRT-PCR and western blotting. RESULTS: I/R-induced renal inflammation was reduced significantly by TDZD-8 pretreatment. Preconditioning with TDZD-8 suppressed NF-κB expression and enhanced Bcl-2 expression in the renal tissue. The upregulated level of malondialdehyde (MDA), and reduced activities of superoxide dismutase (SOD) and glutathione (GSH) in I/R-shocked rats were markedly restored by TDZD-8 pretreatment. Furthermore, pretreatment with TDZD-8 enhanced activation of the Nrf2/HO-1 pathway in the renal tissue of diabetic RI/RI rats. CONCLUSION: These findings suggest that preconditioning with TDZD-8 may protect the kidney from I/R-induced damage via the activation of the Nrf2/HO-1 pathway in STZ-induced diabetic rats. Further detailed studies are needed to further clarify the underlying mechanisms.

Dietary practices of Chinese patients with inflammatory bowel disease: a naturalistic inquiry.

Dietary factors have been linked to the development and symptoms of inflammatory bowel disease. However, little is known about the dietary practices of these patients after being diagnosed and what factors shape those practices. This article reports the findings of a naturalistic inquiry that explored the experience of dietary practices of Chinese patients with inflammatory bowel diseases. Purposive sampling was used and in-depth interviews were conducted with 17 patients with inflammatory bowel disease. Analysis of the transcribed data is presented thematically. Five themes were derived: (a) seeking dietary information, (b) testing out, (c) modifying diet, (d) barriers to diet modification, and (e) fear and stress. Understanding the dietary practice of patients with inflammatory bowel disease from the perspective of those diagnosed is a first step in attempting to assist them with diet management. Healthcare professionals should encourage patients to report diet modification and be aware of both personal and environmental barriers of diet modification.

Improving cell reinfusion to enhance the efficacy of chimeric antigen receptor T-cell therapy and alleviate complications.

Adoptive cell therapy (ACT) is a rapidly expanding area within the realm of transfusion medicine, focusing on the delivery of lymphocytes to trigger responses against tumors, viruses, or inflammation. This area has quickly evolved from its initial promise in immuno-oncology during preclinical trials to commercial approval of chimeric antigen receptor (CAR) T-cell therapies for leukemia and lymphoma (Jun and et al., 2018) [1]. CAR T-cell therapy has demonstrated success in treating hematological malignancies, particularly relapsed/refractory B-cell acute lymphoblastic leukemia and non-Hodgkin's lymphoma (Qi and et al., 2022) [2]. However, its success in treating solid tumors faces challenges due to the short-lived presence of CAR-T cells in the body and diminished T cell functionality (Majzner and Mackall, 2019) [3]. CAR T-cell therapy functions by activating immune effector cells, yet significant side effects and short response durations remain considerable obstacles to its advancement. A prior study demonstrated that the therapeutic regimen can induce systemic inflammatory reactions, such as cytokine release syndrome (CRS), immune effector cell-associated neurotoxicity syndrome (ICANS), tumor lysis syndrome (TLS), off-target effects, and other severe complications. This study aims to explore current research frontiers in this area.

New insights into the interactions between the gut microbiota and the inflammatory response to ulcerative colitis in a mouse model of dextran sodium sulfate and possible mechanisms of action for treatment with PE&AFWE.

BACKGROUND: Inflammatory bowel disease (IBD), comprising Crohn's disease (CD) and ulcerative colitis (UC), is a heterogeneous state of chronic intestinal inflammation. Intestinal innate immunity, including innate immune cells, defends against pathogens and excessive entry of gut microbiota, while preserving immune tolerance to resident intestinal microbiota, and may be characterized by its capacity to produce a rapid and nonspecific reaction. The association between microbiota dysbiosis and the pathogenesis of IBD is complex and dynamic. When the intestinal ecosystem is in dysbiosis, the reduced abundance and diversity of intestinal gut microbiota make the host more vulnerable to the attack of exogenous and endogenous pathogenic gut microbiota. The aim of our study was to comprehensively assess the relationship between microbial populations within UC, the signaling pathways of pathogenic gut microbe therein and the inflammatory response, as well as to understand the effects of using PE&AFWE (poppy extract [Papaver nudicaule L.] and Artemisia frigida Willd. extract) on UC modulation. METHODS: A UC mouse model was established by inducing SPF-grade C57BL/6 mice using dextrose sodium sulfate (DSS). Based on metagenomic sequencing to characterize the gut microbiome, the relationship between gut microbiota dysbiosis and gut microbiota was further studied using random forest and Bayesian network analysis methods, as well as histopathological analysis. RESULTS: (1) We found that the 5 gut microbiota with the highest relative abundance of inflammatory bowel disease UC model gut microbiota were consistent with the top 5 ranked natural bacteria. There were three types of abundance changes in the model groups: increases (Chlamydiae/Proteobacteria and Deferribacteres), decreases (Firmicutes), and no significant changes (Bacteroidetes). The UC model group was significantly different from the control group, with 1308 differentially expressed species with abundance changes greater than or equal to 2-fold. (2) The proportion of the fecal flora in the UC group decreased by 37.5% in the Firmicutes and increased by 14.29% in the proportion of Proteobacteria compared to the control group before treatment. (3) The significantly enriched and increased signaling pathways screened were the 'arachidonic acid metabolic pathway' and the 'phagosomal pathway', which both showed a decreasing trend after drug administration. (4) Based on the causal relationship between different OTUs and the UC model/PE&AFWE administration, screening for directly relevant OTU networks, the UC group was found to directly affect OTU69, followed by a cascade of effects on OTU12, OTU121, OTU93, and OTU7, which may be the pathway of action that initiated the pathological changes in normal mice. (5) We identified a causal relationship between common differentially expressed OTUs and PE&AFWE and UC in the pre- and post-PE&AFWE-treated groups. Thereby, we learned that PE&AFWE can directly affect OTU90, after which it inhibits UC, inhibiting the activity of arachidonic acid metabolic pathway by affecting OTU118, which in turn inhibits the colonization of gut microbiota by OTU93 and OTU7. (6) Histopathological observation and scoring (HS) of the colon showed that there was a significant difference between the model group and the control group (p < 0.001), and that there was a significant recovery in both the sulfasalazine (SASP)and the PE&AFWE groups after the administration of the drug (p < 0.0001). CONCLUSION: We demonstrated causal effects and inflammatory metabolic pathways in gut microbiota dysbiosis and IBD, with five opportunistic pathogens directly contributing to IBD. PE&AFWE reduced the abundance of proteobacteria in the gut microbiota, and histopathology showed significant improvement.

Association between systemic immune-inflammation index and chronic kidney disease: A population-based study.

BACKGROUND: Systemic immune-inflammation index (SII) is a new indicator of inflammation, and chronic kidney disease (CKD) has a connection to inflammation. However, the relationship between SII and CKD is still unsure. The aim of this study was whether there is an association between SII and CKD in the adult US population. METHODS: Data were from the National Health and Nutrition Examination Survey (NHANES) in 2003-2018, and multivariate logistic regression was used to explore the independent linear association between SII and CKD. Smoothing curves and threshold effect analyses were utilized to describe the nonlinear association between SII and CKD. RESULTS: The analysis comprised 40,660 adults in total. After adjusting for a number of factors, we found a positive association between SII and CKD [1.06 (1.04, 1.07)]. In subgroup analysis and interaction tests, this positive correlation showed differences in the age, hypertension, and diabetes strata (p for interaction<0.05), but remained constant in the sex, BMI, abdominal obesity, smoking, and alcohol consumption strata. Smoothing curve fitting revealed a non-linear positive correlation between SII and CKD. Threshold analysis revealed a saturation effect of SII at the inflection point of 2100 (1,000 cells/µl). When SII < 2100 (1,000 cells/µl), SII was an independent risk element for CKD. CONCLUSIONS: In the adult US population, our study found a positive association between SII and CKD (inflection point: 2100). The SII can be considered a positive indicator to identify CKD promptly and guide therapy.

PuRenDan alleviates type 2 diabetes mellitus symptoms by modulating the gut microbiota and its metabolites.

ETHNOPHARMACOLOGICAL RELEVANCE: PuRenDan (PRD) is a traditional Chinese medicine formula comprising five herbs that have been traditionally used to treat type 2 diabetes mellitus (T2DM). While PRD has been shown to be effective in treating T2DM in clinical and animal studies, the mechanisms by which it works on the gut microbiome and metabolites related to T2DM are not well understood. AIM OF THE STUDY: The objective of this study was to partially elucidate the mechanism of PRD in treating T2DM through analyses of the gut microbiota metagenome and metabolome. MATERIALS AND METHODS: Sprague-Dawley rats were fed high-fat diets (HFDs) and injected with low-dose streptozotocin (STZ) to replicate T2DM models. Then the therapeutic effects of PRD were evaluated by measuring clinical markers such as blood glucose, insulin resistance (IR), lipid metabolism biomarkers (total cholesterol, low-density lipoprotein, non-esterified fatty acids, and triglycerides), and inflammatory factors (tumor necrosis factor alpha, interleukin-6 [IL-6], interferon gamma, and IL-1ß). Colon contents were collected, and metagenomics, combined with ultra-high-performance liquid chromatography quadrupole time-of-flight mass spectrometry metabolic profiling, was performed to evaluate the effects of T2DM and PRD on gut microbiota and its metabolites in rats. Spearman analysis was used to calculate the correlation coefficient among different microbiota, clinical indices, and metabolites. RESULTS: PRD exhibited significant improvement in blood glucose and IR, and reduced serum levels of lipid metabolism biomarkers and inflammatory factors. Moreover, the diversity and abundance of gut microbiota undergo significant changes in rats with T2DM that PRD was able to reverse. The gut microbiota associated with T2DM including Rickettsiaceae bacterium 4572_127, Psychrobacter pasteurii, Parabacteroides sp. CAG409, and Paludibacter propionicigenes were identified. The gut microbiota most closely related to PRD were Prevotella sp. 10(H), Parabacteroides sp. SN4, Flavobacteriales bacterium, Bacteroides massiliensis, Alistipes indistinctus, and Ruminococcus flavefaciens. Additionally, PRD regulated the levels of gut microbiota metabolites including pantothenic acid, 1-Methylhistamine, and 1-Methylhistidine; these affected metabolites were involved in pantothenate and coenzyme A biosynthesis, histidine metabolism, and secondary bile acid biosynthesis. Correlation analysis illustrated a close relationship among gut microbiota, its metabolites, and T2DM-related indexes. CONCLUSION: Our study provides insights into the gut microbiota and its metabolites of PRD therapy for T2DM. It clarifies the role of gut microbiota and the metabolites in the pathogenesis of T2DM, highlighting the potential of PRD for the treatment of this disease.

Branched-chain amino acid catabolic defect promotes α-cell proliferation via activating mTOR signaling.

Elevated circulating level of branched-chain amino acids (BCAAs) is closely related to the development of type 2 diabetes. However, the role of BCAA catabolism in various tissues in maintaining glucose homeostasis remains largely unknown. Pancreatic α-cells have been regarded as amino acid sensors in recent years. Therefore, we generated α-cell specific branched-chain alpha-ketoacid dehydrogenase E1α subunit (BCKDHA) knockout (BCKDHA-αKO) mice to decipher the effects of BCAA catabolism in α-cells on whole-body energy metabolism. BCKDHA-αKO mice showed normal body weight, body fat, and energy expenditure. Plasma glucagon level and glucose metabolism also remained unchanged in BCKDHA-αKO mice. Whereas, the deletion of BCKDHA led to increased α-cell number due to elevated cell proliferation in neonatal mice. In vitro, only leucine among BCAAs promoted aTC1-6 cell proliferation, which was blocked by the agonist of BCAA catabolism BT2 and the inhibitor of mTOR Rapamycin. Like Rapamycin, BT2 attenuated leucine-stimulated phosphorylation of S6 in αTC1-6 cells. Elevated phosphorylation level of S6 protein in pancreatic α-cells was also observed in BCKDHA-αKO mice. These results suggest that local accumulated leucine due to defective BCAA catabolism promotes α-cell proliferation through mTOR signaling, which is insufficient to affect glucagon secretion and whole-body glucose homeostasis.

Association between dietary protein intake and mortality among patients with diabetic kidney disease.

AIMS: This study aimed to investigate the association between dietary protein intake and mortality among patients with diabetic kidney disease. METHODS: The research encompassed a total of 2901 participants diagnosed with diabetic kidney disease, drawn from the National Health and Nutrition Examination Survey (NHANES). To determine outcomes related to all-cause and cardiovascular mortality, connections were established with the National Death Index up until December 31, 2019. Estimations of hazard ratios (HRs) and their corresponding 95 % confidence intervals (CIs) were conducted using Cox proportional hazard ratio models. RESULTS: During the 261,239 person-years of follow-up, 1236 deaths were recorded. After multivariate adjustment, the weighted hazard ratio (HR) and 95 % CIs for participants with 1.0-1.2 g/kg of protein intake was 0.65 (0.44, 0.96) for all-cause mortality. A higher proportion of animal protein intake was found to be associated with an increased mortality risk. Stratified analyses showed that higher protein intake benefited older participants. CONCLUSIONS: In diabetic kidney disease patients, 1.0-1.2 g/kg of protein was associated with lower mortality and 0.6-1.2 g/kg of protein especially benefitted patients ≥60 years.

Music Intervention for older adults: Evidence Map of Systematic Reviews.

BACKGROUND: With the increasing aging population, the health problems of the elderly have received increasing attention. As a non-pharmacological interventions, music intervention has been widely used in clinical practice to improve the physical and mental health of the elderly. This article aims to provide a comprehensive review of existing systematic reviews on the health effects of music interventions for older adults in clinical practice. METHODS: The study utilized the evidence map methodology, which involved identifying all relevant systematic reviews, meta-analysis from 7 electronic databases from their inception to November 2022. The studies were analyzed using AMSTAR 2. RESULTS: The researchers identified 67 studies, with the majority published in the past 5 years. The effects of music interventions were categorized into 4 groups of health outcomes: positive (58 results), potentially positive (4 results), inconclusive (2 results), and no effect (3 results). The health outcomes were further classified into 5 groups: psychological well-being, cognitive functioning, physiological responses, quality of life, and overall well-being. CONCLUSIONS: The study revealed that music interventions for older adults can have positive or potentially positive effects on health outcomes, encompassing psychological well-being, cognitive functioning, physiological responses, quality of life, and overall well-being. However, some studies yielded inconclusive or no effect. The study offers valuable insights for healthcare professionals and serves as a visual resource to access evidence-based information on the use of music interventions in promoting health and addressing various conditions in older adults.

Core self-evaluation and innovative behavior: mediating effect of error orientation and self-efficacy of nurses.

Background: Innovation plays a crucial role in advancing nursing and healthcare. Despite its significance, there is a paucity of research examining the interplay among nursing innovative behavior, core self-evaluation, error orientation, and self-efficacy. This study, grounded in Bandura's social cognitive theory, seeks to not only investigate the influence of core self-evaluation on nurses' innovative behavior but also to elucidate the mediating roles of error orientation and self-efficacy within this relationship. By addressing these dynamics, the research aims to provide a comprehensive understanding of the factors shaping nurses' innovative behaviors and contribute to the broader discourse on enhancing healthcare practices. Design: A cross-sectional study using an online questionnaire. Setting: Participants were recruited from 23 hospitals in 6 provinces and 1 municipality directly under the central government in China, namely Zhejiang, Anhui, Jiangxi, Guangdong, Hebei, Henan, and Shanghai. Participants: A total of 741 nurses enrolled in the study. Methods: The participants completed the nurse innovative behavior scale, the core self-evaluation scale, the error orientation questionnaire, and the self-efficacy scale online in 2023. SPSS and AMOS were used for data analysis. The reporting followed the STROBE checklist. Results: A total of 706 valid questionnaires were collected. A positive core self-evaluation was associated with more innovative behavior, and this relation was partially mediated by error orientation and self-efficacy to avoid failure. Core self-evaluation, error orientation and self-efficacy of nurses had a positive predictive effect on innovation behavior, with the path coefficients at 0.09, 0.23, and 0.39, respectively. Conclusion: Our study complements the evidence on the mechanism of action between the core self-evaluation and innovative behavior. Our findings have important clinical implications for promoting innovative behavior in nurses.

Mean-square consensus of a semi-Markov jump multi-agent system based on event-triggered stochastic sampling.

This paper focuses on achieving leader-follower mean square consensus in semi-Markov jump multi-agent systems. To effectively reduce communication costs and control updates, we propose an event-triggered protocol based on stochastic sampling. The stochastic sampling interval randomly switches between finite given values, while the event-triggered function depends on the stochastic sampled data from neighboring agents. Using the event-triggered strategy, we present sufficient conditions to ensure mean square consensus. Finally, we provide a numerical example demonstrating the effectiveness of the theoretical results.

Supervisors' ethical leadership and graduate students' attitudes toward academic misconduct.

Graduate students' academic misconduct has received increasing attention. Although past literature has emphasized university faculty as an important influencing factor on students' moral behaviors, the mechanisms must be further disclosed. We investigated how supervisors' ethical leadership influenced graduate students' attitudes toward academic misconduct. We explained why and how supervisor gender affects post-graduate students' social learning process by integrating social cognitive theory and role congruity theory. Study 1 used a sample of 301 graduate students in 60 academic teams in four Chinese business schools. Study 2 used experimental vignette methodology to enhance the findings' internal and external validity and provided evidence of causality. Based on the two complementary studies, we found that supervisors' ethical leadership significantly inhibited students' acceptance of academic misconduct through students' moral efficacy and the ethical climate of the academic team. The indirect effect via moral efficacy was more significant s for female supervisors. Implications for ethical leadership, academic misconduct, gender differences in leadership, and moral education were discussed.

Morphology, morphogenesis and molecular phylogeny of Lamtostyla granulifera sinensis subsp. nov. (Ciliophora, Hypotrichia) from a wetland in China.

The morphology, morphogenesis and molecular phylogeny of a hypotrichous ciliate, Lamtostyla granulifera sinensis subsp. nov., isolated from northern China, were investigated. This population appeared highly similar in morphology to L. granulifera Foissner, 1997. However, on detailed investigation some non-overlapping features were identified, i.e., the body shape and the arrangement of the cortical granules. These differences suggested the separation at subspecies level. Furthermore, the morphogenesis of the new subspecies is described, which is characterized by: (1) the posterior part of the parental adoral zone of membranelles is renewed; (2) the amphisiellid median cirral row is formed from two anlagen; and (3) the frontoventral-transverse cirral anlagen II to VI generate one transverse cirrus each. Phylogenetic analyses based on SSU rDNA sequence data show that Lamtostyla species are scattered in different clades. The monophyly of the genus Lamtostyla is also rejected by the AU test in this study.

Exogenous melatonin activates the antioxidant system and maintains postharvest organoleptic quality in Hami melon (Cucumis. melo var. inodorus Jacq.).

Hami melon is prone to postharvest perishing. Melatonin is a signaling molecule involved in a variety of physiological processes in fruit, and it improves fruit quality. We hypothesized that melatonin treatment would improve the storage quality of Hami melon by altering its respiration and reactive oxygen species (Graphical abstract). Our results indicated that optimal melatonin treatment (0.5 mmol L-1) effectively slowed the softening, weight loss, and respiratory rate of the Hami melon fruit. Furthermore, melatonin markedly improved the antioxidant capacity of the fruit and protected it from oxidative damage by decreasing its contents of superoxide anions, hydrogen peroxide, and malondialdehyde. Melatonin significantly enhanced the activities of superoxide dismutase, catalase, ascorbate peroxidase, and peroxidase. The total phenol, total flavonoids, and ascorbic acid contents were maintained by melatonin treatment. This treatment also repressed the activities of lipase, lipoxygenase, and phospholipase D, which are related to lipid metabolism. Thus, exogenous melatonin can maintain postharvest organoleptic quality of Hami melon fruit by increasing its antioxidant activity and inhibiting reactive oxygen species production.