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Non-alcoholic fatty liver disease (NAFLD) and myocardial infarction (MI) are two major health burdens with significant prevalence and mortality. This study aimed to explore the co-expressed genes to understand the relationship between NAFLD and MI and identify potential crucial biomarkers of NAFLD-related MI using bioinformatics and machine learning. Functional enrichment analysis was conducted, a co-protein-protein interaction (PPI) network diagram was constructed, and support vector machine-recursive feature elimination (SVM-RFE) and least absolute shrinkage and selection operator (LASSO) techniques were employed to identify one differentially expressed gene (DEG), Thrombospondin 1 (THBS1). THBS1 demonstrated strong performance in distinguishing NAFLD patients (AUC = 0.981) and MI patients (AUC = 0.900). Immuno-infiltration analysis revealed significantly lower CD8+ T cells and higher neutrophil levels in patients with NAFLD and MI. CD8+ T cells and neutrophils were effective in distinguishing NAFLD/MI from healthy controls. Correlation analysis showed that THBS1 was positively correlated with CCR (chemokine receptor), MHC class (major histocompatibility complex class), neutrophils, parainflammation, and Tfh (follicular helper T cells), and negatively correlated with CD8+ T cells, cytolytic activity, and TIL (tumor-infiltrating lymphocytes) in NAFLD and MI patients. THBS1 emerged as a novel biomarker for diagnosing NAFLD/MI in comparison to healthy controls. The results indicate that CD8+ T cells and neutrophils could serve as inflammatory immune features for differentiating patients with NAFLD/MI from healthy individuals.

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BACKGROUND: Guanine-rich RNA sequence binding factor 1 (GRSF1) is an RNA-binding protein, which is eventually localised to mitochondria and promotes the translation of cytochrome C oxidase 1 (COX1) mRNA. However, the role of the miR-19-3p/GRSF1/COX1 axis has not been investigated in an experimental subarachnoid haemorrhage (SAH) model. Thus, we investigated the role of the miR-19-3p/GRSF1/COX1 axis in a SAH-induced early brain injury (EBI) course. METHODS: Primary neurons were treated with oxyhaemoglobin (OxyHb) to simulate in vitro SAH. The rat SAH model was established by injecting autologous arterial blood into the optic chiasma cisterna. The GRSF1 level was downregulated or upregulated by treating the rats and neurons with lentivirus-GRSF1 shRNA (Lenti-GRSF1 shRNA) or lentivirus-GRSF1 (Lenti-GRSF1). RESULTS: The miR-19-3p level was upregulated and the protein levels of GRSF1 and COX1 were both downregulated in SAH brain tissue. GRSF1 silence decreased and GRSF1 overexpression increased the protein levels of GRSF1 and COX1 in primary neurons and brain tissue, respectively. Lenti-GRSF1 shRNA aggravated, but Lenti-GRSF1 alleviated, the indicators of neuronal injury and neurological impairment in both in vitro and in vivo SAH conditions. In addition, miR-19-3p mimic reduced the protein levels of GRSF1 and COX1 in cultured neurons while miR-19-3p inhibitor increased them. More importantly, Lenti-GRSF1 significantly relieved mitochondrial damage of neurons exposed to OxyHb or induced by SAH and was beneficial to maintaining mitochondrial integrity. Lenti-GRSF1 shRNA treatment, conversely, aggravated mitochondrial damage in neurons. CONCLUSION: The miR-19-3p/GRSF1/COX1 axis may serve as an underlying target for inhibiting SAH-induced EBI by maintaining mitochondrial integrity.

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BACKGROUND: A positive work environment can enhance nursing safety and patient satisfaction while alleviating nurse stress. Conversely, a poor work environment can harm nurses' physical and mental health and compromise the quality of care, particularly in the high-intensity and shift-based setting of the ICU. OBJECTIVES: Based on the Job demands-resources (JD-R) model, this study examined the effects of job demands and job resources in the work environment, as well as personal resources, on the night-shift alertness of ICU shift nurses. METHODS: This cross-sectional correlational exploratory study, conducted from July to September 2022, recruited 291 ICU shift nurses from a hospital in Beijing, China. The Copenhagen Psychosocial Questionnaire (COPSOQ), the Self-resilience scale, the General Self-Efficacy Scale (GSES), and the Psychomotor Vigilance Task (PVT) were used to subjectively and objectively measure the job demands, job resources, personal resources, and night-shift alertness. SPSS 26.0 and Mplus 8.3 were used to analyze the data and construct the structural equation model. RESULTS: The night-shift reaction time was 251.0 ms (Median), indicating a relatively high level of alertness. Job demands were negatively correlated with both job resources (r=-0.570, P < 0.001) and personal resources (r=-0.462, P < 0.001), while a positive correlation existed between job resources and personal resources (r = 0.554, P < 0.001). The results show that increased job demands can lead to higher levels of nurse strain (ß = 0.955, P < 0.001), whereas job resources were found that it can decrease strain (ß=-0.477, P = 0.047). Adequate job resources can enhance motivation directly (ß = 0.874, P < 0.001), subsequently reducing reaction time (ß=-0.148, P = 0.044) and improving night-shift alertness among ICU shift nurses. CONCLUSION: Enhancing ICU shift nurses' work motivation through bolstering job resources can boost night-shift alertness. However, it is noteworthy that, in this study, neither strain nor individual resources significantly influenced nurses' night-shift alertness. This may be attributed to the complexity of the ICU environment and individual differences. Future research should explore the relationship between these factors and nurses' work alertness.

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Histone modification is one of the key elements in epigenetic control and plays important roles in regulation of biological processes and disease development. Currently, records of human histone modifications with various levels of confidence in evidence are scattered in various knowledgebases and databases. In the present study, a curated catalogue of human histone modifications, CHHM, was obtained by manual retrieval, evidence assessment, and integration of modification records from 10 knowledgebases/databases and 3 complementary articles. CHHM contains 6612 nonredundant modification entries covering 31 types of modifications (including 9 types of emerging modifications) and 2 types of histone-DNA crosslinks, that were identified in 11 H1 variants, 21 H2A variants, 21 H2B variants, 9 H3 variants, and 2 H4 variants. For ease of visualization and accessibility, modification entries are presented with aligned protein sequences in an Excel file. Confidence level in evidence is provided for each entry. Acylation modifications contribute to the highest number of modification entries in CHHM. This supports that cellular metabolic status plays a very important role in epigenetic control. CHHM reveals modification hotspot regions and uneven distribution of the modification entries across the histone families. Such uneven distribution may suggest that a particular histone family is more susceptible to certain types of modifications. CHHM not only serves as an important and user-friendly resource for biomedical and clinical researches involving histone modifications and transcriptional regulation, but also provides new insights for basic researches in the mechanism of human histone modifications and epigenetic control.

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The complement system is the first defense line of the immune system. However, pathogens have evolved numerous strategies to evade complement attacks. Streptococcus suis is an important zoonotic bacterium, harmful to both the pig industry and human health. ApuA has been reported as a bifunctional amylopullulanase and also contributed to virulence of S. suis. Herein, we found that ApuA could activate both classical and alternative pathways of the complement system. Furthermore, by using bacterial two-hybrid, far-western blot and ELISA assays, it was confirmed that ApuA could interact with complement C3b. The interaction domain of ApuA with C3b was found to be its α-Amylase domain (ApuA_N). After construction of an apuA mutant (ΔapuA) and its complementary strain, it was found that compared to the wild-type strain (WT), ΔapuA had significantly increased C3b deposition and membrane attack complex formation. Additionally, ΔapuA showed significantly lower survival rates in human serum and blood and was more susceptible to engulfment by neutrophils and macrophages. Mice infected with ΔapuA had significantly higher survival rates and lower bacterial loads in their blood, lung and brains, compared to those infected with WT. In summary, this study identified ApuA as a novel factor involved in the complement evasion of S. suis and suggested its multifunctional role in the pathogenesis of S. suis.

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Pancreatic cancer remains one of the most aggressive and lethal malignancies worldwide, with a dismal 5-year relative survival rates of only 12%. Therefore, it is urgent to discover the key molecular markers to improve the therapeutic outcomes in pancreatic cancer. Herein, we first demonstrated that PPM1G is upregulated in pancreatic cancer and that PPM1G depletion decreases pancreatic cancer cell growth in vitro and in vivo. High PPM1G expression was linked to short overall survival of pancreatic cancer patients, which was further validated in the TCGA database. Moreover, by detecting Beclin 1, LC3-II, and SQSTM1/p62 expressions and observing autolysosome under transmission electron microscope, we discovered that PPM1G is a novel positive regulator of macroautophagy/autophagy. Furthermore, by using immunoprecipitation-mass spectrometry (IP-MS) analysis and following systemic molecular biology experiment, we demonstrated PPM1G promotes the autophagy and proliferation of pancreatic cancer by directly upregulating HMGB1. Additionally, patients with both high PPM1G and high HMGB1 exhibited poorer prognosis in our cohort. This study preliminarily investigated the possibility of PPM1G as a potential therapeutic target and prognostic biomarker in pancreatic cancer patients.

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Anaerobic co-digestion was conducted on the solid residues after three-phase separation of kitchen waste (KWS) and waste-activated sludge (WAS), the synergistic effects and process performance were studied during co-digestion at different ratios of KWS to WAS. KWS and WAS mix ratios of 0:1, 1:4, 1:3, 1:2, 1:1, 2:1, 3:1, 4:1 and 1:0 (based on TS). The results showed that a ratio of KWS to WAS of 1:1 got a very high methane recovery with a methane yield of 310.45 ± 30.05 mL/g VSadded. The highest concentration of free ammonia among all reaction systems was only 70.23 ± 5.53 mg/L, which was not enough to produce ammonia inhibition in the anaerobic co-digestion system. However, when the KWS content exceeded 50%, methane inhibition and prolongation of the lag phase were observed due to the accumulation of volatile fatty acids (VFAs), and during the lag phase. Microbial community analysis showed that various bacterial groups involved in acid production and hydrolysis were mainly dominated by phylum Firmicutes, Chloroflexi, Proteobacteria and Bacteroidetes. Hydrogenotrophic methanogen was found to dominate all archaeal communities in the digesters. Co-digestion of KWS with WAS significantly increased the relative abundance of Methanobacterium compared with anaerobic digestion of WAS alone.

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Platelet-derived growth factor receptor α (PDGFRα) is often considered as a general marker of mesenchymal cells and fibroblasts, but also shows expression in a portion of osteoprogenitor cells. Within the skeleton, Pdgfrα+ mesenchymal cells have been identified in bone marrow and periosteum of long bones, where they play a crucial role in participating in fracture repair. A similar examination of Pdgfrα+ cells in calvarial bone healing has not been examined. Here, we utilize Pdgfrα-CreERTM;mT/mG reporter animals to examine the contribution of Pdgfrα+ mesenchymal cells to calvarial bone repair through histology and single-cell RNA sequencing (scRNA-Seq). Results showed that Pdgfrα+ mesenchymal cells are present in several cell clusters by scRNA-Seq, and by histology a dramatic increase in Pdgfrα+ cells populated the defect site at early timepoints to give rise to healed bone tissue overtime. Notably, diphtheria toxin-mediated ablation of Pdgfrα reporter+ cells resulted in significantly impaired calvarial bone healing. Our findings suggest that Pdgfrα-expressing cells within the calvarial niche play a critical role in the process of calvarial bone repair.

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BACKGROUND: This study aimed to investigate functions of GLP-1R agonist by liraglutide (LIRA) and revealing the mechanism related to AGEs/RAGE in chondrocytes. METHODS: To illustrate potential effect of GLP-1R agonist on AGEs induced chondrocytes, chondrocytes were administrated by AGEs with LIRA and GLP-1R inhibitor exendin. Inflammatory factors were assessed using ELISA. Real-time PCR was used to evaluate the catabolic activity MMPs and ADAMTS mRNA level, as well as anabolic activity (aggrecan and collagen II). RAGE expression was investigated by Western blotting. TUNEL, caspase3 activity and immunofluorescence were performed to test the apoptotic activity. RESULTS: Our results showed that treatment with LIRA at > 100 nM attenuated the AGE-induced chondrocyte viability. Western bolt demonstrated that GLP-1R activation by LIRA treatment reduced RAGE protein expression compared with the AGEs groups. ELISA showed that LIRA hindered the AGEs-induced production of inflammatory cytokines (IL-6, IL-12 and TNF-α) in primary chondrocytes. AGEs induced catabolism levels (MMP-1, -3, -13 and ADAMTS-4, 5) are also attenuated by LIRA, causing the retention of more extracellular matrix (Aggrecan and Collagen II). TUNEL, caspase3 activity and immunofluorescence results indicated that LIRA inhibited the AGEs-induced production of inflammatory cytokines in primary chondrocytes and attenuated the caspase 3 level, leading to the reduced apoptotic activity. All the protective effects are reversed by exendin (GLP-1R blockers). CONCLUSIONS: The present study demonstrates for the first time that LIRA, an agonist for GLP-1R which is commonly used in type 2 diabetes reverses AGEs induced chondrocyte inflammation and apoptosis through suppressing RAGE signaling, contributing to reduced catabolism and retention of more extracellular matrix. The above results indicate the possible effect of GLP-1R agonist on treating OA.

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Objective: Observational studies have revealed a link between inflammatory bowel disease (IBD) and sarcopenia. However, it remains unclear whether this correlation between IBD and sarcopenia is causal. Methods: The genetic instrumental variables (IVs) associated with IBD and sarcopenia-related traits were derived from publicly available genome-wide association studies. We employed a two-sample bidirectional Mendelian randomization (MR) method. we obtained genetic IVs for five phenotypes from 34,652 cases in IBD, 27,432 cases in ulcerative colitis (UC), 212356 cases in crohn's disease (CD), 9336415 cases in low hand grip strength (LHGS), and 450243 cases in appendicular lean mass (ALM), respectively. The inverse variance weighting and other MR methods were used to explore the bidirectional causal relationship. Furthermore, we performed heterogeneity test, pleiotropy test, leave-one-out sensitivity test, and multivariate MR to evaluate the robustness of the results. Results: The forward MR results showed that the UC (OR=0.994, 95% CI: 0.9876-0.9998, P = 0.044) and CD (OR=0.993, 95% CI: 0.988-0.998, P = 0.006) was negatively correlated with ALM. In the reverse MR analysis, we also found that LHGS was negatively correlated with the IBD (OR=0.76, 95% CI: 0.61-0.94, P = 0.012) and CD (OR=0.53, 95% CI: 0.40-0.70, P <0.001). Besides, genetically predicted higher ALM reduced IBD (OR=0.87, 95% CI: 0.79-0.95, P = 0.002), UC (OR=0.84, 95% CI: 0.76-0.93, P = 0.001), and CD (OR=0.87, 95% CI: 0.77-0.99, P = 0.029). However, the results of other MR Analyses were not statistically different. Conclusions: We found genetically predicted UC and CD are causally associated with reduced ALM, and higher hand grip strength reduced IBD and CD risk, and higher ALM reduced IBDs risk. This MR study provides moderate evidence for a bidirectional causal relationship between IBD and sarcopenia.

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BACKGROUND: Accurate prognostic assessment is vital for the personalized treatment of endometrial cancer (EC). Although radiomics models have demonstrated prognostic potential in EC, the impact of region of interest (ROI) delineation strategies and the clinical significance of peritumoral features remain uncertain. Our study thereby aimed to explore the predictive performance of varying radiomics models for the prediction of LVSI, DMI, and disease stage in EC. METHODS: Patients with 174 histopathology-confirmed EC were retrospectively reviewed. ROIs were manually delineated using the 2D and 3D approach on T2-weighted MRI images. Six radiomics models involving intratumoral (2Dintra and 3Dintra), peritumoral (2Dperi and 3Dperi), and combined models (2Dintra + peri and 3Dintra + peri) were developed. Models were constructed using the logistic regression method with five-fold cross-validation. Area under the receiver operating characteristic curve (AUC) was assessed, and was compared using the Delong's test. RESULTS: No significant differences in AUC were observed between the 2Dintra and 3Dintra models, or the 2Dperi and 3Dperi models in all prediction tasks (P > 0.05). Significant difference was observed between the 3Dintra and 3Dperi models for LVSI (0.738 vs. 0.805) and DMI prediction (0.719 vs. 0.804). The 3Dintra + peri models demonstrated significantly better predictive performance in all 3 prediction tasks compared to the 3Dintra model in both the training and validation cohorts (P < 0.05). CONCLUSIONS: Comparable predictive performance was observed between the 2D and 3D models. Combined models significantly improved predictive performance, especially with 3D delineation, suggesting that intra- and peritumoral features can provide complementary information for comprehensive prognostication of EC.

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Purpose: Construct an exercise intervention program for patients with sarcopenic obesity. Material and Methods: Based on the COM-B theoretical model and evidence-based principles, the program was constructed using qualitative methods of literature analysis and Delphi method. The Delphi panel consisted of 15 experts from the fields of clinical medicine, rehabilitation medicine, medical technology, and nursing. Results: Fifteen experts were consulted, and the consultation recovery rate was 100%; the authority coefficient of the 1st round was 0.83, with coefficients of variation ranging from 0.00 to 0.27, and importance scores ranging from (4.13±1.13) to (5±0); the authority coefficient of the 2nd round was 0.82, with coefficients of variation ranging from 0.00 to 0.20, and importance scores ranging from (4.53±0.64) to (5±0); Kendall's harmony coefficient was 0.102, 0.115, respectively, and the differences were statistically significant(P < 0.05). The constructed exercise intervention program for patients with sarcopenic obesity included 4 primary indicators, 12 secondary indicators, and 28 tertiary indicators. Conclusion: The constructed exercise intervention program for patients with sarcopenic obesity is scientific, feasible and generalizable, and can provide useful reference for related personnel to develop exercise programs for patients with sarcopenic obesity.

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Palladium hydrides (PdHx) are pivotal in both fundamental research and practical applications across a wide spectrum. PdHx nanocrystals, synthesized by heating in dimethylformamide (DMF), exhibit remarkable stability, granting them widespread applications in the field of electrocatalysis. However, this stability appears inconsistent with their metastable nature. The substantial challenges in characterizing nanoscale structures contribute to the limited understanding of this anomalous phenomenon. Here, through a series of well-conceived experimental designs and advanced characterization techniques, including aberration-corrected scanning transmission electron microscopy (AC-STEM), in situ X-ray diffraction (XRD), and time-of-flight secondary ion mass spectrometry (TOF-SIMS), we have uncovered evidence that indicates the presence of C and N within the lattice of Pd (PdCxNy), rather than H (PdHx). By combining theoretical calculations, we have thoroughly studied the potential configurations and thermodynamic stability of PdCxNy, demonstrating a 2.5:1 ratio of C to N infiltration into the Pd lattice. Furthermore, we successfully modulated the electronic structure of Pd nanocrystals through C and N doping, enhancing their catalytic activity in methanol oxidation reactions. This breakthrough provides a new perspective on the structure and composition of Pd-based nanocrystals infused with light elements, paving the way for the development of advanced catalytic materials in the future.

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Nonalcoholic fatty liver disease (NAFLD) is one of the common causes of chronic liver disease in the world. The problem of NAFLD had become increasingly prominent. However, its pathogenesis is still indistinct. As we all know, NAFLD begins with the accumulation of triglyceride (TG), leading to fatty degeneration, inflammation and other liver tissues damage. Notably, structure of nucleoporin 85 (NUP85) is related to lipid metabolism and inflammation of liver diseases. In this study, the results of researches indicated that NUP85 played a critical role in NAFLD. Firstly, the expression level of NUP85 in methionine-choline-deficient (MCD)-induced mice increased distinctly, as well as the levels of fat disorder and inflammation. On the contrary, knockdown of NUP85 had the opposite effects. In vitro, AML-12 cells were stimulated with 2 mm free fatty acids (FFA) for 24 h. Results also proved that NUP85 significantly increased in model group, and increased lipid accumulation and inflammation level. Besides, NUP85 protein could interact with C-C motif chemokine receptor 2 (CCR2). Furthermore, when NUP85 protein expressed at an extremely low level, the expression level of CCR2 protein also decreased, accompanied with an inhibition of phosphorylation of phosphoinositol-3 kinase (PI3K)-protein kinase B (AKT) signaling pathway. What is more, trans isomer (ISRIB), a targeted inhibitor of NUP85, could alleviate NAFLD. In summary, our findings suggested that NUP85 functions as an important regulator in NAFLD through modulation of CCR2.

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The conversion of methane under ambient conditions has attracted significant attention. Although advancements have been made using active oxygen species from photo- and electro- chemical processes, challenges such as complex catalyst design, costly oxidants, and unwanted byproducts remain. This study exploits the concept of contact-electro-catalysis, initiating chemical reactions through charge exchange at a solid-liquid interface, to report a novel process for directly converting methane under ambient conditions. Utilizing the electrification of commercially available Fluorinated Ethylene Propylene (FEP) with water under ultrasound, we demonstrate how this interaction promote the activation of methane and oxygen molecules. Our results show that the yield of HCHO and CH3OH can reach 467.5 and 151.2 µmol ⋅ gcat -1, respectively. We utilized electron paramagnetic resonance (EPR) to confirm the evolution of hydroxyl radicals (⋅OH) and superoxide radicals (⋅OOH). Isotope mass spectrometry (MS) was employed to analyze the elemental origin of CH3OH, which can be further oxidized to HCHO. Additionally, we conducted density functional theory (DFT) simulations to assess the reaction energies of FEP with H2O, O2, and CH4 under these conditions. The implications of this methodology, with its potential applicability to a wider array of gas-phase catalytic reactions, underscore a significant advance in catalysis.

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Intense inflammatory response impairs bone marrow mesenchymal stem cell (BMSC)-mediated bone regeneration, with transforming growth factor (TGF)-ß1 being the most highly expressed cytokine. However, how to find effective and safe means to improve bone formation impaired by excessive TGF-ß1 remains unclear. In this study, we found that the expression of orphan nuclear receptor Nr4a1, an endogenous repressor of TGF-ß1, was suppressed directly by TGF-ß1-induced Smad3 and indirectly by Hdac4, respectively. Importantly, Nr4a1 overexpression promoted BMSC osteogenesis and reversed TGF-ß1-mediated osteogenic inhibition and pro-fibrotic effects. Transcriptomic and histologic analyses confirmed that upregulation of Nr4a1 increased the transcription of Wnt family member 4 (Wnt4) and activated Wnt pathway. Mechanistically, Nr4a1 bound to the promoter of Wnt4 and regulated its expression, thereby enhancing the osteogenic capacity of BMSCs. Moreover, treatment with Nr4a1 gene therapy or Nr4a1 agonist Csn-B could promote ectopic bone formation, defect repair, and fracture healing. Finally, we demonstrated the correlation of NR4A1 with osteogenesis and the activation of the WNT4/ß-catenin pathway in human BMSCs and fracture samples. Taken together, these findings uncover the critical role of Nr4a1 in bone formation and alleviation of inflammation-induced bone regeneration disorders, and suggest that Nr4a1 has the potential to be a therapeutic target for accelerating bone healing.

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A dual Multi-Dimensional Integration (dMDI) method was proposed and demonstrated for T2* and R2* mapping. By constructing and jointly using both the original MDI term and an inversed MDI term, T2* and R2* mapping can be performed independently with intrinsic background noise suppression and spike elimination, allowing for high quantitative accuracy and robustness over a wide range of T2*. dMDI was compared to original MDI and curve fitting methods in terms of quantitative specificity, accuracy, reliability and computational efficiency. All methods were tested and compared via simulation and in vivo data. With high signal-to-noise-ratio (SNR), the proposed dMDI method yielded T2*and R2* values similar to curve fitting methods. For low SNR and background noise signals, the dMDI yielded low T2* and R2* values, thus effectively suppressing all background noise. Virtually zero spikes were observed in dMDI T2* and R2* maps in all simulation and imaging results. The dMDI method has the potential to provide improved and reliable T2* and R2* mapping results in routine and SNR-challenging scenarios.

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BACKGROUND: China is experiencing an aging population, leading to a significant demand for "Internet + nursing services" tailored for elderly individuals. However, there are many risk problems in the process of nurse service, which hinder the development of the service, and a scale is needed to assess the risk problems faced by nurses in "Internet + nursing services" for the elderly. OBJECTIVE: The purpose of this study is to develop an assessment scale for risk factors and outcomes related to nurses' involvement in the "Internet + Nursing Service" for the elderly and to assess its reliability and validity. METHODS: Based on literature analysis, focus group, the Delphi method, and a presurvey, we designed an initial scale. The initial scale comprised two sections: risk factors and risk outcomes for nurses. In January and February of 2023, nurses engaged in "Internet + nursing services" for the elderly in Shanxi Province were chosen through a convenience sampling technique for a questionnaire survey. Subsequently, item analysis and exploratory factor analysis were employed to refine and develop a test version of the scale further. A follow-up questionnaire survey was carried out in March and April 2023 using a similar approach. The reliability and validity of the scale were assessed through confirmatory factor analysis, culminating in the formation of the final scale. RESULTS: The initial survey yielded 244 valid responses. The cumulative variance contributions of the two segments from the exploratory factor analysis were 84.584% and 90.089%, respectively. A subsequent survey garnered 220 valid responses. The confirmatory factor analysis results indicated: χ2/df = 2.086, comparative fit index (CFI) = 0.918, normative fit index (NLI) = 0.855, root mean square of residuals (RMR) = 0.045, and root mean square of error of approximation (RMSEA) = 0.070. These results demonstrate good structural, convergent, and discriminant validity. The content validity index at the item level (I-CVI) ranged between 0.875 and 1.000, while the content validity index at the scale level (S-CVI/Ave) was 0.941. Cronbach's alpha coefficient for the entire scale stood at 0.970. Moreover, the scale exhibited a split-half reliability of 0.876 and a retest reliability of 0.980 (p < 0.01). CONCLUSION: The risk factors and risk outcomes associated with nurses involved in "Internet + nursing services" for elderly individuals, as developed in this study, demonstrate strong reliability and validity. They are well suited to the Chinese national context.

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Pathogenic bacteria have evolved many strategies to evade surveillance and attack by complements. Streptococcus suis is an important zoonotic pathogen that infects humans and pigs. Hyaluronidase (HylA) has been reported to be a potential virulence factor of S. suis. However, in this study, it was discovered that the genomic region encoding HylA of the virulent S. suis strain SC19 and other ST1 strains was truncated into four fragments when aligned with a strain containing intact HylA and possessing hyaluronidase activity. As a result, SC19 had no hyaluronidase activity, but one truncated HylA fragment, designated as HylS,' directly interacted with complement C3b, as confirmed by western ligand blotting, pull-down, and ELISA assays. The deposition of C3b and membrane attack complex (MAC) formation on the surface of a HylS'-deleted mutant (ΔhylS') was significantly increased compared to wild-type SC19. In human sera and whole blood, ΔhylS' survival was significantly reduced compared to that in SC19. The resistance of ΔhylS' to macrophages and human polymorphonuclear neutrophil PMNs also decreased. In a mouse infection model, ΔhylS' showed reduced lethality and lower bacterial load in the organs compared to that of SC19. We conclude that the truncated hyaluronidase HylS' fragment contributes to complement evasion and the pathogenesis of S. suis.

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Lumbar spinal canal stenosis is primarily caused by ligamentum flavum hypertrophy (LFH), which is a significant pathological factor. Nevertheless, the precise molecular basis for the development of LFH remains uncertain. The current investigation observed a notable increase in thrombospondin-1 (THBS1) expression in LFH through proteomics analysis and single-cell RNA-sequencing analysis of clinical ligamentum flavum specimens. In laboratory experiments, it was demonstrated that THBS1 triggered the activation of Smad3 signaling induced by transforming growth factor ß1 (TGFß1), leading to the subsequent enhancement of COL1A2 and α-SMA, which are fibrosis markers. Furthermore, experiments conducted on a bipedal standing mouse model revealed that THBS1 played a crucial role in the development of LFH. Sestrin2 (SESN2) acted as a stress-responsive protein that suppressed the expression of THBS1, thus averting the progression of fibrosis in ligamentum flavum (LF) cells. To summarize, these results indicate that mechanical overloading causes an increase in THBS1 production, which triggers the TGFß1/Smad3 signaling pathway and ultimately results in the development of LFH. Targeting the suppression of THBS1 expression may present a novel approach for the treatment of LFH.

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