Jiujiang First People's Hospital

The clinical significance of Candida infection in patients with acute exacerbations of chronic obstructive pulmonary disease (AECOPD) remains poorly defined. This multicenter cohort study analyzed 11,925 hospitalized AECOPD patients from ten centers in China, grouped by Candida infection status. Subgroups were analyzed by Candida species and invasiveness. Primary outcome was 3-year all-cause mortality; secondary outcomes included in-hospital mortality, invasive mechanical ventilation (IMV), non-invasive ventilation (NIV), and intensive care unit (ICU) admission. Propensity score matching and Cox regression were used to adjust for confounders. Candida-positive AECOPD patients showed significantly worse short-term outcomes, including increased IMV (7.2% vs 3.8%) and NIV use (31.8% vs 18.2%), more ICU admissions (12.7% vs 8.9%), and prolonged hospitalization (15.97 vs 11.16 days, P < 0.001). No significant difference was observed in 30-day mortality between groups (aHR 1.13, 95% CI 0.63-2.03), but 3-year mortality was significantly higher (41.2% vs 30.5%, P < 0.001) in Candida positive group. Subgroup analyses showed no significant differences by species or invasiveness. Respiratory Candida infection is associated with worse short-term clinical outcomes and increased 3-year mortality in AECOPD patients, but is not an independent risk factor for in-hospital mortality. Neither species nor invasiveness classification offered prognostic value. Screening may identify high-risk patients, but evidence does not support species-specific or β-d-glucan (BDG)-guided therapy among this population.

With the rapid integration of artificial intelligence (AI) into educational practice, its influence on teachers’ innovative teaching behavior has attracted growing attention. However, less is known about the dual psychological mechanisms through which AI use may both facilitate and constrain teaching innovation. Drawing on the cognitive appraisal theory of stress, this study examined whether teachers’ challenge and threat appraisals mediate the relationship between AI use and innovative teaching behavior, and whether school innovation support moderates these pathways. A nationwide survey was conducted among 1275 primary and secondary school teachers in China. Data were collected using validated measures of AI use, challenge appraisal, threat appraisal, innovative teaching behavior, and school innovation support, and were analyzed through confirmatory factor analysis, structural equation modeling, and bootstrapped moderated mediation analysis. The results indicated that AI use was positively associated with both challenge appraisal and threat appraisal. In turn, challenge appraisal was positively associated with innovative teaching behavior, whereas threat appraisal was negatively associated with it. Challenge and threat appraisals both served as significant mediating pathways linking AI use to innovative teaching behavior. In addition, school innovation support moderated the effects of AI use on both appraisals: higher levels of support strengthened the positive association between AI use and challenge appraisal, but unexpectedly also amplified its association with threat appraisal. These findings highlight the double-edged nature of AI use in educational settings and suggest that cognitive appraisal is an important mechanism through which AI use relates to teachers’ innovative teaching behavior. The study further implies that schools should provide supportive conditions that encourage challenge appraisal while carefully managing the pressures that may intensify threat appraisal.

Colon cancer is a common malignancy of the digestive system, tumor disease, and its prevalence in China shows a consistently increasing trend. This study aimed to investigate the role of surfactant associated 2 (SFTA2) in colorectal cancer (CRC) and its molecular mechanism involving ferroptosis.Colon cancer tissues were obtained from patients and normal volunteers from our hospital, and a mouse model of CRC was established using azoxymethane (AOM)/dextran sulfate sodium (DSS) induction.SFTA2 expression was significantly up-regulated at both the messenger RNA (mRNA) and protein levels in CRC tissues and cell lines. Patients with high SFTA2 expression exhibited a shorter survival time compared to those with low SFTA2 expression. SFTA2 was found to be expressed in cancer cells of CRC patients, associated with key signaling molecules.Sh-SFTA2 reduced cancer proliferation in the mice model of CRC. SFTA2 up-regulation promoted cell proliferation of CRC. SFTA2 down-regulation promoted cell proliferation of CRC. SFTA2 up-regulation reduced oxidative stress and ferroptosis of CRC. SFTA2 up-regulation reduced ferroptosis of CRC through mitochondrial damage-tricarboxylic acid cycle (TAC). SFTA2 down-regulation suppressed nuclear factor erythroid 2-related factor 2 (Nrf2) expression in the model of CRC. SFTA2 up-regulation reduced Nrf2 ubiquitination in the model of CRC. Nrf2 reversed the effects of si-SFTA2 on ferroptosis of CRC. Furthermore, SFTA2 down-regulation suppressed Nrf2 expression, while SFTA2 up-regulation decreased Nrf2 ubiquitination in the CRC model. Nrf2 was shown to reverse the pro-ferroptotic effects of si-SFTA2, indicating that SFTA2 activates the Nrf2 pathway by inhibiting its ubiquitination, thereby reducing mitochondrial damage and TCA cycle disruption in CRC.SFTA2 induced the Nrf2 pathway to reduce mitochondrial damage-TAC of the CRC model through the inhibition of Nrf2 ubiquitination. SFTA2 is thus a potentiallyeffective therapeutic strategy for patients with CRC or other cancers.

To investigate the significance of DCUN1D5 in colorectal cancer (CRC) progression and determine the underlying mechanism. We analyzed DCUN1D5 expression levels in CRC tissues using the TCGA and GEO databases and conducted immunohistochemistry and qPCR in retrieved CRC tissues. shRNA-mediated knockdown of DCUN1D5 in CRC cell lines was performed to investigate its effects on cell growth and motility. In addition, DCUN1D5-mediated promotion of CUL1 neddylation was examined using immunoblotting, the antitumor effects of inhibiting the neddylation pathway was evaluated using the inhibitor MLN4924, and the effects of silencing DCUN1D5 and MLN4924 treatment were validated in vivo using xenograft models. DCUN1D5 was found to be significantly overexpressed in CRC tissues, and its knockdown impaired CRC cell proliferation and migration, which was associated with reduced CUL1 neddylation. Inhibition of the neddylation pathway using the NEDD8 inhibitor MLN4924 supported these observations. In vivo, DCUN1D5 silencing and MLN4924 treatment led to reduced tumor growth and metastasis. DCUN1D5 contributes to the growth and motility of CRC in vitro and in vivo.

BACKGROUNDPostoperative recurrence remains a major challenge in gastric cancer management. Monitoring serum biomarkers such as carcinoembryonic antigen (CEA) may enable earlier detection of recurrence and improve patient outcomes.AIMTo evaluate postoperative serum CEA expression and its efficacy in predicting gastric cancer recurrence.METHODSThis retrospective study analyzed clinical data from 120 patients with primary gastric cancer treated between January 2022 and January 2023. Patients were categorized into recurrence and non-recurrence groups. Serum levels of CEA, alpha-fetoprotein (AFP), and carbohydrate antigen 19-9 (CA19-9) were measured at one week, three months, and six months postoperatively. Logistic regression identified independent risk factors for recurrence, Pearson correlation assessed the association with recurrence timing, and receiver operating characteristic (ROC) curves evaluated the predictive performance of combined CEA and AFP levels.RESULTSDuring 24 months of follow-up, 39 patients (32.50%) experienced recurrence. No significant baseline differences were observed between groups (P > 0.05). CEA, AFP, and CA19-9 levels at one week were comparable between groups (P > 0.05), whereas levels at three and six months were significantly higher in the recurrence group (P < 0.05). Logistic regression identified postoperative CEA and AFP as independent risk factors for recurrence (P < 0.05). Pearson correlation showed a negative association between CEA and AFP levels and recurrence interval (P < 0.05). ROC curve analysis demonstrated that combined CEA and AFP yielded an area under the curve of 0.826, with specificity of 94.36% and sensitivity of 90.50%, outperforming either marker alone (P < 0.05).CONCLUSIONDynamic postoperative monitoring of serum CEA and AFP enables early prediction and detection of gastric cancer recurrence.

Chronic pain, marked by nociceptive sensitization and maladaptive neuroplasticity, affects 30% of the global population with escalating socioeconomic burdens. Epidemiological data show a 2-3-fold increase in neuropsychiatric co-morbidities among individuals with chronic pain, where epigenetic dysregulation serves as a key mechanism linking ongoing pain to emotional disorders. This review systematically explores epigenetic signatures in supraspinal integration hubs, notably the limbic-paralimbic networks and prefrontal regulatory circuits. The identified epigenetic signatures encompass dysregulation of DNA methyltransferases (DNMTs), RNA modifications, histone post-translational modifications and locus-specific alterations, including aberrant methylation at the brain-derived neurotrophic factor (BDNF), opioid μ receptor and transient receptor potential ankyrin 1 (TRPA1) gene loci. Additionally, they involve dysfunction of the glucocorticoid receptor (GR)/corticotropin-releasing factor (CRF) axis via epigenetic modulation. Building on these findings, we evaluate therapeutic strategies addressing epigenetic dysregulation. While preclinical data demonstrate the efficacy of histone deacetylase (HDAC) and DNMT inhibitors, clinical translation faces significant barriers, including limited blood-brain barrier permeability. Notably, our analysis highlights the benefits of combining pharmacological interventions with non-invasive neuromodulation for enhanced co-morbidity management. Looking forward, this review proposes innovative approaches that leverage CRISPR-based chromatin editing platforms, biomimetic nanocarriers for neuron-specific delivery and closed-loop neuromodulation integrating real-time biomarker feedback, collectively establishing a precision medicine framework for pain or neuropsychiatric co-morbidities.

School bullying has been recognized as a risk factor for the growth of malevolent creativity. However, its underlying mechanisms and moderators remain under-explored. This study examined the effects of school bullying on malevolent creativity, focusing on the chain mediating effects of anger and hostile attribution bias. Using convenience sampling, we surveyed 1,038 middle school students with the Delaware Bullying Victimization Scale, the Anger Rumination Scale, the Hostile Attribution Bias Scale, and the Malevolent Creativity Scale. A Chain mediation model was estimated in Mplus written by Bengt Muthén and Linda Muthén of the University of California, Los Angeles. Results showed that school bullying significantly is positively associated with malevolent creativity (β = 0.525, p < 0.001, 95% CI=[0.492,1.016]). Besides, school bullying also indirectly was associated with malevolent creativity through anger (β = 0.017, p < 0.001, CI=[0.037, 0.231]), hostile attribution bias (β = 0.318, p < 0.001, CI=[0.042, 0.135]), and the chain-mediated pathway between the above two (β = 0.135, p < 0.001, [0.002,0.009]). These findings indicate that, among victimized adolescents, anger and hostile attribution bias amplify the positive association between school bullying and malevolent creativity. These findings suggest that anger and hostile attribution bias play crucial roles in the relationship between school bullying and malevolent creativity, providing important insights for interventions.

Precision medicine calls for molecular tools that enable high-resolution imaging at depth, accurate lesion localisation and controllable therapy. Small-molecule dyes are widely used in biomedical imaging and treatment, yet their limited photostability, susceptibility to quenching in physiological environments and rapid in vivo clearance continue to hinder clinical translation. Coordination-driven supramolecular chemistry offers a promising route to address these shortcomings. However, progress in in vivo delivery and biodistribution, real-time visual tracking and therapeutic evaluation has often been constrained by short-wavelength excitation and emission. In this context, second near-infrared (NIR-II) metal supramolecular dyes assembled directly from NIR-II ligands have been rapidly developed, furnishing platforms with strong NIR-II performance and tunable photophysical behaviour. This perspective summarises design and construction strategies for NIR-II metal supramolecular dyes, highlights their key photophysical characteristics, and surveys representative applications in cancer, antibacterial and cardiovascular theranostics and imaging. We further discuss outstanding challenges for clinical translation and outline future opportunities for NIR-II metal supramolecular dyes in precision medicine.

Mitochondrial-associated programmed cell death signatures (MPCDS) have emerged as critical indicators of cancer progression and treatment response. In hepatocellular carcinoma (HCC), mitochondrial dysfunction and dysregulated PCD pathways are prevalent, yet the application of MPCDS in HCC remains underexplored. This study aimed to identify and characterize the HCC MPCDS, evaluating its prognostic value. We integrated data from TCGA-LIHC and HCCDB18 cohorts, identifying 351 HCC MPCDS genes through differential expression analysis and intersection with known MPCDS genes. We constructed and validated a prognostic model based on 56 out of the 351 genes, regarding their remarkable influence in HCC survival (Cox p-value < 0.0001) using Cox regression and machine learning algorithms. Our analysis revealed distinct clusters with significant differences in survival outcomes, immune landscapes, somatic mutation, and drug sensitivity. The machine learning model demonstrated robust predictive accuracy for HCC prognosis (1-, 3-, 5-year AUC = 0.976, 0.984, 0.976). Clinical HCC samples were collected for experimental validation of the top-ranked genes, KIF2C and CDK4, using qRT-PCR. The results confirmed that the genes were significantly upregulated in tumor lesions. These findings underscore the importance of HCC MPCDS as a prognostic biomarker and highlight its potential for guiding personalized treatment strategies in HCC.