河北公安警察职业学院

Mental health literacy remains insufficient among university students, even as mental health difficulties grow more prevalent in this population. Blended learning approaches that combine digital and face-to-face components may hold advantages over conventional delivery methods, though empirical evidence supporting their effectiveness is still limited. We conducted a randomized educational evaluation study with 300 university students randomly assigned to either a blended learning program (n = 150) or waitlist control group (n = 150). The eight-week educational curriculum integrated self-paced online modules with weekly face-to-face facilitation sessions. Primary outcomes included educational achievements in mental health literacy measured by the Mental Health Literacy Scale (MHLS), with secondary educational measures assessing stigma awareness, help-seeking knowledge, and factual understanding. Assessments occurred at baseline, immediate post-educational program, and three-month follow-up. Compared with controls, the educational program group showed statistically significant improvements with large effect sizes for total mental health literacy (Cohen’s d = 1.82), though such magnitudes warrant cautious interpretation given the waitlist control design and reliance on self-report measures. Gains were observed across all subscales, including disorder recognition (d = 1.68), knowledge (d = 1.76), and attitudes (d = 1.35), and these improvements remained significant at three-month follow-up. Digital engagement and learning satisfaction partially mediated program effects. No significant moderation was detected by gender, baseline literacy levels, or mental health history. Within this single-institution context, a culturally adapted blended learning program was associated with significant improvements in mental health literacy among university students, with effects persisting over three months. These findings suggest that integrating online flexibility with face-to-face interaction holds promise for mental health education, although replication across diverse settings is needed before broader claims can be made.

The upstream regulators that initiate early transcriptional responses to intestinal stress remain poorly defined. Here, we used germ-free wild-type, Lao1-knockout (LAO1KO), and Lao1/Il4i1 double-knockout (DKO) mice to determine how two l-amino acid oxidases shape acute transcriptional responses to dextran sulfate sodium (DSS). RNA-sequencing performed 24 h after DSS exposure revealed that Lao1 accounted for 80.1% of DSS-induced transcriptional changes, while Il4i1 contributed an additional 14.7%, collectively accounting for 94.8% of the total response. Pathway analysis revealed that Lao1 was required for inducing oxidative phosphorylation (OXPHOS), ATP synthesis, and RNA splicing, while also driving the suppression of nuclear transport and protein localization pathways. At baseline, Lao1 regulated dicarboxylic acid, folic acid, and pteridine metabolism. In contrast, Il4i1 showed minimal baseline activity but was specifically required during DSS exposure to induce lipid metabolism genes and restrain protein homeostasis responses. These findings identify Lao1 as a primary metabolic regulator of early intestinal stress responses, with Il4i1 providing additional stress-specific control. Together, these enzymes link amino acid oxidation to mitochondrial transcriptional programs during intestinal injury.

C 5 H 7 N 3 O 6 Zn, triclinic, P 1 ‾ $\overline{1}$ (no. 2), a = 4.7459(12) Å, b = 6.7043(17) Å, c = 13.648(3) Å, α = 98.303(4)°, β = 98.134(4)°, γ = 103.303(3)°, V = 411.22(18) Å 3 , Z = 2, R gt ( F ) = 0.0244, w R ref ( F 2 ) = 0.0862, T = 296(2) K.

Urbanization has intensified the complexity of urban crimes, rendering traditional empirical prevention models insufficient for precise governance. This study proposes ST-GBT (Spatio-Temporal Gradient Boosting Tree), a multi-source data fusion framework for crime hotspot prediction, using China's LLM-driven street/community crime spatio-temporal dataset to support data-driven public safety decisions. Core predictive features-crime types, spatio-temporal periodicity, spatial grid aggregation, and lag features-are extracted via data cleaning and feature engineering, emphasizing multi-source fusion. The spatio-temporal model, built with Gradient Boosting, is evaluated via regression and classification. The experimental results show that the model's prediction of the number of crimes has a root mean square error (RMSE) of 1.39, a coefficient of determination (R2) of 0.83, and an area under the ROC curve (AUC) over 0.9 for the identification of hot spots (the top 20% of high-crime grids). Feature importance analysis shows that historical crime data (lagging features) and hourly periodic features contribute the most to prediction (60% cumulatively). This study offers a tool for crime control, with fusion strategies and evaluation methods informing other public safety prediction research.

Dysfunction of Schwann cells, including cell apoptosis, autophagy inhibition, dedifferentiation, and pyroptosis, is a pivotal pathogenic factor in induced diabetic peripheral neuropathy (DPN). Histone deacetylases (HDACs) are an important family of proteins that epigenetically regulate gene transcription by affecting chromatin dynamics. Here, we explored the effect of HDAC1 on high glucose-cultured Schwann cells. HDAC1 expression was increased in diabetic mice and high glucose-cultured RSC96 cells, accompanied by cell apoptosis. High glucose also increased the mitochondrial pathway apoptosis-related Bax/Bcl-2 and cleaved caspase-9/caspase-9 ratios and decreased endoplasmic reticulum response-related GRP78, CHOP, and ATF4 expression in RSC96 cells (P < 0.05). Furthermore, overexpression of HDAC1 increased the ratios of Bax/Bcl-2, cleaved caspase-9/caspase-9, and cleaved caspase-3 and reduced the levels of GRP78, CHOP, and ATF4 in RSC96 cells (P < 0.05). In contrast, knockdown of HDAC1 inhibited high glucose-promoted mitochondrial pathway apoptosis and suppressed the endoplasmic reticulum response. Moreover, RNA sequencing revealed that U4 spliceosomal RNA was significantly reduced in HDAC1-overexpressing RSC96 cells. Silencing of U4 spliceosomal RNA led to an increase in Bax/Bcl-2 and cleaved caspase-9 and a decrease in CHOP and ATF4. Conversely, overexpression of U4 spliceosomal RNA blocked HDAC1-promoted mitochondrial pathway apoptosis and inhibited the endoplasmic reticulum response. In addition, alternative splicing analysis of HDAC1-overexpressing RSC96 cells showed that significantly differential intron retention (IR) of Rpl21, Cdc34, and Mtmr11 might be dominant downstream targets that mediate U4 deficiency-induced Schwann cell dysfunction. Taken together, these findings indicate that HDAC1 promotes mitochondrial pathway-mediated apoptosis and inhibits the endoplasmic reticulum stress response in high glucose-cultured Schwann cells by decreasing the U4 spliceosomal RNA/IR of Rpl21, Cdc34, and Mtmr11.