1.Association of personality and sleep quality with psychological distress of junior and senior high school stduents
Chinese Journal of School Health 2026;47(1):65-69
Objective:
To explore the effects of personality and sleep quality with psychological distress of junior and senior high school stduents, so as to provide a reference basis for precise interventions of junior and senior high school students mental health.
Methods:
In October 2023, a convenience sampling method was used to select 9 034 students aged 12-17 from Shiyan City as the study subjects. The Pittsburgh Sleep Quality Index (PSQI) and Kessler Psychological Distress Scale (K10) were used to collect information on sleep quality and psychological distress of junior and senior high school stduents. Between group comparison was conducted by using t-test and Chi-square test. Generalized linear models were employed to analyze the interaction and joint effects of personality and sleep quality on psychological distress.
Results:
The generalized linear model analysis showed that the interaction between personality and sleep quality on psychological distress was statistically significant of junior and senior high school students(effect size=0.80, P <0.01). The general linear model analysis indicated that, after adjusting for variables such as age, gender, screen time, and daily sitting time with the extroverted and good sleep quality group as the reference, the introverted and poor sleep quality group had the largest mean difference in psychological distress scores (difference=0.51, P <0.05). When stratified by sleep quality, psychological distress scores were higher in the introverted and neutral personality groups with both poor and good sleep quality compared to the extroverted group (poor sleep quality: introverted difference=3.71, neutral difference=1.14; good sleep quality: introverted difference=2.23, neutral difference=0.57, all P < 0.05). When stratified by personality, psychological distress scores were higher in the poor sleep quality groups for introverted, neutral, and extroverted individuals compared to their good sleep quality counterparts (differences=8.66, 7.83, 7.34, all P < 0.05 ).
Conclusions
Personality and sleep quality have interactive and joint effects on psychological distress of junior and senior high school stduents. Personalized psychological interventions should be developed based on personality and sleep quality.
2.The SMAD-Pathway Mediates HMGB1-Induced Proliferation and Metastatic Progression in Cutaneous Squamous Cell Carcinoma Cells
De-De LIAN ; Xue Mei LI ; Yu-Xi JIA ; Ming-Wei ZHOU ; Xiang-Ru CHEN ; Yang-Yang TIAN ; Min LI ; Ming-Hui SUN ; Ye ZHAO ; Hong-Jun LI ; Qing-Ling ZHANG
Annals of Dermatology 2026;38(1):51-58
Background:
High-mobility group box protein 1 (HMGB1) is a chromatin-binding protein involved in arthritis, ischemia, sepsis, atherosclerosis, neurodegenerative disorders, meningitis, and cancer. HMGB1 exhibits dual roles in cancer, acting as either a tumor suppressor or oncoprotein depending on context.
Objective:
This research aimed to elucidate HMGB1’s functional significance in cutaneous squamous cell carcinoma (cSCC).
Methods:
We overexpressed HMGB1 in cSCC cell lines using recombinant adenovirus and examined its effects on cell proliferation, colony formation, and cell migration.
Results:
Immunohistochemical analysis revealed elevated HMGB1 expression levels in cSCC tissue relative to normal epidermis. To assess the influence of HMGB1, we employed recombinant adenoviruses expressing HMGB1 to transduce SCC cell lines (SCC12 and SCC13). Enhanced HMGB1 expression significantly promoted cellular proliferation and colony formation capacity.Notably, HMGB1 overexpression elevated the levels of proliferation regulators, including P63, SOX2, CDK4 and CDK6. Furthermore, HMGB1 overexpression substantially enhanced tumor invasiveness, accompanied by upregulation of epithelial-mesenchymal transition (EMT) biomarkers. Mechanistically, overexpression of HMGB1 enhanced transforming growth factor-β signaling by increasing phosphorylation of SMAD2/3, the key mediators of EMT.
Conclusion
These data imply that HMGB1 acts as a tumor-promoting factor in cSCC.
3.SIRT5 Potentiates Hepatocarcinogenesis by Modulating Protein Acylation in Mice
Yu ZHANG ; Feng-Rui REN ; Jia-Yun LI ; Xiang-Yu CHEN ; Zi-Yi WANG ; Qi SUN ; Jun-Cheng ZHAO ; Ye ZHANG ; Zhen HUANG ; Hao HU ; Tao-Tao WEI ; Min XIAO
Progress in Biochemistry and Biophysics 2026;53(6):1712-1722
ObjectiveHepatocellular carcinoma (HCC) represents 90% of all primary liver cancers. The main risk factors associated with HCC include viral hepatitis (B and/or C), alcohol abuse, and metabolic dysfunction-associated steatotic liver disease (MASLD), which progressively advance to liver fibrosis, cirrhosis, and ultimately evolve into HCC. Surgical resection represents the most effective treatment for HCC, while recent advances in immunotherapy, including immune checkpoint inhibitors and adoptive cell therapies, have provided improved treatment prospects for patients with unresectable HCC. However, the complex metabolic heterogeneity of HCC limits the therapeutic efficacy. Metabolic intermediates acyl-CoA not only provide energy and substrates for numerous biochemical reactions but also serve as donors for protein lysine acylation, a major class of post-translational modification (PTM). Therefore, a deeper understanding of the molecular mechanisms underlying protein lysine acylation and hepatocarcinogenesis is urgently needed. MethodsThe levels of protein lysine acylation and silence information regulator 5 (SIRT5) expression levels in clinical HCC samples were analyzed by Western blot. Quantitative malonylome and succinylome of HCC samples were analyzed by antibody-based affinity enrichment coupled with tandem mass spectrometry. The proliferation of HCC cells was analyzed with Cell Counting Kit-8 (CCK-8) assays, the apoptosis was quantified by Annexin V-FITC/propidium iodide (PI) staining coupled with flow cytometry, and the ability of cells to migrate was assayed by Transwell assays. The enzymatic activity of glutathione S-transferase Mu 1 (GSTM1) was quantified. Transgenic mice with hepatic overexpression of SIRT5 were constructed using CRISPR-Cas9, and primary hepatocarcinogenesis was induced by administration of diethylnitrosamine. ResultsWestern blot analysis indicated that the expression level of SIRT5 was elevated in clinical samples from HCC patients, and the levels of lysine malonylation, glutarylation, and succinylation were significantly reduced in HCC tissues. Knockout of SIRT5 in MHCC-97H and MHCC-97L hepatoma cells suppressed cell proliferation, and increased the percentage of apoptotic cells significantly. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses of the differentially malonylome and succinylome of HCC samples revealed significant enrichment in two major classes of biological processes: core energy metabolism (e.g., glycolysis/gluconeogenesis, tricarboxylic acid metabolic process, fatty acid beta oxidation) and detoxification and oxidative stress response (e.g., response to toxic substance, chemical carcinogenesis, reactive oxygen species (ROS)). SIRT5 removes malonylation from lysine residues in GSTM1 and restores its detoxification activity, which is crucial for the survival of hepatocytes under stressed conditions. More importantly, in vivo experiment indicated that hepatic-specific overexpression of SIRT5 in mice accelerated diethylnitrosamine-induced liver fibrosis and hepatocarcinogenesis, indicating the critical role of SIRT5 in HCC progression. ConclusionThis study highlights the previously unrecognized SIRT5-GSTM1 axis as a key regulator in hepatocarcinogenesis, and suggests a potential target for the treatment of patients with HCC.
4.Research on Electrical Impedance and Microwave Dual-modality Tomography Algorithm Based on Conditional Diffusion Models
Jin-Zhen LIU ; Xiang-Qian MENG ; Hui XIONG ; Li-Min ZHOU ; Chun-Chan LI
Progress in Biochemistry and Biophysics 2026;53(6):1780-1792
ObjectiveStroke poses a heavy burden due to its high mortality and morbidity rates. Accurate and real-time detection of lesions is pivotal for prompt clinical intervention and favorable prognosis. Electrical impedance tomography (EIT) and microwave tomography (MWT) have emerged as compelling alternatives for stroke screening, owing to their non-ionizing, non-invasive and portable nature. EIT provides information on tissue conductivity, and MWT offers high sensitivity to changes in dielectric properties. However, single-modality imaging is inherently limited, EIT suffers from low sensitivity to deep-seated tissues and severe ill-posedness of inverse problems, whereas MWT is challenged by strong nonlinearity in inverse scattering and susceptibility to modeling errors. Consequently, the clinical utility of standalone EIT or MWT for stroke diagnosis remains constrained by poor spatial resolution and imaging artifacts. To improve the accuracy and robustness of stroke imaging, a dual-modality fusion conditional denoising diffusion probabilistic model (DM-DDPM) was proposed for high-precision dual-modality image reconstruction. MethodsA dual-encoder network with a symmetric architecture and independently trained parameters was constructed to extract heterogeneous features separately from EIT boundary voltage measurements and MWT scattered field signals. Attentional feature fusion (AFF) is employed to integrate complementary information from the two modalities adaptively, generating robust fused priors that suppress redundant noise while preserving key physical characteristics. Subsequently, the fused priors are embedded into a Transformer-based diffusion model via a cross attention mechanism to guide the reverse denoising process. This approach effectively reduces artifacts and enhances the stability of conductivity distribution reconstruction. Time step embedding is introduced to enable the network to perceive the diffusion stage and further improve the accuracy of noise prediction. ResultsSimulated experiments demonstrated that DM-DDPM significantly outperforms single-modality and multi-modality networks under various noise levels. A head model simulation dataset was constructed based on COMSOL Multiphysics, and tests were carried out under 50 dB, 40 dB and 30 dB signal-to-noise ratio levels. At 30 dB, the average relative error (RE) was below 0.20, while the structural similarity index measure (SSIM) and correlation coefficient (CC) remained above 0.90 and 0.89, respectively. Compared with single-modality and multi-modality networks, artifacts were significantly reduced, lesion edges were clearer, and localization was more accurate. The model maintains high reconstruction quality and strong robustness for single, double, and triple lesions simultaneously. Furthermore, physical experiments were conducted using a 16-electrode EIT system and a 16-antenna MWT system with asynchronous data acquisition. These experiments confirmed the feasibility of the method in real-world scenarios and demonstrated that it can robustly reconstruct simulated lesions despite environmental interference and measurement noise, validating its reliability for practical clinical applications. ConclusionThe proposed method effectively combines complementary dual-modality information with a conditional diffusion model. Low accuracy and poor noise resistance in single-modality imaging were effectively addressed, while the noise amplification issue caused by direct multimodal data fusion was avoided. The proposed algorithm exhibits strong anti-noise interference ability and high imaging stability in both simulation and physical experiments. Precise localization of stroke lesions with different quantities was achieved, providing a high-precision, and practical technical support for clinical stroke detection.
5.Effect of Guilu Taohong Formula on semen quality and spermatogenic cell apoptosis in a varicocele model of rats
Biao WANG ; Yang YANG ; Ze-rui QIU ; En-min FENG ; Xiang ZHAO ; Neng WANG ; Xin HUANG ; Qun-fang LIN ; Qing ZHOU
National Journal of Andrology 2025;31(2):150-156
Objective:To observe the effect of Guilu Taohong Formula on semen quality in varicocele(VC)models of rats,and to explore its possible mechanism.Methods:Forty-eight male SD rats were randomly divided into four groups(sham group,model group,Guilu Taohong Formula group and L-carnitine group).After the establishment of models,the rats were treated with intra-gastric administration for eight consecutive weeks.The general condition of the rats was observed.After the gavage,the testicular and epididymal indices were calculated.Semen quality was assessed using an automatic semen analyzer.Apoptosis of testicular cells was assessed by TUNEL staining.And the expression levels of B-cell lymphocytoma-2(Bcl-2),Bcl-2-associated X protein(Bax)and cys-teine aspartate protease-3(caspase-3)in testicular tissue were detected by Western blot.Results:Compared with the sham group,testicular index,epididymal index,sperm concentration,the percentage of progressive motility of sperm(PR%)and the expression level of Bcl-2 decreased in model group(P<0.01).An increased apoptosis rate of spermatogenic cells and the expression levels of Bax and caspase-3 proteins were observed in model group as well(P<0.01).Compared with the model group,the testicular index,epidid-ymal index,sperm concentration,PR%and the expression level of Bcl-2 in Guilu Taohong Formula group increased significantly(P<0.05,P<0.01).A decreased apoptosis rate of spermatogenic cells and the expression levels of Bax and caspase-3 proteins were de-tected in Guilu Taohong Formula group as well(P<0.01).Similarly,the L-carnitine group showed increased testicular index,epidid-ymal index,sperm concentration,PR%and the expression level of Bcl-2 protein(P<0.05,P<0.01),where showed decreased ap-optosis rate of spermatogenic cells and the expression levels of Bax and caspase-3 proteins compared with model group(P<0.01,P<0.05).Conclusion:Guilu Taohong Formula improves semen quality in VC model rats and reduces the apoptosis rate of spermato-genic cells in testicular tissue,which may be related to the promotion of Bcl-2 protein expression and the inhibition of Bax and caspase-3 protein expression levels.
6.ATIC Promotes Glioma Cell Proliferation by Regulating Cell Cycle Progression Through p21/p-Rb Pathway
Xiaobai WU ; Min XIANG ; Ruonan GUO
Acta Medicinae Universitatis Scientiae et Technologiae Huazhong 2025;54(5):656-664
Objective To investigate 5-aminoimidazole-4-carboxamide ribonucleotide formyl transferase/inosine monophos-phate cyclohydrolase(ATIC),a key regulator of metabolism and cell proliferation,to explore its role in glioma proliferation,e-valuate its association with patient prognosis,and elucidate the underlying molecular mechanisms.Methods Using data from The Cancer Genome Atlas(TCGA),Genotype-Tissue Expression(GTEx),and Chinese Glioma Genome Atlas(CGGA)databas-es,we analyzed differential ATIC expression between tumor tissues and adjacent normal tissues in glioma patients,as well as its correlation with clinical features including pathological grade,isocitrate dehydrogenase(IDH)mutation status,and chromosome 1p/19q deletion.ATIC was knocked down using siRNA transfection.The effect of ATIC on the proliferation of glioma cell lines(LN229,U373,and U251)was evaluated using EdU,CCK-8,and colony formation assays.Furthermore,ATIC overexpression via plasmid transfection was analyzed in conjunction with flow cytometry and Western blotting analysis to assess cell cycle pro-gression and cyclin-related protein expression.Results ATIC expression was significantly elevated in glioma tissues compared to adjacent normal tissues(P<0.01).Patients with high ATIC expression exhibited shorter overall survival(OS)and were asso-ciated with higher pathological grades,wild-type IDH status,and the presence of chromosome 1p/19q deletion.Compared with U373 and U251 glioma cell lines,LN229 and U87 glioma cell lines demonstrated higher ATIC expression.In siRNA-mediated ATIC knockdown models(siATIC-LN229,siATIC-U373),cell proliferation was suppressed as demonstrated by EdU,CCK-8,and colony formation assays,whereas ATIC overexpression in U251 cells promoted proliferation.Flow cytometry revealed G1-phase arrest and impaired S-phase progression in siATIC-LN229 cells.Conversely,ATIC overexpression in U251 cells decreased G1-phase accumulation and increased S-phase progression.Mechanistically,ATIC knockdown decreased the expression of phos-phorylated Rb(p-Rb),upregulated p21,and downregulated key cyclin-related proteins essential for G1/S transition.In contrast,ATIC overexpression facilitated the G1/S transition through p21 downregulation and enhanced phosphorylation of Rb pro-tein.Conclusion High ATIC expression is associated with poor clinical outcomes in glioma patients and may promote tumor progression through regulation of the p21-Rb signaling pathway.Therefore,ATIC represents a promising biomarker for both clinical diagnosis and prognosis in glioma.
7.Expression Level and Proliferation-regulating Function of KCNJ14 in Glioma Cells
Ruonan GUO ; Min XIANG ; Xiaobai WU
Acta Medicinae Universitatis Scientiae et Technologiae Huazhong 2025;54(5):665-671,693
Objective To determine KCNJ14 gene expression in human glioma cells and assess its impact on U251 cell pro-liferation,while exploring the potential mechanism involved.Methods The protein expression levels of KCNJ14 in different hu-man glioma cell lines(U87,U251,SNB19,and LN229)were analyzed by Western blotting.KCNJ14 was knocked down and over-expressed in U251 cells using siRNA and plasmid transfection,respectively.Subsequently,protein expression levels,cell prolif-eration capacity,and the regulation of cell cycle related proteins were measured in each group.The association between KCNJ14 mRNA expression and clinical survival prognosis in glioma patients was evaluated through statistical analysis of public databas-es.Results KCNJ14 protein expression varied across different human glioma cell lines,with the highest level observed in U251 cells.Inhibition of KCNJ14 suppressed U251 cell proliferation and impaired cell cycle progression.Bioinformatics analysis re-vealed that KCNJ14 mRNA expression was significantly associated with clinical characteristics and survival outcomes in glioma patients.Conclusion KCNJ14 exhibits differential expression in glioma cells and is negatively associated with patient prognosis.Mechanistically,it may regulate glioma cell proliferation by modulating cell cycle related proteins.
8.A comparative study on the payment reform for therapeutic value of dominant diseases of Traditional Chinese Medicine at provincial level
Qing-yan WU ; Li-sha LIU ; Min-xi GONG ; Li-xiang ZHAI
Chinese Journal of Health Policy 2025;18(8):63-70
Objective:Through the comparative analysis of the payment program for the therapeutic value of Traditional Chinese Medicine dominant diseases in 8 provinces,we found the shortcomings of the existing program and put forward the perfect policy suggestions.Methods:Comparative analysis of the core content of the programs in various places,the selection of disease types,efficacy evaluation indexes,the application of the payment link and the protection mechanism.Results:The fragmentation of existing programs is an obvious problem,the specific content settings of each item are quite different,reflecting differences in the understanding of the core content of the program,the existence of inconsistent understanding of Chinese medicine's therapeutic value,the failure to link the payment standard to the results of the therapeutic value evaluation,and the lack of recognition of the value of Chinese medicine's technical labor,among other problems.Conclusions:We can select disease types based on the prominent advantages of Traditional Chinese medicine,learn from the evaluation framework of western medicine value-based medical care,construct the evaluation system of Chinese medicine therapeutic value,and carry out"equal price"payment based on the"same effect"of health results,set performance indicators and payment standards in stages,realize the whole process management of disease,and enhance the Traditional Chinese Medicine's therapeutic value,and promote the development of Traditional Chinese Medicine inheritance and innovation.
9.Angiotensin Ⅱ type 1a receptor knockout ameliorates high-fat diet induced cardiac dysfunction by attenuating ferroptosis
Xiao-xiao YIN ; Jin WANG ; Ai-yun LI ; Li-qing WANG ; Min GOU ; Xiang-ying JIAO
Chinese Pharmacological Bulletin 2025;41(11):2105-2112
Aim To investigate the effect of angioten-sin Ⅱ type 1a receptor(AT1aR)knockout on cardiac dysfunction in rats with obesity and its possible molecu-lar mechanism.Methods SD rats(n=24)were used to generated the whole-body AT1 aR-deficiency rats by sgRNA and the CRISPR/Cas9 system,and the obesity model was constructed by feeding with high-fat diet(HFD).They were divided into four groups:wildtype(WT)and knockout(KO)groups with nor-mal feeding and their respective high-fat diets groups.Color ultrasound diagnostic instrument was uses to e-valuate the cardiac function;oil red O staining was a-dopted to stain the myocardial lipids;RT-PCR was used to detect the levels of GPX4 and Ptgs2 genes in myocardial tissue.Western blot was employed to detect the expression of GPX4,ferritin,Nrf2,HO-1 and NQO1 in rat myocardial tissue.ELISA and other kits were used to determine the lipid contents in serum and myocardium.Results It was found that high-fat feed-ing caused cardiac dysfunction,serum lipid disorders,oxidative stress and ferroptosis in SD rats.However,these changes were attenuated in AT1aR knockout rats fed with high-fat diet.Furthermore,compared with WT-HFD group,KO-HFD rats showed enhanced acti-vation of the Nrf2/HO-1 pathway in the myocardium,reduced ferroptosis,decreased lipid accumulation,and reduced cardiac dysfunction.Conclusion AT1aR knockout can improve HFD-induced cardiac dysfunc-tion by enhancing antioxidant capacity and reducing the degree of ferroptosis.
10.Effect of recombinant human natriuretic peptide combined with dopamine on CysC,Hcy and cardiac function in patients with severe heart failure
Rui MENG ; Xiang-nan LI ; Hui-min LIU ; Zhong YI
Chinese Journal of cardiovascular Rehabilitation Medicine 2025;34(2):221-225
Objective:To explore the effect of recombinant human brain natriuretic peptide(rhBNP)combined with dopamine on cystatin C(CysC),homocysteine(Hcy)and cardiac function in patients with severe heart failure(HF).Methods:This randomized controlled study enrolled 110 severe HF patients admitted in Aerospace Center Hospital between December 2021 and December 2022.They were divided into control group(n=55,nitroglycerin combined dopamine)and combined treatment group(n=55,rhBNP combined dopamine).Each group received corresponding therapy based on basic treatment for one week.Therapeutic effect,levels of CysC,Hcy,left ventric-ular end-systolic diameter(LVESd),left ventricular end-diastolic diameter(LVEDd),left ventricular ejection fraction(LVEF),and incidence of adverse reactions were compared between two groups.Results:Compared with patients in control group,those in combined treatment group had significant higher total effective rate(81.82%vs.58.18%)and LVEF[(54.68±4.59)%vs.(44.79±4.37)%],and significant lower CysC[(1.02±0.19)mg/L vs.(1.40±0.21)mg/L],Hcy[(15.98±2.17)μmol/L vs.(21.05±2.82)μmol/L],LVESd[(35.13±3.51)mm vs.(41.71±3.28)mm]and LVEDd[(41.33±4.26)mm vs.(50.51±4.37)mm](P<0.01 all).There was no significant difference in total incidence of adverse reactions between two groups(16.36%vs.7.27%,P=0.180).Conclusion:rhBNP combined with dopamine could significantly improve the clinical therapeutic effect,im-prove levels of CysC,Hcy and cardiac function with good safety in the treatment of severe HF.


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