AIM:To investigate the protective effects of Dendrobium officinale polysaccharide(DOP)on high glucose-induced apoptosis in retinal capillary pericytes and its potential mechanism involving mitochondrial function.METHODS:Retinal capillary pericytes were allocated into five groups: normal control(NC), high glucose(HG), and three DOP treatment groups(low, DOP-L; medium, DOP-M; high, DOP-H). Pericyte ultrastructure was analyzed using transmission electron microscopy(TEM). Apoptotic rate was quantified via Annexin V-FITC staining. Mitochondrial transmembrane potential was assessed using the JC-1 probe. Quantitative real-time polymerase chain reaction(qRT-PCR)and Western blot were employed to measure expression levels of cytochrome C(Cyt C), B-cell lymphoma 2(Bcl-2), Bcl-2-associated X protein(Bax), Caspase-9, and Caspase-3, respectively.RESULTS:Compared to the NC group, pericytes exposed to HG exhibited significant mitochondrial damage, elevated apoptotic rate, increased mRNA and protein expression of Cyt C, Bax, Caspase-9, and Caspase-3(all P<0.01), alongside a marked reduction in mitochondrial transmembrane potential and expression of Bcl-2 mRNA and protein(all P<0.01). In contrast, DOP treatment groups(DOP-M,DOP-H)dose-dependently ameliorated mitochondrial damage, reduced apoptotic rate, downregulated Cyt C, Bax, Caspase-9, and Caspase-3 expression, enhanced mitochondrial transmembrane potential, and upregulated Bcl-2 expression relative to the HG group(all P<0.05).CONCLUSION:DOP attenuates high glucose-induced apoptosis and mitochondrial injury in retinal capillary pericytes. The underlying mechanism may involve the restoration of mitochondrial transmembrane potential.

Background In 2021, chronic obstructive pulmonary disease (COPD) emerged as the forth leading cause of death in the world. However, the impact of air pollutants on COPD is still inconsistent across current studies. Objective To analyze the relationship between ambient sulfur dioxide (SO₂) exposure and hospital admissions for COPD in Lanzhou, and to examine the modified effects of SO₂ across different genders, age groups, and seasons. Methods A total of 20718 hospital admission records for COPD were collected from Lanzhou between 2016 and 2020, alongside synchronized data on SO₂ concentration and meteorological variables. A generalized additive model integrated with a distributed lag nonlinear model was used to assess the relationship and the lag effects between SO₂ exposure and COPD admissions. Potential confounders, including meteorological factors, day-of-the-week effect, and holidays, were controlled for, with a maximum lag period set at 7 d. Two-pollutant models and sensitivity analyses were conducted to ensure robustness. Results are expressed as relative risks (RR) with 95% confidence intervals (95%CI). Results During the study period, the average daily number of COPD admissions was 11.34±7.03. The average mass concentration of SO₂ was (23.72±12.35) μg·m⁻³. SO₂ exposure was positively correlated with COPD admissions; specifically, each 10 μg·m⁻³ increase in SO₂ concentration was associated with an RR of 1.440 (95%CI: 1.317, 1.573). Stratified analyses found that at a cumulative lag of 7 d, the RRs were higher among females, individuals aged ≥65 years, and during the cold season. Conversely, no significant increase in COPD admission risk related to SO₂ was observed during the warm season. For every 10 μg·m⁻³ increase in SO₂ concentration, the RR was 1.483 (95%CI: 1.311, 1.678) for females, 1.441 (95%CI: 1.311, 1.583) for those aged > 65 years， and 1.595 (95%CI: 1.313, 1.937) during the cold season. Conclusion Short-term exposure to ambient SO₂ exposure in Lanzhou is associated with an increased risk of COPD admission. The association is more pronounced among females, the elderly (aged> 65 years) and during the cold season.

Processed electroencephalogram (EEG) indices, such as the Bispectral Index, have markedly influenced anesthesia practice as they translate brain activity into simple numerical indices. Nevertheless, as the manufacturing algorithms are not disclosed, the underlying neurophysiology remains obscured. Additionally, these indices are often affected by electromyographic contamination, pharmacological variability, and patient-specific EEG heterogeneity. In contrast, an EEG spectrogram, or density spectral array, preserves the frequency- and time-resolved structures of cortical oscillations. This information is presented in a form that is both physiologically meaningful and clinically interpretable. In this review, we trace the evolution of anesthesia from an index-based to a spectrogram-guided approach, and summarize the clinical rationale for adopting the latter. Key applications of this approach include the use of frontal alpha power as a biomarker of cortical stability and postoperative brain health, the identification of nociceptive arousal through alpha dropout and beta or delta arousal patterns, and individualized titration of multimodal or age-specific anesthetic management. Although current devices lack standardized quantitative alpha metrics and have limited sensitivity for low-frequency brain wave components, structured EEG education programs have proven to be effective in terms of fostering spectrogram literacy among anesthesiologists. By combining neurophysiological precision with bedside practicality, the EEG spectrogram represents a pivotal advance toward individualized, mechanism-based, and brain-protective anesthesia, transforming anesthetic monitoring from mere algorithmic abstraction to cortical insight.

Background: Surgeons face challenges in selecting cost-effective and biologically active agents for rotator cuff healing, given the numerous commercial products available, such as polydeoxyribonucleotide (PDRN) and atelocollagen (ATC). However, the precise efficacy of PDRN and ATC in rotator cuff healing remains debatable, and there is currently a lack of studies directly comparing the effects of the 2 agents on repaired cuff tendons. Therefore, the purpose of this study was to compare the efficacy of PDRN and ATC on bone-to-tendon interface (BTI) healing using a chronic rotator cuff tear (RCT) model in rabbits. Methods: Forty-eight rabbits were randomly divided into 3 groups. To create chronic RCT models, transected tendons were left untreated for 6 weeks, and then were repaired in a transosseous manner with PDRN and ATC injection into the repair site according to group allocation (group A: saline, group B: PDRN, group C: ATC; n = 16 per group). Genetic and immunofluorescence analyses were performed at 4 weeks after surgery. Furthermore, genetic, histologic, and biomechanical analyses were performed at 12 weeks after surgery. Results: At 4 weeks after surgery, ATC-injected shoulders showed the highest mRNA expression levels of collagen type I alpha 1 and aggrecan compared to the other 2 groups (p < 0.001 and p = 0.002, respectively). Meanwhile, there was more preliminary fibrocartilaginous matrix formation in the ATC-injected group. At 12 weeks after surgery, ATC-injected shoulders demonstrated better collagen fiber continuity and orientation, denser collagen fibers, a more mature bone-to-tendon junction, and greater fibrocartilage layer formation compared to the other 2 groups (all p < 0.001). Furthermore, ATC-injected shoulders also demonstrated a significantly higher load-to-failure value (40.4 ± 4.5 N/kg) than the remaining groups (group A, 26.7 ± 3.0 N/kg; group B, 32.8 ± 4.2 N/kg; p < 0.001). Conclusions ATC demonstrated superior efficacy in promoting BTI healing following surgical repair in a chronic RCT model of rabbits.

Objective Mitochondrial ribosomal proteins(MRPs)that may affect bladder cancer cell proliferation were screened out through bioinformatics analysis. The relevant mechanism of pathogenesis of bladder cancer was explored and verified with clinical samples, cell experiments and functional experiments. Methods Differentially expressed genes(DEGs)in bladder cancer were identified through differential analysis of RNA-seq data downloaded from The Cancer Genome Atlas(TCGA)database. Subsequently, the intersection of these DEGs with MRPs was obtained to screen out MRPs differentially expressed in bladder cancer. Through survival analysis, MRPs possessing both prognostic value and differential expression were identified, and used as the objects of subsequent research. The relative expressions of MRPs were verified using 33 bladder cancer samples from Zhongnan Hospital of Wuhan University. Bladder cancer cells(T24 and UM-UC-3)were transfected with small interfering RNA(siRNA)and plasmids to achieve gene knockdown and overexpression. Changes in the proliferative capacity of bladder cancer cells following knockdown of the genes identified in survival analysis and simultaneous overexpression of cyclin D1(CCND1)were analyzed with 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide(MTT)assay and colony formation assay. The cell cycle status and reactive oxygen species(ROS)level were detected with flow cytometry. The efficiency of gene knockdown or overexpression, as well as changes in the expression of cell cycle-related proteins were verified with quantitative real-time polymerase chain reaction(qRT-PCR)and Western blotting. Results MRPL12 was screened out through bioinformatics and prognosis analysis, which was highly expressed in bladder cancer cells and correlated with poor prognosis. GSEA analysis suggested its association with oxidative phosphorylation, MYC and E2F pathways. When MRPL12 was knocked down, the proliferation of bladder cancer cells weakened and G1 phase arrest occurred. Western blotting showed that the expression of CCND1 and cyclin dependent kinase 4(CDK4)decreased after MRPL12 knockdown. In contrast, overexpression of CCND1 partially rescued the decreased proliferative capacity caused by MRPL12 knockdown and alleviated the G1 phase arrest of cells. Additionally, the ROS level in bladder cancer cells increased when MRPL12 was knocked down. Conclusion MRPL12 is highly expressed in bladder cancer cells and may affect cell proliferation through the cell cycle and mitochondrial function, showing potential application prospects.

Against the backdrop of the "New Medical Education" initiative by the Ministry of Education, higher medical education faces an urgent need to reconstruct its talent cultivation system. Taking the Laboratory Animal Science course at Shandong University of Traditional Chinese Medicine as an example, this paper systematically explores how to construct a teaching system featuring deep integration of scientific research and education, aiming to address the disconnection between theory and practice and the lack of innovative thinking among students in traditional teaching. The construction of this system is based on three pillars: first, the establishment of a high-level, interdisciplinary faculty team that strongly supports teaching innovation; second, reliance on the Laboratory Animal Center of Shandong University of Traditional Chinese Medicine and the Shandong Provincial Engineering Research Center for Prevention and Treatment of Major Brain Diseases with Traditional Chinese Medicine to provide the necessary facilities; third, a systematic restructuring of teaching content and modes through the "multidisciplinary, multi-format, and multilevel" integration approach. The reform has yielded remarkable results, particularly evident in the increase in students' scientific research and innovation capabilities: the proportion of student projects approved at the provincial level or above in undergraduate innovation training programs significantly increased from 11.1% before the reform to 41.6%. Furthermore, student teams have won gold and silver awards in national competitions such as the "National Undergraduate Innovation Forum for Basic Medical Sciences and Experimental Design" and the "National College Students' Medical Innovation Competition". Additionally, the teaching team's faculty members serving as chief editors and editorial board members of the national planning textbook Laboratory Animal Science published by People's Medical Publishing House mark the nationwide recognition of the course construction achievements. Practice has shown that this integrated system effectively transforms scientific research resources into educational advantages, providing an effective pathway for cultivating top-notch talents in traditional Chinese medicine with solid practical skills and advanced innovative capabilities. It also offers a replicable model for teaching reforms in peer institutions.

ObjectiveTo investigate the impact of melanoma-associated antigen D4 （MAGED4） on the malignant biological behavior of hepatocellular carcinoma （HCC）， providing experimental evidence for its evaluation as a potential therapeutic target in HCC. MethodsGenes positively correlated with MAGED4 expression in HCC were screened using the LinkedOmics database， followed by GO functional and KEGG pathway enrichment analyses. Endogenously low-expressing SMMC-7721 and Huh7 cells were selected， with normal hepatic LO2 cells serving as controls. Stable overexpression cell lines were established via lentiviral infection （MAGED4 overexpression group）， with RT-PCR and Western blot validating overexpression efficiency. The effects of MAGED4 overexpression on cell proliferation， cell cycle distribution， migration， and adhesion were systematically analyzed using CCK-8 assays， flow cytometry， scratch healing assays， Transwell migration assays， and cell adhesion assays. ResultsBioinformatics analysis indicated that MAGED4 co-expressed genes were significantly enriched in biological processes closely associated with tumor proliferation and metastasis， including cell-cell adhesion， extracellular matrix organization， and the PI3K-Akt signaling pathway. A stable MAGED4 overexpression cell model was successfully established. In vitro functional assays demonstrated that MAGED4-overexpressing SMMC-7721 and Huh7 cells exhibited a mesenchymal-like morphology， whereas LO2 cells maintained an epithelial-like morphology. Compared with the empty-virus control groups， the MAGED4-overexpressing groups showed significantly increased proliferative activity （48 h： t=3.887， 22.070， 8.866， all P<0.05； 72 h： t=3.231， 23.840， 9.848， all P<0.05； 96 h： t=5.123， 49.800， 5.909， P<0.05， P<0.01， P<0.05）， wound healing rates （12 h： F=40.90， 44.00， 200.50， all P<0.001； 24 h： F=112.00， 34.89， 249.20， all P<0.001）， and numbers of migrated cells （F=239.20， 59.79， 132.80， all P<0.001）， along with significantly decreased numbers of adherent cells （F=73.65， 85.91， 138.00， all P<0.001）， while no significant differences were observed in cell cycle phase distribution in all three cell lines. ConclusionMAGED4 enhances proliferation and migration while suppressing adhesion in both HCC and normal hepatocytes， however， induces mesenchymal-like morphological changes exclusively in HCC cells， suggesting that MAGED4 is capable of driving HCC progression and may serve as a potential therapeutic target for HCC.

The Expert Consensus on Clinical Application of Qinbaohong Zhike Oral Liquid in Treatment of Acute Bronchitis and Acute Attack of Chronic Bronchitis （GS/CACM 337-2023） was released by the China Association of Chinese Medicine on December 13^th， 2023. This expert consensus was developed by experts in methodology， pharmacy， and Chinese medicine in strict accordance with the development requirements of the China Association of Chinese Medicine （CACM） and based on the latest medical evidence and the clinical medication experience of well-known experts in the fields of respiratory medicine （pulmonary diseases） and pediatrics. This expert consensus defines the application of Qinbaohong Zhike oral liquid in the treatment of cough and excessive sputum caused by phlegm-heat obstructing lung， acute bronchitis， and acute attack of chronic bronchitis from the aspects of applicable populations， efficacy evaluation， usage， dosage， drug combination， and safety. It is expected to guide the rational drug use in medical and health institutions， give full play to the unique value of Qinbaohong Zhike oral liquid， and vigorously promote the inheritance and innovation of Chinese patent medicines.

Objective To explore the correlation between the expression of serum microRNA(miR)-1298-5p,miR-625-5p,and miR-155 with the degree of Helicobacter pylori(Hp)infection in elderly gastric cancer patients.Methods From January 2021 to November 2023,120 elderly patients with gastric cancer admitted to the hospital from January 2021 to November 2023 were selected as the gastric cancer group,and 130 non-gas-tric cancer patients who underwent gastroscopy were selected as the control group.The expression levels of miR-1298-5p,miR-625-5p and miR-155 in serum were detected by fluorescence quantitative PCR(qPCR).Car-bon 13 urea breath test was used to detect the positive rate of Hp infection in two groups,and the degree of Hp infection in elderly patients with gastric cancer were evaluated.Receiver operating characteristic(ROC)curve was applied to analyze the diagnostic value of serum miR-1298-5p,miR-625-5p,and miR-155 expression levels for Hp infection in elderly gastric cancer patients.Pearson method was applied to analyze the correlation between serum miR-1298-5p,miR-625-5p,miR-155 expression and positive rate of Hp infection in elderly gas-tric cancer patients.Results Compared with the control group,the expression levels of miR-1298-5p and miR-625-5p in serum of gastric cancer group decreased(P＜0.05),while the positive rate of Hp infection and the expression level of serum miR-155 increased(P＜0.05).The expression levels of serum miR-1298-5p and miR-625-5p in elderly gastric cancer patients with Hp grade Ⅰ,Ⅱ,and Ⅲ infection were lower than those without Hp infection,while the expression level of miR-155 was higher(P＜0.05).Patients with poor differ-entiation,lymph node metastasis,and TNM stage Ⅲ-Ⅳ had lower expressions of serum miR-1298-5p and miR-625-5p(P＜0.05),and higher expression of miR-155(P＜0.05)than those with moderate-high differen-tiation,no lymph node metastasis,and TNM stage Ⅰ-Ⅱ.The expression levels of serum miR-1298-5p and miR-625-5p were negatively correlated with the positive rate of Hp infection in elderly patients with gastric cancer(r=-0.443,-0.386,both P＜0.001),and the expression levels of serum miR-155 were positively correlated with the positive rate of Hp infection(r=0.525,P＜0.001).The area under the curve(AUC)of serum miR-1298-5p,miR-625-5p and miR-155 combined diagnosis of Hp infection in elderly gastric cancer pa-tients was higher than that of single diagnosis(P＜0.05).Conclusion The expression levels of miR-1298-5p and miR-625-5p in serum of elderly gastric cancer patients with Hp infection decrease,while the expression level of miR-155 increases.These three factors are related to the degree of Hp infection and have good diag-nostic value for the occurrence of Hp infection.

Objective To investigate the protective effects of paeonol(PAE)on autophagy in human neuroblastoma cells(SH-SY5Y)induced by overexpression of α-synuclein(α-Syn),and to explore its related mechanism.Methods SH-SY5Y cells served as control group,while those induced with A53T-α-Syn mutation were used as model group.Additional groups included PAE(150 μg/ml)group,3-MA(1 mmol/L)group,and PAE(150 μg/ml)+3-MA(1 mmol/L)group.Cell viability was assessed using CCK-8 method,cell morphology was observed under an optical microscope,and protein expressions of α-Syn,LC3-Ⅱ,p62,Beclin-1,phosphorylated c-Jun N-terminal kinase(p-JNK),and p-Bcl-2 were determined by Western blotting.Results Compared with control group,model control exhibited decreased cell survival(P＜0.01),increased α-Syn expression(P＜0.001),reduced expression of autophagy-related proteins LC3-Ⅱ and Beclin-1(P＜0.01,P＜0.05),elevated autophagy substrate protein p62(P＜0.05),and decreased expression of autophagy pathway-related proteins p-JNK and Bcl-2(P＜0.05,P＜0.01).Compared with model group,PAE group showed increased cell survival(P＜0.01),decreased α-Syn and p62 protein expression(P＜0.01,P＜0.05),and increased expression of LC3-Ⅱ,Beclin-1,p-JNK and Bcl-2(P＜0.05).Compared with PAE group,3-MA+PAE group demonstrated increased α-Syn expression(P＜0.05).Conclusions PAE could attenuate the injury of SH-SY5Y cells induced by A53T-α-Syn and eliminate over-expressed α-Syn by activating autophagy pathway,which may be associated with the upregulation of JNK/Bcl-2 mediated autophagy pathway.