Objective To investigate the effect of knockdown PRTN3 on polarization phenotype and anti-tumor function of macrophages in breast cancer. Methods A mouse monocyte/macrophage cell line(RAW264.7) with knockdown of PRTN3 was constructed. The mRNA and protein levels of PRTN3 were detected by RT-qPCR and flow cytometry. Macrophages were co-cultured with tumor cells, and the polarization phenotypes of macrophages were detected by flow cytometry, and the mRNA levels of polarization and cytokines related genes were detected by RT-qPCR. The tumor phagocytosis and tumor killing ability of macrophages were determined by in vitro phagocytosis assay and tumor killing assay. The effect of macrophages with PRTN3 knockdown on tumor progression and metastasis was compared in an orthotopic transplantation model of mouse breast cancer. Results The mRNA and protein levels of PRTN3 in the RAW264.7 cell line with stable knockdown of PRTN3 were significantly decreased(P＜0.01). Knockdown of PRTN3 in RAW264.7 cells upregulated the expression of M1 phenotype-related genes(CD80, CD86, iNOS, IL-1β, IL-6 and TNF-α)(P＜0.05). After macrophages co-culture with tumor cells, macrophages with knockdown of PRTN3 upregulated the expression of M1 phenotype-related genes(CD80, CD86, iNOS, IL-1β, IL-6 and TNF-α)(P＜0.01). Knockdown of PRTN3 enhanced the phagocytosis(P＜0.05) and tumor killing ability(P＜0.05) of macrophages in vitro. Adoptive transfusion of PRTN3-knockdown macrophages into tumor-bearing mice inhibited the growth of in situ breast cancer and reduced lung metastasis(P＜0.05). Conclusions PRTN3 regulates phenotypic polarization of macrophages, and knockdown of PRTN3 enhances the anti-tumor function of macrophages.

Objective To investigate the effect of ergothioneine(EGT) on tissue metabolism in middle-aged and aged mice. Methods Nine-month-old middle-aged and aged C57BL/6J mice were selected to be gavaged with EGT aqueous solution at the dose and frequency of 35 mg EGT per kg body weight every two days. The control group was gavaged with the same amount of water. Both groups were fed with EGT-free diet. After 7 weeks, the liver, kidney, and small intestine of mice were collected, and untargeted metabolomics analysis was performed using ultra-performance liquid chromatography-mass spectrometry(UHPLC-MS). The differential metabolites were selected for KEGG metabolic pathway enrichment analysis. Results Compared with the control group, the abundances of metabolites related to redox balance in liver, kidney and small intestine of middle-aged and aged mice treated with EGT did not change significantly. However, taurine and hypotaurine metabolism in liver(P＜0.01), purine metabolism in kidney(P＜0.01), and cysteine and methionine metabolism in small intestine(P＜0.001) were affected. Conclusions Non-redox-related metabolic changes in the liver, kidney and small intestine of middle-aged and aged mice by ergothioheine.

Objective To investigate the role of long non-coding RNA-small nucleolar RNA host gene 3(lncRNA-Snhg3) and its regulatory mechanism in the hepatic glucose metabolism of mice. Methods Adenovirus Snhg3 was over-expressed by the tail vein injection in db/db mice, and then glucose tolerance and pyruvate tolerance were measured. The mRNA expression of mouse liver gluconeogenesis-related genes phosphoenolpyruvate carboxylase(Pepck) and glucose-6-phosphatase(G6pc) and stress-inducing protein 2(Sestrin2,Sesn2,a gene adjacent to Snhg3) were detected by RT-qPCR. The dual luciferase reporter assay was used to detect the effect of Snhg3 on the Sesn2 promoter activity in 293T cells. Results Snhg3 over-expression improved glucose tolerance and pyruvate tolerance in db/db mice. Snhg3 over-expression inhibited the mRNA of gluconeogenesis genes of Pepck(P＜0.05) and G6pc(P＜0.05), while promoted the mRNA of Sesn2(P＜0.01). Meanwhile,Snhg3 over-expression promoted Sesn2 promoter activity in 293T cells(P＜0.05). Conclusions Snhg3 improves glucose metabolism in mice by promoting Sestrin2 expression.

Objective To construct a conditional knockout mice model of cysteine-rich angiogenesis inducer 61 (Cyr61, also known as Ccn1) gene in myocardium and skeletal muscle regulated by CRE recombinant enzyme. Methods C57BL/6 mice were used to create CKmm-Cre^+/- Cyr61^flox/flox mice by using CRISPR/Cas9 technology. The successful construction of conditional knockout mice was confirmed by identifying the Cyr61^flox/flox, 3'LoxP and Cre enzyme sequences in mice. The knockout efficiency of Cyr61 was confirmed by Western blot. The skeletal muscle function of Cyr61 knockout mice was evaluated and following related indicators in the myocardium and skeletal muscle were detected by Western blot: Aging (p53, p21),inflammatory response (TNF-α,IL-18,IL-1β),fibrosis (vimentin,TGF-β,α-SMA,COL1). Results The mice were successfully bred and identified. In comparison with the control group, Cyr61 protein level showed a significant decrease in both myocardium and skeletal muscle in the experimental group(P＜0.01). Compared with the control group, the experimental group mice showed increased skeletal muscle grip strength(P＜0.05), enhanced maximum single contraction force (P＜0.01), and increased average cross-sectional area of the anterior tibialis muscle(P＜0.05). The expression level of p21, TNF-α, IL-18, IL-1β, TGF-β, and COL1 proteins in the myocardium and skeletal muscle of the experimental group was all lower than those of the control group (P＜0.05). Conclusions Myocardial and skeletal muscle-specific Cyr61 gene conditional knockout mice were successfully constructed based on Cre-LoxP technology and heritable trait could be passed stably.

Objective To identify the key immune-related genes and potential drug targets of Krabbe disease by using neural stem cells(NSCs) derived from induced pluripotent stem cells(iPSCs) generated from patients with Krabbe disease. Methods 1)The transcriptome data of GLD-NSCs(GSE212512) was analyzed using GEO2R and Sangerbox; 2)Differential expression genes(DEGs) related to immunity were identified through various methods; 3)Functional enrichment and pathway analysis were performed using DAVID; 4)The protein-protein interaction network was constructed and analyzed using STRING and Cytoscape; 5)Key immune-related genes were determined through topological analysis; 6)Potential therapeutic drugs were screened using DGIdb and drug MAP data- bases; 7)Molecular docking was performed using CB-DOCK2. Results 1)Sixty-one immune-related DEGs were identified in patient NSCs, with GDNF, EGF, KDR, FGF10, and MET being identified as key immune-related genes; 2)Drug candidates with high binding affinity to these genes were identified, including gentamicin for GDNF, cetuximab for EGF,tivozanib for KDR, and capmatinib for MET. Conclusions The predictions suggest cetuximab, gentamicin, tivozanib, and capmatinib exhibit high binding affinity with EGF, GDNF, KDR, and MET, respectively, indicating their potential application value in GLD targeted therapy.

Objective To investigate the effect of pseudogene GTF3AP2 in erythroid differentiation. Methods The published high-throughput RNA sequencing(RNA-seq) data were analyzed to identify the functional pseudogene GTF3AP2, which may play a role in erythropoiesis. The endogenous expression of GTF3AP2 was inhibited by shRNA in CD34⁺ hematopoietic stem/progenitor cells to assess the colony-forming ability through colony-forming assay. Flow cytometry analysis was applied to detect changes in the ratio of erythroid/megakaryocytic progenitor cells. Additionally, the role of GTF3AP2 in erythroid differentiation was determined through transcriptome sequencing, which revealed alterations at the cellular and molecular levels following the knockdown of GTF3AP2. Results Compared with the sh-EV group, knockdown of GTF3AP2 resulted in a significant increase in cell expansion, characterized by a significant rise in the number of colony-forming unit erythroid cells(P＜0.001), an increase in the proportion of CD71⁺CD235a⁺ erythroid precursors(P＜0.01), and a decrease in the proportion of CD71^-CD235a⁺ mature erythrocytes(P＜0.05). Furthermore, there was a significant reduction in the expression of key erythroid differentiation genes, including KLF1, HBB, GYPA, EPOR and TFRC. Conclusions Knocking down of GTF3AP2 promotes the expansion of erythroid precursor cells and inhibits erythroid maturation, suggesting that GTF3AP2 plays a regulatory role in erythroid differentiation.

Objective To identify genes regulated by ME2 and to explore their roles as well as underlying mechanisms in liver cancer progression. Methods RNA-seq data of siME2-transfected cells were subjected to differential expression analysis, clustering, GO and KEGG enrichment analyses. The mRNA level of the potential target gene SHCBP1 was measured by quantitative real-time PCR (qPCR) following ME2 knockdown or overexpression in HepG2 cells. The effect of ME2 and SHCBP1 on the downstream pathway was examined by Western blot. Cell proliferation, wound healing, and colony formation assays were conducted to evaluate SHCBP1's role in liver cancer cell proliferation and migration. Survival analysis of the TCGA-LIHC cohort was performed to determine the prognostic value of SHCBP1 in liver cancer patients. Results Differentially expressed genes in siME2-transfected cells were significantly enriched in biological processes including the PI3K-Akt signaling pathway, cell cycle, and serine phosphorylation. In HepG2 cells, ME2 knockdown led to a reduction in SHCBP1 mRNA level, whereas ME2 over-expression resulted in enhanced SHCBP1 mRNA level, demonstrating a positive correlation between ME2 and SHCBP1 expression. Western blot analysis revealed that ME2 enhanced PI3K-Akt signaling pathway activation through SHCBP1. qPCR results confirmed that SHCBP1 was significantly over-expressed in liver cancer cells and promoted both proliferation and migration, contributing to poor prognosis in liver cancer patients. Conclusions ME2 promotes liver cancer progression by regulating SHCBP1 to activate the PI3K-Akt signaling pathway, presenting a novel therapeutic target for liver cancer treatment.

Objective To investigate the inhibitory effect of β-elemonic acid(β-EA)on the proliferation and invasion of colon cancer cells and the underlying mechanisms through PI3K/AKT/mTOR signaling pathway. Methods The effects of β-EA on colon cancer cell proliferation were evaluated using the MTT assay and colony formation assay. Transwell invasion assay were used to assess the impact of β-EA on invasion. Western blot analysis was conducted to detect changes in PI3K/AKT/mTOR pathway proteins after treatment. Results MTT assay showed that β-EA effectively inhibited the proliferation of colon cancer HCT8 and HCT116 cells in a dose-dependent manner. The colony formation assay confirmed its inhibitory effect on cell proliferation. Transwell invasion assays demonstrated that β-elemonic acid reduced the invasion abilities of the cells. Western blot analysis revealed increased expression of apoptosis-related proteins cleaved-caspase 3, cleaved-caspase 9, and Bax, while Bcl-2 expression was decreased. Invasion-related proteins vimentin, snail, MMP2, and MMP9 were downregulated after treatment. Additionally, β-EA reduced the levels of p-PI3K, p-Akt, and p-mTOR, and these reductions were more pronounced after the addition of the PI3K inhibitor LY294002. Conclusions β-EA may inhibit proliferation and invasion in colon cancer cell lines HCT8 and HCT116 through PI3K/AKT/mTOR signaling pathway, and potentially be transformed as a novel therapeutic agent for colon cancer.

Objective To detect the expression of cytochrome c oxidase assembly factor 6(COA6) in breast cancer, study its clinical significance, and analyze the effect of COA6 on immune infiltration in breast cancer. Methods Differential genes were screened by the whole transcriptome sequencing and the expression of COA6 was explored with TCGA(The Cancer Genome Atlas Program) database. The tissues of 125 breast cancer and adjacent tissues were stained by immunohistochemistry to detect COA6 protein expression and analyze the correlation with clinical features. The COA6 mRNA and protein expression in breast cancer cells and tissues were determined by qRT-PCR and Western blot, respectively. The TIMER(Tumor Immune Estimation Resource) database was used to analyze the correlation between high COA6 gene expression and immune cell infiltration. Results The positive expression rate of COA6 in breast cancer tissues was 88%(110/125), which was higher than that of paracarinoma tissues(7.2%, 9/125)(P＜0.05) and was positively correlated with tumor size and histological grade. In fresh breast cancer tissues, COA6 protein expression was significantly higher than that in adjacent tissues. Both COA6 mRNA and protein expression were significantly increased in the breast cancer cell lines. COA6 was positively correlated with the infiltration of helper T cells, NK cells, CD8⁺ T cells, M1 type macrophages, regulatory T cells, dendritic cells, and memory CD4⁺ T cells in the tumor microenvironment. Conclusions The expression level of COA6 is increased in breast cancer and is positively correlated with tumor immune infiltration, which provides a potential therapeutic target for breast cancer treatment.

Objective To explore the association between disease activity and health utility values(HUV) in patients with rheumatoid arthritis(RA) in China, and to analyze other factors that may affect health utility values, providing a basis for individualized treatment and health management for RA patients. Methods Based on the Chinese Registry of Rheumatoid arthritis cohort, this study included 1 017 diagnosed RA patients. The EQ-5D-3L scale was used to assess the health utility values, while clinical data, disease activity, and potential influencing factors(such as age, gender, and comorbidities) were collected. Tobit regression models were employed to analyze the association between disease activity and health utility values, and to investigate other potential influencing factors. Results The median health utility value for RA patients was 0.78[0.59,0.89]. Patients with moderate to high disease activity had significantly lower health utility values as compared to those in remission phase or with low disease activity(median 0.70 vs. 0.87,P＜0.001). Tobit regression analysis showed a significant association between disease activity and health utility values(P＜0.001). Additionally, older age, female gender, use of glucocorticoids, and comorbidity with diabetes were associated with lower health utility values(P＜0.05). Conclusions Health utility values of RA patients are closely related to disease activity, with higher disease activity leading to a significant reduction in health utility values. Early control of RA disease activity may help improve patients' quality of life.

Objective To identify mechanisms regulating disease progression in rat models of pulmonary arterial hypertension (PAH). Methods Rat PAH models were established using subcutaneous monocrotaline (MCT) injection and the SU5416/hypoxia (SU/Hx) method. Transcriptomic sequencing of lung tissues was performed to identify gene expression and pathway alterations in PAH rats, followed by a comparative analysis with transcriptomic data of patients with idiopathic pulmonary arterial hypertension (IPAH) in NCBI database. Results Inflammatory-related genes such as CXCL9, CCL24, and SECTM1 were upregulated in both PAH rat models and IPAH patient lungs, while genes such as DGKG and DOCK9 were downregulated(P＜0.05). Pathways related to endothelial cell proliferation regulation and extracellular matrix (ECM) remodeling were significantly upregulated(P＜0.05). Conclusions The imbalance in endothelial cell proliferation and abnormal ECM remodeling may collectively contribute to PAH pathogenesis. Further exploration of these signaling pathways may provide deep insights for early diagnosis and targeted therapy of PAH.

Objective To prepare a multifunctional mesoporous silica-based nanocarrier system(MMSN@Gem) with gemcitabine and investigate its effect on bladder cancer cells BIU-87. Methods The multifunctional mesoporous silica-based nano drug-carrying system was prepared by a modified method. Transmission electron microscopy, high-performance liquid chromatography, and thermal imaging were used to characterize the morphology, drug-carrying and photothermal properties of MMSN@Gem. The effect of MMSN@Gem on BIU-87 bladder cancer cells was detected by in vitro experiments. Results MMSN@Gem exhibited a well-defined spherical morphology with an average particle size of(102.48±1.03)nm with a drug loading capacity of 25.04%±0.17%, and an average zeta potential of(-24.84±0.07)mV. The photothermal conversion efficiency was 40.7% which significantly enhanced the release of Gem under near-infrared irradiation. In vitro studies showed that MMSN@Gem significantly inhibited BIU-87 cell activity, induced apoptosis of BIU-87 cells, reduced migration and invasion ability, and enhanced its uptake by BIU-87 cells. Conclusions MMSN@Gem exhibits excellent photothermal properties, enhances cellular uptake efficiency, inhibits the proliferation and migration of BIU-87 cells, and promotes apoptosis, providing a promising drug delivery system for the clinical treatment of bladder cancer.

Objective To comprehensively understand the map of transcripts during mitosis and their regulatory mechanisms of HAP1 cells by conducting transcriptome sequencing analysis after being released by mitotic synchronization arrest. Methods HAP1 cells were subjected to mitotic synchronous arrest with nocodazole and samples were collected after 0, 20, 80 min release, and RNA sequencing(RNA-seq) were performed. The transcriptome data was cleaned and the differentially expressed genes, expression trend clustering and functional enrichment combined with the protein interaction network were analyzed to explore the changes of signaling pathways in HAP1 cells during mitosis. Results The transcriptome of HAP1 cells after synchronous release from mitosis underwent significant changes in time series, and differential gene cluster analysis revealed four gene clusters were enriched in important biological processes such as p53 signaling and cytoplasmic translation. Conclusions The transcriptome time-dependent dynamic changes during mitosis in HAP1 cells are coordinated regulation of key signaling pathways including cellular stress response, translational control and chromatin remodeling, ensuring a balance between growth and stress response upon mitotic exit.

Objective To identify potential serum metabolic biomarkers in colorectal cancer (CRC) patients using untargeted metabolomics and to evaluate their diagnostic and staging value. Methods Serum samples from 100 healthy controls and 100 CRC patients were analyzed by ultra-performance liquid chromatography-mass spectrometry (UPLC-MS). After data normalization, differential metabolites were screened using multivariate statistical analyses (PCA, OPLS-DA) and subjected to pathway enrichment analysis. Diagnostic performance was assessed via univariate and multivariate regression, while Mfuzz clustering was applied to analyze stage-related metabolites (Ⅰ-Ⅳ). Results A total of 432 metabolites were identified with 59 showing significant alterations. Starch and sucrose metabolism and glycerophospholipid metabolism pathways were significantly enriched. A three-metabolite panel (4,8- dimethylnonanoyl carnitine, 9,13-dihydroxy-4-megastigmen-3-one 9-glucoside and C17 sphingosine-1-phosphate) achieved a diagnostic AUC of 0.907, while L-Carnitine and L-Norleucine showed an AUC of 0.776 in staging analysis. Conclusions Specific serum metabolite panel exhibit high diagnostic accuracy, and dysregulated metabolic pathways are associated with CRC progression, suggesting their potential value as biomarkers.

Objective To establish a multi-state Markov model of systemic lupus erythematosus(SLE) for patients in China and to explore the transition rule of organ damage accumulation and possible factors affecting the transition between states. Methods A retrospective cohort study was conducted using the data from CSTAR. The Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index(SDI) was divided into five irreversible disease states(SDI=0, 1, 2, ≥3, and death, marked as S0, S1, S2, S3, Death). The R “mstate” package was used for statistical analysis. Results This study included 23 926 cases of SLE patients with cumulative follow-up of 12 030 visits. Among these patients, 21 070 patients had no any organ damage at baseline. At the follow-up period, the transition probabilities of organ damage of S0→S1, S1→S2, S2→S3, S3→Death were 7.01%, 12.58%, 10.64%, and 12.19%, respectively. The multi-state Markov model showed that age, gender, disease duration, SLEDAI score, corticosteroid dosage, and involvement of major organs were associated with the transition of organ damage status, each 1 year increased was associated with a 2%~3% increase in risk of damage accumulation risk(P＜0.01). Also, neurological(S0→S1:HR=1.34;S1→S2:HR=1.53;S2→S3:HR=1.73), cardiopulmonary(S0→S1:HR=3.66;S1→S2:HR=1.51;S2→S3:HR=1.52), renal(S0→S1:HR=1.24)and hematological involvement(S0→S1:HR=1.24)might be the risk factors. Conclusions The probability of organ damage accumulation in SLE patients increases over time. Therefore, in the early stage of the disease, the involvement of important organs needs to be minimized and the treatment strategy should be dynamically adjusted at different stages of treatment.

Objective To explore the effect of sugammadex on safety indicators such as body movement, choking, peak airway pressure during spinal surgery with motor evoked potential monitoring. Methods This study was a retrospective analysis of two randomized controlled trials. Patients undergoing selective thoracic and lumbar spinal surgery with intraoperative motor evoked potential monitoring were included. Rocuronium was continuously infused and the train-of-four stimulation count was maintained at 2. When motor evoked potential monitoring started, stop rocuronium infusion and 2 mg/kg of sugammadex was given. Indicators were compared between administration of sugammadex and 5, 10, 20, 30,60 minutes after administration like body movement, choking, peak airway pressure, allergic reaction, mean arterial pressure, heart rate, end expiratory pressure of CO₂ and the train-of-four stimulation ratio(TOFr). Results A total of 120 patients were finally included in the analysis. Before administering sugammadex, TOFr was 0.2. At 5, 10, 20, 30 and 60 minutes after administration, TOFr were 0.8, 0.8, 0.9, 0.9, 0.9 respectively. No patient experienced intraoperative body movement, choking, or allergy reaction. Compared with the time of sugammadex administration, heart rate was significantly reduced 5, 10, 20, 30 and 60 minutes after administration (P＜0.05), there was no significant change in the remaining indicators. Conclusions Sugammadex can be safely used during spinal surgery with motor evoked potential monitoring.

Objective To analyze the clinical characteristics of 3 patients with Wilson's disease who suffered from skin striae atrophicae after treatment with penicillamine, and to conduct literature review to extensively profile adverse events of penicillamine-induced skin changes. Methods A retrospective analysis was performed on the clinical data of 3 patients with Wilson's disease who developed skin striae atrophicae after administration of penicillamine in the Department of Pediatrics of Peking Union Medical College Hospital from August 2013 to August 2024,and a literature review was performed. Results Three patients with Wilson's disease all developed skin striae atrophicae after taking penicillamine. Among them, 2 patients reduced or stopped using penicillamine shortly after the appearance of striae atrophicae, and their striae atrophicae improved significantly. After taking penicillamine again, their skin changes remained stable. A literature research showed that 48 patients with Wilson's disease experienced penicillamine induced skin changes, and no similar reports of striae atrophicae were found. The reported skin changes included elastosis perforans serpiginosa,skin laxity or wrinkled skin,pseudo-pseudoxanthoma elasticum,increased skin fragility,pigmentation and so on. Among them, 24 patients reduced or stopped penicillamine,and 18 patients (75%) had improved or maintained stable skin changes. Conclusions Penicillamine can cause various skin changes in patients with Wilson's disease, including striae atrophicae, which can be improved after reducing or discontinuing taking penicillamine. And skin striae atrophicae can maintain stable even if they taking penicillamine again.

Obstructive sleep apnea (OSA) is a multifactor respiratory disorder characterized by recurrent episodes of airway collapse, leading to intermittent hypoxemia, hypercapnia, and sleep fragmentation. Intermittent hypoxia (IH) has profound effects on various body systems, particularly the immune system. Additionally, the suppression of the related inflammatory molecules mitigates IH-induced inflammation and tissue injury, presenting new potential targets for treating OSA-related complications. This review aims to explore the mechanisms by which OSA reshapes the immune system and its clinical significance.

Nuclear polyadenosine-binding protein 1(PABPN1)is the only known polyadenosine-binding protein in the cell nucleus of mammals. The first attention was resulted from relevant research on oculopharyngeal muscular dystrophy (OPMD), where mutations and aggregation of PABPN1 were found to be the main pathogenesis of the disease. Recently, PABPN1 is found to be abnormally expressed in some tumor tissues, and confirmed to be involved in regulating selective polyadenylation, which leads to the occurrence and development of various human tumors. This article briefly introduces the structure and function of PABPN1, reviews progress of research related to PABPN1 and tumors in recent years, and provide our thought for exploring point potential pathways for future research on the role and mechanism of PABPN1 in the occurrence and development of tumors.

Objective To explore the application of case-based learning(CBL) approach in the basic medical stage for eight-year clinical medical program. Methods A total of 320 students from the eight-year clinical medicine program at Peking Union Medical College in the grades of 2014—2015 and 2019—2020 were selected as the study subjects. These students were divided into two groups, 162 students in the classes of 2014 and 2015 as the control group, and 158 students in the classes of 2019 and 2020 as the experimental group. The students in the control group received classic teaching in the basic medicine stage characterized by traditional lectures as the main teaching method. The students in the experimental group received traditional lectures supplemented by CBL. In this study, the cardiovascular system was taken as an example, and the assessment scores and questionnaires of the two groups of students were collected in order to evaluate the teaching effectiveness and to obtain timely teaching feedback. Results Traditional lecture combined with CBL method significantly improved the theory assessment scores of students in the experimental group, stimulated learning interest and intrinsic motivation, and enhanced team learning and problem-solving ability. Students believed that CBL teaching could effectively improve the ability to link theory to clinical practice. In addition, CBL teaching method encouraged the interaction between teachers and students and improved teaching efficiency. Conclusions Well-designing and well-organized CBL teaching from multiple levels, including teachers, students, and curricula, can be better accepted and acknowledged by students from eight-year clinical medical program at the stage of basic medical education.

Empathy is a cornerstone in cultivating medical ethics. This article delves into the profound significance of empathy and underscores the importance of promoting it among medical students and practitioners. It also details methods for strengthening empathy and capacity building concerned in students through oral medicine instruction, with the goal of nurturing oral healthcare professionals who provide compassionate care.

Objective To explore the application and effectiveness of the apprenticeship education model in Chinese herbal medicine teaching at Western medical college. Methods By comparing classic lecture-based teaching with a combined approach integrating apprenticeship education, the study assesses the impact on student learning outcomes. Participants included students from the 2018 cohort of the eight-year clinical medicine program and the 2022 cohort of the “4+4” pilot program at Peking Union Medical College, who received classic teaching methods and apprenticeship case-based teaching methods, respectively. Upon course completion, students completed a 14-item multiple-choice questionnaire covering essential theory of Chinese medicine, as well as specific categories such as qi-regulating, blood-activating herbs, among others. Results The overall accuracy rate in the apprenticeship case-based teaching group was significantly higher than that in the classic teaching group (P＜0.01). Conclusions The apprenticeship education model of Traditional Chinese Medicine has a positive effect on teaching of Chinese herbal medicine at Western medical college and warrants further promotion and application.