In recent years， traditional Chinese medicine （TCM） has achieved significant progress in the treatment of inflammatory bowel disease （IBD）. A comprehensive literature search was conducted covering the period from January 1， 2010， to December 30， 2024， across Chinese databases including China National Knowledge Infrastructure （CNKI）， Wanfang Data， VIP China Science and Technology Journal Database， and the Chinese Biomedical Literature Service System， as well as international databases such as PubMed， Web of Science， and Embase. The clinical applications and mechanistic studies of TCM in IBD were systematically reviewed. The current status of TCM research on the etiology and pathogenesis of IBD， innovative clinical practices， and multimodal therapeutic approaches， including Chinese herbal formulas， single herbs or active compounds， acupuncture， herbal retention enema， and acupoint application， were summarized， together with their synergistic effects when combined with western medical treatments. The development and application of Chinese patent medicines for IBD are undergoing a profound transition from efficacy validation to mechanistic exploration. Mechanistic studies on the effects of TCM in IBD mainly focus on regulating gut microbiota homeostasis， repairing the intestinal mucosal barrier， and modulating intestinal immune balance. Furthermore， future research directions for TCM-based IBD management are proposed， including the establishment of TCM diagnostic and treatment models， expanding integrated applications of external and internal TCM therapies， innovating personalized treatment strategies， and advancing drug development. These efforts aim to provide insights for the standardized and precision-oriented development of TCM in the diagnosis and treatment of IBD.

Lung transplantation is a definitive treatment for end-stage lung disease and can significantly improve patient prognosis. However, postoperative complications such as infection, rejection, ischemia-reperfusion injury and chronic lung allograft dysfunction intertwine to form a complex pathological network, posing persistent challenges to long-term patient survival. In 2025, research teams worldwide have made systematic progress in the field of basic lung transplantation research. By integrating cutting-edge technologies including single-cell multi-omics, spatial transcriptomics and novel animal models, significant breakthroughs have been achieved in the evolutionary dynamics of drug-resistant infections, molecular mechanisms of immune regulation, programmed cell death, optimization of donor lung protection strategies and early warning of chronic lung allograft dysfunction. This article systematically reviews the representative advances in basic lung transplantation research worldwide in 2025, and deeply analyzes the implications of mechanistic breakthroughs for optimizing diagnosis and treatment strategies, aiming to anchor the direction for innovative breakthroughs and clinical translation in basic lung transplantation research.

ObjectiveTo construct an interleukin-9 （Il9） gene knockout mouse model on a C57BL/6N background， establish a reliable genotyping method， and provide a standardized animal model for investigating Il9-related immune mechanisms and diseases. MethodsIl9 knockout mouse strain （C57BL/6N-Il9^em1Cya） was generated using conventional gene knockout technology. The method for DNA extraction from mouse tails was optimized to ensure template quality. Two sets of specific primers （F1/R1 and F1/R2） were designed to amplify target fragments by PCR， and mouse genotypes were determined by agarose gel electrophoresis. Specifically， primer pair F1/R1 targeted the knockout sequence with an expected product of 465 bp， while F1/R2 targeted the wild-type sequence with an expected product of 703 bp. Subsequently， Western blot was performed to verify the knockout efficiency of Il9 in primary immune cells and key organs of the offspring mice， and flow cytometry was used to assess the effects of Il9 deficiency on the function of the immune system in major immune cell populations. ResultsIl9 knockout mice were successfully bred and genotyped. PCR identification showed that homozygous mice （-/-） exhibited only a 465 bp band， wild-type mice （+/+） displayed only a 703 bp band， and heterozygous mice （+/-） showed both bands simultaneously. Meanwhile， Western blot analysis revealed significantly decreased IL-9 expression in various organs of the offspring mice （P<0.001）. Flow cytometric results demonstrated that Il9 deficiency exerted no obvious effects on the proportions of peripheral blood lymphocytes， splenic lymphocytes， and peritoneal macrophages. ConclusionAn Il9 gene knockout mouse model on a C57BL/6N background is successfully constructed. The established PCR genotyping system is highly efficient and accurate， which can effectively distinguish mice of different genotypes. This model provides a stable and reliable experimental basis for subsequent functional studies of Il9 and exploration of the mechanisms underlying Il9-related diseases.

ObjectiveTo construct a chimeric antigen receptor macrophage （CAR-M） targeting interleukin-13 receptor α （IL-13Rα） and intracellular domain integration， which can double activate the signal adaptor protein OX40L of macrophages and T cells. MethodsThe CAR molecule targeting IL-13Rα （IL-13Rα-OX40L-CAR） with OX40L as the intracellular signal domain was designed and synthesized， and it was cloned into the adenovirus expression vector. After THP-1 cells were induced to differentiate into macrophages （THP-1-M） by phorbol ester， the cells were infected with recombinant adenovirus to construct THP-1 macrophages stably expressing green fluorescent protein （GFP） labeled anti-IL-13RαCAR. The expression efficiency of CAR molecules was monitored by flow cytometry. The empty vector group was used as the negative control， the CD3ζ group was used as the positive control， and the CD3ζ-OX40L group was used as the experimental group. The phagocytic function of macrophages in each group on IL-13Rα high expression glioma cells （U251） and low expression glioma cells （T98G） was detected by in vitro co-culture experiments. ResultsCAR adenovirus was efficiently transfected into THP-1-M to obtain anti-IL-13RαCAR-M. After co-cultured with glioma cells with different expression levels of IL-13Rα， the results of flow cytometry showed that there was no significant difference among the three groups for T98G cells with low expression of IL-13Rα. After co-culture with U251 cells with high expression of IL-13Rα， the CD3ζ group showed enhanced phagocytosis compared with the empty vector group （P<0.05）. Compared with the CD3ζ group， the phagocytosis ability of the CD3ζ-OX40L group was further enhanced （P<0.05）. ConclusionAnti-IL13Rα- OX40L-CAR-M is successfully constructed by constructing IL-13Rα-OX40L-CAR adenovirus and transfecting PMA-induced differentiated THP-1-M. It can engulf glioma cells with high expression of IL-13Rα by specific targeting， and shows activation of intracellular domain superior to traditional CD3ζ.

Metabolic dysfunction-associated fatty liver disease （MAFLD） is the most common chronic liver disease， and it has become a major global health issue. Excessive lipid accumulation in the liver is the core pathological event of MAFLD， which triggers lipotoxicity and leads to cell apoptosis， necrosis， and inflammatory cascades by mediating endoplasmic reticulum stress， oxidative stress， organelle dysfunction， and ferroptosis， thereby promoting the progression of simple hepatic steatosis to steatohepatitis and fibrosis. In this process， very-long-chain fatty acids （VLCFAs）， as essential components of cell membranes and lipid metabolism， have attracted increasing attention for their role in lipotoxicity mechanisms. This article reviews the role of VLCFAs in lipid metabolism processes and lipotoxicity mechanisms， focusing on how VLCFAs participate in metabolic regulation through key proteins and disrupt cell membranes to induce oxidative stress， and how their metabolites and derivatives drive inflammatory responses， ultimately promoting the progression of MAFLD.

ObjectiveTo obtain a construct chimeric antigen receptor macrophages （CAR-M） targeting disialoganglioside GD2 （GD2） and harboring the intracellular domain of macrophage-specific activating signaling adaptor protein DNAX-activating protein 12 （DAP12）. MethodsA CAR molecule targeting GD2 with the DAP12 intracellular domain as the signaling module ［Anti-GD2 CAR （DAP12）］ was designed， synthesized， and cloned into an adenoviral vector. This virus was used to infect PMA-differentiated THP-1 macrophages to construct green fluorescent protein （GFP）-labeled Anti-GD2 CAR THP-1 cells. CAR expression was confirmed using live-cell imaging. In vitro co-culture assays were performed to evaluate the phagocytic function of empty， Anti-GD2 CAR-M （CD3ζ）， and Anti-GD2 CAR-M （DAP12） groups against glioma cells with high （T98G） and low （U251） GD2 expression. ResultsThe CAR adenovirus efficiently transduced THP-1 macrophages， resulting in successful generation of Anti-GD2 CAR-M. Flow cytometry analysis following co-culture with glioma cells showed that compared to the empty group， the Anti-GD2 CAR-M （CD3ζ） group exhibited significantly enhanced phagocytosis （P<0.05）. Furthermore， compared to the Anti-GD2 CAR-M （CD3ζ） group， the Anti-GD2 CAR-M （DAP12） group demonstrated a further increase in phagocytic capacity specifically against GD2-high T98G cells （P<0.05）. ConclusionAnti-GD2 CAR-M （DAP12） cells are successfully established by transducing PMA-differentiated THP-1-M with recombinant Anti-GD2 CAR （DAP12） adenovirus. The engineered CAR-M can specifically target phagocytose glioma cells with high GD2 expression.

ObjectiveTo obtain stably transfected chimeric antigen receptor macrophages （CAR-M） targeting disialosylganglioside （GD2） based on the constitutive expression of myeloid differentiation factor 88 （MYD88）. MethodsAn Anti-GD2 CAR adenoviral vector incorporating the CD3ζ （cluster of differentiation 3 zeta chain）-MYD88 fusion construct was designed and constructed. THP-1-derived macrophages （THP-1M）， induced by phorbol 12-myristate 13-acetate （PMA） differentiation， were infected with this adenovirus to generate Anti-GD2 CAR THP-1 cells bearing a green fluorescent protein （GFP） tag. CAR expression was monitored using a live-cell imaging system. The phagocytic function of Empty CAR-M， Anti-GD2 CAR-M（CD3ζ）， and Anti-GD2 CAR-M（CD3ζ-MYD88） groups against glioma cells was evaluated in vitro through co-culture experiments， and their polarization status was also analyzed. ResultsCAR adenovirus successfully transfected THP-1 to obtain Anti-GD2 CAR-M. After co-culture with glioma cells， flow cytometry results showed that compared with the Empty CAR-M group and the Anti-GD2 CAR-M（CD3ζ） group， the Anti-GD2 CAR-M（CD3ζ-MYD88） group exhibited enhanced phagocytosis against T98G cells with high GD2 expression （P<0.05） and also showed upregulation of CD86 （P<0.05）. Compared with the Empty CAR-M group and the Anti-GD2 CAR-M（CD3ζ） group， the Anti-GD2 CAR-M（CD3ζ-MYD88）CAR-M group exhibited enhanced phagocytosis against T98G cells with high GD2 expression （P<0.05） and also showed upregulation of CD86 （P<0.05）， and the expression of inflammatory cytokines interleukin （IL）-6 and IL-12 was increased in this group （P<0.05）. ConclusionThis study successfully constructed Anti-GD2 CAR-M cells and verified their phagocytic activity， demonstrating that constitutive expression of MYD88 can promote inflammatory polarization of CAR-M. This provides a potential structural modification approach for the development of pro-inflammatory CAR-M.

Objective To translate the English version of the Acceptance and Action Question-naire-Stigma(AAQ-S)into Chinese and explore its application effect in patients with diabetes.Methods A convenience sampling method was used to select 255 patients with diabetes as the study subjects.Following the Brislin translation principles,the scale was translated,back-translated,cul-turally adapted and pre-tested to develop the Chinese version of the AAQ-S.A self-made general data questionnaire and Chinese version of AAQ-S were used to investigate the patients with diabetes,and the reliability and validity of the scale were tested.Results The scale level-content validity index/u-niversal agreement(S-CVI/UA)of the Chinese version of the AAQ-S was 0.95,and the average scale-level content validity index(S-CVI/Ave)was 0.99.The Chinese version of AAQ-S extracted psycho-logical rigidity and psychological flexibility factors,with a total of 21 items,and the cumulative vari-ance contribution rate of factors was 61.020％.The Cronbach's α of the Chinese version of the AAQ-S was 0.958,the test-retest reliability was 0.890,and the Guttman split-half reliability was 0.882.The item-level content validity index(I-CVI)of each item in the Chinese version of the AAQ-S ranged from 0.86 to 1.00,and the S-CVI/UA of the aggregate table was 0.95.Conclusion The Chinese version AAQ-S has good reliability and validity,and can be used as an evaluation tool to assess the acceptance of stigma in diabetic patients.

For patients with moderate-to-severe functional mitral regurgitation (FMR) who continue to experience heart failure symptoms despite optimized medical and device therapy, transcatheter mitral valve edge-to-edge repair (TEER) is increasingly becoming a reliable treatment option. With the continuous research and development and improvement of TEER-related devices, there are currently dozens of domestically developed TEER devices undergoing clinical trials in China. In this study, we report the first case of a patient with severe FMR treated with the X-Clip® TEER system. The patient, a 60-year-old male, suffered FMR attributed to dilated cardiomyopathy. Preoperative transthoracic echocardiography showed severe mitral regurgitation (4+). He underwent percutaneous repair using the X-Clip® system, and immediate postoperative ultrasound showed mild mitral regurgitation. At the 1-month follow-up, the patient’s symptoms and New York Heart Association (NYHA) functional class improved, and a follow-up transthoracic echocardiogram showed mild mitral regurgitation (1+).

Objective:To investigate the clinical efficacy of two-point localized injection of the depressor anguli oris (DAO) muscle combined with pan-platysma microbotox injection of botulinum toxin type A for improving the aesthetic of mouth corner.Methods:A retrospective analysis was conducted on clinical data from patients who received concomitant DAO localized injection and pan-platysma microbotox of botulinum toxin type A for improving drooping mouth corners at the Facial and Neck Plastic Surgery Center and the Limb and Scar Center of Plastic Surgery Hospital, Chinese Academy of Medical Sciences, between December 2022 and June 2025. Botulinum toxin type A was reconstituted to two concentrations: 40 U/ml and 20 U/ml for the combined injection. Patients were instructed to repeatedly perform upward puckering motions to identify the trapezoidal outline of the DAO muscle. Two injection points were uniformly marked slightly medial to the midline of the DAO muscle for dual-target injection (1.5 U each at the middle one-third and lower one-third of the muscle belly). The pan-platysma microbotox for the platysma muscle extended superiorly to a line parallel and 3-4 cm above the mandibular border, innerly to 1 cm beyond the lateral edge of the DAO muscle, inferiorly to the submental area and the anterior neck region above the clavicle, and laterally to the anterior border of the sternocleidomastoid muscle. The injection dose was 0.6 U per point, with 1 cm spacing between points, administered at the superficial subcutaneous layer. Complications were recorded. At 1-month postoperatively, efficacy was evaluated using the global aesthetic improvement scale (GAIS, scores ranging from 5 to 1, representing "much worse" to "very much improved" ) and subjective patient satisfaction (categorized as very satisfied, satisfied, dissatisfied, or very dissatisfied; satisfaction rate was calculated as the percentage of patients reporting very satisfied or satisfied among the total). Patients’ willingness to receive the same treatment in the future was also surveyed. Descriptive statistics were used for analysis.Results:A total of 21 patients were included (1 male, 20 females), with a mean age of (37.1±3.2) years (range: 34-45 years). The treatment procedures were successful. Post-treatment, 4 cases experienced pain and swelling, 8 had neck ecchymosis, and 1 had temporary asymmetry in mouth corner movement, all of which resolved within 2 weeks. The follow-up period ranged from 1 to 6 months (mean: 1.4 months). At short-term follow-up (4-6 weeks after treatment), patients reported a skin "tightening" sensation in the lower face and neck region, noting significant improvement in lower facial and neck contour, sharper bilateral jawlines, and reduced neck wrinkles. Drooping mouth corners were improved. The satisfaction survey showed that 17 patients were "very satisfied" and 5 were "satisfied", resultsing in a subjective satisfaction rate of 100%. Nineteen patients (90.5%) expressed willingness to undergo repeat treatment. The mean GAIS score was 1.45±0.69, with 14 patients achieving "very much improved", 5 patients "much improved", and 2 patients "improved" .Conclusion:The combination of two-point localized injection of the DAO muscle and pan-platysma microbotox injection of botulinum toxin into the platysma muscle effectively improve the aesthetic of mouth corners and lower facial contour through synergistic middle and superficial layer treatment. This approach aligns with anatomical and physiological merits and offers advantages such as minimal invasiveness and rapid recovery, making it applicable for patients with early signs of lower facial aging.