OBJECTIVE To investigate the protective effect of 2-dodecyl-6-methoxy-2，5-diene-1，4-cyclohexanedione （DMDD）， an active component from Averrhoa carambola root， on myocardial injury in diabetic mice based on the nuclear receptor coactivator 4/ferritin heavy chain 1/autophagy-related protein 8 （NCOA4/FTH1/ATG8） axis. METHODS The successfully modeled diabetic mice were randomly divided into model group and DMDD low-， medium-， and high-dose （12.5， 25， 50 mg/kg） groups， while an additional non-modeled control group was established， with 6 mice in each group. Each group received the corresponding drug solution or an equal volume of normal saline intragastically once daily for 21 consecutive days. After the administration， the levels of fasting blood glucose （FBG）， serum lactate dehydrogenase （LDH）， and creatine kinase isoenzyme MB （CK-MB） were measured. Myocardial pathological changes， degree of fibrosis， and myocardial cell ultrastructure were observed. Myocardial cell death index and NCOA4 protein positive index were detected. The protein expression levels of NCOA4， FTH1， ATG8， solute carrier family 7 member 11 （SLC7A11）， and glutathione peroxidase 4 （GPX4） in cardiac tissue were measured. RESULTS Compared with model group， each DMDD group showed significant alleviation of cardiac pathological injury and varying degrees of improvement in the myocardial cell ultrastructure. The FBG and serum LDH and CK-MB levels， the myocardial cell death index and NCOA4 protein positive index，the protein expression levels of NCOA4， FTH1， and ATG8 in cardiac tissue were significantly decreased （ P ＜0.001）， while the protein expression levels of SLC7A11 and GPX4 were significantly increased （ P ＜0.001）. CONCLUSIONS DMDD can reduce blood glucose levels， alleviate myocardial histopathological injury， and inhibit cell death in diabetic mice. The mechanism is associated with inhibiting excessive activation of the NCOA4/FTH1/ATG8 axis and reducing ferritinophagy.

Intelligent prescription recommendation has become an important research direction in traditional Chinese medicine (TCM), offering new opportunities to support clinical decision-making and promote the modernization of TCM practice. With the rapid development of artificial intelligence (AI), a variety of computational approaches have been proposed to learn prescription patterns from clinical data and generate personalized treatment recommendations. However, despite increasing research activity, systematic and comprehensive reviews of AI-driven methods for TCM prescription recommendation remain limited. In this study, we present a comprehensive review of computational approaches for herbal prescription recommendation (HPR) in TCM. Existing methods are systematically categorized into several major paradigms, including traditional machine learning methods, topic model methods, sequential generative methods, deep learning and graph-based methods, and large language model–based frameworks. In addition to summarizing methodological developments, we also review commonly used public datasets and evaluation metrics in this field. Furthermore, representative models with publicly available implementations are experimentally evaluated on multiple benchmark datasets to provide a comparative analysis of their performance on the HPR task. Finally, we discuss the key challenges that hinder the practical deployment of intelligent prescription recommendation systems, including data heterogeneity, limited interpretability, and insufficient integration of TCM domain knowledge. Future research directions are outlined to facilitate the development of more reliable, interpretable, and clinically applicable AI-assisted HPR systems for TCM.

Lung transplantation is currently the only effective treatment for end-stage lung disease. However, the field of lung transplantation still faces numerous challenges, including donor shortage, primary graft dysfunction, rejection, infection and others. In 2025, scholars worldwide have made remarkable progress in clinical research on lung transplantation. This article systematically reviews the cutting-edge developments in clinical research on lung transplantation in 2025, focusing on the application of novel evaluation tools in donor lung screening, optimization of lung perfusion techniques, exploration of extracorporeal membrane oxygenation and robot-assisted minimally invasive surgery, as well as mechanistic research and intervention strategies for primary graft dysfunction, acute kidney injury and chronic lung allograft dysfunction. Meanwhile, hot topics such as the management of special populations, prevention and control of postoperative infections, and improvement of quality of life are summarized. This review aims to conclude the important annual research findings and provide references for the clinical practice and research development of lung transplantation in China.

Background Silicosis is a progressive pulmonary fibrotic disease caused by long-term inhalation of silica (SiO₂) dust, and abnormal fibroblast activation is a central pathological mechanism. Galectin 3 (LGALS3) plays a significant role in fibrosis across multiple organs; however, its specific molecular mechanism in SiO₂-induced pulmonary fibrosis remains unclear. Objective To investigate the role of LGALS3 in silica (SiO₂) induced pulmonary fibrosis and its potential molecular mechanisms. Methods Differentially expressed genes in mouse lung fibroblasts treated with SiO₂ for 56 d were analysed using the GSE183682 single-cell RNA sequencing dataset, followed by pathway enrichment analysis. A mouse model of pulmonary fibrosis was established by intratracheal instillation of SiO₂ suspension (50 mg·mL⁻¹, 100 μL). Lung index, hydroxyproline content, and histopathological changes (HE staining) were assessed. Western blot and immunofluorescence staining were used to evaluate the expression of LGALS3, MAPK pathway proteins, and fibrosis markers [collagen type I alpha 1 chain (COL1A1) and α-smooth muscle actin (ACTA2)]. Results Single-cell RNA sequencing analysis identified 53 differentially expressed genes in fibroblasts, and Lgals3 was significantly upregulated in the SiO₂ group. SiO₂ exposure successfully induced pulmonary fibrosis in mice, as indicated by weight loss, elevated hydroxyproline content, alveolar structural disruption, and collagen deposition. Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses showed that Lgals3-associated genes were enriched in Toll-like receptor/chemokine signaling pathways. After SiO₂ exposure, LGALS3 expression was increased in fibrotic lung tissue and co-localized with ACTA2, an activated fibroblast and myofibroblast marker. This was accompanied by activation of the MAPK signaling pathway. Conclusion LGALS3 may be involved in fibroblast activation and collagen deposition, potentially through activation of the MAPK signalling pathway. These findings suggest that LGALS3 may represent a potential regulatory target in SiO₂-induced pulmonary fibrosis.

ObjectiveTo investigate the effects of different antiplatelet therapy regimens （aspirin versus clopidogrel at specific doses） on cognitive function， blood biomarkers and brain imaging biomarkers when used prophylactically in patients with cerebral small vessel disease （CSVD）. MethodsA randomized controlled trial was conducted involving 160 CSVD patients who were randomly assigned to four groups： aspirin group （ASA）， low-dose clopidogrel group （CLOP-50）， standard-dose clopidogrel group （CLOP-75）， and control group （HC）. Cognitive function ［auditory verbal learning test-immediate recall （AVLT-IR）， auditory verbal learning test-short-delay recall （AVLT-SDR）， auditory verbal learning test-long-delay recall （AVLT-LDR）， hamilton anxiety rating scale （HAMA）， and hamilton depression rating scale （HAMD）， ADL（activities of daily living scale ）， （ascertain dementia 8-item questionnaire，AD8）］， blood biomarkers ［platelet count （PLT） and mean platelet volume （MPV）］， and CSVD-related imaging biomarkers ［white matter hyperintensities （WMH） and cerebral microbleeds （CMB）］ were assessed in all groups at baseline and at the 6-month follow-up. ResultsAfter 6 months of treatment， within-group comparisons showed that， compared with baseline， the ASA group had significantly increased scores on the AVLT immediate recall （AVLT-IR）， short-delay recall （AVLT-SDR）， and long-delay recall （AVLT-LDR） （P<0.05）. The CLOP-75 group showed significantly decreased HAMA and HAMD scores （P<0.05）， along with a significant increase in AVLT-LDR scores （P<0.05）. The number of CMBs increased from baseline in both the ASA and CLOP-75 groups （P<0.05）， whereas no statistically significant changes in blood biomarkers were observed in either group. By contrast， the CLOP-50 and HC groups showed no significant changes in cognitive function， blood biomarkers， or CSVD-related imaging biomarkers compared with baseline （all P<0.05）. Comparisons between groups showed that the AVLT-LDR scores and the number of CMBs increased faster in the ASA group than in the HC group （β=-0.187， P=0.04； β=-0.805， P<0.001）. In addition， the rate of CMB increase was also faster in the ASA group than in the CLOP-50 group （β=-0.695， P<0.01）. The ADL scores increased faster in the HC group than in the ASA group （β=0.170， P=0.02）. The AD8 scores decreased faster in the CLOP-75 group than in the HC group （β=-0.128， P=0.04）， but the rate of CMB increase in the CLOP-75 group was also faster than that in the HC group （β=0.604， P=0.04）. ConclusionIn CSVD patients， aspirin 100 mg or clopidogrel 75 mg improves cognitive function but increases the risk of cerebral hemorrhage. Clopidogrel 50 mg shows no short-term clinical benefit or imaging improvement.

Oral submucous fibrosis (OSF), characterized by excessive deposition of extracellular matrix (ECM) that causes oral mucosal tissue sclerosis, and even cancer transformation, is a chronic, progressive fibrosis disease. However, despite some advancements in recent years, no targeted antifibrotic strategies for OSF have been approved; likely because the complicated mechanisms that initiate and drive fibrosis remain to be determined. In this review, we briefly introduce the epidemiology and etiology of OSF. Then, we highlight how cell-intrinsic changes in significant structural cells can drive fibrotic response by regulating biological behaviors, secretion function, and activation of ECM-producing myofibroblasts. In addition, we also discuss the role of innate and adaptive immune cells and how they contribute to the pathogenesis of OSF. Finally, we summarize strategies to interrupt key mechanisms that cause OSF, including modulation of the ECM, inhibition of inflammation, improvement of vascular disturbance. This review will provide potential routes for developing novel anti-OSF therapeutics.
Humans ; Oral Submucous Fibrosis/immunology* ; Extracellular Matrix/metabolism* ; Myofibroblasts

Diannan Su's bone-setting school is one of the orthopedic schools of traditional Chinese medicine(TCM),and Su Caichen,a famous bone-setting physician in Diannan,is the key figure of Diannan Su's bone-setting school.This paper systematically summarized Su Caichen's bone-setting academic thoughts of"adaptation","harmonization"and"recovery",presented his core bone-setting concepts of"original traumatic chamber","bone-setting prior to activating blood and vessles,bone-setting together with soothing tendons and then fracture healing naturally after the removal of stasis",and introduced his five kinds of bone-setting manipulations for treating the common upper limb fractures in detail,namely shaking and pushing manipulations for distal radius fracture,floating manipulations for fracture of both ulna and radius,five-step manipulations for supracondylar fractures of humerus,staging manipulations for humeral shaft fracture,and degloving manipulations for proximal humeral fractures complicated with shoulder dislocation.Su Caichen's bone-setting academic thoughts,bone-setting concepts and his specific TCM bone-setting manipulations have constructed the academic and theoretical system of Diannan Su's bone-setting school,which will provide an approach for TCM treatment of orthopedic diseases,and will promote the inheritance and development of the specific TCM orthopedic schools.

AIM:To explore the effect of sinomenine hydrochloride(SH)on microcirculation and renal func-tion in type 2 diabetic db/db mice with a focus on the diacylglycerol(DAG)/protein kinase C(PKC)signaling pathway.METHODS:Eighteen 6-week-old male db/db mice were randomly divided into three groups:model group(saline),LY group(administered with 1 mg·kg-1·d-1 LY333531),and SH group(administered with 124.8 mg·kg-1·d-1 SH).Addi-tionally,6 age-matched db/m mice comprised the control group(saline).Daily intragastric administration lasted 6 weeks.Body mass,fasting blood glucose(FBG),urinary microalbumin(mALB),urinary creatinine(UCr)and urinary β2-micro-globulin(β2-MG)were measured in each group.The serum levels of endothelin-1(ET-1),endothelial nitric oxide syn-thase(eNOS),collagen type Ⅳ(Col Ⅳ)and laminin(LN),and the levels of DAG and PKC in renal tissues were ana-lyzed by enzyme-linked immunosorbent assay(ELISA).The morphological changes of renal tissues were assessed using HE and PAS staining,and kidney ultrastructure was examined via transmission electron microscopy.Immunohistochemis-try and Western blot were used to detect PKC and p-PKC levels in renal tissues.RESULTS:Compared with model group,the mice in both LY and SH groups showed decreased body mass(P＜0.05),with significantly reduced FBG level in LY group(P＜0.01).In addition,the urinary mALB and β2-MG levels were markedly decreased(P＜0.01),while UCr level was significantly increased(P＜0.01).Serum ET-1,Col Ⅳ and LN levels were significantly lower(P＜0.01),whereas eNOS level was notably higher(P＜0.01).Renal tissue DAG and PKC levels,as well as p-PKC expression were significantly reduced(P＜0.01).Improvements in renal tissue pathology and ultrastructure were observed.CONCLU-SION:Sinomenine hydrochloride improves microcirculation in diabetic db/db mice by modulating DAG/PKC signaling pathway,thus exerting protective effect on the kidney.

Background and Aims:Laparoscopic pancreaticoduodenectomy(LPD)has become a preferred approach for periampullary tumors,yet delayed gastric emptying(DGE)remains a frequent complication that hampers postoperative recovery.The nasojejunal feeding tube(NJT)is commonly used for early enteral nutrition,but its impact on DGE is controversial.This study aimed to evaluate whether intraoperative NJT placement increases the risk of DGE after LPD and to assess its influence on postoperative recovery outcomes.Methods:A retrospective cohort of 319 patients who underwent LPD at Provincial Hospital Affiliated to Shandong First Medical University from April 2017 to November 2023 was analyzed.Patients were divided into two groups based on intraoperative NJT placement(NJT group,n=200;non-NJT group,n=119).The incidence of DGE and postoperative outcomes were compared.Multivariate logistic regression and propensity score matching(PSM)were performed to identify independent risk factors for DGE.Results:The incidence of grade B/C DGE was significantly higher in the NJT group than in the non-NJT group(36.5%vs.21.8%,P=0.006).NJT placement was associated with longer postoperative hospital stay and higher hospitalization costs(both P<0.05).Multivariate analysis revealed intraoperative NJT placement(OR=1.960,95%CI=1.142-3.363,P=0.015)and intraoperative blood loss>400 mL(OR=1.921,95%CI=1.155-3.194,P=0.012)as independent risk factors for DGE.These findings were consistent after PSM.Conclusions:Prophylactic intraoperative NJT placement confers no additional benefit for postoperative recovery after LPD and is associated with a higher risk of DGE,prolonged hospitalization,and increased medical costs.Routine NJT placement should therefore be avoided,and individualized strategies should be adopted to minimize postoperative complications and enhance recovery.