As one of the most common malignant tumors， digestive system tumors exhibit an increase in the incidence and mortality year by year. Its pathogenesis is complex， making it difficult to carry out early prevention. Autophagy is a process in which cells use lysosomes to degrade their organelles and macromolecules to maintain cellular homeostasis under the regulation of autophagy-related genes. Cellular autophagy has a dual regulatory effect on the tumor microenvironment， which always affects the occurrence and development of digestive system tumors. Therefore， the effect and mechanism of action of cellular autophagy on digestive system tumors have become a hot topic in tumor therapy in recent years. Meanwhile， the remarkable research results of targeted autophagy drugs indicate that cellular autophagy may become an important target for anti-digestive system tumors. Traditional Chinese medicine （TCM） has been widely used in the comprehensive treatment of digestive system tumors with good efficacy. A variety of active ingredients in TCM， such as flavonoids， glycosides， terpenoids， quinones， and alkaloids， can increase the expression of autophagy-associated proteins microtubule-associated protein 1 light chain 3 （LC3）Ⅱ/Ⅰ， autophagy-related gene （ATG）5， ATG7， inhibit the expression of autophagy-related protein p62 ， and induce autophagy in digestive system tumor cells， thereby exerting the anti-digestive system tumor effect. By summarizing the research results in recent years on the modulation of cell autophagy by active ingredients in TCM to fight against digestive system tumors， this paper analyzed the relevant signaling pathways， regulatory factors， and functional characteristics of cell autophagy modulation， so as to elucidate the mechanism by which active ingredients of TCM induce autophagy and to provide ideas and references for clinical application.

As one of the most common malignant tumors， digestive system tumors exhibit an increase in the incidence and mortality year by year. Its pathogenesis is complex， making it difficult to carry out early prevention. Autophagy is a process in which cells use lysosomes to degrade their organelles and macromolecules to maintain cellular homeostasis under the regulation of autophagy-related genes. Cellular autophagy has a dual regulatory effect on the tumor microenvironment， which always affects the occurrence and development of digestive system tumors. Therefore， the effect and mechanism of action of cellular autophagy on digestive system tumors have become a hot topic in tumor therapy in recent years. Meanwhile， the remarkable research results of targeted autophagy drugs indicate that cellular autophagy may become an important target for anti-digestive system tumors. Traditional Chinese medicine （TCM） has been widely used in the comprehensive treatment of digestive system tumors with good efficacy. A variety of active ingredients in TCM， such as flavonoids， glycosides， terpenoids， quinones， and alkaloids， can increase the expression of autophagy-associated proteins microtubule-associated protein 1 light chain 3 （LC3）Ⅱ/Ⅰ， autophagy-related gene （ATG）5， ATG7， inhibit the expression of autophagy-related protein p62 ， and induce autophagy in digestive system tumor cells， thereby exerting the anti-digestive system tumor effect. By summarizing the research results in recent years on the modulation of cell autophagy by active ingredients in TCM to fight against digestive system tumors， this paper analyzed the relevant signaling pathways， regulatory factors， and functional characteristics of cell autophagy modulation， so as to elucidate the mechanism by which active ingredients of TCM induce autophagy and to provide ideas and references for clinical application.

ObjectiveTo explore the effect of the medical-community linkage model on activities of daily living, psychological status and motor function of stroke patients in the community. MethodsA total of 60 stroke patients admitted to two community health service centers and their affiliated stations in Fengtai District, Beijing, from January, 2024 to August, 2025 were enrolled and randomly divided into control group (n = 30) and intervention group (n = 30). The control group received routine medicine, dietary care and rehabilitation management, while the intervention group underwent rehabilitation with the medical-community linkage model, for twelve weeks. They were assessed with modified Barthel Index (MBI), Hamilton Anxiety Scale (HAMA), Hamilton Depression Scale (HAMD) and Fugl-Meyer Assessment (FMA) before and after intervention. ResultsAfter intervention, the MBI, HAMA, HAMD and FMA scores of patients improved in both groups (|t| > 5.599, P < 0.001), and improved more in the intervention group than in the control group (P < 0.05), except MBI. The HAMA and HAMD scores of family members decreased in both groups (|t| > 10.333, P < 0.001), and decreased more in the intervention group than in the control group (t > 5.681, P < 0.001). ConclusionThe medical-community linkage model can further improve the motor function of stroke patients in community, as well as the psychological status of both patients and their family members.

ObjectiveTo investigate the effect of interfering with long noncoding RNA （LncRNA） small nucleolar RNA host gene16 （SNHG16） on improving angiogenesis of ectopic endometrial stromal cells （EScs） in adenomyosis （AM） by targeting upregulation of miRNA （miR）-141-3p and inhibition of high mobility group box-1 protein （HMGB1）. MethodsThe expression levels of SNHG16， miR-141-3p and HMGB1 mRNA in endometrial tissues of 52 patients with adenomyosis （AM group） and 52 patients who needed hysterectomy due to cervical cancer or ovarian cancer （control group） were detected by quantitative reverse transcription polymerase chain reaction （qRT-PCR）. Y14 cells were divided into small hairpin RNA （shRNA） NC group， shRNA SNHG16 group， shRNA SNHG16+miR-141-3p inhibitor （inhibitor） group， shRNA SNHG16+inhibitor NC group and blank group. The targeting relationship between miR-141-3p and SNHG16 as well as HMGB1 was verified. The expression levels of SNHG16， miR-141-3p and HMGB1 mRNA in Y14 cells were detected by qRT-PCR. CCK-8 and Transwell assay were used to detect cell proliferation， invasion and migration. Microvascular density （MVD） was determined by immunofluorescence. The expressions of hypoxia-inducing factor α （HIF-1α）， cyclooxygenase-2 （Cox-2）， vascular endothelial growth factor （VEGF） and HMGB1 were detected by Western blot. ResultsThe expression of SNHG16 and HMGB1 mRNA in AM group was higher than that in control group， but the expression of miR-141-3p was lower than that in control group （P0.05）. The expression of SNHG16， HMGB1 mRNA， proliferation rate， migration， invasion number， MVD， expression of VEGF， HIF-1 α， Cox-2， and HMGB1 proteins in the shRNA SNHG16 group were lower than those in the blank group and shRNA NC group， while the expression of miR-141-3p was higher than that in the blank group and shRNA NC group （P0.05）. Inhibition of miR-141-3p reversed the improvement of EScs angiogenesis by interfering with SNHG16. ConclusionInterference with LncRNA SNHG16 improves EScs angiogenesis and inhibits proliferation， migration， and invasion of EScs by targeting upregulation of miR-141-3p and inhibition of HMGB1.

Gastrointestinal tumors （GTs）， including colorectal cancer， gastric cancer， liver cancer， pancreatic cancer， and esophageal cancer， are increasing in incidence worldwide and have become one of the major diseases threatening human health. Tumor stem cells （TSCs）， an undifferentiated subpopulation within tumor tissues， possess biological characteristics such as self-renewal， multidirectional differentiation， high tumorigenicity， and resistance to radiochemotherapy. They play an important role in the occurrence， progression， recurrence， and metastasis of GTs and have increasingly become a research hotspot in GT treatment. Although modern medicine has made remarkable progress， there remain many problems in therapeutic approaches targeting TSCs. In this context， traditional Chinese medicine （TCM）， with its favorable safety profile and multi-target mechanisms， has shown potential advantages and value in regulating TSCs. It can reduce TSC drug resistance， enhance the sensitivity of tumor cells to chemotherapeutic agents， inhibit tumor growth and metastasis， and has shown unique advantages in improving the quality of life and prolonging the survival of GT patients. Studies have found that active components of Chinese medicine， such as terpenoids， polyphenols， flavonoids， glycosides， and quinones， and Chinese medicine compound formulas， including Zuojin pills， Sijunzi decoction， Biejiajian pills， and Xuanfu Daizhe decoction， can inhibit TSCs-related signaling pathways such as the Notch signaling pathway， the Wnt/β-catenin signaling pathway， the phosphatidylinositol 3-kinase/protein kinase B （PI3K/Akt） signaling pathway， and the Hippo signaling pathway. They also reduce the expression of TSC surface markers， including sex-determining region Y-box 2 （SOX2）， sex-determining region Y-box 9 （SOX9）， octamer-binding transcription factor 4 （OCT4）， prominin-1 （CD133）， cluster of differentiation 44 （CD44）， cluster of differentiation 24 （CD24）， and thyroid transmembrane protein 1 （CD90）， thereby hindering TSC differentiation， accelerating their metabolic processes， improving the tumor microenvironment， and consequently inhibiting GT growth. This study collects and analyzes recent research on the regulation of TSCs by TCM in the treatment of GT， aiming to provide a new theoretical basis for tumor therapy with TCM， expand its application in the comprehensive treatment of GT， and offer new therapeutic ideas and methods for clinical practice.

BACKGROUND: Senescent human skin primary fibroblast (FB) models have been established for studying aging-related, proliferative, and inflammatory skin diseases. The aim of this study was to compare the transcriptome characteristics of human primary dermal FBs from children and the elderly with four senescence models. METHODS: Human skin primary FBs were obtained from healthy children (FB-C) and elderly donors (FB-E). Senescence models were generated by ultraviolet B irradiation (FB-UVB), D-galactose stimulation (FB-D-gal), atazanavir treatment (FB-ATV), and replication exhaustion induction (FB-P30). Flow cytometry, immunofluorescence staining, real-time quantitative polymerase chain reaction, co-culturing with immune cells, and bulk RNA sequencing were used for systematic comparisons of the models. RESULTS: In comparison with FB-C, FB-E showed elevated expression of senescence-related genes related to the skin barrier and extracellular matrix, proinflammatory factors, chemokines, oxidative stress, and complement factors. In comparison with FB-E, FB-UVB and FB-ATV showed higher levels of senescence and expression of the genes related to the senescence-associated secretory phenotype (SASP), and their shaped immune microenvironment highly facilitated the activation of downstream immune cells, including T cells, macrophages, and natural killer cells. FB-P30 was most similar to FB-E in terms of general transcriptome features, such as FB migration and proliferation, and aging-related characteristics. FB-D-gal showed the lowest expression levels of senescence-related genes. In comparisons with the single-cell RNA sequencing results, FB-E showed almost complete simulation of the transcriptional spectrum of FBs in elderly patients with atopic dermatitis, followed by FB-P30 and FB-UVB. FB-E and FB-P30 showed higher similarity with the FBs in keloids. CONCLUSIONS Each senescent FB model exhibited different characteristics. In addition to showing upregulated expression of natural senescence features, FB-UVB and FB-ATV showed high expression levels of senescence-related genes, including those involved in the SASP, and FB-P30 showed the greatest similarity with FB-E. However, D-galactose-stimulated FBs did not clearly present aging characteristics.
Humans ; Fibroblasts/drug effects* ; Cellular Senescence/physiology* ; Skin/metabolism* ; Child ; Transcriptome/genetics* ; Aged ; Ultraviolet Rays ; Cells, Cultured ; Galactose/pharmacology*

Although cancer immunotherapy has made great strides in the clinic, it is still hindered by the tumor immunosuppressive microenvironment (TIME). The stimulator of interferon genes (STING) pathway which can modulate TIME effectively has emerged as a promising therapeutic recently. However, the delivery of most STING agonists, specifically cyclic dinucleotides (CDNs), is performed intratumorally due to their insufficient pharmacological properties, such as weak permeability across cell membranes and vulnerability to nuclease degradation. To expand the clinical applicability of CDNs, a novel pH-sensitive polycationic polymer-modified lipid nanoparticle (LNP-B) system was developed for intravenous delivery of CDNs. LNP-B significantly extended the circulation of CDNs and enhanced the accumulation of CDNs within the tumor, spleen, and tumor-draining lymph nodes compared with free CDNs thereby triggering the STING pathway of dendritic cells and repolarizing pro-tumor macrophages. These events subsequently gave rise to potent anti-tumor immune reactions and substantial inhibition of tumors in CT26 colon cancer-bearing mouse models. In addition, due to the acid-sensitive property of the polycationic polymer, the delivery system of LNP-B was more biocompatible and safer compared with lipid nanoparticles formulated with an indissociable cationic DOTAP (LNP-D). These findings suggest that LNP-B has great potential in the intravenous delivery of CDNs for tumor immunotherapy.

Objective:To investigate the independent risk factors of recurrent laryngeal nerve(RLN)injury after microwave ablation(MWA)for thyroid nodules of different malignant stratification.Methods:The medical records of 240 patients,who underwent microwave ablation for thyroid nodules in the department of ultrasound,Beijing Friendship Hospital Affiliated to Capital Medical University from September 2022 to August 2024,were retrospectively selected.All thyroid nodule cases were categorized based on the American College of Radiology Thyroid Imaging Reporting and Data System(TI-RADS)classification criteria and whether occurred RLN injury during the ablation procedure.A total of 54 patients with RLN injury and 65 patients without RLN injury,who were classified as TI-RADS 4a or higher than that,were divided into the high-risk group,and 35 patients with RLN injury and 86 patients without RLN injury,who were classified below TI-RADS 4a,were divided into the low-risk group.And then,a series of parameters included the benign and malignant nodules,the upper diameter of nodules,the left and right diameters of nodules,anteroposterior diameters of nodules,the aspect ratio(>1,≤1),overall echo,calcification,location,cystic solidity,and ablation parameters were analyzed.The risk factors of RLN injury of two groups were analyzed by using single factor and multi factor analysis.Results:There were not significant differences in the benign and malignant nodules,the upper diameters of nodules,the left and right diameters of nodules,anteroposterior diameters of nodules,the volume of nodules,overall echo,calcification,ldiametersocation,and cystic solidity between high and low-risk groups(P>0.05).In high-risk group,the distance between nodules and esophageal groove of trachea was less or equal to 2mm,and the increase of nodule volume were independent risk factors for RLN injury(OR=4.199,1.002,P<0.05),respectively.In the low-risk group,the nodule,which location was on the Zuckerkandl tubercle(Z-nodule),was risk factor that significantly increased RLN injury(OR=3.296,P<0.05).Conclusion:For nodules with differently malignant risk,the anatomical location,volume parameters and optimized ablation plan should be paid special attention before surgery,so as to reduce the risk of RLN injury.

The incidence and mortality rates of malignant tumors continue to rise,which posing a serious threat to the physical and mental health of the global population,and becoming a significant scientific problem in urgent need of resolution.Tumor immuno-therapy,as a novel anti-tumor treatment,optimizes the treatment modalities for tumors.Currently,combination of immunotherapy with chemotherapy and targeted therapy has shown promising results in anti-tumor treatment.Traditional Chinese medicine is widely used in comprehensive anti-tumor treatments,demonstrating significant effectiveness and distinct advantages.Among them,monomeric saponins in Chinese herbal medicine exhibit remarkable anti-tumor effects with the notable advantages of high efficiency and low tox-icity.This has made them a focal point of research for many oncologists.Studies have revealed that a large number of monomeric sapo-nins from Chinese herbal medicine can directly or indirectly affect the functions of immune cells by regulating the innate immune sys-tem,adaptive immune system,and related immune cell factors.This enhances the immune cytotoxicity against tumor cells,thereby better exerting the anti-tumor immune effects.This paper summarizes the research findings on the anti-tumor effects of monomeric sapo-nins in recent years.It elaborates on the specific mechanisms by which monomeric saponins from Chinese herbal medicine regulate im-mune cells to exert anti-tumor effects.The aim of this paper is to provide new research perspectives for tumor immunotherapy,further harness the crucial role of traditional Chinese medicine in anti-tumor treatment,and propel the modernization of traditional Chinese medicine.

Objective To explore the effects and mechanisms of Changpu Yujin Tang(CPYJT)on the NOD-like receptor thermal protein domain associated protein 3/cysteinyl aspartate specific proteinase-1/Gasdermin D(NLRP3/Caspase-1/GSDMD)signaling pathway-mediated neuroinflammation in rats with Tourette syndrome(TS).Methods SPF-grade male SD rats were randomly divided into the Control and TS groups.After successful modeling in the TS group,the rats were randomly divided into the Model,Tiapride,and CPYJT groups,and were treated with the corresponding drugs for 4 weeks.After the treatment,the rats' behavior was scored,H & E staining was used to observe pathological changes in the striatum,ELISA was used to measure the content of IL-1β and IL-18,RT-qPCR was used to detect the expression of NLRP3 and ASC mRNA,and Western blot was used to detect the expression of NLRP3,ASC,Caspase-1,Cleaved-Caspase-1,GSDMD,and GSDMD-NT proteins.Results Compared with the Control group,the Model group showed increased scores of stereotyped and motor behaviors(P＜0.01),pathological changes in the striatal tissue,increased content of IL-1β and IL-18(P＜0.01),and upregulated expression of NLRP3,ASC mRNA,and NLRP3,ASC,Caspase-1,Cleaved-Caspase-1,GSDMD,and GSDMD-NT proteins(P＜0.01).Compared with the Model group,the Tiapride group and the CPYJT group showed decreased scores of stereotyped and motor behaviors(P＜0.01),improved pathological damage in the striatal tissue,reduced content of IL-1β and IL-18(P＜0.01),and inhibited expression of NLRP3,ASC mRNA,and NLRP3,ASC,Caspase-1,Cleaved-Caspase-1,GSDMD,and GSDMD-NT proteins(P＜0.01).Conclusion The therapeutic effect of CPYJT on TS is related to the inhibition of the neuroinflammatory response mediated by the NLRP3/Caspase-1/GSDMD signaling pathway.