ObjectiveTo explore the effectiveness of traditional Chinese medicine （TCM） chronic disease management programme in preventing postoperative recurrence of colorectal polyps. MethodsThe clinical data of 447 postoperative colorectal polyp patients were retrospectively collected， and the patients were divided into an exposure group and a control group taking the acceptance of TCM chronic disease management programme as exposure factor， and the polyp recurrence rate as the main outcome indicator， comparing the differences in baseline characteristics， outcome events， and safety assessment between the two groups， and conducting correlation analysis between the length of medication and polyp recurrence. Multifactorial logistic regression was used to analyse the effects of receiving the TCM chronic disease management programme （TCM treatment and life management for spleen deficiency and dampness stasis syndrome， dampness and stasis obstruction in collaterals syndrome， and intestinal dampness and heat syndrome）， gender， age， co-morbidities， TCM syndrome， and dietary and exercise factors on the outcome events. ResultsAmong 257 postoperative patients with colorectal polyps， there were 172 in the exposure group and 85 in control group. The recurrence rate of polyps in exposure group was 22.7% （39/172）， while the recurrence rate in control group was 57.6% （49/85）， and the difference between groups was statistically significant （P＜0.01）. The diameter of recurrent polyps in exposure group （median= 4.0 mm） was smaller than that in control group （median= 5.0 mm， P＜0.01）. The correlation analysis between the duration of medication taking and the recurrence of polyps in the spleen deficiency and dampness stasis syndrome group showed Phi value as -0.345 （P＜0.001）； the correlation analysis within the group of dampness and stasis obstruction in collaterals syndrome showed Phi value as -0.361 （P＜0.05）， indicating a negative correlation between the duration of medication taking and polyp recurrence. The results of multivariate logistic regression analysis indicated that the positive effect of accepting TCM chronic disease management programme on preventing polyp recurrence is statistically significant （OR=0.224， P＜0.01）. ConclusionAccepting TCM chronic disease management programme for colorectal polyps can help reducing the recurrence rate after polyp surgery， which is a protective factor for patients to the outcome event.

The core pathogenesis of disease caused by latent toxin is deficiency of healthy qi and lingering pathogen, which is characterized by lingering and recurrent courses, and onset upon exogenous induction. The biological mechanisms of disease caused by latent toxin present multi-dimensional and synergistic characteristics. Immune dysfunction and inflammatory response serve as the core links, involving the abnormal activation of signaling pathways such as Wnt/β-catenin, PI3K/Akt/mTOR, TLR, and NF-κB; the accumulation of metabolites, as the microscopic carrier of latent toxin, participates in chronic complications of diabetes by damaging vascular endothelium and inhibiting repair pathways; immune escape and tolerance, as well as weakened tumor suppressor function, supplement the potential mechanisms of latent toxin from the perspectives of pathogen/tumor cell latency and congenital insufficiency; the imbalance of tissue repair and remodeling, and the imbalance of protein metabolism and cellular homeostasis further improve the mechanism network of latent toxin. Among these, immune dysfunction, tumor suppressor gene mutation, and regulatory dysfunction may be the microscopic manifestations of "healthy qi deficiency"; inflammatory factors, metabolites, viruses, and tumor cells may be the microscopic manifestations of "latent toxin". Current studies have limitations, such as unclear specific biomarkers for different types of latent toxin, insufficient research on the interaction of multiple mechanisms, and lack of clinical verification. It is suggested that future research should be further carried out around "latent toxin classification-mechanism-efficacy".

Objective To explore the research status and hotspots of umbilical acupuncture over the past 20 years using bibliometric methods,thus to providing references for the subsequent clinical treatment of umbilical acupuncture and studies of the therapeutic mechanism.Methods Literature on umbilical acupuncture published between 2004 and 2024 was retrieved from the CNKI,Wanfang Data Knowledge Service Platform,and VIP Chinese Journal Service Platform.Duplicate check was conducted using NoteExpress 3.9.0 software,and then manual screening was performed.The included literature data were imported into VOSviewer for visualized analysis,including institutional collaboration,author collaboration,and keyword co-occurrence.Results A total of 388 articles were included,comprising 286 original research articles,23 reviews,and 79 dissertations.Annual publication analysis revealed a significant upward trend in umbilical acupuncture research output starting from 2017.Zhejiang Chinese Medical University and Hangzhou Hospital of Traditional Chinese Medicine ranked first in publication volume,and Bao Yehua was the most prolific author.Inter-institutional collaboration remained limited,and author collaborations usually occurred in small-team models.Clinical research was the most commonly-seen keyword,and insomnia and stroke were the diseases being frequently studied.Conclusion Clinical research has become the focus of umbilical acupuncture studies over the past two decades,while mechanism research is still in its early stages.Current research hotspots include the research about insomnia and stroke.

ObjectiveTo observe the effects of Wendantang on the expression of inflammatory cytokines， autophagy markers， and key molecules of phosphatidylinositol-3-kinase/protein kinase B/mammalian target of rapamycin （PI3K/Akt/mTOR） signaling pathway in the adipocytes of the rat model of obesity （syndrome of phlegm-dampness） and to explore the material basis of inflammation in obesity （syndrome of phlegm-dampness） and the underlying mechanism of Wendantang intervention. MethodA total of 126 SD rats were randomized into 2 groups： 16 rats in the blank group and 110 rats in the modeling group. The blank group was fed with a basic diet while the modeling group with a high-fat diet to establish the animal model of obesity （syndrome of phlegm-dampness） for 8 weeks. After successful modeling， 48 obese rats were selected according to their body mass and randomized into a model control group， an orlistat （ORLI， 32.40 mg·kg^-1） group， a rapamycin （RAPA， 2 mg·kg^-1） group， and low-， medium-， and high-dose （4.45， 8.90， 17.80 g·kg^-1， respectively） Wendantang groups， with 8 rats in each group. In addition， 8 rats were randomly selected from the blank group to be set as the normal control group. The corresponding agents in each group were administrated by gavage and the model and control groups were administrated with equal amounts of distilled water once daily for 6 weeks. The body mass， Lee's index， body fat ratio， and obesity rate were measured or calculated. The expression of UNC51-like kinase-1 （ULK1）， Beclin1， human autophagy-related protein 5 （Atg5）， p62， and microtubule-associated protein 1 light chain 3 （LC3） Ⅰ/Ⅱ （markers of autophagy in adipocytes） was detected by the immunohistochemical two-step method. Enzyme-linked immunosorbent assay （ELISA） was employed to determine the expression of tumor necrosis factor （TNF）-α， interleukin-6 （IL-6）， IL-1β， monocyte chemotactic protein-1 （MCP-1）， IL-4， IL-10， IL-13， and transforming growth factor （TGF）-β in adipocytes. Western blot was employed to measure the protein levels of classⅠ-PI3K， phosphatidylinositol triphosphate （PIP3）， Akt， mTORC1， ULK1， TSC1， and TSC2 in adipocytes. ResultCompared with the blank group， the modeling group showed increased body mass and Lee's index （P<0.01）， the obesity rate >20%， and phlegm-dampness syndrome manifestations such as physical obesity， decreased mobility， decreased appetite， lusterless and tight fur， loose stools， decreased responsiveness to the outside world， and decreased water intake. Compared with the normal control group， the model control group showed increased body mass， Lee's index， body fat ratio， adipocyte autophagy marker expression， pro- and anti-inflammatory cytokine levels （P<0.05， P<0.01）， down-regulated protein levels of classⅠ-PI3K， PIP3， Akt， mTORC1， TSC1， and TSC2 （P<0.01）， and up-regulated protein level of ULK1 （P<0.01）. The intervention groups showed lower body mass， body fat ratio， adipocyte autophagy marker protein expression， and protein levels of TNF-α， IL-6， IL-1β， MCP-1， IL-4， and IL-13 than the model control group （P<0.05， P<0.01）. Moreover， the RAPA and Wendantang （medium and high dose） groups showed lowered levels of IL-10 and TGF-β （P<0.01）， and the ORLI group showed down-regulated expression of TGF-β （P<0.01）. The expression of key molecules of the signaling pathway was up-regulated （P<0.05， P<0.01） while that of ULK1 was down-regulated （P<0.01） in all the intervention groups. Compared with the RAPA group， the Wendantang groups showed up-regulated expression of all autophagy marker proteins in adipocytes （P<0.01）. In addition， the low-dose Wendantang group showed elevated levels of inflammatory cytokines （except TNF-α） （P<0.05， P<0.01） and down-regulated expression of all key molecules of the signaling pathway （P<0.05， P<0.01）. The levels of inflammatory cytokines （except IL-16， MCP-1， and IL-10） were elevated in the medium-dose Wendantang group （P<0.05， P<0.01）. The expression of key molecules except PI3K of the signaling pathway was down-regulated in the medium- and high-dose Wendantang groups （P<0.05， P<0.01）. Compared with the ORLI group， low- and medium-dose Wendantang groups showed up-regulated expression of autophagy markers in adipocytes （P<0.01）， and the low-dose group showed elevated levels of inflammatory cytokines （IL-6， IL-4， and TGF-β） （P<0.01） and down-regulated expression of all key molecules of the signaling pathway （P<0.01）. The medium-dose Wendantang group showed up-regulated expression of IL-4 （P<0.01） and down-regulated expression of key molecules except PI3K of the signaling pathway （P<0.05， P<0.01）. The high-dose Wendantang group showed increased body mass， up-regulated expression levels of autophagy markers （ULK1， LC3 Ⅰ/Ⅱ） （P<0.05， P<0.01）， down-regulated expression of PIP3， mTORC1， and TSC1 （P<0.05， P<0.01）， and lowered levels of Beclin1， Atg5， TNF-α， and IL-13 （P<0.05， P<0.01）. ConclusionThe inflammation in obesity （syndrome of phlegm-dampness） is closely associated with the PI3K/Akt/mTOR pathway-mediated adipocyte autophagy. Wendantang can treat the chronic inflammation in obese rats with the syndrome of phlegm-dampness by regulating this signaling pathway and thus improve adipocyte autophagy.