ObjectiveThe development trend and knowledge structure of the research on human use experience （HUE） of traditional Chinese medicine （TCM） were systematically reviewed， and the core challenges and future directions were identified. This study aims to provide reference for the construction of a scientific and feasible research and development framework and evidence transformation system. MethodsLiterature related to "human use experience" published from January 1， 2019 to July 31， 2025 was retrieved from the China National Knowledge Infrastructure （CNKI）， Wanfang， China Science and Technology Journal Database （VIP）， and PubMed databases. Bibliometric visualization was conducted using Excel， VOSviewer， and CiteSpace， followed by in-depth reading and thematic summarization of core literature. ResultsA total of 181 papers were included for bibliometric analysis， with 45 articles used for in-depth thematic mining. The analysis showed that the number of publications on HUE research has increased in a stepwise manner over the past five years. Yang Zhongqi （24 times） was the core of the author network， the journal with the highest number of publications was China Journal of Chinese Materia Medica， the institutions publishing the most articles were mainly research institutions， regulatory agencies， hospitals， and universities， high-frequency keywords included "new TCM drugs"， "real-world studies"， and "clinical comprehensive evaluation"， keyword clustering analysis formed three major clusters： Policy orientation， application fields， and methodological approaches. Thematic analysis reveals that HUE-based evaluation should be integrated throughout the research and development process， encompassing three dimensions： TCM theory， clinical value， and pharmaceutical fundamentals， with toxic herbs and compatibility contraindications being key foci. Data collection primarily relies on empirical data， while real-world data constitute the primary source for clinical research， with efficacy and safety as the shared core. Data management emphasizes quality control and statistical analysis； however， the management of bias and confounding remains a critical bottleneck in evidence transformation. In practice， HUE-based approaches have successfully supported the registration and evaluation of multiple categories of new TCM drugs. ConclusionThe research on HUE of TCM has formed a policy-driven pattern characterized by， rapid development and close link with regulatory practice. A technical framework covering the whole chain of research and development has been constructed with clinical value as the core， which provides methodological basis and strategy reference for the scientific transformation of HUE of TCM from "experience" to "evidence".

ObjectiveTo investigate the effects and underlying mechanisms of polydatin in delaying the progression of colitis-associated colorectal cancer （CAC） by constructing an azoxymethane （AOM）/dextran sulfate sodium （DSS）-induced CAC mouse model and conducting in vitro experiments. MethodsFifty-four male C57BL/6J mice were randomly divided into normal， model， and polydatin groups （0.045 g·kg^-1）. The CAC mouse model was established using AOM/DSS， and samples were collected at 4， 7， and 10 weeks. Body weight change rate， disease activity index （DAI）， and tumor formation were assessed. Hematoxylin-eosin （HE） staining was used to observe pathological injury in intestinal tissues. Immunohistochemistry （IHC） was performed to detect zonula occludens-1 （ZO-1） expression in colonic tissues， and Western blot was used to detect the expression of E-cadherin， N-cadherin， and Vimentin in colonic epithelial cells. Real-time PCR was used to measure mRNA expression of interleukin-17A （IL-17A）， Wnt3a， β-catenin， T cell factor 1 （Tcf1）， E-cadherin， N-cadherin， and Vimentin in colonic tissues. Flow cytometry was used to analyze the proportion of CD8⁺T cells and the expression of exhaustion-related molecules in tumors. Human colon cancer DLD-1 cells were cultured in a polydatin-containing medium， and wound healing assays were performed to observe migration changes. Real-time PCR was used to detect mRNA expression of interleukin-17 receptor A （IL-17RA）， Wnt3a， β-catenin， Tcf1， E-cadherin， N-cadherin， and Vimentin in DLD-1 cells. ResultsCompared with the normal group， the model group at all three time points showed significantly decreased body weight change rate （P<0.01）， significantly shortened colon length （P<0.01）， and markedly increased DAI scores （P<0.01）. HE staining revealed significant inflammatory cell infiltration in the submucosa of the colon in the model group， accompanied by epithelial dysplasia. ZO-1 expression in colonic tissues was significantly reduced （P<0.01）. The mRNA expression of the pro-inflammatory factor IL-17A and key molecules of the Wnt/β-catenin pathway （Wnt3a， β-catenin， Tcf1） was significantly elevated （P<0.05）. The mRNA and protein expression of epithelial-mesenchymal transition （EMT） markers N-cadherin and Vimentin was significantly upregulated （P<0.05）， while E-cadherin expression was significantly downregulated （P<0.05）. The proportion of tumor-infiltrating CD8⁺T cells expressing immunosuppressive molecules （TIM-3， LAG-3， PD-1） was significantly increased （P<0.05）. Compared with the model group， the polydatin group showed significant improvement in body weight and DAI score （P<0.01）， as well as recovery of colon length and tissue injury. ZO-1 expression in colonic tissue was significantly increased （P<0.01）， while IL-17A， Wnt3a， β-catenin， Tcf1， N-cadherin， and Vimentin expression levels were significantly decreased （P<0.05）， and E-cadherin expression was significantly increased （P<0.01）. Tumor-infiltrating CD8⁺ T cells expressing immunosuppressive molecules were significantly reduced （P<0.05）. In vitro experiments showed that polydatin significantly inhibited migration of DLD-1 cells （P<0.01） and reversed the upregulation of IL-17RA， Wnt3a， β-catenin， N-cadherin， and Vimentin mRNA， as well as the downregulation of E-cadherin mRNA （P<0.05）. ConclusionPolydatin inhibits IL-17A secretion and IL-17RA expression， improves the immune microenvironment， blocks activation of the Wnt/β-catenin signaling pathway， suppresses EMT markers （N-cadherin and Vimentin）， and restores tight junction protein expression in intestinal epithelial cells， thereby delaying the progression from colitis to colorectal cancer in mice.

AIM: To analyze the pathological features, immunophenotype, and imaging findings of conjunctival lymphangiectasia(CL), and to explore the etiological mechanisms and provide a theoretical basis for clinical diagnosis and treatment. METHODS:This single-center descriptive cross-sectional study enrolled postoperative specimens from patients with CL who underwent surgical treatment in the hospital between Feb. 2023 and Sept. 2025. Routine hematoxylin and eosin(HE)staining and immunohistochemical staining(D2-40, CD31, CD34, CK)were performed. Anterior segment optical coherence tomography(AS-OCT)was used to observe the lesion morphology. The pathological results were comprehensively analyzed combined with clinical data. RESULTS: A total of postoperative specimens from 32 eyes of 32 patients with CL were enrolled, including 23 females(72%)and 9 males(28%), with a mean age of 53.03±12.47 y. All patients presented with single or multiple transparent cystic elevations beneath the bulbar conjunctiva. The postoperative pathological manifestations were characterized by dilation of conjunctival lymphatic vessels lined with a single layer of flattened endothelial cells, accompanied by edema and inflammatory infiltration in the surrounding stroma. All cases were positive for D2-40, confirming a lymphatic origin; some cases also expressed CD31 and CD34. AS-OCT revealed the lesions as unilocular or multilocular cystic spaces with low reflectivity. After complete surgical resection, the mean follow-up period was 16.2 mo with no recurrence.CONCLUSION:CL is a benign ocular surface lesion characterized by lymphatic vessel dilation. The endothelium co-expresses lymphatic and some vascular markers, suggesting that CL may belong to the spectrum of vascular malformations. AS-OCT has adjunctive diagnostic value, and surgical resection has definitive therapeutic efficacy.

OBJECTIVE To evaluate the long-term efficacy of intra-articular injection of hyaluronic acid （HA）， platelet-rich plasma （PRP）， and micro-fragmented adipose tissue （MFAT） in treatment of knee osteoarthritis （KOA）. METHODS Randomized controlled trials （RCTs） of KOA patients receiving intra-articular injection of the three agents were collected from PubMed， Web of Science， Embase， Cochrane Library， CNKI， Wanfang Data， VIP， Chinese Biomedical Literature Service System，and clinical trial registration platforms. The retrieval time limit was from January 2016 to December 2025. After screening the literature， extracting the data，and evaluating the quality of the literature， network meta-analysis was performed using RevMan 5.3 and Stata MP 16.0 software. RESULTS A total of 31 RCTs involving 2 964 patients were included. For pain relief， after 6 months of treatment， the Visual Analogue Scale （VAS） scores in the PRP+HA and PRP groups were significantly lower than those in the saline and HA groups （ P ＜0.05）， PRP+HA and PRP were ranked as the top two by surface under the cumulative ranking curve （SUCRA）. After 12 months of treatment， the VAS scores in the PRP group were significantly lower than those in the HA and saline groups （ P ＜0.05）， PRP and PRP+HA were ranked as the top two by SUCRA. For functional recovery， after 6 months of treatment， the Western Ontario and McMaster Universities Osteoarthritis Index （WOMAC） scores in the PRP group were significantly lower than those in the HA or saline groups （ P ＜0.05）. After 12 months of treatment， the WOMAC scores in the MFAT， PRP and PRP+HA groups were significantly lower than those in the HA or saline groups （ P ＜0.05）. After 6 and 12 months of treatment， International Knee Documentation Committee （IKDC） scores in the MFAT and PRP groups were significantly higher than the saline group （ P ＜0.05）， and after 12 months of treatment， the PRP group was significantly higher than the HA group （ P ＜0.05）. MFAT and PRP were ranked as the top two by SUCRA for both the WOMAC and IKDC scores. CONCLUSIONS For pain relief， PRP+HA showed a significant advantage at 6 months after treatment， whereas PRP alone demonstrated a notable superiority at 12 months after treatment. For functional recovery， MFAT exhibited a marked advantage at both 6 and 12 months after treatment.

Based on the modern understanding that lipid metabolism disorders mediate tumor microenvironmental imbalance in esophageal carcinoma， this paper proposes that failure of spleen and kidney warming and internal accumulation of phlegm-toxin constitute the core pathogenesis of esophageal carcinoma. Deficiency of spleen and kidney yang qi serves as the root cause， while impaired transformation and transportation of lipids and the accumulation of phlegm-toxin represent the superficial manifestations. Phlegm originates from the transformation of lipids， while toxin arises from and attaches to phlegm. Their interaction forms a sticky and persistent pathological state that runs throughout the entire disease process. The evolution of pathogenesis follows a dynamic and progressive pattern. In the early stage， failure of spleen and kidney warming and dysfunction of lipid metabolism mediate abnormalities in a lipid-enriched microenvironment； in the middle stage， lipid turbidity condenses into phlegm， and phlegm-toxin stasis promotes the formation of an inflammatory and hypercoagulable microenvironment； in the late stage， dysfunction of the sanjiao （三焦） warming function and impaired qi transformation lead to an imbalance in the hypoxic and metabolically dysfunctional microenvironment. Accordingly， a staged therapeutic approach is proposed， including warming the kidney and strengthening the spleen， transforming phlegm and resolving toxin， and warming and unblocking the sanjiao. By regulating lipid metabolism to restore tumor microenvironmental homeostasis， this approach provides a new theore-tical perspective and practical strategy for the intervention of esophageal cancer progression through traditional Chinese medicine.

Based on the modern understanding that lipid metabolism disorders mediate tumor microenvironmental imbalance in esophageal carcinoma， this paper proposes that failure of spleen and kidney warming and internal accumulation of phlegm-toxin constitute the core pathogenesis of esophageal carcinoma. Deficiency of spleen and kidney yang qi serves as the root cause， while impaired transformation and transportation of lipids and the accumulation of phlegm-toxin represent the superficial manifestations. Phlegm originates from the transformation of lipids， while toxin arises from and attaches to phlegm. Their interaction forms a sticky and persistent pathological state that runs throughout the entire disease process. The evolution of pathogenesis follows a dynamic and progressive pattern. In the early stage， failure of spleen and kidney warming and dysfunction of lipid metabolism mediate abnormalities in a lipid-enriched microenvironment； in the middle stage， lipid turbidity condenses into phlegm， and phlegm-toxin stasis promotes the formation of an inflammatory and hypercoagulable microenvironment； in the late stage， dysfunction of the sanjiao （三焦） warming function and impaired qi transformation lead to an imbalance in the hypoxic and metabolically dysfunctional microenvironment. Accordingly， a staged therapeutic approach is proposed， including warming the kidney and strengthening the spleen， transforming phlegm and resolving toxin， and warming and unblocking the sanjiao. By regulating lipid metabolism to restore tumor microenvironmental homeostasis， this approach provides a new theore-tical perspective and practical strategy for the intervention of esophageal cancer progression through traditional Chinese medicine.

Objective To investigate the association between single nucleotide polymorphisms (SNPs) in the nicotinamide adenine dinucleotide phosphate-oxidase (NOX) 2 and NOX4 genes and susceptibility to noise-induced hearing loss (NIHL). Methods A total of 439 noise-exposed workers were recruited using a convenience sampling method. Based on pure-tone air conduction hearing threshold tests, participants were categorized into normal hearing, mild hearing loss, and moderate hearing loss groups, with 147, 154, 138 individuals, respectively. Peripheral venous blood samples of the workers were collected for DNA extraction. Genotyping of nine SNPs loci in NOX2 and NOX4 genes was performed using multiplex polymerase chain reaction, single-base extension, and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. Results A total of seven of the nine SNPs loci conformed to Hardy-Weinberg equilibrium among the workers in the normal hearing group (all P>0.05). There was no significant difference in the genotype distribution or allele frequencies for these seven SNPs loci among workers in these three groups (all P>0.05). Ordinal logistic regression analysis showed that, after adjusting for confounders including age, sex, cumulative noise exposure, smoking, alcohol consumption, and earplug use, individuals carrying the GG genotype at rs200522762 had a lower risk of NIHL compared with those carrying the TT genotype under the codominant model (P<0.05). In the recessive model, individuals carrying the GG genotype at the rs200522762 locus had a lower risk than those carrying the GT+TT genotypes (P<0.05). Polymorphisms at the other six SNPs loci were not associated with NIHL risk (all P>0.05). Conclusion The NOX4 rs200522762 polymorphism is associated with susceptibility to NIHL.

Conjunctival lymphangiectasia is a low-incidence ocular surface disease that is currently rarely reported in the relevant literature. It may be related to cosmetic eyelid surgery, tumor, radiation or chemotherapy and other factors and often causes a foreign body sensation, lacrimation, eye pain, visual fatigue and other discomfort. These symptoms of constant eye irritation affect the patient's quality of life. At present, anterior segment optical coherence tomography can be used for clinical diagnosis, and the novel monoclonal antibody D2-40, as a marker of lymphatic endothelial cell dilatation, has high specificity in pathological diagnosis. Previous studies have not fully defined the pathogenesis of the disease, and treatment methods vary. Conventional treatment has resulted in varying degrees of damage to the conjunctiva in patients. In recent years, anti-vascular endothelial growth factor drugs have been reported to be effective in treating the disease with few complications. This article reviews the pathogenesis, diagnosis and treatment of this rare disease in order to gain a better understanding of conjunctival lymphangiectasia and provide more support for clinical diagnosis and treatment.

The Department of Thoracic Surgery of Shanghai Chest Hospital has performed esophageal function testing for over 30 years, being the only department of its kind in China with this capability. The pressure testing and 24-hour pH/impedance monitoring of the esophagus is of great help to assist in the diagnosis and treatment of benign and malignant esophageal diseases related to it. Thanks to the esophageal function test, in addition to the routine various endoscopic anti-reflux procedures, our hospital has taken the lead in China in recent years to carry out a series of clinical and research work for benign esophageal diseases, such as the development of magnetic ring, double nedoscopic combination and new anti-reflux endoscopic techniques. In recent years, we have carried out high-resolution esophageal manometry and 24-hour pH/impedance monitoring for patients with interstitial pneumonia and pulmonary fibrosis suspected to be caused by gastroesophageal acid reflux. We can better assess the correlation between gastroesophageal reflux and pulmonary fibrosis, and to provide the different clinical treatments and even surgical interventions. The Bravo capsule is used more often in the United States, and it has obvious advantages over traditional approach for acid measurement. We strongly call for the collaboration between industry and academic institutions in this field, and the development of our own related products with independent intellectual property rights.

ObjectiveTo clarify the repair effect of Mume Fructus on the intestinal mucosal epithelial barrier in the mouse model of inflammatory bowel disease （IBD） and explore the repair mechanism. MethodsThirty-six male C57BL/6 mice were randomly assigned into six groups： normal， model， low-， medium-， and high-dose （200， 400， and 800 mg·kg^-1） Mume Fructus， and sulfasalazine （300 mg·kg^-1）. Except the normal group， the rest groups had free access to 2% dextran sulfate sodium （DSS） solution for seven days to establish the IBD model， followed by a seven-day drug intervention. The body weight change and disease activity index （DAI） were recorded. After the last administration， spleen and colon tissue samples were collected to analyze the differences in colon length and spleen index. Hematoxylin-eosin staining was used to observe the morphology of the colon tissue. The level of diamine oxidase （DAO） in the serum was measured by the DAO assay kit. Immunohistochemistry was employed to determine the expression of tight junction proteins such as Claudin-1， Occludin， and zonula occludens-1 （ZO-1） in the colon tissue. Real-time PCR was performed to measure the mRNA levels of tumor necrosis factor-α （TNF-α） and interleukin-1β （IL-1β） in the colon tissue. Finally， Western blot was employed to determine the protein levels of mitogen-activated protein kinase kinase （MEK）， extracellular signal-regulated kinase （ERK）， phosphorylated （p）-MEK， and phosphorylated ERK in the colon tissue. ResultsCompared with the normal group， the model group exhibited decreases in body weight and colon length （P<0.01）， increases in DAI， spleen index， and serum DAO level （P<0.01）， damaged colonic epithelium and goblet cells， and obvious infiltration of inflammatory cells. In addition， the model group exhibited higher positive expression of Claudin-1， Occludin， and ZO-1 （P<0.01）， higher mRNA levels of TNF-α and IL-1β （P<0.01）， and higher protein levels of p-MEK and p-ERK （P<0.05， P<0.01） than the normal group. However， sulfasalazine and three doses of Mume Fructus markedly decreased the body weight and DAI （P<0.05）， recovered the colon length and spleen index， alleviated colon tissue damage， lowered the level of DAO in the serum （P<0.01）， and down-regulated the mRNA levels of TNF-α and IL-1β （P<0.01） and the protein levels of p-MEK and p-ERK （P<0.05）. Sulfasalazine and low- and medium-dose Mume Fructus increased the positive expression of Occludin， Claudin-1， and ZO-1 （P<0.05， P<0.01）. Furthermore， high-dose Mume Fructus elevated the protein expression of Occludin （P<0.05）. ConclusionMume Fructus can restore the expression of intestinal epithelial tight junction proteins by inhibiting the phosphorylation of proteins in the MEK/ERK signaling pathway and down-regulating the levels of TNF-α and IL-1β， thus repairing the intestinal mucosal barrier in the mouse model of IBD.