ObjectiveThis study aimed to investigate the action mechanism by which Banxia Xiexintang （BXT） inhibits epithelial-mesenchymal transition （EMT） in chronic atrophic gastritis （CAG） rats by regulating the interleukin-17（IL-17）/extracellular regulated protein kinases（ERK）/CCAAT enhancer binding protein β（C/EBPβ）signaling pathway， thereby providing new theoretical evidence for the treatment of CAG with classic traditional Chinese medicine formulas. MethodsA CAG rat model was established by using the combined factor method. After successful modeling， the rats were randomly divided into the model group， low-， medium-， and high-dose groups （0.549， 1.098， 2.196 g·kg^-1， respectively） of BXT， and the positive drug group （vitacoenzyme， 0.3 g·kg^-1）. A normal control group was also set up. After 8 weeks of intervention， the pathological changes of gastric tissue were evaluated. The enzyme-linked immunosorbent assay （ELISA） was used to detect the contents of IL-17， tumor necrosis factor-α （TNF-α）， cyclooxygenase-2 （COX-2）， and C/EBPβ in serum， as well as the contents of EMT markers in gastric mucosal tissue including E-cadherin， N-cadherin， and vimentin. The immunohistochemistry method was employed to determine the localization and protein expression levels of IL-17， p-ERK， and C/EBPβ in gastric mucosal tissue. Western blot was used to detect the protein expressions of C/EBPβ， ERK， and its phosphorylated form （p）-ERK in gastric mucosa. Real-time polymerase chain reaction （Real-time PCR） was applied to measure the mRNA expression levels of ERK， COX-2， and C/EBPβ in gastric mucosa. ResultsCompared with those in the normal control group， the rats in the model group showed gastric mucosal glandular atrophy and inflammatory cell infiltration. The protein and their related mRNA expressions of C/EBPβ， ERK， and p-ERK in gastric mucosa were significantly increased （P<0.05，P<0.01）. The levels of IL-17， TNF-α， COX-2， and C/EBPβ in serum were significantly increased （P<0.01）. The contents of N-cadherin and vimentin in gastric mucosal tissue were significantly increased， while the content of E-cadherin was significantly decreased （P<0.01）. Compared with the model group， after intervention with different doses of BXT， the pathological damage of the gastric mucosa was improved to varying degrees. The protein and mRNA expressions of C/EBPβ， ERK， and p-ERK in gastric mucosa were significantly reduced （P<0.05，P<0.01）. The levels of IL-17， TNF-α， COX-2， and C/EBP β in serum were significantly decreased （P<0.01）. The contents of N-cadherin and vimentin in gastric mucosa tissue were decreased， while the content of E-cadherin was increased （P<0.05，P<0.01）. ConclusionBXT can effectively improve the pathological damage of gastric mucosal tissue in CAG rats. Its action mechanism may be related to reducing the levels of IL-17 and TNF-α in serum， regulating the IL-17/ERK/C/EBPβ signaling pathway and inhibiting the EMT process.

Stroke is one of the leading causes of disability and mortality worldwide. Research into its mechanisms and the development of therapeutic strategies heavily rely on animal models that accurately replicate the pathological features of human disease. An ideal animal model for stroke should not only reproduce the neurological deficits and pathological changes observed in clinical patients but also demonstrate good reproducibility and translational value. This review focuses on the preparation and evaluation methods of ischemic stroke animal models. Firstly, it elaborates on the selection criteria, advantages, and disadvantages of experimental animals, including rodents (rats, mice) and non-rodents (non-human primates, miniature pigs, rabbits, zebrafish). Secondly, it provides a detailed overview of the modeling principles, key procedures, and application scopes for ischemic stroke models and hemorrhagic stroke models. Furthermore, the review summarizes advances in the applications of emerging technologies—including gene editing [e.g., clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9) gene editing], multimodal imaging (e.g., two-photon microscopy, photoacoustic imaging), artificial intelligence, optogenetics, 3D bioprinting, organoid models, and multi-omics–in model optimization, precise assessment, and mechanistic investigation. Finally, based on a systematic analysis of relevant domestic and international literature from 2019 to 2024, this review discusses model selection strategies based on research objectives, a multidimensional evaluation system encompassing behavioral, imaging, and molecular pathological assessments, and envisions future directions involving technological integration to achieve model precision and individualization. This article aims to provide a comprehensive methodological reference to help researchers select appropriate animal models of stroke according to specific scientific questions.

This paper summarizes the experience of professor LIU Shangyi in differentiating and treating rectal carcinoma from the perspective of "treating ulcers as tumors". It is believed that the manifestations of rectal cancer， such as anal itching， cauliflower-like or ulcerative tumors， and bloody stools， are similar to external skin itching， skin ulceration， swelling， and skin bleeding. Therefore， the treatment principles of sores and ulcers department can be applied to treat tumors. Following the diagnostic and treatment approach of dermatology regarding the clinical typical symptoms， for anal itching， the main treatment is to dispel wind and remove dampness， clear heat to relieve itching， using "skin medicinals" such as Difuzi （Fructus Kochiae） and Baixianpi （Cortex Dictamni）， as well as wind medicinals such as Shengma （Rhizoma Cimicifugae） and Fangfeng （Radix Saposhnikoviae）. For constipation， the method of clearing heat and resolving toxins， unblocking the bowels and discharging heat can be used， commonly using Baitouweng （Radix Pulsatillae）， Donglingcao （Herba Rabdosiae Rubescentis） and Dahuang （Radix et Rhizoma Rhei）. In terms of mucosal ulcers， it is critical to differentiate between yin and yang； the treatment of yang ulcers should focus on clearing heat and resolving toxins， commonly using modified Xianfang Huoming Beverage （仙方活命饮）； for yin ulcers， emphasis should be placed on removing dampness and resolving phlegm， commonly with modified Yiyi Fuzi Baijiang Powder （薏苡附子败酱散）. For bloody stool， differentiation is made between deficiency and excess， with the use of Diyu （Radix Sanguisorbae） and Huaihua （Flos Sophorae） for excess syndrome to cool and stop blee-ding， and both herbs dry-fried until charred combined with liver-tonifying medicinals for deficiency syndrome

This paper explores the immune-inflammatory regulatory mechanism of colorectal cancer cachexia and corresponding traditional Chinese medicine （TCM） intervention strategies based on the TCM theory of reinforcing healthy qi and dispelling pathogenen. It is proposed that depletion of healthy qi is the root cause of colorectal cancer cachexia， while cancer toxins exuberance is the symptomatic manifestation of the disease， and failure of the spleen and stomach is the core pathogenesis. In terms of treatment， a TCM treatment system is constructed based on the principles of reinforcing healthy qi to consolidate the foundation and regulate immunity， and dispelling pathogen to remove toxins and alleviate inflammation. The system clarifies the healty qi-reinforcing method as fortifying spleen and boosting qi to enhance immune function， and nourishing blood and enriching yin to consolidate yin essence and healthy qi. It also emphasizes the pathogen-dispelling method as clearing heat and removing toxins to regulate the secretion of inflammatory cytokines， and promoting blood circulation and resolving stasis to improve the immune microenvironment and microcirculation. This therapeutic approach may provide valuable insights for TCM interventions in colo-rectal cancer cachexia.

Cardiotoxicity induced by antineoplastic agents is an important factor affecting the prognosis of cancer patients. This article systematically summarizes the clinical manifestations of cardiotoxicity caused by chemotherapeutic drugs, molecular targeted cancer therapies, and immunotherapeutic drugs, and identifies the core injury mechanisms, including cardiomyocyte apoptosis, oxidative stress, and mitochondrial dysfunction. In Traditional Chinese Medicine (TCM) theory, anticancer drug-induced cardiotoxicity falls under the category of “heat toxins” characterized by dual deficiency of qi and blood, upward flaming of heart heat, stagnation of the heart vessels, and meridian obstruction induced by phlegm-dampness. Therefore, by reviewing the preventive and therapeutic effects and the underlying mechanisms of tonic medicines, interior heat-clearing medicines, blood-circulating and stasis-resolving medicines, phlegm-transforming, cough-suppressing and panting-relieving medicines, and interior-warming medicines, this paper concludes that TCM prevention and treatment of this condition adheres to the formulation principle of “reinforcing healthy qi, removing toxins, and resolving blood stasis”. Its mechanisms of action—including antioxidation effects, regulation of autophagic balance, antagonism of inflammatory responses, and improvement of microcirculation—are highly consistent with modern medical treatment strategies (e.g., dexrazoxane for inhibiting iron-dependent oxidative stress, statins for anti-inflammatory effects). This study provides theoretical support and practical guidance for the collaborative and precise prevention and treatment of anticancer drug-induced cardiotoxicity through the integration of traditional Chinese and Western medicine.

Based on the theory of traditional Chinese medicine （TCM） chronomedicine， this paper explores the pathogenesis and treatment strategies of colorectal cancer mediated by circadian rhythm disorders. It is believed that the imbalance of yin and yang is isomorphic to the disorder of biological clock genes， which is the root cause of the disease. The disharmony of ying and wei （营卫） corresponds to the imbalance of immunity and metabolism， which is the pivot of the disease. The disorder of qi movement is related to the imbalance of intestinal barrier， which is the manifestation of the disease. Accordingly， relevant strategies are proposed， including chronochemotherapy regimen that aligns with biological rhythms to enhance efficacy and reduce toxicity， acupuncture based on the ebb and flow of midnight and midday which selects acupoints along meridians to harmonize qi and blood， and a timed medication strategy that matches the disease mechanism by administering drugs at optimal times. These strategies aim to deepen the understanding of the pathogenesis of colorectal cancer mediated by circadian rhythm disorders from the perspective of TCM chronomedicine， thereby providing new ideas for clinical practice.

Based on the pathogenesis of earth congestion and wood constraint， internal accumulation of turbid toxin， this paper analyzes the evolution characteristics and therapeutic methods of the traditional Chinese medicine （TCM） pathogenesis of cancer cachexia. Based on the progressive process of cancer cachexia， characterized by earth congestion， wood constraint， turbidity accumulation， and disease progression， earth congestion is considered as the initiating factor， which initially attacks the body and leads to qi constraint and stagnation. Over time， middle jiao （焦） fails to transport properly， and the internal accumulation of turbid toxin hinders the ascent and descent of qi. Consequently， earth congestion and wood constraint mutually affect each other， causing the turbid toxin to become increasingly profound and persistent throughout the entire course of cancer cachexia. Combined with the progressive evolution process of the disease， it is proposed that in the early stage， treatment should focus on fortifying the spleen， resolving stagnation， and unblocking fu （腑） organs to restore the transportation and transformation functions of the spleen and stomach， increase appetite， and promote muscle recovery. In the middle stage， harmonizing the liver and spleen and smoothing the qi movement should be taken as the key therapeutic principles to reverse the disease progression. In the late stage， treatment should focus on resolving turbid toxin and unblocking stagnated stasis in the collaterals to halt the progression of the disease and prolong the survival period of cancer patients.

Objective:To investigate the association between photodynamic diagnosis(PDD)and treatment efficacy of 5-aminolevu-linic acid(ALA)photodynamic therapy(PDT)in patients with cutaneous squamous cell carcinoma in situ(cSCCis).Methods:A pro-spective cohort study was conducted among the patients with cSCCis who underwent ALA-PDT in Department of Dermatology,Huashan Hospital,Fudan University,from January 2020 to November 2024.All patients were diagnosed with cSCCis based on biopsy,and invasive squamous cell carcinoma was excluded.Clinical information was collected and PDD was performed before treatment,and the patients were divided into moderate fluorescence group and strong fluorescence groups based on fluorescence intensity.All patients received six sessions of PDT treatment at an interval of 1-2 weeks.The primary endpoint was the initial complete clearance rate at 3 months after the last treatment session,and secondary endpoints were the sustained complete clearance rate at 12 months after the last treatment session and treatment failure rate.The multivariate regression analysis,the survival curves,and the Cox regression analysis were used to investigate the association between PDD fluorescence intensity and treatment efficacy,as well as other influencing factors for treatment efficacy.Results:Compared with the strong fluorescence group,the moderate fluorescence group had significantly lower initial complete clearance rate[57.14%(8/14)vs.93.33%(28/30),odds ratio OR=0.100,P=0.010]and sustained complete clearance rate[42.86%(6/14)vs.76.67%(23/30),OR=0.230,P=0.030)].The multivariate regression analysis showed that moderate fluores-cence was an independent risk factor for initial complete clearance(OR=0.030,P=0.030).The moderate fluorescence group had a significantly higher treatment failure rate than the strong fluorescence group[57.14%(8/14)vs.23.33%(7/30),P=0.030].The survival analysis and the Cox regression analysis showed that moderate fluo-rescence was an independent risk factor for PDT treatment failure(hazard ratio=3.040,P=0.048).There were no significant differences in adverse reactions between the two groups.Conclusion:PDD fluorescence intensity can predict the efficacy of ALA-PDT in patients with cSCCis.Moderate fluorescence indicates a higher risk of treatment failure,which can help to guide clinicians in develop-ing individualized treatment strategies.

Background The Inner Mongolia Autonomous Region is a vast area with a wide array of ecological environments, resulting in considerable regional variations in air pollution characteristics. Current research is limited by a scarcity of systematic, region-wide studies and risk assessments. Objective To assess the health risks associated with inhalation exposure to nine heavy metal and metalloid elements in atmospheric fine particulate matter (PM_2.5) for the population of the Inner Mongolia Autonomous Region. Methods From the 10th to the 16th of each month throughout 2023, atmospheric PM_2.5 samples were collected at designated monitoring sites in 12 leagues (cities) across the Inner Mongolia Autonomous Region to analyze the characteristics and trends in concentration. The health risk assessment model developed by the United States Environmental Protection Agency was employed to evaluate both the non-carcinogenic and carcinogenic risks associated with the heavy metal elements beryllium (Be), cadmium (Cd), chromium (Cr), hydrargyrum (Hg), plumbum (Pb), manganese (Mn), and nickel (Ni) and the metalloid elements stibium (Sb) and arsenic (As). Results In 2023, a total of 1206 valid PM_2.5 samples were analyzed from the Inner Mongolia Autonomous Region. The annual average PM_2.5 concentrations in Inner Mongolia, as well as in the cities of Ordos, Wuhai, and the Alxa League, all exceeded the national limit of 35 μg·m⁻³. The PM_2.5 concentrations across the leagues (cities) exhibited a clear seasonal variation, peaking in winter, followed by spring, and reaching a minimum in summer and autumn. The median PM_2.5 concentration in Ordos throughout the year was higher than that in the other leagues (cities) of the region. Concerning health risks, the non-carcinogenic risks associated with the 9 elements detected in each league (city) were all below 1, indicating acceptable levels. However, the non-carcinogenic risk values for Mn, Cr, and As were relatively high; specifically, Ordos City displayed the highest non-carcinogenic risk values for Mn (7.74×10⁻¹) and Cr (2.97×10⁻²), while Chifeng City recorded the highest value for As (2.34×10⁻³). The carcinogenic risk values for As, Cd, Cr, and Ni fell within the range of 1×10⁻⁹ to 1×10⁻⁵, representing an acceptable level. The health risks varied with age, and the elderly residents faced the highest non-carcinogenic and carcinogenic health risks. Conclusion While the carcinogenic and non-carcinogenic risks from heavy metals and metalloids within atmospheric PM_2.5 in the Inner Mongolia Autonomous Region are generally within acceptable limits, the potential risks that Mn, As, and Cr pose to the health of elderly people warrants particular attention, and Ordos and Chifeng cities exhibit notably higher health risks among other areas. It is recommended that regular, long-term monitoring be conducted, taking into account the specific conditions at monitoring sites across each league (city), and that targeted air quality management strategies be implemented to protect public health.

Objective·To investigate the differential gene expression of microglia in the gray and white matter of multiple sclerosis(MS)using single-nucleus transcriptomic analysis,aiming to explore their roles in disease progression,and identify key transcriptional regulatory networks associated with the disease.Methods·snRNA-seq data of frozen human brain tissue samples from MS patients and control individuals were obtained from the Gene Expression Omnibus(GEO)database.R language,along with R packages such as Seurat,was employed to identify cell types based on specific cell markers.Microglia were extracted from the identified cell populations and classified based on their anatomical origin,either gray matter or white matter.Dimensionality reduction and clustering techniques were utilized to identify distinct microglial subpopulations with differential characteristics.Differentially expressed genes(DEGs)between the MS and control groups at the subpopulation level were analyzed by using the Seurat package.Gene set enrichment analysis of Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)was conducted on the DEGs to further explore the biological significance of these differences.Monocle3 was used for pseudotime analysis to study dynamic changes in microglia subpopulations during disease progression.Single cell regulatory network inference and clustering(SCENIC)method was applied to analyze transcription factor(TF)regulatory networks,aiming to identify key transcription factors potentially involved in MS regulation.Results·After quality control,a total of 149 062 nuclei were retained for analysis.Following dimensional reduction and clustering,12 238 microglia were identified by using key markers,including DOCK8,CSF1R,P2RY12,and CD74.The results of GO and KEGG pathway analysis showed that in gray matter microglia,functions such as endocytosis,ion homeostasis,and lipid localization were downregulated during disease progression,while in white matter microglia,functions such as protein folding,cytoplasmic translation,and response to thermal stimuli were upregulated.SCENIC analysis revealed that the expression of transcription factors such as FLI1,MITF,and FOXP1 was upregulated in MS.Conclusion·Microglia play a critical role in MS,with white matter microglia being more significantly impacted by MS than their gray matter counterparts.Transcription factors such as FLI1,MITF,and FOXP1 are identified as key regulators involved in disease modulation,with their associated transcriptional regulatory networks playing a central role in disease modulation.