This paper systematically reviews the core concepts and lines of theoretical inheritance of major spleen-stomach theories in traditional Chinese medicine （TCM）， including spleen deficiency theory， spleen-stomach damp-heat theory， and liver-spleen disharmony theory. It is found that these theories have all undergone a developmental trajectory characterized by classical foundation， refinement of therapeutic methods， systematization of pathogenesis， and modern innovation. The evolution of spleen-stomach theory has achieved a shift from a singular focus on tonifying the spleen to regulating dynamic middle-jiao （焦） balance， and from localized spleen-stomach regulation to the circular movement of qi involving all five zang organs. In terms of modern disease-syndrome integrative research， spleen deficiency syndrome is shown to be closely associated with impairment of the gastrointestinal mucosal barrier， metabolic disorders， and gene polymorphisms related to Helicobacter pylori-associated gastric diseases. Spleen-stomach damp-heat syndrome is closely linked to hyperactive energy metabolism， inflammatory cytokines， and abnormal expression of aquaporins. Liver-spleen disharmony syndrome is mainly associated with dysregulation of the brain-gut axis and microbiota-related metabolic disorders. It is proposed that future research on spleen-stomach diseases and syndromes should further elucidate their potential multidimensional differential biological characteristics， thereby promoting the modernization of the TCM discipline of spleen-stomach studies.

Objective: To systematically review the modeling strategies, primary outcomes, and quantifiable effects in animal models of transfusion-related acute lung injury (TRALI), transfusion-associated circulatory overload (TACO), acute hemolytic transfusion reaction (AHTR), and related transfusion paradigms. Subgroup meta-analysis was designated as the primary analytical framework, with the overall pooled effect treated as exploratory. Methods: We searched PubMed, Embase, Web of Science, and the Cochrane Central Register of Controlled Trials (CENTRAL) from inception to December 30, 2025. Eligible studies utilized animal models to simulate transfusion-related adverse reactions and provided extractable quantitative outcomes. The SYRCLE tool was used to assess the risk of bias. Random-effects models were employed to calculate odds ratios (ORs) and 95% confidence intervals (CIs). Prespecified subgroup analyses were conducted for TRALI, TACO, AHTR, and donor sex-related transfusion paradigms. Additional analyses included funnel plots, Egger/Begg tests, leave-one-out sensitivity analyses, and meta-regression based on publication year. Results: Twenty-one studies comprising 24 independent comparisons were included in the quantitative synthesis. The overall pooled estimate was OR=1.07 (95% CI:0.69-1.66), with substantial heterogeneity (I =96%). Subgroup analyses yielded the following estimates: TRALI, OR=0.83 (95%CI:0.57-1.21, I =97%); TACO, OR=1.85 (95%CI:0.54-6.34, I =93%); donor sex-related paradigms, OR=1.49 (95%CI:1.02-2.17, I =85%); and AHTR, OR=0.26 (95%CI:0.10-0.64, I =0%). Between-subgroup differences were statistically significant (P<0.000 1). Publication year was positively correlated with effect size (P=0.001 4). Most studies demonstrated unclear risk of bias across several SYRCLE domains due to incomplete methodological reporting. Conclusion: Animal models of transfusion-related adverse reactions exhibit significant structural heterogeneity across syndrome categories. Therefore, subgroup-specific and narrative syntheses are recommended as the primary presentation framework, rather than relying on a single overall pooled effect. Complement-targeted interventions in AHTR models demonstrated a consistent protective signal. In contrast, TRALI and TACO models require greater standardization in modeling protocols and endpoint definitions to reduce methodological variability.

Bladder tumor within inguinal bladder hernia is rare. This article reports a case of a male patient who was admitted to hospital due to gross hematuria，accompanied by lower abdominal pain when straining to urinate for two months. Physical examination revealed a irreducible mass in the left inguinal region. Ultrasound and MRI examinations suggested an inguinal bladder hernia complicated by multiple bladder lesions. Cystoscopy revealed extensive tumors，and pathological examination indicated high-grade urothelial carcinoma with carcinoma in situ. PET-CT confirmed pelvic lymph node metastasis. The patient underwent three cycles of neoadjuvant therapy followed by laparoscopic radical cystectomy combined with hernia repair. There was no evidence of recurrence of the hernia or tumor after one year of follow-up.

Bladder tumor within inguinal bladder hernia is rare. This article reports a case of a male patient who was admitted to hospital due to gross hematuria，accompanied by lower abdominal pain when straining to urinate for two months. Physical examination revealed a irreducible mass in the left inguinal region. Ultrasound and MRI examinations suggested an inguinal bladder hernia complicated by multiple bladder lesions. Cystoscopy revealed extensive tumors，and pathological examination indicated high-grade urothelial carcinoma with carcinoma in situ. PET-CT confirmed pelvic lymph node metastasis. The patient underwent three cycles of neoadjuvant therapy followed by laparoscopic radical cystectomy combined with hernia repair. There was no evidence of recurrence of the hernia or tumor after one year of follow-up.

Hepatocellular carcinoma is the most common malignancy of the liver and poses serious health burdens on China and the whole world. However， most patients with hepatocellular carcinoma are already in the advanced stage at the time of diagnosis， with fewer opportunities for surgery and limited treatment options. In recent years， the advances in molecular targeted therapies have brought new hope for patients with advanced hepatocellular carcinoma. Among these therapies， lenvatinib is the second first-line drug after sorafenib approved by the US Food and Drug Administration for the treatment of advanced hepatocellular carcinoma， and it has attracted widespread attention for its powerful anti-tumor properties. However， the efficacy of lenvatinib is severely limited by its drug resistance. This article reviews the research advances in the molecular mechanisms of lenvatinib resistance in hepatocellular carcinoma and discusses possible ways to improve the efficacy of lenvatinib， so as to improve its efficacy.

OBJECTIVE To explore the action mechanism of kushenol F （KSCF） in treating ulcerative colitis （UC） in mice. METHODS The potential targets of KSCF intervening in UC were predicted with network pharmacology and molecular docking. C57BL/6J mice were randomly divided by body weight into model group， positive control group （sulfasalazine， 703 mg/kg）， KSCF group （100 mg/kg）， and normal group， with 6 mice per group. The UC model of mice was induced by dextran sulfate sodium solution. During the modeling period， the mice were given relevant medicine intragastrically， once a day， for 7 consecutive days. After the last administration， the disease activity index （DAI） of the mice was scored； the length of the mice’s colon was measured； pathological changes in the colon tissue of mice were observed； the levels of lipopolysaccharide （LPS） in serum， myeloperoxidase （MPO）， nitric oxide （NO） and superoxide dismutase （SOD） in the colon were detected in mice； the expression levels of occludin and ZO-1 in colon tissue of mice were detected； the proportions of CD3+T， CD4+T， and CD8+T lymphocytes in the spleen and the ratio of CD4+/CD8+ were detected； changes in colonic microbiota were analyzed by 16S rDNA sequencing. RESULTS Results of network pharmacology indicated that KSCF may treat UC by regulating signaling pathways such as phosphatidylinositol-3 kinase/protein kinase B （PI3K/AKT） and nuclear factor kappa B （NF- κB）. Molecular docking results showed that KSCF bound most stably with NF-κB p65 protein. Animal experiment results demonstrated that， compared with the model group， the pathological characteristics of colon tissue in mice were improved in KSCF group. DAI scores， serum levels of LPS， the levels of MPO，NF-κB p65 phosphorylation and NLRP3 protein expression in the colon， and the proportion of CD8+T lymphocytes in the spleen were reduced significantly （P＜0.05）. Body weight， SOD levels， expression levels of occludin and ZO-1 in the colon， proportions of CD3+T and CD4+T lymphocytes， and the CD4+/CD8+ ratio in the spleen were significantly increased （P＜0.05）； the abundance of Firmicutes， Actinobacteria， Akkermansia， and Lactobacillus genera were increased， while Proteobacteria decreased； the microbial community structure tended towards that of the normal group. CONCLUSIONS KSCF alleviates UC by restoring intestinal microbial imbalance， enhancing immune response， and inhibiting colonic inflammatory responses， thereby improving intestinal barrier integrity.

OBJECTIVE To investigate the intervention effect of kushenol F （KSC-F） on ulcerative colitis （UC） mice. METHODS Totally 30 male C57BL/6J mice were randomly divided into the normal group， model group， positive drug group （sulfasalazine， 703 mg/kg）， KSC-F 50 mg/kg group （KSC-F50 group）， and KSC-F 100 mg/kg group （KSC-F100 group）， with 6 mice in each group. Except for the normal group， the mice in the remaining groups were given 3% dextran sulfate sodium solution continuously for 7 days to induce UC model. Concurrently， administration groups received corresponding drug solution intragastrically， once a day， for 10 consecutive days. During the experiment， the changes in body weight and bowel movements of the mice were observed. Disease activity index scoring was performed after the last administration. The histopathological morphology of colonic tissue was examined. The levels of inflammatory factors in the serum and colon tissue were measured. Additionally， the mRNA expression of inflammatory factors， and the protein expressions of inflammation-related proteins [interleukin-1β （IL-1β）， forkhead box O1（FOXO1）， phosphoinositide 3-kinase（PI3K）， phosphorylated PI3K（p-PI3K）， p38 mitogen-activated protein kinase（p38 MAPK）， phosphorylated p38 MAPK（p-p38 MPAK） and phosphorylated protein kinase B（p- Akt）] were determined in colonic tissue. RESULTS KSC-F could alleviate weight loss and colonic tissue damage in UC mice. KSC- F reduced the levels of IL-1β， IL-6， IL-8 and tumor necrosis factor-α （TNF-α） in serum， as well as IL-1β， IL-6， IL-17 and TNF- α in colonic tissue to varying degrees and increased the levels of IL-10 in both serum and colonic tissue （P＜0.05 or P＜0.01）. Moreover， KSC-F decreased the expression levels of IL-1β， IL-17 and TNF-α mRNA， as well as p-PI3K， p-p38 MAPK， and p- Akt proteins in colonic tissue to varying degrees， and increased the expression levels of IL-10 mRNA and FOXO1 protein in colonic tissue （P＜0.05 or P＜0.01）. CONCLUSIONS KSC-F effectively alleviates UC symptoms in mice by inhibiting PI3K， Akt and p38 MAPK activation， mitigating the release of pro-inflammatory factors such as IL-1β， IL-6， TNF- α，promoting the anti-inflammatory factor IL-10 secretion， and reducing inflammation-induced colonic tissue damage.

Objective To investigate the clinicopathological characteristics and the factors affecting the prognosis of patients with resectable sarcomatoid carcinoma of the bladder(SCB).Methods A retrospective analysis was conducted with the clinical data of patients with resectable SCB treated at the Second Hospital of Tianjin Medical University between September 2008 and December 2023.The patients were divided into two groups,a bladder-preserving surgery(BPS)group and a radical cystectomy(RC)group,according to the specific surgical approach used for each patient.Kaplan-Meier survival curves were used to evaluate overall survival(OS)in both groups,and Cox regression models were employed to identify risk factors affecting survival.Results A total of 77 patients with resectable SCB were included.Among them,35 patients(45.5％)underwent BPS,while 42 patients(54.5％)underwent RC.Ki-67 expression≥30％was observed in 91.7％of the patients.A total of 92.2％of the patients was tested positive for cytokeratin(CK)and 98.1％for vimentin.In addition,62.5％and 37.5％of patients had the human epidermal growth factor receptor 2(Her-2)scores of 0 and 1+,respectively.The median follow-up time was 23.2 months(ranging from 0.4 to 164.7 months).The 1-year,3-year,and 5-year survival rates for the BPS group and the RC group were as follows,76.2％vs.84.9％,46.7％vs.61.1％,and 35.6％vs.43.2％,respectively.Multivariate Cox regression analysis revealed that in the RC group,age ≥ 75 years old(hazard ratio[HR]=3.836,95％confidence interval[CI]:1.168-12.595,P=0.027),tumor multiplicity(HR=3.439,95％CI:1.235-9.574,P=0.018),and lack of adjuvant therapy(HR=3.164,95％CI:1.015-9.862,P=0.047)were independent risk factors affecting survival.In the BPS group,female sex was identified as an independent risk factor for survival(HR=3.601,95％CI:1.200-10.804,P=0.022).Conclusion Ki-67,CK,and vimentin are significantly overexpressed in SCB patients,while Her-2 is either unexpressed or expressed at low levels.In the RC group,tumor multiplicity,age ≥75 years,and lack of postoperative adjuvant therapy are independent risk factors for overall survival.Female sex is an independent risk factor affecting prognosis in the BPS group.

Dendritic cell-based cancer vaccines (DC vaccines) have been proved efficient and safe in immunotherapy of various cancers, including melanoma, ovarian and prostate cancer. However, the clinical responses were not always satisfied. Here we proposed a novel strategy to prepare DC vaccines. In the present study, a fusion protein SNU containing a secretin-penetratin (SecPen) peptide, NY-ESO-1 and ubiquitin was designed and expressed. To establish the DC vaccine (DC-SNU), the mouse bone marrow-derived DCs (BMDCs) were isolated, pulsed with SNU and maturated with cytokine cocktail. Then peripheral blood mononuclear cells (PBMCs) from C57BL/6 mice inoculated intraperitoneally with DC-SNU were separated and cocultured with MC38/MC38

Objective: To investigate the etiologic and epidemiologic features of an infectious diarrhea outbreak in a boarding school in Fuyang city, Anhui province. Methods: Traceability hypothesis of this study was tested according to the epidemiological characteristics of the cases. Feces, anal swabs, water samples and food residues related to the patients and chefs were collected for pathogen isolation and detection. Biochemical identification, virulence gene detection, drug susceptibility test, PFGE and multilocus sequence typing were performed. Results: The incidence rate (3.41%) of different dormitory buildings within the water supply area by shallow wells was higher than that (0.98%) of the deep wells, with statistical significance (χ²=17.215, P<0.001). Sixteen strains belonged to the Shigella Sonneri family were isolated from the patient’s samples, and all carrying the ipaH gene. Seven strains belonged to sen and ial genes. Set1 gene that did not appear in all the 16 strains were highly resistant to ampicillin, tetracycline, compound xinnomine, cefazoline, cefotaxime, gentamicin, naphthidinic acid and streptomycin, including 9 strains to doxycycline. The pulse field pattern of the 16 strains of Shigella sonneri appeared the same, with the ST type as ST152. Conclusion When combined data from the etiological and epidemiological investigation, it was confirmed that Shigella sonneri was the pathogen of this outbreak, and water from the shallow wells might be responsible for the source of infection.