This paper outlines the development of artificial intelligence （AI） and its applications in traditional Chinese medicine （TCM） research， and elucidates the roles and advantages of large language models， knowledge graphs， and natural language processing in advancing syndrome identification， prescription generation， and mechanism exploration. Using spleen-stomach diseases as an example， it demonstrates the empowering effects of AI in classical literature mining， precise clinical syndrome differentiation， efficacy and safety prediction， and intelligent education， highlighting an upgraded research paradigm that evolves from data-driven and knowledge-driven approaches to intelligence-driven models. To address challenges related to privacy protection and regulatory compliance in cross-institutional data collaboration， a "trusted federated evidence-based analysis platform for TCM spleen-stomach diseases" is proposed， integrating blockchain-based smart contracts， federated learning， and secure multi-party computation. The deep integration of AI with privacy-preserving computing is reshaping research and clinical practice in TCM spleen-stomach diseases， providing feasible pathways and a technical framework for building a high-quality， trustworthy TCM big-data ecosystem and achieving precision syndrome differentiation.

OBJECTIVE To comprehensively evaluate the efficacy， safety and cost-effectiveness of insulin icodec in treating type 2 diabetes mellitus （T2DM）， providing evidence-based guidance for new drug selection in hospital and clinical medication decision-making. METHODS PubMed， Cochrane Library， Embase， CNKI， Wanfang， VIP and foreign health technology assessment （HTA） websites were searched by using rapid health technology assessment from inception to 15 July 2025 for systematic reviews/meta-analyses， pharmacoeconomic studies， and HTA reports on insulin icodec in the treatment of T2DM. After data extraction and quality assessment， the findings of the included studies were analyzed descriptively. RESULTS Ten systematic reviews/meta-analyses and three pharmacoeconomic studies were included. Among them， 4 systematic reviews/meta-analyses were of high quality； the overall quality of the 3 pharmacoeconomic studies was relatively good. Regarding efficacy， insulin icodec was superior to once-daily basal insulin in reducing glycated hemoglobin （HbA1c） and in achieving the target of HbA1c＜7% （P＜0.05）. No significant differences were observed between icodec insulin and comparators in lowering fasting plasma glucose （P＞0.05）. For safety， insulin icodec did not increase the incidence of any adverse events （AEs）， serious AEs， clinically significant hypoglycemia （random glucose＜3 mmol/L）， injection-site reactions， or allergic reactions， compared with once-daily basal insulin overall （P＞ 0.05）； however， insulin icodec was associated with a significant increase in body weight （P＜0.05）. Domestic economic evaluations indicated that insulin icodec was more cost-effective than insulin glargine and insulin degludec when its annual costs were in the range of 784.90-1 145.96 and 597.66-736.34 US dollars， respectively. CONCLUSIONS Insulin icodec demonstrates favorable efficacy and safety profiles in the treatment of T2DM； however， attention should be paid to the risk of weight gain. Under China’s healthcare system， insulin icodec demonstrates greater economic value only when the patient’s weekly required basal insulin dose falls within a specific range，and clinical practice requires individualization.

Objective To investigate the function and mechanism of miR-29 family in trauma induced coagulopathy(TIC).Methods Bioinformatics was used to analyze the targeting relationship between miR-29 family members and hepatocyte nuclear factor-4α(HNF-4α).HE staining results,TEG parameters and coagu-lation parameters were used to verify the TIC rat model construction.Real-time quantitative fluorescent PCR(RT-qPCR)and Western blot were used to detect the expression of miR-29 family,HNF-4α and coagulation factor Ⅹ(FⅩ)in rat liver tissues.Overexpression of miR-29b-3p(miR-29b-3p mimics)or silence of miR-29b-3p(miR-29b-3p inhibitor)was transfected into hepatocytes,and the levels of miR-29b-3p,HNF-4α and FⅩ in hepatocytes were detected by RT-qPCR and Western blot.Double lucifase reporter gene assay verified the targeted regulation of miR-29b-3p on HNF-4α.The miR-29b-3p mimics and/or HNF-4α overexpression vector were transfected into hepatocytes,and the levels of miR-29b-3p,HNF-4α and FⅩ in hepatocytes were detected by RT-qPCR and Western blot.Results Bioinformatic prediction results from the miRDIP database identified that multiple members of the miR-29 family(miR-29a-3p,miR-29b-3p,miR-29b-5p,and miR-29c-3p)contain potential binding sites with HNF-4α.Histopathological evaluation through HE staining,combined with TEG parameters and coagulation profiles,confirmed successful establishment of the TIC rat model.Quantitative analyses using RT-qPCR and Western blot revealed that compared to controls,both HNF-4α and coagulation FⅩ expression levels were markedly suppressed in the model group,while miR-29b-3p expression showed significant elevation in TIC rats(P＜0.01).In vitro functional studies demonstrated that neither overexpression nor silencing of miR-29b-3p significantly influenced hepatocyte proliferation(P＞0.05).How-ever,forced expression of miR-29b-3p effectively downregulated HNF-4α and its downstream target FⅩ,whereas miR-29b-3p knockdown substantially upregulated these molecules(P＜0.05).This regulatory rela-tionship was further validated by dual luciferase reporter assays confirming direct targeting between HNF-4α and miR-29b-3p.Notably,exogenous HNF-4α overexpression significantly rescued FⅩ suppression induced by miR-29b-3p overexpression(P＜0.05).Conclusion miR-29b-3p is up-regulated in TIC,which can promote the progression of TIC by targeting HNF-4α to regulate FⅩ expression.

Objective To explore the effects and mechanisms of bone marrow mesenchymal stem cell(BMMSC)-derived exosomes(BMMSC-Exo)on hypoxia/reoxygenation(H/R)-induced injury in rat cardiomyocyte cell line(H9c2).Methods BMMSC-Exosomes were isolated by ultracentrifugation.The cells were divided into three groups:control,H/R,and H/R+BMMSC-Exo(H/R+Exo).A hypoxia/reoxygenation(H/R)injury model was es-tablished by exposing cells to 12 hours of hypoxia followed by 6 hours of reoxygenation.Flow cytometry was used to detect cell apoptosis,DHE staining was used to assess cellular ROS levels,JC-1 immunofluorescence staining was used to evaluate mitochondrial membrane potential,and Western blot was used to detect mitochondrial autophagy-re-lated proteins.Results BMMSC-Exo treatment significantly alleviated oxidative stress,restored mitochondrial mem-brane potential,reduced mitochondrial autophagy levels,and effectively decreased cardiomyocyte apoptosis.Conclu-sions Bone marrow mesenchymal stem cell-derived exosomes alleviate H/R-induced cardiomyocyte injury.

A U-Net incorporating improved Transformer and convolutional channel attention module is designed for biventricular segmentation in MRI image.By replacing the high-level convolution of U-Net with the improved Transformer,the global feature information can be effectively extracted to cope with the challenge of poor segmentation performance due to the complex morphological variation of the right ventricle.The improved Transformer incorporates a fixed window attention for position localization in the self-attention module,and aggregates the output feature map for reducing the feature map size;and the network learning capability is improved by increasing network depth through the adjustment of multilayer perceptron.To solve the problem of unsatisfactory segmentation performance caused by blurred tissue edges,a feature aggregation module is used for the fusion of multi-level underlying features,and a convolutional channel attention module is adopted to rescale the underlying features to achieve adaptive learning of feature weights.In addition,a plug-and-play feature enhancement module is integrated to improve the segmentation performance which is affected by feature loss due to channel decay in the codec structure,which guarantees the spatial information while increasing the proportion of useful channel information.The test on the ACDC dataset shows that the proposed method has higher biventricular segmentation accuracy,especially for the right ventricle segmentation.Compared with other methods,the proposed method improves the DSC coefficient by at least 2.83%,proving its effectiveness in biventricular segmentation.

Objective:To investigate the role of an inflammatory microenvironment induced by Porphyromonasgingivalis ( P. gingivalis) in the occurrence of esophageal squamous cell carcinoma (ESCC) in mice. Methods:A total of 180 C57BL/6 mice were randomly divided into 6 groups, i.e. control group, P. gingivalis group, 4NQO group, 4NQO + P. gingivalis group, 4NQO + P. gingivalis + celecoxib group, and 4NQO + P. gingivalis + antibiotic cocktail (ABC, including metronidazole, neomycin, ampicillin, and vancomycin) group, with 30 mice in each group, using the random number table. All mice were normalized by treatment with ABC in drinking water for 2 weeks. In the following 2 weeks, the mice in the control group and the P. gingivalis group were given drinking water, while the other 4 groups were treated with 30 μg/ml 4NQO in the drinking water. In weeks 11-12, the mice in the P. gingivalis group, the 4NQO + P. gingivalis group, the 4NQO + P. gingivalis + celecoxib group, and the 4NQO + P. gingivalis + ABC group were subjected to ligation of the second molar in oral cavity followed by oral P. gingivalis infection thrice weekly for 24 weeks in weeks 11-34. In weeks 13-34, the mice in 4NQO + P. gingivalis+celecoxib group and 4NQO + P. gingivalis + ABC group were administered with celecoxib and ABC for 22 weeks, respectively. At the end of 34 weeks, gross and microscopic alterations were examined followed by RT-qPCR and immunohistochemistry to examine the expression profiles of inflammatory- and tumor-molecules in esophagi of mice. Results:At 34 weeks, 4NQO treatment alone did not affect the foci of papillary hyperproliferation, diseased area, and the thickness of the esophageal wall, but significantly enhanced the foci of hyperproliferation (median 1.00, P＜0.05) and mild/moderate dysplasia (median 2.00, P＜0.01). In addition, the expression levels of IL-6 [8.35(3.45,8.99)], IL-1β [6.90(2.01,9.72)], TNF-α [12.04(3.31,14.08)], c-myc [2.21(1.80,3.04)], pSTAT3, Ki-67, and pH2AX were higher than those in the control group. The pathological changes of the esophageal mucosa were significantly more overt in the 4NQO + P. gingivalis group in terms of the foci of papillary hyperproliferation (median 2.00), diseased area (median 2.51 mm 2), the thickness of the esophageal wall (median 172.52 μm), the foci of hyperproliferation (median 1.00, P＜0.05), and mild/moderate dysplasia (median 1.00, P＜0.01). In mice of the 4NQO + P. gingivalis group, the expression levels of IL-6 [12.27(5.35,22.08)], IL-1β [13.89(10.04,15.96)], TNF-α [19.56(6.07,20.36)], IFN-γ [11.37(8.23,20.07)], c-myc [2.62(1.51,4.25)], cyclin D1 [4.52(2.68,7.83)], nuclear pSTAT3, COX-2, Ki-67, and pH2AX were significantly increased compared with the mice in the control group. In mice of the 4NQO + P. gingivalis group, the diseased area, invasive malignant foci as well as pSTAT3 and pH2AX expression were significantly blunted by celecoxib. Treatment with ABC markedly reduced the papillary hyperproliferative foci, invasive malignant foci, and pSTAT3 expression but not pH2AX. Conclusions:P. gingivalis promotes the occurrence of esophageal squamous cell carcinoma in mice by inducing an inflammatory microenvironment primed with 4NQO induced DNA damage. Clearance of P. gingivalis with ABC or anti-inflammatory intervention holds promise for prevention of esophageal squamous cell malignant pathogenesis via blockage of IL-6/STAT3 signaling and amelioration of inflammation.

Objective To assess the value of cone-beam computed tomography (CBCT) in evaluating the response of unresectable liver cancer to transarterial chemoembolization (TACE). Methods A total of 55 unresectable liver cancer patients with 90 lesions who received TACE at the First People’s Hospital of Liangshan Yi Autonomous Prefecture between July 2021 and July 2023 were enrolled in the study. The response to TACE was evaluated using the modified Response Evaluation Criteria in Solid Tumors one month post-treatment. The value of lesion diameter, volume, and density on CBCT images in predicting the response to TACE was assessed using the area under the receiver operating characteristic curve. Results Of the 55 patients treated with TACE, 26 achieved complete response, 17 achieved partial response, 9 showed stable disease, and 3 had progressive disease. Of the 90 lesions, 48 achieved complete response, 20 achieved partial response, 17 showed stable disease, and 5 had progressive disease. On CBCT images, the mean diameter, volume, and density of lesions with complete and non-complete responses were (20.9 ± 9.9) mm, (1719.3 ± 777.9) mm³, and (143.7 ± 87.9) HU, versus (10.9 ± 7.7) mm, (890.0 ± 327.4) mm³, and (38.8 ± 33.3) HU, respectively, with significant differences between the two groups (t=10.6, 79.8, and 65.5; all P < 0.01). One month post-treatment, CT scans displayed no enhanced areas in lesions with complete response and visible enhanced areas in lesions with non-complete response, with mean lesion diameter and density of (14.1 ± 6.2) mm and (78.8 ± 30.3) HU, respectively. In addition, the areas under the receiver operating characteristic curves of lesion diameter, volume, and density on CBCT images were 0.935, 0.955, and 0.981, respectively, in distinguishing between complete and non-complete responses following TACE. Using a cut-off value of 82.5 HU for predicting response to TACE, the lesion density had sensitivity, specificity, positive predictive value, and negative predictive value of 95.5%, 100.0%, 100.0%, and 95.0%, respectively. Conclusion CBCT is effective in predicting the short-term response of liver cancer to TACE.

Objective: The study aimed to investigate the role of N6-methyladenosine (m6A) modification in spinal cord injury (SCI) and its underlying mechanism, focusing on the interplay between m6A methyltransferase-like 3 (METTL3), miR-30c, and autophagy-related proteins. Methods: An SCI model was established in rats, and changes in autophagy-related proteins, m6A methylation levels, and miR-30c levels were analyzed. Hydrogen peroxide (H2O2)-stimulated spinal cord neuron cells (SCNCs) were used to assess the impact of METTL3 overexpression. The effects of STM2457, an antagonist of METTL3, were evaluated on cell viability, apoptosis, and autophagy markers in H2O2-stimulated SCNCs. Results: In the SCI model, decreased levels of autophagy markers and increased m6A methylation, miR-30c levels, and METTL3 were observed. Overexpression of METTL3 in SCNCs led to reduced cell viability, increased apoptosis, and suppressed autophagy. Conversely, co-overexpression of autophagy-related protein 5 (ATG5) or miR-30c inhibition reversed these effects. Knocking out METTL3 yielded opposite results. STM2457 treatment improved cell viability, reduced apoptosis, and upregulated autophagy markers in SCNCs, which also enhanced functional recovery in rats as measured by the Basso-Beattie-Bresnahan score and inclined plate test. Conclusion STM2457 alleviated SCI by suppressing METTL3-mediated m6A modification of miR-30c, which in turn induces ATG5-mediated autophagy. This study provides insights into the role of m6A modification in SCI and suggests a potential therapeutic approach through targeting METTL3.

Objective:To explore the value of conventional magnetic resonance imaging (MRI), diffusion weighted imaging (DWI), diffusion kurtosis imaging (DKI) sequence and pathological examination in predicting the efficacy of neoadjuvant chemotherapy (NAC) in advanced breast cancer.Methods:The clinical data of 65 cases of advanced breast cancer with NAC confirmed by pathology in the Affiliated Hospital of Jining Medical University from March 2022 to May 2023 were retrospectively analyzed, including 20 cases in the pathological complete remission (pCR) group and 45 cases in the non pCR group; All patients underwent routine MRI, DWI, DKI examinations and pathological analysis. The clinical pathological data, routine MRI features, apparent diffusion coefficient (ADC) values, mean kurtosis coefficient (MK), and mean diffusion coefficient (MD) between the two groups were analyzed; We compared the differences in various parameters between two groups and plotted receiver operating characteristic (ROC) curves to compare their diagnostic efficacy of NAC in breast cancer.Results:There were significant differences in molecular typing, estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor 2 (Her-2) and Ki-67 between pCR group and non pCR group (all P<0.05). In pCR group, Her-2 overexpression type and triple negative breast cancer (TNBC) type breast cancer were more common. ER and PR were mostly negative, Her-2 was mostly positive, and Ki 67 was mainly positive. The difference in tumor T2WI signal between the pCR group and the non pCR group was statistically significant ( P<0.05), with the pCR group showing mostly moderate/low T2WI signal. The ADC and MD values of the pCR group were lower than those of the non pCR group, while the MK value of the pCR group was higher than that of the non pCR group, and the differences were statistically significant (all P<0.001). The area under the ROC curve (AUC) for predicting the efficacy of NAC using a clinical pathological model was 0.829, which was higher than the AUC of molecular subtypes, ER, PR, Her-2, and Ki-67 ( Z=3.008, 2.697, 2.815, 2.131, 2.376, all P<0.05); The AUC of the DKI+ DWI predicting the efficacy of NAC was 0.934, which was higher than that of the DWI single sequence model, and the difference in type was statistically significant ( Z=2.396, P=0.017). The diagnostic efficacy of the DKI+ DWI model was higher than that of the single parameter ADC, MD, and MK, and the differences were statistically significant ( Z=2.396, 2.219, 2.161, all P<0.05); The AUC of the combined imaging and pathology model was 0.983, and its diagnostic efficacy was higher than that of the conventional MRI feature model, pathology model, DWI model, and DKI model, with statistically significant differences ( Z=5.877, 2.961, 3.240, 2.264, all P<0.05). Conclusions:The results of pathology, conventional MRI, DWI and DKI parameters of pCR and non pCR breast cancer patients are significantly different, and the combined model is better than the single model in predicting the efficacy of NAC.