ObjectiveTo explore the potential mechanism of Xianglian Huazhuo prescription （XLHZ） in treating chronic atrophic gastritis （CAG） by regulating cell cycle and inhibiting proliferation， using bioinformatics technology and animal experiments. MethodsDifferential expressed genes （DEGs） related to CAG were screened using GEO database and GEO2R tool. Weighted gene co-expression network analysis （WGCNA） was employed to search for hub genes of CAG. These hub genes were intersected with cell cycle proliferation based on GeneCards database. Eenrichment analysis of the intersecting genes was performed to obtain signaling pathways and biological processes related to CAG. Protein protein interaction （PPI） analysis of genes was conducted using the Protein Interaction Platform （STRING） database to search the super hub gene （hub 2.0）， and animal experiments were conducted for further validation. Fourteen of 70 male Wistar rats were randomly selected as the normal group， and the remaining 56 rats were prepared by the combined modeling method of "starvation disorder+N-methyl-N-nitro-N-nitrosoguanidine （MNNG） + sodium salicylate". The successfully modeled rats were randomly divided into the model group， XLHZ-H， XLHZ-M， and XLHZ-L groups （36， 18， 9 g·kg^-1， respectively）， and Morodan group （1.4 g·kg^-1）. Each group was given corresponding intervention for 60 days. Hematoxylin-eosin （HE） staining was used to observe the histopathological changes of gastric mucosa in rats. The ultrastructure of gastric mucosal tissue cells was observed by transmission electron microscopy. The relative expression levels of TGF-β₁， Smad2 and Smad3 proteins， S/G₂/M phase marker geminin and proliferation marker MCM2 were detected by Western blot in gastric mucosal tissue， and Spearman correlation analysis was performed. ResultsA total of 15 hub 2.0 genes were identified， including TGF-β₁， suggesting the involvement of the TGF-β₁ signaling pathway in the CAG pathogenesis. Compared with the normal group， the expressions of TGF-β₁， Smad2， geminin and MCM2 proteins in the gastric mucosa tissue of the model group were increased （P<0.05）， and the expression of Smad3 protein was decreased （P<0.05）. Compared with the model group， the expressions of TGF-β₁ and geminin in the gastric mucosa were decreased in the drug groups （P<0.05）. The XLHZ-M group， XLHZ-H group and Morodan group had significantly decreased protein expression of Smad2 and MCM2 （P<0.05）. The protein expression of Smad3 was significantly increased in XLHZ-M， XLHZ-H， and Morodan groups （P<0.05）. Spearman correlation analysis showed that Smad3 was negatively correlated with other indicators， and positively correlated with other indicators （P<0.01）. ConclusionXLHZ may inhibit TGF-β₁/Smads signaling pathway， regulate cell cycle， and inhibit proliferation in the treatment of CAG.

ObjectiveTo explore the potential mechanism of Xianglian Huazhuo prescription （XLHZ） in treating chronic atrophic gastritis （CAG） by regulating cell cycle and inhibiting proliferation， using bioinformatics technology and animal experiments. MethodsDifferential expressed genes （DEGs） related to CAG were screened using GEO database and GEO2R tool. Weighted gene co-expression network analysis （WGCNA） was employed to search for hub genes of CAG. These hub genes were intersected with cell cycle proliferation based on GeneCards database. Eenrichment analysis of the intersecting genes was performed to obtain signaling pathways and biological processes related to CAG. Protein protein interaction （PPI） analysis of genes was conducted using the Protein Interaction Platform （STRING） database to search the super hub gene （hub 2.0）， and animal experiments were conducted for further validation. Fourteen of 70 male Wistar rats were randomly selected as the normal group， and the remaining 56 rats were prepared by the combined modeling method of "starvation disorder+N-methyl-N-nitro-N-nitrosoguanidine （MNNG） + sodium salicylate". The successfully modeled rats were randomly divided into the model group， XLHZ-H， XLHZ-M， and XLHZ-L groups （36， 18， 9 g·kg^-1， respectively）， and Morodan group （1.4 g·kg^-1）. Each group was given corresponding intervention for 60 days. Hematoxylin-eosin （HE） staining was used to observe the histopathological changes of gastric mucosa in rats. The ultrastructure of gastric mucosal tissue cells was observed by transmission electron microscopy. The relative expression levels of TGF-β₁， Smad2 and Smad3 proteins， S/G₂/M phase marker geminin and proliferation marker MCM2 were detected by Western blot in gastric mucosal tissue， and Spearman correlation analysis was performed. ResultsA total of 15 hub 2.0 genes were identified， including TGF-β₁， suggesting the involvement of the TGF-β₁ signaling pathway in the CAG pathogenesis. Compared with the normal group， the expressions of TGF-β₁， Smad2， geminin and MCM2 proteins in the gastric mucosa tissue of the model group were increased （P<0.05）， and the expression of Smad3 protein was decreased （P<0.05）. Compared with the model group， the expressions of TGF-β₁ and geminin in the gastric mucosa were decreased in the drug groups （P<0.05）. The XLHZ-M group， XLHZ-H group and Morodan group had significantly decreased protein expression of Smad2 and MCM2 （P<0.05）. The protein expression of Smad3 was significantly increased in XLHZ-M， XLHZ-H， and Morodan groups （P<0.05）. Spearman correlation analysis showed that Smad3 was negatively correlated with other indicators， and positively correlated with other indicators （P<0.01）. ConclusionXLHZ may inhibit TGF-β₁/Smads signaling pathway， regulate cell cycle， and inhibit proliferation in the treatment of CAG.

Chronic heart failure （CHF） is a clinical syndrome characterized by impaired ventricular ejection function due to cardiac abnormalities， representing the terminal stage of most cardiovascular diseases. With its rising prevalence and significant impact on patients' quality of life， CHF has emerged as a major global public health concern. Current Western medicine treatments mainly involve the oral administration of the "new quadruple therapy" drugs and diuretics. Despite substantial progress in pathological research and clinical treatment， challenges persist， including considerable side effects， drug resistance， and marked interindividual variability in therapeutic response. Therefore， exploring and leveraging the advantages of traditional Chinese medicine （TCM） in treating CHF has become an urgent research priority. TCM has a millennia-long history in the prevention and treatment of heart failure， accumulating extensive clinical experience. Characterized by its multi-component and multi-target properties， TCM enables holistic regulation of multiple systemic functions and intervention in the progression of heart failure， demonstrating significant clinical relevance in its management. By employing therapeutic strategies such as warming Yang， promoting diuresis， replenishing Qi， nourishing Yin， and activating blood circulation， TCM effectively improves myocardial fibrosis， inhibits oxidative stress responses， enhances myocardial contractility， and ameliorates ventricular remodeling. Modern proprietary Chinese medicines derived from classic formulas， based on the theoretical foundation of traditional prescriptions， not only exhibit favorable clinical efficacy but also offer notable advantages in convenience， stability， and safety. This review systematically examined the significant therapeutic effects and underlying mechanisms of classical TCM formulas in the treatment of CHF， and provided an overview of the clinical application of modern proprietary Chinese medicines. It aims to provide new strategies for the clinical diagnosis and treatment of CHF.

Objective To explore the mechanism by which breast cancer-derived LncRNA OIP5-AS1 regulates the migration, invasion, and epithelial-mesenchymal transition of breast cancer cells through the M2 polarization of tumor-associated macrophages (TAM). Methods MDA-MB-231 cells were divided into the control group (blank control), the NC group (transfected with NC siRNA), and the si-OIP5 group (transfected with LncRNA OIP5-AS1 siRNA). The mRNA expression levels of LncRNAs OIP5-AS1, IL-4, and IL-13 were detected by RT-qPCR. The protein expression levels of IL-4 and IL-13 in the culture supernatant were detected by ELISA. The culture supernatant from the control group was added to RPMI 1640 medium at different volume ratios to induce the polarization of M0 macrophages into TAMs. The mRNA expression of CD206 in TAMs was detected by RT-qPCR. M0-type macrophages were induced with the medium supernatant of the NC group/si-OIP5 group, and the expression of CD206 was detected by Western blot. Subsequently, a co-culture model of macrophage and MDA-MB-231 was constructed to evaluate the migration and invasion abilities of MDA-MB-231 cells and detect the expression changes in Vimentin, N-cadherin and E-cadherin. Results Compared with the control and NC groups, the si-OIP5 group showed significantly downregulated expression of LncRNA OIP5-AS1 (P<0.001) and significantly decreased IL-13 mRNA and protein levels (P<0.05). Meanwhile, no significant difference was observed in the expression of IL-4 among the groups. Conditioned medium induced CD206 expression in M0 macrophages in a volume-dependent manner, with the strongest effect at a 40% volume ratio (P<0.001). The CD206 protein level in the si-OIP5 group significantly decreased (P<0.01). In the co-culture system, the migration and invasion abilities of MDA-MB-231 cells in the si-OIP5 group significantly weakened (P<0.001), the expression of E-cadherin was upregulated, and the expression levels of N-cadherin and Vimentin were downregulated (both P<0.01). Conclusion Breast cancer-derived LncRNA OIP5-AS1 can induce TAM M2 polarization mediated by IL-13, thereby promoting the migration, invasion, and EMT of breast cancer cells.

ObjectiveTo observe the activation patterns and functional connectivity in the prefrontal cortex of patients with post-stroke anxiety (PSA) using functional near-infrared spectroscopy, in order to explore the underlying neural mechanism. MethodsFrom December, 2024 to September, 2025, 120 stroke patients were selected in Changzhou De'an Hospital. They were divided into PSA group (n = 60) and non-PSA group (n = 60) according to the score of Hamilton Anxiety Scale (HAMA). All patients wore an 18-channel fNIRS acquisition cap for detection. The differences in resting-state functional connectivity between the frontopolar cortex (FPC) and dorsolateral prefrontal cortex (DLPFC) were examined in both groups, as well as task-related activation in these brain regions. ResultsResting-state functional connectivity analysis revealed no statistically significant difference in network connectivity between two groups in the FPC and DLPFC regions (|t| < 1.301, P > 0.05). Task-related activation results revealed significantly reduced activation in the contralateral FPC of PSA group compared to the non-PSA group (Z = -2.063, P < 0.05). Activation levels in this region showed a negative correlation with the scores of HAMA (ρ = -0.201, P = 0.028). ConclusionActivation decreased in the contralateral frontal pole during the task state for patients with PSA, and the activation levels negatively correlates with anxiety severities.

ObjectiveTo observe the activation patterns and functional connectivity in the prefrontal cortex of patients with post-stroke anxiety (PSA) using functional near-infrared spectroscopy, in order to explore the underlying neural mechanism. MethodsFrom December, 2024 to September, 2025, 120 stroke patients were selected in Changzhou De'an Hospital. They were divided into PSA group (n = 60) and non-PSA group (n = 60) according to the score of Hamilton Anxiety Scale (HAMA). All patients wore an 18-channel fNIRS acquisition cap for detection. The differences in resting-state functional connectivity between the frontopolar cortex (FPC) and dorsolateral prefrontal cortex (DLPFC) were examined in both groups, as well as task-related activation in these brain regions. ResultsResting-state functional connectivity analysis revealed no statistically significant difference in network connectivity between two groups in the FPC and DLPFC regions (|t| < 1.301, P > 0.05). Task-related activation results revealed significantly reduced activation in the contralateral FPC of PSA group compared to the non-PSA group (Z = -2.063, P < 0.05). Activation levels in this region showed a negative correlation with the scores of HAMA (ρ = -0.201, P = 0.028). ConclusionActivation decreased in the contralateral frontal pole during the task state for patients with PSA, and the activation levels negatively correlates with anxiety severities.

Objective: To construct gene recombinant expression plasmids of human anti-P antibody with IgG1 and kappa chain based on the human hybridoma cell line. Methods: Starting from the specific RT-PCR products encoding the variable regions of the IgH chain and IgL chain of the anti-P monoclonal cell line, appropriate restriction enzyme digestion sites were introduced at both ends of the VH and VL fragments through nested PCR. The plasmids carrying the antibody constant region and the nested PCR products of VH and VL were ligated by the action of T4 ligase and subsequently transferred into competent E. coli DH5ɑ, and positive clones were selected in the antibiotic resistant LB medium. After sequence confirmation, recombinant plasmids DNA were transfected into HEK293T cells, and the recombinant antibody obtained in the culture supernatant. The characteristics of recombinant expression antibodies were determined by using rapid antibody isotying kit, serological agglutination tests and flow cytometry. Results: Recombinant gene expression vectors, pFUSEss-CHIg-hG1+VH, pFUSE2ss-CLIg-hκ+VL, were successfully constructed. Human IgG1 kappa light chain antibodies were detected in the supernatant of HEK293T cells transient transfected with recombinant plasmids. After the supernatant was ultra-filtered and concentrated, it could cause agglutination reactions with P antigen-positive red blood cells. The mean fluorescence intensity (MFI) of the reaction between recombinant antibodies and antigen-positive red blood cells in flow cytometry experiments was higher than that of antigen-negative red blood cells. Conclusion: The experimental study on the conversion of red blood group antibody types by genetic engineering technology represents a beneficial exploration towards establishing a feasible technical route for the development of genetic recombination and modification of antibodies reagent.

OBJECTIVE To introduce the development of an intelligent prescription review decision-support system for anti-tumor drugs and assess its clinical application outcomes. METHODS Relevant data sources， including national and local pharmaceutical administration policies， clinical practice guidelines/consensus， hospital information systems data， and genetic testing results， were integrated. Adhering to the principles of structure， standardization and dynamic updating， a knowledge base covering chemotherapeutic， targeted and immunotherapeutic agents was constructed using a dual-dimensional modeling approach that combined “drug attributes” and “clinical contexts”. This knowledge base was then embedded into the hospital’s electronic medical order system to establish the prescription review decision-support system. The application and performance of the system were evaluated at Shanghai Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University School of Medicine. RESULTS A knowledge base containing 18 318 prescription review rules for anti-tumor drugs was constructed， and a closed-loop prescription review system was successfully established， encompassing pre-prescription real-time intervention， in-process interactive review， and post-prescription evaluation and analysis. From 2021 to 2024， the system generated a total of 57 879 alerts for prescriptions of five typical categories of anti-tumor drugs. For platinum-containing prescriptions， 22 577 alerts were generated， with Cisplatin for injection （lyophilized） being the most frequently alerted drug （13 445 alerts）， and “ototoxicity risk due to combined use” alerts remained high （7 682 alerts）. For methotrexate-containing prescriptions， 3 721 alerts were recorded， primarily related to “precaution-related issues” （76.4%， 2 843/3 721）. For doxorubicin-containing prescriptions， 17 301 alerts were triggered， primarily related to “dosage and administration” （14 315 alerts）. For human epidermal growth factor receptor 2-targeted agents-containing prescriptions， 1 007 alerts were issued， mostly related to “reimbursement restrictions” （956 alerts）. For programmed death-1/programmed death-ligand 1 inhibitors-containing prescriptions， the alerts increased year by year， totaling 13 273 alerts， primarily related to “inappropriate indication” （9 118 alerts）. Over the 4 years， the physician response rates to system alerts were 21.4%， 27.1%， 33.5% and 51.6%， respectively. CONCLUSIONS An intelligent decision-support system for anti-tumor drug prescription review， encompassing a closed-loop process of “real-time pre-event intervention， interactive in-event prescription review， post-event evaluation and analysis”， has been successfully constructed and implemented throughout the entire workflow. There is a discernible trend in this hospital， where the focus on monitoring anti-tumor drugs is shifting towards immunotherapy drugs. Additionally， the acceptance rate of physicians regarding prescription review opinions has been steadily increasing year by year.

ObjectiveTo observe the activation patterns and functional connectivity in the prefrontal cortex of patients with post-stroke anxiety (PSA) using functional near-infrared spectroscopy, in order to explore the underlying neural mechanism. MethodsFrom December, 2024 to September, 2025, 120 stroke patients were selected in Changzhou De'an Hospital. They were divided into PSA group (n = 60) and non-PSA group (n = 60) according to the score of Hamilton Anxiety Scale (HAMA). All patients wore an 18-channel fNIRS acquisition cap for detection. The differences in resting-state functional connectivity between the frontopolar cortex (FPC) and dorsolateral prefrontal cortex (DLPFC) were examined in both groups, as well as task-related activation in these brain regions. ResultsResting-state functional connectivity analysis revealed no statistically significant difference in network connectivity between two groups in the FPC and DLPFC regions (|t| < 1.301, P > 0.05). Task-related activation results revealed significantly reduced activation in the contralateral FPC of PSA group compared to the non-PSA group (Z = -2.063, P < 0.05). Activation levels in this region showed a negative correlation with the scores of HAMA (ρ = -0.201, P = 0.028). ConclusionActivation decreased in the contralateral frontal pole during the task state for patients with PSA, and the activation levels negatively correlates with anxiety severities.

ObjectiveThis paper aims to explore the risk factors for chronic atrophic gastritis （CAG） with turbidity toxin accumulation syndrome and establish a prediction model. MethodsClinical data of 180 patients with CAG who participated in the "clinical study of Xianglian Huazhuo Particles blocking CAG cancer transformation" of Hebei Sheng Zhong Yi Yuan from July 2021 to March 2022 were collected. After confounding factors were controlled by propensity score matching， patients were divided into a training set （namely dev） and a validation set （namely vad） in a seven to three ratio. The risk factors for CAG with turbidity toxin accumulation syndrome in the training set were investigated by using univariate Logistic regression analysis and least absolute shrinkage and selection operator （namely Lasso） regression algorithms. Subsequently， a model， named model 1se， was developed by using the training set data to predict the risk factors for CAG with turbidity toxin accumulation syndrome. The accuracy of the prediction model was assessed by using various methods， including the receiver operating characteristic （ROC） curve， Hosmer-Lemeshow test （H-L）， calibration plot， and decision curve analysis （DCA）. ResultsAge， body mass index （BMI）， family history of cancer， job and life satisfaction， yellow and greasy fur with slippery pulse， and heavy body sensation were independent risk factors of the model. The prediction model showed excellent predictive value for both the training and validation sets. ConclusionThe established prediction model for CAG with turbidity toxin accumulation syndrome has high discrimination and excellent calibration， which could provide an excellent clinical basis for disease diagnosis and individualized treatment of patients.