ObjectiveTo investigate the mechanism of action of Jiedu Huayu granules in improving liver injury in mice with acute liver failure （ALF） by observing its effect on a mouse model of ALF after prophylactic administration， and to provide a basis for clinical medication. MethodsA total of 60 specific pathogen-free male C57BL/6J mice were divided into normal group， model group， Jiedu Huayu granules group （JDHY group）， and farnesoid X receptor （FXR） agonist （GW4064） group using a random number table， with 15 mice in each group. The model of ALF was induced by a single intraperitoneal injection of D-galactosamine combined with lipopolysaccharide. The mice in the JDHY group were given prophylactic administration of 0.3 g/mL drug solution of Jiedu Huayu granules by gavage for 3 days before modeling， those in the normal group and the model group were given 0.9% NaCl solution by gavage， and those in the GW4064 group were given intraperitoneal injection of GW4064 for 3 consecutive days before modeling. The mice were sacrificed after modeling， and serum and liver tissue samples were collected. A veterinary automatic biochemical analyzer was used to measure the serum levels of total bilirubin （TBil）， total bile acids （TBA）， gamma-glutamyl transferase （GGT）， alanine aminotransferase （ALT）， and aspartate aminotransferase （AST） in mice from each group； HE staining was used to observe liver pathological changes； RT-PCR was used to measure the mRNA expression levels of FXR， fibroblast growth factor 15 （FGF15）， fibroblast growth factor receptor 4 （FGFR4）， small heterodimer partner （SHP）， and bile salt export pump （BSEP） in mice， and Western blot was used to measure the protein expression levels of FXR， FGF15， FGFR4， SHP， and BSEP. A one-way analysis of variance was used for comparison between groups， and the Dunett method was used for further comparison between two groups. ResultsCompared with the normal group， the model group had significant increases in the serum levels of TBil， ALT， AST， TBA， and GGT （all P<0.01）， and compared with the model group， the JDHY group and the GW4064 group had significant reductions in the serum levels of TBil， ALT， AST， TBA， and GGT （all P <0.01）. HE staining showed that compared with the model group， the JDHY group and the GW4064 group had milder pathological injury， a reduction in the area of hepatocyte necrosis， and alleviation of cellular swelling and edema. Compared with the normal group， the model group had significant reductions in the mRNA and protein expression levels of FXR， FGF15， FGFR4， SHP， and BSEP in liver tissue （all P <0.01）， and compared with the model group， the JDHY group and the GW4064 group had significant increases in the mRNA and protein expression levels of FXR， FGF15， FGFR4， SHP， and BSEP in liver tissue （all P <0.05）. ConclusionJiedu Huayu granules may alleviate liver injury in mice with ALF through the FXR/SHP axis.

This study aimed to investigate the protective effects of Huangqi Guizhi Wuwu decoction (HGWD) against cerebral ischemic injury and the underlying mechanisms. A middle cerebral artery occlusion (MCAO) model was established in C57BL/6 mice to evaluate the effects of HGWD on neurobehavioral scores, cerebral infarction rate, brain water content, and oxidative stress and inflammatory markers. The mRNA and protein expression levels of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), B-cell lymphoma-2 (Bcl-2), and Bcl-2-associated X protein (Bax) in brain tissue were assessed. In addition, Nrf2 knockout mice were used to verify the role of Nrf2 in the protective effects of HGWD against MCAO-induced injury. Additionally, an oxygen-glucose deprivation/reperfusion (OGD/R) model in primary neuronal cells was employed to further confirm the pharmacological effects of HGWD in vitro. The results showed that HGWD significantly ameliorated cerebral ischemic injury in MCAO mice, alleviated oxidative stress, suppressed the release of inflammatory factors, and markedly upregulated the expression of Nrf2, HO-1, and Bcl-2 while downregulating Bax expression, with consistent trends being observed at both mRNA and protein levels. The protective effects of HGWD were significantly attenuated in Nrf2 knockout mice, indicating the pivotal role of Nrf2 in HGWD-mediated protection against cerebral ischemic injury. In vitro experiments revealed that HGWD significantly increased neuronal cell viability, reduced lactate dehydrogenase(LDH) leakage, and decreased apoptosis in OGD/R-treated cells, accompanied by upregulation of Nrf2, HO-1, and Bcl-2 and downregulation of Bax. In conclusion, HGWD protects against cerebral ischemic injury by activating the Nrf2/HO-1 pathway to enhance antioxidant capacity and modulating the Bcl-2/Bax signaling pathway to inhibit apoptosis, thereby protecting brain cells from ischemic damage.

Objective:To identify independent risk factors for early recurrence following curative resection of resectable pancreatic cancer and establish a nomogram prediction model.Methods:Clinical data from 405 patients with resectable pancreatic cancer treated at Renji Hospital, Shanghai Jiao Tong University School of Medicine from February 2010 to December 2020 were retrospectively reviewed. Patients were stratified into a training cohort (265 patients form February 2010 to December 2018) and a validation cohort (140 patients from January 2019 to December 2020) based on surgery dates. Optimal cutoff values for clinical variables were determined using X-tile software. Independent risk factors were identified through univariate and multivariate Cox proportional hazards regression analyses. Kaplan-Meier curves for recurrence-free survival (RFS) were generated across subgroups, and a nomogram was developed to predict early recurrence (within 1 year post-surgery). Time-dependent receiver operating characteristic (tROC) curves was drawn and area under the curve (AUC) metrics were utilized to evaluate predictive accuracy, while model reliability was assessed by calibration curves. Individualized risk scores derived from the nomogram were stratified into high- and low-risk groups using X-tile-derived cutoff values. Survival differences between groups were analyzed via log-rank tests. The clinical application value was judged by decision curve analysis (DCA) compared to TNM staging. Results:In the training cohort, 139 patients (52.45%) experienced early recurrence, with a median RFS of 11.1 months [interquartile range ( IQR): 6.0-26.0]. The validation cohort reported 70 early recurrences (50.00%) and a median RFS of 11.8 months ( IQR: 4.9-21.4). Univariate analysis revealed significant associations between early recurrence and tumor diameter, carcinoembryonic antigen (CEA), carbohydrate antigen 19-9 (CA19-9), carbohydrate antigen 125 (CA125), systemic immune-inflammation index (SⅡ), and prognostic nutritional index (PNI). Multivariate analysis identified tumor diameter ≥3.75 cm ( HR=1.718, 95% CI 1.223-2.412, P=0.002), CA19-9≥218 U/ml ( HR=1.567, 95% CI 1.107-2.220, P=0.011), CA125≥20.98 U/ml ( HR=2.501, 95% CI 1.768-3.539, P<0.001), SⅡ≥388.28 ( HR=1.708, 95% CI 1.096-2.662, P=0.018), and PNI<53.18 ( HR=0.596, 95% CI 0.404-0.879, P=0.009) as independent risk factors for early recurrence. The nomogram achieved AUC values of 0.771 and 0.708 in the training and validation cohorts, respectively. Calibration curves demonstrated strong agreement between predicted and observed survival probabilities. Kaplan-Meier analysis revealed significantly lower 1-year RFS rates in high-risk versus low-risk groups for both cohorts (training: HR=3.65, 95% CI 2.45-5.44, P<0.001; validation: HR=2.37, 95% CI 1.39-4.06, P=0.001). DCA indicated superior net benefit of the nomogram over TNM staging across threshold probabilities of 0.2-0.9. Conclusions:The proposed nomogram effectively integrates clinical and serological biomarkers to preoperatively assess early recurrence risk in resectable pancreatic cancer patients, offering enhanced precision for clinical decision-making.

The pathogenesis and progression of depression are closely associated with functional dysregula-tion in the brain's reward and emotion-modulating circuits.As the central hub of the reward system,the nucleus accumbens(NAc)forms aberrant neural circuits with multiple brain regions-including the ventral tegmental area(VTA),medial prefrontal cortex(mPFC),amygdala(AMY),hippocampus(HIP),and paraventricular nucleus of the thalamus(PVT)-which have been empirically linked to depressive symptomatology.Acupuncture,with its multi-target therapeutic profile,aligns well with the multifactorial and multisystem dysregulation characteristic of depressive disorders.This review systematically examines the functional alterations of the NAc-centered neural circuitry in depression and explores the potential mechanisms of acupuncture intervention.Evidence suggests that acupuncture holistically ameliorates depression by:modulating dopaminergic transmission in the VTA-NAc pathway,enhancing neurotransmitter equilibrium in the mPFC-NAc circuit,bidirectionally regulating emotional stability via the AMY-NAc loop,attenuating HIP-NAc glutamatergic hyperactivity,and optimizing excitatory signaling in the thalamus-NAc circuit.Furthermore,this synthesis emphasizes a systems-level integration of circuit mechanisms,highlighting both the clinical applicability of acupuncture in depression treatment and recent advances in mechanistic research.The findings provide robust theoretical foundations and practical guidance for clinical practice,bridging translational neuroscience with therapeutic innovation.

The pathogenesis and progression of depression are closely associated with functional dysregula-tion in the brain's reward and emotion-modulating circuits.As the central hub of the reward system,the nucleus accumbens(NAc)forms aberrant neural circuits with multiple brain regions-including the ventral tegmental area(VTA),medial prefrontal cortex(mPFC),amygdala(AMY),hippocampus(HIP),and paraventricular nucleus of the thalamus(PVT)-which have been empirically linked to depressive symptomatology.Acupuncture,with its multi-target therapeutic profile,aligns well with the multifactorial and multisystem dysregulation characteristic of depressive disorders.This review systematically examines the functional alterations of the NAc-centered neural circuitry in depression and explores the potential mechanisms of acupuncture intervention.Evidence suggests that acupuncture holistically ameliorates depression by:modulating dopaminergic transmission in the VTA-NAc pathway,enhancing neurotransmitter equilibrium in the mPFC-NAc circuit,bidirectionally regulating emotional stability via the AMY-NAc loop,attenuating HIP-NAc glutamatergic hyperactivity,and optimizing excitatory signaling in the thalamus-NAc circuit.Furthermore,this synthesis emphasizes a systems-level integration of circuit mechanisms,highlighting both the clinical applicability of acupuncture in depression treatment and recent advances in mechanistic research.The findings provide robust theoretical foundations and practical guidance for clinical practice,bridging translational neuroscience with therapeutic innovation.

Objective To investigate and analyze the current situation of the construction of Smart Hospital in the dis-trict-level hospital of Beijing,and to provide reference for thedistrict-level hospitals to promote the construction of Smart Hospitals.Methods A questionnaire survey was conducted in Beijing district-level hospitals,and the construc-tion of Smart Hospital was analyzed by descriptive statistical analysis.Results The overall construction rate of Beijing district-level hospitals smart service business function was 50.98％,and the overall average construction rate of hos-pital smart management business function was 46.72％.93.75％hospitals thought that the investment in Smart Hos-pital construction was insufficient.The functions of smart service and management in different grades and categories of hospitals were different.Conclusion In order to promote the construction of Smart Hospital in Beijingdistrict-level hospitals,we should improve the top-level system such as strategic planning for the construction of smart hospi-tals,increase the investment in hospital informatization and talent teams,strengthen the standardization of intercon-nection between different hospitals,enhance the sharing and utilization of medical data and information,and strengthen the application of new hospital technologies and hospital information security.

Objective To investigate and analyze the current situation of the construction of Smart Hospital in the dis-trict-level hospital of Beijing,and to provide reference for thedistrict-level hospitals to promote the construction of Smart Hospitals.Methods A questionnaire survey was conducted in Beijing district-level hospitals,and the construc-tion of Smart Hospital was analyzed by descriptive statistical analysis.Results The overall construction rate of Beijing district-level hospitals smart service business function was 50.98％,and the overall average construction rate of hos-pital smart management business function was 46.72％.93.75％hospitals thought that the investment in Smart Hos-pital construction was insufficient.The functions of smart service and management in different grades and categories of hospitals were different.Conclusion In order to promote the construction of Smart Hospital in Beijingdistrict-level hospitals,we should improve the top-level system such as strategic planning for the construction of smart hospi-tals,increase the investment in hospital informatization and talent teams,strengthen the standardization of intercon-nection between different hospitals,enhance the sharing and utilization of medical data and information,and strengthen the application of new hospital technologies and hospital information security.

OBJECTIVE To investigate the improvement mechanism of hyperoside （HYP） on non-alcoholic fatty liver disease （NAFLD）. METHODS Male C57BL/6 mice were randomly divided into normal （NFD） group， model （HFD） group and HYP group， with 8 mice in each group. Except for NFD group， the mice in other groups were fed with HF60 high-fat diet to establish NAFLD model； HYP group was simultaneously given HYP 100 mg/kg intragastrically every day， for 16 consecutive weeks. The body weight and liver weight of mice in each group were recorded 16 h after the last medication； the histopathological changes and lipid accumulation in the liver were observed， and the contents of triglyceride （TAG） in liver tissue and serum contents of TAG， aspartate transaminase （AST） and alanine transaminase （ALT） were measured； LC-MS/MS method was adopted to detect lipid changes in the liver tissue of mice for lipidomics analysis， and protein expressions of lipid synthesis-associated proteins peroxisome proliferator-activated receptor α （PPARα） were also tested. Human hepatocellular carcinoma cell line HepG2 was divided into normal control group， model group， HYP low-concentration group （50 μmol/L）， HYP high-concentration group （100 μmol/L）， HYP low-concentration+GW6471 （PPARαinhibitor） group， and HYP high-concentration+GW6471 group. Except for normal control group， the remaining cells were induced with oleic acid and palmitic acid to establish a high-fat cell model. The accumulation of lipid droplets in each group of cells was observed， and the TAG content was detected. RESULTS Compared with HFD group， HYP group exhibited significant reductions in liver fat vacuoles， lipid accumulation， liver weight， and TAG content in liver tissue， as well as serum contents of ALT， AST and TAG （P＜0.05）. Additionally， the expression of PPARα protein in liver tissue was significantly increased （P＜0.05）， and the pathological morphological changes associated with NAFLD were alleviated. Lipidomic analysis revealed that HYP significantly reduced the levels of TAG， diacylglycerol and other lipids in the liver. Compared with model group， cellular lipid droplet accumulation and TAG content decreased significantly in HYP low- and high-concentration groups （P＜0.05）； GW6471 could significantly reverse the improvement effect of HYP on above indicators （P＜0.05）. CONCLUSIONS HYP can effectively ameliorate NAFLD induced by a high-fat diet in mice， and the mechanism may be related to the activation of PPARα to regulate hepatic lipid synthesis.

Traditional Chinese Medicine (TCM), as a treasure of the Chinese nation, plays a significant role in maintaining public health. In 2019, the Central Committee of the Communist Party of China and the State Council proposed for the first time the establishment of a TCM registration and evaluation evidence system that integrates TCM theory, "personal experience" and clinical trials (referred to as the "Three-in-One" System) to promote the inheritance and innovation of TCM. Subsequently, the National Medical Products Administration issued several guiding principles to advance the improvement and implementation of this system. Owing to the complexity of its implementation, there are still differing understandings within the TCM industry regarding the positioning of the "Three-in-One" Registration and Evaluation Evidence System, as well as the connotation and value orientation of the "personal experience." To address this, Academician WANG Qi, President of the TCM Association, China International Exchange and Promotion Association for Medical and Healthcare and TCM master, led a group of academicians, TCM masters, TCM pharmacology experts and clinical TCM experts to convene a "Seminar on Promoting the Implementation of the ′Three-in-One′ Registration and Evaluation Evidence System for Chinese Medicinals." Through extensive discussions, an expert consensus was formed, clarifying the different roles of the TCM theory, "personal experience" and clinical trials within the system. It was further emphasized that the "personal experience" is the core of this system, and its data should be derived from clinical practice scenarios. In the future, the improvement of this system will require collaborative efforts across multiple fields to promote the high-quality development of the Chinese medicinal industry.

Objective To explore the role and mechanism of HJT-sRNA-m7(M7)bencaosome in a silicosis mouse model.Methods C57BL/6J mice were randomly divided into four groups:blank,control,negative control(NC)oligonucleotide,and M7 treatment(HJT-sRNA-m7 bencaosome)groups.After three rounds of pretreatment with HJT-sRNA-m7 bencaosome,all groups except the blank one were modeled via a single intratracheal exposure.Each mouse received 50 μL of a silica suspension at a dose of 200 mg/kg body weight via intratracheal instillation.From day 6 to day 26,the bencaosome was administered every other day via oral gavages.On day 28,pulmonary function tests were performed.Bronchoalveolar lavage fluid was collected for flow cytometry and cytokine analysis.The left lung was harvested for histopathological examination and Masson's trichrome staining to evaluate collagen fiber dep-osition.The right lung was used for hydroxyproline quantification to assess collagen accumulation.Results The re-sults of pulmonary function test,pathological analysis and hydroxyproline measurements all indicated that M7 ben-caosome treatment significantly alleviated silica-induced pulmonary fibrosis.Moreover,flow cytometry analysis of BALF confirmed that M7 bencaosome inhibited the silica-induced inflammatory response,that was supported by cy-tokine analysis.Conclusions HJT-sRNA-m7 bencaosome is quite effective to treat silicosis and inhibits mitigating pulmonary fibrosis progression in mouse models.