Objective To analyze the risk factors of venous thromboembolism(VTE)after endoscopic surgery in elderly patients with urinary system calculi,construct a prediction model and validate it.Methods A retrospective analysis was conducted on the clinical data of 402 elderly patients(≥ 60 years)with urinary system calculi who underwent endoscopic surgery in our hospital during Jan.2018 and Jan.2023.The patients were divided into VTE group(n=43)and non-VTE group(n=359)based on whether VTE occurred after surgery.Risk factors of VTE were screened with univariate and multivariate logistic regression analyses.Based on the screening results(P＜0.05 for the factor),a nomogram prediction model was established,the receiver operating characteristic(ROC)curve was drawn,the area under the curve(AUC)was calculated to determine the efficacy of the model,and a calibration chart was drawn to determine the accuracy of the model.Results Univariate analysis showed that age＞70 years,body mass index(BMI)≥30,VTE history,history of malignant tumors,diabetes,operation time＞180 min,diuretic use during operation,and postoperative ambulation time＞24 h were risk factors of VTE(P＜0.05).Logistic regression analysis showed that age＞70 years,BMI ≥ 30,history of VTE,history of malignant tumors,and operation time＞180 min were independent risk factors of VTE(P＜0.05).The AUC in the ROC curve of the validation set data was 0.789(95％CI:0.731-0.848,P＜0.001).The calibration chart showed that the calibration curve was close to the standard curve(Brier=0.13).Conclusion Age＞70 years,BMI ≥30,history of VTE,history of malignant tumors,and surgery time＞180 min are independent risk factors of postoperative VTE in elderly patients with urinary system calculi undergoing endoscopic surgery.The prediction model can effectively predict the risk factors of postoperative VTE.

Liquid chromatography-tandem mass spectrometry (LC-MS/MS) technology has the characteristics of high specificity and high throughput, making it rapidly applied and developed in the field of clinical testing. Its application in the monitoring of therapeutic drugs can effectively improve the quantitative accuracy and sensitivity, and formulate a personalized and optimal dosing plan for patients. However, this technology still faces some challenges, and automation, quality control, and quantitative traceability will be the future development direction.

To summarize the experience of Professor CAO Hongxin in syndrome differentiation and treatment of allergic rhinitis. Based on the clinical and pathological characteristics of allergic rhinitis， it is believed that its main pathogenesis is zang-fu organs deficiency or retention of latent pathogens， and affected by external pathogens， resulting in a decrease in the body's adaptability to the external environment， so the body showed as healthy qi deficiency and pathogenic qi excess， accumulation of pathogens in the nasal cavity， and unfavorable clearing of the cavity， leading to allergic rhinitis. In clinic， it is often divided into three syndromes for treatment： deficiency of lung and spleen qi， and disharmony between ying and wei qi； kidney deficiency and lung heat， and wind pathogen invading the lungs； liver and gallbladder stagnation and heat， and wind pathogen attacking the exterior. The prescriptions were recommended to apply Yupingfeng Powder （玉屏风散） plus Guizhi Decoction （桂枝汤）， self-prescribed Jingfang Guishao Dihuang Decoction （荆防桂芍地黄汤）， and modified Qingkong Decoction （清空汤）， respectively.

OBJECTIVE To investigate the antidepressant mechanism of Shugan hewei tang （SGHWT） based on the metabolomics of prefrontal cortex （PFC）-nucleus accumbens （NAc）-ventral tegmental area （VTA） neural circuit. METHODS Male SD rats were randomly divided into blank group， model group， SGHWT low-， medium- and high-dose groups [3.67， 7.34， 14.68 g/（kg·d）， by raw material]， and fluoxetine group [1.58 mg/（kg·d）， positive control]， with 12 rats in each group. Except for the blank group， the depression model was established by chronic unpredictable mild stress combined with individual cage housing in the remaining groups， and the corresponding drug solution or normal saline was administered via gavage during modeling， once a day， for 6 consecutive weeks. After the last administration， the body weight， sucrose preference rate， total moving distance， frequency into the center and immobility time of rats in each group were detected. Samples of PFC， NAc and VTA areas of rats in the blank group， model group， SGHWT medium-dose group and fluoxetine positive control groups were collected，and their histomorphological features were observed， and non-targeted metabolomics analysis （except for fluoxetine group）were performed and validated. RESULTS Compared with model group， the cytolysis， structural damage and other pathological damages in three brain regions of rats were significantly alleviated in each drug group， while their body weight， sucrose preference rate， total moving distance and frequency into the center were all significantly higher or longer （P＜0.05）， and immobility time was significantly shorter （P＜0.05）. The results of non-targeted metabolomics showed that a total of 78 endogenous differential metabolites were identified， with 40， 35 and 24 in the PFC， NAc and VTA regions respectively， mainly involved in amino acid， lipid and sphingolipid metabolism. The results of metabolic pathway enrichment analysis showed that SGHWT affected the neural circuits of depressed rats by regulating sphingolipid metabolism， alanine， aspartic acid and glutamic acid metabolism， saturated fatty acid biosynthesis， among which alanine， aspartic acid and glutamic acid metabolism was predominantly involved. Validation experiments showed that SGHWT significantly increased the phosphorylation levels of protein kinase B （Akt） and mammalian target of rapamycin （mTOR）， and decreased the protein expression of N-methyl-D-aspartic acid receptor 1 （NMDAR1） in the NAc region of rats. CONCLUSIONS SGHWT significantly improves the depression-like behavior and attenuates pathological damage of PFC-NAc-VTA neural circuit of model rats， the mechanism of which is associated with inhibiting NMDAR1 expression and activating the Akt/mTOR signaling pathway.