ObjectiveTo address the challenges of unstructured classical Chinese expressions， nested entity relationships， and limited annotated data in famous traditional Chinese medicine（TCM） case records， this study proposes a joint relation extraction framework that integrates data augmentation and entity mapping， aiming to support the construction of TCM diagnostic knowledge graphs and clinical pattern mining. MethodsWe developed an annotation structure for entities and their relationships in TCM case texts and applied a data augmentation strategy by incorporating multiple ancient texts to expand the relation extraction dataset. A cascade binary tagging framework for relation triple extraction（CasRel） model for TCM semantics was designed， integrating a pre-trained bidirectional encoder representations from transformers（BERT） layer for classical TCM texts to enhance semantic representation， and using a head entity-relation-tail entity mapping mechanism to address entity nesting and relation overlapping issues. ResultsExperimental results showed that the CasRel model， combining data augmentation and entity mapping， outperformed the pipeline-based Bert-Radical-Lexicon（BRL）-bidirectional long short-term memory（BiLSTM）-Attention model. The overall precision， recall， and F₁-score across 12 relation types reached 65.73%， 64.03%， and 64.87%， which represent improvements of 14.26%， 7.98%， and 11.21% compared to the BRL-BiLSTM-Attention model， respectively. Notably， the F₁-score for tongue syndrome relations increased by 22.68%（69.32%）， and the prescription-syndrome relations performed the best with the F₁-score of 70.10%. ConclusionThe proposed framework significantly improves the semantic representation and complex dependencies in TCM texts， offering a reusable technical framework for structured mining of TCM case records. The constructed knowledge graph can support clinical syndrome differentiation， prescription optimization， and drug compatibility， providing a methodological reference for TCM artificial intelligence research.

Humans ; East Asian People ; Surveys and Questionnaires ; Vitiligo/epidemiology*

OBJECTIVE To investigate the effects of astilbin （AST） on myocardial ischemia-reperfusion injury （MIRI） in rats and its potential mechanism. METHODS SD male rats were randomly divided into sham operation group， model group， positive control group （Compound Salvia miltiorrhiza tablets， 240 mg/kg）， AST low-dose and high-dose groups （30， 90 mg/kg）， and high- dose of AST+hypoxia-inducible factor-1α（HIF-1α） inhibitor group （AST 90 mg/kg+2ME2 15 mg/kg）， with 25 rats in each group. Except for sham operation group， MIRI model was induced in other groups， and then given relevant drug or normal saline intragastrically or intraperitoneally， for consecutive 28 d. Serum contents of cardiac troponin I （cTnI） and creatine kinase isoenzyme （CK-MB） were detected； volume ratio of myocardial infarction was measured； the pathological changes of myocardium， the apoptotic rate of myocardial cells and ultrastructure of mitochondria in myocardial tissue were all observed. The contents of tumor necrosis factor α （TNF-α）， interleukin 6 （IL-6） and malondialdehyde （MDA）， the activity of superoxide dismutase （SOD）， the expressions of HIF-1α， adenovirus E1B interacting protein 3 （BNIP3） and myosin-like Bcl-2 interacting protein （Beclin1） were determined in myocardium. The ratio of microtubule-associated protein light chain 3 （LC3） Ⅱ to Ⅰ （LC3 Ⅱ/Ⅰ） in rat myocardium was calculated. RESULTS Compared with model group， no obvious swelling was found in the myocardial tissue of rats in positive control group， AST low-dose and high-dose groups， and the myocardial fibers were arranged regularly； the volume ratio of myocardial infarction， the contents of cTnI， CK-MB， TNF-α， IL-6 and MDA， the apoptotic rate were decreased significantly （P＜0.05）， while SOD activity， protein expressions of HIF-1α， BNIP3 and Beclin1， LC3Ⅱ/Ⅰ were increased significantly （P＜0.05）. HIF-1α inhibitor could significantly weaken the improvement effect of AST on the above indicators in MIRI model rats （P＜0.05）. CONCLUSIONS AST enhances mitochondrial autophagy by activating HIF-1α/BNIP3 signaling pathway， thereby reducing MIRI in rats.

Objective:To investigate the value of fibroblast growth factor 2 (FGF-2) and microRNA-206 (miR-206) in predicting postoperative delayed union of closed tibial shaft fractures.Methods:The clinical data of 136 patients who underwent closed tibial shaft fracture surgery in Hospital of the 80 th Group Army of Chinese People's Liberation Army Ground Forces from May 2018 to May 2021 were retrospectively analyzed. Eighty-six patients who had delayed union of closed tibial shaft fractures were included in the observation group, and fifty patients who had normal union of closed tibial shaft fractures were included in the control group. Serum FGF-2 level was measured using the enzyme-linked immunosorbent assay, and serum miR-206 expression was detected using the real-time fluorescence polymerase chain reaction. The relationship between FGF-2 expression and miR-206 expression and closed tibial shaft fractures was analyzed. Results:At 1 day, 1, and 4 weeks after surgery, serum FGF-2 level was significantly lower in the observation group than the control group [(14.24 ± 2.15) ng/L vs. (20.36 ± 3.42) ng/L, (21.38 ± 3.27) ng/L vs. (30.45 ± 4.29) ng/L, (23.59 ± 4.36) ng/L vs. (36.67 ± 4.51) ng/L, t = 7.42, 8.42, 16.66, all P < 0.001]. Serum FGF-2 level gradually increased with time in each group. At 1 day after surgery, serum miR-206 expression was significantly lower in the observation group than the control group ( t = 7.50, P < 0.001). At 4 weeks after surgery, serum miR-206 expression was significantly higher in the observation group than the control group ( t = 17.24, P < 0.001). At 1 week after surgery, there was no significant difference in serum miR-206 expression between the two groups ( P > 0.05). Univariate analysis results showed that postoperative infection, FGF-2, and miR-206 were closely related to the delayed union of closed tibial shaft fractures after surgery (all P < 0.05). Multivariate logistic regression analysis results showed that postoperative infection ( OR = 1.93, 95% CI: 1.20-3.07), FGF-2 ( OR = 2.10, 95% CI: 1.31-3.36), miR-206 ( OR = 2.30, 95% CI: 1.35-3.89) were independent risk factors for delayed union of closed tibial shaft fractures after surgery (all P < 0.05). The receiver operating characteristic (ROC) curves plotting serum FGF-2 level and serum miR-206 expression after closed tibial shaft fractures showed that at 4 weeks after surgery, the optimal cut-off value of FGF-2 for predicting delayed union of closed tibial shaft fractures was 29.83 ng/L, with the area under the curve, sensitivity, and specificity of 0.76 (95% CI: 1.23-3.25), 79.34%, and 68.82%, respectively; at 4 weeks after surgery, the optimal cut-off value of miR-206 for predicting delayed union of closed tibial shaft fractures was 0.63, with the area under the curve, sensitivity and specificity of 0.72 (95% CI: 1.10-2.45), 75.33%, and 67.25%, respectively. The area under the curve, the sensitivity, and specificity of combined use of FGF-2 and miR-206 in predicting delayed union of closed tibial shaft fractures were 0.81 (95% CI: 1.35-3.26), sensitivity and specificity were 83.45% and 67.36% respectively. Conclusion:The decrease in serum FGF-2 level and the increase in serum miR-206 expression at 4 weeks after surgery are independent risk factors for delayed union of closed tibial shaft fractures. Combined use of FGF-2 and miR-206 can better predict the delayed union of closed tibial shaft fractures.

OBJECTIVE To investigate the effects of a spirin （Asp） on myocardia l ischemia/reperfusion （I/R） injury by regulating microRNA -340-5p （miR-340-5p）/high mobility group box 1 （HMGB1）/Toll-like receptor 4 （TLR4） pathway. METHODS Male SD rats were divided into sham operation （Sham）group（thoracotomy without ligation ），I/R group （I/R injury model was constructed ），and Asp pretreatment （I/R+Asp）group（7 d of Asp pretreatment+modeling ），I/R+Asp+in-miR-340-5p group [Asp pretreatment 7 d+transfection with miR -340-5p inhibitor 48 h before modeling+modeling ] and I/R+Asp+HMGB 1 group （7 d of Asp pretreatment+transfection with overexpression of HMGB 1 48 h before modeling+modeling ），with 20 rats in each group. The levels of myocardial injury indexes [lactate dehydrogenase ，creatine kinase isoenzyme -MB，cardiac troponin Ⅰ]， inflammation and oxidative stress indexes [myeloperoxidase，superoxide dismutase ，glutathione peroxidase ，malondialdehyde] were detected in each group ，and the pathological changes of myocardial tissue were observed . The myocardial infarction area ，cell apoptosis and the expression of miR -540-5p，HMGB1 and TLR 4 in myocardial tissue were detected . Cardiomyocyte H 9C2 of rats was used as the object to investigate the targeting relationship between miR -340-5p and HMGB 1. RESULTS Asp pretreatment could significantly inhibit the increase of serum myocardial injury indexes in I/R model rats ，reduce inflammation and inhibit oxidative stress ，reduce myocardial infarct size and apoptosis ，and significantly up -regulated the expression of miR -340-5p and down-regulated the expression of HMGB 1 and TLR 4 proteins（P＜0.05）；inhibition of miR -340-5p or overexpression of HMGB 1 could reverse the above protective effects of Asp （P＜0.05）. miR-340-5p could target and negatively regulate HMGB 1 expression （P＜0.05）. CONCLUSIONS Asp can reduce inflammation and oxidative stress by regulating the miR -340-5p/HMGB1/TLR4 pathway，reduce apoptosis i n myocardial tissue ，and play a protective role against myocard ial I/R injury .

BACKGROUND:Insufficient blood supply after major bone defects leads to osteocyte necrosis;therefore, the tissue-engineered bone cannot meet the clinical requirements. OBJECTIVE:To construct an artificial vessel using in vitro cultured rabbit bone marrow stromal stem cel s and human umbilical vein endothelial cel s combined with the rabbit aortic decel ularized vascular matrix. METHODS:Rabbit bone marrow stromal stem cel s were cultured by adherent method, human umbilical vein endothelial cel s were cultured in vitro and isolated, and rabbit aortic decel ularized vascular stent was prepared. The stent-cel composite was constructed, and its biocompatibility was observed under scanning electron microscope. There were three groups:blank control, control (bone marrow stromal stem cel-stent) and experimental (stent-cel composites) groups (n=10 per group), fol owed by implantation around the smal vessels. Three months later, the vascular samples were col ected for gross observation and hematoxylin-eosin staining. RESULTS AND CONCLUSION:Fibroblast-like cel clones were formed by adherent method, and were positive for CD44+and STRO-1+after climbing;calcified nodule formed in the ossification. Flow cytometry showed CD34+accounting for 43.83%, and visible VIII factor in the endothelial cel s. In the experimental group, endothelial cel s formed a single cel layer onto the scaffold under scanning electron microscope;the artificial vessel grew wel and tubular structure presented and eight angiod structures were found. Thin film-like vessels formed in the blank control group and there were only endothelial-like tissues in the control group. These results suggest that angiod structures can form after the stent-cel composite implantation, causing no immune reaction, but the artificial vessel is visible in absence of muscular layer.

Objective To analyze the effects of the " Clinic-pharmacy separation" reform in Beijing. Methods Following the chronological order, 60-month operational data of a pilot hospital from 2012 to 2016 were analyzed. These data included medical statistics reports, financial information, HIS information,authority information,and patients′satisfaction on site. Results Pilot hospital showed that its medical work efficiency continued to grow. During 2013 -2016, its outpatients volume growth rate ranged 3.53% ~15.20%, and its number of discharged patients growth rate ranged 3. 12% -8. 48%. The hospital harvested 12.21 million yuan of converted income from September 2012 (when the reform was in place to cancel the drug markup and collect medical service fees) to August 2013,scoring a smooth shift of revenue sources. Medical insurance fund expenditure did not increase as a result. The percentage of drug expense was significantly decreased,dropping over 15% in 5 years. Outpatient drug fees and inpatient drug fees continued to decline year by year. Patients expressed higher satisfaction over medical services due to longer time of consultation with physicians. Conclusions " Clinic-pharmacy separation" reform has achieved the following objectives. The revenue is maintained stable; Patients flow is diverted under guidance, with less financial burden; and medical insurance expenditure is under control. We propose to improve the performance incentive and constraint mechanism for drug prescriptions by physicians.

Objective To investigate the effects of nicardipine on apoptosis in ischemia?reperfusion myocardium of rabbits. Methods Forty New Zealand rabbit were randomly divided into 4 groups:control group(group A),ischemia group(group B),ischemia?reperfusion group(group C),ni?cardipine treatment group(group D). Ischemia?reperfusion model was established by left circumflex branch coronary artery ligation for 40 min,fol?lowed by 120 min reperfusion. Apoptotic cardiomyocyte was detected using the analysis for the exposure of phosphatidyl?serine ( Annexin V)meth?od. Results Myocardial cell damage was lower in D group than that in group B and group C from pathology(P<0.01). The myocardial cell apopto?sis in group D is less than that of group B and group C(P<0.01),but higher than that of group A(P<0.05). Myocardial cell necrosis is lower than group B and group C(P<0.01),and no difference was found comparing with group A(P>0.05). Conclusion Nicardipine horizon can reduce the myocardial cell apoptosis in rabbits with myocardial ischemic reperfusion injury.

A new series of 2-(5-methyl-2,3-dioxoindolin-1-yl)acetamide derivatives were synthesized and evaluated for their anticonvulsive activity in a pentylenetetrazole (PTZ)-evoked convulsion model and antidepressant activity in the forced swimming test (FST) model. Eleven synthesized compounds were found to be protective against PTZ-induced seizure and showed the anticonvulsant activity. In addition, four of the synthesized compounds (4l, 4m, 4p and 4q) showed potent antidepressant-like activity. Among these compounds, compound 4l was found to have the most potent antidepressant-like activity, and significantly reduced the duration of immobility time at 100 mg/kg dose level when compared to the vehicle control, which is similar to the reference drug fluoxetine.

BACKGROUND:Central pancreatectomy is a surgical treatment for tumors at the neck or the middle part of the pancreas, which can reserve more normal pancreas, not cut adjacent organs, and reduce the incidence of postoperative internal and external pancreatic secretion deficiency with respect to the expanded proximal and distal pancreatectomy. OBJECTIVE: To systematicaly evaluate the clinical efficacy of the central pancreatectomy and distal pancreatectomy. METHODS: A computer-based search of Chinese and English databases was performed, and then 15 controled clinical trials were included and systematicaly evaluated using RevMa5.2 software. RESULTS AND CONCLUSION: Totaly 1 079 cases were included in this study, which consisted of 436 central pancreatectomy cases and 643 distal pancreatectomy cases. Meta-analysis showed that compared with the distal pancreatectomy group, the incidences of postoperative pancreatic fistula and complications were significantly higher, the risk of postoperative endocrine and exocrine insufficiency were significantly lower, while the surgical time (SMD: 59.23, 95%CI: 22.41-96.05, P < 0.01) and hospital stays (SMD: 7.01, 95%CI: 1.94-12.09,P< 0.01) were longer in the central pancreatectomy group. These findings indicate that although the central pancreatectomy has a high postoperative complication incidence, it can be accepted clinicaly, which may be a reasonable operation method to preserve pancreatic exocrine and endocrine function.