ObjectiveTo explore the effect and mechanism of Taishan Panshi powder （TSPSP） on inhibiting oxidative stress injury in human chorionic trophoblast cells （HTR-8/SVneo）， and to uelucidate the underlying mechanism of TSPSP in the treatment of spontaneous abortion （SA）. MethodsGene differential analysis of SA was performed using the Gene Expression Omnibus （GEO） database and correlated with oxidative stress. Network pharmacology was employed to screen the active components of TSPSP， and a "Chinese medicine-component-target-disease" network was constructed to predict the mechanism of action of TSPSP. For in vitro validation experiments， HTR-8/SVneo cells were divided into blank group， model group， TSPSP-containing serum 2.5%， 5%， 10% groups， and nuclear factor E₂-related factor 2 （Nrf2） inhibitor group （ML385， 30 μmol·L^-1）. Except for the blank group， other groups were stimulated with 150 μmol·L^-1 H₂O₂ for 3 h to establish a cell oxidative stress injury model. After successful modeling， the blank group and model group were given 10% blank serum， each TSPSP-containing serum group was treated with the corresponding concentration of drug-containing serum， and the Nrf2 inhibitor group was additionally given 30 μmol·L^-1 ML385 on the basis of 10% TSPSP-containing serum. All groups of cells were continuously cultured under the above conditions for 24 h， and then samples were collected for subsequent detection. Cell viability in each group was detected by CCK-8 assay. Cell migration rate was detected by scratch test. The contents of malondialdehyde （MDA）， Fe²⁺， and Glutathione （GSH） were detected by enzyme-linked immunosorbent assay （ELISA）. Intracellular reactive oxygen species （ROS） level was detected by a fluorescent probe （DCF-DA）. The protein and mRNA expression levels of Kelch-like ECH-associated protein 1 （KEAP1）， Nrf2， and forkhead box protein O3 （FoxO3） in cells were detected by immunofluorescence （IF） and real-time quantitative polymerase chain reaction （Real-time PCR）. The protein expression levels of KEAP1， Nrf2， FoxO3， Glutathione peroxidase 4 （GPX4）， and superoxide dismutase （SOD） in cells were detected by Western blot. ResultsThe GSE76862 and GSE22490 datasets were obtained from the GEO database. Differential gene analyses showed that the KEAP1， Nrf2， and FoxO3 genes were all associated with the disease. After matching with the oxidative stress pathway， nine significantly differential pathways were identified （P<0.05）， among which three contained the target genes Nrf2 and FoxO3. A total of 246 active ingredient targets of TSPSP and 2 804 SA-related targets were obtained through network pharmacology， and 154 potential action targets were obtained after taking the intersection. Topological analysis showed that targets such as KEAP1 and Nrf2 exhibited high degree values. GO and KEGG enrichment analyses indicated that the intersection targets were mainly involved in oxidative stress response， FOXO and MAPK signaling pathways， etc. In in vitro experiments， compared with the blank group， the cell viability in the model group was significantly decreased （P<0.01）. Compared with the model group， the cell viability in each TSPSP-containing serum group was significantly increased （P<0.01）. Compared with the 10% TSPSP-containing serum group， the cell viability in the ML385 group decreased to approximately 70% （P<0.01）. Compared with the blank group， the model group showed significantly increased contents of MDA， Fe²⁺， and ROS， decreased GSH expression （P<0.01）， significantly reduced cell migration rate （P<0.01）， and increased protein and mRNA expression levels of KEAP1 and FoxO3 （P<0.01）， while decreased protein and mRNA expression levels of Nrf2， GPX4， and SOD （P<0.01）. Compared with the model group， each TSPSP-containing serum group showed significantly decreased contents of MDA， Fe²⁺， and ROS， increased GSH expression （P<0.01）， significantly increased migration rate （P<0.01）， significantly decreased protein and mRNA expression levels of KEAP1 and FoxO3 （P<0.05， P<0.01）， and significantly increased protein and mRNA expression levels of Nrf2， GPX4， and SOD （P<0.05， P<0.01）. Compared with the 10% TSPSP-containing serum group， the ML385 group showed reversed trends in all indicators （P<0.05， P<0.01）. ConclusionTSPSP can inhibit H₂O₂-induced oxidative stress injury of trophoblast cells， and its mechanism of action may be related to the drug activating the KEAP1/Nrf2/FoxO3 signaling pathway.

ObjectiveTo explore the effect and mechanism of Taishan Panshi powder （TSPSP） on inhibiting oxidative stress injury in human chorionic trophoblast cells （HTR-8/SVneo）， and to uelucidate the underlying mechanism of TSPSP in the treatment of spontaneous abortion （SA）. MethodsGene differential analysis of SA was performed using the Gene Expression Omnibus （GEO） database and correlated with oxidative stress. Network pharmacology was employed to screen the active components of TSPSP， and a "Chinese medicine-component-target-disease" network was constructed to predict the mechanism of action of TSPSP. For in vitro validation experiments， HTR-8/SVneo cells were divided into blank group， model group， TSPSP-containing serum 2.5%， 5%， 10% groups， and nuclear factor E₂-related factor 2 （Nrf2） inhibitor group （ML385， 30 μmol·L^-1）. Except for the blank group， other groups were stimulated with 150 μmol·L^-1 H₂O₂ for 3 h to establish a cell oxidative stress injury model. After successful modeling， the blank group and model group were given 10% blank serum， each TSPSP-containing serum group was treated with the corresponding concentration of drug-containing serum， and the Nrf2 inhibitor group was additionally given 30 μmol·L^-1 ML385 on the basis of 10% TSPSP-containing serum. All groups of cells were continuously cultured under the above conditions for 24 h， and then samples were collected for subsequent detection. Cell viability in each group was detected by CCK-8 assay. Cell migration rate was detected by scratch test. The contents of malondialdehyde （MDA）， Fe²⁺， and Glutathione （GSH） were detected by enzyme-linked immunosorbent assay （ELISA）. Intracellular reactive oxygen species （ROS） level was detected by a fluorescent probe （DCF-DA）. The protein and mRNA expression levels of Kelch-like ECH-associated protein 1 （KEAP1）， Nrf2， and forkhead box protein O3 （FoxO3） in cells were detected by immunofluorescence （IF） and real-time quantitative polymerase chain reaction （Real-time PCR）. The protein expression levels of KEAP1， Nrf2， FoxO3， Glutathione peroxidase 4 （GPX4）， and superoxide dismutase （SOD） in cells were detected by Western blot. ResultsThe GSE76862 and GSE22490 datasets were obtained from the GEO database. Differential gene analyses showed that the KEAP1， Nrf2， and FoxO3 genes were all associated with the disease. After matching with the oxidative stress pathway， nine significantly differential pathways were identified （P<0.05）， among which three contained the target genes Nrf2 and FoxO3. A total of 246 active ingredient targets of TSPSP and 2 804 SA-related targets were obtained through network pharmacology， and 154 potential action targets were obtained after taking the intersection. Topological analysis showed that targets such as KEAP1 and Nrf2 exhibited high degree values. GO and KEGG enrichment analyses indicated that the intersection targets were mainly involved in oxidative stress response， FOXO and MAPK signaling pathways， etc. In in vitro experiments， compared with the blank group， the cell viability in the model group was significantly decreased （P<0.01）. Compared with the model group， the cell viability in each TSPSP-containing serum group was significantly increased （P<0.01）. Compared with the 10% TSPSP-containing serum group， the cell viability in the ML385 group decreased to approximately 70% （P<0.01）. Compared with the blank group， the model group showed significantly increased contents of MDA， Fe²⁺， and ROS， decreased GSH expression （P<0.01）， significantly reduced cell migration rate （P<0.01）， and increased protein and mRNA expression levels of KEAP1 and FoxO3 （P<0.01）， while decreased protein and mRNA expression levels of Nrf2， GPX4， and SOD （P<0.01）. Compared with the model group， each TSPSP-containing serum group showed significantly decreased contents of MDA， Fe²⁺， and ROS， increased GSH expression （P<0.01）， significantly increased migration rate （P<0.01）， significantly decreased protein and mRNA expression levels of KEAP1 and FoxO3 （P<0.05， P<0.01）， and significantly increased protein and mRNA expression levels of Nrf2， GPX4， and SOD （P<0.05， P<0.01）. Compared with the 10% TSPSP-containing serum group， the ML385 group showed reversed trends in all indicators （P<0.05， P<0.01）. ConclusionTSPSP can inhibit H₂O₂-induced oxidative stress injury of trophoblast cells， and its mechanism of action may be related to the drug activating the KEAP1/Nrf2/FoxO3 signaling pathway.

Objective: To analyze the trends, gender, and age differences in the incidence of lip and oral cavity cancer in Chinese population from 1990 to 2021 and predict future incidence trends, providing a scientific basis for disease prevention and public health policy. Methods: Incidence data of lip and oral cavity cancer in Chinese population from the Global Burden of Disease (GBD) database from 1990 to 2021 were analyzed. The Joinpoint regression model was used to assess temporal trends, the age-period-cohort model was used to evaluate the independent effects of age, period, and cohort, and the Bayesian age-period-cohort model (BAPC) model was used to predict incidence trends from 2022 to 2044. Results: From 1990 to 2021, the age-standardized incidence rate of lip and oral cavity cancer in Chinese population increased from 2.39/100 000 to 3.76/100 000, and the crude incidence rate rose from 1.71/100 000 to 4.85/100 000. The incidence rate in males was higher and increased more rapidly than in females. Higher incidence rates were prevalent among older populations, a rapid increase in incidence rates occurred during 2003 to 2012, and earlier birth cohorts showed overall higher risks. BAPC predictions indicated a continued rise in incidence from 2022 to 2044. During this period, male incidence stabilized while female incidence increased at a relatively faster rate. Conclusion The incidence of lip and oral cavity cancer in Chinese population has revealed a continuous upward trend, particularly among males and older populations. Future prevention strategies should focus on these high-risk populations.

ObjectiveTo analyze the epidemiological trends and characteristics of brucellosis in humans (hereinafter referred to as brucellosis) in Tangshan City, Hebei Province from 2016 to 2023, and to provide a scientific basis for formulating brucellosis prevention and control strategies in the region. MethodsThe incidence data of human brucellosis in Tangshan City from 2016 to 2023 were collected from the China Disease Prevention and Control Information System. The diagnosis time, infection route, and clinical characteristics of the cases were obtained from the case investigation reports. Descriptive epidemiological methods were used to analyze the temporal, spatial, demographic distributions, and clinical characteristics of human brucellosis. Brucella species were identified using agglutination tests with bacterial suspension and A/M antigen-positive serum. ResultsA total of 2 193 cases of human brucellosis were confirmed and clinically diagnosed in Tangshan City from 2016 to 2023, with the peak incidence occured from March to August, and which exhibited distinct geographic distribution patterns. The highest incidence rate was found in people aged 60‒<70 years. The occupation of cases were primarily farmers. The incidence rate in males (528/100 000) was higher than that in females (184/100 000). All cases had confirmed exposure to infected animals or contaminated animal products. ConclusionThe epidemic of human brucellosis in Tangshan exhibited an overall steady downward trend from 2016 to 2023, except for a slight increase in 2016 and 2021, with the incidence rate controlled at 289/100 000‒335/100 000. The prevention and control situation of human brucellosis still remains severe, with the highest incidence rate in the eastern region of Tangshan, which are characterized by the breeding, slaughtering, and processing of cattle and sheep. Therefore, it it is necessary to enhance the prevention and control of human brucellosis among the personnel engaged in these industries in the eastern areas.

Objective To elucidate the role of let-7 in the pathogenesis of oral squamous cell carcinoma(OSCC)and its underlying molecular mechanism.Methods The expression of let-7 in human oral keratinocyte(HOK),OSCC tissues,and OSCC cells(CAL-27,SCC-25,and SCC-9)was detected by quantitative real-time PCR.Colony formation,scratch,Transwell,and flow cytometry assays were used to examine the effects of let-7 on the proliferation,migration,invasion,and apoptosis of SCC-25 cells.Western blotting was used to detect the expression of Wnt and β-catenin proteins.The correlation between let-7 expression and the clinicopathological cha-racteristics and prognosis of OSCC patients was analyzed.Results let-7 was downregulated in OSCC tissues and cells.let-7 over-expression effectively inhibited the proliferation,migration,and invasion of SCC-25 cells while promoting apoptosis by suppressing acti-vation of the Wnt/β-catenin pathway.let-7 expression was closely associated with tumor stage,lymph node metastasis,and patient survival status.Patients with low let-7 expression exhibited lower overall survival rate.Conclusion let-7 targets and regulates the Wnt/β-catenin pathway,thereby inhibiting proliferation,migration,and invasion of OSCC cells while promoting apoptosis.

Objective To elucidate the role of let-7 in the pathogenesis of oral squamous cell carcinoma(OSCC)and its underlying molecular mechanism.Methods The expression of let-7 in human oral keratinocyte(HOK),OSCC tissues,and OSCC cells(CAL-27,SCC-25,and SCC-9)was detected by quantitative real-time PCR.Colony formation,scratch,Transwell,and flow cytometry assays were used to examine the effects of let-7 on the proliferation,migration,invasion,and apoptosis of SCC-25 cells.Western blotting was used to detect the expression of Wnt and β-catenin proteins.The correlation between let-7 expression and the clinicopathological cha-racteristics and prognosis of OSCC patients was analyzed.Results let-7 was downregulated in OSCC tissues and cells.let-7 over-expression effectively inhibited the proliferation,migration,and invasion of SCC-25 cells while promoting apoptosis by suppressing acti-vation of the Wnt/β-catenin pathway.let-7 expression was closely associated with tumor stage,lymph node metastasis,and patient survival status.Patients with low let-7 expression exhibited lower overall survival rate.Conclusion let-7 targets and regulates the Wnt/β-catenin pathway,thereby inhibiting proliferation,migration,and invasion of OSCC cells while promoting apoptosis.

Objective To investigate the risk factors associated with post traumatic cerebral infarction (PTCI) after craniotomy hematoma evacuation for severe traumatic brain injury (sTBI) so as to provide clinical reference for the early prevention of postoperative PTCI.Methods A retrospective case control study was conducted to analyze the clinical data of 558 sTBI patients who received craniotomy hematoma evacuation admitted to Changsha Hospital of Traditional Chinese Medicine from October 2006 to June 2016.There were 340 males and 218 females,aged 15-71 years,with an average of 47.8 years.Among them,75 patients were at the age of less than 30 years,315 were at 30-50 years,and 168 were above 50 years.According to the Glasgow coma score (GCS),there were 127 patients with 3-4 points,124 with 5-6 points,and 307 with 7-8 points.The patients were divided into PTCI group (51 patients)and non-PTCI group (507 patients).The related indicators of the two groups of patients after admission were collected,including gender,age,injury cause,GCS,skull base fracture,traumatic subarachnoid hemorrhage (tSAH),cerebral hernia,hypotension,the time from injury to craniotomy,and whether decompressive craniectomy was performed.Univariate analysis was first performed for these factors,followed by multivariate logistic regression analysis.Results There were no significant differences in gender,age,injury cause,skull base fracture,and decompressive craniectomy between PTCI group and control group (P ＞ 0.05).In the PTCI group,there were 29 patients with GCS of 3-4 points,17 with 5-6 points,and five with 7-8 points;there were 48 patients with tSAH,37 patients with cerebral hernia,and 18 patients with hypotension.In terms of the time from injury to craniotomy,it took ＜ 3 hours in 30 patients,3-6 hours in 12,6-12 hours in five,and ＞ 12 hours in four.In the non-PTCI group,there were 98 patients with GCS of 3-4 points,107 with 5-6 points,and 302 with 7-8 points.There were 34 patients with tSAH,117 with cerebral hernia,and 35 with hypotension.In terms of the time from injury to craniotomy,it took ＜3 hours in 294 patients,3-6 hours in 130,6-12 hours in 68,and ＞ 12 hours in 15.The differences between the two groups were statistically significant (P ＜ 0.05).Multivariate logistic regression analysis indicated that GCS of 3-6 points,tSAH,cerebral hernia,time from injury to craniotomy,and hypotension were significantly associated with PTCI after operation for sTBI (P ＜ 0.01).Conclusions GCS of 3-6 points,tSAH,cerebral hernia,duration from injury to craniotomy,and hypotension time ＞ 3 hours are the high risk factors of PTCI in sTBI patients after craniotomy.For patients with these high risk factors,craniotomy should be performed in time,and the perioperative blood pressure and intracranial pressure stability should be maintained so as to relieve vasospasm.

Objective To summarize the clinicopathological characteristic,diagnosis and treatment of iatrogenic biliary tree destruction.Methods The retrospective cross-sectional study was conducted.The clinical data of 11 patients with iatrogenic biliary tree destruction who were admitted to the Chinese PLA General Hospital (9 patients) between January 1990 and December 2013 and Beijing Tsinghua Changgung Hospital (2 patients) between December 2014 and May 2017 were collected.Observation indicators:(1) causes and parts of destruction;(2) clinical manifestation;(3) imaging performance;(4) treatment;(5) follow-up.Follow-up using outpatient examination and telephone interview was performed to detect long-term prognosis of patients up to April 2018.Measurement data with skewed distribution were described as M (range).Results (1) Causes and parts of iatrogenic biliary tree destruction:causes of iatrogenic biliary tree destruction in 11 patients:transcatheter arterial embolization for hepatic hemangioma was performed in 7 patients,high intensity focused ultrasound for hepatic hemangioma in 1 patient,arterial embolization for false aneurysm in 1 patient,sclerosant injection for hepatic echinococcosis in 1 patient,and cyberknife radiotherapy for hepatocellular carcinoma in 1 patient.Parts of biliary tree destruction of 11 patients:5,3,2 and 1 respectively involved bilateral biliary tree,right biliary tree,bilateral main biliary ducts in hepatic port and left biliary tree.(2) Clinical manifestation:11 patients had symptoms of recurrent chills and fever,and combined with different degrees of jaundice.The initial symptom occurred in 2 weeks to 3 months after iatrogenic biliary tree destruction.Of 11 patients,7 were complicated by different degrees of hepatic abscess,and abscess involving left and right half liver were detected in 4 patients,aggregating in right half liver in 2 patients and aggregating in left half liver in 1 patient.Eight patients had secondary biliary cirrhosis,portal hypertension,splenomegaly and hypersplenism during the late course of disease.(3) Imaging performance:magnetic resonanced cholangio-pancreatography (MRCP) and cholangiography examinations showed missing bile duct in necrosis area,beading-like stricture and dilation of damaged biliary tree,reducing proximal bile duct branches and associated gallbladder necrosis.CT and MRI examinations showed that structure of distribution area of damaged biliary tree disappeared or bile duct wall was thickened,and hepatic abscesses of patients were scattered and multiple.Five patients had significantly secondary liver atrophy-hypertrophic syndrome,showing atrophy of right liver and hyperplasia of left liver.Radiotherapy-induced biliary tree destruction showed a characteristic of continued progress,localized abnormality in the early stage and typical imaging changes after the damage stability in the late stage.(4) Treatment:of 11 patients,4 didn't undergo surgery,and 7 underwent 18 intentional and conclusive surgeries (1-4 times / per case).(5) Follow-up:11 patients were followed up for 2-132 months,with a median time of 73 months.During the follow-up,2,1 and 8 patients had respectively excellent,good and poor prognoses.Among 11 patients,4 died (2 died of severe infection and 2 died of biliary cirrhosis),and 7 survived.Conclusions Iatrogenic biliary tree destruction is easy to cause hepatic abscess,liver atrophy-hypertrophic syndrome or biliary cirrhosis,and it can be diagnosed by imaging examination.The definitive treatment should be followed by liver resection or liver transplantation of involving area according to the extent of damage.

Due to the theoretical and technique limitation of traditional surgery,surgical treatment of complex intrahepatic biliary diseases was left for an unresolved difficult problem of the last century.Uncertainties of the anatomical,physiological,pathological changes and surgical techniques in the intrahepatic biliary tract contribute to this complexity.Through integrated application of modern scientific technology and traditional medicine methods and systematic optimization and innovation of biliary surgical theories and techniques,authors have developed a paradigm of precision biliary surgery which is characterized by high quantification,visualization and controllability.The establishment of the precise biliary surgical system solves the difficulty in surgeries for intrahepatic biliary diseases,puts forward the biliary surgery from extrahepatic ducts,hilar ducts to intrahepatic ducts,entering a new segment era of the biliary surgery marked by precision treatment of intrahepatic biliary diseases.

MicroRNA (miRNA),sharing the character of regulating the transcriptional level and expression level of mRNAs,is one kind of small non-coded RNAs.At present,innate immune has become one of the hot topics for researchers,and miRNAs as a sort of bioactive substance greatly take part in the whole regulation progress.In detailed,miRNAs can influence the immune state of immune cells during innate immune period and further regulate inflammatory conditions in whole body.By systematically summarizing miRNA function during innate immunity,this present review may provide a reference for peer researchers.