Objective To explore the mechanism of Fufangbiejiaruanganpian(FFBJRGP) treating liver fibrosis. Methods Needle biopsies before and after treatment with FFBJRGP were done in 65 patients with chronic viral hepatitis B, and the liver tissues were studied with Ishak scoring system to evaluate the effects of treatment. The activation, proliferation and apoptosis of hepatic stellate cells (HSCs) in the liver specimens were determined by using the double immunohistochemical staining of in situ terminal deoxynucleotidyl transferase mediated dUTP nick end labelling method (TUNEL) and smooth muscle actin (SMA). Results Compared with the specimens before treatment, the stages of liver fibrosis and histological activity grades in liver tissues were significantly improved after treatment with FFBJRGP for 6 months (mean value: P

Objective To study the effect of the traditional Chinese medicinal herbs, Fufangbiejiaruanganpian (FFBJRGP), in an experimental model of hepatic fibrosis and its pharmacodynamics. Methods An experimental model of hepatic fibrosis induced by carbon tetrachloride in rat was reproduced, and FFBJRGP was given in high, moderate, and low dosage for 0, 1, 3 and 6 months respectively. Six months after the treatment, matrix metalloproteinase MMP-2, MMP-13, MT-MMP-1, MT-MMP-2 and their inhibitor TIMP-1 and TIMP-2, total extracellular matrix and collagen I, Ⅲ and Ⅳ, and active hepatic stellate cells in the fibrotic livers were qualitatively and quantitatively examined at the protein and/or mRNA expression levels by using immunohistochemistry, in situ hybridization, image analysis and Chevallier's scoring system. Meanwhile, enzyme-degrading activities of MMP-2 and MMP-13 were assessed with gelatin or collagen substrate zymography respectively. Results Compared with the control group, in which rats with hepatic fibrosis were not treated with FFBJRGP, the histological examination of rat livers in the treatment groups showed that the total scores of hepatic fibrosis in treatment groups with varions dosage were significantly decreased 3,6 months after the treatment and 3,6 months after the termination of treatment (P

Objective To explore the mechanism of fibrosis in autoimmune hepatitis(AIH). Methods By using synaptophysin (SYN) as a new marker for hepatic stellate cells (HSCs),HSCs,collagen I,collagen IV,and MT-MMP-1 were detected by immunohistochemistry,and the expressions of MT-MMP-1 and TIMP-1 mRNA were assessed by in situ hybridization in liver tissues obtained by needle biopsy from 36 AIH patients. Results The HSCs were observed in the portal tracts,fibrotic septa and lobules of AIH liver tissues where inflammation was active,especially in the interface of inflammatory and non-inflammatory areas. The number of HSCs increased in proportion to the increase in histoligical active index (HAI,Knodell),while the deposition of Col I and Col IV were increased with increase in hepatic fibrosis stages (Knodell). MT-MMP-1 and its mRNA were mainly expressed in mesenchymal cells which were distributed in the areas of interface of inflammation and borders of fibrotic septa. It was also observed in a few hepatocytes. The expression of MT-MMP-1 was parallel to collagen IV distribution,and increased with advancement of HAI and fibrosis stages,reaching the peak at S4-5 stage. In addition,the expression of TIMP-1 mRNA was similar to that of MT-MMP-1 mRNA. Conclusions The results of immunohistochemistry and in situ hybridization suggested persistant active inflammation,triggering the activation and proliferation of HSC,and the resultant deposition of extracellular matrix such as collagen IV and I might be one of pathogenetic mechnisms of hepatic fibrosis in AIH. The increased expression of MT-MMP-1 in liver tissues of AIH in parallel with the advancement fibrotic stages also suggested that the relative lower level of ECM degeneration due to metalloproteinase suppression might be another reason for fibrogenesis and development of fibrosis in AIH. In addition,it was shown that synaptophysin was another good marker for HSC.

Objective To explore the clinical pathological features of Wilson's disease and the pathogenesis of liver fibrosis. Methods The clinical data and liver biopsy specimens obtained from 48 children with Wilson's disease were analysed. The pathological changes were studied with light microscopy, electron microscopy, combined with rhodanine and rubeanic acid for copper staining, Gordon-Sweet's staining for reticular fibers and Masson's staining for collagen fibers. Meanwhile, immunohistochemistry was used to investigate the expression of tissue inhibitors of metalloproteinase (TIMP) -1 and TIMP-2. The apoptosis of activated hepatic stellate cells (HSC) in liver tissues was illustrated with in situ end labeling (ISEL)(TUNEL POD method) and ?-SMA double staining. Results In all the cases, the mean onset age was 10.0?3.8 years, and the positive rates of family history, Kayser-Fleischer’s ring and decreased serum ceruloplasmin level were 29.2%, 68.8% and 93.0%, respectively. The levels of serum ALT, AST, ALP and ?-Glo were 3.6, 3.0, 2.7 and 2.0 fold of normal cutoff values. The major pathological changes in childhood patients with Wilson’s disease presented various chronic inflammatory changes in hepatic acini and portal tracts, interface hepatitis, focal or diffuse vesicular/ microvesicular steatosis, with large and irregular apoptotic bodies, Mallory's bodies, glycogenated nuclei, and eosinophilc granular hepatocytes. Among all the cases, 77.0% of liver specimens were positive for rhodanine and rubeanic acid staining for copper in hepatocyts, especially in the zone I of acinus. Ultrastructural observation showed swollen and unusual giant mitochondria, increased lysosomes and vesicular inclusions in hepatocytes. The incidence of hepatic fibrosis was 100%, presenting expanded portal tracts in the early, fibrotic septa in the moderate and cirrhosis in the late stage. The extent of TIMP-1 and TIMP-2 expression and number of activated HSC were increased in various degrees in all the liver specimens, while apoptotic HSCs were obviously decreased in the majority of cases. Conclusions The clinical and pathological changes of children with Wilson’s disease are varied and relatively obscure, and liver fibrosis appears early and progressive. Excessive activation and proliferation of HSC stimulated by liver injury and inflammation due to copper deposition and the decrease in activity of matrix degradation enzymes might be the important mechanisms underlying the occurrence and progression of hepatic fibrosis in Wilson's disease.

Objective The study aimed to analyze the clinical features and the causes of hospital death among the 5720 acute myocardial infarction(AMI)patients from Cardiology Center,Beijing Chao-Yang Hospital during the last 8 years. Methods A total of 5720 AMI patients received treatment in the Cardiology Center from January 1st ,2002 to December 31th ,2009 were retrospectively reviewed. All patients were classified according to age into 3 groups of ≤45,46 -75,and ＞ 75 years old. The morbidity,cause of death ,whether they had the PCI therapy,mortality after PCI and the impact of gender on the cause of death were observed respectively. Results The morbidity rate of male was significantly higher than female in all three groups,and the study also found that the morbidity rate of female was significantly higher in the group of ＞ 75 years old,which however was still lower than that of male. The AMI patients were more likely to accept PCI therapy,which could significantly reduce the mortality rate. The top 3 causes of death included acute heart failure(AHF),cardiogenic shock(CGS)and AHF combined with CGS. In addition,AHF caused significantly more death in female and older(＞ 75 years old)patients. Conclusions The morbidity rate of AMI patients in Beijing Chao-Yang Hospital increased year by year. And PCI therapy could reduce the mortality rate of all groups. Revascularization treatment seems to be feasible and safe for the patients older than 75 years old.

ObjectiveTo investigate the role of OPN in human breast cancer cell line ( MDA-MB-231) by using small interfering RNA to specifically knockdown OPN expression. MethodsOPN ShRNA expression vector was stably transfected to MDA-MB-231 cell line.The expression of OPN mRNA and protein were analyzed using reverse transcription polymerase chain reaction (RT-PCR)and Western blot,respectively.The growth of MDA-MB-231 cells were observed by MTT.The effect of OPN siRNA on the transplanted tumor growth and tumor hypoxia were assessed in nude mice. ResultsThe expression level of OPN in MDA-MB-231 cells were significantly lower under hypoxia or normoxia(P ＜ 0.05 ).OPN silence with RNAi significantly inhibited the invasion ability and proliferation of MDA-MB-231 cell lines (P ＜ 0.01 ).Inhibition of OPN with RNAi significantly inhibited the growth ability of MDA-MB-231 cells in vivo(P ＜0.05).The tumor hypoxia significantly decreased(P ＜ 0.05). ConclusionsOPN silence with RNAi can effectively inhibit cell proliferation and tumor growth of MDA-MB-231 cells,and decrease the bypoxia level of MDA-MB-231 transplanted tumor in nude mice.

Objective To study the clinicopathological features of primary and metastatic hepatic neuroendocrine carcinoma.Methods The records of 35 patients with primary hepatic neuroendocrine carcinoma and 35 patients with metastatic hepatic neuroendocrine carcinoma were retrospectively reviewed.These patients served as the primary group(priNET,n=35)and the metastasis group (metNET,n=35),respectively.Results There were significant differences between the two groups of patients in gender,site,size and number of tumor(P＜0.05).Although there was no significant difference between the two groups in the distribution of the tumors in the two lobes of liver (P＞0.05),priNET had more tumors localized to one lobe of liver while metNET had more tumors involving both lobes of liver(P＜0.05).Conclusions Gender,size,site and number of tumor may play an important role in the differentiation of primary or metastatic hepatic neuroendocrine tumor.

ObjectiveTo explore the in-hospital mortality and its determinants for very eldly (80 + years of age) patients with acute myocardial infarction (AMI).MethodsA retrospective cohort method was used.The 499 study subjects were very eldly patients with newly diagnosed AMI consecutively admitted into our department between January 1,2002 and February 22,2010.ResultsNinety-seven out of 499 patients died during hospitalization period,with total in-hospital mortality of 19.4％.Multivariable logistic regression analysis showed the independent determinants for mortality of very elderly AMI patients were cardiac Killip grades,complete A-V block,renal dysfunction,stent implant,and the type of AMI.Conclusions The independent determinants for mortality of elderly AMI patients are as following,cardiac Killip grade,complete A-V block,renal dysfunction,stent implant,and the type of MAI.Urgent PCI is safe and effective for some very elderly with AMI,which could improve their survival rate within hospitalization period.

Objective:To improve the performance of ECG arrhythmia classification algorithm and provide auxiliary basis for clinical ECG diagnosis.Methods:The one-dimensional ECG data was segmented according to the R point, and the segmented data was generated into a 2D image. The samples were expanded by data augmentation technology, and the image features were extracted by the 2D convolutional layer, 2D maximum pooling layer, Flatten layer and fully connected layer in 2D-CNN. Then, the samples were classified with Softmax classifier. The loss function with weight coefficients was used to enhance the model's learning of class S and class V. The MIT-BIH data set was used for model training and algorithm performance evaluation.Results:Sample expansion and the use of loss functions with weight coefficients can improve the recall rate and specificity index of the model, while maintaining the model's accuracy index of the classificatio on VEB and SVEB.Conclusions:The accuracy of the proposed model is 99.02%, and the recall rate of SVEB is 96.4%, indicating that this classification method can assist medical staff in diagnosing heart diseases.

Objective To evaluate the clinical value of 3D reconstruction in the single utility-port thoracoscopic segmentectomy of early stage NSCLC by propensity score matching (PSM). Methods We retrospectively analyzed clinical data of 150 early stage NSCLC patients undergoing single utility-port thoracoscopic segmentectomy. The patients were divided into reconstruction group (n=58) and non-reconstruction group (n=92) according to 3D reconstruction. PSM was performed on two groups to compare perioperative outcomes. Results Procedures were successfully completed on all patients, without perioperative death. In each group, 43 patients were successfully matched after PSM on the basis of 8 confounding factors, age, gender, smoking status, BMI, maximum tumor diameter on CT, tumor location, % FEV1 and type of planned segmentectomy. After PSM, in complex segmentectomy, the patients in the reconstruction group had shorter operation time (155.77±30.17 vs. 212.94±66.49min, P < 0.001) and less blood loss (46.00±25.94 vs. 88.79±68.36ml, P=0.002), compared with the non- reconstruction group. Conclusion Preoperative 3D reconstruction could help improve the efficiency of single utility-port thoracoscopic surgery for complex segmentectomy and reduce intraoperative bleeding.