Objective To observe the effect of glutathione on bleomycin-induced pulmonary fibrosis in rats .Methods Fifty-four SD rats in good conditions were divided into three groups at random:control group ,BLM group,glutathione(GSH) group.On experimental day(day 0),the rats were intratracheally instilled with bleomycin(5mg?kg -1 .body weight),and then treated with intraperitoneal injection of glutathione .On days 7,14,28 after instillation ,six rats of each group were sacrified respectively and the lungs were harvested for histopathological examination and determinations of GSH and hydroxyproline(HYP).Results Pathological findings of GSH group were the same as BLM group,but compared with BLM group,pathomorphologic changes in GSH group was a small extent.The content of GSH in lung tissue was increased significantly(P0 05).Conclusions Glutathione has anti-oxidation and may protect lung tissue free from oxidation injury, but it has no protecting effect on collagen deposition caused by bleomycin.

Objective Liver function in perioperative periods, postoperative complications, and pathological changes in the liver were studied and compared between patients undergoing emergent and elective surgical intervention (extensive esophagogastric devascularization, EED) for portal hypertension (PTH), with the purpose to elucidate the pathogenesis of PTH. Methods The clinical data and liver biopsies from 150 cases of inpatients with hepatis cirrhosis and PTH who underwent either emergent (28 cases) or elective (100 cases) surgical intervention including extensive esophagogastric devascularization (EED) in 302 th Hospital of PLA were analysed. Liver biopsy was done in 128 patients, and the expression of ?-smooth muscle actin (?-SMA), tubulin?and ?in hepatic stellate cells (HSCs), and endothelin-1 (ET-1) was histochemically studied in the liver tissue. Results It was found that the mean internal diameter of portal veins before surgery was larger and the incidence of pre-operative acute variceal haemorrhage was significantly higher in the emergent EED group than those in the elective EED group (P

Breast Neoplasms ; drug therapy ; pathology ; surgery ; Chemotherapy, Adjuvant ; Female ; Humans ; Mammaplasty ; Mastectomy, Segmental ; methods ; Neoadjuvant Therapy ; Sentinel Lymph Node Biopsy ; methods

OBJECTIVE To emphasize the management of personnel and articles during operations with infective diseases,so to control the incidence of hospital infection.METHODS To establish an integrated and strict management of sterilization-isolation system,enhance the medical crew′s understanding of medical refuse′s harm during operations with infective diseases and intensify career training and supervising.RESULTS Hospital infection had been prevented effectively with procedure management and learning in operations with infective diseases.CONCLUSIONS The important procedures to prevent hospital infection are all medical crew take part in execution of perioperative antisepsis system strictly.

Objective To assess the efficacy of extensive esophagogastric devascularization with splenectomy for surgical treatment of portal hypertension complicating cirrhosis of liver, and to explore the pathogenesis of chronic congestive splenomegaly. Methods A retrospective analysis of clinical data of 232 patients of portal hypertension complicating cirrhosis of liver having undergone extensive esophagogastric devascularization with splenectomy was made. Pathological alterations and extracellular matrix productive cells of the congestive splenomegaly were studied both immunohistochemically and histologically. Results The functional markers including the numbers of PLT, WBC, and PTA in the peripheral blood and serum Alb were significantly improved after the operation compared with that of before the operation. Careful pre-operation preparation, replenishment of blood loss during the operation, postoperative drainage of the splenic bed, and prevention of complications were efficiently carried out. The mean volume of CCS spleens was 1 423.67?738.69cm 3. There was an obvious increase in the numbers of vimentin-, ?-SMA-positive cells in the CCS tissues, as well as CD68-positive macrophages. Conclusions The results indicated that extensive esophagogastric devascularization with splenectomy was a reasonably effective alternative therapy for patients with portal hypertension complicated by esophageal varices and congestive splenomegaly. Adequate replacement of blood lost in prevention of operation and postoperative complications were essential for satisfactory recovery of the petient. The activation of macrophagic system, with proliferation of fibroblasts and myofibroblasts, might participate in the pathogenesis of congestive splenomegaly.

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.

AIM: To investigate the inhibitory effect of arsenic trioxide on human glioma cell line U251 growth, change of gene expression and intracellular calcium content. METHODS: MTT method was used to observe the growth inhibition effect. Cell cycle, positive rate of proliferation cell nuclear antigen (PCNA), apoptosis associated protein Fas and Bcl-2, and intracellular calcium ion (IECa~ 2+ ) levels were measured by flow cytometry in U251 cells treated with different doses of As_2O_3. Apoptosis was detected with annexin V-FITC+PI dual parameter. RESULTS: As_2O_3 inhibited the growth of U251 cells dramatically. There were obvious dosage-effect and time-effect correlations (P0.05). The cell cycle was arrested in G_2M phase. Apoptosis occurred in U251 cells treated with As_2O_3 by annexin V-FITC+PI dual parameter detection. CONCLUSION: As_2O_3 inhibits the growth of U251 cells in vitro dramatically and induces apoptosis. The mechanism is probably associated with the improvement of Fas expression and IECa~ 2+ levels, decrease in PCNA protein expression and cell cycle arrest.