AIM: To explore protective and therapeutic effects of the shenfu injection (SF) against renal ischemia reperfusionand and its possible mechanisms by studying the impact of SF on P38 mitogen activated protein kinase (P38MAPK), tumor necrosis factor alpha (TNF-?) and intercellular adhensive molecule-1 (ICAM-1). METHODS: 36 male SD rats were randomly divided into control group, ischemia reperfusion (IR) group and SF group. Rats were subjected to left renal pedicle occlusion followed by reperfusion with contralateral nephrectomy. The expression of P38MAPK and ICAM-1 were evaluated by Imunohistochemistry. The expression of TNF-? in the kidney tissue and plasma were analyzed by enzyme-linked immunoadsordent assay (ELISA). RESULTS: The expression of P38MAPK and ICAM-1, concentration of TNF-? in IR group were higher than that in the control group (P

Oxidative stress is one of the important pathogenesis of diabetic nephropathy.In recent years,the role of oxidized low-density lipoprotein(Ox-LDL) in the occurrence and progress of diabetic nephropathy has been more and more concerned about,and becomes a hot spot once again.This paper makes a review of the formation and metabolic mechanism of Ox-LDL,the changes of Ox-LDL in the progress of diabetic nephropathy and its clinical significance,and a number of new treatments for Ox-LDL in recent years to further understand the role of Ox-LDL in the occurrence and progress of diabetic nephropathy,then to provide new ideas for effective clinical treatment of diabetic nephropathy. Abstract:Summ ary:Oxidative stress is one of the important pathogenesis of d iabetic nephropathy.In recent years,the role of oxi-d ized low-density lipoprote in(Ox-LDL) in the occurrence and progress of d iabetic nephropathy has been more and more concerned about,and becom es a hot spot once again.Th is paperm akes a review of the form ation and m etabolic m echan ism of Ox-LDL,the changes of Ox-LDL in the progress of d iabetic nephropathy and its c lin ical sign ificance,and a number of new treatm ents forOx-LDL in recent years to further understand the role ofOx-LDL in the occurrence and progress of d ia-betic nephropathy,then to provide new ideas for effective c lin ical treatm ent of d iabetic nephropathy.

That sparkplugs and cognizances caution of medical morality base line is a realistic proposition that to spurn mammonism phenomenon filters medical service industry and enhances diathesis of medical affairs personnel.Medical service incited by mammonism phenomenon forms a menace to the medical base line,it is important inducement of medical action of getting out of line,and duties of medical risk and complaints of medical comsumer.Mammonism phenomenon form a nubbin quoted by medical morality base line and duties of medical risk.

Objective To explore the significance of cellular apoptosis induced by severe acute respiratory syndrome cronovirus (SARS-CoV) in the pathogenesis of SARS. Methods TdT-mediated biotinylated-dUTP nick end ladelling method (TUNEL), and the double immunochemical staining with cytokeratin and CD3, CD8, CD20 and CD68 monoclonal antibodies were used to study the cellular apoptosis in tissue specimens from six patients who died from SARS. Meanwhile, the expression of Fas, Fas ligand (FasL), P53 and Bcl-2 proteins was detected by immunohistochemical method. Results The number of cellular apoptosis was obviously increased in multiple organs from the six patients died from SARS. The cellular apoptosis occurred predominantly in cytokeratin-positive pneumoncytes, terminal bronchiolar epithelium, CD3 + and CD8 + lymphocytes, as well as a part of CD20 + lymphocytes and CD68 + macrophages. Fas protein was mainly expressed in the infiltrated mononuclear cells, while FasL was chiefly expressed in SARS-CoV target cells, especially in the apoptotic cells. In the lung and immune organs, down-regulation of P53 and Bcl-2 expression was found. Conclusion The occurrence of increased and rapid cell apoptosis induced by SARS-CoV might be the main cause of the injuries to the lung and immune system. That the activated lymphocytes which expressed Fas and FasL attack SARS-CoV target cells might be the underlying mechanism of cell apoptosis in SARS. Down-expression of Bcl-2 and P53 proteins might also participate in cell apoptosis induced by SARS-CoV.

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 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.

Cancer/testis(CT) antigens,of which more than 40 kinds have now been identified,are encoded by genes that are expressed normally in the human germ line,and are also expressed in various tumor types,including melanoma,and carcinomas of the bladder,lung and liver.These immunogenic proteins are being vigorously pursued as targets for therapeutic cancer vaccines.In this paper,the classification,expression and function of CT antigens are reviewed.

Objective To investigate the expressions of pivotal cytokines such as TNF-? and TGF-?_1, and leptin in human nonalcoholic lipoid hepatitis (NALH), and to explore their potential roles in the pathogenesis of NALH. Methods Liver tissue obtained from 59 patients pathologically diagnosed as nonalcoholic lipoid hepatitis and 10 healthy adult liver tissues were examined in the present study. The respective expression of TNF-?, TGF-?_1 and Leptin was qualitatively and semi-quantitatively determined at the protein expression levels by using immunohistochemical method and image analysis. Results In NALH liver tissue the expression of TNF-? appeared mainly in inflammatory cells and lining cells of liver sinusoids in zone 3, lipogranulomas and portal tract, where obvious inflammation was found. The expression was parallel to different degrees of inflammation in NALH, significant correlation was found between degree of inflammation and fibrosis and extent of expression (P

Objective To investigate the role of ERK1/2 signal pathway in the apoptosis of rat mesangial cells inhibited by TIMP-1.Methods The human TIMP-1 sense and antisense plasmid were transferred into rat mesangial cells through liposome,while mesangial cells transfected with pcDNA3 and non-transfected mesangial cells were used as control.After being stimulated with high glucose(HG 25mmol/L D-glucose)and PD98059(50 ?mol/L)for 24 hours,the apoptosis rate was measured by flow cytometry.The expression of ERK1mRNA was assayed by RT-PCR.The protein expression of p-ERK1/2 in the cell was analyed by ELISA.Results(1)The apoptosis rates of the non-transfected group,transfect pcDNA3 group,sense group and antisense group in the culture medium of high glucose withact PD98059,were(12.10?2.21)%,(11.90?3.34)%,(5.50?0.50)%and(20.70?3.41)%,respectively.The apoptosis rate of the sense group was significantly lower than that without transfection(P

Objective To explore the expression of leptin and its receptors in liver tissue of nonalcoholic steatohepatitis(NASH)patient and its significance in pathogenesis.Methods Samples of 59 liver biopsies of NASH patients were divided into three groups G,S and F according to their degree of inflammation and steatosis and stage of fibrosis.The expression of leptin and its receptors including Ob-R,the short form of Ob-R(Ob-Ra)and the long form of Ob-R(Ob-Rb)were semi-quantitatively determined at the protein and/or mRNA expression levels by using immunohistochemistry,in situ hybridization and image analysis.Results The expressions of leptin in NASH liver tissues were found in KC,HSC and MNC,which were mainly situated in zone 3 near steatotic hepatocytes and perisinusoidal or portal fibrosis areas.Leptin mRNA(Ob)positive cells were distributed in hepatocytes in zone 3.The expression of leptin at protein and mRNA levels in the NASH liver tissues was significantly increased in NASH compared with normal liver tissues(P