inflammatory pseudotumor. Conclusions The number of pleural is closely relative to the shape size and position. The occurrence rate of pleural indentation is closely relative to the distance between SPN and pleural,and the nature of SPN has correlation with pulling pleural.

AIM:To analyse sequences of p62 dok amino acid and cDNA and to investigate p62 dok tyrosine phosphorylation and its relation with p21 ras GAP. METHODS:The purified p62 dok was extracted from CHO/IR cells. The peptide sequence of p62 dok was carried out on a high performance analyzer. PCR was performed with the primers designed from the sequence of p62 dok amino acid. Western blot and immunoprecipitation were used to identify tyrosine phosphorylation of p62 dok and the binding of p62 dok with p21 ras GAP. RESULTS:The p62 dok cDNA is a 1863 bp sequence and code 481 amino acid with 15 tyrosine residues and a putative pleckstrin homology domain. The p62 dok protein is rich in PxxP motif. The tyrosine-phosphorylated p62 dok can bind p21 ras GAP. CONCLUSION:Perhaps p62 dok is a new signaling molecule and play an important role in insulin signaling networks through RAS/MAPK pathway.

Objective To observe the function of recombinant human tissue factor pathway inhibitor1(rTFPI-1)in acute myocardial infarction in rabbit. Method Forty New Zealand White rabbits were subjected to coronary artery occlusion for 120 min and followed by reperfusion for 60 min,then they were ranlow dose rTFPI-1 group(n=10/group).The extent of ischemic area and the extent of myocardial infarction area were measured by Evan's blue stain and TTC stain,respectively.The degrees of infarction severity and ischemic severity were expressed as the ratios of the total left ventrieular wall area.The degrees of infarction severity and ischemic severity in different groups were compared by using one-way ANOVA and then followed by LSD procedure.Results The degree of infarction severity in the larger dose rTFPI-1 group was significantly lessened than that in low dose RTFPI-1 group and control group(P<0.001),and than that in modcrate dose rTFPI-1 group as well(P<0.05).The degree of infarction severity in the moderate dose rTFPI1 group was significantly lessened than that in low dose rTFPI-1 group and control group(P<0.001).There was no significant difference in degree of infarction severity between low dose rTFPI-1 group and control group(P>0.05).Conclusions Human rTFPI-1 might decrease myocardial infarction severity and save the survival myocardial tissue.

Sixty male SD rats were separately fed by normal diet or high-fat diet.After eight weeks of highfat diet,these rats were injected low dose streptozotocin (30 mg/kg).Diazoxide or glipizide was administered to the diabetic rats for 4 weeks.The results showed that body weight,serum insulin,and insulin sensitive index were decreased in the obese diabetic rats while the fasting blood glucose,total cholesterol,and triglyceride levels were increased compared with the high-fat diet group ( all P＜0.01 ).Consistent with the results of glipizide,diazoxide treatment lowered blood glucose,improved glucose tolerance,and decreased islet cell apoptosis compared with the diabetes mellitus group ( all P＜0.05 ).The results suggest that diazoxide can improve islet function of obese type 2 diabetic rats via decreasing insulin secretion and thus lessening the load on islet cells.

AIM：To analyse sequences of p62dok amino acid and cDNA and to investigate p62dok tyrosine phosphorylation and its relation with p21ras GAP. METHODS：The purified p62dok was extracted from CHO/IR cells. The peptide sequence of p62dok was carried out on a high performance analyzer. PCR was performed with the primers designed from the sequence of p62dok amino acid. Western blot and immunoprecipitation were used to identify tyrosine phosphorylation of p62dok and the binding of p62dok with p21ras GAP. RESULTS：The p62dok cDNA is a 1863 bp sequence and code 481 amino acid with 15 tyrosine residues and a putative pleckstrin homology domain. The p62dok protein is rich in PxxP motif. The tyrosine-phosphorylated p62dok can bind p21ras GAP. CONCLUSION：Perhaps p62dok is a new signaling molecule and play an important role in insulin signaling networks through RAS/MAPK pathway.

Objective To establish a sensitive and specific LC-MS/MS method for measurement of notoginsenoside R1, ginsenoside Rg1, ginsenoside Re, ginsenoside Rb1, ginsenoside Rd, tanshinone Ⅰ, astragaloside Ⅳ and harpagosidein of Fufang Xueshuantong Capsule in rat plasma. Methods The HPLC separation was performed on Thermo Hypersil GOLD column (2.1 mm× 100mm, 5 μm) at 30 ℃, injecting 10 μL and using acetonitrile-water (0.1% formic acid) as the mobile phrase (B was acetonitrile, A was 0.1%formic acid;0-10 min, 25%-55%B;10-20 min, 55%-70%B) with the flow rate of 0.2 mL/min. Detection was performed on a tandem quadrapole mass spectrometer using positive electrospray ionization, SRM scan mode. Results The eight compounds showed good linearity in wide ranges (notoginsenoside R1 1.00-800 ng/mL, ginsenoside Rg1 0.950-760 ng/mL, ginsenoside Re 1.44-1440 ng/mL, ginsenoside Rb1 1.33-1330 ng/mL, ginsenoside Rd 9.90-990 ng/mL, harpagosidein 1.01-1010 ng/mL, astragaloside Ⅳ 1.16-928 ng/mL, tanshinone Ⅰ 10.0-800 ng/mL). In addition, the accuracy and recovery were around 85%-115%and 50%-70%. The RSD of intra and inter day precision were lower than 15%. Conclusion The method is specific, rapid and sensitive. Therefore, it can be applied to pharmacokinetic study of eight effective compounds in Fufang Xueshuantong Capsule.

Objective To analyze the changes of the intima-media thickness(IMT)of carotid and femoral arteries, serum advanced glycosylation end-products(AGEs),and AGEs soluble receptor(sRAGE)after intensively controlling blood glucose, blood pressure, and lipid. Methods One hundred and thirty-two type 2 diabetic patients were divided into 3 groups and followed for 5 years: 20 patients were treated with intensive control of blood glucose and blood pressure, 80 patients with intensive control of blood glucose, blood pressure, and lipid; and 32 patients with conventional therapy. AGEs, sRAGE, and IMT of carotid and femoral arteries were measured and compared among different groups. Results The IMT of carotid and femoral arteries and serum level of AGEs were significantly decreased after intensive treatment. The ratio of sRAGE and HbA1C(sRAGE/HbA1C)were negatively correlated with the mean of HbA1Cin the past five years(r=-0.417, P＜0.001)and the fluctuation of HbA1C(r=-0.309,P＜0.001). Multinomial regression analysis showed that AGEs were the important risk factors of IMT of femoral artery(β=0.152,P=0.068). Conclusion Intensive treatment is significant in controlling the growing IMT of carotid and femoral arteries, while decreasing serum level of AGEs.

OBJECTIVETo identify the risk factors for no-reflow (NR) phenomenon after primary percutaneous coronary intervention (PCI) in patients with acute myocardial infarction.

METHODSA total of 843 patients with AMI underwent primary PCI within 12 h following onset of the ischemic symptoms. According to TIMI flow grade and myocardial blush grade, the patients were divided into reflow group and NR group after primary PCI, and the clinical data, angiography findings and surgical data were compared to analyze the factors contributing to NR.

RESULTSNR occurred in 15.9% of the AMI patients after primary PCI. Univariate analysis showed that previous myocardial infarction, Killip classes of MI, time to reperfusion, IABP use before PCI, TIMI flow grade before primary PCI, long target lesion, pre-PCI thrombus score and method of reperfusion were correlated to NR (P<0.05 ). Multiple logistic analysis identified the time to reperfusion (OR=1.60; 95% CI: 1.02-2.73), TIMI flow grade before primary PCI (OR=1.1; 95% CI: 1.04-1.16), long target lesion (OR=1.40; 95% CI: 1.19-1.69), and pre-PCI thrombus score (OR=2.02; 95% CI: 1.47-2.76) as the independent predictors of NR after primary PCI.

CONCLUSIONThe time to reperfusion, TIMI flow grade before primary PCI, long target lesion, and pre-PCI thrombus score are independent predictors of NR after primary PCI for AMI.

Aged ; Angioplasty, Balloon, Coronary ; China ; epidemiology ; Female ; Humans ; Male ; Middle Aged ; Myocardial Infarction ; therapy ; No-Reflow Phenomenon ; epidemiology ; etiology ; Percutaneous Coronary Intervention ; Risk Factors

OBJECTIVETo investigate the inhibitory activities of norcantharidin (NCTD), a demethylated analogue of cantharidin, on Hep3B cells (a human hepatoma cell line) with deficiency of p53.

METHODSThe survival rate of the Hep3B cells after treating with NCTD was measured by MTT assay. Cell cycle of treated cells was analyzed by flow cytometry, and DNA fragmentation was observed by electrophoresis. The influence of inhibitors for various caspases and anti-death receptors antibodies on the NCTD-induced apoptosis in the cells was determined.

RESULTSNCTD treatment resulted in growth inhibition of Hep3B cells in a dose- and time-dependent manner. Cell cycle analysis of the cells after treatment with NCTD for 48 h shows that NCTD induced G(2)M phase arrest occurs at low concentration ([Symbol: see text] 25 μmol/L) but G(0)G(1) phase arrest at high concentration (50 μmol/L). The addition of both caspase-3 and caspase-10 inhibitors completely inhibited DNA fragmentation. Addition of anti-TRAIL/DR5 antibody significantly inhibited DNA fragmentation.

CONCLUSIONNCTD may inhibit the proliferation of Hep3B cells by arresting cell cycle at G(2)M or G(0)G(1) phase, and induce cells apoptosis via TRAIL/DR5 signal transduction through activation of caspase-3 and caspase-10 by a p53-independent pathway.

Antibodies, Neoplasm ; pharmacology ; Antibodies, Neutralizing ; pharmacology ; Apoptosis ; drug effects ; Bridged Bicyclo Compounds, Heterocyclic ; pharmacology ; Carcinoma, Hepatocellular ; enzymology ; pathology ; Caspase 10 ; metabolism ; Caspase 3 ; metabolism ; Caspase Inhibitors ; pharmacology ; Cell Cycle Checkpoints ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; DNA Fragmentation ; drug effects ; Humans ; Immunohistochemistry ; Liver Neoplasms ; enzymology ; pathology ; Receptors, TNF-Related Apoptosis-Inducing Ligand ; metabolism ; Signal Transduction ; drug effects ; TNF-Related Apoptosis-Inducing Ligand ; metabolism ; Tumor Suppressor Protein p53 ; metabolism

It has been demonstrated that APPL1 (adaptor protein, phosphotyrosine interacting with PH domain and leucine zipper 1) is involved in the regulation of several growth-related signaling pathways and thus closely associated with the development and progression of some cancers. Diallyl trisulfide (DAT), a garlic-derived bioactive compound, exerts selective cytotoxicity to various human cancer cells through interfering with pro-survival signaling pathways. However, whether and how DAT affects survival of human hepatocellular carcinoma (HCC) cells remain unclear. Herein, we tested the hypothesis of the involvement of APPL1 in DAT-induced cytotoxicity in HCC HepG2 cells. We found that Lys 63 (K63)-linked polyubiquitination of APPL1 was significantly decreased whereas phosphorylation of APPL1 at serine residues remained unchanged in DAT-treated HepG2 cells. Compared with wild-type APPL1, overexpression of APPL1 K63R mutant dramatically increased cell apoptosis and mitigated cell survival, along with a reduction of phosphorylation of STAT3, Akt, and Erk1/2. In addition, DAT administration markedly reduced protein levels of intracellular TNF receptor-associated factor 6 (TRAF6). Genetic inhibition of TRAF6 decreased K63-linked polyubiquitination of APPL1. Moreover, the cytotoxicity impacts of DAT on HepG2 cells were greatly attenuated by overexpression of wild-type APPL1. Taken together, these results suggest that APPL1 polyubiquitination probably mediates the inhibitory effects of DAT on survival of HepG2 cells by modulating STAT3, Akt, and Erk1/2 pathways.