Human coagulation Factor V(FV), together with Factor Xa, assembles to prothrombinase complex on activated cell surface, which converts prothrombin into thrombin, leading to fibrin deposition. The C2 domain of FV is ...Human coagulation Factor V(FV), together with Factor Xa, assembles to prothrombinase complex on activated cell surface, which converts prothrombin into thrombin, leading to fibrin deposition. The C2 domain of FV is believed to be a primary anchor for the assembly of pro- thrombinase on the cell surface, and was proposed as a target to intervene with pathological thrombotic events. We report here the crystal structure of the C2 domain of FV fused to maltose-binding protein(MBP). The fusion tag of MBP is critical to generate the crystal for this study. There is no strong interaction between MBP and FVC2. The overall structure of FVC2 is similar to the previous FVC2 structures, suggesting the MBP fusion does not perturb the molecular structure of FVC2. This crystal form of FVC2 can be used for future study of molecular interaction between FVC2 and its inhibitors.展开更多
Objective To investigate the clinical significances of CD44v6 protein expression in human gallbladder carcinoma(GBC).Methods The immunohistochemical technique was used to detect the CD44v6 protein expression in 40 cas...Objective To investigate the clinical significances of CD44v6 protein expression in human gallbladder carcinoma(GBC).Methods The immunohistochemical technique was used to detect the CD44v6 protein expression in 40 cases of GBC,12 cases of chronic cholecystitis,6 cases of adenoma and 4 cases of adenomyomatous hyperplasia.Results The positive rate of CD44v6 expression in gallbladder carcinoma and benign lesions was 72.5% and 0%,respectively( P <0.01),and it also correlated with the lymph node metastasis,pathologic differentiation and clinic staging,but there was no correlation among pathological types.Conclusion Detecting CD44v6 expression might be severed as an objective indicator for differential diagnosis,lymph node metastatic potency,tumor progress and prognosis in gallbladder carcinoma.展开更多
Background: As life expectancy of HIV-infected patients increases with use of highly active antiretroviral therapy (HAART), protean haematologic manifestation including decreased activity of natural anticoagulants suc...Background: As life expectancy of HIV-infected patients increases with use of highly active antiretroviral therapy (HAART), protean haematologic manifestation including decreased activity of natural anticoagulants such as protein C may occur in the absence of genetic risk factors. Based on this preposition, we assessed the plasma level of protein C, and prevalence of factor V Leiden mutation among HIV-infected individuals. Our cohort consisted of 499 HIV-infected patients, of which 250 had AIDS, while 249 were either asymptomatic or had minor mucocutaneous infection consistent with WHO clinical stages I and II without features of AIDS. We also evaluated 251 healthy, HIV-negative subjects as controls. All participants were tested for plasma protein C levels and factor V Leiden (FVL) mutation (Arg 506 Gln) by automation and amplification created restriction enzyme site (ACRES) polymerase chain reaction, respectively. The prevalence of reduced protein C plasma levels among HIV positive patients was 20%;it was more prevalent among those that had AIDS compared with those without features of AIDS, but within WHO clinical stage I and II, (93.3% vs 6.7%) respectively. None of the control patients had either reduced protein C nor FVL mutation. All participants that demonstrated reduced protein C plasma levels demonstrated normal FVL genotype (1691G/G). Conclusion: Decreased protein C plasma levels can occur in HIV-infected patients in the absence of factor V Leiden mutation. The risk increases with severity of the disease. Deranged protein C plasma level increases the risk of hypercoagulable state in patients with advanced HIV disease;it should be considered among the causes of thrombo embolism in this group of patients.展开更多
基金Supported by the National Natural Science Foundation of China(31161130356)
文摘Human coagulation Factor V(FV), together with Factor Xa, assembles to prothrombinase complex on activated cell surface, which converts prothrombin into thrombin, leading to fibrin deposition. The C2 domain of FV is believed to be a primary anchor for the assembly of pro- thrombinase on the cell surface, and was proposed as a target to intervene with pathological thrombotic events. We report here the crystal structure of the C2 domain of FV fused to maltose-binding protein(MBP). The fusion tag of MBP is critical to generate the crystal for this study. There is no strong interaction between MBP and FVC2. The overall structure of FVC2 is similar to the previous FVC2 structures, suggesting the MBP fusion does not perturb the molecular structure of FVC2. This crystal form of FVC2 can be used for future study of molecular interaction between FVC2 and its inhibitors.
文摘Objective To investigate the clinical significances of CD44v6 protein expression in human gallbladder carcinoma(GBC).Methods The immunohistochemical technique was used to detect the CD44v6 protein expression in 40 cases of GBC,12 cases of chronic cholecystitis,6 cases of adenoma and 4 cases of adenomyomatous hyperplasia.Results The positive rate of CD44v6 expression in gallbladder carcinoma and benign lesions was 72.5% and 0%,respectively( P <0.01),and it also correlated with the lymph node metastasis,pathologic differentiation and clinic staging,but there was no correlation among pathological types.Conclusion Detecting CD44v6 expression might be severed as an objective indicator for differential diagnosis,lymph node metastatic potency,tumor progress and prognosis in gallbladder carcinoma.
文摘Background: As life expectancy of HIV-infected patients increases with use of highly active antiretroviral therapy (HAART), protean haematologic manifestation including decreased activity of natural anticoagulants such as protein C may occur in the absence of genetic risk factors. Based on this preposition, we assessed the plasma level of protein C, and prevalence of factor V Leiden mutation among HIV-infected individuals. Our cohort consisted of 499 HIV-infected patients, of which 250 had AIDS, while 249 were either asymptomatic or had minor mucocutaneous infection consistent with WHO clinical stages I and II without features of AIDS. We also evaluated 251 healthy, HIV-negative subjects as controls. All participants were tested for plasma protein C levels and factor V Leiden (FVL) mutation (Arg 506 Gln) by automation and amplification created restriction enzyme site (ACRES) polymerase chain reaction, respectively. The prevalence of reduced protein C plasma levels among HIV positive patients was 20%;it was more prevalent among those that had AIDS compared with those without features of AIDS, but within WHO clinical stage I and II, (93.3% vs 6.7%) respectively. None of the control patients had either reduced protein C nor FVL mutation. All participants that demonstrated reduced protein C plasma levels demonstrated normal FVL genotype (1691G/G). Conclusion: Decreased protein C plasma levels can occur in HIV-infected patients in the absence of factor V Leiden mutation. The risk increases with severity of the disease. Deranged protein C plasma level increases the risk of hypercoagulable state in patients with advanced HIV disease;it should be considered among the causes of thrombo embolism in this group of patients.