Japanese Journal of Thrombosis and Hemostasis
Online ISSN : 1880-8808
Print ISSN : 0915-7441
ISSN-L : 0915-7441
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Volume 13, Issue 2
Displaying 1-11 of 11 articles from this issue
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Reviews
Original Articles
  • Role of Endothelin in LPS-induced Rat DIC Model
    Yukio SUGA, Hidesaku ASAKURA, Tomotaka YOSHIDA, Eriko MORISHITA, Masah ...
    2002 Volume 13 Issue 2 Pages 169-174
    Published: 2002
    Released on J-STAGE: March 31, 2009
    DOIhttps://doi.org/10.2491/jjsth.13.169
    JOURNAL FREE ACCESS
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    We studied to see whether or not endothelin, a potent vasoconstrictive peptide, is involved in the propagation of DIC in rats induced with lipopolysaccharide (LPS) by simultaneously giving animals an endothelin receptor antagonist, TAK-044. Fifty mg/kg of LPS and TAK-044 (2, 10 and 50 mg/kg) were given to the Wistar strain rats via their tail vein over a period of 4 hours for LPS and 4 1/2 hours for TAK-044, the start of administration of the latter having been 1/2 hour prior to administraion of LPS. The prothrombin time, platelet counts and plasma levels of the thrombin-antithrombin complex (TAT) and fibrinogen remained unchanged, but that of the D-dimer increased significantly. On the other hand, the levels in plasma of creatinine and alanine aminotransferase (ALT), known as markers for the organ damages, were found to be decreased in a dose-dependent fashion of TAK-044. Fibrin deposition in the glomeruli was also found to be decreased. The data altogether suggest that endothelin plays a certain role in the development of organ injuries in the LPS-induced DIC in rats.
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  • Recombinant Missense Mutant Factor VIII (R2159C, R2209Q) in Patients with Hemophilia A Exhibit Decreased Secretion of Abnormal Proteins
    Kou YAMANAKA, Kagehiro AMANO, Keiko NAGAIZUMI, Hiroshi INABA, Morio AR ...
    2002 Volume 13 Issue 2 Pages 175-182
    Published: 2002
    Released on J-STAGE: March 31, 2009
    DOIhttps://doi.org/10.2491/jjsth.13.175
    JOURNAL FREE ACCESS
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    We introduced 2 different mutations, i.e CGC to TGA in codon 2159 and CGA to CAA in codon 2209 within the C-domain of factor VIII(FVIII) gene that had previously been reported as genetic defects in hemophilia A. The FVIII gene mutants corresponding to R2159C and R2209Q were made by site-directed mutagenesis. Synthesis and secretion of abnormal FVIII were analyzed by immunoprecipitation of cell extracts (CE) and condi-tioned media (CM) from 35S-methionine pulse-labeled and chased transfected cells. SDS-PAGE analysis demonstrated that both mutants were normally synthesized, but disappear-ed from the CE during 4 hours of chase. Addition of ALLN, an inhibitor of cysteine-protease, increased the intracellular accumulation of the R2159C mutant in the CE, without affecting the amount recovered in the CM. These results indicate that defective secretion with subsequent intracellular degradation is responsible for the loss of the mutant FVIII from the CE, leading to the hemophilia A phenotype for both mutants.
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Letter to the Editor
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