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  • Book
    edited by Hamilton I. McCubbin & Charles R. Figley.
    Contents:
    v. 1. Coping with normative transitions
    v. 2. Coping with catastrophe.
    Print Access Request
    Location
    Version
    Call Number
    Items
    Stored offsite. Please request print.
    v. 1-2, 1983.
    HQ734 .S9735 1983
    2
  • Article
    Moriwaki C, Miyazaki K, Matsuda Y, Moriya H, Fujimoto Y.
    J Biochem. 1976 Dec;80(6):1277-85.
    The contents of kallikrein [EC 3.4.21.8] in the kidneys of various animals were estimated and the activity was found to be most potent in dogs. The dog renal kallikrein (DRK) was located mainly in the kidney cortex. Following the activation of a dog kidney cortex homogenate with acetone, kallikrein was purified about 2,000-fold with an overall yield of 18% by diethylaminoethyl (DEAE)-cellulose adsorption, acetone fractionation, and chromatography on Sephadex G-75 and DEAE-Sephadex A-50. The final purified preparation of dog renal kallikrein had a vasodilator activity of 65.5 KU per A280, and appeared to be homogeneous both in disc electrophoresis and ultracentrifugal analysis. Its molecular weight was estimated to be approximately 3.8 X 10(4) from the sedimentation coefficient obtained by ultracentrifugation, and by Sephadex gel filtration. However, isoelectric fractionation of the purified DRK preparation gave three isoelectric point, 3.9, 4.1, and 4.3. The DRK had an optimum pH of about 8.6 and was stable at pH 8. This enzyme was hardly inhibited by Trasylol, soybean trypsin inhibitor, ovomucoid trypsin inhibitor or potato kallikrein inhibitors. These properties were compared with those of kallikrein from other sources; DRK appeared to be similar to urinary kallikrein.
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