Paul Didisheim
University of Pittsburgh
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Featured researches published by Paul Didisheim.
Experimental Biology and Medicine | 1956
Paul Didisheim; Jessica H. Lewis
Summary Of the 16 snake venoms studied, 11 actively lysed human blood clots. However, only one of these, C. basiliscus, was devoid of thrombic, hemolytic, and hemaggluti-nating properties. This venom was fibrino-genolytic as well as fibrinolytic. The possible therapeutic use of certain venoms as dissolving agents for intravascular clots presents a theoretical advantage over most other fibrinolytic agents in that their fibrinolytic activity is not readily inhibited by human serum. Fractionation of a pure fibrinolytic principle may be possible.
Journal of Clinical Investigation | 1958
Jessica H. Lewis; Denny Walters; Paul Didisheim; William R. Merchant
Continuous flow filter paper electrophoresis, as developed by Svensson and Brattsen (1), Grassmann and Hannig (2-4) and Durrum (5), offers a method of plasma fractionation in which protein denaturation appears minimal. This study involves the testing of such fractions for biological activity in various coagulation systems. With the exception of fibrinogen, the coagulation proteins are present in plasma in minute amounts which, at the present time, can be assayed only by their activities in specific clotting systems. Many of these coagulation factors are readily denatured; thus, rigid control with particular attention to temperature is necessary to obtain good recovery of biological activity. Previous electrophoretic studies concerning distribution of plasma coagulation proteins have employed paper electrophoresis with elutions from cut strips. Owen and McKenzie (6) found pro
Experimental Biology and Medicine | 1956
Jessica H. Lewis; Paul Didisheim
Summary Rabbits injected with human serum “PTC” developed inhibitors to human PTC and also to human proconvertin. These two activities could be separated by differential adsorption.
Experimental Biology and Medicine | 1957
Jessica H. Lewis; Paul Didisheim
Summary 1. A lengthening of saline-re-calcification time beyond normal occurred in plasma deficient in any one of the following: platelets, AHF, PTC, PTA, Hageman factor, proaccelerin, or proconvertin. It also occurred in certain acquired multiple factor deficiencies, and in heparinized plasma. 2. Brain thromboplastin recalcification times were normal in platelet, AHF, PTC, PTA and Hageman factor deficiencies, but prolonged in proconvertin or proaccelerin deficiency or heparinized plasma. 3. Plasma thromboplastin recalcification times were normal in these same deficiencies and, in addition, in proconvertin or proaccelerin deficiency. This latter activity seemed due to incorporation of (pro) convertin and (pro) accelerin into the plasma thromboplastin complex, rather than to any free proconvertin and proaccelerin in solution. 4. Formed plasma thromboplastin is inactive in absence of optimal calcium concentration.
JAMA Internal Medicine | 1957
Jessica H. Lewis; Paul Didisheim
JAMA Internal Medicine | 1958
Paul Didisheim; John H. Ferguson; Jessica H. Lewis
American Journal of Human Genetics | 1963
Jessica H. Lewis; Paul Didisheim; John H. Ferguson; C. C. Li
JAMA Internal Medicine | 1962
Paul Didisheim
Pediatrics | 1958
Paul Didisheim; Jessica H. Lewis
Archive | 2017
Jessica H. Lewis; Paul Didisheim