Arnold G. Ware
University of Southern California
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Featured researches published by Arnold G. Ware.
Annals of Internal Medicine | 1952
George C. Griffith; Robert Stragnell; David C. Levinson; Frederick J. Moore; Arnold G. Ware
Excerpt Thromboemboli are a frequent cause of death in patients with congestive heart failure. In 565 patients with rheumatic heart disease and congestive heart failure, autopsied at the Los Angele...
Experimental Biology and Medicine | 1960
Sandra Schiffman; Samuel I. Rapaport; Arnold G. Ware; John W. Mehl
Summary 1) Hageman factor and plasma thromboplastin antecedent have been separated from human plasma and each other by ion exchange chromatography. 2) The defect in “exhausted plasma” is not corrected by purified PTA, purified HF, or a combination of the two.
Experimental Biology and Medicine | 1953
Merle Lovell Lewis; Arnold G. Ware
Summary A simple one-stage procedure has been devised for the determination of accelerator globulin activity in human plasma. The components of the assay system are of human origin. The test is specific for accelerator globulin activity, and is unaffected by large fluctuations in prothrombin or fibrinogen content of the material to be tested.
Experimental Biology and Medicine | 1953
Merle Lovell Lewis; Arnold G. Ware
Summary A simple and rapid procedure is described for the separation of prothrombin of high specific activity and partially purified accelerator globulin from fresh citrated human plasma. Each product appears to be free from other known clotting factors.
Annals of Internal Medicine | 1957
Arnold G. Ware; Robert Stragnell
Excerpt The theoretic possibility of controlling thrombo-embolic disease with agents that inhibit blood clotting is well recognized. There is no question that undesirable thrombotic complications c...
Experimental Biology and Medicine | 1952
John B. Field; Martin S. Goldfarb; Arnold G. Ware; George C. Griffith
Summary 1. A new anticoagulant, Dipaxin (diphenylacetyl-1,3 -indandione), has been studied in man. This agent induces an effective hypoprothrombinemia in single doses of as little as 4 mg. It appears to be more potent on a weight basis than any other known agent. After single doses of 20 mg a marked hypoprothrombinemia was usually evident in 48 hours which persisted from 6 to 10 days. Its effects were usually reproducible and predictable. 2, The drug was successfully administered therapeutically. The recommended starting dose is about 20 mg. A schedule of dosages is given. The maintenance of adequate clinical hypoprothrombinemia was obtained with daily doses of 2 to 4 mg. Hypoprothrombinemia was readily overcome with vit. K, the natural vitamin being more effective than the synthetic. No bleeding or other toxic phenomena were encountered. 3. The advantages and disadvantages of Dipaxin as a clinically useful hypoprothrombinemic anticoagulant are briefly discussed.
Circulation | 1955
John B. Field; Martin S. Goldfarb; Arnold G. Ware; George C. Griffith
In the course of development of new anticoagulants, an indandione derivative has been subjected to a clinical evaluation. The new agent is one of the most potent hypoprothrombinemic substance known but it is readily counteracted with vitamin K. The agent was administered to a large series of patients with thromboembolic diseases and control of anticoagulant therapy was observed to be simple, reproducible, with a good predictability of response as well as with absence of toxic phenomena and a low order of bleeding complications. It has been administered to 11 patients for ambulant anticoagulant care for periods up to 18 months with satisfactory results and it appears to be especially suitable for long-term maintenance therapy.
Standard Methods of Clinical Chemistry | 1963
Arnold G. Ware; Clifford B. Walberg; Rex E. Sterling; David Seligson
The Journal of Urology | 1955
Jay J. Crane; Arnold G. Ware; Jack Hamilton
American Journal of Obstetrics and Gynecology | 1961
Charles F. Langmade; Solomon Notrica; James A. Demetriou; Arnold G. Ware