Biomedical subjects
Publications and source records attributed to C V DeShazo.
An axillofemoral bypass was used to preserve a functioning renal allograft after excision of a mycotic abdominal aortic aneurysm in a diabetic patient. In the presence of continued immunosuppression the aortic wall infection progressed and the patient expired after rupture of the proximal aortic closure.
The knee joint in rabbits has been used as an arthritis model for the study of acute immunologic injury. Histologic examination of synovium plus a standardized procedure for irrigating inflammatory exudate from the joint allowed study of damage due to immune complexes, urate crystals, and Arthus type vascular lesions by multiple parameters. With this model Arthus lesions could be abolished with neutrophil depletion and reconstituted with intra-articular injection of neutrophil suspension. The rate and degree of injury could also be diminished by depletion of complement components.
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Mediators of acute immunologic injury have been studied in vivo by producing arthritis in rabbit knee joints. A reversed passive Arthus lesion was produced by injecting antibody into the joint space and antigen intravenously. Injury was assessed by measuring leakage of serum proteins and circulating radiolabeled proteins into the joint space and by the accumulation of neutrophils in the joint fluid. Inflammatory exudate was recovered for study by a standardized irrigation technique.Maximal vascular permeability developed 2 hr after injection as neutrophils accumulated about immune complexes in venule walls to produce structural injury. After 5 hr the number of neutrophils in the joint space rose rapidly, followed by a second rise in permeability at 8 hr. Neutrophil depletion abolished both peaks of permeability. It was then possible to reconstitute the synovial lesion in neutrophil-depleted rabbits by intra-articular injection of purified suspensions of neutrophils.A requirement for complement was demonstrated in development of the lesion. Rabbits genetically deficient in C6 showed delay in vascular permeability, appearance of neutrophils, and histologic lesions. The delay was longer in normal rabbits depleted of C3. In C6-deficient rabbits depleted of C3, still further reduction in injury occurred. Evidence was obtained as well for a chemotactic attraction of neutrophils in vivo. Antigen-antibody-complement complexes in the walls of blood vessels attracted neutrophils placed in the joint space of neutrophil-depleted rabbits. Omission of either antigen or antibody from this replacement reaction prevented the migration of neutrophils.
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This article examines some of the problems of the health care organizations we serve and that support us. While external problems can besiege an organization, the fundamental building block for success is to develop physician buy-in and a well-functioning team. The author describes how his IPA failed because the physicians in his organization didn't bond sufficiently, and for a sustained period, to carry out business operations. What are the warning signals that might help you decide whether to stay or move on? An IPA must have: (1) A clearly articulated vision of what success will look like, one that is accepted by its members; (2) effective leadership; (3) clear evidence of adaptability and flexibility; (4) financial stability; and (5) good data available to physicians. There can be other evidence of trouble you need to watch for. In some areas, hospitals and health plans are hostile to physician initiatives. Don't rely on politically motivated decisions--they are too easily changed. If you plan to be a leader for your physician organization, focus on creating or revising the internal architecture of the group.