Electrical measurements on endomembranes.
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Biomedical subjects
Publications and source records attributed to R Eisenberg.
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We have investigated the mechanism of monovalency of the 7S subunit of a mouse IgA myeloma protein (MOPC 315) against a large antigen. This subunit, although it clearly can bind two molecules of a small hapten, fails to precipitate or hemagglutinate the relevant multivalent antigen. In an equilibrium Farr assay, we have shown that the subunit has only one valence for a univalent 40,000 molecular weight antigen (dinitrophenyl-dextran). We have investigated how various levels of affinity labeling quantitatively affect (a) the valence observed in the equilibrium Farr assay against a large antigen, and (b) the binding of the MOPC 315 to an insoluble antigenic matrix. Our results indicate that the Fab regions of the 7S subunit are arranged symmetrically and that the inactivity of one of them toward a large antigen is probably due to steric hindrance caused by the antigen bound to the adjacent site.
To define the natural history of the asymptomatic, nonstenotic, ulcerative lesion involving the carotid artery bifurcation, the arteriograms and clinical course of 67 patients with 72 asymptomatic ulcerative lesions of the carotid artery were reviewed. The angiographic appearance of ulceration was classified into three groups: minimal (group A), large (group B), and compound (group C). Using life-table methods, the clinical course of these patients was compared between groups and was also compared to a nonrandomized surgically treated group of patients with nonstenotic ulcerative lesions in whom operation was performed for hemispheric or monocular symptoms. There were no significant (P greater than .1) differences in mortality, but the differences in stroke incidence was highly significant (P less than .001). The annual stroke rate, averaged over seven years, was 0.4% per year for group A, 1.47% per year for the surgically treated group, and 12.5% per year for groups B and C. The data indicate that group A ulcers have a benign prognosis, in noticeable contrast to group B and C ulcers which incur a high risk for subsequent stroke.
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A thrombotic thrombocytopenic purpura (TTP)-like syndrome was the chief presenting feature in two patients with infective endocarditis. Clinical and laboratory aberrations of the syndrome were rapidly reversed by specific antimicrobial therapy. Hypocomplementemia and high levels of circulating immune complexes were detected initially in both patients. Because these returned to normal as the TTP syndrome abated, an immunopathologic mechanism may have been operative.
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To examine further the role of immune-complex deposition in infective endocarditis, we studied 29 patients with infective endocarditis for presence of complement-containing circulating immune complexes. Ninety-seven per cent (28 of 29) had serum levels of immune complexes greater than 12 mug per milliliter. Mean levels in these patients were significantly higher than in patients with sepsis without endocarditis or in normal controls (P less than 0.05). Circulating immune-complex levels were correlated with longer duration of illness (P less than 0.025), extravalvular manifestations of endocarditis (P less than 0.025) and hypocomplementemia (P less than 0.05). Patients with right-sided endocarditis had significantly higher circulating immune-complex levels than patients with left-sided involvement (P less than 0.025). In general, levels fell to zero with successful antimicrobial or surgical therapy. This drop was concurrent with disappearance of extravalvular signs, blood cultures becoming sterile, and rise in serum complement levels. These findings support the concept that immune complexes may be important in the pathogenesis of infective endocarditis.
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