Biomedical subjects
Publications and source records attributed to G W Miller.
The polytome should be used as an adjunct to conventional roentgenograms of the temporal bone and not as a substitute. The purpose of this paper is to demonstrate how the polytome has been used to great advantage in a private otologic practice.
There are presently two schools of thought on the proper surgical management of cholesteatoma associated with chronic ear disease: one feels that the ear should be exteriorized and left "open"; the other takes the position that the disease can be removed, and the ear left in its normal anatomical and functional state. The latter group are known to favor a "closed" or more conservative procedure. The purpose of this paper is to review a series of patients who have had cholesteatoma managed by an intact canal wall procedure that prevents a postoperative cavity. Out of a series of 590 chronic ear surgeries performed between January 1, 1970, and December 31, 1974, there were 179 done for cholesteatoma (30 percent). There were 153 patients, 26 of whom had bilateral disease. Twenty-three patients were lost to follow-up, giving an overall total of 154 surgeries with from one to five-year information. The overall follow-up rate was 85 percent. Recurrent cholesteatoma was the most bothersome complication and occurred in 14 percent of the series. Residual cholesteatoma was managed by doing all procedures in two stages. The authors feel that the intact canal wall tympanoplasty is a procedure that will gain acceptance and will be more widely used in the future.
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The subjects, 120 college students, sorted cards for 42 sec with instructions to process 0, 1, or 2 bits of information per card (response uncertainty) and then were asked to make an absolute judgement of the interval's duration. Half of the subjects knew this judgement would be required before the interval (prospective paradigm); half did not (retrospective paradigm). Judged time was an inverse linear function of response uncertainty under the prospective paradigm, whereas no significant function was obtained under the retrospective paradigm.
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The complement (C) system can solubilize immune precipitates prepared with antibodies of the IgG class, and apparently also of the IgM class. This paper shows that C can also solubilize immune precipitates prepared with two different antigen-binding IgA myeloma proteins. Immune precipitates were prepared with a) mouse myeloma protein TEPC 15 and PC-KLH, and b) mouse myeloma protein MOPC 315 and DNP-BSA. The precipitates could be solubilized by fresh mouse serum, but not by zymosan- or heat-inactivated serum. The rate of solubilization was not affected by the removal of of Ca++ ions. These results verify that the C-mediated solubilization effect can proceed entirely via the alternative C pathway, and lend increased support to the view that the effect is a general phenomenon, not restricted to a particular antibody class or type of antigen.
Antigen-antibody aggregates are solubilized when incubated with fresh serum at 37 degrees, yielding immune-complexes of relatively small molecular weight which contain antigen, antibody, and complement (C3)determinants. Solubilization is complement-dependent,requires free Mg++ but not Ca++, and proceeds in sera from C4- or C5-deficient animals. It is accelerated in the presence of Ca++ in normal or C4-deficient guinea pig serum, suggesting involvement of the Cl-bypass activation of the properdin system. Immune precipitates can also be solubilized by monovalent fragments (Fab) of antibodies directed against determinants of the antibody molecules included in the antigen-antibody lattice. Similarly, it is suggested that complement-mediated solubilization might be induced by the combination of a complement fragment with the antibody in the immune-aggregate.
Serum of normal mammals contains factors which can release antigen-antibody complexes from the surfaces of leukocytes and platelets. This "complex release activity" (CRA) is mediated by the alternative pathway of complement activation, and is measured by a kinetic assay of the release of lymphocyte-bound soluble immune complexes. CRA activity was measured in the sera of NZB/W mice, which develop an autoimmune disease with aging. CRA in these mice declined rapidly after 16 weeks of age, and by 32 weeks was barely detectable. Serum C3 levels also declined in these mice. An association test correlating CRA and C3 concentration was highly significant. The decreased complement levels in the older mice led to profound changes in their handling of injected soluble immune complexes, as demonstrated in studies of the kinetics of distribution of the complexes between plasma and circulating cells. These abnormalities may be related to the diseases which occurs spontaneously in NZB/W mice, as well as in human immune complex diseases.
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Soluble antigen-antibody-complement complexes bound to mouse B lymphocytes are rapidly released from the cell membrane in the presence of normal serum from several mammalian species. The release is not the result of antigen-antibody dissociation or extensive degradation of the complexes. However, the released complexes have been altered because they will no longer bind to fresh lymphocytes. The release is not the result of lymphocyte damage mediated by complement. It is complement-dependent, and is generated either preferentially or exclusively via the alternate pathway, since it occurs in C4-deficient serum, is Mg(++) but not Ca(++) dependent, and requires C3 proactivator. C3 inactivator is not involved. The release activity of the serum, once generated, is unstable at 37 degrees C. The release of complexes from the lymphocyte membrane by serum provides a convenient assay for the functioning of the alternate pathway in the mouse and in other species.
Human peripheral blood lymphocytes have membrane receptors for EAC43b (sheep erythrocytes sensitized with antibody and complement) and also for EAC43d, obtained by treating EAC43b with C3b inactivator. Human granulocytes bind only EAC43b, C3 fragments obtained by limited trypsin digestion of purified human C3 display both C3b and C3d sites, since they inhibit rosette formation of lymphocytes with EAC43b and EAC43d. These findings raise the possibility that C3b and C3d receptor sites may be selectively distributed among normal subpopulations of B lymphocytes as well as among leukemic leukocytes.
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