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Biomedical subjects

J M Corson

Publications and source records attributed to J M Corson.

6 recordsLinked to original sources
PubMed1979

Renal metastases from well differentiated follicular thyroid carcinoma: a case report with light and electron microscopic findings.

The second case of metastatic follicular carcinoma of the thyroid presenting during life as bilateral renal masses is described. Metastases appeared 18 years after resection of the primary and on clinical evaluation were confined to the kidneys. Although most malignant tumors which present clinically in the kidney are primary there, a review of the literature indicates that the possibility of metastatic tumor must be kept in mind, particularly when the renal tumor is bilateral.

Adenocarcinoma↗
PubMed1975

Modification of the rat alloimmune response by enhancing antibodies and the role of blocking factors in the survival of renal grafts.

Correlation of morphological and immunological events ocurring in control and passively enhanced rat renal allograft recipients has revealed an important role for vasculitis in rejection, whereas the tempo and severity of graft lymphocyte infiltration and tubular damage was comparable in both groups during the first 5 days. Thereafter, the degree of cellular infiltration in enhanced allografts progressed and actually exceeded that in control grafts. 2-Mercaptoethanol-sensitive lymphocytotoxic antibodies were present in both groups with comparable titers and appearance times; however, the presence of a severe IgG-containing necrotizing arteritis and glomerulitis in control, but not enhanced, grafts suggests that passive enhancement protects by interfereing with the cooperative T cell-dependent inductive response. Further support for this possibility comes from the fact that the development of cytotoxic lymphocytes against donor target cells was delayed for 48 hr in the enhanced group. While controls died at days 9-11, enhanced animals entered a period of prolonged survival with stable renal function. This state of "autoenhancement" was characterized by a low degree of cell-mediated cytotoxicity and the appearance of serum factors that blocked the in vitro cellular assay. Blocking factors have a low affinity for the attacking cell population, suggesting that they are immune complexes or anti-idiotypic antibodies, and not free alloantibody of high affinity.

Animals↗
PubMed1975

Immunologic enhancement of rat renal allografts. III. Immunopathologic lesions and rejection in long-surviving passively enhanced grafts.

Immunologic enhancement of renal allografts from (Lewis times Brown Norway) F1 to Lewis rats was achieved by administering a single dose of antidonor serum at the time of transplantation. A series of grafts functioning for 1 to 4 months after transplantation were examined by light and immunofluorescence microscopy to evaluate the long-term protective effects of the enhancing serum and to determine if previously unobserved lesions appeared in long survivors. Despite the absence of detectable circulating cytotoxic alloantibody, long-term allografts showed necrotizing glomerular and arterial lesions which resembled those seen in acutely rejecting grafts and were compatible with humoral rejection. Thus, in this model, there is a late decline in the ability of passive enhancement to inhibit humoral rejection. Long-term grafts also developed tubular lesions with deposition of immunoglobulin and complement on the tubular basement membranes (TBM). Anti-TBM antibodies were demonstrated in recipients' sera and found to be organ specific but not major histocompatibility antigen or species specific. This tubular lesion is therefore a unique form of allograft injury in which the immune response is directed against tissue antigen(s) which are distinct from the major histocompatibility antigens that induce rejection.

Animals↗
PubMed1975

Rheumatoid synovitis: complement and immune complexes.

The pattern of complement component utilization within the joint space of patients with RA is consistent with activation by immune complexes. Immunogluorescent studies of SF leukocytes revealed intracytoplasmic inclusions of immunoglobulins and complement components, particularly in cells from SF with low complement levels and containing materials which precipitated with either C1q and/or rheumatoid factor. RA patients with low levels of SF complement tended to have an unremitting course, subcutaneous nodules, and to have been treated with gold. Their joints had more periarticular demineralization, joint space narrowing, cortical impaction by X-ray; and synoviocytic giant cells, fibrosis, lymphocytes, congestion, and fibrin exudation by pathologic examination than did joints of RA patients without low levels of SF complement. Patients with systemic hypocomplementemia had active classical RA with evidence of severe joint involvement and vasculitis. These findings suggest that rheumatoid inflammation of joints is mediated by immunologic activation of the complement system.

Antigen-Antibody Complex↗
PubMedDate not supplied

Giant cell synovitis associated with failed polyethylene patellar replacements.

Destroyed patellar articular surfaces were replaced with a high molecular weight polyethylene prosthesis in two patients. The patellofemoral articulation of the femur consisted of eburnated bone in one case and degenerative cartilage in the other. Both operations failed within one year because of a giant cell synovitis caused by a high volume (0.2 cc) of fine polyethylene (1-100 mu) wear particles. Ultra high molecular weight polyethylene should not be used as a prosthetic bearing surface to articulate against cortical, cancellous or eburnated bone or against degenerative articular cartilage in a major joint.

Aged↗