The role of afferent blood supply in regeneration of liver isografts in rats.
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Biomedical subjects
Publications and source records attributed to T S Edgington.
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A renal tubular epithelial antigen is deposited in association with gamma globulin and complement in glomeruli from rats with experimental allergic glomerulonephritis induced by immunization with renal tubular antigens. Apparently, in normal kidneys this antigen is concentrated in the distal segment of the proximal convoluted tubular epithelium, and the principal source of this antigen in the glomerular deposits is autologous. This form of glomerulonephritis provides an experimental prototype for what may be termed "autologous immunecomplex" diseases.
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The functioning and survival of orthotopic liver allotransplants in toto were compared with heterotopic partial and whole allotransplants in inbred rats. In contrast to the rapid and aggressive rejection of the heterotopic allografts, the orthotopic whole-liver allografts survived for prolonged periods. These latter grafts were subjected to mild cellular attack 11 to 12 days following transplantation, but they survived without the massive cellular infiltration and hepatocytolysis seen in the heterotopic partial grafts. Biliary secretion by the orthotopic whole-liver allografts was functional throughout the survival period and was markedly increased during the final stages of survival, whereas the heterotopic liver grafts ceased to excrete normal bile by day 9, after which they were completely depigmented.
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Carcinoembryonic antigen (CEA) is heterogeneous and may represent a set of closely related glycoproteins which have been referred to as isomeric species of CEA. The existence of other CEA-related glycoproteins such as non-specific cross reacting antigen (NCA) has been recognized. Recently a highly purified homogeneous isomeric species of CEA described as CEA-S has shown differences in diagnostic results upon analysis of clinical sera as well as quantitative immunochemical differences. In a blind study of 308 sera, the CEA and CEA-S assays were compared. A significant difference in false positive results was observed between the CEA and CEA-S assay results. In contrast to the low but significant evidence of elevated CEA in sera of random normal persons and patients with liver disease or inflammatory disease of the gastrointestinal tract or lung, none of the sera had elevated concentrations of CEA-S. Among patients with tumor of the gastrointestinal tract that were considered surgically resectable, 46 percent were elevated using the CEA-S assay and only 34.7 percent were elevated above 5 nanograms per ml by the CEA assay. The CEA assays detect CEA-related molecules produced by lung, breast and other tumors; the CEA-S assay appears equally sensitive to CEA of gastrointestinal origin but detects only a small subgroup of breast, lung and, rarely, other types of tumors.
Infection of man and chimpanzees with the hepatitis B virus (HBV) is associated with diffuse hepatocellular infection and variable manifestations of disease which may not only reflect the character of the host immune response, but also depend upon differences in the cellular biology of this minimally cytopathic or noncytopathic agent. The presence of hepatocellular injury and the course of disease do not appear to be related to the presence of viral antigens in hepatocytes or to the specific pattern of genome expression. HBV infection is typically associated with both humoral and cellular immune responses to viral and hepatocellular antigens. Whereas cellular effector systems may be responsible for immunologically mediated hepatocellular injury, the patterns of viral antigen synthesis and expression may be modulated by the humoral immune response. Aberration of lymphocyte function occurs during acute hepatitis type B. Thymus-derived lymphocyte function is abnormal and is associated with persistent humoral suppression of T lymphocyte function during the development of the chronic carrier state. Extrahepatic disease appears attributable to the formation and deposition of HBS Ag-antibody complexes. Current information of the biology and immunology of HBV and other viruses has been integrated into a hypothesis to explain the pathogenesis of injury and events associated with persistent infection. Hepatocellular injury and persistence of viral synthesis may be determined by the regulation of synthesis and hepatocyte surface expression of viral and cellular antigens as well as by the specificity and character of the host immune response. Termination of HBV infection is viewed as suppression of viral genome rather than eradication of infected cells.