Biomedical subjects
Publications and source records attributed to J S Fong.
A crude muscle extract infused into rats produced oliguria, a precipitous drop in total hemolytic complement, and in circulating white cell and platelets counts. A mild vaso-depressor effects was noted. These changes were not produced by myoglobin or saline infusion. Muscle constituents other than myoglobin are responsible for the systemic and renal nephrotoxic effects observed.
The effects of endotoxin (lipopolysaccharide [LPS]) on the pathogenesis of canine endotoxin shock were compared with those of LPS which had interacted with polymyxin B sulfate prior to administration. Both LPS and polymyxin B-modified LPS caused comparable early decreases in aortic blood pressure, leukocyte and platelet numbers, and serum complement levels. However, in dogs receiving polymyxin B-modified LPS the late hypotensive phase was significantly ameliorated and lethality was significantly decreased. These data indicate that polymyxin B-modified LPS, though significantly less lethal than unmodified LPS, was capable of major interactions with several components of the humoral defense system, and support the concept that such interactions are not determinative in the pathogenesis of canine endotoxin shock.
A new hemolytic plate method for the functional assessment of alternative-pathway complement activity is described. The plates are easy to prepare and the method simple to perform. Analysis of 23 normal serum samples showed a mean lysis diameter of 4.1 +/- 0.2 mm (1 standard deviation).
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Endotoxin-platelet interactions are thought to be of major importance in the response of dogs and other species to bacterial endotoxin; the mechanisms postulated are: (i) the release of vasoactive substances, (ii) the formation of occlusive platelet aggregates, and (iii) induction of intravascular coagulation. The role of platelets in canine endotoxin shock was examined in animals with thrombocytopenia induced by estrogen pretreatment (less than 10,000 platelets/mm3) and in controls. After intravenously administered endotoxin, the hemodynamic responses, mortality, and gross necropsy findings were similar in both groups. These data indicate that endotoxin-platelet interactions are not determinative in the pathogenesis of canine endotoxin shock.
Two patients, a 4-month-old infant girl with congenital syphilis and a 45-year-old man with secondary syphilis, had the nephrotic syndrome with glomerulonephritis. Immunoglobulins and treponemal antigenic material were seen in the glomeruli of both patients by immunofluorescence microscopic studies of renal tissue. Electron micrographs showed subepithelial electron dense deposits along the glomerular basement membrane. This confirms earlier suggestions that the renal injury is of an immune-complex type.
Deficiency of the sixth component of complement in rabbits is an autosomal recessive defect which also renders C7-9 functionally unavailable. The function of C6-9 appears to be that of amplification of immunologic processes. Defective animals are associated with a subtle disadvantage. Normal rabbits injected with cobra-venom-anticomplementary-factor show primary C3-9 and secondary polymorphonuclear leukocyte and platelet functional deficiency. Animals treated with cobra venom showed striking deficits in manifestations of some immunologic functions. Thus the complement system plays a vital role in maintaining integrity of immunologic mechanisms.
Based on recent evidence of a genetic influence on prognosis (1) and the existence of red cell membrane phospholipid depletion with low or absent serum alpha-tocopherol (2) levels in three children with the Hemolytic Uremic Syndrome (H.U.S.), we wish to suggest the existence of an inborn error of antioxident capacity as the basic pathogenetic mechanism in the development of the hemolytic uremic syndrome (H.U.S.).