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Biomedical subjects

J S Fong

Publications and source records attributed to J S Fong.

33 records · Page 2Linked to original sources
PubMed1976

Role of platelets in the pathogenesis of canine endotoxin shock.

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.

Animals↗
PubMed1976

Treponemal antigens in congenital and acquired syphilitic nephritis: demonstration by immunofluorescence studies.

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.

Antigens, Bacterial↗
PubMed1975

Congenital and experimentally induced complement deficiency in rabbits.

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.

Animals↗
PubMed1971

Prevention of the localized and generalized Shwartzman reactions by an anticomplementary agent, cobra venom factor.

Both localized and generalized Shwartzman reactions were induced in the same rabbits by simultaneous administration of preparatory intravenous and intradermal doses of endotoxin followed in 24 hr by the provocative dose. Control rabbits with more than 80% positive responses showed corresponding changes of platelet, white blood cell, fibrinogen, and hemolytic complement levels. Circulating fibrinogen and fibrin degradation products were detected shortly after the preparatory dose and persisted for at least 3 days. Rabbits given cobra venom anticomplementary factor showed hypocomplementemia (less than 10% of normal), leukocytosis, and elevated fibrinogen levels. After the administration of endotoxin, only one of 15 CVF-treated animals developed a Shwartzman reaction and that was mild. These rabbits showed only minor changes of platelet and fibrinogen levels throughout the experiment although their white blood cell responses were similar to those of the control group. No detectable fibrinogen and fibrin degradation products appeared in circulation, and the hemolytic complement activity increased gradually beginning with the preparatory dose of endotoxin. Thus depletion of terminal complement components (mainly C3) in rabbits is protective against the development of both localized and generalized Shwartzman reactions; its mechanism of action is probably through the sparing of platelets by inhibiting platelet-endotoxin interaction. The essential role of the complement system in Shwartzman reaction indicates that this coagulopathy probably represents a manifestation of immunologic injury.

Animals↗
PubMedDate not supplied

Lipid peroxidation in the hemolytic uremic syndrome.

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.).

Animals↗