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Biomedical subjects

C S Koh

Publications and source records attributed to C S Koh.

At least 163 records · Page 9Linked to original sources
PubMed1985

Peripheral nervous tissue injury induced by galactocerebroside and galactocerebroside immune complexes.

It was demonstrated that New Zealand Albino rabbits sensitized to galactocerebroside had high levels of anti-galactocerebroside antibody and of immune complexes. The rabbits was high titers of immune complexes developed demyelination in the peripheral nerves. Lesion were produced in the peripheral nerves of mice by the i.m. injection of galactocerebroside immune complexes. The lesions were characterized by axonal degeneration, infiltrating macrophages containing myelin debris, and an inflammatory infiltrate of polymorphonuclear and mononuclear cells. Rabbit immunoglobulin and mouse C3 were observed around the endoneural blood vessels. These results suggest that galactocerebroside immune complexes may play a role in the pathogenesis of mouse peripheral nerve lesions, due to the production of vasculomyelinopathy.

Animals↗
PubMed1984

Detection of immune complexes in experimental allergic neuritis.

Circulating immune complexes were assayed in the sera of animals with experimental allergic neuritis (EAN), and immunofluorescent staining and immunohistological examination were performed to clarify the role of immune complexes in the pathogenesis of EAN. The level of immune complexes in the sera of animals with clinical signs of EAN was from 1:32 to 1:64. Control animals showed a titer of immune complexes from 1:2 to 1:4. Animals with EAN showed deposition of immune complexes, which were detected by FITC-conjugated anti-rat IgG or C3-complement, in the vessels of the peripheral nerve. These findings suggest that immune complexes may contribute to the immunopathogenesis of EAN.

Animals↗
PubMed1983

Chronic neuropathy associated with immune complexes of hepatitis B virus.

In 7 patients, including one autopsied case, with neuropathy associated with hepatitis B virus infection, histologic examination of sural nerve biopsies revealed small vessel vasculitis in the vasa nervorum. In all cases, immunofluorescent deposits of hepatitis B surface antigen, immunoglobulin and C3 complement were detected in the vasa nervorum. That these deposits could represent immune complexes composed of hepatitis B virus was supported by the serologic demonstration of high serum-level of immune complexes and by the ultrastructural demonstration of electron-dense deposits around the endoneural capillary and in the endoneurium. The densities of large myelinated fibers were significantly lower than controls (P less than 0.01) in 6 of 7 cases. These results suggest that immune complexes composed of hepatitis B virus might play a significant role in the pathogenesis of endoneural and epineural vascular lesions, through which neuropathy may be induced in patients with hepatitis B virus infection.

Adult↗
PubMed1981

Mild encephalitogenic activity of basic protein--acidic lipid complex from myelin and detection of immune complexes in experimental allergic encephalomyelitis.

Further biochemical and pathological investigation of basic protein--acidic lipid complex from canine cerebral myelin show the presence of sulfatide, phosphatidylserine, ganglioside and basic protein in the molar ratio of approximately 6 : 3 : 1 : 1 and that it is associated with mild encephalitogenic activity in guinea pigs in comparison to intact myelin and basic protein. Circulating immune complexes were detected in the sera of guinea pigs with clinical signs of experimental allergic encephalomyelitis and immunofluorescent staining showed the deposition of immune complexes of immunoglobulin and complement in vessels of white matter and meninges and in the choroid plexus.

Animals↗
PubMedDate not supplied

Spontaneous hypoglycemia and insulin autoantibodies in a patient with Graves' disease.

A 31-year-old woman with Graves' disease developed fasting hypoglycemia after treatment for 3 weeks with methimazole. Although the patient had not received exogenous insulin, high titers of insulin autoantibodies were found in serum and large amounts of total and free insulin (1550 and 82 microU/ml, respectively) and C-peptide reactivity (CPR, 22 ng/ml) were detected in serum. After glucose loading, blood glucose and total insulin levels increased abnormally. The immunoglobulin class of the autoantibodies was IgG and the light chains were of the kappa type. The titers of insulin autoantibodies, elevated serum total and free insulin, and CPR levels decreased gradually, but insulin autoantibodies and elevated insulin levels were still present in the serum 8 months after the episode of hypoglycemia. These findings suggest that the patient's fasting hypoglycemia was due to excess free insulin released from antibody-bound insulin, and that methimazole might play a role in the initiation of production of insulin autoantibodies.

Adult↗
PubMedDate not supplied

Glucose, insulin and C-peptide kinetics during intravenous glucose tolerance test in chronic liver disease.

To elucidate the mechanism of glucose intolerance in chronic liver disease (CLD), the kinetics of plasma glucose, insulin and C-peptide were studied after intravenous glucose loading in patients with CLD. Fasting plasma insulin levels were higher in patients with CLD than in normal subjects. This hyperinsulinemia was attributed primarily to an increased pancreatic secretion of insulin. Patients with CLD were divided into two groups, one with normal fasting plasma glucose (FBS less than 100 mg/dl (Group I) and the other with higher FBS (Group II). In Group I, the glucose disappearance rate was normal and a brisk acute insulin response (AIR) to glucose was noted. The glucose disappearance rate in Group II was lower than that in normal subjects, and AIR to glucose was blunted. It is suggested that normal glucose tolerance in Group I patients could be interpreted as a state of compensation by hypersecretion of insulin. On the other hand, the glucose intolerance in Group II patients could be due to inadequate insulin secretion to overcome insulin resistance of CLD.

Adult↗