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S Stenman

Publications and source records attributed to S Stenman.

74 records · Page 5Linked to original sources

Cytoskeleton antibodies in chronic active hepatitis, primary biliary cirrhosis, and alcoholic liver disease.

Antibodies to cytoplasmic microfilaments, intermediate filaments (vimentin filaments), and microtubules which comprise the cytoskeleton of the cell were assayed in sera from 23 patients with HBsAg-negative chronic active hepatitis and 1 with HBsAg-positive chronic active hepatitis, 15 patients with primary biliary cirrhosis, 20 patients with alcoholic liver disease, and 32 healthy controls. The cytoskeleton antibodies were assayed by indirect immunofluorescence technique using vinblastine-treated cultured human embryonic fibroblasts as substrates. There was a significantly increased incidence of cytoskeleton antibodies in patients with liver disease as compared to the control group. Antibodies to microfilaments were found frequently in sera from patients with chronic active hepatitis (67%) and primary biliary cirrhosis (53%) but were rare in sera from patients with alcoholic liver disease (25%) and in control sera (3%). On the other hand, antibodies to microtubules were found in 50% of sera from patients with alcoholic liver disease but in only 7 to 13% of sera from other groups. Intermediate filament antibodies of IgG or IgA class were found only in patient sera whereas intermediate filament antibodies of IgM class were found in the majority of sera in all groups including control sera. The highest titers of intermediate filament antibodies were seen in primary biliary cirrhosis and chronic active hepatitis. The production of cytoskeleton antibodies may be due to the reorganization or destruction of cytoskeletal structures in the liver.

Adult↗

Comparison of pharmacokinetics, metabolic effects and mechanisms of action of glyburide and glipizide during long-term treatment.

Fourteen non-insulin-dependent diabetic (NIDDM) patients continued their previous medication (7 on glyburide, 7 on glipizide) for 6 mo, after which they switched to the alternate treatment for another 6 mo. The treatment periods were followed by 1 mo of placebo. The sulfonylurea dose was increased to achieve fasting plasma glucose levels less than 9 mM or to a total maximum daily dose of 25 mg. The mean final doses of glyburide (14.7 +/- 2.4 mg/day) and glipizide (15.2 +/- 2.2 mg/day) were similar. Postprandial (postdose) glipizide levels were higher than those of glyburide, whereas fasting (predose) glyburide concentrations were higher than those of glipizide. Both treatments improved glucose control by 25% compared with placebo. Glipizide therapy evoked higher postprandial insulin concentrations than did glyburide, whereas basal insulin concentrations were higher during glyburide. Insulin sensitivity, assessed by an insulin tolerance test, was more improved with glyburide than with glipizide. In conclusion, overall glucose control is similarly improved by glyburide and glipizide. However, glipizide amplifies the plasma insulin response to meals more than glyburide, whereas glyburide enhances basal insulin secretion more than glipizide. Both pharmacokinetic and pharmacodynamic factors may contribute to these differences.

Blood Glucose↗