Gene Literature Dashboard

1. The metabolism of human antithrombin III (ATIII) was studied by using 125I-labelled tracer. 2. The plasma half-life (t0.5) was 2.71 +/- 0.26 days in normal subjects and was similar in patients with cirrhosis or primary carcinoma of liver. 3. Patients with cirrhosis had low ATIII levels, decreased intravascular mass, total body mass and decreased absolute catabolic rate, suggesting decreased synthesis. The positive correlation of ATIII level with fractional catabolic rate (K10) indicated that the decreased catabolic might exert a positive inhibition on ATIII production. 4. These abnormalities were more exaggerated in patients with macronodular cirrhosis associated with hepatitis surface antigen or in those with ascites. 5. In cirrhotic patients with ascites an additional extravascular pool of ATIII was present which did not turn over at the same rate as the intravascular pool. 6. Patients with primary carcinoma of liver had moderately low ATIII, but normal intravascular mass and total body mass because of the increased plasma volume and normal absolute catabolic rate. 7. The negative correlation of ATIII levels with K10 suggested that the low levels could be due to increased catabolism or consumption. 8. One patient with disseminated malignancy and active superficial thrombophlebitis had normal ATIII metabolism.

The sex steroid hormone receptor levels of uterine cytosol were assayed in the course of experimental induction of endometrial carcinoma in rats. Effects of administration of various hormones on the receptor levels were examined with each histological pattern of endometrium. 1) The dissociation constants for E2 and R5020 bindings with uterine cytosol were almost fixed in spite of various histological patterns of endometrium. 2) The influence of administrated hormones on the receptor assay system could be neglected by the preincubation of uterine cytosol with DCC for five times. 3) By the administration of DES for six weeks, estrogen receptor levels were increased significantly in adenocarcinoma, while progesterone receptor levels did not show the tendency of decreasing. 4) By the administration of MPA combined with DES, estrogen receptor levels were not decreased significantly in both atypical adenomatous hyperplasia and adenocarcinoma; progesterone receptor levels were decreased in all groups. 5) By the administration of MPA, estrogen receptor levels were decreased significantly in adenocarcinoma. These data suggest that receptor levels can be controlled by the administration of sex hormones in the course of development of endometrial carcinoma.

The following inborn errors of metabolism may show corneal changes: A. Inborn errors of metabolism affecting the corneal epithelium: (1) familial dysautonomia, (2) tyrosinaemia type II, (3) Fabry's glycolipidosis. B. Inborn errors of metabolism affecting the corneal stroma: I. Localized amyloidosis (lattice dystrophy of the cornea), II. Defects in carbohydrate metabolism: (1) localized mucopolysaccharidosis (macular dystrophy of the cornea), (2) systemic mucopolysaccharides, (3) glycogen storage disease. III. Defects in lipid metabolism: (1) localized from (Schnyder's crystalline dystrophy), (2) systemic forms (hyperlipoproteinaemia, hypolipoproteinaemia, Lecithin-cholesterol acyl transferase deficiency, Wolman's disease, Gaucher's disease). IV. Combined defects in lipid and carbohydrate metabolism (mucolipidoses). V. Other inherited metabolic disorders: (1) aminoacidopathies (cystinosis, Wilson's disease, ochronosis, Chediak-Higashi syndrome), (2) hemochromatosis.