[A case report of perineurial sacral cyst associated with a mosaic of Turner's syndrome (author's transl)].
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Biomedical subjects
Publications and source records attributed to M Fukase.
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The adenylate cyclase responses of the human GH or ACTH producing pituitary adenomas and ectopic ACTH producing tumors to TRH, LH-RH, biogenic amines, peptides hormones, PGE1 and rat median eminence extract (MEE) have been examined. Out of 4 GH producing pituitary adenomas obtained from patients with active acromegaly at hypophysectomy two were stimulated by TRH, two by LH-RH, three by norepinephrine, one by dopamine, four by PGE1 and none by serotonin. Glucagon stimulated the adenylate cyclase in one of three and MEE in both of two tested. The positive responses of paradoxical GH release after TRH and/or LH-RH before surgery in these patients coincidentally related to the response of adenylate cyclase of each pituitary adenoma. There seems, however, to be no consistent correlation between the adenylate cyclase responses to biogenic amines and the GH release after L-Dopa or 5-hydroxytroptophan tested. The adenylate cyclase of a pituitary adenoma from case of Cushing's disease was stimulated by LH-RH, norepinephrine glucagon and MEE but not by TRH. Plasma levels of ACTH, beta-MSH and cortisol increased after LH-RH but not after TRH in this patient before hypophysectomy. The adenylate cyclase of two ectopic ACTH producing tumors (gastric carcinoid and malignant thymoma) was activated by TRH, LH-RH, norepinephrine, epinephrine, serotonin, PGE1 and MEE. These results indicate the presence of multiple hormone receptors in GH or ACTH producing pituitary adenomas and ectopic ACTH producing tumors, and suggest that the paradoxical GH or ACTH release after TRH and/or LH-RH injection in acromegaly and Cushing's syndrome might be caused by an alteration of the cellular membrane receptors of the pituitary adenomas.
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1. A new experimental system has been used to analyse factors involved in the initiation of atherosclerosis in rats. 2. Arterial fat deposition in the cerebral arteries was affected by blood pressure, serum cholesterol concentrations, strain difference and age, of which high blood pressure was the most important. 3. A genetic factor independent of hypertension was shown to be involved in acute arterial fat deposition in spontaneously hypertensive rats.
Cytosol-binding proteins for L-thyroxine (T4) and triiodo-L-thyronine (T3) were studied in human liver specimens obtained at autopsy from 5 male and 2 female subjects. The liver cytosol containing 131I-T4 or T3, together with or without added stable hormones, was fractionated by Pevikon thin-layer electrophoresis at pH 8.6, 8.0, and7.4. It was demonstrated in all the specimens that besides a small amount of serum T4-binding globulin, there existed three T4-binding proteins, termed hT4-1, hT4-2 and hT4-3, with the electrophoretic mobilities of alpha2- and beta-globulins, and two T3-binding proteins, termed hT3-1 and hT3-2, with the mobilities of gamma-globulin. Binding of hormones by the cytosol proteins was pH-dependent, and a preliminary dialysis had no effect on the hormone binding. The major band of T4, hT4-2, bound more than half the tracer T4, and possessed the maximal binding capacity of 110 mug/100 ml of 33% cytosol at pH 7.4. However, it showed no apparent affinity for T3, because the bound T4 could not be displaced with a T3 load of 600 mug/100 ml. The major band of T3, hT3-2, bound more than 70% of the tracer T3, and appeared to have a large capacity for the hormone although secondary binding sites on the same molecule might be responsible for the large capacity. The binding sites appeared almost specific for T3, because only a small, insignificant displacement was noted with a T4 load of 600 mug/100 ml. The results provide evidence for distinct binding proteins for T4 and T3 in the human liver cytosol, though their physiological roles remain to be elucidated.
An autopsy case of Behçet disease which was considered to be typical both clinically and histopathologically was reported. Cerebral abscess was also noted. Consequently it was presumed that some of the findings which had been called softening, demyelination, cavitation among others as the lesions of Neuro-Behçet might be closely related to abscess. Besides suppurative endoaortitis which was thought to be of interest as the lesions of Vascular-Behçet was observed. In order to substantiate the above, a general review of the literature of Behçet disease was made.
One hundred microgram of luteinizing hormone releasing hormone was intravenously injected into 19 female patients with systemic lupus erythematosus and plasma luteinizing hormone levels before and after the injection were determined with a method of solid phase radioimmunoassay. In 4 patients among them, the basal levels of luteinizing hormone were abnormaly high. A question about the existence of autoantibodies to luteinizing hormone in the patient's plasma raised to explain the reason for the high level of luteinizing hormone. The results from 3 experiments for solution of this question were as follows. 1) The patient's plasma was proved to have a binding activity with labeled luteinizing hormone. 2) This binding activity is specifically inhibited by purified luteinizing hormone. 3) This binding activity was located in gamma-globulin fraction. From the results, the existence of autoantibodies to luteinizing hormone in the 2 patients' plasma was concluded.
We have already reported a high rate of occurrence of antimicrosomal antibodies in diabetes mellitus. Thirteen of 507 diabetics (2.5%) were positive with antithyroglobulin antibodies and thirty-one (6.1%) were positive with antimicrosomal antibodies compared to 2.3% and 2.5% respectively in normal controls. Two of 34 insulin dependent diabetics (5.9%) were positive with antithyroglobulin antibodies and ten (29.4%) were positive with antimicrosomal antibodies compared to 2.3% and 4.4% respectively in 473 insulin independent diabetics. To clarify the association of insulin antibodies and thyroid antibodies in diabetics, antithyroid antibodies in 507 diabetics were tested by tanned red cell hemagglutination test and insulin antibodies were demonstrated by using a method descrived by Wright in a modified form. Twelve of 482 diabetics negative-insulin antibody (2.5%) were positive with antithyroglobulin antibodies and thirty(6.2%)were positive with antimicrosomal antibodies. Only one of 25 positive-insulin antibody (4%) was positive with antithyroid antibodies respectively. No evident correlation was observed between antithyroid antibodies and insulin antibodies.
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In the course of studies on the occurrence of antithyroid antibodies in various thyroid disorders, serum antibodies to microsome of thyroid epithelial cells, as well as circulating antibodies to thyroglobulin, are demonstrated by tanned red cell hemaggulutination. These thyroglobulin and microsome-coated tanned red blood cells can be efficiently demonstrated with a commercially prepared reagent. (Fuji-Zoki Co.) The sera of 2,350 normal subjects were tested by these thryoid autoantibodies tests. Fifty-one (2.3 per cent) of the sera of 2,350 normal subjects showed a positive reaction for thyroglobulin antibodies, and fifty-nine (2.5 per cent) persons showed a positive reaction for microsomal antibodies. The incidence of thyroglobulin and microsomal antibodies in males and females were progressively greater with age, particularly between ages 60 to 69.
A 32-year-old woman, patient of chronic glomerulonephritis whose total clinical course was 3 years. During this period intensive peritoneal and hemodialyses were performed. Autopsy revealed deposition of calcium oxalate in the kidneys and the other main organs as well as chronic glomerulonephritis. And it was thought that the patient was accompanied by secondary hyperoxaluria.