Biomedical subjects
Publications and source records attributed to K Endo.
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When secretin was given by continuous intravenous infusion in the control subjects, the dose of secretin inducing maximal bicarbonate output was found to be around 6.0 CHR U/kg/hr. Then the pancreatic exocrine secretory response to sequential standard (1.2 CHR U/kg/hr) and augmented (6.0 CHR U/kg/hr) dose of secretin was studied in the controls, in patients with chronic pancreatitis and in its suspected cases. This new method for exocrine pancreatic function did not offer advantage for the diagnosis of well established chronic pancreatitis. But from the results obtained in suspected chronic pancreatitis it was supposed that the decline of increasing rate of bicarbonate output with augmentation of dose and the decrease of response to augmented dose of secretin might be one of functional disorders occurred in the early stage of chronic pancreatitis.
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TSH-binding inhibitor immunoglobulins (TBII) have been detected in patients with Graves' disease and Hashimoto's thyroiditis by using the radioreceptor assay of TSH. In untreated Graves' patients, TBII levels correlated well with thyroidal 99mTc uptake at 30 min and the grade of epithelial hyperplasia of thyroid follicles. There were many Graves' patients whose sera contained high TBII levels but no detectable bioassayable thyroid-stimulating activity (LATS), and in these patients, close correlation was observed between serum levels of TBII and bioassayable LATS-protector activity. TBII were detectable in 2 (10%) of 20 patients with Hashimoto's thyroiditis, both of whom were clinically hypothyroid. The serum or IgG fraction from one of them, however, did not contain any significant LATS, LATS-protector, or human thyroid adenylate cyclase-stimulating activity and caused inhibition of adenylate cyclase stimulation by TSH. In that patient, TBII may be acting to block TSH binding to TSH receptors, thus causing TSH unresponsiveness and hypothyroidism.
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The electric capacitance of isolated rat mast cells and its change under the influence of either n-decylamine or toluidine blue was investigated. Since the electric circuit employed in the detection unit is the one merely sensitive for the capacitance changes, output signals pertain to the capacitance of the tested cell alone. N-decylamine released histamine without accompanying degranulation; and it caused a marked swelling of mast cells and a striking decrease of capacitance, although electric capacitance is usually proportional to the size of the cell. Morphological changes induced by toluidine blue are seemingly correlated with the changes in capacitance. At the concentrations (25-50 microgram/ml) in which the mast cell became enlarged, electric capacitances exceeded the control value. However, at the concentrations higher than 100 microgram/ml in which the cell became shrunken, the capacitance values were less than control value. Pretreatment with DNP (0.1 mM) or oxyphenbutazone (0.05-0.2 mM) was of little effect in inhibiting the histamine release, morphological alterations and capacitance changes due to n-decylamine, but pretreatment with either prevented all of those changes produced by toluidine blue. The mechanism of the capacitance changes in mast cells induced under influence of those compounds is discussed.
In one case of untreated Hashimoto's thyroiditis, the serum thyroxine (T4) value, obtained by radioimmunoassay (RIA) employing resin to separate bound and free T4, was significantly lower than that obtained by competitive protein binding analysis (CPBA). The discrepancy was found to be due to the presence of anti-thyroxine autoantibody in the serum. This phenomenon is considered to be of practical importance in interpreting the T4 value by RIA in cases with autoimmune thyroid diseases.
Antibodies against thyroxine (T4) and/or triiodothyronine (T3) were detected in 3 patients with Hashimoto's thyroiditis. One of the patients had both anti-T4 and anti-T3 antibodies and the other 2 patients had only anti-T3 antibody. Serum T4 or T3 antibodies and the other 2 patients had only anti-T3 antibody. Serum T4 or T3 values measured by the single antibody radioimmunoassay (RIA), were low or nil in these patients. One patient was mildly hypothyroid. The other 2 patients were clinically euthyroid, but they were considered latent hypothyroid because of a slight elevation in serum TSH. On extraction of the sera with ethanol, high or normal values of T3 were obtained in all cases. Recovery of T4 or T3 added to the patients' sera determined by RIA was significantly low. The binding of [125I]T4 or [125I]T3 to the patients' sera was demonstrated by the polyethylene glycol method and by using RIA kits without adding the antibody provided. The binding activity was localized in the IgG fraction by column chromatography and by immunoprecipitation. T4- or T3-binding protein in two sera migrated in the gammaglobulin region on paper electrophoresis and was found in 7S fraction on Sephadex G-200 chromatography. In one serum containing both anti-T4 and anti-T3 antibodies, the association constants (Ka) for binding of T4 and T3 were 3.8 x 10(8) l/mol and 1.7 x 10(8) l/mol, respectively. The binding capacities in the serum were 8.2 microgram of T4 and 1.9 microgram of T3 per 100 ml of serum. For two sera containing anti-T3 antibody, Ka were 5.5 x 10(8) l/mol and 7.4 x 10(10) l/mol, and the binding capacities were 0.6 microgram/100 ml serum and 0.7 microgram/100 ml serum respectively. The clinical significance of these antibodies is discussed.
In order to study the disposition which is thought to be latent in chronic pancreatitis, we investigated the sweat chloride concentration of 95 normal subjects, 43 cases of chronic pancreatitis, 12 cases of cholelithiasis, 15 cases of peptic ulcers, 16 cases of hepatic diseases and 23 cases of diabetes mellitus with the sweat test, using the method of pilocarpine iontophoresis. We obtained the following results. (1) In normal subjects, the sweat chloride concentration was inclined to rise gradually with age from childhood to adulthood; the mean value of sweat chloride concentration was 30.0 mEq/liter in adults from 20 years old, and the upper limit was about 60 mEq/liter. (2) The mean value of sweat chloride concentration was 60.0 mEq/liter in chronic calcifying pancreatitis; this value was markedly higher than that of control subjects of the same age (p is less than 0.001). (3) The mean value of sweat chloride concentration in cholelithiasis, peptic ulcer and hepatic diseases did not differ significantly from control subjects. The mean value of sweat chloride concentration in diabetes mellitus was significantly higher than that of control subjects (p is less than 0.01), but was significantly lower than that in chronic pancreatitis (p is less than 0.01). (4) It was supposed that some cases of chronic pancreatitis have a congenital disposition toward abnormal secretion of sweat glands and epithelium in the pancreatic duct, resembling cystic fibrosis, and this disposition leads easily to pancreatic disorders when the individual is exposed to various external factors.
Biopsy specimens of the duodenal mucosa were assayed to determine their secretin-like activity in 9 controls, 9 patients with gastric ulcer, 19 patients with duodenal ulcer, 4 patients with gastric and duodenal ulcer, and 13 patients with chronic pancreatitis. The bioassay of secretin was done on the pancreatic secretion in anesthetized rats. The sensitivity was in the orcer of 0.0625 CHR unit/rat (4 ng/rat). In the range between 0.0625 and 0.5 CHR units a satisfactory dose dependency was recognized. The following results were obtained. 1) The level of duodenal mucosal secretin-like activity in patients with gastric ulcer was the same as that in the controls, but was elevated in 32% of the patients with duodenal ulcer, 50% of those with gastric and duodenal ulcer, and 8% of those with chronic pancreatitis. 2) The high level of secretin-like activity noted in patients with duodenal ulcer was suspected to be related to the hypersecretion of gastric acid which is characteristic of this disease, but there was no correlation between gastric acid secretion and secretin-like activity in the duodenal mucosa.
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