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Y Koizumi

Publications and source records attributed to Y Koizumi.

At least 19 recordsLinked to original sources
PubMed1992

High-performance affinity chromatography system for the rapid, efficient assay of glycated albumin.

A high-performance affinity chromatographic system was constructed and shown to permit highly reproducible, rapid, automatic assays of serum glycated albumin (GA) by separation of albumin (Alb) on an anion-exchange column (Asahipak ES-502N) packed with a vinyl alcohol copolymer bearing diethylamino groups and consecutive separation of GA on a column packed with a vinyl alcohol copolymer bearing boronate groups. The first column selectively retained Alb free of other serum proteins and permitted at least a 95% recovery of sample Alb. The purity of the Alb peak was confirmed by two-dimensional electrophoresis. Chromatographic analyses of human serum Alb incubated with glucose on the second column showed that the peak area for GA increased in accordance with the incubation time and suggested selective adsorption of GA on the second column. Optimization of the conditions for the two-column system reduced the analysis time to 10 min. Analyses of human sera with the present system showed GA to be 16.1 +/- 1.1% (mean +/- S.D.) of total Alb in non-diabetic children and 39.9 +/- 9.1% (mean +/- S.D.) in diabetic children (0-17 years old).

Adolescent↗
PubMed1992

Disappearance of thyrotropin-blocking antibodies and spontaneous recovery from hypothyroidism in autoimmune thyroiditis.

BACKGROUND: Hypothyroidism may result from the production of antibodies that block the actions of thyrotropin. How often these thyrotropin-blocking antibodies are a cause of hypothyroidism and whether their production may cease, causing hypothyroidism to disappear, have not been extensively studied. METHODS: We determined the frequency with which thyrotropin-blocking antibodies were present in 172 hypothyroid patients with goitrous autoimmune thyroiditis (Hashimoto's disease) and 64 hypothyroid patients with atrophic autoimmune thyroiditis (idiopathic primary hypothyroidism). For 6 to 11 years we then followed 21 of these patients who were found to have thyrotropin-blocking antibodies. They received levothyroxine therapy for 3.5 to 8 years, after which it was discontinued. At frequent intervals during this time we measured the patients' serum concentrations of thyroxine, triiodothyronine, thyrotropin, and thyrotropin-blocking antibodies (measured as immunoglobulins that inhibit thyrotropin binding and immunoglobulins that inhibit thyrotropin bioactivity). RESULTS: Thyrotropin-blocking antibodies were detected in 9 percent of the patients with goitrous autoimmune thyroiditis and in 25 percent of those with atrophic autoimmune thyroiditis. Among the 21 patients studied serially while receiving levothyroxine, thyrotropin-blocking antibodies disappeared in 15 (group 1), 7 of whom had goiter initially, and persisted in 6 (group 2), none of whom had goiter initially. Levothyroxine therapy was subsequently discontinued in these 21 patients. Six of those in group 1 (four with goiter) remained euthyroid (mean follow-up after discontinuation of therapy, 2.1 years), and nine became hypothyroid again within 3 months. All six patients in group 2 remained hypothyroid. CONCLUSIONS: Hypothyroidism in some patients with autoimmune thyroiditis may be due to thyrotropin-blocking antibodies. The production of thyrotropin-blocking antibodies may subside, producing remissions of hypothyroidism. Chronic autoimmune thyroiditis may therefore cause transient as well as permanent hypothyroidism.

Adult↗
PubMed1992

A case of autoimmune insulin antibody syndrome associated with polymyositis, empty sella and apparent high urinary output of immunoreactive insulin.

Patients with autoimmune insulin antibody are characterized by hypoglycemic attacks and antibodies to insulin in serum without prior insulin administration. In the present report, a patient with hypoglycemia due to autoimmune insulin antibody associated with primary empty sella syndrome and polymyositis appeared to have high urinary immunoreactive insulin (IRI) in the face of normal urinary C peptide. Consequently, the urinary IRI/C peptide ratio was apparently high. The amelioration of hypoglycemic attacks and polymyositis by prednisolone treatment was accompanied by the disappearance of the antibodies and complete normalization of the urinary IRI and IRI/C peptide ratio. No comparable rise in the urinary IRI and IRI/C peptide ratio was observed in the patients with other disorders studied. Glucose clamp and glucose tolerance study showed decreased sensitivity to exogenous or newly secreted insulin, prolonged half disappearance time of serum insulin, and normal disappearance of blood glucose. These results were consistent with the idea that autoantibodies buffered the effect of exogenous or newly secreted insulin and maintained a relatively constant level of serum free insulin which was not high enough when a large amount of glucose was loaded, but was too high after prolonged fasting, which eventually caused hypoglycemic attacks.

Autoantibodies↗
PubMed1991

Possible involvement of dopamine D-1 and D-2 receptors in diazepam-induced hyperphagia in rats.

Possible involvement of dopamine receptors in diazepam-induced (1 mg/kg, subcutaneous (sc] hyperphagia was studied in nondeprived rats. Pretreatment with the selective D-1 antagonist, SCH23390 (0.03 mg/kg, sc) inhibited diazepam-induced hyperphagia. In addition, pretreatment with the preferential D-2 antagonists, haloperidol (0.1 to 0.3 mg/kg, sc) and clebopride (0.1 to 0.3 mg/kg, sc) inhibited diazepam-induced hyperphagia in a dose-dependent manner. Pretreatment with co-administration of SCH23390 (0.1 mg/kg, sc) and clebopride (0.03 mg/kg, sc) completely inhibited this hyperphagia. The selective D-2 antagonist, sulpiride (40 mg/kg, sc) and the peripheral D-2 antagonist, domperidone (10 mg/kg, sc) did not affect diazepam-induced hyperphagia. However, sulpiride (10 micrograms, icv) or domperidone (2 micrograms, icv) administered centrally inhibited this hyperphagia. The highest dose of haloperidol (0.3 mg/kg, sc) or clebopride (0.3 mg/kg, sc) and higher doses of SCH23390 (0.01 and 0.03 mg/kg, sc) or SCH23390/clebopride (0.01/0.03 and 0.01/0.1 mg/kg, sc) tended to decrease spontaneous feeding in non-deprived rats. In addition, the highest dose of haloperidol, clebopride or SCH23390/clebopride inhibited spontaneous feeding in deprived rats. Interestingly, diazepam-induced hyperphagia was inhibited significantly by doses of haloperidol (0.1 mg/kg, sc), clebopride (0.1 mg/kg, sc) and SCH23390/clebopride (0.003/0.03 and 0.003/0.1 mg/kg, sc) which did not affect spontaneous feeding in non-deprived or deprived rats. Pretreatment with alpha-methyl-p-tyrosine (40 mg/kg, IP x 2, 6 and 2 h prior to diazepam administration) failed to inhibit this hyperphagia. Furthermore, pretreatment with a large dose of haloperidol (5 mg/kg, sc, 4 days before diazepam administration) augmented the sub-hyperphagic effect to diazepam (0.5 mg/kg, sc). Thus, these findings suggest that hyperphagia to diazepam is mediated in part by both dopamine D-1 and D-2 receptors in non-deprived rats.

Animals↗
PubMed1990

Serum thyroglobulin concentration as an indicator for assessing thyroid stimulation in patients with Graves' disease during antithyroid drug therapy.

PURPOSE: The purpose of this study was to elucidate the mechanism of regulation of serum thyroglobulin concentration in patients with Graves' disease and to establish the clinical usefulness of this measurement. PATIENTS AND METHODS: Serum thyroglobulin concentration was analyzed in relation to serum thyrotropin receptor antibody (TRab) titer and thyrotropin concentration in 166 patients with Graves' disease without thyroglobulin antibody. RESULTS: A total of 113 patients were treated and had been kept euthyroid for at least 10 months with methimazole and underwent a triiodothyronine (T3) suppression test. At the time of the T3 suppression test, the serum thyroglobulin concentration (ng/mL) was 33 +/- 31 in 80 of them with T3-suppressible (radioiodine uptake less than 12%) thyroids, negative TRab titers (less than 15% displacement), and normal serum thyrotropin concentrations (0.1 to 3.0 mU/L). Patients with T3-non-suppressible thyroids were divided into three subgroups according to serum TRab titers and thyrotropin concentrations: those with a negative TRab titer and a normal serum thyrotropin concentration (n = 9), those with a positive TRab titer and a normal thyrotropin concentration (n = 18), and those with a positive TRab titer and undetectable thyrotropin (n = 6). Serum thyroglobulin concentrations (ng/mL) were 116 +/- 40 in the first group, 249 +/- 194 in the second group, and 399 +/- 205 in the third group. In the other 39 methimazole-treated patients, 72 determinations of serum thyroglobulin concentration were performed either before or during treatment without the T3 suppression test, and it correlated well with the TRab titer but not with the serum thyrotropin concentration. In 14 patients who became hypothyroid due to excess methimazole, the serum thyroglobulin concentration increased concurrently with elevation of the serum thyrotropin concentration and normalized during thyroxine supplementation. In treated patients with T3-suppressible thyroids, the serum thyroglobulin concentration was similar among those with positive (n = 54) and negative (n = 26) microsomal antibody, indicating that the presence of Hashimoto's thyroiditis does not profoundly affect the serum thyroglobulin level. Among 80 patients with T3-suppressible thyroids who were followed without methimazole for a mean period of 31.1 months, eight (10%) experienced a clinically overt recurrence of hyperthyroidism. Serum thyroglobulin concentration and TRab titer (%) in these eight patients were 188.1 +/- 101.7 and 27.8 +/- 12.6, respectively. Thyroglobulin and TRab did not increase in the patients who remained euthyroid (n = 71) or who experienced subclinical recurrence (n = 1). CONCLUSIONS: Abnormal thyroid stimulator(s) and thyrotropin synergistically (if both are present in the serum) or independently (if either one is present) stimulate thyroglobulin secretion in patients with Graves' disease. Therefore, serum thyroglobulin concentration can be a useful means of assessing the degree of thyroidal stimulation and, if serum thyrotropin is normal or suppressed, correlates well with thyroidal stimulation even in patients with a negative TRab titer.

Adult↗
PubMed1990

[Diphtheria antitoxin levels in Japanese adults (10-20 years after the last vaccination)].

The serum diphtheria antitoxin levels in Japanese adults were investigated and the persistence of diphtheria toxoid effect was evaluated. The subjects consisted of 56 volunteers (20-31 years of age) who had received regular inoculations of diphtheria and pertussis vaccine (I and II or III phases). They had been immunized according to the Vaccination Law (old version) revised in 1958. The length of time after the last inoculation of diphtheria toxoid was speculated to range from 10 to 20 years. Serum diphtheria antitoxin was determined by passive hemagglutination method. Antitoxin level was 0.025 HAU/ml in 1 subject (1.8%), 0.05 in 2 (3.6%), 0.1 in 2 (3.6%), 0.2 in 8 (14.3%), 0.4 in 7 (12.5%), 0.8 in 12 (21.4%), 1.6 in 7 (12.5%) and more than 1.6 in 17 (30.4%). Results indicated that 55 of 56 (98.2%) possessed a higher level than the prophylaxis standard (0.05 HAU/ml). Since the current Vaccination Law prescribes a lower amount and fewer inoculations than the old law, the number of adults possessing prophylactic antitoxin level may decrease in the future. Further investigation of antitoxin level in adults needs to be continued.

Adult↗
PubMed1990

[Effects of the synthetic proteinase inhibitor, FOY, on hypercoagulability after surgery for esophageal carcinoma].

Hypercoagulability develops after surgery for esophageal carcinoma, and it related closely to postoperative complications. This study evaluated the effects of the synthetic proteinase inhibitor, Cabexate Mesilate (FOY), on this hypercoagulability. The subjects used were 25 patients with a mean age of 63 who had undergone surgery for esophageal carcinoma. Of these, eight patients (test group) received FOY (2,000 mg/day) for three to 23 days after surgery, but 17 (control group) did not. In the test group, FOY controlled aggregation and release of the platelets and minimized their exhaustion. FOY almost completely checked the abnormal increase in thrombin activity which might trigger the hypercoagulability. Also, FOY suppressed the fibrinolytic activity slightly. These results indicate that FOY is effective in controlling hypercoagulability after surgery for esophageal carcinoma and in suppressing activity of the proteinases that cause both blood coagulation and fibrinolysis.

Adult↗
PubMed1990

[Hypercoagulability after surgery of esophageal carcinoma].

The purpose of this study was to determine hypercoagulability in patients surgically treated for thoracic esophageal cancer. Twenty-four patients were evaluated; 19 subjected to open chest esophagectomy and 5 closed chest blunt dissection. Six patients subjected to gastrectomy served as controls. In all test patients, preoperative coagulability was within the normal range. Immediately after surgery, however, they were in a hypercoagulable state, showing a marked decrease in platelet count, prothrombin time, antithrombin III level and plasminogen level and an increase in activated partial thromboplastin time and fibrinopeptide B beta 15-42. The controls showed almost no change. There was a close correlation between hypercoagulability on one hand and the time needed for surgery and hemorrhage during 3rd to 7th postoperative day except those with multiple organ failure whose recovery was delayed and those with leakage of anastomosis whose condition did not improve even on the 10th postoperative day.

Adult↗
PubMed1989

Cholecystokinin antagonism by anthramycin, a benzodiazepine antibiotic, in the central nervous system in mice.

Anthramycin (ATM) which is a product of some streptomyces micro-organisms was shown to antagonize the central effects of cholecystokinin (CCK) such as antinociception and satiety and to displace CCK bound to the slices from the brains of mice. Sulfated octapeptide CCK (CCK8) was administered intracisternally to mice at doses of 1 microgram/mouse for inducing antinociception and 200 ng/mouse for satiety. ATM was administered intraperitoneally to mice at doses such as 0.3 and 0.5 mg/kg. CCK8-induced antinociception and satiety were significantly reversed by ATM in those doses. [125I]CCK8 binding to the brain slices was observed autoradiographically. The autoradiograms from the slices were converted to false color images by using a microcomputer. The radioactivity in the autoradiograms was expressed by color spectra in the false color images. Comparison of the binding of [125I]CCK8 to the brain slices in the presence and the absence of ATM revealed that ATM (10(-6) M) clearly displaced the CCK8 binding in the various regions, especially in the cortex, of the brain. These findings suggest that ATM acts as an potent antagonist of CCK in the central nervous system in mice.

Animals↗
PubMed1989

Presence of anti-DNA antibody in diabetes mellitus: its relation to the duration of diabetes and diabetic complications.

In seven patients with insulin-dependent diabetes mellitus (IDDM) and 86 patients with non-insulin-dependent diabetes mellitus (NIDDM), serum anti-DNA antibody was measured by a semiquantitative radioimmunoassay (RIA) method. Prevalence of positive anti-DNA antibody (more than 20 U/mL) was five of seven in IDDM patients, 15 of 36 in NIDDM patients with insulin therapy, and seven of 50 in NIDDM patients without insulin therapy. None of normal subjects or patients with impaired glucose tolerance (IGT) showed positive anti-DNA antibody. The titer of anti-DNA antibody was higher in IDDM patients than in age-matched normal subjects (mean +/- SD; 22.1 +/- 15.3 v 6.5 +/- 2.2 U/mL, P less than .05). In patients with NIDDM, the antibody titer regardless of insulin treatment, was higher than in age-matched subjects with IGT (18.5 +/- 13.1 U/mL in NIDDM patients receiving insulin, 14.8 +/- 8.1 U/mL in NIDDM patients not receiving insulin, and 8.8 +/- 3.9 U/mL in IGT patients [P less than .001] for either of NIDDM groups v IGT). The titer of anti-DNA antibody was positively correlated with the duration of diabetes (r = .413, P less than .001) and with the postprandial blood glucose level (r = .311, P less than .01) in NIDDM patients when all of them were combined and analyzed as a group.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Antinuclear↗
PubMed1989

[Effects of transfer factor on chronic hepatitis B in childhood].

Nine children, 1 to 13 years of age, with HBeAg positive chronic hepatitis B received transfer factor (T.F.) monotherapy for 3 to 17 months, and were monitored by check-ups every six months from serum HBeAg, anti-HBe and GPT. In 12 months, 4 subjects became HBeAg negative and had normal serum GPT. In 22 to 48 months, 6 of the nine subjects had negative HBeAg and normal GPT, 2 had positive HBeAg and high GPT values. The remaining 1 subject who was observed for six months after T.F. therapy remained HBeAg positive with a high GPT values. No side effects were observed. These preliminary observations may indicate beneficial effects of T.F. on the natural course of chronic hepatitis B in childhood, though the ultimate effects awaits longer and well controlled clinical trials.

Adolescent↗
PubMed1989

[Background of low-level gamma-ray spectrometer due to the atmospheric 220Rn and 222Rn].

In connection with low-level gamma-ray counting of natural samples, background due to 220Rn- and 222Rn-daughters was monitored. The results obtained for 4 months showed that the background gamma-ray from 222Rn-daughters was more variable than that of 220Rn-daughters. An efficient air-conditioning was helpful to keep the background stable. It was practically equivalent to the use of N2-gas. Radiometric data for dust samples filtered from the laboratory air suggested that Rn-daughters tended to be removed by air-conditioning.

Air Pollutants↗
PubMed1989

[Bone scintigraphy of metastatic calcifications].

The bone scintigrams of 4 cases with metastatic calcification in the lung, stomach and myocardium were presented. These four cases were malignancy with hypercalcemia. Metastatic calcifications were not able to be detected by radiographs and CT. Therefore, bone scan seems to be the most useful method for detection of metastatic calcification.

Aged↗
PubMed1989

[Factor analysis of bone mineral dynamics in patients with renal osteodystrophy].

Remarkably high accumulation of Tc-99m-MDP is seen in the skull on bone scintigraphy of patients with renal osteodystrophy (ROD), especially with secondary hyperparathyroidism. For the quantitative evaluation, the Factor Analysis (FA) was used for the early phase of bone scan. Tc-99m-MDP (14.8 MBq/body weight kg) was injected as a bolus through the medial antecubital vein. Dynamic acquisition of 40 x 30 sec frames were performed in a 64 x 64 matrix. For pre-processing, nine points smoothing was carried out, and then the region of interest was set on the frontal image of the head for the FA. The FA was performed with an 8 x 8 sampling corresponding to 64 dixels from 4,096 dixels. Bone factor was clearly extracted by the FA. Then, two original parameters were calculated. One is the bone radionuclide uptake counts (Bu) which is the product of the total radionuclide counts of skull and the contribution ratio, the other is the uptake ratio (Br) derived by the time activity curve (physiological component) of the FA. These parameters of ROD were significantly different compared to those of controls. The FA seems to be useful in quantitative evaluation of bone mineral dynamics.

Adult↗
PubMed1988

Effects of naloxone and picrotoxin on diazepam- or pentobarbital-induced hyperphagia in nondeprived rats.

Diazepam and pentobarbital administered intravenously increased food intake in a dose-dependent manner in nondeprived rats. Low doses of naloxone inhibited diazepam-induced feeding, but did not inhibit pentobarbital-induced feeding. On the other hand, picrotoxin inhibited feeding induced by both drugs. These findings suggest that diazepam-induced hyperphagia is related to endogenous opioid mechanisms, but pentobarbital-induced hyperphagia is not. Hyperphagia induced by both drugs may be related to GABAergic neurons.

Animals↗