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Biomedical subjects

I Matsuda

Publications and source records attributed to I Matsuda.

At least 379 records · Page 21Linked to original sources
PubMed1985

Detection of vitamin K deficiency by use of an enzyme-linked immunosorbent assay for circulating abnormal prothrombin.

A monoclonal antibody was raised against an abnormal decarboxylated prothrombin by a cell fusion technique. A cell line which produces an IgG1 murine antibody to the abnormal prothrombin, but not to prothrombin, was selected. Using this antibody we developed an enzyme-linked sandwich immunoassay for the abnormal prothrombin. The detection range was 0.5 X 10(-1) approximately 0.5 X 10(-3) micrograms protein of decarboxylated prothrombin and 0.5 approximately 0.5 X 10(-2) micrograms protein of abnormal prothrombin in vitamin K-deficient subjects. This discrepancy is attributable to a heterogeneity of decarboxylated prothrombin, depending on the number of gamma-carboxyglutamic acid residues. The antibody obtained had a higher affinity to a protein possessing less gamma-carboxyglutamic acid residues. The assay system developed may be useful for the detection of vitamin K deficiency, since a severe deficiency may result in less gamma-carboxyglutamic acid residues in the protein.

1-Carboxyglutamic Acid↗
PubMed1985

Reversal of antinociceptive effect of cholecystokinin by benzodiazepines and a benzodiazepine antagonist, Ro 15-1788.

Intraperitoneally administered benzodiazepines, chlordiazepoxide (2-5 mg/kg), diazepam (1 mg/kg), flurazepam (1 mg/kg) and a benzodiazepine antagonist, Ro 15-1788 (0.5 mg/kg), reversed the antinociceptive effect in mice which was induced by intracisternal administration of 1 microgram of sulfated cholecystokinin octapeptide. The antinociceptive effect of cholecystokinin was reversed by naloxone, suggesting that the antinociceptive action involves endogenous opioid peptides in its production. On the other hand, morphine-induced analgesia was not reversed by diazepam and Ro 15-1788. These facts rule out opioid receptors as the site of the antagonism between the benzodiazepines or Ro 15-1788 and cholecystokinin on the antinociceptive effect. Benzodiazepines and Ro 15-1788 seem to inhibit the release of opioid peptides induced by cholecystokinin.

Analgesics↗
PubMed1985

Caerulein antagonism by benzodiazepines in the food intake in mice.

Intracisternal administration of caerulein inhibited the food intake in mice, but the caerulein action was antagonized by benzodiazepines such as chlordiazepoxide, diazepam and flurazepam which were administered intraperitoneally in low doses (0.2 to 2 mg/kg). The antagonism mechanism between caerulein and benzodiazepines remains unclear, but the characteristics of the antagonism were similar to those which had been observed with cholecystokinin and benzodiazepines.

Animals↗
PubMed1985

Inhibition of hypothermic effect of cholecystokinin by benzodiazepines and a benzodiazepine antagonist, Ro 15-1788, in mice.

Intracisternally administered cholecystokinin produced long lasting hypothermia in mice, and the hypothermic effect was significantly antagonized by benzodiazepines like chlordiazepoxide and diazepam and by a benzodiazepine antagonist, Ro 15-1788, that were administered intraperitoneally. Proglumide, a cholecystokinin antagonist, failed to prevent the hypothermia induced by cholecystokinin at a dose of 200 mg/kg. Benzodiazepines and Ro 15-1788 revealed a considerably strong hypothermic effect, but they still prevented the hypothermic effect of cholecystokinin. The precise mechanism of the antagonism between cholecystokinin and benzodiazepines remains unclear at present.

Animals↗
PubMed1985

Erythrocyte insulin receptor and glucose tolerance test in children treated with prednisolone.

Insulin receptors of erythrocytes and oral glucose tolerance test (O-GTT) were investigated in sixteen children treated with prednisolone for various diseases. Ten patients (Group 1) received low doses of prednisolone (0.2-0.5 mg/kg body weight/day) and six patients (Group 2) received higher doses of prednisolone (1.5-2.0 mg/kg body weight/day). Compared to the values for controls, the sums of blood glucose (sigma BS) at O-GTT in both group 1 and group 2 patients were significantly elevated. (422 +/- 75 mg/dl, p less than 0.01 Group 1; 419 +/- 39 mg/dl, p less than 0.01 Group 2; 338 +/- 41 mg/dl controls) Significant differences were not observed in the sums of insulin concentration at O-GTT, fasting blood concentration and basal insulin levels among these two groups and the controls. There was a significant increase in the maximum insulin binding in group 2 (9.13 +/- 0.68% in group 2, 7.97 +/- 1.06% in controls, p less than 0.05), but not in group 1 (8.59 +/- 1.82%). There is no significant difference in binding affinity or the number of receptors between any of these two patients' groups and the controls. When patients in group 1 and group 2 were combined, sigma IRI levels were significantly elevated in the patients (p less than 0.05). These results suggested that prednisolone treatment with a smaller dosage as well as with the higher dosage resulted in a carbohydrate intolerance, the main cause of which is located in a postreceptor step (or steps) of insulin action.

Adolescent↗
PubMed1985

Cellular hypersensitivity to human pancreatic B-cell clone in diabetes mellitus and its relationship to the presence of islet cell antibodies.

A leukocyte migration inhibition test on the human pancreatic B-cell clone (JHPI-1) was performed in 13 IDDM patients with islet cell cytoplasmic antibody (ICCA) and/or islet cell surface antibody (ICSA), 15 IDDM patients without ICCA or ICSA, 34 NIDDM patients and 17 healthy controls. The mean values for the migration index (M.I. %) in each group were 85.4 +/- 6.9, 89.1 +/- 10.9, 98.3 +/- 7.9 and 100.0 +/- 8.5. The M.I. values were significantly decreased in IDDM patients than in NIDDM patients and controls irrespective of whether or not there were islet cell antibodies in the patients' sera. When M.I. values less than 0.83 (Mean-2 S.D.) were taken as indicative of inhibition, the percentage of IDDM and NIDDM patients with migration inhibition were 32% and 0% respectively. And the decreased M.I. values in IDDM patients proved not to be due to non-specific migration inhibition by normal M.I. values, with the human fetal lung fibroblast cells (W 138) as antigen. Our data suggested that the lymphocytes of IDDM patients might be sensitized by pancreatic B-cell antigen(s) present in the JHPI-1 cells, which promoted leukocyte migration inhibition. No correlation between the migration indices and duration of diabetes mellitus in IDDM patients was observed (r = 0.254, Y = 84.9 + 0.49 X). LMT to JHPI-1 seems to be useful in detecting the abnormal cell-mediated immunity even in patients with longstanding IDDM.

Adolescent↗
PubMed1985

The negative correlation between prolactin and ionic calcium in cord blood of full term infants.

Total serum calcium (Ca), ionic calcium (Ca++), phosphorus, magnesium, total protein, immunoreactive parathyroid hormone (iPTH), calcitonin (iCT) and prolactin (iPRL) were measured in 30 paired samples of cord and maternal blood obtained at term delivery. In the cord blood, the concentrations of Ca, Ca++, phosphorus, magnesium, albumin, iCT and iPRL were all higher, and the concentrations of total protein and iPTH lower than in the maternal blood. The calcium binding capacity of albumin assessed with the equation (Ca-Ca++)/albumin, was similar at a given concentration of Ca in both the maternal and fetal circulations. There was a significant positive correlation between cord Ca++ and maternal Ca or Ca++, and a significant negative correlation between Ca++ and iPRL in cord blood. These data suggest that there is an active system transporting calcium from mother to fetus through the placenta, and PRL is the only one of the three hormones which was correlated with ionic calcium values in the fetus. The negative relationship between Ca++ and iPRL in the cord blood suggests an inhibitory effect of the relative hypercalcemia on PRL secretion in the fetus.

Calcitonin↗
PubMed1985

Serum zinc and copper concentrations in low birth weight infants during first three months of life: correlation to birth weight and different feedings.

Serum zinc (Zn) and copper (Cu) concentrations were measured in infants weighing 740 g to 2,500 g at birth. They were divided into three groups depending on their birth weight; Group I ranged from 740 to 1,500 g (N = 35), Group II from 1,501 to 2,000 g (N = 26), and Group III from 2,001 to 2,500 g (N = 19). They were fed breast milk (N = 24), commercially available non-supplemented formula with low Zn and low Cu content (N = 42), or Zn- and Cu-supplemented formula (N = 14). Serum Zn levels of breast fed infants were apparently higher than those of the other two different formula fed infants, the difference being significant at 1 month of age in Group I. After the decline of serum Zn level during the first month of life, the level in Groups II and III remained unchanged, whereas the level in Group I further declined progressively until 3 months of age. An incidence of hypozincemia (0.65 micrograms/ml) was highest in Group I, medium in Group II, and lowest in Group III. The serum Cu level was elevated progressively after birth in all groups, but the mean level was consistently highest in Group III, medium in Group II and lowest in Group I. No difference in serum Cu level was found among the infants with different feedings.

Birth Weight↗
PubMed1985

Regulation of receptors and digestive activity toward synthesized formyl-chemotactic peptide in human polymorphonuclear leukocytes.

A receptor binding and digestive activity of human polymorphonuclear leukocytes (PMNs) toward formyl-methionyl-leucyl-[3H]phenylalanine (3H-FMLP) was examined with the following results: Up- and down-regulation and recovery of 3H-FMLP binding activity were demonstrated. Both intact PMN and a lysate prepared from them cleaved the carboxyl terminal amino acid (phenylalanine) of 3H-FMLP. The digestive activity decreased as the receptor binding was inhibited by n-ethylmaleimide and 4-chloromercuribenzoate. Little digestive activity was found in the supernatant from PMN stimulated by FMLP. The released phenylalanine was found in the pellet and supernatant of PMNs. Digestive activity with cathepsin A-like characteristics was found in the lysate of PMN. These observations suggest that FMLP is internalized in lysosomes in a receptor-mediated manner and cleaved by the cathepsin A-like enzyme, the free phenylalanine is released extracellularly, and a part of the dissociated receptors with FMLP may return to the surface or to an intracellular receptor pool. Another finding was that the digestive activity of the lysate of cord blood granulocytes was decreased compared with that of adult blood granulocytes. This decrease may explain in part the impaired chemotaxis of cord blood granulocytes.

Cell Membrane↗
PubMed1984

Immunologic studies of peripheral blood in a child with hypogammaglobulinemia. Suggested mechanism for the development of malignant B-cell lymphoma.

A case of a 7-year-old boy with common variable hypogammaglobulinemia who developed B-cell-type non-Hodgkin's lymphoma is reported. Immunologic studies of his peripheral blood before the development of lymphoma revealed: (1) although peripheral T-cell and B-cell counts were normal, serum IgG and IgA levels were remarkably reduced; (2) DNA synthesis in response to phytohemagglutinin-P (PHA), concanavalin A (Con A), and pokeweed mitogen (PWM) stimulation were decreased; (3) DNA synthesis in response to EBV was enhanced; (4) in vitro IgG production with the patient's peripheral blood lymphocytes was significantly depressed; and (5) helper and suppressor activities of the patient's T-cells did not differ from that of normal controls. Six months after the investigation systemic involvement of malignant lymphoma appeared. The lymphoma was diagnosed as a lymphoblastic diffuse one. Lymph node cell marker analysis revealed that the lymphoblasts had surface mu and kappa chain, cytoplasmic IgM, and HLA-DR antigen. Blastogenesis of B-cell series may be suppressed by a feedback mechanism with the B-cells and antibody. In the current case, impairment of such a mechanism with defect of immunoglobulin production might finally induce malignant B-lymphoid proliferation.

Agammaglobulinemia↗
PubMed1984

Siblings with renal tubular acidosis and nerve deafness. The first family in Japan.

Two siblings with renal tubular acidosis (RTA) and nerve deafness were examined. It was found by ammonium chloride and bicarbonate loading tests that the 6-year-old brother had a hybrid type of RTA and his 4-year-old sister, a distal type of RTA. Enzyme activity and amount of enzyme protein of carbonic anhydrase isoenzyme I and II in red blood cells, measured using an immunoadsorbent method, were normal in both cases. Although this indicated that the RTAs of these patients are not generated by the carbonic anhydrase deficiency, an investigation with renal tissue is necessary to arrive at a final conclusion.

Acidosis, Renal Tubular↗
PubMed1984

Study on established lymphoid cells in maple syrup urine disease. Correlation with clinical heterogeneity.

Branched-chain keto acid dehydrogenase complex (BCKAD) was measured in lymphoid cells established from five patients with maple syrup urine disease (MSUD) and six control subjects. Two other MSUD lymphoid cell lines obtained from The Human Genetic Mutant Cell Repository were used as references. One day after subculture, the cells grew logarithmically up to 4-5 days. With this cell growth, BCKAD activity increased greatly in controls, but not in MSUD cells. The maximum BCKAD activity of MSUD cells was less than 7% and 13%-16% of the control in classic and variant types, respectively. Leucine added to culture medium at the concentration of 10-20 mM significantly inhibited cell growth in MSUD cells alone, and with increasing concentration and impaired enzyme activity in a cell line, the effect became more prominent. The effects of isoleucine and valine were mild and did not differ between control and MSUD cells.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗
PubMed1984

Complementation analysis in lymphoid cells from five patients with different forms of maple syrup urine disease.

The possibility of genetic heterogeneity in maple syrup urine disease was investigated by measuring branched-chain ketoacid dehydrogenase in polyethylene glycol-induced heterokaryons of lymphoid cells. The lymphoid cell lines from five patients with varying forms of the disease were established after incubation with Epstein-Barr virus. The results suggested that there are at least two genetic complementation groups in the disease.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗