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Biomedical subjects

I Matsuda

Publications and source records attributed to I Matsuda.

At least 325 records · Page 18Linked to original sources
PubMed1987

Spread of epidural analgesia following a constant pressure injection--an investigation of relationships between locus of injection, epidural pressure and spread of analgesia.

(1) The spread of epidural analgesia following injection of 15 ml of 2% mepivacaine was 17.3 +/- 0.6, 14.3 +/- 0.4, and 13.3 +/- 0.7 spinal segments in cervical, thoracic, and lumbar epidural analgesia, respectively. The patient's age showed significant correlation with the spread of epidural analgesia in cervical (r = 0.5776, p < 0.001), thoracic (r = 0.3758, p < 0.01), and lumbar area (r = 0.8195, p < 0.001). The spread of cervical epidural analgesia was more caudad than cephalad (p < 0.05), but in lumbar epidural analgesia it was more cephalad than caudad (p < 0.05). There was no difference between the cephalad and caudad spread in thoracic epidural analgesia. (2) The epidural pressure immediately after injection of 15 ml of 2% mepivacaine into the lumbar epidural space at a constant pressure (80 mmHg) correlated to the patient's age (r = -0.5714, p < 0.001) and the spread of analgesia (r = -0.3904, p < 0.05). The lower epidural pressure associated with higher age, the wider spread of analgesia. There was no significant correlation between the residual pressure at 60 seconds and the age or the spread of analgesia.

Journal Article↗
PubMed1987

The patient with combined deficiency of neuraminidase and 21-hydroxylase.

To investigate the possibility that deletion en block in the HLA region had caused the combined deficiency of neuraminidase and 21-hydroxylase in a female patient, genetic markers on the short arm of chromosome 6 were examined in the patient and her parents, and 21-hydroxylase genes of the patient were analyzed by the Southern blot technique. The affected "extended haplotype" identical by descent might have been recombined at two sites, between HLA-A and C and between HLA-DQ and GLO. This suggests that the neuraminidase gene is mapped between HLA-A and GLO. Southern blot analysis revealed the existence of two 21-hydroxylase genes, so that we found no evidence to support the possibility that deletion en bloc in the HLA class III region had caused the combined deficiency of neuraminidase and 21-hydroxylase.

Adrenal Hyperplasia, Congenital↗
PubMed1987

Molecular cloning and nucleotide sequence of cDNA for human liver arginase.

Arginase (EC 3.5.3.1) catalyzes the last step of the urea cycle in the liver of ureotelic animals. Inherited deficiency of the enzyme results in argininemia, an autosomal recessive disorder characterized by hyperammonemia. To facilitate investigation of the enzyme and gene structures and to elucidate the nature of the mutation in argininemia, we isolated cDNA clones for human liver arginase. Oligo(dT)-primed and random primer human liver cDNA libraries in lambda gt11 were screened using isolated rat arginase cDNA as a probe. Two of the positive clones, designated lambda hARG6 and lambda hARG109, contained an overlapping cDNA sequence with an open reading frame encoding a polypeptide of 322 amino acid residues (predicted Mr, 34,732), a 5'-untranslated sequence of 56 base pairs, a 3'-untranslated sequence of 423 base pairs, and a poly(A) segment. Arginase activity was detected in Escherichia coli cells transformed with the plasmid carrying lambda hARG6 cDNA insert. RNA gel blot analysis of human liver RNA showed a single mRNA of 1.6 kilobases. The predicted amino acid sequence of human liver arginase is 87% and 41% identical with those of the rat liver and yeast enzymes, respectively. There are several highly conserved segments among the human, rat, and yeast enzymes.

Amino Acid Sequence↗
PubMed1987

Screening for late neonatal vitamin K deficiency by acarboxyprothrombin in dried blood spots.

Acarboxyprothrombin (protein induced by vitamin K absence or antagonist-II (PIVKA-II] concentrations in dried blood spots were determined in 19,029 infants at about 1 month of age as an indicator of vitamin K deficiency. We observed 51 cases with raised blood concentrations of PIVKA-II (greater than 4 AU/ml), nine of whom showed very high concentrations (greater than 20 AU/ml). For infants who did not receive vitamin K prophylaxis at birth, the incidence of the PIVKA-II test yielding positive results was significantly higher in those solely breast fed (0.51%) compared with those fed formula milk (0.18%). Among solely breast fed infants, the incidence of a very high result of the PIVKA-II test was 0.14% in those who had not received vitamin K prophylaxis at birth, 0.04% in those who received 2 mg orally, and 0.03% in those who received 2 mg orally plus a further dose of 2-4 mg orally at 7 days. Thus vitamin K prophylaxis at birth did not completely prevent vitamin K deficiency at 1 month. We administered vitamin K therapeutically to all infants whose PIVKA-II test yielded a positive result at 1 month. Only one infant with a positive result developed late neonatal intracranial haemorrhage.

Biomarkers↗
PubMed1987

Analysis of cell proteins in lymphoblasts of acute lymphocytic leukemia by two-dimensional gel electrophoresis.

The two-dimensional gel electrophoresis (2-DE) method developed by O'Farrell was used to analyze the differences of major proteins between lymphoblasts from children with acute lymphocytic leukemia (ALL) at diagnosis (lymphoblasts, n = 6), normal lymphocytes (n = 6) and lymphocytes from children with ALL in complete remission (lymphocytes in CR, n = 12). Among all the spots, those which were deeply stained and large were termed 'major spots'. Their number was 118. Two spots (No. B1 and B2) were characteristic of lymphoblasts, three spots (No. N1-N3) were characteristic of normal lymphocytes. In lymphocytes in CR, the latter spots were not always detected, and furthermore, the former spots were detected in several gels. These findings may relate to the insufficient recovery of functions of lymphocytes in CR. Several spots (No. 6, 55 and 57) in lymphoblasts were remarkably larger than those in normal lymphocytes. Spot No. 67, an actin spot, in lymphoblasts was smaller than that in normal lymphocytes. Spots No. 6, 55 and 57 in lymphocytes in CR were relatively small in size.

Adolescent↗
PubMed1987

Zinc status and delayed cutaneous hypersensitivity in handicapped children treated with anticonvulsants.

Delayed cutaneous hypersensitivity and hair zinc contents were investigated in 68 children treated with anticonvulsants and 14 untreated children, and serum zinc contents were also measured in 21 of the treated and 13 of the untreated children. Serum zinc levels in the treated and untreated children were 82.7 +/- 7.1 and 85.1 +/- 18.2 micrograms/dl, respectively. Hair zinc levels in the treated and untreated children were 145.4 +/- 27.0 and 144.3 +/- 20.1 micrograms/g, respectively. These two parameters were not significantly different between the two groups. However, a significantly depressed skin reaction and a higher incidence of hypozincnemia (below 70 micrograms/dl) were found in the treated children (p less than 0.05). The results indicated that phenytoin-induced zinc deficiency might be one of the possible factors or exacerbatory factors in suppressed cellular immunity found with anticonvulsant therapy.

Adolescent↗
PubMed1987

Molecular aspects of urea cycle enzymes and related disorders.

Amino acid sequence of rat ornithine transcarbamylase (OTC) precursor containing an NH2-terminal presequence of 32 residues was deduced from the cDNA sequence. Comparison with the human and Escherichia coli enzymes indicated that regions containing the putative binding sites for the substrates are highly conserved among the three species. cDNA clones for rat and human liver arginase were isolated and predicted amino acid sequences were compared with that of the yeast enzyme. There are several regions highly conserved among the three species which may be important for catalysis. Several cases of carbamyl phosphate synthetase I and OTC deficiencies were analyzed for enzyme activity, enzyme amount and mRNA activity.

Amino Acid Metabolism, Inborn Errors↗
PubMed1987

Hyperammonemia related to carnitine metabolism with particular emphasis on ornithine transcarbamylase deficiency.

Carnitine status was evaluated in 8 patients with partial ornithine transcarbamylase (OTC) deficiency and 19 patients with secondary carnitine deficiency, who were used as positive references. Laboratory findings indicated that all patients with OTC deficiency had secondary carnitine deficiency especially in hyperammonemic attack. After L-carnitine administration in 2 patients with OTC deficiency, the number of attacks was significantly reduced in both cases.

Amino Acid Metabolism, Inborn Errors↗
PubMed1987

Treatment of phenylketonuria with a formula consisting of low-phenylalanine peptide. A collaborative study.

A method of preparation of a more palatable therapeutic formula for phenylketonuria (PKU), consisting of low-phenylalanine peptide (LPP), was reported. There were no adverse effects and, in fact, there was a reduced frequency of diarrhea in patients who received LPP formula for more than 6 months. The LPP formula can be used not only as a more palatable therapeutic milk for PKU, but also as an ingredient to make more palatable foods of low-phenylalanine content.

Adolescent↗
PubMed1987

Altered kinetic properties of the branched-chain alpha-keto acid dehydrogenase complex due to mutation of the beta-subunit of the branched-chain alpha-keto acid decarboxylase (E1) component in lymphoblastoid cells derived from patients with maple syrup urine disease.

Branched-chain alpha-keto acid dehydrogenase (BCKDH) complexes of lymphoblastoid cell lines derived from patients with classical maple syrup urine disease (MSUD) phenotypes were studied in terms of their catalytic functions and analyzed by immunoblotting, using affinity purified anti-bovine BCKDH antibody. Kinetic studies on three cell lines derived from patients with the classical phenotype showed sigmoidal or near sigmoidal kinetics for overall BCKDH activity and a deficiency of the E1 component activity. An immunoblot study revealed a markedly decreased amount of the E1 beta subunit accompanied by weak staining of the E1 alpha subunit. The E2 and E3 component exhibited a cross-reactive peptide. Thus, in at least some patients with MSUD, mutations of the E1 beta subunit might provide an explanation for the altered kinetic properties of the BCKDH complex.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗
PubMed1987

Immunochemical studies of human prolidase with monoclonal and polyclonal antibodies: absence of the subunit of prolidase in erythrocytes from a patient with prolidase deficiency.

Prolidase was highly purified from human liver and erythrocytes. NaDodSO4/acrylamide gel electrophoresis revealed that these preparations contained a major protein with MW = 56,000. The mass of prolidase was estimated on gel filtration to be MW = 97,000, for both enzyme preparations. A monoclonal antibody was raised against the liver enzyme and a specific antiserum against the erythrocyte enzyme. The monoclonal antibody (EP-2) recognized prolidase from erythrocytes and liver, in equal proportions. The antiserum also recognized the enzyme from erythrocytes and liver. Immunoprecipitation studies with these antibodies suggested only a single species of prolidase in erythrocytes and liver. Using an immobilized monoclonal antibody (EP-2) as an immunoadsorbent, prolidase was partially purified from crude extracts, and the protein of the partially purified enzyme was identified by immunoblotting using antiserum. A protein band with a MW = 56,000 was demonstrated specifically when crude extracts from the liver and erythrocytes were examined using NaDodSO4/acrylamide gel electrophoresis. The subunit protein was absent in erythrocytes from a patient with prolidase deficiency. We propose that the absence of the subunit is one cause of the prolidase deficiency.

Antibodies, Monoclonal↗
PubMed1987

Heterogeneous phenotypes of mitochondrial encephalomyopathy in a single kindred.

Five patients with mitochondrial disorders in a single family showed marked heterogeneity of clinical signs and symptoms. Two patients had the syndrome of mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes; one had blepharoptosis, seizures, and diabetes insipidus; and two had a nonspecific encephalomyopathic disorder. This family supports the concept of a "mitochondrial cytopathy."

Acidosis, Lactic↗
PubMed1987

Possible involvement of the CCK receptor in the benzodiazepine antagonism to CCK in the mouse brain.

In mice, intraperitoneally injected chlordiazepoxide and proglumide, both of which are regarded as cholecystokinin (CCK) receptor antagonists in the peripheral tissues, dose-dependently inhibited the satiety induced by 200 ng of intracisternally administered CCK octapeptide (CCK8). Intraperitoneally administered diazepam (1 mg/kg) and/or Ro 15-1788 (5 mg/kg), a benzodiazepine antagonist, both prevented the elevation in the pain threshold induced by 1 microgram of CCK8. However, Ro 15-1788 did not antagonize the effect of diazepam that reversed the CCK-induced antinociception. Ro 15-1788 also inhibited the satiety induced by CCK8. From these results, it was considered that the antagonism, which was observed in the present work, of benzodiazepines and proglumide to CCK8 seemed to occur at the CCK receptor and not at the benzodiazepine receptor in the brain.

Animals↗