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Biomedical subjects

I Matsuda

Publications and source records attributed to I Matsuda.

At least 235 records · Page 13Linked to original sources
PubMed1991

Use of drugs during pregnancy in Japanese women.

The use of drugs during pregnancy was studied in 890 women, who were delivered of their babies in 11 obstetric departments of general hospitals in Japan, during the one month period of November 1989. Of these women, 889 (99.9%) took one or more drugs during the whole period of pregnancy and the number of drugs taken averaged 9.6. During pregnancy 172 women (19.3%) did not take drugs, and the remaining 718 (80.7%) took a total of 1766 medications. The most commonly used drugs were anti-anemic, anti-abortion medications, digestives, and antimicrobials. Bronchodilators, psychotropic agents, anticonvulsants, and steroids were each prescribed during pregnancy for about 1% of the women. Malformations were found at birth in 12 infants (1.3%). No significant relations were found between these anomalies and ingestion of particular drugs. During pregnancy, 9.3% of the women continued to smoke, and 1.9% continued to consume moderate amounts or more of alcohol. (Tab. 8, Ref. 7.)

Abnormalities, Drug-Induced↗
PubMed1991

[The influence of exercise loading for a long period on the renal function of the children with mesangial proliferative glomerulonephritis].

We have studied the influence of exercise on renal function in chronic glomerulonephritis with mesangial proliferation. The mesangial proliferative glomerulonephritis consisted of (1) IgA nephropathy (Mild group), (2) IgA nephropathy (Moderate group), (3) diffuse proliferative glomerulonephritis = DPGN (Mild group), were divided 2 groups between (A) exercise loading groups and (B) control groups, respectively. The period of observation was one or one year 6 months. None of cases deteriorated in the renal function during the period of observation were found in the exercise loading groups. The prescription of exercise for permits with mesangial proliferative glomerulonephritis indicates approximately 130 values of %BMR, which is estimated by calorie counter.

Adolescent↗
PubMed1991

Molecular basis of prolidase (peptidase D) deficiency.

Human prolidase (PEPD, iminodipeptidase, EC 3.4.13.9) and related deficiencies were analyzed in terms of the nature and molecular biology of the enzyme and the molecular events seen in patients with this deficiency. The analyses were based on findings concerning isolation of the enzyme, development of specific antibodies and molecular cloning of cDNA and genome DNA of human prolidase. The studies revealed that human prolidase is a homo-dimer of an identical subunit 492 amino acid residues. The gene for prolidase (PEPD gene) was localized on chromosome 19, spanned more than 130 x 10(3) base-pairs and split into 15 exons. Molecular defects in prolidase deficiency were then analyzed. Two patients with the polypeptide-positive phenotype of the disease carried a mis-sense mutation of exon 12. Two siblings with a polypeptide-negative phenotype carried a gene deletion that encompassed exon 14. These mutations were not found in ten other patients with the disease, hence the molecular defects in prolidase deficiency are apparently highly heterogeneous.

Base Sequence↗
PubMed1991

A murine model for type III tyrosinemia: lack of immunologically detectable 4-hydroxyphenylpyruvic acid dioxygenase enzyme protein in a novel mouse strain with hypertyrosinemia.

We have characterized a new mutant strain of mouse that has hypertyrosinemia. The blood tyrosine level was persistently high, and increased amounts of 4-hydroxyphenylpyruvic acid and its derivatives were excreted into the urine. Succinylacetone was not detected in urine samples from these mice. All the animals were apparently healthy, and there was no evidence of hepatorenal dysfunction. The hypertyrosinemia was transmitted through an autosomal recessive inheritance. Analyses of hepatic enzymes related to tyrosine metabolism revealed that 4-hydroxyphenylpyruvic acid dioxygenase activity was virtually absent, while fumarylacetoacetase and tyrosine aminotransferases (cytosolic and mitochondrial forms) were normal in these mutant mice. Immunoblot analysis of 4-hydroxyphenylpyruvic acid dioxygenase protein in the liver indicated that the subunit protein of the enzyme was absent. It would appear that hypertyrosinemia in this mutant strain was caused by a genetic defect in 4-hydroxyphenylpyruvic acid dioxygenase. These features are similar to type III tyrosinemia in humans. Analysis of this mutant strain of mouse is expected to provide valuable information on the pathogenesis of human type III tyrosinemia and can also serve as a useful system for studies on tyrosine metabolism.

4-Hydroxyphenylpyruvate Dioxygenase↗
PubMed1990

A T-to-A substitution in the E1 alpha subunit gene of the branched-chain alpha-ketoacid dehydrogenase complex in two cell lines derived from Menonite maple syrup urine disease patients.

We cloned and sequenced cDNAs of the E1 alpha and E1 beta subunits of the branched chain alpha-ketoacid dehydrogenase complex (BCKDH) in two cell lines derived from two different Menonite MSUD patients (GM 1655, GM 1099). A T-to-A substitution which generates an asparagine in place of a tyrosine at amino acid 394 of the mature E1 alpha subunit was present in both alleles in these two cell lines, whereas cDNAs of the E1 beta subunit in these cell lines were identical to that of normal human lymphoid cell line and that of the clone from a human placenta cDNA library. It is suggested that the Menonite MSUD is caused by the missense mutation of the E1 alpha subunit of the BCKDH complex.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗
PubMed1990

Structural organization of the gene for human prolidase (peptidase D) and demonstration of a partial gene deletion in a patient with prolidase deficiency.

Prolidase (peptidase D) catalyzes hydrolysis of the di- and tripeptide with carboxyl-terminal proline and plays an important role in recycling proline in various cells and tissues. By using human prolidase cDNA as a probe, a chromosomal gene related to prolidase was isolated from human gene libraries. The human prolidase gene is over 130 kilobases long and is split into 15 exons. All of the splice donor and acceptor sites conform to the GT/AG rule. The transcription initiation site was determined by nuclease S1 mapping and primer extension and was located 131 bases upstream from the initiation codon. A "CAAT" box-like sequence was present 67 bases upstream from the cap site, but there was no "TATA" box-like sequence. There were seven sets of sequences resembling the transcription factor Sp1 binding sites. Four were upstream from the cap site, and three were downstream. We also analyzed findings in patients with prolidase deficiency with respect to major gene re-arrangement. Several hundred base deletions, including the 14th exon, were identified. Knowledge of the gene structure of human prolidase will facilitate further studies on the expression and regulation of this gene and provide necessary information for analyses of mutations in patients with this deficiency.

Base Sequence↗
PubMed1990

Isolation and characterization of a complementary DNA clone coding for the E1 beta subunit of the bovine branched-chain alpha-ketoacid dehydrogenase complex: complete amino acid sequence of the precursor protein and its proteolytic processing.

A 1.7-kb cDNA clone encoding the entire precursor of the E1 beta subunit of the branched-chain alpha-ketoacid dehydrogenase (BCKDH) complex was isolated from a bovine liver cDNA library by screening with a mixture of synthetic oligonucleotide probes corresponding to the C-terminal five-residue sequence of the mature E1 beta subunit. A partial amino acid sequence was determined by Edman degradation of the intact subunit and the peptides generated by cleavage at the lysyl bonds. Nucleotide sequence analysis revealed that the isolated cDNA clone contained the 5'-untranslated sequence of 186 nucleotides, the translated sequence of 1176 nucleotides, and the 3'-untranslated sequence of 306 nucleotides with a poly(A) tail. A type AATAAA polyadenylation signal was located 17 nucleotides upstream of the start of a poly(A) tail. Comparison of the amino acid sequence predicted from the nucleotide sequence of the cDNA insert of the clone with the partial amino acid sequence of the mature BCKDH E1 beta subunit showed that the cDNA insert encodes for a 342 amino acid subunit with Mr 37,745 and that the subunit is synthesized as the precursor with a leader sequence of 50 amino acids and processed at the N-terminus. Northern blot analysis using the cDNA insert as a probe showed the presence of a 1.8-1.9-kb mRNA in bovine liver, suggesting that the insert covers nearly a full length of mRNA. Alignment of the deduced amino acid sequence of bovine BCKDH E1 beta with that of the human pyruvate dehydrogenase (PDH) complex E1 beta subunit revealed a high degree of sequence homology throughout the two enzymes.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗
PubMed1990

A disease with immune deficiency, skin abscesses, pancytopenia, abnormal bone marrow karyotype, and increased sister chromatid exchanges: an autosomal recessive chromosome instability syndrome?

A 19-year-old girl is described with microcephaly, short stature, mental retardation, pigmentation of the skin, and recurrent skin abscesses over the whole body. Her elder brother and sister both showed growth and developmental retardation, microcephaly, and anemia. Both died during childhood. Their parents were first cousins. Laboratory studies of the proband revealed hyperchromic erythrocytes with an increased HbF content, thrombocytopenia, an impaired mitogenic response of the PHA-stimulated lymphocytes, and partial impairment of humoral and cellular immunity. She developed pancytopenia in the terminal stage of the disease. Cytogenetic studies of the bone marrow revealed 46,XX, 15p+, -18, +mar karyotype, increased chromosomal aberrations and sister chromatid exchanges, in cultured lymphocytes and skin fibroblasts. She died at age 20. Thus, the disorder in the patient was deduced as an unclassified chromosomal breakage syndrome with an apparently autosomal recessive inheritance.

Abscess↗
PubMed1990

Superoxide dismutase activity and chromosome damage in cultured chromosome instability syndrome cells.

The basal levels of superoxide dismutase (SOD) activity and chromosome aberration (CA) and sister-chromatid exchange (SCE) frequencies were examined in cultured fibroblasts or Epstein-Barr virus (EBV)-transformed lymphoblastoid cell lines (LCLs). These cells were derived from patients with chromosome instability syndromes (CISs) including Bloom's syndrome (BS), Fanconi's anemia (FA) and ataxia telangiectasia (AT). Embryonal fibroblasts and LCLs from normal subjects served as controls. Although LCLs tended to exhibit a higher SOD level than fibroblasts due to an elevation of Cu/Zn-SOD activity, BS and FA fibroblasts with increased frequencies of CAs and/or SCEs showed abnormally elevated SOD activity due to the manifold increase of Mn-SOD levels compared with control cells. However, BS and AT LCLs with almost control levels of CA and SCE frequencies showed no, or a slightly elevated, SOD activity, suggesting a possible selection of such cells during EBV transformation. The observed parallelism between the SOD activity and the cytogenetic manifestation may imply an involvement of active oxygen species, especially superoxide radicals, in the increased chromosome damage of CIS cells.

Ataxia Telangiectasia↗
PubMed1990

Effect of extradural compliance and resistance on spread of extradural analgesia.

We have studied the effect of extradural compliance and extradural resistance on the spread of extradural analgesia. In 111 patients aged 21-75 yr, compliance and resistance of the extradural space were calculated by a mathematical analysis (using the Windkessel theory) of the extradural pressure-response curve to injection of a given volume of local anaesthetic. The calculated mean extradural compliance was 0.39 (SD 0.13) ml mm Hg-1 and this increased with advancing age (P less than 0.01). The total number of analgesic segments blocked was related to extradural compliance (P less than 0.01). Segmental dose requirement was related inversely to extradural compliance (P less than 0.01). Calculated extradural resistance was 26.8 (14.5) mm Hg s ml-1 and this decreased with advancing age (P less than 0.05). The total number of analgesic segments blocked was related inversely to extradural resistance (P less than 0.05). Segmental dose requirement was related to extradural resistance (P less than 0.05).

Adult↗