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Biomedical subjects

Y Matsuda

Publications and source records attributed to Y Matsuda.

At least 451 records · Page 25Linked to original sources
PubMed1996

EI-1507-1 and -2, novel interleukin-1 beta converting enzyme inhibitors produced by Streptomyces sp. E-1507.

EI-1507-1 and -2, novel interleukin-1 beta converting enzyme (ICE) inhibitors, were isolated from the culture broths of Streptomyces sp. E-1507. EI-1507-1 and EI-1507-2 selectively inhibited the recombinant human ICE activity with IC50 values of 0.23 and 0.42 microM, respectively. EI-1507-1 and EI-1507-2 also inhibited mature interleukin-1 beta secretion from THP-1 cells with IC50 values of 1.1 and 1.4 microM, respectively.

Amino Acid Sequence↗
PubMed1996

[The perinatal risk factors and periventricular leukomalacia (PVL) in premature infants--relationship between fetal heart rate decelerations and PVL].

Periventricular leukomalacia (PVL) has recently been recognized as an important risk factor of neurological impairment in premature infants. We studied 29 PVL cases on perinatal risk factors comparing with a non-PVL matched control group retrospectively. Variable decelerations were more frequently observed with statistical significance in the PVL group in the intrapartum period. Then another study was conducted to evaluate the relationship between fetal heart rate (FHR) decelerations and cystic PVL prospectively. Since January 1993 through December 1994 we studied 209 low birth weight infants (31.1 +/- 3.2 weeks, 1,424 +/- 419 g) who had been subjected to intrapartum FHR monitoring and postnatal sonographic intracranial examinations sequentially every 7 days until discharge. Cystic PVL was detected in 6 of 209 cases (2.9%) and occurred only in infants who had revealed severe variable deceleration or prolonged deceleration (6/37, 16%) in intrapartum FHR monitoring. We conclude that in low birth weight infants intrapartum severe variable deceleration or prolonged deceleration might play a causal role in cystic PVL.

Bradycardia↗
PubMed1996

Localization of choline acetyltransferase and calcitonin gene-related peptide immunoreactivities in the vestibular end-organs of the guinea pig.

The localization of choline acetyltransferase (ChAT) and calcitonin gene-related peptide (CGRP) immunoreactivities in the vestibular end-organs of the guinea pig was examined using immunohistochemistry. A large number of ChAT immunoreactive (ChAT-IR) terminals were found adjacent to the base of vestibular sensory cells. ChAT-IR terminals frequently formed synapses with the chalices of afferent nerves receiving synaptic inputs from type I cells and also formed direct contacts with type II cells. ChAT-IR terminals were filled with small clear vesicles, indicating that they are associated with the vestibular efferent system. All the vestibular efferent terminals were identified to be ChAT immunoreactive by electron microscopy. On the other hand, vestibular efferent terminals did not always show CGRP immunoreactivity. CGRP-immunoreactive (CGRP-IR) efferent terminals frequently made synaptic contacts with the chalices and type II cells. These results suggest that acetylcholine (ACh) and CGRP frequently coexist in the vestibular efferent system and may participate in the regulation of the vestibular function.

Animals↗
PubMed1995

Isolation and characterization of a pseudoautosomal region-specific genetic marker in C57BL/6 mice using genomic representational difference analysis.

Representational difference analysis was used to identify strain-specific differences in the pseudoautosomal region (PAR) of mouse X and Y chromosomes. One second generation (C57BL/6 x Mus spretus) x Mus spretus interspecific backcross male carrying the C57BL/6 (B6) PAR was used for tester DNA. DNA from five backcross males from the same generation that were M. spretus-type for the PAR was pooled for the driver. A cloned probe designated B6-38 was recovered that is B6-specific in Southern analysis. Analysis of genomic DNA from several inbred strains of laboratory mice and diverse Mus species and subspecies identified a characteristic Pst I pattern of fragment sizes that is present only in the C57BL family of strains. Hybridization was observed with sequences in DBA/2J and to a limited extent with Mus musculus (PWK strain) and Mus castaneus DNA. No hybridization was observed in DNA of different Mus species, M. spretus, M. hortulanus, and M. caroli. Genetic analyses of B6-38 was conducted using C57BL congenic males that carry M. spretus alleles for distal X chromosome loci and the PAR and outcrosses of heterozygous congenic females with M. spretus. These analyses demonstrated that the B6-38 sequences were inherited with both the X and Y chromosome. B6-38 sequences were genetically mapped as a locus within the PAR using two interspecific backcrosses. The locus defined by B6-38 is designated DXYRp1. Preliminary analyses of recombination between the distal X chromosome gene amelogenin (Amg) and the PAR loci for either TelXY or sex chromosome association (Sxa) suggest that the locus DXYRp1 maps to the distal portion of the PAR.

Animals↗
PubMed1995

Biochemical and pharmacological studies with KT7692 and LY294002 on the role of phosphatidylinositol 3-kinase in Fc epsilon RI-mediated signal transduction.

Wortmannin inhibited phosphatidylinositol 3-kinase (P13-kinase) and Fc epsilon RI-mediated histamine secretion in RBL-2H3 cells to a similar degree, with IC50 values of 3 and 2 nM, respectively. Although P13-kinase is an acknowledged regulator of intracellular trafficking and secretion, wortmannin has proved to be a difficult drug to use in assessing the role of P13-kinase because it inhibits another important enzyme, myosin light-chain kinase (MLCK; IC50 = 200 nM). In the present study we synthesized a unique derivative of wortmannin, O-acetyl-delta 16-wortmannin-17-ol (KT7692), that has an inhibitory potency against PI3-kinase one-hundredth that of wortmannin, but retains a similar potency to wortmannin against MLCK. Histamine secretion was influenced 100-fold more by wortmannin than by KT7692.2-(4-Morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (LY294002), a structurally different PI3-kinase inhibitor from wortmannin, inhibited PI3-kinase with an IC50 of 2 microM but had little effect on MLCK activity in this concentration range. LY294002 also inhibited histamine secretion in RBL-2H3 cells with an IC50 of 5 microM. These results provide further evidence that PI3-kinase is involved in the signal transduction pathway responsible for histamine secretion after stimulation of Fc epsilon RI. Furthermore KT7692 in combination with wortmannin and LY294002 would be a powerful tool for clarifying the involvement of PI3-kinase as distinct from that of MLCK in signal transduction systems of various cellular responses.

Androstadienes↗
PubMed1995

Atlanto-occipital hypermobility in subjects with Down's syndrome.

STUDY DESIGN: The upper cervical spines of 57 subjects with Down's syndrome were retrospectively examined, with special attention to atlanto-occipital mobility. OBJECTIVE: To examine the magnitude of atlanto-occipital mobility and its clinical significance in subjects with Down's syndrome. SUMMARY OF BACKGROUND DATA: Atlanto-occipital translation of more than 1 mm in adults implies instability. However, the normal value in children with Down's syndrome has not been established, and the value in Down's syndrome has not been evaluated based on a comparison between subjects with Down's syndrome and control subjects. METHODS: Measurements were made by Wiesel and Rothman's method in 38 subjects with Down's syndrome and 34 control subjects. RESULTS: Atlanto-occipital translation in the Down's syndrome group ranged from 0-6.4 mm (mean, 2.3 mm), whereas in the control group it ranged from 0-2.1 mm (mean, 0.61 mm). The difference was statistically significant. Of the 38 subjects with Down's syndrome, 37 were asymptomatic. CONCLUSION: The magnitude of atlanto-occipital translation, as expected, apparently was greater in subjects with Down's syndrome than in control subjects. Although the possibility of neurologic complications should be considered whenever unusually high atlanto-occipital mobility is seen, a majority of the subjects with Down's syndrome were asymptomatic.

Adolescent↗
PubMed1995

Genomic cloning and chromosomal assignment of rat regucalcin gene.

The gene for a Ca(2+)-binding protein regucalcin was cloned from a rat genomic library which was constructed in lambda FIX II by screening with radiolabeled probe (complementary DNA of rat liver regucalcin). Positive clone had 19.9 kb insert of size and contained four exons of the gene coding for a rat regucalcin. These exons included the partial coding sequence (61.2% of open reading frame) and the entire 3'-untranslated region of the gene. The nucleotide sequence of exons completely agreed with that of a rat regucalcin cDNA clone. The sequence analysis of the clone showed that the identifier sequence and two simple repeated sequences exist in the intron of the gene. Moreover, chromosomal location of the rat regucalcin gene was determined by direct R-banding fluorescence in situ hybridization (FISH) method with the 19.9 kb clone containing four exons. The regucalcin gene was localized on rat chromosome Xq11.1-12 proximal end.

Amino Acid Sequence↗
PubMed1995

An inhibitory role for phosphatidylinositol 3-kinase in insulin secretion from pancreatic B cell line MIN6.

Phosphatidylinositol 3-kinase (PI3-kinase) has been implicated in the regulation of vesicular transport. We examined the roles of PI3-kinase in the glucose-induced insulin secretion from the pancreatic beta cell line MIN6 by using wortmannin, a potent inhibitor of PI3-kinase. Low concentrations of wortmannin markedly potentiated the glucose-induced insulin secretion. This effect was probably mediated by PI3-kinase inhibition. Furthermore, wortmannin completely canceled the suppressive effect of insulin-like growth factor-I on insulin secretion from MIN6 cells. On the basis of these results, we discuss a possible role of PI3-kinase in the negative feed-back regulation of insulin secretion.

Androstadienes↗
PubMed1995

Complementary DNA sequence and chromosomal localization of xpg, the mouse counterpart of human repair gene XPG/ERCC5.

We have molecularly cloned and sequenced the mouse counterpart of the human repair gene XPG/ERCC5 cDNA. The mouse xpg cDNA had a single long open reading frame predicted to encode 1170 amino acid residues (predicted M(r) of 130,753). Northern blot analysis has been carried out to determine the size and tissue transcription specificity of the mouse xpg mRNA. The xpg gene expressed one species of transcript with 4.3 kb at similar levels in five mouse tissues examined. We have determined the chromosomal location of the xpg gene by both in situ hybridization and molecular linkage analysis. The xpg gene was localized at 2.3 cM proximal to the microsatellite locus D1Mit18 on the R-positive B band of mouse chromosome 1. By in situ hybridization with the mouse xpg probe, the rat homolog of the mouse xpg was localized on q22.3 band of rat chromosome 9, which has been known to have a conserved linkage homology to mouse chromosome 1. In the case of human, the XPG/ERCC5 gene has been reported to be assigned to human chromosome 13q32.3-q33.1, where any conserved linkage homology to mouse chromosome 1 has not been found so far. Thus, these results show new regions of conserved linkage homology among mouse chromosome 1, rat chromosome 9, and human chromosome 13q.

Amino Acid Sequence↗
PubMed1995

Construction of YAC contigs at human chromosome 11q22.3-q23.1 region covering the Ataxia telangiectasia locus.

Ataxia telangiectasia (AT) is an autosomal recessive disease of unknown etiology associated with cerebellar ataxia, telangiectasia, immune dysfunction, higher cancer risk, genomic instability and hypersensitivity to ionizing radiation. The major AT loci, AT-A and AT-C, are shown to be closely linked at chromosome 11q22-q23. The most recent genetic linkage mapping and linkage disequilibrium analysis have localized the major AT loci to a sequence of approximately 850 kb between the markers D11S1819 and D11S1818. The isolation of yeast artificial chromosomes spanning the AT region is an essential step to identify the gene or genes responsible for the mutation(s). We isolated a total of 20 YAC clones from three independent YAC libraries, using sequence tagged sites mapped in the AT region as primers for PCR-based YAC screening. The PCR assay for the presence or absence of 16 different DNA markers allowed us to construct and to order four YAC contigs at the AT region. One of the contigs which consists of the 10 YAC clones, covers about 2 Mb of DNA at the boundary between Giemsa-positive band 11q22.3 and Giemsa-negative band 11q23.1 and includes the entire region of the major AT locus between D11S1819 and D11S1818. Thus, the YAC contigs will facilitate the positional cloning approach for searching transcribed sequences from the defined genomic region.

Ataxia Telangiectasia↗
PubMed1995

Isolation and characterization of mutants affected in lipid metabolism of Chlamydomonas reinhardtii.

Two mutants affected in lipid metabolism of Chlamydomonas reinhardtii were isolated by treating cells with ultraviolet light. Both mutants showed high chlorophyll fluorescent yields, as compared with parents, and were designated as hf-2 and hf-9 (for high fluorescence). hf-2 was shown to be defective in the synthesis of a chloroplast-specific lipid, sulfoquinovosyl diacylglycerol. hf-9 was shown to be defective in desaturation at the omega 6 position of fatty acids of monogalactosyl diacylglycerol, digalactosyl diacylglycerol, sulfoquinovosyl diacylglycerol and phosphatidylglycerol. The mutants exhibited alterations in photosynthetic activity and chloroplast ultrastructure.

Animals↗
PubMed1995

Coupling of the endothelin ETA and ETB receptors to Ca2+ mobilization and Ca2+ sensitization in vascular smooth muscle.

Effects of endothelins on cytosolic Ca2+ level ([Ca2+]i) and contraction were examined in the swine pulmonary artery and vein. In the artery, endothelin-1 and endothelin-3, but not sarafotoxin S6c and IRL 1620 (300 nM each), induced transient increase followed by sustained increase in [Ca2+]i and sustained contraction. These effects were inhibited by the ETA receptor antagonist, BQ-123. In the vein, endothelin-1 and endothelin-3 (300 nM each) induced sustained increase in [Ca2+]i and sustained contraction whereas sarafotoxin S6c and IRL 1620 (300 nM each) transiently increased both [Ca2+]i and contractile tension. The ETB receptor in the vein was desensitized by pretreatment with sarafotoxin S6c, abolishing the effects of sarafotoxin S6c and IRL 1620 without changing the effects of endothelin-1 and endothelin-3. In contrast, an ETB antagonist, RES-701-1, antagonized the effects of IRL 1620 without changing the effects of other stimulants. In both artery and vein, the maximum contraction induced by these stimulants was greater than that induced by KCl at a given [Ca2+]i. In the absence of external Ca2+, endothelin-1 and endothelin-3 induced transient increase in [Ca2+]i and slow sustained contraction in both artery and vein. In the vein, sarafotoxin S6c induced small sustained contraction without changing [Ca2+]i. In the permeabilized artery and vein, endothelin-1 augmented the contraction induced by Ca2+. These results suggest that the ETA receptors in the artery and vein are coupled to Ca2+ release (which does not seem to trigger contraction), Ca2+ influx and Ca2+ sensitization.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Characterization of mouse and human GTP cyclohydrolase I genes. Mutations in patients with GTP cyclohydrolase I deficiency.

GTP cyclohydrolase I is the first and rate-limiting enzyme for the biosynthesis of tetrahydrobiopterin in mammals. Previously, we reported three species of human GTP cyclohydrolase I cDNA in a human liver cDNA library (Togari, A., Ichinose, H., Matsumoto, S., Fujita, K., and Nagatsu, T. (1992) Biochem. Biophys. Res. Commun. 187, 359-365). Furthermore, very recently, we found that the GTP cyclohydrolase I gene is causative for hereditary progressive dystonia with marked diurnal fluctuation, also known as DOPA-responsive dystonia (Ichinose, H., Ohye, T., Takahashi, E., Seki, N., Hori, T., Segawa, M., Nomura, Y., Endo, K., Tanaka, H., Tsuji, S., Fujita, K., and Nagatsu, T. (1994) Nature Genetics 8, 236-242). To clarify the mechanisms that regulate transcription of the GTP cyclohydrolase I gene and to generate multiple species of mRNA, we isolated genomic DNA clones for the human and mouse GTP cyclohydrolase I genes. Structural analysis of the isolated clones revealed that the GTP cyclohydrolase I gene is encoded by a single copy gene and is composed of six exons spanning approximately 30 kilobases. We sequenced all exon/intron boundaries of the human and mouse genes. Structural analysis also demonstrated that the heterogeneity of GTP cyclohydrolase I mRNA is caused by an alternative usage of the splicing acceptor site at the sixth exon. The transcription start site of the mouse GTP cyclohydrolase I gene and the 5'-flanking sequences of the mouse and human genes were determined. We performed regional mapping of the mouse gene by fluorescence in situ hybridization, and the mouse GTP cyclohydrolase I gene was assigned to region C2-3 of mouse chromosome 14. We identified missense mutations in patients with GTP cyclohydrolase I deficiency and expressed mutated enzymes in Escherichia coli to confirm alterations in the enzyme activity.

Amino Acid Sequence↗