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Biomedical subjects

M Yoshida

Publications and source records attributed to M Yoshida.

At least 1,225 records · Page 68Linked to original sources
PubMed1995

Mutations in the dystrophin-associated protein gamma-sarcoglycan in chromosome 13 muscular dystrophy.

Severe childhood autosomal recessive muscular dystrophy (SCARMD) is a progressive muscle-wasting disorder common in North Africa that segregates with microsatellite markers at chromosome 13q12. Here, it is shown that a mutation in the gene encoding the 35-kilodalton dystrophin-associated glycoprotein, gamma-sarcoglycan, is likely to be the primary genetic defect in this disorder. The human gamma-sarcoglycan gene was mapped to chromosome 13q12, and deletions that alter its reading frame were identified in three families and one of four sporadic cases of SCARMD. These mutations not only affect gamma-sarcoglycan but also disrupt the integrity of the entire sarcoglycan complex.

Amino Acid Sequence↗
PubMed1995

Mucopolysaccharidosis type VI in rats: isolation of cDNAs encoding arylsulfatase B, chromosomal localization of the gene, and identification of the mutation.

Mucopolysaccharidosis (MPS) type VI, the lysosomal storage disorder caused by the deficiency of arylsulfatase B (ARSB) activity, occurs in humans, cats, and rats. To characterize the molecular lesion(s) causing MPS VI in rats, cDNAs encoding rat ARSB were isolated from a rat liver cDNA library. The nucleotide and deduced amino acid sequences of rat ARSB had approximately 80 and 85% identity with the human ARSB sequences, respectively. The chromosomal location of the rat ARSB gene was determined by PCR analysis of rat-mouse somatic cell hybrid panel. The ARSB gene was assigned to rat chromosome 2, where the locus for the MPS VI phenotype in rats has been localized by linkage analysis. To identify the mutation(s) within the ARSB gene causing MPS VI in rats, the ARSB sequence were amplified from affected animals and completely sequenced. Notably, a homoallelic one-base insertion at nucleotide 507 (507insC) was identified, resulting in a frame shift mutation and premature termination at codon 258. The presence of the insertion completely correlated with the occurrence of the MPS VI phenotype among 66 members of the MPR rat colony. Thus, we conclude that 507insC is the causative mutation in these animals and that the MPS VI rats are an authentic model of human MPS VI.

Amino Acid Sequence↗
PubMed1995

Analysis of time-dependent change of Escherichia coli F1-ATPase activity and its relationship with apparent negative cooperativity.

Except for the case of gradual activation of EF1 (F1-ATPase from Escherichia coli) caused by the dissociation of the epsilon subunit [Laget, P. P. and Smith, J. B. (1979) Arch. Biochem. Biophys. 197, 83-89], EF1 has long been thought not to show a time-dependent change in activity [Senior, A.E. et al. (1992) Arch. Biochem. Biophys. 297, 340-344]. Here, we report the time-dependent inactivation and activation of EF1, which are apparently similar to those of mitochondrial F1-ATPases [Vasilyeva, E.A. et al. (1982) Biochem. J. 202, 15-23]. Analysis of these changes as a function of ATP concentrations in relation to negative cooperativity revealed that the initial inactivation phase was attributable to the decrease in the Vmax associated with the low Km (around 10 microM), and the following activation, probably due to the dissociation of the epsilon subunit, corresponded to the increase in the Vmax associated with the high Km (in the order of 100 microM). Thus, the time-dependent change in EF1 activity is closely related to the apparent negative cooperativity (multiple Km values) of ATP hydrolysis.

Adenosine Triphosphate↗
PubMed1995

A histologically distinctive interstitial pneumonia induced by overexpression of the interleukin 6, transforming growth factor beta 1, or platelet-derived growth factor B gene.

Interstitial pneumonia is characterized by alveolitis with resulting fibrosis of the interstitium. To determine the relevance of humoral factors in the pathogenesis of interstitial pneumonia, we introduced expression vectors into Wistar rats via the trachea to locally overexpress humoral factors in the lungs. Human interleukin (IL) 6 and IL-6 receptor genes induced lymphocytic alveolitis without marked fibroblast proliferation. In contrast, overexpression of human transforming growth factor beta 1 or human platelet-derived growth factor B gene induced only mild or apparent cellular infiltration in the alveoli, respectively. However, both factors induced significant proliferation of fibroblasts and deposition of collagen fibrils. These histopathologic changes induced by the transforming growth factor beta 1 and platelet-derived growth factor B gene are partly akin to those changes seen in lung tissues from patients with pulmonary fibrosis and markedly contrast with the changes induced by overexpression of the IL-6 and IL-6 receptor genes that mimics lymphocytic interstitial pneumonia.

Adenoviridae↗
PubMed1995

Expression of the wild-type and the Cys-/Trp-less alpha 3 beta 3 gamma complex of thermophilic F1-ATPase in Escherichia coli.

The alpha, beta and gamma subunits of F1-ATPase from thermophilic Bacillus PS3 were expressed in Escherichia coli cells simultaneously in large amounts. Most of the expressed subunits assembled into a form of alpha 3 beta 3 gamma complex in E. coli cells and this complex was easily purified to homogeneity. The recombinant alpha 3 beta 3 gamma complex thus obtained showed similar enzymatic properties to the alpha 3 beta 3 gamma complex obtained by in vitro reconstitution from individual subunits (Yokoyama, K. et al. (1989) J. Biol. Chem. 264, 21837-21841) except that the former had several-fold higher ATPase activity than the latter. Using this expression system, a mutant alpha 3 beta 3 gamma complex with no Trp and Cys was generated by replacing alpha Cys193 and alpha Trp463 with Ser and Phe, respectively. This mutant complex was functionally intact, indicating both residues are not essential for catalysis. The Cys-/Trp-less complex is a convenient 'second wild type' enzyme from which one can generate mutants with Trp (as a fluorescent probe) or Cys (as an acceptor of a variety of probes) at desired positions without concern for 'background' Trp and Cys residues.

Bacillus↗
PubMed1995

Expression of Fas/Apo-1 (CD95) and apoptosis in tumor cells from patients with plasma cell disorders.

Fas/Apo-1 antigen (CD95) is a cell surface molecule that directly mediates apoptosis. Fas expression was studied in five plasma cell lines, 11 multiple myeloma cases, and three plasma cell leukemia (PCL) cases. Induction of apoptosis by anti-Fas antibody was studied in five plasma cell lines and fresh plasma cells from eight patients. Apoptosis was confirmed by morphologic analysis alone or in combination with DNA electrophoresis analysis. Four of the five cell lines showed Fas expression, three of which showed induction of apoptosis by anti-Fas antibody. One cell line, RPMI 8226, showed the highest sensitivity for Fas-mediated apoptosis. High bcl-2 expression was found in KMS12PE, which showed resistance to Fas-mediated apoptosis despite its Fas expression. Plasma cells from seven fresh cases, including all five cases with high serum lactate dehydrogenase (LDH), showed expression of Fas antigen. Fas-induced apoptosis was found in five cases at various levels, although significant induction of apoptosis was found in only one case. Interestingly, Fas-independent apoptosis was induced during culture without anti-Fas antibody in cases with high serum LDH. These results indicate that plasma cells from aggressive myeloma with high LDH express Fas antigen and undergo apoptosis through either Fas-mediated or Fas-independent pathways. An understanding of the mechanism of apoptosis in malignant plasma cells should contribute to investigations of the pathophysiology of and therapy for myeloma/PCL.

Adult↗
PubMed1995

Kinetic analysis of interactions between GroEL and reduced alpha-lactalbumin. Effect of GroES and nucleotides.

The real-time analysis of the association and dissociation of chaperonin with respect to its substrate protein was carried out using the BIAcore system. We immobilized alpha-lactalbumin (LA) as a substrate protein on the sensor chip and the GroEL solution was passed over it. Whereas GroEL did not bind to the immobilized native LA, it associated with the immobilized Ca(2+)-depleted, disulfide bond-reduced form of LA (rLA) rapidly (kon = 1.96 x 10(5) M-1 S-1) and dissociated extremely slowly (koff = 2.08 x 10(-4) S-1), giving a low dissociation constant (KD = 1.06 nM). MgATP greatly accelerated the dissociation (koff = 0.15 +/- 0.02 S-1). The KD value remained almost unchanged when GroES and/or 10 microM ADP was included in the GroEL solution. However, when 1 mM ADP was included, the KD value of GroEL increased by 2 orders of magnitude solely due to the change in koff. When GroES and 1 mM ADP were included, no interaction with rLA was detected due to changes in both kon and koff. These results indicate that GroEL/ES has high and low affinity ADP binding sites and that occupation of the low affinity sites by ADP was responsible for the loss of ability to interact with the substrate protein. The effect of excess GroES on the preformed GroEL.rLA and GroEL/ES.rLA complexes was also examined. With increasing GroES, the dissociation of GroEL and GroEL/ES from rLA was accelerated, and thus the possibility is suggested that the substrate protein and GroES compete for the same site on GroEL.

Adenine Nucleotides↗
PubMed1995

Induction of endometrial adenocarcinomas by a single intra-uterine administration of N-ethyl-N'-nitro-N-nitrosoguanidine to aged Donryu rats showing spontaneously persistent estrus.

Induction of endometrial adenocarcinomas by a single intra-uterine administration of N-ethyl-N'-nitro-N-nitrosoguanidine (ENNG) to aged rats was examined. Donryu rats showing spontaneously persistent estrus were given a single intra-uterine administration of ENNG (20 mg/kg) at 10 months (44 weeks) of age. At the termination of the experiment (week 34 after the ENNG-treatment), 22% and 13% incidences of endometrial adenocarcinomas were observed in the experimental and control groups, respectively, the difference being without significance. No variation was found in the endocrine environment between experimental and non carcinogen-treated control animals throughout the experimental period. These results show that ENNG-treatment alone is not sufficient in aged rats for high induction of endometrial carcinomas. Comparison of the data with those from our previous studies, in which ENNG was given at a young age (10 weeks of age), indicates that young rats may be more sensitive than their old counterparts.

Adenocarcinoma↗
PubMed1995

Spinal and parachordal neurons in the eel leptocephali, Anguilla japonica revealed by labeling with a fluorescent dye.

The spinal and parachordal neurons innervating the trunk muscles and skin in the Japanese eel leptocephali, Anguilla japonica, were retrogradely labeled with a fluorescent dye, DiI (1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate). The spinal motoneurons innervating the trunk muscles were located in the medioventral part of the spinal cord and were divided into two populations on the basis of their soma sizes and position. The sensory neurons were labeled in the well-developed dorsal root ganglia, that were situated just peripheral to the meeting of the dorsal and ventral roots. Presumable postganglionic sympathetic neurons were also labeled in the sympathetic ganglia which were located ventrally to the notochord. Thus, the spinal and parachordal neurons innervating the trunk muscles and skin were firstly identified in the anguilliform leptocephalus.

Anguilla↗
PubMed1995

A K-252a-resistance gene, sks1+, encodes a protein similar to the Caenorhabditis elegans F37 A4.5 gene product and confers multidrug resistance in Schizosaccharomyces pombe.

A gene named sks1+ was cloned as a suppressor of the K-252a-sensitivity phenotype of Schizosaccharomyces pombe (Sp) from a gene library of the parental Sp chromosomal DNA constructed with a multicopy vector pDB248'. The gene encoded a 308-amino-acid (aa) protein similar to the Caenorhabditis elegans F37 A4.5 gene product and to the mouse and Drosophila Mov34 gene products. The sks1+ null mutants obtained by gene disruption were non-viable, indicating that sks1+ is essential for vegetative growth. The parental Sp strain carrying multiple copies of sks1+ showed distinct cross-resistance to staurosporine, thiabendazole and vanadate in addition to K-252a, although Sks1 has no similarity in aa sequence to those of ATP-binding cassette (ABC)-type transporters. The multicopy plasmid containing sks1+ conferred multidrug resistance (MDR), even in a mutant cell defective in pmd1+ encoding an ABC-type transporter. It is therefore unlikely that the function of pmd1+ is involved in MDR conferred by sks1+. These results suggest that sks1+ is a functionally novel MDR gene.

Amino Acid Sequence↗
PubMed1995

Detection of 1-phenyl-N-methyl-1,2,3,4-tetrahydroisoquinoline and 1-phenyl-1,2,3,4-tetrahydroisoquinoline in human brain by gas chromatography-tandem mass spectrometry.

1-Phenyl-N-methyl-1,2,3,4-tetrahydroisoquinoline and 1-phenyl-1,2,3,4-tetrahydroisoquinoline were detected for the first time in parkinsonian human brain using gas chromatography-tandem mass spectrometry (GC-MS-MS). Since these compounds are structural analogues of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) that produces parkinsonism in humans, they might be candidates for endogenous MPTP-like neurotoxins.

Aged↗
PubMed1995

Transition from ischemic neuronal necrosis to infarction in repeated ischemia.

To study morphological changes in the cortex that follow repeated ischemia, one, two, and three 7-min unilateral occlusions of the carotid artery at 6-h intervals, and three, four, and five 7-min similar occlusions at 12-h intervals were produced in gerbils. Animals with one and two 7-min occlusions at 6-h intervals showed selective neuronal necrosis in the cortex; those with three 7-min occlusions at 6-h intervals showed focal infarction in the third layer of the cortex. Animals with three 7-min occlusions at 12-h intervals showed selective neuronal necrosis; those with four 7-min occlusions at 12-h intervals showed focal infarction in the third layer. In animals with five 7-min occlusions at 12 h intervals, infarction affecting all layers of the cortex was seen. Results of the present study indicate that cortical infarction occurred when a brief ischemic insult that does not cause any visible morphological damage in cortical neurons was inflicted repeatedly, and that development of infarction in the cortex following repeated episodes of ischemia depended on both the number of insults and the time intervals between them. This finding suggests that there is a threshold of infarction in repeated ischemia. In our model, various stages of ischemic brain injury could be achieved more easily than in transient ischemia by altering the number of insults or the intervals between them. This model is suitable for studying the pathophysiology on transition from ischemic neuronal necrosis to infarction.

Animals↗
PubMed1995

A minimum catalytic unit of F1-ATPase shows non-cooperative ATPase activity inherent in a single catalytic site with a Km 70 microM.

F1-ATPase has three interacting catalytic sites and shows complicated kinetics. Here, we report reconstitution of a complex, most likely composed of one alpha subunit and one beta subunit, with a single catalytic site from thermophilic Bacillus PS3 F1-ATPase on the solid surface. The complex has an ATPase activity which obeys a simple non-cooperative kinetics with a Km(ATP) of 70 microM and a Vmax of 0.1 unit/mg. Different from F1-ATPase, the complex is not inactivated by 7-chrolo-4-nitrobenzofrazan. Thus, the inherent activity attributable to a single catalytic site unaffected by other catalytic sites of F1-ATPase is characterized.

4-Chloro-7-nitrobenzofurazan↗
PubMed1995

Dystrophin-associated protein A0 is a homologue of the Torpedo 87K protein.

We raised a monoclonal antibody, MA0, which reacts with A0, a 94-kDa rabbit skeletal muscle dystrophin-associated protein (DAP) bound to the syntrophin-binding domain of dystrophin. The antibody also reacted with the 62-kDa DAP which was moved to the locus close to beta-syntrophins by 2-dimensional PAGE, but the DAP did not coincide with any known beta-syntrophins. We have cloned a fragment of cDNA which codes the protein reacting with MA0 from a neonatal rabbit heart cDNA library. Based on the coincidence of cDNA sequences and the similarity in molecular mass, we concluded that the proteins reacting with MA0 are rabbit homologues of the Torpedo 87K protein.

Amino Acid Sequence↗
PubMed1995

Repression of cell cycle progression by antisense HMG2 RNA.

The expression level of the HMG2 gene during the cell cycle of rat fibroblast cell lines was analyzed. Northern analysis demonstrated that the level of HMG2 mRNA was markedly enhanced in the post-S phase and reached a maximum at G2 phase, suggesting that expression of the HMG2 gene is not coupled with DNA synthesis. Progression of the cell cycle of COS-1 cells was repressed during G1 to S phase by expression of the antisense RNA for HMG2, resulting in a decrease of cell growth. These results suggest that the fluctuation of the HMG2 message during the cell cycle is not a consequence of but a prerequisite for cell proliferation.

Animals↗