Biomedical subjects
M Matsuo
Publications and source records attributed to M Matsuo.
[Urinary hydroxy-proline in patients with urolithiasis].
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[Basic studies on the cause of urolithiasis. I. Stone producing substances and experimental stone formation with administration of drugs].
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[Basic studies on the cause of urolithiasis. II. Experimental foreign body stone formation].
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Basic studies on the cause of urolithiasis. 3. Role of urinary citrate in urolithiasis.
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Biosynthesis of lichen depsides, lecanoric acid and atranorin.
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Biosynthesis of sinigrin. II.
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p53 adenoviral vector (Ad-CMV-p53) induced prostatic growth inhibition of primary cultures of human prostate and an experimental rat model.
BACKGROUND: Benign prostatic hyperplasia (BPH) is the most common proliferative disease affecting men. Numerous minimally invasive technologies are being developed or are currently in use to obviate the need for transurethral surgery. The goal of the present study was to develop a novel molecular based approach for the treatment of BPH using recombinant p53 adenoviral vector. The over-expression of wt-p53 can cause cell apoptosis or cell growth arrest, thus preventing the uncontrolled cell proliferation underlying BPH pathophysiology. METHODS: Ad-CMV-p53, a replication-deficient recombinant adenovirus containing cytomegalovirus promoter driving p53 gene, was used. Human prostate stromal (PS) cells were evaluated for apoptosis (TUNEL assay), mRNA levels of key cell cycle regulators influencing apoptosis (p-53, Bax and Bcl-2) using quantitative RT-PCR and cytotoxicity after Ad-CMV-p53. Ad-CMV-p53 was unilaterally injected into rat ventral prostates and growth inhibition was measured by prostate weight 3 weeks after injection. RESULTS: In vitro exposure to Ad-CMV-p53 significantly inhibited the proliferation of PS cells, induced mRNA over-expression of both wt-p53 and Bax, and increased the proportion of apoptotic cells. A 30% decrease in average prostate weight was demonstrated in rodents after Ad-CMV-p53 injection. CONCLUSIONS: The results suggest that further investigation of molecular gene therapy with recombinant wt-p53 adenovirus for the treatment of BPH is warranted.
Confluent hepatic fibrosis in cirrhosis: ferumoxides-enhanced MR imaging findings.
We describe ferumoxides-enhanced magnetic resonance imaging findings in a 60-year-old man with confluent hepatic fibrosis in advanced cirrhosis. The extension and internal structure of confluent fibrosis were well demonstrated with ferumoxides-enhanced proton-density spin-echo magnetic resonance images, showing a wedge-shaped area of high signal intensity corresponding to the extension of fibrosis and internal focal areas of low signal intensity, presumably corresponding to residual functioning liver parenchyma. This case suggests a potential utility of ferumoxides-enhanced magnetic resonance imaging for characterizing this tumor-mimicking disorder.
Age-related change in the amount of ubiquitinated histones in the mouse brain.
We investigated age-related changes in the ubiquitination of histones in mouse brains. By Western blot analysis using rabbit anti-ubiquitin antibodies, histone H2A and H2B were found to be the only proteins that are ubiquitinated in the acid-extractable nuclear proteins of both young (4-month-old) and senescent (29-month-old) mouse brains. The proportion of ubiquitinated histones was about 30% higher in senescent mice than in young ones. When total brain homogenates were analyzed similarly using somewhat different age groups of the animals, the proportion in the old animals was about 2-fold higher than that in the young.
Severe neonatal nemaline myopathy with delayed maturation of muscle.
A Japanese infant with a severe neonatal form of nemaline myopathy showed features of muscle immaturity as well as rods in the biopsied quadriceps femoris muscle, and involvement of diaphragm was first confirmed at autopsy. The biopsied muscle showed numerous rods in 80% of muscle fibers, and an increased number of type 2C fibers (23.2%). Electron microscopic findings were characterized by the presence of many small, immature round fibers with central nuclei and sparse myofibrils, and an increased number of satellite cells in close association with the small muscle fibers, as well as numerous rod structures. These microscopic and electron microscopic findings are interpreted as immature muscle fibers. Maturational delay or arrest implies deprivation of a development promoting factor such as a neuronal signal. Severe involvement with numerous rods was demonstrated in both diaphragm and intercostal muscles at the time of the postmortem examination, compatible with the patient's respiratory failure.
An MRI study of the myelination pattern in West syndrome.
Using magnetic resonance imaging (MRI), we studied the myelination of the brains of 8 patients with West syndrome. All cases were symptomatic, 2 having severe asphyxia, 1 lissencephaly, 1 Leigh encephalopathy, 2 tuberous sclerosis, 1 multiple anomalies and 1 microcephaly. Myelination of the pons, cerebellum, thalamus, internal capsules, optic radiation, centrum semiovale and cerebral white matter was separately assessed. The 2 cases with tuberous sclerosis exhibited normal myelination patterns, although asymmetry of the cerebral white matter was noted. These cases had a moderate degree of mental retardation and persistent seizures. The other 6 cases exhibited a marked delay of myelination throughout the central nervous system except for the midbrain. These cases had severe psychomotor retardation and persistent seizures. Although the difference in the outcome may simply reflect the different etiological disorders, these results suggest that the myelination pattern is related to the psychomotor retardation but not to the severity of the seizures in West syndrome. Atrophy of the corpus callosum developed during ACTH therapy and disappeared after the therapy. It was thus suggested that the callosal atrophy caused by the ACTH therapy was reversible.
Duchenne/Becker muscular dystrophy: from molecular diagnosis to gene therapy.
Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD) are X-linked muscular dystrophies. The recent isolation of the defective gene in DMD/BMD and the identification of its protein product, dystrophin, have revolutionized our ability to diagnose DMD/BMD and promoted speculation regarding the application of gene therapy. The purpose of this review is to present progress made in this area of research, with particular reference to dystrophin Kobe, which is caused by exon skipping during splicing due to the presence of an intra-exon deletion. On the basis of result of molecular analysis of dystrophin Kobe we propose a novel way of gene therapy for DMD, in which antisense oligonucleotides transform DMD into BMD phenotype by inducing exon skipping.
Vascular involvement in benign infantile mitochondrial myopathy caused by reversible cytochrome c oxidase deficiency.
A 1-month-old Japanese girl had profound generalized weakness, hypotonia, and severe lactic acidosis. The infant improved gradually: she held her head at 9 months, learned to walk by 15 months. At the first muscle biopsy at 11 weeks of age, the specimen was characterized by numerous ragged-red fibers and decreased enzyme activity on cytochrome c oxidase (COX) staining. Electron microscopic findings were characterized by the presence of excessive abnormal mitochondria not only in skeletal muscle fibers but also in blood vessels. Vascular abnormalities consisted of an increased number of enlarged mitochondria in endothelial and smooth muscle cells of small arteries. Biochemical analysis showed an isolated defect of COX activity, which was only 16% of the mean control level. At the second biopsy at 44 months of age, the COX activity had increased to normal in the entire specimen. On electron microscopy, the abnormal mitochondria present on the first biopsy specimen had disappeared both in muscle fibers and blood vessels; nearly all mitochondria were morphologically normal at the second biopsy. Now at 5 years of age she can run and does not show muscle weakness. We report reversibility of abnormal mitochondria with age not only in skeletal muscle fibers but also in blood vessels in a patient, who had reversible COX deficiency with a benign clinical course.
Increased susceptibility of late passage human diploid fibroblasts to oxidative stress.
Three strains of human diploid fibroblasts, TIG-3, TIG-7, and MRC-5, were serially cultivated. The susceptibility of early-passage and late-passage cells at 20-30 and 60-70 population doubling levels, respectively, to hydrogen peroxide, the superoxide radical (exposure to the hypoxanthine-xanthine oxidase system), or linoleic acid hydroperoxide was examined for lactate dehydrogenase release. The susceptibility of late-passage cells to such oxidative stress was considerably enhanced compared with early-passage cells. The concentration of reduced glutathione in late-passage cells was lower by 24-44% on a per-cell-number basis and by 86.0-94.5% on a per-protein-quantity basis than in early-passage cells. In addition, the activity of catalase in late-passage cells was lower by 19-46% compared with early-passage cells. There was, however, no difference between the mRNA levels of catalase in early-passage and late-passage cells. The activities and mRNA levels of copper/zinc superoxide dismutase, manganese superoxide dismutase, and glutathione peroxidase in late-passage cells were all higher than in early-passage cells. These results suggest that late-passage cells are more susceptible to oxidative stress than early-passage cells presumably because of decreases in cellular reduced glutathione concentration and catalase activity, and that their primary defense against oxidative stress is reduced glutathione.
Supraclinoid carotid dissection in a pediatric patient.
The authors present the case of a 13-year-old boy with a left temporal lobe infarction that developed during a 400-m run. Magnetic resonance (MR) angiography showed segmental narrowing of the left supraclinoid internal carotid artery (ICA) and a duplicated left middle cerebral artery (MCA). MR angiographic source images revealed a crescent-shaped left carotid lumen, indicative of a supraclinoid carotid dissection.
Reactions of vitamin E and its model compound 2,2,5,7,8-pentamethylchroman-6-ol with ozone.
Reaction of vitamin E [(R,R,R)-alpha-tocopherol] with ozone in acetonitrile yielded alpha-tocopheryl quinone and its precursor 8a-hydroxytocopherone, which accounted for approximately 30% of the products at < 50% alpha-tocopherol oxidation. In addition, two novel products were identified as epimers of 10-acetyl-7-(4',8',12'-trimethyltridecyl)-3,4,7-trimethyl-2-oxo- 1,6-dioxaspiro[4.5]-deca-3,9-diene. These spiro products were formed in equal amounts in a combined yield of approximately 33% after complete alpha-tocopherol oxidation. Ozonation of the vitamin E model compound 2,2,5,7,8-pentamethylchroman-6-ol yielded an analogous spiro product, 10-acetyl-3,4,7,7-tetramethyl-2-oxo-1,6-dioxaspiro[4.5]deca-3,9-di ene, whose structure was confirmed by X-ray crystallography. The spiro products may be formed by ozone addition to the chroman ring and subsequent rearrangement to ring-opened hydroxyacid products, which yield spiro products by ring closure due to dehydration. Novel spiro products formed by ozonation of vitamin E may be unique markers of ozone interaction with lipid structures that contain vitamin E.
Reactions of the vitamin E model compound 2,2,5,7,8-pentamethylchroman-6-ol with peroxyl radicals.
The vitamin E model compound 2,2,5,7,8-pentamethylchroman-6-ol (1b) was oxidized by peroxyl radicals generated by thermolysis of 2,2'-azobis(2,4- dimethylvaleronitrile) in oxygenated solvents. Oxidation of 1b yielded 4a,5-epoxy-4a,5-dihydro-8a-hydroperoxy- 2,2,5,7,8-pentamethylchroman-6(8aH)-one (5b), 7,8-epoxy-7,8-dihydro-8a-hydroperoxy-2,2,5,7,8-pentamethylchroman- 6(8aH)- one (6b), 8a-[(2,4-dimethyl-1-nitrilopent-2-yl)dioxy]-2,2,5,7,8- pentamethylchroman-6(8aH)-one (3b), and a 5,5'-spirodimer product (7b). In otherwise identical reactions, yields of chromanone 3b and epoxides 5b/6b increased with increasing solvent polarity, whereas the yield of spirodimer 7b decreased. Deuterium substitution at C5a inhibited oxidation of 1b to spirodimer 7b and favored the formation of a novel 5,7'-spirodimer 11. The results demonstrate that the reaction medium controls the balance between competing reactions of chromanoxyl radical 2b and are consistent with the formation of epoxides and 8a-substituted tocopherones as the predominant products of alpha-tocopherol oxidation in biological membranes.