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Biomedical subjects

G Takada

Publications and source records attributed to G Takada.

At least 55 records · Page 3Linked to original sources
PubMed1999

Acute cerebellitis caused by Coxiella burnetii.

We report a childhood case of severe acute cerebellitis caused by Coxiella burnetii. After 10 days of fever and headache, the patient fell into a drowsy state. Examination of the cerebrospinal fluid (CSF) revealed pleocytosis, an increased level of protein, and negative results in bacterial and viral studies. Magnetic resonance imaging demonstrated a herniated tonsil compressed by the swollen vermis. Administration of minocycline relieved the patient's clinical symptoms. C. burnetii was isolated from the CSF obtained during convalescence.

Acute Disease↗
PubMed1999

Immunohistochemical study on transforming growth factor-beta1 expression in liver fibrosis of Down's syndrome with transient abnormal myelopoiesis.

A case of Down's syndrome associated with liver fibrosis is reported. The fibrosis was diffusely distributed along sinusoids, and an excess of megakaryocytes was also found in the liver. To determine the mechanism of liver fibrosis in Down's syndrome, we immunohistochemically stained the liver with markers of myofibroblast-like cells, antialpha smooth muscle actin antibodies and antidesmin antibodies. The myofibroblast-like cells were found along sinusoids, suggesting that liver fibrosis in Down's syndrome is caused by the myofibroblast-like cells derived from Ito cells/lipocytes. The expression of transforming growth factor (TGF)-betal, which is an important mediator of the activation of lipocytes, was immunohistochemically examined. The accumulation of TGF-betal was observed in cells in the sinusoidal spaces, which involve the intracellular expression of megakaryocytes. Together, these findings suggest that megakaryocyte-derived TGF-betal is one of the likely candidates in the lipocyte activation of liver fibrogenesis in Down's syndrome.

Actins↗
PubMed1999

Serial echocardiographic and Doppler evaluation of left ventricular systolic performance and diastolic filling in premature infants.

To examine the effects of somatic growth on left ventricular systolic and diastolic functions in premature infants, we performed serial two-dimensional, M-mode and Doppler echocardiograms of 18 premature infants in the early neonatal period (mean of 14 days) and on the day when they were discharged from the hospital (mean of 94 days). The relation between rate-corrected mean velocity of fiber shortening and end-systolic wall stress relation was used as a load-independent estimate of contractility. Diastolic function was assessed by transmitral Doppler filling velocity patterns. The end-systolic wall stress was significantly lower in the first examination than in the second examination (38+/-8 vs. 46+/-10 g/cm2, P < 0.005). However, there was no significant difference in the rate-corrected velocity of fiber shortening between the two examinations. An inverse linear relation between the end-systolic wall stress and the rate-corrected mean velocity of fiber shortening was found in each examination. The slopes of these two regression lines showed no significant difference, suggesting that the left ventricular contractility is on the same level during this study period. The transmitral Doppler flow velocity patterns markedly altered between the two observations. The peak E wave, peak A wave, peak E/A ratio, flow velocity time integral of E/A wave, the first third filling fraction, and the normalized peak filling rate to stroke volume increased significantly during the study period (78+/-14 vs. 31+/-9 cm/s, 61+/-12 vs. 33+/-7 cm/s, 1.29+/-0.18 vs. 0.93+/-0.19, 1.75+/-0.58 vs. 1.17+/-0.24, 0.42+/-0.07 vs. 0.37+/-0.05, and 9.48+/-1.71 vs. 7.30+/-0.96/s, respectively, P < 0.001), suggesting a relative shift of Doppler filling into the early diastole. We demonstrated that the age- and growth-related alterations in the transmitral Doppler filling patterns occurred dramatically without changes in contractility during the first 3 months after birth. This diastolic filling change may be related to the age-related maturation in the left ventricular diastolic properties.

Analysis of Variance↗
PubMed1999

SSPE following neonatal measles infection.

The authors report a case of subacute sclerosing panencephalitis in a child who had measles during the neonatal period. At 3 years, 6 months of age, over a period of a few weeks, the patient lost the ability to sit unaided as a result of progressive truncal ataxia, without apparent cognitive changes, simulating acute cerebellar ataxia. His symptoms improved in 1 month, and he was able to walk again with support, but mental alteration and periodic mild head nodding on awakening followed. His illness was diagnosed as subacute sclerosing panencephalitis on the basis of the elevated titers of measles antibodies in the cerebrospinal fluid. Measles infection before 1 year of age is a risk factor of subacute sclerosing panencephalitis, but reports about patients with neonatal measles infection are rare. Immaturity of the brain at the time of measles infection may not only be a risk factor but may also influence the clinical course of the disease.

Age of Onset↗
PubMed1999

Anoxic and hypoxic immature rat model for measurement of monoamine using in vivo microdialysis.

The immature brain is considered relatively resistant to anoxia and ischemia. Although hypoxia without ischemia has not been considered to produce brain damage in immature rats as well as in adult rats (S. Levine, Anoxic-ischemic encephalopathy in rats, Am. J. Pathol., 36 (1960) 1-17 [8]; D.E. Levy, J.B. Brieley, D.G. Silverman, F. Plum, Brief hypoxia-ischemia initially damages cerebral neurons, Arch. Neurol., 32 (1975) 450-456 [9]; J.E. Rice, R.C. Vannucci, J.B., Brieriey, The influence of immaturity on hypoxic-ischemic brain damage in rat, Ann. Neurol., 9 (1981) 131-141 [14]), hypoxia in postnatal period is possible to cause a functional brain damage (T. Hender, P. Lundborg, Regional changes in monoamine synthesis in the developing rat brain during hypoxia, Acta. Physiol. Scand., 106 (1979) 139-143 [3]; W. Ihle, J. Gross, R. Moller, Effect on chronic postnatal hypoxia on dopamine uptake by synaptosomes from striatum of adult rats, Biomed. Biochem. Acta., 44 (1985) 433-437 [7]; A. Lun, J. Gross, M. Beyer, H.D. Fischer, C. Wustmann, J. Schmidt, K. Hecht, The vulnerable period of perinatal hypoxia with regard to dopamine release and behavior in adult rats, Biomed. Biochem. Acta., 45 (1986) 619-627 [10]). Using microdialysis, we studied the anoxic or hypoxic effect on catecholamine metabolism in immature rat brain by measuring extracellular concentrations of norepinephrine (NE), dopamine (DA), and its metabolites and also 5-hydroxyindole-3-acetic acid (5-HIAA), the serotonin metabolite. DA is a well established excitatory neurotransmitter (R.C. Vannucci, Experimental biology of cerebral hypoxia-ischemia: relation to perinatal brain damage, Pediatr. Res., 27 (1990) 317-326 [16]), and in the previous report using hypoxic 7-day-old rat pups increase of DA was not detected without additional stimulations (K. Gordon, D. Johnston, M.V. Robinson, T.E. Statman, J.B. Becker, F. Silverstein, Transient hypoxia alters striatal catecholamine metabolism in immature brain: An in vivo microdialysis study, J. Neurochem., 54 (1990) 605-611 [2]). Whereas recently in newborn piglets, hypoxic hypoxia produced increase of extracellular DA (C.-C. Huang, N.S. Lajevardi, O. Tammela, A. Pastuszko, Relationship of extracellular dopamine in striatum of newborn piglets to cortical oxygen pressure, Neurochem. Res., 19 (1994) 649-655 [6]; Olano, M., Song, D., Murphy, S., Wilson, D. F. and Pastuszko, A., Relationships of dopamine, cortical oxygen pressure, and hydroxyl radicals in brain of newborn piglets during hypoxia and posthypoxic recovery, J. Neurochem., 65 (1995) 1205-1212 [13]). We consider that hypoxic ischemic brain damage of human newborns that we can treat is a damage, which does not show overt neuropathological changes. We therefore tried to show that transient anoxia and hypoxia caused biochemical alteration if the exposure did not produce marked morphological changes. This rodent model is adequate to study perinatal asphyxia and alteration of monoamine level could be useful for evaluation of brain damage, even if it is not detected histologically.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1999

Production of D-lyxose from D-glucose by microbial and enzymatic reactions.

D-arabitol was first prepared from D-glucose using Candida famata R28. The reaction gave 5.0% D-arabitol from 10.0% D-glucose. D-arabitol was then almost completely converted to D-xylulose using Acetobacter aceti IFO 3281. Finally, D-lyxose was prepared from D-xylulose enzymatically using L-ribose isomerase from toluene-treated cells of Acinetobacter sp. strain DL-28. The isomerization reaction progressed steadily and the concentration of D-xylulose increased from 1.0 to 10.0%. About 70% of D-xylulose was converted to D-lyxose in all cases. Separation of residual D-xylulose from the reaction mixture is very difficult to achieve by column chromatography, but D-xylulose could be selectively degraded easily using Saccharomyces cerevisiae IFO 0841. The product was crystallized and was confirmed to be D-lyxose by HPLC, 13C-NMR spectra, IR spectra analysis, and optical rotation measurement.

Journal Article↗
PubMed1999

Preparation of L-talose and D-gulose from L-tagatose and D-sorbose, respectively, using immobilized L-rhamnose isomerase.

L-rhamnose isomerase of Pseudomonas sp. LL172 immobilized on BCW 2603 Chitopearl beads was used to produce L-talose and D-gulose. At equilibrium, the production yields of L-talose and D-gulose were determined to be 12 and 10% from L-tagatose and D-sorbose, respectively. The crystallized products were confirmed by HPLC, IR and NMR spectra, and optical rotation measurement analyses.

Journal Article↗
PubMed1999

Biochemical preparation of L-ribose and L-arabinose from ribitol: a new approach.

L-ribose and L-arabinose were prepared biochemically from ribitol via a two-step reaction, by which the complete oxidation of ribitol to L-ribulose (approximately 98%) was achieved by the reaction of washed cells of Acetobacter aceti IFO 3281. The produced L-ribulose was then used as a substrate for the production of L-ribose and L-arabinose. The isomerization of L-ribulose to L-ribose and L-arabinose was carried out using L-ribose isomerase (L-RI) of Acinetobacter sp. strain DL-28 and L-arabinose isomerase (L-AI) of Mycobacterium smegmatis, respectively. At equilibrium, the ratio of L-ribose: L-ribulose was 70:30 and that of L-arabinose: L-ribulose was 90: 10. After a simple purification treatment, both pentoses could be crystallized without the use of column chromatography. The crystals were confirmed as L-ribose and L-arabinose by High-performance liquid chromatography (HPLC), Infrared (IR), Nuclear magnetic resonance (NMR) and optical rotation measurements.

Journal Article↗
PubMed1999

Fatal neonatal hypertrophic cardiomyopathy with severe stenosis of the right ventricular outflow tract: echocardiographic diagnosis and potential therapy.

We discuss the clinical course of aneonate with idiopathic hypertrophic cardiomyopathy who showed rapid progression of stenosis of the right ventricular outflow tract and reduction in size of the right ventricular cavity due to thicken ing of the ventricular septum. Medical treatment proved unsuccessful. We suggest that balloon atrial septostomy combined with construction of a Blalock-Taussig shunt may be effective in view of the hemodynamics, which mimic pulmonary atresia with intact interventricular septum.

Cardiac Output, Low↗
PubMed1999

3-Methylglutaconic aciduria type I: clinical heterogeneity as a neurometabolic disease.

3-Methylglutaconic (3-MGC) aciduria with 3-methylglutaconyl-CoA hydratase deficiency (3-MGC aciduria type I) is a rare inherited metabolic disease of L-leucine catabolism. We describe a 9-month-old Japanese boy with this disorder who showed progressive neurological impairments presented as quadriplegia, athetoid movements and severe psychomotor retardation from 4 months of age. This finding indicates the existence of clinical heterogeneity in 3-MGC aciduria type I, suggesting it may present as a neurometabolic disease.

Acidosis, Renal Tubular↗
PubMed1999

Primary systemic carnitine deficiency is caused by mutations in a gene encoding sodium ion-dependent carnitine transporter.

Primary systemic carnitine deficiency (SCD; OMIM 212140) is an autosomal recessive disorder characterized by progressive cardiomyopathy, skeletal myopathy, hypoglycaemia and hyperammonaemia. SCD has also been linked to sudden infant death syndrome. Membrane-physiological studies have suggested a defect of the carnitine transport system in the plasma membrane in SCD patients and in the mouse model, juvenile visceral steatosis. Although the responsible loci have been mapped in both human and mouse, the underlying gene has not yet been identified. Recently, we cloned and analysed the function of a novel transporter protein termed OCTN2. Our observation that OCTN2 has the ability to transport carnitine in a sodium-dependent manner prompted us to search for mutations in the gene encoding OCTN2, SLC22A5. Initially, we analysed the mouse gene and found a missense mutation in Slc22a5 in jvs mice. Biochemical analysis revealed that this mutation abrogates carnitine transport. Subsequent analysis of the human gene identified four mutations in three SCD pedigrees. Affected individuals in one family were homozygous for the deletion of a 113-bp region containing the start codon. In the second pedigree, the affected individual was shown to be a compound heterozygote for two mutations that cause a frameshift and a premature stop codon, respectively. In an affected individual belonging to a third family, we found a homozygous splice-site mutation also resulting in a premature stop codon. These mutations provide the first evidence that loss of OCTN2 function causes SCD.

Amino Acid Sequence↗
PubMed1999

Mass screening for Wilson's disease: results and recommendations.

Wilson's disease is a treatable inherited disorder of copper metabolism. Established treatments include the use of oral chelating agents and the establishment of a minimum copper diet, although prognosis mainly depends on the extent of liver or nervous system damage present before treatment. Once irreversible damage has occurred, the effect of these treatments is diminished and the patient's quality of life compromised. Therefore, the establishment of a mass screening system able to detect Wilson's disease patients presymptomatically has been discussed. Recently, a monoclonal antibody specific to holoceruloplasmin has been developed. This antibody was used in a nationwide screening trial of 126,810 newborn infants, but no Wilson's disease patients were identified. However, three patients out of 24,165 were diagnosed with Wilson's disease using this specific antibody in a screening performed during the period from late infancy to elementary school. The age of 3 years is thought to be the best point for Wilson's disease mass screening. In this paper, a review of mass screening for Wilson's disease in Japan using a specific monoclonal antibody to holoceruloplasmin is presented.

Antibodies, Monoclonal↗
PubMed1999

Evaluation of efficacy in platelet collection by the Haemonetics Component Collection System.

Platelet concentrate product derived from plateletpheresis from a single donor is preferable in terms of reducing the risks of adverse reactions in platelet transfusion. This study evaluated the status of platelet transfusion and the efficacy and safety of plateletpheresis machines. The average number of donors of platelet product per patient has been decreasing and recently reached nearly 1.0; however, some patients still receive multiple random donor platelet products. Platelet collection efficacy was comparable between the Haemonetics Component Collection System (CCS) and the Multi Component System (Multi). However, the CCS has been shown to be effective in terms of processed blood volume and procedure time, especially in donors with lower hematocrits. These results suggest that the CCS may be preferable and safer for donors with lower hematocrits and lighter body weights. Blood centers should collect platelets more effectively to achieve platelet transfusion with the use of platelets derived from a single donor using effective equipment.

Blood Donors↗
PubMed1999

Genetic epidemiology of the carnitine transporter OCTN2 gene in a Japanese population and phenotypic characterization in Japanese pedigrees with primary systemic carnitine deficiency.

Serum free-carnitine levels were determined in 973 unrelated white collar workers in Akita, Japan. Fourteen of these participants consistently had serum free-carnitine levels below the fifth percentile (28 microM for females and 38 microM for males). The OCTN2 (organic cation transporter) gene was sequenced for these 14 subjects, for 22 subjects whose carnitine levels were below the fifth percentile in the first screening but were normal in the second measurement and in 69 individuals with normal carnitine levels for two separate measurements. Polymorphic sequences defined three major haplotypes with equal frequency. Mutations were identified in nine subjects with low carnitine levels: Trp132X (three individuals), Ser467Cys (four), Trp283Cys (one) and Met179Leu (one). In vitro expression studies in HEK cells indicated that Ser467Cys and Trp283Cys, but not Met179Leu, significantly reduced L-carnitine uptake relative to the normal control. Trp132X and Ser467Cys were associated with specific haplotypes, suggesting a founder effect. A conservative estimate of the overall prevalence of heterozygotes was 1.01% in the Akita prefecture, Japan, giving an estimated incidence of primary systemic carnitine deficiency (MIM 212140) as 1 in 40 000 births. An echocardiographic study of the families of patients with primary carnitine deficiency revealed that the heterozygotes for OCTN2 mutations were predisposed to late onset benign cardiac hypertrophy (odds ratio 15.1, 95% CI 1.39-164) compared with the wild-types. Sequencing of DNA isolated from three deceased siblings (1.5-8 years) in two families retrospectively confirmed that all three deceased subjects were homozygous for the OCTN2 mutations.

Base Sequence↗
PubMed1999

Cloning and sequencing of beta-mannosidase gene from Aspergillus aculeatus no. F-50.

The manB gene, coding for a unique beta-mannosidase (MANB) of Aspergillus aculeatus, was cloned from genomic and cDNA libraries, and sequenced. The gene consists of 2,811 bp encoding a polypeptide of 937 amino acid residues with a molecular mass of 104,214 Da. The A. aculeatus MANB shared amino acid sequence identity with MANB of human (24%), goat (24%), bovine (24%), and Caenorhabditis elegans (22%). When the A. aculeatus MANB was compared with other related enzymes, a Glu residue corresponding to the active site identified by the Escherichia coli beta-galactosidase and the human beta-guclonidase was conserved. This is the first fungal gene that encodes MANB.

Amino Acid Sequence↗
PubMed1999

Morphological adaptation of the cardiovascular system in fetal rats during late gestation.

The aim of this study was to evaluate morphological changes of the cardiovascular system in fetal rats during late gestation. We used the rapid whole-body freezing technique for rats of day 17 through 21 of gestation. The right and left ventricular volumes increased markedly and significantly during this period by about 11- and 24-fold, respectively. Although the right ventricular volume was 108% larger with statistical significance than the left ventricular volume on day 17, they were almost equal after day 19. The length of the primum septum of the atrium significantly increased by 92% within 4 days, but the opening distance of foramen ovale significantly decreased by 14%. The ratio of the inner diameter (the sum of right and left pulmonary arteries to ductus arteriosus) significantly increased from 0.72+/-0.03 on day 17 to 1.17+/-0.07 on day 21. There was also a significant increase in the ratio of the inner diameters of the ascending to descending aorta. These observations suggest that the reduction of the opening distance of foramen ovale reflect the growth of pulmonary arteries.

Adaptation, Physiological↗
PubMed1999

Right ventricular diastolic filling assessed by conventional doppler and tissue Doppler imaging in normal children.

To examine age-related changes in right ventricular filling dynamics, we performed conventional pulsed Doppler (n=99) and tissue Doppler (n=30) echocardiographic studies in normal subjects aged 7 days to 273 months. The tricuspid flow velocity during early diastole (peak E) wave correlated significantly but weakly with the logarithm of age. The peak E wave in the early neonatal period was almost 80% of the older children's values and increased to 100% by 36 months of age. In the right ventricular tissue Doppler imaging, the peak myocardial velocity during early diastole also increased significantly with the logarithm of age. However, the tissue Doppler peak A did not change with age. There was a significant correlation between the tissue Doppler peak E wave and the tricuspid peak E wave and between the tissue Doppler peak E/A wave and the tricuspid peak E/A wave. The age-related changes in the tricuspid inflow velocity patterns were similar to the age-related alterations in the right ventricular myocardial velocity patterns. Age-related changes in the tricuspid inflow velocity and myocardial velocity patterns may be related to age-related maturation in the right ventricular diastolic performance.

Adolescent↗