Hitomi Ueno

Tokyo Metropolitan Institute of Gerontology, Tokyo, Tokyo-to, Japan

Are you Hitomi Ueno?

Claim your profile

Publications (10)30.11 Total impact

  • Article: Phylogenetic analysis of urease-positive thermophilic Campylobacter (UPTC) strains based on the molecular characterization of the flaA gene.
    [show abstract] [hide abstract]
    ABSTRACT: Molecular cloning, nucleotide sequencing, and characterization of the flaA gene from additional isolates of urease-positive thermophilic Campylobacter (UPTC) were performed. These isolates were obtained from the natural environment in Northern Ireland (n = 9 from mussels) and in England (n = 1 from sea water). All isolates carried the shorter flaA gene, [open reading frames (ORFs), 1,461 to 1,503 base pairs], without any internal termination codons, and did not carry any flaA pseudogenes. The UPTC isolates were well discriminated by the neighbor joining (NJ) phylogenetic tree constructed based on the putative flaA genes ORFs nucleotide sequence information. In addition, the NJ tree constructed based on the flaA-short variable region sequence information discriminated the Campylobacter lari isolates with a similar degree of discrimination power.
    Folia Microbiologica 08/2011; 56(5):397-406. · 0.68 Impact Factor
  • Article: Demonstration of the absence of intervening sequences (IVSs) within 16S rRNA genes of Taylorella equigenitalis and Taylorella asinigenitalis isolates.
    [show abstract] [hide abstract]
    ABSTRACT: A total of 57 Taylorella equigenitalis (n=22) and Taylorella asinigenitalis (n=35) isolates was shown not to carry any intervening sequences (IVSs) within 16S rRNA gene sequences. By contrast, we have already shown the genus Taylorella group to carry several kinds of IVSs within the 23S rRNA gene sequences.
    Research in Veterinary Science 05/2011; 92(3):435-7. · 1.65 Impact Factor
  • Article: Extensive screening system using suspension array technology to detect mitochondrial DNA point mutations.
    [show abstract] [hide abstract]
    ABSTRACT: We established an extensive and rapid system using suspension array to detect 61 representative mitochondrial DNA (mtDNA) heteroplasmic or homoplasmic point mutations (29 for Series A and 32 for Series B) in 22 genes: 1 each in MT-RNR1, -TV, -ND1, -TQ, -TW, -TC, and -TH genes; 2 each in MT-TN, -TG, -ND4, -TL2, -TE, and -CYB genes; 3 each in MT-ATP6, -ND3, and -ND5 genes; 4 each in MT-CO1 and -TK genes; 5 each in MT-TI, -TS1, and -ND6 genes; and 10 in the MT-TL1 gene. We carefully selected 5'-biotinylated primers and pooled primers for use in two sets of multiplex-PCR amplifications. To detect both mutant and wild-type mtDNA, even when polymorphisms were present near the target mutation sites, we designed specific oligonucleotide probes. By using the mtDNA point mutation detection system of Series A (29 mutations) and Series B (32 mutations), we screened a total of 3103 mutant sites in 107 DNA samples for Series A and 13,101 mutant sites in 397 DNA samples for Series B. We succeeded in determining 99.4% (Series A) and 99.6% (Series B) of the targeted mutant sites by use of the system. The 22 samples with the m.3243A>G heteroplasmic mutation revealed positive signals with both mutant- and wild-type-specific probes in this detection system with a detection limit of approximately 2%. This genetic screening platform is useful to reach a definitive diagnosis for mitochondrial diseases.
    Mitochondrion 04/2010; 10(3):300-8. · 3.62 Impact Factor
  • Article: Extensive and rapid screening for major mitochondrial DNA point mutations in patients with hereditary hearing loss.
    [show abstract] [hide abstract]
    ABSTRACT: Sensorineural hearing loss (HL) is one of the most frequent clinical features in patients with mitochondrial diseases caused by mitochondrial DNA (mtDNA) mutations, and hearing is impaired in over half of all cases with mitochondrial disorders. This study analyzed 373 patients with suspected hereditary HL using an extensive and rapid suspension-array screening system for 29 major mtDNA mutations, including the m.1555A>G homoplasmic mutation in the MT-RNR1 gene, which causes non-syndromic sensorineural HL and aminoglycoside-induced HL, and the m.3243A>G heteroplasmic mutation in the MT-TL1 gene. This method is rapid and suitable for large-scale screening because universal 96-well plates are available for use, and because an analysis of each plate can be completed within 1 h. This system detected five different mtDNA mutations in 24 of the 373 (6.4%) patients. The m.1555A>G and m.3243A>G mutations were detected in 11 (2.9%) and 9 (2.7%) patients, respectively. In addition, three mutations, that is, m.8348A>G in the MT-TK gene, m.11778G>A in the MT-ND4 gene and 15498G>A in the MT-CYB gene were detected in one patient for each. This screening system is useful for the genetic diagnosis and epidemiological study of both syndromic and non-syndromic HL.
    Journal of Human Genetics 03/2010; 55(3):147-54. · 2.57 Impact Factor
  • Article: Analysis of mitochondrial DNA variants in Japanese patients with schizophrenia.
    [show abstract] [hide abstract]
    ABSTRACT: To test the hypothesis that mitochondrial DNA (mtDNA) variants contribute to the susceptibility to schizophrenia, we sequenced the entire mtDNAs from 93 Japanese schizophrenic patients. Three non-synonymous homoplasmic variants in subunit six of the ATP synthase (MT-ATP6) gene that were detected only in patients but not in controls were suggested to be slightly deleterious, because (1) their original amino acid residues (AA) were highly conserved and (2) the physicochemical differences between the original and altered AA were relatively high. In addition, we detected three novel heteroplasmic variants that were potentially pathogenic. Although functional analysis is needed, rare variants in the mtDNA may convey susceptibility to schizophrenia.
    Mitochondrion 07/2009; 9(6):385-93. · 3.62 Impact Factor
  • Source
    Article: Mitochondrial DNA haplogroup D4a is a marker for extreme longevity in Japan.
    [show abstract] [hide abstract]
    ABSTRACT: We report results from the analysis of complete mitochondrial DNA (mtDNA) sequences from 112 Japanese semi-supercentenarians (aged above 105 years) combined with previously published data from 96 patients in each of three non-disease phenotypes: centenarians (99-105 years of age), healthy non-obese males, obese young males and four disease phenotypes, diabetics with and without angiopathy, and Alzheimer's and Parkinson's disease patients. We analyze the correlation between mitochondrial polymorphisms and the longevity phenotype using two different methods. We first use an exhaustive algorithm to identify all maximal patterns of polymorphisms shared by at least five individuals and define a significance score for enrichment of the patterns in each phenotype relative to healthy normals. Our study confirms the correlations observed in a previous study showing enrichment of a hierarchy of haplogroups in the D clade for longevity. For the extreme longevity phenotype we see a single statistically significant signal: a progressive enrichment of certain "beneficial" patterns in centenarians and semi-supercentenarians in the D4a haplogroup. We then use Principal Component Spectral Analysis of the SNP-SNP Covariance Matrix to compare the measured eigenvalues to a Null distribution of eigenvalues on Gaussian datasets to determine whether the correlations in the data (due to longevity) arises from some property of the mutations themselves or whether they are due to population structure. The conclusion is that the correlations are entirely due to population structure (phylogenetic tree). We find no signal for a functional mtDNA SNP correlated with longevity. The fact that the correlations are from the population structure suggests that hitch-hiking on autosomal events is a possible explanation for the observed correlations.
    PLoS ONE 02/2008; 3(6):e2421. · 4.09 Impact Factor
  • Article: Novel conformation-sensitive antibodies specific to three- and four-repeat tau.
    [show abstract] [hide abstract]
    ABSTRACT: Two types of tau isoform, three- and four-repeat tau, are found in neurofibrillary tangles--a pathological hallmark of tauopathies. Which isoform is deposited in the affected tissues depends on the tauopathy. To study how and which tau isoforms contribute to neuronal degeneration, we have developed and characterized two novel conformation-sensitive antibodies, T3R and T4R. Two closely related synthetic peptides, PGGGKVQIVYK and PGGGSVQIVYK, respectively, were designed as antigens. The isoform-specific residues, (305)K in three-repeat tau or (305)S in four-repeat tau, and the PHF6 motif (VQIVYK) were identified as critical sequences. Despite the high similarity of the antigens, there was no cross-reactivity between T3R and T4R. Furthermore, T3R and T4R showed reduced binding to the thioflavin-positive beta-structural form of their target. These features may enable these antibodies to act as novel indicators that allow us to observe and evaluate conformational changes in each distinct isoform of tau.
    Biochemical and Biophysical Research Communications 07/2007; 358(2):602-7. · 2.48 Impact Factor
  • Article: Enrichment of longevity phenotype in mtDNA haplogroups D4b2b, D4a, and D5 in the Japanese population.
    [show abstract] [hide abstract]
    ABSTRACT: We report new results from the re-analysis of 672 complete mitochondrial (mtDNA) genomes of unrelated Japanese individuals stratified into seven equal sized groups by the phenotypes: diabetic patients, diabetic patients with severe angiopathy, healthy non-obese young males, obese young males, patients with Alzheimer's disease, patients with Parkinson's disease and centenarians. Each phenotype had 96 samples over 27 known haplogroups: A, B4a, B4b, B4c, B*, B5, D*, F1, F2, M*, M7a, M7b, M8, M9, D4a, D4b1, D4b2, D4d, D4e, D4g, D4h, D5, G, Z, M*, N9a, and N9b. A t-test comparing the fraction of samples in a haplogroup to healthy young males showed a significant enrichment of haplogroups D4a, D5, and D4b2 in centenarians. The D4b2 enrichment was limited to a subgroup of 40 of 61 samples which had the synonymous mutation 9296C > T. We identified this cluster as a distinct haplogroup and labeled it as D4b2b. Using an exhaustive procedure, we constructed the complete list of "mutation patterns" for centenarians and showed that the most significant patterns were in D4a, D5, and D4b2b. We argue that if a selection for longevity appeared only once, it was probably an autosomal event which could be dated to after the appearance of the D mega-group but before the coalescent time of D4a, D5, and D4b2b. Using a simple procedure, we estimated that this event occurred 24.4 +/- 0.9 kYBP.
    Human Genetics 05/2007; 121(3-4):347-56. · 5.07 Impact Factor
  • Article: Genetic heterogeneity of urease gene loci in urease-positive thermophilic Campylobacter (UPTC).
    [show abstract] [hide abstract]
    ABSTRACT: Degenerate PCR primers in silico based on the two urease structural genes, ureA and ureB, were designed for urease-positive thermophilic Campylobacter (UPTC). Resultant PCR amplification employing these primers generated an amplicon of approximately 2kb, which was cloned and sequenced in UPTC (n=12) isolated from various parts of Europe and Japan. Overall, sequence similarities were shown to be 96.7 to 99.9%. Following sequence alignment analysis, the approximate 1.96kb regions were deduced to consist of parts of ureA (about 570bps) and ureB (about 1390bps) with an overlapping region between the ureA and ureB gene loci. Although a total of 144 heterogeneous sites of all substitutions were located throughout this region, the substitution ratio was higher in the ureA region (1/Omega10bases) than in the ureB region (1/Omega15bases). A resulting dendrogram was constructed, which was based on the nucleotide sequence data of 12 UPTC isolates and demonstrated that the UPTC were genetically variable. They formed a major cluster with Helicobacter, separate from the other urease-producing bacteria examined, suggesting a shared ancestry between UPTC and Helicobacter.
    International Journal of Hygiene and Environmental Health 12/2006; 209(6):541-5. · 3.81 Impact Factor
  • Article: Major depression and heat shock protein 70-1 gene.
    [show abstract] [hide abstract]
    ABSTRACT: Heat shock protein (HSP) expression can be induced by any stress such as with adrenocorticotropic hormones and catecholamines. It has been reported that patients with major depression have a 162-base deletion in the 5'-flanking region of heat shock protein 70 (HSP70)-1 gene mRNA. To detect the HSP70-1 gene mRNA, total RNA was isolated and amplified by RT-PCR, and the sequence was confirmed in all five patients by DNA direct sequencing analysis. RT-PCR produced was no deletions of 162 bp in the human heat shock protein 70-1 gene in any of the patients with major depression or the nine controls. This finding is inconsistent with previous reports. We suggest that the 162-base deletion in the 5'-flanking region of the HSP70-1 gene mRNA is not associated with major depression. Further studies are required to determine the amounts of HSP70 and its mRNA in stress disorders such as major depression.
    Clinica Chimica Acta 07/2003; 332(1-2):133-7. · 2.54 Impact Factor

Institutions

  • 2009–2010
    • Tokyo Metropolitan Institute of Gerontology
      Tokyo, Tokyo-to, Japan
  • 2008
    • Rutgers, The State University of New Jersey
      New Brunswick, NJ, USA
  • 2007
    • Broad Institute of MIT and Harvard
      Cambridge, MA, USA
    • Azabu University
      • Laboratory of Molecular Biology
      Sagamihara, Kanagawa-ken, Japan