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Articles by M Suzuki
Total Records ( 6 ) for M Suzuki
  M Suzuki , A Tatsumi , T Otsuka , K Kikuchi , A Mizuta , K Makino , A Kimoto , K Fujiwara , T Abe , T Nakagomi , T Hayashi and T. Saruhara

Tactile massage is a soft massage that improves physical relaxation and psychological well-being. The purpose of this study was to clarify the effects of a 6-week tactile massage on changes in physical and mental function, symptoms of behavioral and psychological symptoms of dementia (BPSD) among elderly patients with dementia. In addition, chromogranin A (CgA) levels as an index of stress examined the effects of tactile massage intervention. A tactile massage group consisting of elderly patients with dementia received tactile massage therapy a total of 30 times each for about 20 minutes between 16:00 and 17:00 hours. In the control group, the mean scores for ‘‘intellectual’’ and ‘‘emotional function’’ score decreased significantly after 6 weeks (P < .05); however, no change was observed in the tactile massage group. Both the ‘‘aggressiveness’’ score (P < .05) and CgA levels decreased significantly after 6 weeks in the tactile massage group. These results suggest that tactile massage reduces aggressiveness and stress level in patients with dementia.

  R. F Thompson , M Suzuki , K. W Lau and J. M. Greally

Motivation: DNA cytosine methylation is an important epigenetic regulator, critical for mammalian development and the control of gene expression. Numerous techniques using either restriction enzyme or affinity-based approaches have been developed to interrogate cytosine methylation status genome-wide, however these assays must be validated by a more quantitative approach, such as MALDI-TOF mass spectrometry of bisulphite-converted DNA (commercialized as Sequenom's EpiTYPER assay using the MassArray system). Here, we present an R package (‘MassArray’) that assists in assay design and uses the standard Sequenom output file as the input to a pipeline of analyses not available as part of the commercial software. The tools in this package include bisulphite conversion efficiency calculation, sequence polymorphism flagging and visualization tools that combine multiple experimental replicates and create tracks for genome browser viewing.

  T. S Kim , M Kawaguchi , M Suzuki , C. G Jung , K Asai , Y Shibamoto , M. F Lavin , K. K Khanna and Y. Miura
  Tae-Sun Kim, Makoto Kawaguchi, Mitsuko Suzuki, Cha-Gyun Jung, Kiyofumi Asai, Yuta Shibamoto, Martin F. Lavin, Kum Kum Khanna, and Yutaka Miura

Ataxia telangiectasia (A-T) is a neurodegenerative disease caused by mutations in the large serine-threonine kinase ATM. A-T patients suffer from degeneration of the cerebellum and show abnormal elevation of serum alpha-fetoprotein. Here, we report a novel signaling pathway that links ATM via cAMP-responsive-element-binding protein (CREB) to the transcription factor ZFHX3 (also known as ATBF1), which in turn promotes survival of neurons by inducing expression of platelet-derived growth factor receptor β (PDGFRB). Notably, AG1433, an inhibitor of PDGFRB, suppressed the activation of ATM under oxidative stress, whereas AG1433 did not inhibit the response of ATM to genotoxic stress by X-ray irradiation. Thus, the activity of a membrane-bound tyrosine kinase is required to trigger the activation of ATM in oxidative stress, independent of the response to genotoxic stress. Kainic acid stimulation induced activation of ATM in the cerebral cortex, hippocampus and deep cerebellar nuclei (DCN), predominately in the cytoplasm in the absence of induction of -H2AX (a marker of DNA double-strand breaks). The activation of ATM in the cytoplasm might play a role in autophagy in protection of neurons against oxidative stress. It is important to consider DCN of the cerebellum in the etiology of A-T, because these neurons are directly innervated by Purkinje cells, which are progressively lost in A-T.

  T Nakakura , A Soda , K Unno , M Suzuki and S. Tanaka

The number of corticotrophs increases in the anterior pituitary (AP) gland in adrenalectomized (AdX) rats. In this study, aimed at identifying the growth factor implicated in this proliferation, we analyzed proteins secreted from a cDNA library of the AP of AdX rats, using the signal sequence trap method. A PCR analysis of several cDNAs that coded for insulin-like growth factor binding protein (IGFBP) 5, IGFBP7, and vacuolar H+-ATPase accessory subunit Ac45 revealed an increased and decreased expression level of IGFBP7 mRNA in the AP of AdX rats and AdX rats injected with dexamethasone, respectively. IGFBP7 mRNA was predominately expressed in the corticotrophs of the APs of both sham-operated and AdX rats. The AP of AdX rats contained an increased number of IGFBP7 mRNA–expressing cells and corticotrophs compared with that of sham-operated rats, but the ratio of IGFBP7 mRNA–positive corticotrophs per total number of corticotrophs did not significantly change in either group. Histochemical analysis of labeled proliferating cell nuclear antigen (PCNA) and sex-determining region Y box-2 (SOX2) revealed the presence of several PCNA-positive signals and the absence of SOX2 cells among the corticotrophs, suggesting that IGFBP7 mRNA–expressing corticotrophs are derived from in situ corticotrophs and that they increase in number as corticotrophs increase. The possible roles of IGFBP7 in the corticotrophs are also discussed. (J Histochem Cytochem 58:969–978, 2010)

  T Takahashi , S. J Wood , A. R Yung , M Walterfang , L. J Phillips , B Soulsby , Y Kawasaki , P. D McGorry , M Suzuki , D Velakoulis and C. Pantelis


Morphological abnormalities of the superior temporal gyrus have been consistently reported in schizophrenia, but the timing of their occurrence remains unclear.


To determine whether individuals exhibit superior temporal gyral changes before the onset of psychosis.


We used magnetic resonance imaging to examine grey matter volumes of the superior temporal gyrus and its subregions (planum polare, Heschl’s gyrus, planum temporale, and rostral and caudal regions) in 97 antipsychotic-naive individuals at ultra-high risk of psychosis, of whom 31 subsequently developed psychosis and 66 did not, and 42 controls.


Those at risk of psychosis had significantly smaller superior temporal gyri at baseline compared with controls bilaterally, without any prominent subregional effect; however, there was no difference between those who did and did not subsequently develop psychosis.


Our findings indicate that grey matter reductions of the superior temporal gyrus are present before psychosis onset, and are not due to medication, but these baseline changes are not predictive of transition to psychosis.

  M Suzuki , A Niimi , S Limsirichaikul , S Tomida , Q Miao Huang , S Izuta , J Usukura , Y Itoh , T Hishida , T Akashi , Y Nakagawa , A Kikuchi , Y Pavlov , T Murate and T. Takahashi

Translesion DNA synthesis (TLS) involves PCNA mono-ubiquitination and TLS DNA polymerases (pols). Recent evidence has shown that the mono-ubiquitination is induced not only by DNA damage but also by other factors that induce stalling of the DNA replication fork. We studied the effect of spontaneous DNA replication errors on PCNA mono-ubiquitination and TLS induction. In the pol1L868F strain, which expressed an error-prone pol , PCNA was spontaneously mono-ubiquitinated. Pol L868F had a rate-limiting step at the extension from mismatched primer termini. Electron microscopic observation showed the accumulation of a single-stranded region at the DNA replication fork in yeast cells. For pol errors, pol participated in a generation of +1 frameshifts. Furthermore, in the pol1L868F strain, UV-induced mutations were lower than in the wild-type and a pol mutant strain (pol3-5DV), and deletion of the RAD30 gene (pol ) suppressed this defect. These data suggest that nucleotide misincorporation by pol induces exposure of single-stranded DNA, PCNA mono-ubiquitination and activates TLS pols.

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