Researchers Database

tokitowa rina

    Anestheesiology Research Associate
Last Updated :2021/11/23

Researcher Information

Research funding number

  • 20644371

J-Global ID

Research Interests

  • 自然免疫細胞   HLA   サイトカイン   疾患モデル動物   アルツハイマー病   内耳   うつ病   脳腸相関   消化管   がん   酸化ストレス   代謝   

Research Areas

  • Life sciences / Allergies and connective tissue disease
  • Life sciences / Neuroscience - general
  • Life sciences / Tumor biology
  • Life sciences / Developmental biology

Association Memberships


Published Papers

  • Wei Chen, Kazunori Hashimoto, Yasuhiro Omata, Nobutaka Ohgami, Akira Tazaki, Yuqi Deng, Lisa Kondo-Ida, Atsushi Intoh, Masashi Kato
    Environmental health and preventive medicine 24 (1) 36 - 36 1342-078X 2019/05 [Refereed][Not invited]
    BACKGROUND: Melanin is detectable in various sense organs including the skin in animals. It has been reported that melanin adsorbs toxic elements such as mercury, cadmium, and lead. In this study, we investigated the adsorption of molybdenum, which is widely recognized as a toxic element, by melanin. METHODS: Molybdenum level of the mouse skin was measured by inductively coupled plasma mass spectrometry. The pigmentation level of murine skin was digitalized as the L* value by using a reflectance spectrophotometer. An in vitro adsorption assay was performed to confirm the interaction between molybdenum and melanin. RESULTS: Our analysis of hairless mice with different levels of skin pigmentation showed that the level of molybdenum increased with an increase in the level of skin pigmentation (L* value). Moreover, our analysis by Spearman's correlation coefficient test showed a strong correlation (r = - 0.9441, p < 0.0001) between L* value and molybdenum level. Our cell-free experiment using the Langmuir isotherm provided evidence for the adsorption of molybdenum by melanin. The maximum adsorption capacity of 1 mg of synthetic melanin for molybdenum was 131 μg in theory. CONCLUSION: Our in vivo and in vitro results showed a new aspect of melanin as an adsorbent of molybdenum.
  • Comparison of gut tight junction gene expression in C57BL/6J and BALB/c mice after chronic social defeat stress
    Yamagishi N, Omata Y, Aoki-Yoshida A, Moriya N, Goto T, Toyoda A, Aoki R, Suzuki C, Takayama Y
    JARQ 53 (1) 41 - 46 2019/01 [Refereed][Not invited]
  • Omata Y, Yoshinaga M, Yajima I, Ohgami N, Hashimoto K, Higashimura K, Tazaki A, Kato M
    Chemosphere 210 384 - 391 0045-6535 2018/11 [Refereed][Not invited]
    At present, beneficial effects of melanin and harmful effects of barium have been reported. However, little is known about the adsorption of barium, and even less is known about the biological significance of adsorption of barium by melanin. In this study, we showed that there was a strong correlation between the digitalized level of skin pigmentation and barium level in murine skin compared to the correlations between skin pigmentation level and levels of homologous elements of barium (magnesium, calcium and strontium). The concentration of subcutaneously injected barium in skin with a high level of pigmentation was higher than that in skin with a low level of pigmentation. Our cell-free experiment using the Langmuir isotherm for adsorption of barium in synthetic melanin also provided direct evidence of adsorption of barium by melanin. We then investigated the biological significance of melanin-mediated barium adsorption. We found barium-mediated increase in transforming activity in pigmented melanocytes (melan-a) but not in unpigmented melanocytes (melan-c) after confirming that the barium level in melan-a melanocytes was 3.4-fold higher than that in melan-c melanocytes after culture of 5 μM barium for 24 h. Taken together, our results not only indicate adsorption of barium by melanin in mice, cells and cell-free systems but also suggest a disadvantageous effect of adsorption of barium by melanin on transforming activity in cultured cells.
  • Yasuhiro Omata, Reiji Aoki, Ayako Aoki-Yoshida, Keiko Hiemori, Atsushi Toyoda, Hiroaki Tateno, Chise Suzuki, Yoshiharu Takayama
    Scientific reports 8 (1) 13199 - 13199 2018/09 [Refereed][Not invited]
    Psychological stress can cause dysfunction of the gastrointestinal tract by regulating its interaction with central nervous system (brain-gut axis). Chronic social defeat stress (CSDS) is widely used to produce a rodent model of stress-induced human mood disorders and depression. We previously showed that CSDS significantly affects the intestinal ecosystem including cecal and fecal microbiota, intestinal gene expression profiles and cecal metabolite profiles. Here, we investigated whether the glycosylation pattern in the intestinal epithelium was affected in C57BL/6 mice exposed to CSDS (hereinafter referred to as CSDS mice). A lectin microarray analysis revealed that CSDS significantly reduced the reactivity of fucose-specific lectins (rAOL, TJA-II, rAAL, rGC2, AOL, AAL, rPAIIL and rRSIIL) with distal intestinal mucosa, but not with mucosa from proximal intestine and colon. Flow cytometric analysis confirmed the reduced TJA-II reactivity with intestinal epithelial cells in CSDS mice. In addition, distal intestine expression levels of the genes encoding fucosyltransferase 1 and 2 (Fut1 and Fut2) were downregulated in CSDS mice. These findings suggest that CSDS alters the fucosylation pattern in the distal intestinal epithelium, which could be used as a sensitive marker for CSDS exposure.
  • Leo Tsuda, Yasuhiro Omata, Yasutoyo Yamasaki, Ryunosuke Minami, Young-Mi Lim
    HUMAN MOLECULAR GENETICS 26 (23) 4642 - 4656 0964-6906 2017/12 [Refereed][Not invited]
    Alzheimer's disease (AD) is the most common neurodegenerative disorder among the elderly. During the progression of AD, massive neuronal degeneration occurs in the late stage of the disease; however, the molecular mechanisms responsible for this neuronal loss remain unknown. A beta(pE3-42) (an N-terminal-truncated amyloid-beta peptide that begins with pyroglutamate at the third position) is produced during late-stage AD. It also aggregates more rapidly in vitro and exhibits greater toxicity in neurons than full-length A beta(1-42). In the present study, we established a Drosophila melanogaster model that expresses A beta(E3Q)(3-42), which effectively produces A beta(pE3-42), and investigated the function of A beta(pE3-42) using the photoreceptor neurons of Drosophila. A beta(pE3-42) induced caspase-dependent apoptosis and caused progressive degeneration in photoreceptor neurons. Mutations in ER stress response genes or the administration of an inhibitor of the ER stress response markedly suppressed the degeneration phenotype, suggesting that the ER stress response plays an important role in neurodegeneration caused by A beta(pE3-42). We also confirmed that human Tau-dependent apoptotic induction was strongly enhanced by A beta(pE3-42). Thus, A beta(pE3-42) expression system in the fly may be a promising new tool for studying late-onset neurodegeneration in AD.
  • Xiang Li, Nobutaka Ohgami, Yasuhiro Omata, Ichiro Yajima, Machiko Iida, Reina Oshino, Shoko Ohnuma, Nazmul Ahsan, Anwarul Azim Akhand, Masashi Kato
    SCIENTIFIC REPORTS 7 (1) 6844  2045-2322 2017/07 [Refereed][Not invited]
    There is no information on the association between oral exposure to arsenic (As) and hearing loss in humans or mice. In this combined epidemiological study and experimental study, the association of oral exposure to As with hearing loss in people aged 12-29 years and young mice was examined. Subjects in the exposure group (n = 48), who were drinking tube well water contaminated with As, showed significantly higher risks of hearing loss at 4 kHz [odds ratio (OR) = 7.60; 95% confidence interval (CI): 1.56, 57.88], 8 kHz (OR = 5.00; 95% CI: 1.48, 18.90) and 12 kHz (OR = 8.72; 95% CI: 2.09, 47.77) than did subjects in the control group (n = 29). We next performed an experiment in which young mice were exposed to As via drinking water at 22.5 mg/L, which is a much greater concentration than that in human studies. The exposure group showed hearing loss and accumulation of As in inner ears. Ex vivo exposure of the organ of Corti from mice exposed to As significantly decreased the number of auditory neurons and fibers. Thus, our combined study showed that oral exposure to As caused hearing loss in young people and young mice.
  • Yasuhiro Omata, Suganya Tharasegaran, Young-Mi Lim, Yasutoyo Yamasaki, Yasuhito Ishigaki, Takanori Tatsuno, Mitsuo Maruyama, Leo Tsuda
    AGING-US 8 (3) 427 - 440 1945-4589 2016/03 [Refereed][Not invited]
    Increasing evidence indicates that defects in the sensory system are highly correlated with age-related neurodegenerative diseases, including Alzheimer's disease (AD). This raises the possibility that sensory cells possess some commonalities with neurons and may provide a tool for studying AD. The sensory system, especially the auditory system, has the advantage that depression in function over time can easily be measured with electrophysiological methods. To establish a new mouse AD model that takes advantage of this benefit, we produced transgenic mice expressing amyloid-beta (A beta), a causative element for AD, in their auditory hair cells. Electrophysiological assessment indicated that these mice had hearing impairment, specifically in high-frequency sound perception (>32 kHz), at 4 months after birth. Furthermore, loss of hair cells in the basal region of the cochlea, which is known to be associated with age-related hearing loss, appeared to be involved in this hearing defect. Interestingly, overexpression of human microtubule-associated protein tau, another factor in AD development, synergistically enhanced the A beta-induced hearing defects. These results suggest that our new system reflects some, if not all, aspects of AD progression and, therefore, could complement the traditional AD mouse model to monitor A beta-induced neuronal dysfunction quantitatively over time.
  • Yasuhiro Omata, Machiko Iida, Ichiro Yajima, Nobutaka Ohgami, Masao Maeda, Hiromasa Ninomiya, Reina Oshino, Toyonori Tsuzuki, Masaru Hori, Masashi Kato
    INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY 9 (2) 1061 - + 1936-2625 2016 [Refereed][Not invited]
    Development of therapy for melanomas without BRAF(V600E) mutation, which account for about half of all melanomas, is an urgent issue because effective therapy is currently being developed for patients who have melanomas with BRAF(V600E) mutation. RET-transgenic mice (RET-mice) carrying the RFP-RET oncogene under the control of metallothionein-I promoter spontaneously developed skin melanomas without Braf(V600E) mutation from benign melanocytic tumors. We previously showed decreased expression levels of cell cycle regulators and matrix metalloproteinases in melanoma from RET-transgenic mice by single irradiation of non-equilibrium atmospheric pressure plasmas (NEAPPs). In this study, we focused on RFP-RET, c-Ret, Epidermal growth factor receptor (Egfr), Vascular endothelial growth factor receptor 2 (Vegfr2) and c-Src kinases, which are correlated with melanoma. We first confirmed significantly increased transcript expression levels of the 5 kinases in melanomas compared to those in benign tumors in RET-mice. We then found that transcript expression levels of c-Ret and Egfr, but not those of RFP-RET, Vegfr2 and c-Src, were significantly decreased by single irradiation of NEAPP. Since EGFR-mediated promotion of melanoma has been reported, we further focused on the mechanism of NEAPP-mediated decrease in the level of Egfr. Transcript expression level of Y box protein 1 (Ybx1), but not those of p53, Early growth factor 1 (Egr1), GC-rich sequence DNA binding factor 2 (Gcf2) and Kluppel-like factor 10 (Klf10), was significantly decreased by single irradiation of NEAPP. These results suggest that NEAPP decreased Egfr expression level through decrease of Ybx1 expression. Our results indicate that NEAPP irradiation to melanoma without BRAF(V600E) mutation is a possible novel therapy.
  • Sahabudeen Sheik Mohideen, Yasutoyo Yamasaki, Yasuhiro Omata, Leo Tsuda, Yuji Yoshiike
    SCIENTIFIC REPORTS 5 10821  2045-2322 2015/06 [Refereed][Not invited]
    Methylene blue (MB) inhibits the aggregation of tau, a main constituent of neurofibrillary tangles. However, MB's mode of action in vivo is not fully understood. MB treatment reduced the amount of sarkosyl-insoluble tau in Drosophila that express human wild-type tau. MB concurrently ameliorated the climbing deficits of transgenic tau flies to a limited extent and diminished the climbing activity of wild-type flies. MB also decreased the survival rate of wild-type flies. Based on its photosensitive efficacies, we surmised that singlet oxygen generated through MB under light might contribute to both the beneficial and toxic effects of MB in vivo. We identified rose bengal (RB) that suppressed tau accumulation and ameliorated the behavioral deficits to a lesser extent than MB. Unlike MB, RB did not reduce the survival rate of flies. Our findings indicate that singlet oxygen generators with little toxicity may be suitable drug candidates for treating tauopathies.
  • Ichiro Yajima, Mayuko Y. Kumasaka, Shoko Ohnuma, Nobutaka Ohgami, Hisao Naito, Hossain U. Shekhar, Yasuhiro Omata, Masashi Kato
    JOURNAL OF INVESTIGATIVE DERMATOLOGY 135 (4) 1147 - 1156 0022-202X 2015/04 [Refereed][Not invited]
    Various cancers including skin cancer are increasing in 45 million people exposed to arsenic above the World Health Organization's guideline value of 10 mu gl(-1). However, there is limited information on key molecules regulating arsenic-mediated carcinogenesis. Our fieldwork in Bangladesh demonstrated that levels of placental growth factor (PIGF) in urine samples from residents of cancer-prone areas with arsenic-polluted drinking water were higher than those in urine samples from residents of an area that was not polluted with arsenic. Our experimental study in human nontumorigenic HaCaT skin keratinocytes showed that arsenite promoted anchorage-independent growth with increased expression and secretion of PIGF, a ligand of vascular endothelial growth factor receptor1 (VEGFR1), and increased VEGFR1/mitogen-activated protein kinase/ERK kinase (MEK)/extracellular signal-regulated kinase (ERK) activities. The arsenite-mediated promotion of anchorage-independent growth was strongly inhibited by PIGF depletion with decreased activities of the PIGF/VEGFR1/MEK/ERK pathway. Moreover, arsenite proteasome-dependently degrades metal-regulatory transcription factor-1 (MTF-1) protein, resulting in a decreased amount of MTF-1 protein binding to the PIGF promoter. MTF-1 negatively controlled PIGF transcription in HaCaT cells, resulting in increased PIGF transcription. These results suggest that arsenite-mediated MTF-1 degradation enhances the activity of PIGF/VEGFR1/MEK/ERK signaling, resulting in promotion of the malignant transformation of keratinocytes. Thus, this study proposed a molecular mechanism for arsenite-mediated development of skin cancer.
  • Ohgami N, Iida M, Omata Y, Nakano C, Wenting W, Li X, Kato M
    Nihon eiseigaku zasshi. Japanese journal of hygiene 70 (2) 100 - 104 0021-5082 2015 [Refereed][Not invited]
  • Yajima I, Zou C, Li X, Nakano C, Omata Y, Kumasaka MY
    Nihon eiseigaku zasshi. Japanese journal of hygiene 70 (2) 105 - 109 0021-5082 2015 [Refereed][Not invited]
  • Kato M, Omata Y, Iida M, Kumasaka MY, Ohgami N, Li X, Zou C, Nakano C, Kato Y, Ohgami K, Ohnuma S, Yajima I
    Nihon eiseigaku zasshi. Japanese journal of hygiene 70 (3) 176 - 180 0021-5082 2015 [Refereed][Not invited]
  • Machiko Iida, Yasuhiro Omata, Chihiro Nakano, Ichiro Yajima, Toyonori Tsuzuki, Kenji Ishikawa, Masaru Hori, Masashi Kato
    INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY 8 (8) 9326 - 9331 1936-2625 2015 [Refereed][Not invited]
    Since effective therapies for melanoma with BRAFV600E mutation are being developed, interest has been shown in the development of therapies for melanoma without BRAFV600E mutation. Recently, interest has also been shown in medical application of non-nequilibrium atmospheric pressure plasmas (NEAPPs). We previously suggested that repeated NEAPP irradiation to spontaneously developed benign melanocytic tumors in RFP-RET-transgenic mice (RET-mice) not only suppresses tumor growth but also prevents malignant transformation. In this study, we first confirmed that transcript expression levels of tumor growth regulators (CyclinD1, D2, E1, E2, G2 and PCNA but not CyclinG1) and tumor invasion regulators [Matrix metalloproteinase (MMP)-2, -9 and -14 and melanoma cell adhesion molecule (MCAM)] in melanomas were significantly higher than those in benign melanocytic tumors in RET-mice. We then showed that transcript expression levels of CyclinE1, G1 and G2 and MMP-2 and -9 in melanomas from RET-mice were significantly decreased by single NEAPP irradiation, whereas transcript expression levels of CyclinD1, D2, E2, PCNA, MCAM and MMP-14 were comparable in untreated and NEAPP-treated melanomas. Since no BrafV600E mutation melanomas have been found in RET-mice, our results suggest that single NEAPP irradiation is a potential therapeutic tool for melanoma without BRAFV600E mutation through modulation of the expression levels of tumor growth and invasion regulators.
  • Kozue Takeda, Yoshiyuki Kawamoto, Machiko Iida, Yasuhiro Omata, Cunchao Zou, Masashi Kato
    ARCHIVES OF TOXICOLOGY 88 (12) 2319 - 2320 0340-5761 2014/12 [Refereed][Not invited]
  • Yasuhiro Omata, Machiko Iida, Ichiro Yajima, Kozue Takeda, Nobutaka Ohgami, Masaru Hori, Masashi Kato
    ENVIRONMENTAL HEALTH AND PREVENTIVE MEDICINE 19 (5) 367 - 369 1342-078X 2014/09 [Refereed][Not invited]
    Due to the increased ultraviolet radiation, the incidence of melanoma is increasing worldwide more than that of any other cancer. In this study, the effects of irradiation of non-thermal atmospheric pressure plasmas (NEAPPs) on benign melanocytic tumors from our original hairless model mice (HL-RET-mice), in which benign melanocytic tumors and melanomas spontaneously develop in the skin stepwise, were examined. Expression levels of melanoma cell adhesion molecule (MCAM) and matrix metalloproteinase-2 (MMP-2) mRNA in melanomas were higher than those in benign melanocytic tumors in the mice. Repeated irradiation of non-thermal atmospheric pressure plasmas (NEAPPs) for the benign tumors decreased the expression levels of MCAM and MMP-2 mRNA in the tumors from the mice. Previous studies showed that MCAM sites are upstream of MMP-2, that MCAM regulates transcription of MMP-2 in melanoma cells and that MMP-2 is associated with the conversion of a benign tumor to a malignant tumor. Therefore, our results suggest that the NEAPP irradiation-mediated decrease in the expression level of MMP-2 in benign melanocytic tumors is associated with decreased expression levels of MCAM. Moreover, NEAPP irradiation might be a potential candidate for therapy to prevent melanoma development through suppression of malignant conversion in benign melanocytic tumors.
  • Ichiro Yajima, Machiko Iida, Mayuko Y. Kumasaka, Yasuhiro Omata, Nobutaka Ohgami, Jie Chang, Sahoko Ichihara, Masaru Hori, Masashi Kato
    EXPERIMENTAL DERMATOLOGY 23 (6) 424 - 425 0906-6705 2014/06 [Refereed][Not invited]
    The incidence of cutaneous malignant melanoma is increasing at a greater rate than that of any other cancer in the world. However, an effective therapy for malignant melanoma has not been established. Recently, some studies have shown an antitumor effect of non-equilibrium atmospheric pressure plasmas (NEAPPs) in vitro. Here, we examined the in vivo effect of NEAPP on cell cycle regulators, key elements for malignant transformation, in spontaneously developed benign melanocytic tumors in a hairless animal model. NEAPP irradiation decreased expression levels of cell cycle promoters, Cyclin D1, E1 and E2, and increased expression level of a cell cycle repressor, p27KIP1. Cyclin D1, E1 and E2 and p27KIP expression levels were associated with malignant transformation of the benign tumor in the animal model. Our results suggest that NEAPP irradiation suppresses malignant transformation of a benign melanocytic tumor via control of the expression levels of cell cycle regulators.
  • Mayuko Y. Kumasaka, Ichiro Yajima, Nobutaka Ohgami, Hisao Naito, Yasuhiro Omata, Masashi Kato
    ARCHIVES OF TOXICOLOGY 88 (5) 1185 - 1186 0340-5761 2014/05 [Refereed][Not invited]
    Krishna et al. (Arch Toxicol 88(1): 47-64, 2014) recently published the results of a study in which adult C57BL/6 mice were subchronically exposed to 400,000 mu g/L manganese (Mn) using manganese chloride via drinking water for 8 weeks and examined the neurotoxic effects. After 5 weeks of Mn exposure, significant deposition of Mn in all of the brain regions examined by magnetic resonance imaging was detected. After 6 weeks of Mn exposure, neurobehavioral deficits in an open field test, a grip strength test, and a forced swim test were observed. Eight weeks of Mn exposure increased striatal 5-hydroxyindoleacetic acid (a serotonin metabolite) levels, but did not alter the levels of striatal dopamine, its metabolites and serotonin. Krishna et al. also reported significant increases in mRNA levels of GFAP (an astrocyte activation marker), HO-1 (an oxidative stress marker) and NOS2 (a nitrosative stress marker), and in protein expression level of GFAP in the substantia nigra pars reticulata after 8 weeks of Mn exposure. These results suggest that 400,000 mu g/L Mn exposure via drinking water in mice induces neurobehavioral deficits, serotonergic imbalance, and glial activation accompanied by an increase in brain Mn deposition. The report by Krishna et al. is interesting because the studies on the neurobehavioral effect of Mn exposure by drinking water in mice are very limited. However, Mn concentrations previously reported in well drinking water (Agusa et al. in Vietnam Environ Pollut 139(1): 95-106, 2006; Buschmann et al. in Environ Int 34(6): 756-764, 2008; Hafeman et al. in Environ Health Perspect 115(7): 1107-1112, 2007; Wasserman et al. in Bangladesh Environ Health Perspect 114(1): 124-129, 2006) were lower than 400,000 mu g/ L.
  • Omata Y, Lim YM, Akao Y, Tsuda L
    American journal of neurodegenerative disease 3 (3) 134 - 142 2014 [Refereed][Not invited]
  • Yasuhiro Omata, Yasuhiro Nojima, Satomi Nakayama, Hitoshi Okamoto, Harukazu Nakamura, Jun-ichi Funahashi
    DEVELOPMENT GROWTH & DIFFERENTIATION 49 (9) 711 - 719 0012-1592 2007/12 [Refereed][Not invited]
    Bone morphogenetic proteins (BMPs) are known to play roles in inner ear development of higher vertebrates. In zebrafish, there are several reports showing that members of the BMP family are expressed in the otic vesicle. We have isolated a novel zebrafish mutant gallery, which affects the development of the semicircular canal. Gallery merely forms the lateral and the immature anterior protrusion, and does not form posterior and ventral protrusions. We found that the expression of bmp2b and bmp4, both expressed in the normal optic vesicle at the protrusion stage, are extremely upregulated in the otic vesicle of gallery. To elucidate the role of BMPs in the development of the inner ear of zebrafish, we have applied excess BMP to the wild-type otic vesicle. The formation of protrusions was severely affected, and in some cases, they were completely lost in BMP4-treated embryos. Furthermore, the protrusions in gallery treated with Noggin were partially rescued. These data indicate that BMP4 plays an important role in the development of protrusions to form semicircular canals.

Conference Activities & Talks

  • 精神的ストレスは腸管上皮細胞のフコシル化糖鎖を減少させる  [Not invited]
    小又尉広, 青木玲二, 青木(吉田)綾子, 比江森恵子, 豊田淳, 舘野浩章, 鈴木チセ, 高山喜晴
    SAT 2019 テクノロジー・ショーケース  2019/01
  • パルミトイル-L-カルニチンは大腸がん細胞株においてアポトーシスを誘導し、浸潤を抑制する  [Not invited]
    小又尉広, 山岸直子, 高山喜晴
    第41回日本分子生物学会  2018/11
  • Palmitoyl-L-carnitine induces apoptosis and suppresses invasion of colorectal cancer caco2  [Not invited]
    Omata Y, Yamagishi N, Takayama Y
    第40回日本分子生物学会年会  2017/12
  • 個体レベルのスクリーニングによるアルツハイマー病治療薬の開発  [Not invited]
    津田玲生, 小又尉広, 山崎泰豊, 市原沙織, 林永美
    第34回日本認知症学会学術集会  2015/10
  • 創薬開発に資する新規アルツハイマー解析モデルマウスの作製  [Not invited]
    津田玲生, 小又尉広, 山崎泰豊, 林永美
    第33回日本認知症学会学術集会  2014/12
  • アルツハイマー病モデルショウジョウバエにおけるAβペプチドの経時的挙動:治療薬開発のための基礎解析  [Not invited]
    山崎泰豊, 小又尉広, 鈴木枝里子, 林永美, 柳澤勝彦, 津田玲生
    第37回日本分子生物学会年会  2014/11
  • 聴覚細胞を用いた新規アルツハイマー病解析モデルマウスの作製  [Not invited]
    津田玲生, 小又尉広, 山崎泰豊, 林永美
    日本神経化学会第57回大会  2014/09
  • Analysis on the use of oxidative eustress for potential Alzheimer's therapy  [Not invited]
    Yoshiike Y, Tsuda L, Tsuda L, Yamasaki Y, Omata Y, Sugimoto M, Hashimoto M, Takashshima A, Mohideen SS
    日本基礎老化学会第37回大会  2014/06
  • The effect of aging in Alzheimer disease formation  [Not invited]
    Tsuda L, Omata Y, Yamasaki Y, Lim YM
    日本基礎老化学会第37回大会  2014/06
  • ショウジョウバエを用いたアルツハイマー病治療薬の定量的評価系  [Not invited]
    山崎泰豊, 小又尉広, 鈴木枝里子, 林永美, 柳澤勝彦, 津田玲生
    第36回日本分子生物学会年会  2013/12
  • アルツハイマー重篤化メカニズムの解析  [Not invited]
    小又尉広, 山崎泰豊, 林永美, 津田玲生
    第32回日本認知症学会学術集会  2013/11
  • Molecular study of age-related hearing disorders  [Not invited]
    Lim YM, Omata Y, Yamasaki Y, Tsuda L
    54th Drosophila Research Conference  2013/04
  • Chemical Genetic approach to evaluate the toxicity of Amyloid beta using Drosophila  [Not invited]
    Tsuda L, Omata Y, Yamasaki Y, Lim YM
    11th International Conference on Alzheimer & Parkinson’s Disease (AD/PD 2013)  2013/03
  • HDAC 制御によるタウ代謝機構の解析  [Not invited]
    吉池裕二, 小又尉広, 津田玲生
    第31回日本認知症学会学術集会  2012/12
  • 感覚細胞を用いた認知症モデルの作製  [Not invited]
    認知症研究を知る若手研究者の集まり  2011/07
  • 三半規管形成に異常を示すゼブラフィッシュ突然変異体galleryとBMPシグナルについて  [Not invited]
    小又尉広, 野島康弘, 中山里実, 岡本仁, 仲村春和, 舟橋淳一
    日本発生生物学会第39回大会  2006/06
  • 三半規管形成に影響を与えるゼブラフィッシュ突然変異体の解析  [Not invited]
    小又尉広, 野島康弘, 中山里実, 岡本仁, 仲村春和, 舟橋淳一
    日本発生生物学会第38回大会  2005/06
  • ゼブラフィッシュ内耳に関する突然変異体のスクリーニング  [Not invited]
    小又尉広, 野島康弘, 岡本仁, 仲村春和, 舟橋淳一
    日本発生生物学会第37回大会  2004/06
  • 培養したニワトリ胚網膜色素上皮の神経性網膜への分化転換様式の解析  [Not invited]
    小又尉広, 和気由里枝, 恒松康彦
    日本細胞生物学会第56回大会  2003/05
  • 培養した網膜色素上皮から神経性網膜又は水晶体への分化転換におけるbFGFの役割  [Not invited]
    小又尉広, 佐藤 渉, 中川俊徳, 恒松康彦
    日本細胞生物学会第55回大会  2002/05


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