|山座 治義（やまざ はるよし）||データ更新日：2020.05.26|
|1.||Haruyoshi Yamaza, Soichiro Sonoda, Kazuaki Nonaka, Toshio Kukita, Takayoshi Yamaza, Pamidronate decreases bilirubin-impaired cell death and improves dentinogenic dysfunction of stem cells from human deciduous teeth, Stem Cell Research and Therapy, 10.1186/s13287-018-1042-7, 9, 1, 2018.11, [URL], BACKGROUND: Hyperbilirubinemia that occurs in pediatric liver diseases such as biliary atresia can result in the development of not only jaundice in the brain, eyes, and skin, but also tooth abnormalities including green pigmentation and dentin hypoplasia in the developing teeth. However, hyperbilirubinemia-induced tooth impairments remain after liver transplantation. No effective dental management to prevent hyperbilirubinemia-induced tooth impairments has been established. METHODS: In this study, we focused on pamidronate, which is used to treat pediatric osteopenia, and investigated its effects on hyperbilirubinemia-induced tooth impairments. We cultured stem cells from human exfoliated deciduous teeth (SHED) under high and low concentrations of unconjugated bilirubin in the presence or absence of pamidronate. We then analyzed the effects of pamidronate on the cell death, associated signal pathways, and dentinogenic function in SHED. RESULTS: We demonstrated that a high concentration of unconjugated bilirubin induced cell death in SHED via the mitochondrial pathway, and this was associated with the suppression of AKT and extracellular signal-related kinase 1 and 2 (ERK1/2) signal pathways and activation of the nuclear factor kappa B (NF-κB) signal pathway. The high concentration of unconjugated bilirubin impaired the in vitro and in vivo dentinogenic capacity of SHED, but not the low concentration. We then demonstrated that pamidronate decreased the bilirubin-induced cell death in SHED via the altered AKT, ERK1/2, and NF-κB signal pathways and recovered the bilirubin-impaired dentinogenic function of SHED. CONCLUSIONS: Our findings suggest that pamidronate may prevent tooth abnormalities in pediatric patients with hyperbilirubinemia..|
|2.||Haruyoshi Yamaza, E. Tomoda, S. Sonoda, K. Nonaka, Toshio Kukita, Takayoshi Yamaza, Bilirubin reversibly affects cell death and odontogenic capacity in stem cells from human exfoliated deciduous teeth, Oral Diseases, 10.1111/odi.12827, 24, 5, 809-819, 2018.01, [URL], Objective: Hyperbilirubinemia in patients with biliary atresia causes deciduous tooth injuries such as green pigmentation and dentin hypoplasia. In patients with biliary atresia who received liver transplantation, tooth structure appears to be recovered radiographically. Nevertheless, little is known about cellular mechanisms underlying bilirubin-induced damage and suppression of deciduous tooth formation. In this study, we examined the effects of bilirubin in stem cells from human exfoliated deciduous teeth (SHED) in vitro. Materials and Methods: SHED were cultured under exposure to excess of bilirubin and then interruption of bilirubin stimulation. Results: Bilirubin induced cell death and inhibited the odontogenic capacity of SHED by suppressing AKT and extracellular signal-regulated kinase 1 and 2 (ERK1/2) pathways and enhancing nuclear factor kappa B p65 (NF-κB p65) pathway. The interruption of bilirubin stimulation reduced cell death and recovered the inhibited odontogenic capacity of bilirubin-damaged SHED. The bilirubin interruption also normalized the impaired AKT, ERK1/2, and NF-κB p65 signaling pathways. Conclusion: These findings suggest that tooth hypodontia in patients with hyperbilirubinemia might be due to bilirubin-induced cell death and dentinogenic dysfunction of odontogenic stem cells via AKT, ERK1/2, and NF-κB pathways and also suggested that bilirubin-induced impairments in odontogenic stem cells were reversible when bilirubin stimulation is interrupted..|
|3.||Jingxian Fang, Haruyoshi Yamaza, Takeshi Uchiumi, Yoshihiro Hoshino, Keiji Masuda, Yuta Hirofuji, Frank A.D.T.G. Wagener, Dongchon Kang, Kazuaki Nonaka, Dihydroorotate dehydrogenase depletion hampers mitochondrial function and osteogenic differentiation in osteoblasts, European Journal of Oral Sciences, 10.1111/eos.12270, 124, 3, 241-245, 2016.06, [URL], Mutation of the dihydroorotate dehydrogenase (DHODH) gene is responsible for Miller syndrome, which is characterized by craniofacial malformations with limb abnormalities. We previously demonstrated that DHODH was involved in forming a mitochondrial supercomplex and that mutated DHODH led to protein instability, loss of enzyme activity, and increased levels of reactive oxygen species in HeLa cells. To explore the etiology of Miller syndrome in more detail, we investigated the effects of DHODH inhibition in the cells involved in skeletal structure. Dihydroorotate dehydrogenase in MC3T3-E1 cells derived from mouse calvaria osteoblast precursor cells was knocked down by specific small interfering RNAs (siRNAs), and cell proliferation, ATP production, and expression of bone-related genes were investigated in these cells. After depletion of DHODH using specific siRNAs, inhibition of cell proliferation and cell cycle arrest occurred in MC3T3-E1 cells. In addition, ATP production was reduced in whole cells, especially in mitochondria. Furthermore, the levels of runt-related transcription factor 2 (Runx2) and osteocalcin (Ocn) mRNAs were lower in DHODH siRNA-treated cells compared with controls. These data suggest that depletion of DHODH affects the differentiation and maturation of osteoblasts. This study shows that mitochondrial dysfunction by DHODH depletion in osteoblasts can be directly linked to the abnormal bone formation in Miller syndrome..|
|4.||山座 治義, 増田 啓次, 柳田 憲一, 西垣 奏一郎, 小笠原 貴子, 廣藤 雄太, 野中 和明, Angelman症候群の患児に多数歯齲蝕を認めた1例, 小児歯科学会雑誌, 52, 4, 559-564, 2014.10.|
|5.||増田 啓次, 山座 治義, 西垣 奏一郎, 小笠原 貴子, 大隈 由紀子, 柳田 憲一, 野中 和明, Hallermann, Streiff症候群に歯肉腫瘤を伴う先天歯を認めた1例, 小児歯科学会雑誌, 51, 4, 461-466, 2013.10.|
|6.||Haruyoshi Yamaza, Toshimitsu Komatsu, Saori Wakita, Carole Kijogi, Seongjoon Park, Hiroko Hayashi, Takuya Chiba, Ryoichi Mori, Tatsuo Furuyama, Nozomu Mori, Isao Shimokawa, FoxO1 is involved in the antineoplastic effect of calorie restriction, Aging Cell, 10.1111/j.1474-9726.2010.00563.x, 9, 3, 372-382, 2010.06, [URL], The FoxO transcription factors may be involved in the antiaging effect of calorie restriction (CR) in mammals. To test the hypothesis, we used FoxO1 knockout heterozygotic (HT) mice, in which the FoxO1 mRNA level was reduced by 50%, or less, of that in wild-type (WT) mouse tissues. The WT and HT mice were fed ad libitum (AL) or 30% CR diets from 12 weeks of age. Aging- and CR-related changes in body weight, food intake, blood glucose, and insulin concentrations were similar between the WT and HT mice in the lifespan study. The response to oxidative stress, induced by intraperitoneal injection of 3-nitropropionic acid (3-NPA), was evaluated in the liver and hippocampus at 6 months of age. Several of the selected FoxO1-target genes for cell cycle arrest, DNA repair, apoptosis, and stress resistance were up-regulated in the WT-CR tissues after 3-NPA injection, while the effect was mostly diminished in the HT-CR tissues. Of these gene products, we focused on the nuclear p21 protein level in the liver and confirmed its up-regulation only in the WT-CR mice in response to oxidative stress. The lifespan did not differ significantly between the WT and HT mice in AL or CR conditions. However, the antineoplastic effect of CR, as indicated by reduced incidence of tumors at death in the WT-CR mice, was mostly abrogated in the HT-CR mice. The present results suggest a role for FoxO1 in the antineoplastic effect of CR through the induction of genes responsible for protection against oxidative and genotoxic stress..|
|7.||Ming Zhan, Haruyoshi Yamaza, Yu Sun, Jason Sinclair, Huai Li, Sige Zou, Temporal and spatial transcriptional profiles of aging in Drosophila melanogaster, Genome Research, 10.1101/gr.6216607, 17, 8, 1236-1243, 2007.08, [URL], Temporal and tissue-specific alterations in gene expression have profound effects on aging of multicellular organisms. However, much remains unknown about the patterns of molecular changes in different tissues and how different tissues interact with each other during aging. Previous genomic studies on invertebrate aging mostly utilized the whole body or body parts and limited age-points, and failed to address tissue-specific aging. Here we measured genome-wide expression profiles of aging in Drosophila melanogaster for seven tissues representing nervous, muscular, digestive, renal, reproductive, and storage systems at six adult ages. In each tissue, we identified hundreds of age-related genes exhibiting significant changes of transcript levels with age. The age-related genes showed clear tissue-specific patterns: <10% of them in each tissue were in common with any other tissue; <20% of the biological processes enriched with the age-related genes were in common between any two tissues. A significant portion of the age-related genes were those involved in physiological functions regulated by the corresponding tissue. Nevertheless, we identified some overlaps of the age-related functional groups among tissues, suggesting certain common molecular mechanisms that regulate aging in different tissues. This study is one of the first that defined global, temporal, and spatial changes associated with aging from multiple tissues at multiple ages, showing that different tissues age in different patterns in an organism. The spatial and temporal transcriptome data presented in this study provide a basis and a valuable resource for further genetic and genomic investigation of tissue-specific regulation of aging..|
|8.||Haruyoshi Yamaza, Toshimitsu Komatsu, Kazuo To, Hiroaki Toyama, Takuya Chiba, Yoshikazu Higami, Isao Shimokawa, Involvement of insulin-like growth factor-1 in the effect of caloric restriction
Regulation of plasma adiponectin and leptin, Journals of Gerontology - Series A Biological Sciences and Medical Sciences, 10.1093/gerona/62.1.27, 62, 1, 27-33, 2007.01, [URL], Insulin-like growth factor (IGF)-1 signaling might partly mediate effects of caloric restriction (CR), an experimental intervention for increasing longevity in mammals. The present study evaluated effects of recombinant human (rh)IGF-1 infusion on adipokine levels in CR and transgenic (Tg) dwarf rats with the reduced growth hormone-IGF-1 axis, which shared similar body weight and food intake. At 9 months of age, each rat received a continuous infusion of rhIGF-1 for 14 days, and rats received an injection of glucose after overnight fasting. Infusion of rhIGF-1 had metabolic effects in all rat groups although it did not affect insulin sensitivity in any of the groups. In addition, plasma adiponectin was decreased to the control group levels and plasma leptin was further reduced in CR and Tg rats. The similarity of phenotypes and adipokine responses to rhIGF-1 between CR and Tg rats supports a role for reduced IGF-1 signaling in the CR effect..
|9.||Haruyoshi Yamaza, Toshimitsu Komatsu, Takuya Chiba, Hiroaki Toyama, Kazuo To, Yoshikazu Higami, Isao Shimokawa, A transgenic dwarf rat model as a tool for the study of calorie restriction and aging, Experimental Gerontology, 10.1016/j.exger.2003.11.001, 39, 2, 269-272, 2004.01, [URL], We have previously reported a long-lived transgenic dwarf rat model, in which the growth hormone (GH)-insulin like growth factor (IGF)-1 axis was selectively suppressed by overexpression of antisense GH transgene. Rats heterozygous for the transgene (tg/-) manifest phenotypes similar to those in calorie-restricted (CR) rats. To further characterize the transgenic rat in comparison with CR rats, the present study evaluated glucose and insulin tolerance in tg/- and control Wistar (-/-) rats at 6-9 months of age. Rats were fed ad libitum (AL) or 30% CR from 6 weeks of age. In CR rats, glucose disposal after glucose load was facilitated without any significant surge of serum insulin, and insulin tolerance test also indicated increased insulin sensitivity. In transgenic rats, similar findings were observed after glucose and insulin load, and CR in tg/- rats further facilitated glucose disposal during glucose and insulin tolerance tests. These findings suggest the presence of both common and separate mechanisms regulating the glucose-insulin system between CR and the reduced GH-IGF-1 axis paradigms. The transgenic rat model is, therefore, a useful one for studies of CR and aging..|
|10.||Haruyoshi Yamaza, Takuya Chiba, Yoshikazu Higami, Isao Shimokawa, Lifespan extension by caloric restriction
An aspect of energy metabolism, Microscopy Research and Technique, 10.1002/jemt.10212, 59, 4, 325-330, 2002.11, [URL], Caloric restriction (CR) may retard aging processes and extend lifespan in organisms by altering energy-metabolic pathways. In CR rodents, glucose influx into tissues is not reduced, as compared with control animals fed ad libitum (AL), although plasma concentrations of glucose and insulin are lower. Gene expression profiles in rodents have suggested that CR promotes gluconeogenesis and fatty acid biosynthesis in skeletal muscle. In the liver, CR promotes gluconeogenesis but decreases fatty acid synthesis and glycolysis. In lower organisms such as yeasts and nematodes, incomplete blocks in steps of insulin/insulin-like growth factor-1 (IGF-1) signal pathway extend lifespan. The life-prolonging effect of CR in yeasts requires NPT1 and SIR2 genes, both of which relate to sensing energy status and silencing genes. These findings stress the substantial role of energy metabolism on CR. Future studies on metabolic adaptation and gene silencing with regard to lower caloric intake will be warranted to understand the mechanisms of the anti-aging and life-prolonging effects of CR..
|11.||Haruyoshi Yamaza, K. Matsuo, Tamotsu Kiyoshima, Noriatsu Shigemura, I. Kobayashi, Hiroko Wada, A. Akamime, H. Sakai, Detection of differentially expressed genes in the early developmental stage of the mouse mandible, International Journal of Developmental Biology, 45, 4, 675-680, 2001.08, We previously examined the development of the mouse mandible, and demonstrated that odontogenesis occurs between embryonic day 10.5 (E10.5) and E12. Based on the histological findings, we performed cDNA subtraction between the E10.5 and E12 mandibles to detect any differentially expressed genes which might be involved in the initiation of odontogenesis. By sequencing, homology search and semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR), we thus found Pgk-1, Ccte, Hsp86, Nucleolin, Hsc73, Frg1, N-ras, Set alpha and Hsj2 from the E10.5 mandible, and E25, ATPase6, Mum2, Thymosin beta4 and L21 from the E12 mandible to be differentially expressed genes. These genes are functionally related to protein transport, signal transduction, transcription, translation and molecular chaperon activity. In situ hybridization analyses of Set alpha and E25 showed that Set alpha was detected in the tooth germ at E12 and E14.5, thus indicating a close relationship of this gene to odontogenesis. Meanwhile, the in situ signal of E25 was found in the muscular layer of the tongue, thus suggesting E25 to be related to the differentiation of muscular tissue. In conclusion, we found 15 differentially expressed genes in the course of the early developmental stage of the mouse mandible using a combination of the cDNA subtraction and semi-quantitative RT-PCR methods, while in addition, two genes were demonstrated to be related to the initiation and the development of both tooth germ and the tongue according to the in situ hybridization technique..|
|12.||Haruyoshi Yamaza, Kou Matsuo, Ieyoshi Kobayashi, Hiroko Wada, Tamotsu Kiyoshima, Merina Akhtar, Yukiko Ishibashi, Takako Sakai, Akifumi Akamine, Hidetaka Sakai, Expression of Set-α during morphogenesis of mouse lower first molar, Histochemical Journal, 10.1023/A:1014491111628, 33, 8, 437-441, 2001.12, [URL], The detailed in situ expression pattern of the Set-α gene has been studied. Previously we showed that Set-α is a differentially expressed gene in the embryonic mouse mandible at day 10.5 (E10.5) gestational age. Cells expressing Set-α were widely distributed in both the epithelial and underlying ectomesenchymal cells at E10.5. At E12, they were slightly aggregated in an area where tooth germ of the lower first molar is estimated to be formed. At E13.5, Set-α was strongly expressed in the tooth germ. At the cap stage, Set-α was expressed in the enamel organ and dental papilla. At the bell stage, Set-α was distinctly expressed in the inner enamel epithelial and dental papilla cells facing the inner enamel epithelial layer, which were intended to differentiate into ameloblasts and odontoblasts, respectively. Interestingly, Set-α was also expressed in several embryonic craniofacial tissues derived from the ectoderm. This study is the first report that Set-α is distinctly expressed in the developing tooth germ, and suggests that Set-α plays an important role in both the initiation and the growth of the tooth germ, as well as in the differentiation of ameloblasts and odontoblasts..|
主要総説, 論評, 解説, 書評, 報告書等
|1.||増田啓次，山座治義，山口 登，野中和明, 口唇口蓋裂への対応, 小児科臨床, 2010.11.|
|2.||山座治義，千葉卓哉，下川 功, メタボリックシンドロームとカロリー制限：糖代謝を中心に, 新しい眼科学, 2008.01.|
|3.||山座治義，下川 功, カロリーリストリクション仮説と抗老化医学への応用, 眼科プラクティス, 2008.07.|
2020.02～2022.02, 日本外傷歯学会, 理事.
2017.04～2019.03, 日本小児歯科学会, 評議員.
2015.04～2017.03, 日本小児歯科学会九州地方会, 幹事.
2013.04～2015.03, 日本小児歯科学会, 評議員.
2011.05, 九州学校保健学会, 評議員.
2010.04～2012.03, 日本小児歯科学会九州地方会, 幹事.
2010.04～2012.03, 日本小児歯科学会, 評議員.
2020.02.09～2020.02.09, 第30回西日本小児口腔外科学会総会・学術大会, 座長.
2019.09.04～2019.09.04, 小児外科再生医療セミナー, 座長.
2018.10.21～2018.10.21, 第36回日本小児歯科学会九州地方会大会および総会, 座長.
2018.08.27～2018.08.27, 第15回市民公開講座, 座長.
2018.02.04～2018.02.04, 日本小児歯科学会専門医セミナー, 座長.
2015.11.15～2015.11.15, 第33回日本小児歯科学会九州地方会大会, 座長（Chairmanship）.
2014.03.08～2014.03.09, Kyudai Oral Bioscience 2013 -7th International Symposium, 座長（Chairmanship）.
2013.08.31～2013.08.31, The 24th Fukuoka International Symposium on Pediatric/Maternal-Child Health Research, 座長（Chairmanship）.
2011.03.04～2011.03.05, The 6th international joint symposium on “dental and craniofacial morphogenesis and tissue regeneration” and “oral health science”, 座長（Chairmanship）.
2010.10.03～2011.10.03, 第28回日本小児歯科学会九州地方会大会, 準備委員長補佐.
2010.10.03～2010.10.03, 第28回日本小児歯科学会九州地方会大会, 抄録編集担当.
2010.10.03～2010.10.09, 第28回日本小児歯科学会九州地方会大会, 司会.
2010.10.03～2010.10.03, 第28回日本小児歯科学会九州地方会大会, 座長（Chairmanship）.
2010.10.03～2010.10.03, 第28回日本小児歯科学会九州地方会大会, 司会（Moderator）.
2010.02.05～2010.02.05, The 5th International Symposium on “Dental and Craniofacial Morphogenesis and Tissue Regeneration: A View from Stem Cell Research”, 会場設営.
2010.02.05～2010.02.05, The 5th International Symposium on “Dental and Craniofacial Morphogenesis and Tissue Regeneration: A View from Stem Cell Research”, 座長（Chairmanship）.
2008.09.04～2008.09.06, The Japan-Korea Joint Seminar (AACL2008)-Toward the establishment of Asian Aging Research and Education Center, 司会.
2008.09.04～2008.09.06, he Japan-Korea Joint Seminar (AACL2008)-Toward the establishment of Asian Aging Research and Education Center, 司会（Moderator）.
2013.04, International Journal of Dentistry, 国際, 査読委員.
2010.04～2012.03, 日本小児歯科学会九州地方会 News Letter, 国内, 編集委員長.
ASCB|EMBO 2018 meeting, UnitedStatesofAmerica, 2019.03～2019.03.
Gordon Research Conferences, Italy, 2014.03～2014.04.
U.S.-Japan Research Institute, UnitedStatesofAmerica, 2013.09～2013.09.
National Instirute on Aging, UnitedStatesofAmerica, 2013.09～2013.09.
National Institute on Health, UnitedStatesofAmerica, 2012.09～2012.09.
U.S.-Japan Research Institute, UnitedStatesofAmerica, 2012.09～2012.09.
University of Hawaii, UnitedStatesofAmerica, 2012.05～2013.06.
University of Hawaii, UnitedStatesofAmerica, 2012.05～2013.06.
32nd Annual Meeting and Scientific Symposium, UnitedStatesofAmerica, 2009.10～2009.10.
The American Aging Assosiation, UnitedStatesofAmerica, 2009.05～2009.06.
Yeungnam University, Korea, 2008.05～2008.05.
National Institute on Aging, UnitedStatesofAmerica, 2004.11～2007.03.
Workshop of Current Perspectives on the Mechanism of Caloric Restriction, UnitedStatesofAmerica, 2002.10～2002.10.
若手奨励賞受賞, 日本基礎老化学会, 2004.06.
Travel Award, The American Aging Association, 2006.06.
2016年度～2017年度, 萌芽研究, 分担, 乳歯で染色体異常疾患を克服するトランスレーショナル研究.
2016年度～2018年度, 基盤研究(C), 分担, 酸化ストレスからみた口唇裂口蓋裂発症機序解明と予防法の開発.
2016年度～2018年度, 基盤研究(C), 代表, ヒト乳歯幹細胞を基盤とした新規アンチエイジング機構の解明.
2015年度～2017年度, 基盤研究(C), 分担, ヒト乳歯歯髄幹細胞によるヒルシュスプルング病類縁疾患に対する新規再生医療の開発.
2015年度～2017年度, 基盤研究(C), 分担, 薬剤抵抗性小腸移植片拒絶反応に対する細胞治療法の確立.
2013年度～2019年度, 基盤研究(A), 分担, ヒルシュスプルング病および類縁疾患における乳歯幹細胞による病因解明と新規治療開発.
2013年度～2015年度, 基盤研究(B), 分担, 患者由来歯髄幹細胞を応用した口唇口蓋裂の発症機序の解明と治療法の開発.
2013年度～2014年度, 挑戦的萌芽研究, 分担, ヒルシュスプルング病および類縁疾患の乳歯歯髄幹細胞を用いた新規治療法の開発 .
2013年度～2014年度, 萌芽研究, 分担, 孫が祖父母を救う.
2013年度～2015年度, 基盤研究(A), 分担, 小児外科領域の難治性疾患における脱落乳歯幹細胞を用いた新規治療法の開発.
2013年度～2015年度, 基盤研究(C), 代表, 早老症をモデルとした老化制御機構の解明に関する小児歯科的アプローチ.
2012年度～2014年度, 基盤研究(C), 分担, ミトコンンドリアの形態変化と口腔顎顔面組織発生との関係解明.
2012年度～2013年度, 挑戦的萌芽研究, 分担, ヒト乳歯幹細胞を用いた造血機能再生医療へのチャレンジ.
2011年度～2012年度, 挑戦的萌芽研究, 分担, 先天性代謝異常症および凝固異常症に対する乳歯幹細胞を用いた肝再生療法の開発.
2011年度～2012年度, 挑戦的萌芽研究, 分担, 乳歯による高齢者の若返り医療を開拓する発生・細胞学的研究.
2011年度～2012年度, 若手研究(B), 代表, 生物学的母子関係の解明に関する研究.
2008年度～2010年度, 若手研究(B), 代表, カロリー制限における新規の血糖制御機構と糖毒性への小胞体ストレス反応について.
2007年度～2008年度, 基盤研究(C), 分担, カロリー制限の抗老化機構:Neuropeptide Yと受容体サブタイプの解析.
2004年度～2004年度, 若手研究(B), 代表, 哺乳類における長寿モデル動物の解析.
2004年度～2005年度, 基盤研究(C), 分担, 白色脂肪組織での肥満やインシュリン感受性を制御する遺伝子群の同定.
2003年度～2005年度, 基盤研究(B), 分担, ほ乳類における老化制御機構:インスリン/IGF-1抑制とカロリー制限との相違
2015年度～2015年度, 橋渡し研究加速ネットワークプログラムシーズＢ, 分担, 脱落乳歯幹細胞を用いた立体肝組織移植による小児代謝性肝疾患根治療法の開発.
2014年度～2014年度, 厚生労働科学研究費補助金 (厚生労働省), 分担, ヒルシュスプルング病及び類縁疾患の幹細胞を用いた病因病態解明と新規治療法の開発.
2002年度～2002年度, 長崎医学同窓会医学研究助成金, 代表, カロリー制限による老化遅延機構の解明－神経内分泌系の役割－.
2009年度～2009年度, 国際学会等派遣事業, 代表, TISSUE-SPECIFIC VARIATION OF INSULIN SIGNAL IN CALORIC RESTRICTION.
QIR 九州大学学術情報リポジトリ システム情報科学研究院