Tokushima University / Educator and Researcher Directory --- Mizusawa, Noriko

Field of Study

○	Dentistry

Subject of Study

○

Book / Paper

Book:

1.	Katsuhiko Yoshimoto, Takeo Iwata and Noriko Mizusawa : 遺伝性・家族性下垂体腫瘍, 株式会社診断と治療社, Tokyo, Nov. 2016.
2.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa, Zhi-Rong Qian, Shima Wan Nazatul Shahidan, Shinji Ono and Kyoko Ishimoto : Pituitary adenomas: role of cyclin-dependent kinase inhibitors, Springer, Oct. 2013.
3.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa and 小野信二 : アクロメガリーの病態生理, Medical Review Co.,Ltd, Jul. 2013.
4.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa and Shinji Ono : アクロメガリーの発症にかかわる遺伝子異常, Medical Review Co.,Ltd, Jul. 2013.
5.	Katsuhiko Yoshimoto, Takeo Iwata and Noriko Mizusawa : 遺伝性・家族性下垂体腫瘍, 株式会社診断と治療社, Apr. 2012.
6.	Katsuhiko Yoshimoto, Noriko Mizusawa, Takeo Iwata, Daisuke Nagao, Hossain Md.Golam, 露口勝, Toshiaki Sano and 内野眞也 : 【内分泌クリニカル・カンファランス】副甲状腺家族性副甲状腺機能亢進症2家系におけるHRPT2遺伝子変異の解析, Sep. 2006.
7.	Katsuhiko Yoshimoto, Xu Bing, Noriko Mizusawa, Takeo Iwata, Daisuke Nagao, Golam Md. Hossain, Akira Miyauchi, Seiji Kuma, Mitsuyoshi Hirokawa and Toshiaki Sano : Somatic mutations of the CTNNB1 gene in cribriform-morular variant of papillary thyroid carcinoma., Transworld Research Network, Kerala, India, 2006.

Academic Paper (Judged Full Paper):

1.	Fumiya Kano, Noboru Hashimoto, Yao Liu, Linze Xia, Takaaki Nishihara, Wakana Oki, Keita Kawarabayashi, Noriko Mizusawa, Keiko Aota, Takayoshi Sakai, Masayuki Azuma, Hideharu Hibi, Tomonori Iwasaki, Tsutomu Iwamoto, Nobuyasu Horimai and Akihito Yamamoto : Therapeutic benefits of factors derived from stem cells from human exfoliated deciduous teeth for radiation-induced mouse xerostomia, Scientific Reports, Vol.13, No.1, 2706-2719, 2023. (Summary) Radiation therapy for head and neck cancers is frequently associated with adverse effects on the surrounding normal tissue. Irreversible damage to radiation-sensitive acinar cells in the salivary gland (SG) causes severe radiation-induced xerostomia (RIX). Currently, there are no effective drugs for treating RIX. We investigated the efficacy of treatment with conditioned medium derived from stem cells from human exfoliated deciduous teeth (SHED-CM) in a mouse RIX model. Intravenous administration of SHED-CM, but not fibroblast-CM (Fibro-CM), prevented radiation-induced cutaneous ulcer formation (p < 0.0001) and maintained SG function (p < 0.0001). SHED-CM treatment enhanced the expression of multiple antioxidant genes in mouse RIX and human acinar cells and strongly suppressed radiation-induced oxidative stress. The therapeutic effects of SHED-CM were abolished by the superoxide dismutase inhibitor diethyldithiocarbamate (p < 0.0001). Notably, quantitative liquid chromatography-tandem mass spectrometry shotgun proteomics of SHED-CM and Fibro-CM identified eight proteins activating the endogenous antioxidant system, which were more abundant in SHED-CM than in Fibro-CM (p < 0.0001). Neutralizing antibodies against those activators reduced antioxidant activity of SHED-CM (anti-PDGF-D; p = 0.0001, anti-HGF; p = 0.003). Our results suggest that SHED-CM may provide substantial therapeutic benefits for RIX primarily through the activation of multiple antioxidant enzyme genes in the target tissue. (Keyword) Mice / Humans / Animals / Antioxidants / Stem Cells / Disease Models, Animal / Xerostomia / Tooth, Deciduous (Tokushima University Institutional Repository) ● Metadata: 118051 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41598-023-29176-w (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36792628 ● Summary page in Scopus @ Elsevier: 2-s2.0-85148115146 (Tokushima University Institutional Repository: 118051, DOI: 10.1038/s41598-023-29176-w, PubMed: 36792628, Elsevier: Scopus)
2.	Noriko Mizusawa, Nagakatsu Harada, Takeo Iwata, Izumi Ohigashi, Mitsuo Itakura and Katsuhiko Yoshimoto : Identification of protease serine S1 family member 53 as a mitochondrial protein in murine islet beta cells, Islets, Vol.14, No.1, 1-13, 2021. (Keyword) Prss53 / pancreatic β-cell / mitochondria (Tokushima University Institutional Repository) ● Metadata: 117033 (Link to Publication Site) ● Publication site (DOI): 10.1080/19382014.2021.1982325 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34636707 ● Summary page in Scopus @ Elsevier: 2-s2.0-85116882945 (Tokushima University Institutional Repository: 117033, DOI: 10.1080/19382014.2021.1982325, PubMed: 34636707, Elsevier: Scopus)
3.	Takeo Iwata, Kyoko Kuribayashi, Masahiko Nakasono, Noriko Saito-Tarashima, Noriaki Minakawa, Noriko Mizusawa, Rie Kido and Katsuhiko Yoshimoto : The AMPK/mTOR pathway is involved in D-dopachrome tautomerase gene transcription in adipocytes differentiated from SGBS cells, a human preadipocyte cell line, Cytokine, Vol.96, 195-202, 2017. (Summary) In adipose tissue, D-dopachrome tautomerase (DDT), a cytokine with structural similarity to macrophage migration inhibitory factor, is mainly expressed in adipocytes rather than preadipocytes and acts as an anti-obesity adipokine in an autocrine manner. However, its transcriptional regulation is largely unknown. In order to explore molecules affecting DDT transcription, a chemical library screening using HEK293 cells stably expressing a DDT promoter-reporter construct was performed. Several derivatives of 5-aminoimidazole-4-carboxamide-1--d-ribofuranoside (AICAR), an AMP-activated protein kinase (AMPK) activator, were identified as transcriptional activators of the DDT gene. Furthermore, DDT mRNA levels were reduced in SGBS adipocytes treated with compound C, an AMPK inhibitor, suggesting involvement of AMPK in DDT transcription. Overexpression of the FOXO1 constitutive active form reduced transcriptional activity of the DDT gene in SGBS cells, but increased it in HEK293 cells. Cell-type specific effects were also observed in the DDT gene expression of cells treated with AS1842856, a FOXO1 inhibitor. Finally, involvement of the mammalian target of rapamycin (mTOR) signaling in DDT transcription in SGBS adipocytes was investigated. Rapamycin, an inhibitor of mTOR, increased DDT mRNA levels and attenuated the inhibitory effects of compound C on DDT mRNA levels in SGBS adipocytes. In conclusion, DDT transcription may be regulated in a cell-dependent manner, and were enhanced by AMPK activation in SGBS adipocytes through inhibiting the mTOR signaling. (Tokushima University Institutional Repository) ● Metadata: 111466 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.cyto.2017.04.017 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28445821 ● Summary page in Scopus @ Elsevier: 2-s2.0-85018474373 (Tokushima University Institutional Repository: 111466, DOI: 10.1016/j.cyto.2017.04.017, PubMed: 28445821, Elsevier: Scopus)
4.	Otsuka Ryo, Nagakatsu Harada, Aoki Shouhei, Shirai Kanna, Kazuchika Nishitsuji, Nozaki Ayane, Hatakeyama Adzumi, Masayuki Shono, Noriko Mizusawa, Katsuhiko Yoshimoto, Yutaka Nakaya, Hiroshi Kitahata and Hiroshi Sakaue : C-terminal region of GADD34 regulates eIF2alpha dephosphorylation and cell proliferation in CHO-K1 cells., Cell Stress & Chaperones, Vol.21, No.1, 29-40, 2016. (Summary) GADD34 is a member of a growth arrest and DNA damage (GADD)-inducible gene family. Here, we established a novel Chinese hamster ovary (CHO)-K1-derived cell line, CHO-K1-G34M, which carries a nonsense mutation (termed the Q525X mutation) in the GADD34 gene. The Q525X mutant protein lacks the C-terminal 66 amino acids required for GADD34 to bind to and activate protein phosphatase 1 (PP1). We investigated the effects of GADD34 with or without the Q525X mutation on the phosphorylation status of PP1 target proteins, including the subunit of eukaryotic initiation factor 2 (eIF2) and glycogen synthase kinase 3 (GSK3). CHO-K1-G34M cells had higher levels of eIF2 phosphorylation compared to the control CHO-K1-normal cells both in the presence and absence of endoplasmic reticulum stress. Overexpression of the wild-type GADD34 protein in CHO-K1-normal cells largely reduced eIF2 phosphorylation, while overexpression of the Q525X mutant did not produce similar reductions. Meanwhile, neither wild type nor Q525X mutation of GADD34 affected the GSK3 phosphorylation status. GADD34 also did not affect the canonical Wnt signaling pathway downstream of GSK3. Cell proliferation rates were higher, while expression levels of the cyclin-dependent kinase inhibitor p21 were lower in CHO-K1-G34M cells compared to the CHO-K1-normal cells. The GADD34 Q525X mutant had a reduced ability to inhibit cell proliferation and enhance p21 expression of the CHO-K1-normal cells compared to the wild-type GADD34 protein. These results suggest that the GADD34 protein C-terminal plays important roles in regulating not only eIF2 dephosphorylation but also cell proliferation in CHO-K1 cells. (Tokushima University Institutional Repository) ● Metadata: 110106 (Link to Publication Site) ● Publication site (DOI): 10.1007/s12192-015-0633-9 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26318739 ● Summary page in Scopus @ Elsevier: 2-s2.0-84951905379 (Tokushima University Institutional Repository: 110106, DOI: 10.1007/s12192-015-0633-9, PubMed: 26318739, Elsevier: Scopus)
5.	Yuki Iwawaki, Noriko Mizusawa, Takeo Iwata, Nobuaki Higaki, Takaharu Goto, Megumi Watanabe, Yoritoki Tomotake, Tetsuo Ichikawa and Katsuhiko Yoshimoto : MiR-494-3p induced by compressive force inhibits cell proliferation in MC3T3-E1 cells., Journal of Bioscience and Bioengineering, Vol.120, No.4, 456-462, 2015. (Summary) Mechanical stimuli regulate fundamental cell processes such as proliferation, differentiation, and morphogenesis. We attempted to identify microRNA (miRNA) whose expression is changed during compressive treatment in MC3T3-E1, a pre-osteoblastic cell line. Microarray analysis followed by reverse transcription-quantitative polymerase chain reaction revealed that compressive force at 294 Pa for 24 h in MC3T3-E1 cells increased levels of miR-494-3p, miR-146a-5p, miR-210-3p, and miR-1247-3p. Among these miRNAs, miR-494-3p was found to inhibit cell proliferation in MC3T3-E1 cells. Furthermore, cells subjected to compressive force showed slower cell growth compared with control cells. Levels of mRNA for fibroblast growth factor receptor 2 (FGFR2) and Rho-associated coiled-coil kinase 1 (ROCK1), which were predicted to be targets of miR-494-3p, were decreased by compressive force or overexpression of miR-494-3p mimics in MC3T3-E1 cells. Furthermore, binding sites of miR-494-3p within 3'-untranslated regions of Fgfr2 and Rock1 were determined using luciferase reporter assay. In conclusion, compressive force affected expressions of several miRNAs including miR-494-3p in MC3T3-E1 cells. Compressive force might inhibit cell proliferation in osteoblasts by up-regulating miR-494-3p followed by FGFR2 and ROCK1 gene repressions. (Keyword) 3' Untranslated Regions / Cell Line / Cell Proliferation / Down-Regulation / Gene Expression Regulation / Humans / Luciferases / MicroRNAs / Oligonucleotide Array Sequence Analysis / Osteoblasts / RNA, Messenger / Receptor, Fibroblast Growth Factor, Type 2 / Reverse Transcriptase Polymerase Chain Reaction / Stress, Mechanical / Up-Regulation / rho-Associated Kinases (Tokushima University Institutional Repository) ● Metadata: 109479 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jbiosc.2015.02.006 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25795570 ● Summary page in Scopus @ Elsevier: 2-s2.0-84938332268 (Tokushima University Institutional Repository: 109479, DOI: 10.1016/j.jbiosc.2015.02.006, PubMed: 25795570, Elsevier: Scopus)
6.	Takeo Iwata, T Tamanaha, R Koezuka, M Tochiya, H Makino, I Kishimoto, Noriko Mizusawa, S Ono, N Inoshita, Shozo Yamada, A Shimatsu and Katsuhiko Yoshimoto : Germline deletion and a somatic mutation of the PRKAR1A gene in a Carney complex-related pituitary adenoma., European Journal of Endocrinology, Vol.172, No.1, K5-K10, 2015. (Summary) The objective was to assess involvement of loss of the PRKAR1A gene encoding a type 1α regulatory subunit of cAMP-dependent protein kinase A located on 17q24 in a Carney complex (CNC)-related pituitary adenoma. We investigated aberrations of the PRKAR1A gene in a CNC patient with a GH-producing pituitary adenoma, whose family has three other members with probable CNC. A gene mutation was identified by a standard DNA sequencing method based on PCR. DNA copy number was measured to evaluate allelic loss on 17q24 by quantitative PCR. The breakpoints of deletion were determined by cloning a rearranged region in the deleted allele. A PRKAR1A mutation of c.751_758del8 (p.S251LfsX16) was found in genomic DNA obtained from a pituitary adenoma, but not leukocytes from the patient. Reduced DNA copy number at loci including the PRKAR1A gene on 17q24 was detected in both the tumor and leukocytes, suggesting a deletion at the loci at the germline level. The deletion size was determined to be ∼ 0.5 Mb and this large deletion was also found in two other family members. This is the first case showing a CNC-related pituitary adenoma with the combination of somatic mutation and a large inherited deletion of the PRKAR1A gene. Biallelic inactivation of PRKAR1A appears to be necessary for the development of CNC-related pituitary adenoma. (Keyword) Adenoma / Aged / Carney Complex / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit / Female / Gene Deletion / Germ-Line Mutation / Humans / Middle Aged / Pedigree / Pituitary Neoplasms / Young Adult (Tokushima University Institutional Repository) ● Metadata: 109643 (Link to Publication Site) ● Publication site (DOI): 10.1530/EJE-14-0685 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25336503 ● Summary page in Scopus @ Elsevier: 2-s2.0-84920365005 (Tokushima University Institutional Repository: 109643, DOI: 10.1530/EJE-14-0685, PubMed: 25336503, Elsevier: Scopus)
7.	Takeo Iwata, Shozo Yamada, Junko Ito, Naoko Inoshita, Noriko Mizusawa, Shinji Ono and Katsuhiko Yoshimoto : A Novel C-terminal Nonsense Mutation, Q315X, of the Aryl Hydrocarbon Receptor-Interacting Protein Gene in a Japanese Familial Isolated Pituitary Adenoma Family., Endocrine Pathology, Vol.25, No.3, 273-281, 2014. (Summary) Although the cause of familial isolated pituitary adenoma (FIPA) remains unknown in many cases, germline mutations in the aryl hydrocarbon receptor-interacting protein (AIP) gene were identified in approximately 20 % of families with FIPA. We investigated the AIP gene mutation by a standard sequencing method in 12 members of a Japanese two-generation FIPA family, which includes 3 patients with early-onset acromegaly. Multiplex ligation-dependent probe amplification analysis in a tumor sample was attempted to examine the loss of heterozygosity (LOH) in the locus. The effect of the detected mutation on cell proliferation was investigated. A germline mutation of c.943C > T (p.Q315X) generating an AIP protein with the C-terminal end deleted was found in the FIPA family. Biallelic inactivation of AIP by a combination of the germline mutation and LOH at 11q13 was confirmed in the tumor. The nonsense mutation disrupted the ability to inhibit cell proliferation. We conclude that p.Q315X mutation in the AIP gene is a pathogenic variant and the C-terminal region of AIP plays an important role in the predisposition to pituitary adenomas. (Tokushima University Institutional Repository) ● Metadata: 109644 (Link to Publication Site) ● Publication site (DOI): 10.1007/s12022-014-9318-7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24789813 ● Search Scopus @ Elsevier (PMID): 24789813 ● Search Scopus @ Elsevier (DOI): 10.1007/s12022-014-9318-7 (Tokushima University Institutional Repository: 109644, DOI: 10.1007/s12022-014-9318-7, PubMed: 24789813)
8.	Guangfei Xu, Jiao Liu, Katsuhiko Yoshimoto, Gang Chen, Takeo Iwata, Noriko Mizusawa, Zhiqing Duan, Chunhua Wan and Junkang Jiang : 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induces expression of p27(kip¹) and FoxO3a in female rat cerebral cortex and PC12 cells., Toxicology Letters, Vol.226, No.3, 294-302, 2014. (Summary) 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a potent toxin that alters normal brain development, producing cognitive disability and motor dysfunction. Previous studies in rats have proved that female rats are more sensitive to TCDD lethality than male ones. Recent studies have shown that TCDD induces cell cycle arrest and apoptosis, but the regulatory proteins involved in these processes have yet to be elucidated. In this study, we constructed an acute TCDD injury female rat model, and investigated the effects of TCDD on apoptosis and expression of cell cycle regulators, forkhead box class O 3a (FoxO3a) and p27(kip1), in the central nervous system (CNS). Increased levels of active caspase-3 were observed in the cerebral cortex of female rats treated with TCDD, suggesting that TCDD-induced apoptosis occurs in the CNS. The terminal deoxynucleotidyl transferase-mediated biotinylated-dUTP nick-end labeling assay showed that apoptosis primarily occurred in neurons. Furthermore, Western blot analysis, reverse transcription-polymerase chain reaction, and immunohistochemistry showed a significant up-regulation of FoxO3a and p27(kip1) in the cerebral cortex. Immunofluorescent labeling indicated that FoxO3a and p27(kip1) were predominantly localized in apoptotic neurons, but not in astrocytes. In vitro experiments using PC12, a rat neuron-like pheochromocytoma cell line, also revealed that TCDD induced apoptosis and an increase in FoxO3a and p27(kip1) expression. Furthermore, knockdown of FoxO3a expression inhibited p27(kip1) transcription and TCDD-induced apoptosis. Based on our data, induction of FoxO3a may play an important role in TCDD-induced neurotoxicity. (Keyword) Animals / Apoptosis / Cerebral Cortex / Cyclin-Dependent Kinase Inhibitor p27 / Female / Forkhead Transcription Factors / PC12 Cells / Rats / Rats, Sprague-Dawley / Receptors, Aryl Hydrocarbon / Tetrachlorodibenzodioxin (Link to Publication Site) ● Publication site (DOI): 10.1016/j.toxlet.2014.02.019 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24594276 ● Search Scopus @ Elsevier (PMID): 24594276 ● Search Scopus @ Elsevier (DOI): 10.1016/j.toxlet.2014.02.019 (DOI: 10.1016/j.toxlet.2014.02.019, PubMed: 24594276)
9.	Guangfei Xu, Yuanye Li, Katsuhiko Yoshimoto, Qiyun Wu, Gang Chen, Takeo Iwata, Noriko Mizusawa, Chunhua Wan and Xiaoke Nie : 2,3,7,8-Tetrachlorodibenzo-p-dioxin stimulates proliferation of HAPI microglia by affecting the Akt/GSK-3/cyclin D1 signaling pathway., Toxicology Letters, Vol.224, No.3, 362-370, 2013. (Summary) 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is an environmental toxin that induces apoptosis of neurons and a pro-inflammatory response in microglial cells. First, we found that TCDD induced proliferation of HAPI microglial cells in a dose- and time-dependent manner. Flow cytometry analysis showed that this proliferation by TCDD was due to mainly enhancing the G1 to S phase transition. Next, it was found that TCDD treatment led to up-regulation of cyclin D1, which induces cell cycle progression from G1 to S phase, in a time-dependent manner. As for molecular mechanism, we revealed that TCDD was capable of inducing Akt phosphorylation and activation, resulting in phosphorylation and inactivation of glycogen synthase kinase-3 (GSK-3). Inactivated GSK-3 attenuated proteasomal degradation of cyclin D1 by reducing Thr(286)-phosphorylated cyclin D1 levels. Moreover, inactivated GSK-3 increased cyclin D1 gene transcription by increasing its transcription factor -catenin in the nucleus. Further, blockage of phosphoinositide 3-kinase/Akt kinase with their specific inhibitors, LY294002 and Akt 1/2 kinase inhibitor, significantly reduced TCDD-enhanced proliferation of HAPI microglial cells. In conclusion, TCDD stimulates proliferation of HAPI microglial cells by affecting the Akt/GSK-3/cyclin D1 signaling pathway. (Keyword) Cell Adhesion / Cell Count / Cell Cycle / Cell Line / Cell Proliferation / Cyclin D1 / Deoxyuridine / Environmental Pollutants / Enzyme-Linked Immunosorbent Assay / Glycogen Synthase Kinase 3 / Humans / Microglia / Oncogene Protein v-akt / Phosphorylation / RNA / RNA, Small Interfering / Real-Time Polymerase Chain Reaction / Signal Transduction / Tetrachlorodibenzodioxin / beta Catenin (Link to Publication Site) ● Publication site (DOI): 10.1016/j.toxlet.2013.11.003 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24231000 ● Search Scopus @ Elsevier (PMID): 24231000 ● Search Scopus @ Elsevier (DOI): 10.1016/j.toxlet.2013.11.003 (DOI: 10.1016/j.toxlet.2013.11.003, PubMed: 24231000)
10.	Guangfei Xu, Yuanye Li, Katsuhiko Yoshimoto, Gang Chen, Chunhua Wan, Takeo Iwata, Noriko Mizusawa, Zhiqing Duan, Jiao Liu and Junkang Jiang : 2,3,7,8-Tetrachlorodibenzo-p-dioxin-induced inflammatory activation is mediated by intracellular free calcium in microglial cells, Toxicology, Vol.308, 158-167, 2013. (Summary) 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) has been known to induce inflammatory signaling in a number of cell types and tissues. However, the adverse effects of TCDD on the central nervous system (CNS) have not been entirely elucidated. In this study, using reverse transcriptase PCR (RT-PCR) and ELISA, we showed that TCDD up-regulated the expression and secretion of tumor necrosis factor-alpha (TNF-α) in a time-dependent manner in cultured HAPI microglial cells. TCDD also caused a fast (within 30min as judged by the increase in its mRNA level) activation of cytosolic phospholipase A2 (cPLA2). This initial action was accompanied by up-regulation of cyclooxygenase-2 (COX-2), an important inflammation marker within 1h after TCDD treatment. These pro-inflammatory responses were inhibited by two types of Ca(2+) blockers, bis-(o-aminophenoxy) ethane-N,N,N',N'-tetra-acetic acid acetoxymethyl ester (BAPTA-AM) and nifedipine, thus, indicating that the effects are triggered by initial increase in the intracellular concentration of free Ca(2+) ([Ca(2+)]i). Further, TCDD exposure could induce phosphorylation- and ubiquitination-dependent degradation of I Bα, and the translocation of NF-κB p65 from the cytosol to the nucleus in this microglial cell line. Thus, the NF-κB signaling pathway can be activated after TCDD treatment. However, Ca(2+) blockers also obviously attenuated NF-κB activation and transnuclear transport induced by TCDD. In concert with these results, we highlighted that the secretion of pro-inflammatory cytokine and NF-κB activation induced by TCDD can be mediated by elevation of [Ca(2+)]i in HAPI microglial cells. (Keyword) Animals / Calcium / Inflammation / Intracellular Fluid / Microglia / Rats / Rats, Sprague-Dawley / Tetrachlorodibenzodioxin (Link to Publication Site) ● Publication site (DOI): 10.1016/j.tox.2013.04.002 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23583884 ● Summary page in Scopus @ Elsevier: 2-s2.0-84877349038 (DOI: 10.1016/j.tox.2013.04.002, PubMed: 23583884, Elsevier: Scopus)
11.	Kyoko Ishimoto, Takeo Iwata, Hisaaki Taniguchi, Noriko Mizusawa, Eiji Tanaka and Katsuhiko Yoshimoto : d-Dopachrome tautomerase promotes IL-6 expression and inhibits adipogenesis in preadipocytes., Cytokine, Vol.60, 772-777, 2012. (Summary) We previously identified d-dopachrome tautomerase (DDT) as a novel adipokine whose mRNA levels in adipocytes are negatively correlated with obesity-related clinical parameters, and which acts on adipocytes to regulate lipid metabolism. Here we investigated functions of DDT on preadipocytes. Recombinant DDT (rDDT) enhanced both the expression and secretion of interleukin-6 (IL-6) in SGBS cells, a human preadipocyte cell line. Treatment with rDDT increased levels of phosphorylated ERK1/2, but not p38, in SGBS cells, and rDDT-induced IL-6 mRNA expression was attenuated by pretreatment with an ERK inhibitor, U0126. Knockdown of CD74, but not CD44, inhibited rDDT-induced IL-6 mRNA expression in SGBS cells. These results suggested that the rDDT-induced IL-6 expression in preadipocytes occurred through the CD74-ERK pathway. Furthermore, in SGBS cells subjected to adipogenic induction, rDDT decreased the amount of triacylglycerol, number of cells with oil droplets, and levels of mRNA encoding adipocyte marker proteins. Increased expression of CCAAT/enhancer binding protein families and peroxisome proliferator-activated receptor 2 during adipogenesis was inhibited in the cells treated with rDDT. These results suggested DDT to inhibit adipogenesis by suppressing the expression of genes encoding adipogenic regulators in preadipocytes. (Tokushima University Institutional Repository) ● Metadata: 109657 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.cyto.2012.07.037 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22951300 ● Search Scopus @ Elsevier (PMID): 22951300 ● Search Scopus @ Elsevier (DOI): 10.1016/j.cyto.2012.07.037 (Tokushima University Institutional Repository: 109657, DOI: 10.1016/j.cyto.2012.07.037, PubMed: 22951300)
12.	Takeo Iwata, Hisaaki Taniguchi, Masamichi Kuwajima, Takako Taniguchi, Okuda Yuko, Akiko Sukeno, Kyoko Ishimoto, Noriko Mizusawa and Katsuhiko Yoshimoto : The action of D-dopachrome tautomerase as an adipokine in adipocyte lipid metabolism, PLoS ONE, Vol.7, No.3, e33402, 2012. (Summary) Adipose tissue is a critical exchange center for complex energy transactions involving triacylglycerol storage and release. It also has an active endocrine role, releasing various adipose-derived cytokines (adipokines) that participate in complex pathways to maintain metabolic and vascular health. Here, we found D-dopachrome tautomerase (DDT) as an adipokine secreted from human adipocytes by a proteomic approach. DDT mRNA levels in human adipocytes were negatively correlated with obesity-related clinical parameters such as BMI, and visceral and subcutaneous fat areas. Experiments using SGBS cells, a human preadipocyte cell line, revealed that DDT mRNA levels were increased in an adipocyte differentiation-dependent manner and DDT was secreted from adipocytes. In DDT knockdown adipocytes differentiated from SGBS cells that were infected with the adenovirus expressing shRNA against the DDT gene, mRNA levels of genes involved in both lipolysis and lipogenesis were slightly but significantly increased. Furthermore, we investigated AMP-activated protein kinase (AMPK) signaling, which phosphorylates and inactivates enzymes involved in lipid metabolism, including hormone-sensitive lipase (HSL) and acetyl-CoA carboxylase (ACC), in DDT knockdown adipocytes. The AMPK phosphorylation of HSL Ser-565 and ACC Ser-79 was inhibited in DDT knockdown cells and recovered in the cells treated with recombinant DDT (rDDT), suggesting that down-regulated DDT in adipocytes brings about a state of active lipid metabolism. Furthermore, administration of rDDT in db/db mice improved glucose intolerance and decreased serum free fatty acids levels. In the adipose tissue from rDDT-treated db/db mice, not only increased levels of HSL phosphorylated by AMPK, but also decreased levels of HSL phosphorylated by protein kinase A (PKA), which phosphorylates HSL to promote its activity, were observed. These results suggested that DDT acts on adipocytes to regulate lipid metabolism through AMPK and/or PKA pathway(s) and improves glucose intolerance caused by obesity. (Keyword) AMP-Activated Protein Kinases / Adipocytes / Adipokines / Animals / Blotting, Western / Body Mass Index / Cell Differentiation / DNA Primers / Gene Knockdown Techniques / Humans / Intramolecular Oxidoreductases / Lipid Metabolism / Mice / Microscopy, Fluorescence / Phosphorylation / Proteomics / Reverse Transcriptase Polymerase Chain Reaction / Signal Transduction (Tokushima University Institutional Repository) ● Metadata: 109634 (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0033402 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22428043 ● Search Scopus @ Elsevier (PMID): 22428043 ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0033402 (Tokushima University Institutional Repository: 109634, DOI: 10.1371/journal.pone.0033402, PubMed: 22428043)
13.	Setsuko Hatakeyama, Noriko Mizusawa, Reiko Tsutsumi, Katsuhiko Yoshimoto, Harumi Mizuki, Shigeru Yasumoto, Shigehiro Sato and Yasunori Takeda : Establishment of human dental epithelial cell lines expressing ameloblastin and enamelin by transfection of hTERT and cdk4 cDNAs., Journal of Oral Pathology & Medicine, Vol.40, No.3, 227-234, 2010. (Summary) We established three cell lines by transfection of hTERT and cdk4 cDNAs, which were characterized as dental epithelial progenitor cells containing ameloblast-lineage cell phenotype. (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1600-0714.2010.00950.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20923449 ● Search Scopus @ Elsevier (PMID): 20923449 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1600-0714.2010.00950.x (DOI: 10.1111/j.1600-0714.2010.00950.x, PubMed: 20923449)
14.	Golam Md Hossain, Takeo Iwata, Noriko Mizusawa, Nazatul Shahidan Wan Shima, Toru Okutsu, Kyoko Ishimoto and Katsuhiko Yoshimoto : Compressive force inhibits adipogenesis through COX-2-mediated down-regulation of PPARgamma2 and C/EBPalpha., Journal of Bioscience and Bioengineering, Vol.109, No.3, 297-303, 2010. (Summary) Various mechanical stimuli affect differentiation of mesoderm-derived cells such as osteoblasts or myoblasts, suggesting that adipogenesis may also be influenced by mechanical stimulation. However, effects of mechanical stimuli on adipogenesis are scarcely known. Compressive force was applied to a human preadipocyte cell line, SGBS. Levels of gene expression were estimated by real-time reverse transcription-polymerase chain reaction. The accumulation of lipids was evaluated by Sudan III or Oil Red O staining. In SGBS cells subjected to a compressive force of 226 Pa for 12 h before adipogenic induction, adipogenesis was inhibited. Compressive force immediately after adipogenic induction did not affect the adipogenesis. The expression of peroxisome proliferator-activated receptor (PPAR) gamma2 and CCAAT/enhancer binding protein (C/EBP) alpha mRNA during adipogenesis was inhibited by compressive force, whereas C/EBPbeta and C/EBPdelta mRNA levels were unaffected. In preadipocytes, compressive force increased mRNA levels of Krüppel-like factor 2, preadipocyte factor 1, WNT10b, and cyclooxygenase-2 (COX-2) which are known as negative regulators for the PPARgamma2 and C/EBPalpha genes. Furthermore, a COX-2 inhibitor completely reversed the inhibition of adipogenesis by compressive force. In conclusion, compressive force inhibited adipogenesis by suppressing expression of PPARgamma2 and C/EBPalpha in a COX-2-dependent manner. (Keyword) Adipocytes / Adipogenesis / CCAAT-Enhancer-Binding Protein-alpha / Cells, Cultured / Compressive Strength / Cyclooxygenase 2 / Down-Regulation / Humans / Mechanotransduction, Cellular / PPAR gamma / Physical Stimulation / Stress, Mechanical (Tokushima University Institutional Repository) ● Metadata: 109655 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jbiosc.2009.09.003 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20159581 ● Search Scopus @ Elsevier (PMID): 20159581 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jbiosc.2009.09.003 (Tokushima University Institutional Repository: 109655, DOI: 10.1016/j.jbiosc.2009.09.003, PubMed: 20159581)
15.	Golam M Hossain, Takeo Iwata, Noriko Mizusawa, Zhi-Rong Qian, Nazatul Shahidan Wan Shima, Toru Okutsu, Shozo Yamada, Toshiaki Sano and Katsuhiko Yoshimoto : Expression of p18(INK4C) is down-regulated in human pituitary adenomas., Endocrine Pathology, Vol.20, No.2, 114-121, 2009. (Summary) Cyclin-dependent kinase inhibitors represented by the INK4 family comprising p16(INK4A), p15(INK4B), p18(INK4C), and p19(INK4D) are regulators of the cell cycle shown to be aberrant in many types of cancer. Mice lacking p18(Ink4c) exhibit a series of phenotypes including the development of widespread organomegaly and pituitary adenomas. The objective of our study is to examine the role of p18(INK4C) in the pathogenesis of human pituitary tumors. The protein and mRNA levels of p18(INK4C) were examined by immunohistochemistry and real-time reverse transcription-polymerase chain reaction, respectively. The methylation status of the p18(INK4C) gene promoter and somatic mutations of the p18(INK4C) gene were also investigated. p18(INK4C) protein expression was lost or significantly reduced in 64% of pituitary adenomas compared with levels in normal pituitary glands. p18(INK4C) mRNA levels were low in all ACTH adenomas and non-functioning (NF)-FSH and in 42%, 70% and 66% of GH, PRL, and subtype 3 adenomas, respectively. p18(INK4C) mRNA levels were significantly associated with p18(INK4C) protein levels. Neither methylated promoters in pituitary adenomas, except in one NF-FSH adenoma, nor somatic mutations of the p18(INK4C) gene in any pituitary adenomas were detected. The down-regulation of p18(INK4C) expression may contribute to the tumorigenesis of pituitary adenomas. (Keyword) Adenoma / Adult / Aged / Aged, 80 and over / Cyclin-Dependent Kinase Inhibitor p18 / DNA Methylation / Down-Regulation / Female / Gene Expression Regulation, Neoplastic / Humans / Male / Middle Aged / Mutation / Pituitary Neoplasms / RNA, Messenger (Tokushima University Institutional Repository) ● Metadata: 109645 (Link to Publication Site) ● Publication site (DOI): 10.1007/s12022-009-9076-0 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19401813 ● Search Scopus @ Elsevier (PMID): 19401813 ● Search Scopus @ Elsevier (DOI): 10.1007/s12022-009-9076-0 (Tokushima University Institutional Repository: 109645, DOI: 10.1007/s12022-009-9076-0, PubMed: 19401813)
16.	Takeo Iwata, Masamichi Kuwajima, Akiko Sukeno, Naozumi Ishimaru, Yoshio Hayashi, Martin Wabitsch, Noriko Mizusawa, Mitsuo Itakura and Katsuhiko Yoshimoto : YKL-40 secreted from adipose tissue inhibits degradation of type I collagen., Biochemical and Biophysical Research Communications, Vol.388, No.3, 511-516, 2009. (Summary) Obesity is considered a chronic low-grade inflammatory status and the stromal vascular fraction (SVF) cells of adipose tissue (AT) are considered a source of inflammation-related molecules. We identified YKL-40 as a major protein secreted from SVF cells in human visceral AT. YKL-40 expression levels in SVF cells from visceral AT were higher than in those from subcutaneous AT. Immunofluorescence staining revealed that YKL-40 was exclusively expressed in macrophages among SVF cells. YKL-40 purified from SVF cells inhibited the degradation of type I collagen, a major extracellular matrix of AT, by matrix metalloproteinase (MMP)-1 and increased rate of fibril formation of type I collagen. The expression of MMP-1 in preadipocytes and macrophages was enhanced by interaction between these cells. These results suggest that macrophage/preadipocyte interaction enhances degradation of type I collagen in AT, meanwhile, YKL-40 secreted from macrophages infiltrating into AT inhibits the type I collagen degradation. (Keyword) Adipocytes / Adipose Tissue / Adult / Aged / Cells, Cultured / Coculture Techniques / Collagen Type I / Female / Glycoproteins / Humans / Inflammation / Lectins / Macrophages / Male / Matrix Metalloproteinase 1 / Middle Aged / Obesity / Stromal Cells (Tokushima University Institutional Repository) ● Metadata: 109641 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2009.08.024 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19666003 ● Search Scopus @ Elsevier (PMID): 19666003 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2009.08.024 (Tokushima University Institutional Repository: 109641, DOI: 10.1016/j.bbrc.2009.08.024, PubMed: 19666003)
17.	Zhi-Rong Qian, Toshiaki Sano, Katsuhiko Yoshimoto, Asa L Sylvia, Shozo Yamada, Noriko Mizusawa and Eiji Kudo : Tumor-specific down-regulation and methylation of the CDH13 (H-cadherin) and CDH1 (E-cadherin) genes correlate with aggressiveness of human pituitary adenomas, Modern Pathology, Vol.20, No.12, 1269-1277, 2007. (Summary) The gene products of CDH13 and CDH1, H-cadherin and E-cadherin, respectively, play a key role in cell-cell adhesion. Inactivation of the cadherin-mediated cell adhesion system caused by aberrant methylation is a common finding in human cancers, indicating that the CDH13 and CDH1 function as tumor suppressor and invasion suppressor genes. In this study, we analyzed the expression of H-cadherin mRNA and E-cadherin protein in 5 normal pituitary tissues and 69 primary pituitary adenomas including all major types by quantitative real-time RT-PCR (qRT-PCR) and immunohistochemistry, respectively. Reduced expression of H-cadherin was detected in 54% (28/52) of pituitary tumors and was significantly associated with tumor aggressiveness (P<0.05). E-cadherin expression was lost in 30% (21 of 69) and significantly reduced in 32% (22 of 69) of tumors. E-cadherin expression was significantly lower in grade II, III, and IV than in grade I adenomas (P=0.015, P=0.029, and P=0.01, respectively). Using methylation-specific PCR (MSP), promoter hypermethylation of CDH13 and CDH1 was detected in 30 and 36% of 69 adenomas, respectively, but not in 5 normal pituitary tissues. Methylation of CDH13 was observed more frequently in invasive adenomas (42%) than in non-invasive adenomas (19%) (P<0.05) and methylation of CDH1 was more frequent in grade IV adenomas compared with grade I adenomas (P<0.05). Methylation of either CDH13 or CDH1 was identified in 35 cases (51%) and was more frequent in grade IV invasive adenomas than in grade I non-invasive adenomas (P<0.05 and P<0.05, respectively). Downregulation of expression was correlated with promoter hypermethylation in CDH13 and CDH1. In conclusion, the tumor-specific downregulation of expression and methylation of CDH13 and CDH1, alone or in combination, may be involved in the development and invasive growth of pituitary adenomas. (Keyword) Adenoma / Adult / Cadherins / DNA Methylation / Down-Regulation / Female / Gene Expression / Humans / Immunohistochemistry / Male / Middle Aged / Pituitary Neoplasms / Promoter Regions, Genetic / Reverse Transcriptase Polymerase Chain Reaction / Tumor Markers, Biological (Link to Publication Site) ● Publication site (DOI): 10.1038/modpathol.3800965 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17873891 ● Search Scopus @ Elsevier (PMID): 17873891 ● Search Scopus @ Elsevier (DOI): 10.1038/modpathol.3800965 (DOI: 10.1038/modpathol.3800965, PubMed: 17873891)
18.	Takeo Iwata, Noriko Mizusawa, Yutaka Taketani, Mitsuo Itakura and Katsuhiko Yoshimoto : Parafibromin tumor suppressor enhances cell growth in the cells expressing SV40 large T antigen., Oncogene, Vol.26, No.42, 6176-6183, 2007. (Summary) Parafibromin (PF) is a 531-amino acid protein encoded by HRPT2, a putative tumor suppressor gene recently implicated in the autosomal-dominant hyperparathyroidism-jaw tumor familial cancer syndrome and sporadic parathyroid carcinoma. To investigate effects of PF's overexpression on cell proliferation, we performed assays in four different cell lines. The transient overexpression of PF inhibited cell growth in HEK293 and NIH3T3 cells, but enhanced cell growth in the SV40 large T antigen-expressing cell lines such as 293FT and COS7 cells. In 293FT cells, PF was found to interact with SV40 large T antigen and its overexpression promoted entry into the S phase, implying that the interaction enhanced progression through the cell cycle. The tumor suppressor protein PF acts as a positive regulator of cell growth similar to an oncoprotein in the presence of SV40 large T antigen. (Keyword) Animals / Antigens, Polyomavirus Transforming / COS Cells / Cell Line / Cell Proliferation / Cercopithecus aethiops / Fibroblasts / Humans / Mice / NIH 3T3 Cells / Simian virus 40 / Tumor Suppressor Proteins (Tokushima University Institutional Repository) ● Metadata: 109649 (Link to Publication Site) ● Publication site (DOI): 10.1038/sj.onc.1210445 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17404568 ● Search Scopus @ Elsevier (PMID): 17404568 ● Search Scopus @ Elsevier (DOI): 10.1038/sj.onc.1210445 (Tokushima University Institutional Repository: 109649, DOI: 10.1038/sj.onc.1210445, PubMed: 17404568)
19.	Takeo Iwata, Shozo Yamada, Noriko Mizusawa, HM Golam, Toshiaki Sano and Katsuhiko Yoshimoto : The aryl hydrocarbon receptor-interacting protein gene is rarely mutated in sporadic GH-secreting adenomas, Clinical Endocrinology, Vol.66, No.4, 499-502, 2007. (Summary) Recently, germline mutations of aryl hydrocarbon receptor-interacting protein (AIP) gene located on 11q13 were identified in patients with pituitary adenoma predisposition. AIM/PATIENTS AND METHODS: We investigated the involvement of the AIP gene in one family with isolated familial somatotropinomas (IFS). To investigate the role of AIP in sporadic GH-secreting adenomas, we first analysed somatic mutations in 40 tumours. Second, DNA from corresponding leucocytes was analysed in tumours showing genetic changes of the AIP gene. Germline mutation of AIP was found in an IFS family. Bi-allelic inactivation of AIP by a combination of germline mutation and loss of heterozygosity were confirmed in two pituitary adenomas. Mutation analysis of the AIP gene in the 40 sporadic GH-secreting adenomas showed no mutations except for a missense mutation, suggesting that germline mutations in patients diagnosed with sporadic acromegaly or gigantism were rare. In a patient with gigantism, a missense mutation of V49M was identified at the germline level. Based on these results, we conclude that the loss of function of AIP contributes to IFS, but not for most Japanese sporadic GH-secreting adenomas. (Keyword) Adult / Aged / Female / Growth Hormone-Secreting Pituitary Adenoma / Humans / Intracellular Signaling Peptides and Proteins / Loss of Heterozygosity / Male / Middle Aged / Mutation / Pedigree / Pituitary Neoplasms / Proteins / Sequence Analysis, DNA (Tokushima University Institutional Repository) ● Metadata: 109642 (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1365-2265.2007.02758.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17371465 ● Search Scopus @ Elsevier (PMID): 17371465 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1365-2265.2007.02758.x (Tokushima University Institutional Repository: 109642, DOI: 10.1111/j.1365-2265.2007.02758.x, PubMed: 17371465)
20.	Y Yamashia, T Akiyama, Noriko Mizusawa, Katsuhiko Yoshimoto and M Goto : A case of hyperparathyroidism-jaw tumour syndrome found in the treatment of an ossifying fibroma in the maxillary bone, International Journal of Oral and Maxillofacial Surgery, Vol.36, No.4, 365-369, 2007. (Summary) Hyperparathyroidism-jaw tumour (HPT-JT) syndrome is characterized by parathyroid tumours as well as by ossifying fibromas of the mandible and maxilla, renal cysts, or Wilms' tumours. Recently, the gene responsible for HPT-JT syndrome has been identified as the HRPT2 tumour suppressor gene. In an 18-year-old male, a tumour in the maxilla was first diagnosed as an ossifying fibroma. During biochemical screening before surgery, the patient received a diagnosis of primary hyperparathyroidism. Neck computed tomography scanning showed a parathyroid tumour. Surgical excisions to remove the jaw tumour and parathyroid adenoma were performed. The postoperative course has been uneventful and a follow up at 2 years revealed no evidence of recurrence. The HRPT2 germline mutation of 39delC was detected in the proband, but not in his unaffected parents. These results suggested that the germline mutation occurred de novo. (Keyword) Adenoma / Adolescent / Diagnosis, Differential / Fibroma, Ossifying / Follow-Up Studies / Gene Deletion / Germ-Line Mutation / Humans / Hyperparathyroidism, Primary / Male / Maxillary Neoplasms / Parathyroid Neoplasms / Syndrome / Tomography, X-Ray Computed / Tumor Suppressor Proteins (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ijom.2006.08.007 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17052894 ● Search Scopus @ Elsevier (PMID): 17052894 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ijom.2006.08.007 (DOI: 10.1016/j.ijom.2006.08.007, PubMed: 17052894)
21.	Kiyoshi Kunika, Toshihito Tanahashi, Eiji Kudo, Noriko Mizusawa, Eiichiro Ichiishi, Naoto Nakamura, Toshikazu Yoshikawa, Takashi Yamaoka, Hiroaki Yasumo, Kazue Tsugaw, Maki Moritani, Hiroshi Inoue and Mitsuo Itakura : Effect of +36T > C in intron 1 on the glutamine: fructose-6-phosphate amidotransferase 1 gene and its contribution to type 2 diabetes in different populations., Journal of Human Genetics, Vol.51, No.12, 1100-1109, 2006. (Summary) Glutamine: fructose-6-phosphate amidotransferase 1 (GFPT1) acts as a rate-limiting enzyme in the hexosamine biosynthetic pathway, which is an alternative branch of glucose metabolism. To evaluate GFPT1 as a susceptibility gene to type 2 diabetes, we surveyed the polymorphisms related with the gene function of GFPT1 and assessed its contribution to type 2 diabetes with a case-control association study. Screening of the 5'-flanking and all coding regions of GFPT1 revealed eight polymorphisms, one in the 5'-flanking region, one synonymous polymorphism in exon 8, five in introns and one in 3'-UTR, but no mis-sense or non-sense polymorphism. With in silico simulation, a putative promoter region was apparently predicted between 1 kb upstream and 1 kb downstream of the start codon. In this region, +36T>C polymorphism was located on the GC box sequence in intron 1, and its functional effect on promoter activity was confirmed by luciferase reporter assay, introducing a new functional polymorphism of the GFPT1 gene. To examine its association with type 2 diabetes, we analyzed 2,763 Japanese (1,461 controls and 1,302 cases) and 330 Caucasians (190 controls and 140 cases). One possible association of +36T>C was observed in Caucasians, but no association of polymorphisms including +36T>C in intron 1 or haplotypes was observed in Japanese. Although we could not completely rule out a contribution to specific sub-groups or other populations, genetic variation of GFPT1 is unlikely to have a major role in the susceptibility to type 2 diabetes in Japanese. (Keyword) 5' Flanking Region / Adult / Aged / Aged, 80 and over / Asian Continental Ancestry Group / Base Sequence / Case-Control Studies / Diabetes Mellitus, Type 2 / European Continental Ancestry Group / Female / Genetic Predisposition to Disease / Glutamine-Fructose-6-Phosphate Transaminase (Isomerizing) / Humans / Introns / Male / Middle Aged / Molecular Sequence Data / Polymorphism, Single Nucleotide / Promoter Regions, Genetic (Link to Publication Site) ● Publication site (DOI): 10.1007/s10038-006-0072-7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17024311 ● Search Scopus @ Elsevier (PMID): 17024311 ● Search Scopus @ Elsevier (DOI): 10.1007/s10038-006-0072-7 (DOI: 10.1007/s10038-006-0072-7, PubMed: 17024311)
22.	Noriko Mizusawa, Shinya Uchino, Takeo Iwata, Masaru Tsuyuguchi, Yasuyo Suzuki, Tsunenori Mizukoshi, Yoshio Yamashita, Akihiro Sakurai, Shinichi Suzuki, Mutsuo Beniko, Hideki Tahara, Masato Fujisawa, Nobuyuki Kamata, Kenji Fujisawa, Tohru Yashiro, Daisuke Nagao, Golam Md. Hossain, Toshiaki Sano, Shiro Noguchi and Katsuhiko Yoshimoto : Genetic analyses in patients with familial isolated hyperparathyroidism and hyperparathyroidism-jaw tumour syndrome., Clinical Endocrinology, Vol.65, No.1, 9-16, 2006. (Summary) A subset of familial isolated primary hyperparathyroidism (FIHP) is a variant of hyperparathyroidism-jaw tumour syndrome (HPT-JT). AIM/PATIENTS AND METHODS: We investigated the involvement of the HRPT2, MEN1 and CASR genes in 11 provisional FIHP families and two HPT-JT families. Germline mutations of HRPT2 were found in two of the 11 FIHP families and one of the two HPT-JT families. One FIHP family with parathyroid carcinoma and atypical adenomas and another FIHP family with cystic parathyroid adenoma had novel frameshift mutations of 518-521del and 62-66del, respectively. In a patient with HPT-JT, a de novo germline mutation of 39delC was detected. Novel somatic HRPT2 mutations of 70-73del and 95-102del were found in two of five parathyroid tumours in a family with a 518-521del mutation. Biallelic inactivation of HRPT2 by a combination of germline and somatic mutation was confirmed in the parathyroid tumours. The finding that two families diagnosed with FIHP carried HRPT2 mutations suggests that they have occult HPT-JT. In the remaining 10 families, one family had a missense MEN1 mutation. No mutations of CASR were detected. Our results confirm the need to test for HRPT2 in FIHP families, especially those with parathyroid carcinomas, atypical adenomas or adenomas with cystic change. (Keyword) Adenoma / Adult / Aged / DNA Mutational Analysis / Female / Frameshift Mutation / Gene Deletion / Genes, Tumor Suppressor / Genotype / Germ-Line Mutation / Humans / Hyperparathyroidism, Primary / Jaw Neoplasms / Loss of Heterozygosity / Male / Methylation / Microsatellite Repeats / Middle Aged / Multiple Endocrine Neoplasia Type 1 / Mutation / Parathyroid Neoplasms / Pedigree / Promoter Regions, Genetic / Receptors, Calcium-Sensing / Sequence Analysis, DNA / Tumor Suppressor Proteins (Tokushima University Institutional Repository) ● Metadata: 113299 (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1365-2265.2006.02534.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16817812 ● Summary page in Scopus @ Elsevier: 2-s2.0-33745207986 (Tokushima University Institutional Repository: 113299, DOI: 10.1111/j.1365-2265.2006.02534.x, PubMed: 16817812, Elsevier: Scopus)
23.	Zhi-Rong Qian, Toshiaki Sano, Katsuhiko Yoshimoto, Shozo Yamada, Akira Ishizuka, Noriko Mizusawa, Hidehisa Horiguchi, Mitsuyoshi Hirokawa and L Sylvia Asa : Inactivation of RASSF1A tumor suppressor gene by aberrant promoter hypermethylation in human pituitary adenomas., Laboratory Investigation; a Journal of Technical Methods and Pathology, Vol.85, No.4, 464-473, 2005. (Summary) Aberrant promoter methylation and resultant silencing of several tumor suppressor genes play an important role in the pathogenesis of many tumor types. The human Ras association domain family 1A gene (RASSF1A), recently cloned from the lung tumor locus at 3p21.3, was shown to be frequently inactivated by hypermethylation of its promoter region in a number of malignancies. We have investigated the expression and epigenetic changes of this novel universal tumor suppressor gene in pituitary adenomas and correlated the data with clinicopathologic findings. Fresh frozen normal pituitary tissues and 52 primary pituitary adenomas including all major types were examined. Methylation-specific polymerase chain reaction (MSP), combined bisulfite restriction analysis (COBRA), bisulfite sequencing and semiquantitative reverse transcription-polymerase chain reaction were used to analyze DNA promoter methylation status and the mRNA expression of RASSF1A, respectively. High levels of RASSF1A transcript and no methylation of the RASSF1A promoter were found in normal pituitary tissues. RASSF1A promoter methylation was detected in 20 of 52 (38%) adenomas including all major types of pituitary adenomas. However, a lower frequency of methylation of the RASSF1A promoter was found in gonadotroph cell adenomas (15%) compared with growth hormone cell, prolactin cell, or adrenocorticotropic hormone cell adenomas (54, 46 and 50%, respectively). Methylation frequency was higher in the most aggressive adenomas (87% in grade IV tumors, P=0.0163). In addition, methylation of the RASSF1A promoter potentially correlated with higher labeling index of the proliferation marker Ki-67 (P=0.1475). Loss or significant reduction of RASSF1A messenger RNA transcripts was identified in 18 of 20 (90%) adenomas with hypermethylation of RASSF1A (P<0.0001). Our data suggest that promoter hypermethylation of RASSF1A and resultant alterations of RASSF1A expression may play a critical role in pituitary tumorigenesis and may be involved in tumor progression. (Keyword) Adenoma / Base Sequence / DNA Methylation / Female / Humans / immunohistochemistry / Male / Molecular Sequence Data / Pituitary Neoplasms / Promoter Regions, Genetic / Reverse Transcriptase Polymerase Chain Reaction / Tumor Suppressor Proteins (Link to Publication Site) ● Publication site (DOI): 10.1038/labinvest.3700248 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15711568 ● Search Scopus @ Elsevier (PMID): 15711568 ● Search Scopus @ Elsevier (DOI): 10.1038/labinvest.3700248 (DOI: 10.1038/labinvest.3700248, PubMed: 15711568)
24.	Noriko Mizusawa, Tomoko Hasegawa, Izumi Ohigashi, Chisato Kosugi, Nagakatsu Harada, Mitsuo Itakura and Katsuhiko Yoshimoto : Differentiation Penotypes of Pancreatic Islet β- and α-cells are Closely Related with Homeotic Genes and a Group of Differentially Expressed Genes., Gene, Vol.331, No.28, 53-63, 2004. (Summary) To identify the genes that determine differentiation phenotypes, we compared gene expression of pancreatic islet beta- and alpha-cells, which are derived from the common precursor and secrete insulin and glucagon, respectively. The expression levels of homeotic genes including Hox genes known to determine region specificity in the antero-posterior (AP) body axis, tissue-specific homeobox genes, and other 8,734 genes were compared in a beta- and alpha-cell line of MIN6 and alpha TC1.6. The expression of homeotic genes were surveyed with reverse transcription-polymerase chain reaction (RT-PCR) using degenerate primers corresponding to invariant amino acid sequences within the homeodomain and subsequently with specific primers. Expression of Hoxc6, Hoxc9, Hoxc10, Pdx1, Cdx2, Gbx2, Pax4, and Hlxb9 genes in MIN6 was higher than those in alpha TC1.6, while expression of Hoxa2, Hoxa3, Hoxa5, Hoxa6, Hoxa7, Hoxa9, Hoxa10, Hoxa13, Hoxb3, Hoxb5, Hoxb6, Hoxb13, Hoxb8, and Brain4 genes in alpha TC1.6 was higher than those in MIN6. Out of 8,734 mouse genes screened with high-density mouse cDNA microarrays for MIN6- and alpha TC1.6-derived cDNA, 58 and 25 genes were differentially over- and under-expressed in MIN6, respectively. GLUTag, which is derived from a large bowel tumor and expresses the proglucagon gene, showed a comparatively similar expression profile to that of alpha TC1.6 in both homeotic and other genes analyzed in cDNA microarray. Our results are consistent with the interpretation that not only the tissue-specific homeotic genes, but also Hox genes are related to differentiation phenotypes of pancreatic beta- and alpha-cells rather than their regional specification of the body in vertebrates. (Keyword) Animals / Blotting, Northern / cell differentiation / Cell Line, Transformed / Cell Line, Tumor / DNA, Complementary / Gene Expression Profiling / Genes, Homeobox / Islets of Langerhans / Mice / NIH 3T3 Cells / Oligonucleotide Array Sequence Analysis / Phenotype / RNA, Messenger / Reverse Transcriptase Polymerase Chain Reaction (Tokushima University Institutional Repository) ● Metadata: 112035 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.gene.2004.01.016 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15094191 ● Search Scopus @ Elsevier (PMID): 15094191 ● Search Scopus @ Elsevier (DOI): 10.1016/j.gene.2004.01.016 (Tokushima University Institutional Repository: 112035, DOI: 10.1016/j.gene.2004.01.016, PubMed: 15094191)
25.	Hiroyuki Yamasaki, Noriko Mizusawa, Shinji Nagahiro, Shozo Yamada, Toshiaki Sano, Mitsuo Itakura and Katsuhiko Yoshimoto : GH-Secreting Pituitary Adenomas Infrequently Contain Inactivating Mutations of PRKAR1A and LOH of 17q23-24., Clinical Endocrinology, Vol.58, No.4, 464-470, 2003. (Summary) The molecular events leading to the development of GH-secreting pituitary tumours remain largely unknown. Gsalpha (GNAS1) mutations are found in 27-43% of sporadic GH-secreting adenomas in the Caucasian population, but the frequency of GNAS1 mutations in Japanese and Korean acromegalic patients was reported to be lower, 4-9% and 16%, respectively. Other genes responsible for the tumourigenesis of GH-secreting pituitary adenomas have not been detected yet. PRKAR1A, which codes for the RIalpha regulatory subunit of cyclic AMP-dependent protein kinase A (PKA) on 17q23-24, was recently reported to contain inactivating mutations in some Carney complex families, which involved GH-secreting adenomas in about 10%. We re-evaluated the frequency of GNAS1 mutations and investigated PRKAR1A on the hypothesis that it might play a role in the tumourigenesis of GH-secreting adenomas. We analysed exons 8 and 9 of GNAS1 and all exons and the exon-intron boundaries of PRKAR1A with the PCR and by direct sequencing using genomic DNA extracted from 32 GH-secreting pituitary adenomas (30 GH-secreting adenomas, two GH and PRL-secreting adenomas) and 28 corresponding peripheral blood samples, and performed loss of heterozygosity (LOH) analysis of 17q23-24 with four microsatellite markers and intragenic markers of PRKAR1A. Seventeen of 32 (53.1%) tumours showed somatic-activating mutations of GNAS1: 16 (53.3%) of 30 GH-secreting adenomas and one of two GH and PRL-secreting adenomas. Neither inactivating somatic mutations of PRKAR1A nor LOH of 17q23-24 were detected in any of the tumours examined. We reconfirm the important role of activating mutations of GNAS1 in GH-secreting adenomas, and conclude that PRKAR1A does not play a significant role in the tumourigenesis. (Keyword) Adenoma / Adult / Aged / Chromosomes, Human, Pair 17 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit / Cyclic AMP-Dependent Protein Kinases / Female / Gene Silencing / Growth Hormone / Growth Hormone-Releasing Hormone / Humans / Loss of Heterozygosity / Male / Middle Aged / Pituitary Neoplasms / Polymerase Chain Reaction / Statistics, Nonparametric (Link to Publication Site) ● Publication site (DOI): 10.1046/j.1365-2265.2003.01740.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12641630 ● Search Scopus @ Elsevier (PMID): 12641630 ● Search Scopus @ Elsevier (DOI): 10.1046/j.1365-2265.2003.01740.x (DOI: 10.1046/j.1365-2265.2003.01740.x, PubMed: 12641630)
26.	Bing Xu, Katsuhiko Yoshimoto, Akira Miyauchi, Seiji Kuma, Noriko Mizusawa, Mitsuyoshi Hirokawa and Toshiaki Sano : Cribriform-Morular Variant of Papillary Thyroid Carcinoma: A Pathological and Molecular Genetics Study with Evidence of Frequent Somatic Mutations in exon 3 of the b-catenin Gene., The Journal of Pathology, Vol.199, No.1, 58-67, 2003. (Summary) The cribriform-morular variant (C-MV), an unusual and peculiar subtype of papillary thyroid carcinoma (PTC), has been observed frequently in familial adenomatous polyposis (FAP)-associated thyroid carcinoma and also in sporadic thyroid carcinoma. In this paper, five young women with the C-MV of PTC, aged 22-34 years at cancer diagnosis, are reported; two of them had attenuated FAP. Grossly, one FAP-associated tumour and one sporadic tumour were multicentric and the others were solitary. Histologically, the tumours were encapsulated and exhibited a combination of cribriform, follicular, trabecular, solid, and papillary patterns of growth, with morular areas. Immunohistochemically, the tumour cells showed cytoplasmic expression of thyroglobulin, neuron-specific enolase, epithelial membrane antigen, high- and low-molecular-weight cytokeratins, vimentin, and bcl-2 protein; nuclear expression of oestrogen and progesterone receptors, and retinoblastoma protein; and cytoplasmic and nuclear accumulation of beta-catenin. Germline mutations of the adenomatous polyposis coli (APC) gene were investigated using the protein truncation test in four subjects, including two FAP individuals. Germline APC mutation was identified in only one FAP patient with the multicentric C-MV of PTC, who had a thymidine deletion at codon 512, resulting in a frameshift leading to a premature stop codon. No loss of heterozygosity of loci close to the APC gene was detected in tumour tissues from these four patients. Somatic mutation analysis of exon 3 of the beta-catenin gene (CTNNB1) revealed alterations in seven tumours from all five individuals: one at a serine residue (codon 29), three at amino acids adjacent to serine or threonine residues (codons 22, 39, and 44), and three at other amino acids (codons 49, 54, and 56). Moreover, each of two different tumours examined from two patients with the multicentric C-MV of PTC, had different somatic mutations of the CTNNB1 gene. Taken together, these data suggest that accumulation of mutant beta-catenin contributes to the development of the C-MV of PTC. (Keyword) Adenocarcinoma, Papillary / Adenomatous Polyposis Coli / Adult / Cytoskeletal Proteins / Exons / Female / Genes, APC / Humans / Immunohistochemistry / Loss of Heterozygosity / Mutation / Thyroid Gland / Thyroid Neoplasms / Trans-Activators / beta Catenin (Link to Publication Site) ● Publication site (DOI): 10.1002/path.1225 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12474227 ● Search Scopus @ Elsevier (PMID): 12474227 ● Search Scopus @ Elsevier (DOI): 10.1002/path.1225 (DOI: 10.1002/path.1225, PubMed: 12474227)
27.	Zhi-Rong Qian, Chei Chiun Li, Hiroyuki Yamasaki, Noriko Mizusawa, Katsuhiko Yoshimoto, Shozo Yamada, Takashi Tashiro, Hidehisa Horiguchi, Shingo Wakatsuki, Mitsuyoshi Hirokawa and Toshiaki Sano : Role of E-cadherin, alpha-, beta-, and gamma-catenins, and p120 (cell adhesion molecules) in prolactinoma behavior., Modern Pathology, Vol.15, No.12, 1357-1365, 2002. (Summary) E-cadherin/catenin complex regulates cellular adhesion and motility and is believed to function as an invasion suppressor system. In a number of cancers, abnormal and reduced expression of E-cadherin/catenin complex is associated with tumor invasion and metastasis. Prolactinomas show frequent invasion on the surrounding structures, despite their histologically benign nature. Furthermore, gender-based differences in endocrine and surgical findings are found in patients with prolactinoma. To understand biological factors governing prolactinoma behavior, this study analyzed the expression of E-cadherin; alpha-, beta-, and gamma-catenins; p120; and cell proliferation marker MIB-1 labeling index in 13 invasive tumors (9 in men, 4 in women), 26 noninvasive tumors (4 in men, 22 in women), and 8 normal anterior pituitaries by immunohistochemistry. Immunostaining of E-cadherin; alpha-, beta-, and gamma-catenins; and p120 showed a membranous pattern of reactivity and generally stronger in normal pituitaries than in prolactinomas. Expression of E-cadherin and beta-catenin was significantly lower in invasive than in noninvasive prolactinomas (P <.002 and P <.005, respectively), and reduced expression of E-cadherin and beta-catenin was more frequent in invasive than in noninvasive prolactinomas (P <.001 and P <.05, respectively); in contrast, gamma-catenin expression showed higher in invasive than in noninvasive prolactinomas (P <.05). Expression of E-cadherin was significantly lower in macroprolactinomas than in microprolactinomas (P <.01), and decreased expression of E-cadherin and beta-catenin predicted high MIB-1 expression (P <.05). Moreover, the expression of E-cadherin and beta-catenin was significantly lower in macroprolactinomas in men than in those in women (P <.01 and P <.02, respectively). No statistical correlations were observed between expression of alpha-catenin, p120, and clinicopathologic features. In conclusion, the reduction of E-cadherin and beta-catenin expression was related to invasiveness and proliferative status of prolactinomas and correlated with the more aggressive behavior of prolactinomas in men compared with in women. (Keyword) Adolescent / Adult / Aged / Cadherins / Cell Adhesion Molecules / Cytoskeletal Proteins / Desmoplakins / Female / Humans / immunohistochemistry / Ki-67 Antigen / Male / Middle Aged / Phosphoproteins / Pituitary Neoplasms / Prolactinoma / Trans-Activators / alpha Catenin / beta Catenin / gamma Catenin (Link to Publication Site) ● Publication site (DOI): 10.1097/01.MP.0000039572.75188.1A (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12481018 ● Search Scopus @ Elsevier (PMID): 12481018 ● Search Scopus @ Elsevier (DOI): 10.1097/01.MP.0000039572.75188.1A (DOI: 10.1097/01.MP.0000039572.75188.1A, PubMed: 12481018)
28.	Hiroyuki Iwahana, Takashi Yamaoka, Masakazu Mizutani, Noriko Mizusawa, Setsuko Ii, Katsuhiko Yoshimoto and Mitsuo Itakura : Molecular Cloning of Rat Amidophosphoribosyltransferase., The Journal of Biological Chemistry, Vol.268, No.10, 7225-7237, 1993.
29.	Hiroyuki Iwahana, Jun Oka, Noriko Mizusawa, Eiji Kudo, Setsuko Ii, Katsuhiko Yoshimoto, Edward W Holmes and Mitsuo Itakura : Molecular Cloning of Human Amidophosphoribosyltransferase., Biochemical and Biophysical Research Communications, Vol.190, No.1, 192-200, 1993.
30.	Hiroyuki Iwahana, Noriko Mizusawa, Katsuhiko Yoshimoto and Mitsuo Itakura : Detection of a New Polymorphism of the Human Prothrombin (F2) Gene by Combination of PASA and Mutated Primer-Mediated PCR-RFLP., Human Genetics, Vol.90, 325-326, 1992.

Review, Commentary:

1.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa and Shinji Ono : Carney complex (CNC), 臨床画像, Vol.31, No.10, 31-32, 2015. (Tokushima University Institutional Repository) ● Metadata: 111702 (Tokushima University Institutional Repository: 111702)
2.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa and 小野信二 : Hyperparathyroidism-Jaw Tumor Syndrome, Shikoku Dental Research, Vol.27, No.1, 35-39, Jun. 2014. (Tokushima University Institutional Repository) ● Metadata: 109852 (Tokushima University Institutional Repository: 109852)
3.	Katsuhiko Yoshimoto, Noriko Mizusawa, Takeo Iwata and Shinji Ono : Familial hyperparathyroidism, Endocrinology, Diabetology & Metabolism, Vol.37, No.4, 380-386, Oct. 2013. (Keyword) familial isolated hyperparathyroidism / familial hypocalciuric hypercalcemia / hyperparathyroidism-jaw tumor syndrome / CDC73 / parafibromin (Tokushima University Institutional Repository) ● Metadata: 111716 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050845762396554368 (Tokushima University Institutional Repository: 111716, CiNii: 1050845762396554368)
4.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa and Shinji Ono : The AIP gene and pituitary tumors, ホルモンと臨床, Vol.60, No.8, 627-632, Aug. 2012. (Tokushima University Institutional Repository) ● Metadata: 114320 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050846637597795968 (Tokushima University Institutional Repository: 114320, CiNii: 1050846637597795968)
5.	Noriko Mizusawa, Takeo Iwata and Katsuhiko Yoshimoto : 【遺伝性内分泌腫瘍の基礎と臨床遺伝カウンセリングに必要な知識】家族性副甲状腺機能亢進症の基礎と臨床, ホルモンと臨床, Vol.57, No.3, 255-261, Mar. 2009. (Keyword) 顎腫瘍(病理学) カルシウム代謝障害(診断,遺伝学) 甲状腺機能亢進症(実験的) *上皮小体機能亢進症(診断,遺伝学) 上皮小体腫瘍(病理学) 免疫組織化学ノックアウトマウス遺伝学的検査腫瘍抑制蛋白質低カルシウム尿性高カルシウム血症-家族性(診断,遺伝学) HRPT2 Protein ヒトマウス動物特集 (Tokushima University Institutional Repository) ● Metadata: 114318 (Tokushima University Institutional Repository: 114318)
6.	Katsuhiko Yoshimoto, Takeo Iwata and Noriko Mizusawa : アディポサイトカインと生活習慣病, Shikoku Dental Research, Vol.20, No.2, 261-263, 2008. (Tokushima University Institutional Repository) ● Metadata: 109771 (Tokushima University Institutional Repository: 109771)
7.	HM Golam, Takeo Iwata, Noriko Mizusawa, Zhi-Rong Qian, Shozo Yamada, Toshiaki Sano and Katsuhiko Yoshimoto : Role of cyclin-dependent kinase inhibitors in pituitary tumorigenesis: an update, Shikoku Acta Medica, Vol.64, 225-231, 2008. (Tokushima University Institutional Repository) ● Metadata: 110181 (Tokushima University Institutional Repository: 110181)
8.	Takeo Iwata, Noriko Mizusawa, Golam Md Hossain and Katsuhiko Yoshimoto : 癌抑制因子パラフィブロミンはSV40 large T抗原存在下では細胞増殖促進に働く, ホルモンと臨床増刊号, Vol.56, 147-155, 2008. (Tokushima University Institutional Repository) ● Metadata: 114317 (Tokushima University Institutional Repository: 114317)
9.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa, 長尾大輔, Md.Golam Hossain, 露口勝, Toshiaki Sano and 内野眞也 : 家族性副甲状腺機能亢進症2家系におけるHRPT2遺伝子変異の解析,, ホルモンと臨床, Vol.54, 138-142, 2006. (Tokushima University Institutional Repository) ● Metadata: 114316 (Tokushima University Institutional Repository: 114316)

Proceeding of International Conference:

1.	Yuki Iwawaki, Noriko Mizusawa, Yoritoki Tomotake, Tetsuo Ichikawa and Katsuhiko Yoshimoto : Mechanical stress - responsive microRNA, The 3rd ASEAN plus and TOKUSHIMA Joint International Conference, Makassar, Indonesia, Dec. 2014.
2.	Noriko Mizusawa, Takeo Iwata and Katsuhiko Yoshimoto : Profile of microRNA inhuman saliva, Asean Plus Tokushima Joint International Conference, Dec. 2012.
3.	Shima Nazatul Wan, Noriko Mizusawa, Takeo Iwata and Katsuhiko Yoshimoto : Analysis of microRNA in saliva and submandibular gland cell lines., International Joint Symposium: The University of Tokushima, Universitas Gadjah Mada, Niigata University, Denpasar, Bali, Dec. 2010.
4.	Katsuhiko Yoshimoto, Md. Golam Hossain, Takeo Iwata, Noriko Mizusawa, Shima Wan Nazatul Schadan, Toru Okutsu, Kyoko Ishimoto, Zhi-Rong Qian, Toshiaki Sano and Shozo Yamada : Down-regulated expression of p18INK4C in pituitary adenomas., 14th International Congress of Endocrinology, Kyoto, Mar. 2010.
5.	Takeo Iwata, Masamichi Kuwajima, Akiko Sukeno, Naozumi Ishimaru, Yoshio Hayashi, M Wabitsch, Noriko Mizusawa, Mitsuo Itakura and Katsuhiko Yoshimoto : YKL-40 secreted from macrophages infiltrating into adipose tissue inhibits degradation of type I collagen., International symposium on diabetes, Tokyo, Mar. 2009.
6.	Shima Nazatul Wan, Noriko Mizusawa, Takeo Iwata and Katsuhiko Yoshimoto : Effect of Liver X Receptor (LXR) Agonist on GLP-1 Expression., The International Symposium on Oral Sciences to Improve The Quality of Life, Tokushima, Sep. 2008.
7.	Golam Md. Hossain, Takeo Iwata, Noriko Mizusawa and Katsuhiko Yoshimoto : Compressive force-induced inhibition of adipocyte differentiation is mediated through down-regulatioin of PPAR2., The International Symposium on Oral Sciences to Improve The Quality of Life, Tokushima, Sep. 2008.
8.	Golam Md. Hossain, Takeo Iwata, Noriko Mizusawa, Shozo Yamada, Zhi-Rong Qian, Toshiaki Sano and Katsuhiko Yoshimoto : Mutational analysis and gene expression profile of CDKN2C/p18INK4C in pituitary adenomas., TThe 2nd International Symposium on "The Future Direction of Oral Sciences in the 21st Century"-Oral Sciences for Our Healthy Life-, Tokushima, Dec. 2007.
9.	Golam Md. Hossain, Takeo Iwata, Shozo Yamada, Noriko Mizusawa, Toshiaki Sano and Katsuhiko Yoshimoto : Mutation analysis of AIP in isolated familial somatotropinomas and sporadic growth hormone-secreting adenomas., The 1st International Symposium and Workshop The Future Direction of Oral Sciences in the 21st Century, Awaji, Mar. 2007.
10.	Yamasaki Hiroyuki, Noriko Mizusawa, Shinji Nagahiro, Shozo Yamada, Toshiaki Sano, Mitsuo Itakura and Katsuhiko Yoshimoto : GH-secreting pituitary adenomas infrequently contain inactivating mutations of PRKAR1A and LOH of 2p16 and 17q23-24., 85th annual meeting of the endocrine society, Philadelphia, Jun. 2003.

Proceeding of Domestic Conference:

1.	Jin Shengjian, Takaaki Tsunematsu, Taigo Horiguchi, Yasuhiro Mouri, Wenhua Shao, Keiko Miyoshi, Noriko Mizusawa, Hagita Hiroko, Sarubo Motoharu, Yoshida Kayo, Kaya Yoshida, Natsumi Fujiwara, Kazumi Ozaki, Naozumi Ishimaru and Yasusei Kudo : The role of deubiquitinating enzyme, OTUB1 in head and neck squamous cell carcinoma (HNSCC) progression, 第82回日本癌学会学術集会, Sep. 2023.
2.	Jin Shengjian, Takaaki Tsunematsu, Taigo Horiguchi, Yasuhiro Mouri, Wenhua Shao, Keiko Miyoshi, Noriko Mizusawa, Hiroko Hagita, YOSHIDA Kayo, Kaya Yoshida, Natsumi Fujiwara, Kazumi Ozaki, Naozumi Ishimaru and Yasusei Kudo : The role of Deubiquitinating enzyme, OTUB1 in head and neck squamous cell carcinoma (HNSCC) progression, 第61回四国歯学会, Mar. 2023.
3.	Nanaka Murata, Mima Hashimoto, Noriko Mizusawa and Katsuhiko Yoshimoto : マイクロRNAの細胞増殖への影響, 四国歯学会第56回例会・徳島県歯科医学大会, Feb. 2020.
4.	Mima Hashimoto, Nanaka Murata, Noriko Mizusawa and Katsuhiko Yoshimoto : 唾液マイクロRNAの機能解析, 四国歯学会第56回例会・徳島県歯科医学大会, Feb. 2020.
5.	Noriko Mizusawa, Yuki Iwawaki and Katsuhiko Yoshimoto : 唾液中に存在するマイクロRNAのプロファイリング, 四国歯学会第56回例会・徳島県歯科医学大会, Feb. 2020.
6.	Noriko Mizusawa and Katsuhiko Yoshimoto : マイクロRNAプロファイリングによるヒト顎下腺細胞株での上皮間葉系変換の解析, 第11回日本RNAi研究会, Aug. 2019.
7.	Noriko Mizusawa, Nagakatsu Harada, Takeo Iwata and Katsuhiko Yoshimoto : 膵beta細胞機能に関与するPrss53の解析, 第62回日本糖尿病学会年次学術集会, May 2019.
8.	Noriko Mizusawa, Nagakatsu Harada, Takeo Iwata and Katsuhiko Yoshimoto : Prss53は膵ベータ細胞のミトコンドリア機能を介した細胞維持に関与する, 第22回日本臨床内分泌病理学会学術総会, Sep. 2018.
9.	Noriko Mizusawa, Takeo Iwata and Katsuhiko Yoshimoto : ヒト顎下腺細胞株 NS-SV-AC における miR-1290 の機能解析, 第59回歯科基礎医学会学術大会・総会, Sep. 2017.
10.	Shinji Ono, Takeo Iwata, Noriko Mizusawa, Shozo Yamada and Katsuhiko Yoshimoto : 非機能性腺腫および ACTH 腺腫における 14q32 領域遺伝子の発現低下, 第27回間脳下垂体腫瘍学会, Feb. 2017.
11.	Ohtuka Ryo, Nagakatsu Harada, Noriko Mizusawa, Katsuhiko Yoshimoto, Kazuchika Nishitsuji, Kazumi Takaishi, 豊中屋, Hiroshi Sakaue and Hiroshi Kitahata : GADD34のC末端領域を欠損したCHO-K1細胞の樹立, 第253回徳島医学会学術集会, Jul. 2016.
12.	Noriko Mizusawa, Takeo Iwata and Katsuhiko Yoshimoto : miR-222はRNA-binding protein 24 を標的として顎下腺細胞株NS-SV-ACの細胞増殖に関与する, 第38回日本分子生物学会年会, Dec. 2015.
13.	Shinji Ono, Takeo Iwata, Noriko Mizusawa, 岩脇有軌 and Katsuhiko Yoshimoto : ACTH 産生腺腫で低発現を認めた miR-551b の腺腫発症への関与, 第56回歯科基礎医学会学術大会・総会福岡, Sep. 2014.
14.	岩脇有軌, Noriko Mizusawa, Takeo Iwata, Shinji Ono, Yoritoki Tomotake, Tetsuo Ichikawa and Katsuhiko Yoshimoto : メカニカルストレス応答性 miR-494-3p による FGFR2 発現の抑制, 第56回歯科基礎医学会学術大会・総会福岡, Sep. 2014.
15.	Shinji Ono, Takeo Iwata, Noriko Mizusawa, Shozo Yamada and Katsuhiko Yoshimoto : 成長ホルモン産生腺腫におけるPRKACA遺伝子活性化変異の検討, 第14回日本内分泌学会四国地方会徳島, Sep. 2014.
16.	Noriko Mizusawa, 岩脇有軌, Takeo Iwata and Katsuhiko Yoshimoto : ヒト顎下腺細胞株を用いた miRNA 標的遺伝子の解析, 第6回日本RNAi研究会・第1回細胞外小胞学会広島, Aug. 2014.
17.	Takeo Iwata, Hisaaki Taniguchi, Masamichi Kuwajima, Noriko Mizusawa and Katsuhiko Yoshimoto : D-dopachrome tautomeraseの脂肪細胞への作用, 第17回日本内分泌病理学会学術総会横浜, Oct. 2013.
18.	Takeo Iwata, Kyoko Ishimoto, Noriko Mizusawa and Katsuhiko Yoshimoto : D-dopachrome tautomeraseのインスリン抵抗性改善機序に関連する分子の探索, 第55回歯科基礎医学会学術大会・総会岡山, Sep. 2013.
19.	小野信二, Takeo Iwata, Noriko Mizusawa and Katsuhiko Yoshimoto : 下垂体腺腫における miRNA 発現解析, 第55回歯科基礎医学会学術大会・総会岡山, Sep. 2013.
20.	岩脇有軌, Noriko Mizusawa, Takeo Iwata, 小野信二, Yoritoki Tomotake, Tetsuo Ichikawa and Katsuhiko Yoshimoto : 機械的刺激応答性miRNAの同定, 第5回日本RNAi研究会広島, Aug. 2013.
21.	安藤明彦, 長坂昌一郎, 高橋仁麗, 野牛宏晃, 大須賀淳一, Noriko Mizusawa, Katsuhiko Yoshimoto and 石橋俊 : 原発性アルドステロン症・サブクリニカルCushing症候群を合併した家族性副甲状腺機能亢進症の1例, 第85回日本内分泌学会学術総会, Apr. 2012.
22.	安藤明彦, 長坂昌一郎, 齋藤芽里, 山崎智行, 高橋仁麗, 野牛宏晃, 大須賀淳一, Noriko Mizusawa, Katsuhiko Yoshimoto and 石橋俊 : 原発性アルドステロン症・サブクリニカルCushing症候群を合併した家族性副甲状腺機能亢進症の一例, 第39回内分泌代謝研究会, Dec. 2011.
23.	Takeo Iwata, Kyoko Ishimoto, Noriko Mizusawa and Katsuhiko Yoshimoto : D-dopachrome tautomeraseは肥満マウスでのインスリン抵抗性を改善する, 第53回歯科基礎医学会学術大会(岐阜), Oct. 2011.
24.	Nazatul Wan Shima, Noriko Mizusawa, Takeo Iwata and Katsuhiko Yoshimoto : Analysis of miRNAs in saliva, 第84回日本生化学会大会, Sep. 2011.
25.	Noriko Mizusawa, Takeo Iwata, Nagakatsu Harada, Shima Nazatul Wan, Mitsuo Itakura and Katsuhiko Yoshimoto : マウス膵島におけるisletasinの機能解析, 第54回日本糖尿病学会年次学術集会(札幌), May 2011.
26.	Takeo Iwata, Hisaaki Taniguchi, Masamichi Kuwajima, Kyoko Ishimoto, Noriko Mizusawa and Katsuhiko Yoshimoto : D-dopachrome tautomeraseは脂肪細胞での脂質代謝を制御する, 第54回日本糖尿病学会年次学術集会(札幌), May 2011.
27.	Rie Kido, Noriko Mizusawa, Shima Nazatul Wan, Takeo Iwata and Katsuhiko Yoshimoto : マウス膵島の単離, 126回徳島生物学会, Dec. 2010.
28.	Shima Nazatul Wan, Noriko Mizusawa, Takeo Iwata and Katsuhiko Yoshimoto : 唾液microRNAの解析, 第52回歯科基礎医学会学術大会・総会, Sep. 2010.
29.	Takeo Iwata, Kyoko Ishimoto, Noriko Mizusawa and Katsuhiko Yoshimoto : D-dopachrome tautomeraseは脂肪細胞での中性脂肪量を制御する, 第52回歯科基礎医学会学術大会・総会, Sep. 2010.
30.	Takeo Iwata, Md. Golam Hossain, Noriko Mizusawa and Katsuhiko Yoshimoto : 持続的圧縮力は前駆脂肪細胞からの脂肪細胞への分化を抑制する, 第53回日本糖尿病学会年次学術集会, May 2010.
31.	Noriko Mizusawa, Takeo Iwata, Shima Nazatul Wan and Katsuhiko Yoshimoto : LXRアゴニストによるプログルカゴン遺伝子産生への影響, 第53回日本糖尿病学会年次学術集会, May 2010.
32.	Takeo Iwata, Naozumi Ishimaru, Yoshio Hayashi, Noriko Mizusawa and Katsuhiko Yoshimoto : 脂肪組織におけるYKL-40の役割, 第51回歯科基礎医学会学術大会, Sep. 2009.
33.	Shima Nazatul Wan, Noriko Mizusawa, Takeo Iwata and Katsuhiko Yoshimoto : Liver X receptorアゴニストによる消化管ホルモン発現調節, 第51回歯科基礎医学会学術大会, Sep. 2009.
34.	Noriko Mizusawa, Takeo Iwata, Shima Nazatul Wan and Katsuhiko Yoshimoto : LXRアゴニスト T0901317によるプログルカゴン遺伝子発現への影響, 第52回日本糖尿病学会年次学術集会, May 2009.
35.	畠山節子, 堤玲子, Noriko Mizusawa, Katsuhiko Yoshimoto, 安本茂 and 武田泰典 : hTERTおよびcdk4遺伝子導入による不死化歯原性上皮細胞の樹立, 日本組織培養学会第82回大会, May 2009.
36.	Golam Md. Hossain, Takeo Iwata, Noriko Mizusawa, Shozo Yamada, Zhi-Rong Qian, Toshiaki Sano and Katsuhiko Yoshimoto : Mutations, gene expression and CpG methylation status of cyclin-dependent kinase inhibitor p18INK4C in human pituitary adenomas., 第238回徳島医学会学術集会, Feb. 2009.
37.	Takeo Iwata, Noriko Mizusawa, Mitsuo Itakura and Katsuhiko Yoshimoto : YKL-40とMMP-1は脂肪組織のリモデリングに関与する, 第29回日本肥満学会, Oct. 2008.
38.	小野信二, Shima Nazatul Wan, Noriko Mizusawa and Katsuhiko Yoshimoto : インクレチン発現におけるLXR合成アゴニストの影響, 第50回歯科基礎医学会学術大会・総会, Sep. 2008.
39.	安永佳世, Noriko Mizusawa, 畠山節子 and Katsuhiko Yoshimoto : isletasinの機能解析, 第50回歯科基礎医学会学術大会・総会, Sep. 2008.
40.	Golam Md. Hossain, Takeo Iwata, Noriko Mizusawa, Shozo Yamada, Zhi-Rong Qian, Toshiaki Sano and Katsuhiko Yoshimoto : Mutations, gene expression and CpG methylation status of cyclin-dependent kinase inhibitor p18INK4C in human pituitary adenomas., 第237回徳島医学会学術集会, Aug. 2008.
41.	Noriko Mizusawa, Takeo Iwata and Katsuhiko Yoshimoto : LXRアゴニストによるインクレチン発現への影響,, 第81回日本内分泌学会学術総会, May 2008.
42.	Katsuhiko Yoshimoto, Golam Hossain, Takeo Iwata, Noriko Mizusawa, 内野眞也, 鈴木やすよ, 水越常徳, 田原英樹, 櫻井晃洋, 紅粉睦男, 八代享, 鈴木眞一, 松野彰, 西岡宏 and 田村哲郎 : 家族性副甲状腺機能亢進症家系および家族性下垂体腺腫家系におけるp27Kip1遺伝子解析, 第81回日本内分泌学会学術総会, May 2008.
43.	Takeo Iwata, Noriko Mizusawa, Toshiaki Sano, Mitsuo Itakura and Katsuhiko Yoshimoto : マクロファージ培養上清が脂肪前駆細胞株SGBSのMMP発現に与える影響, 第28回日本肥満学会, Oct. 2007.
44.	Takeo Iwata, Noriko Mizusawa, Yutaka Taketani, Mitsuo Itakura and Katsuhiko Yoshimoto : 副甲状腺癌抑制因子パラフィブロミンはSV40 large T抗原存在下では細胞増殖促進に働く, 第32回日本比較内分泌学会大会, Oct. 2007.
45.	Noriko Mizusawa, 畠山節子 and Katsuhiko Yoshimoto : isletasin遺伝子の膵β細胞特異的発現と細胞内局在, 第49回歯科基礎医学会学術大会・総会, Aug. 2007.
46.	Golam Md. Hossain, Takeo Iwata, Noriko Mizusawa, Katsuhiko Yoshimoto, Shozo Yamada and Toshiaki Sano : Mutation analysis of AIP gene in isolated familial somatotropinomas and sporadic growth hormone-secreting adenomas., 第235回徳島医学会学術集会, Aug. 2007.
47.	Takeo Iwata, Shozo Yamada, Noriko Mizusawa, Golam Md. Hossain, 西岡宏, 松野彰, Toshiaki Sano and Katsuhiko Yoshimoto : 家族性および孤発性 GH産生腺腫におけるAIP遺伝子解析, 第80回日本内分泌学会学術総会, Jun. 2007.
48.	Noriko Mizusawa, Takeo Iwata and Katsuhiko Yoshimoto : 膵β細胞に高発現するisletasin遺伝子の解析, 第50回日本糖尿病学会年次学術集会, May 2007.
49.	Takeo Iwata, Noriko Mizusawa, Yutaka Taketani, Mitsuo Itakura and Katsuhiko Yoshimoto : 癌抑制因子パラフィブロミンはSV40 large T抗原存在下では細胞増殖促進に働く, 第10回日本内分泌病理学会学術総会, Nov. 2006.
50.	Katsuhiko Yoshimoto, Noriko Mizusawa, Takeo Iwata, Toshiaki Sano and 露口勝 : 副甲状腺機能亢進症-顎腫瘍症候群におけるHRPT2変異, 第6回日本内分泌学会四国地方会, Sep. 2006.
51.	Noriko Mizusawa, Nagakatsu Harada, Takeo Iwata, 国香清, Maki Moritani, Yutaka Taketani, Mitsuo Itakura and Katsuhiko Yoshimoto : 膵β細胞に高発現する新規蛋白Isletasinの機能解析, 第49回日本糖尿病学会年次学術集会, May 2006.
52.	Katsuhiko Yoshimoto, Noriko Mizusawa, Takeo Iwata, Toshiaki Sano, 露口勝, 内野眞也, 野口志郎, 鈴木やすよ, 水越常徳, 田原英樹, 櫻井晃洋, 紅粉睦男, 八代享, 鈴木眞一 and 藤澤正人 : 家族性副甲状腺機能亢進症家系および孤発性副甲状腺腺腫症例におけるHRPT2遺伝子変異,, 第79回日本内分泌学会学術総会, May 2006.
53.	Takeo Iwata, Noriko Mizusawa, Yutaka Taketani, Mitsuo Itakura and Katsuhiko Yoshimoto : 副甲状腺癌抑制遺伝子産物パラフィブロミンとSV40 large T抗原の相互作用による癌化機構, 第79回日本内分泌学会学術総会, May 2006.
54.	Takeo Iwata, Noriko Mizusawa, Yutaka Taketani, Mitsuo Itakura and Katsuhiko Yoshimoto : Under40 Panel Discussion 副甲状腺癌抑制遺伝子産物パラフィブロミンと相互作用する蛋白の同定, 第78回日本内分泌学会学術総会, Jul. 2005.
55.	Katsuhiko Yoshimoto, Noriko Mizusawa, Takeo Iwata, 露口勝, Toshiaki Sano and 内野眞也 : 家族性副甲状腺機能亢進症2家系におけるHRPT2遺伝子変異の解析, 第78回日本内分泌学会学術総会, Jul. 2005.
56.	Noriko Mizusawa, Takeo Iwata, Mitsuo Itakura and Katsuhiko Yoshimoto : ヒトインスリン遺伝子発現調節におけるGC2-GC1配列の役割, 第48回日本糖尿病年次学術集会, May 2005.
57.	Noriko Mizusawa, Chisato Kosugi, Nagakatsu Harada, Mitsuo Itakura and Katsuhiko Yoshimoto : 膵β細胞とα細胞のHox遺伝子およびホメオティック遺伝子発現の差異, 第47回日本糖尿病学会年次学術総会, May 2004.
58.	Zhi-Rong Qian, Toshiaki Sano, Katsuhiko Yoshimoto, Shozo Yamada, Noriko Mizusawa, 石塚明, Hidehisa Horiguchi and Mitsuyoshi Hirokawa : Aberrant methylation of the CDH13 gene in pituitary adenomas, 第14回日本間脳下垂体腫瘍学会, Feb. 2004.
59.	Zhi-Rong Qian, Toshiaki Sano, Katsuhiko Yoshimoto, Shozo Yamada, Noriko Mizusawa, Ishizuka Akira, Hidehisa Horiguchi and Mitsuyoshi Hirokawa : Inactivation of RASSF1A tumor suppressor gene by aberrant promoter methylation in human pituitary adenomas, 第7回日本内分泌病理学会総会, Oct. 2003.
60.	Noriko Mizusawa, Nagakatsu Harada and Katsuhiko Yoshimoto : 膵β細胞特異的に発現するisletasin遺伝子の解析, 第46回日本糖尿病学会年次学術総会, May 2003.
61.	Noriko Mizusawa, 友成章, Chisato Kosugi, 小倉真琴, Nagakatsu Harada, Izumi Ohigashi, Mitsuo Itakura and Katsuhiko Yoshimoto : ヒトインスリン遺伝子のグルコ-ス応答性転写調節に及ぼすGG配列の役割, 第45回日本糖尿病学会年次学術総会, May 2002.
62.	Zhi-Rong Qian, Li Chei Chiun, 山崎弘幸, Noriko Mizusawa, Katsuhiko Yoshimoto, Shozo Yamada, Hidehisa Horiguchi, Shingo Wakatsuki, Mitsuyoshi Hirokawa and Toshiaki Sano : Expression of E-cadherin and alpha-, beta-, and gamma-catenins in Human Pituitary Prolactinomas, 第91回日本病理学会総会, Mar. 2002.
63.	Zhi-Rong Qian, Li Chei Chiun, 山崎弘幸, Noriko Mizusawa, Katsuhiko Yoshimoto, Shozo Yamada and Toshiaki Sano : Expression of E-cadherin and alpha-, beta-, and gamma-catenins in Human Pituitary Prolactinomas, 第12回日本間脳下垂体腫瘍学会, Feb. 2002.
64.	山崎弘幸, Noriko Mizusawa, Chisato Kosugi, Nagakatsu Harada, Izumi Ohigashi, 本田壮一, Shozo Yamada, Toshiaki Sano, Teruyoshi Kageji, Shinji Nagahiro and Katsuhiko Yoshimoto : GH下垂体腺腫におけるPRKAR1A遺伝子異常の解析, 第12回日本間脳下垂体腫瘍学会, Feb. 2002.
65.	本田壮一, Chisato Kosugi, Shozo Yamada, 木村敏彦, Nagakatsu Harada, Izumi Ohigashi, Noriko Mizusawa, 山崎弘幸, Toshiaki Sano and Katsuhiko Yoshimoto : 下垂体腺腫における網膜芽細胞腫 (RB)遺伝子異常の解析, 第12回日本間脳下垂体腫瘍学会, Feb. 2002.
66.	Zhi-Rong Qian, Li Chei Chiun, 山崎弘幸, Noriko Mizusawa, Katsuhiko Yoshimoto, Shozo Yamada and Toshiaki Sano : Expression of E-cadherin and alpha-, beta-, and gamma-catenins in Human Pituitary Prolactinomas, 第224回徳島医学会学術集会 (平成13年度冬期), Feb. 2002.
67.	Noriko Mizusawa, 友成章, Chisato Tanaka, Nagakatsu Harada, Izumi Ohigashi, Mitsuo Itakura and Katsuhiko Yoshimoto : インスリン遺伝子のグルコース応答性転写調節に及ぼすCG配列の役割, 第24回日本分子生物学会年会, Dec. 2001.
68.	Noriko Mizusawa, Katsuhiko Yoshimoto, Hiroyuki Iwahana, 清水新司, 久保田美子, 平野浩子, Mitsuo Itakura and 堀内三郎 : ヒトCAD遺伝子上流調節領域の構造決定と解析, 第66回日本生化学会東北支部会例会, Jun. 2000.
69.	Noriko Mizusawa, 藤村美和, Hiroyuki Iwahana, Rumi Katashima, Katsuhiko Yoshimoto, 堀内三郎 and Mitsuo Itakura : ヒトCAD遺伝子のゲノム構造の解析, 第70回日本生化学会(金沢), Sep. 1997.
70.	Hiroyuki Iwahana, 岡純, Noriko Mizusawa, Rumi Katashima, 村上大輔, Eiji Kudo, Setsuko Ii, Takashi Yamaoka, Katsuhiko Yoshimoto, Edward W. Holmes and Mitsuo Itakura : ヒト・アミドホスホリボシルトランスフェラーゼ(ATase)蛋白の精製とcDNAクローニング, 第67回日本生化学会大会(大阪), Sep. 1994.
71.	Hiroyuki Iwahana, 岡純, Noriko Mizusawa, Rumi Katashima, 村上大輔, Eiji Kudo, Setsuko Ii, Katsuhiko Yoshimoto, Edward W. Holmes and Mitsuo Itakura : ヒト・アミドホスホリボシルトランスフェラーゼ(ATase)蛋白の精製とcDNAクローニング, 第27回日本プリン・ピリミジン代謝学会総会(名古屋), Feb. 1994.
72.	田中正喜, Rumi Katashima, Noriko Mizusawa, 村上大輔, 大塚理司, Katsuhiko Yoshimoto, Hiroyuki Iwahana and Mitsuo Itakura : Random sequencingによるマウス膵ランゲルハンス島B細胞(膵B細胞)の発現遺伝子群の解析, 第16回日本分子生物学会年会(千葉), Dec. 1993.
73.	Hiroyuki Iwahana, Katsuhiko Yoshimoto, Noriko Mizusawa, Eiji Kudo and Mitsuo Itakura : 多種類の蛍光色素とコンピューター画像を用いたMF-PCR-SSCP解析, 第16回日本分子生物学会年会(千葉), Dec. 1993.
74.	岩花弘之, Takashi Yamaoka, 水谷正一, Noriko Mizusawa, Eiji Kudo, Setsuko Ii, Katsuhiko Yoshimoto and Mitsuo Itakura : ラット・アミドホスホリボシルトランスフェラーゼ(ATase)酵素蛋白のアミノ酸配列とmRNAの組織別発現, 第26回日本プリン・ピリミジン代謝学会総会(仙台), Feb. 1993.
75.	岩花弘之, Noriko Mizusawa, Eiji Kudo, Setsuko Ii, Katsuhiko Yoshimoto and Mitsuo Itakura : ラット・アミドホスホリボシルトランスフェラーゼ(ATase)cDNAのPCRを用いた遺伝子クローニング, 第26回日本プリン・ピリミジン代謝学会総会(仙台), Feb. 1993.
76.	Noriko Mizusawa, 岩花弘之, Takashi Yamaoka, Eiji Kudo, Setsuko Ii, Katsuhiko Yoshimoto and Mitsuo Itakura : ラット・アミドホスホリボシルトランスフェラーゼ(ATase)のcDNAクローニング, 第64回日本生化学会大会(福岡), Oct. 1992.

Report:

1.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa, Shozo Yamada and 井下尚子 : 頭蓋咽頭腫の各タイプにおける遺伝子異常, 成長科学協会研究年報, No.40, 163-166, Sep. 2017. (Tokushima University Institutional Repository) ● Metadata: 114139 (Tokushima University Institutional Repository: 114139)
2.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa and Shozo Yamada : cAMP-protein kinase Aシグナル異常によるGH細胞腫瘍化機構, 成長科学協会研究年報, No.39, 157-160, Sep. 2016. (Tokushima University Institutional Repository) ● Metadata: 114138 (Tokushima University Institutional Repository: 114138)
3.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa, Shozo Yamada, 西岡宏 and 井下尚子 : 頭蓋咽頭腫の腫瘍化機構の解析, 成長科学協会研究年報, No.38, 149-152, Aug. 2015. (Tokushima University Institutional Repository) ● Metadata: 114137 (Tokushima University Institutional Repository: 114137)
4.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa, Shinji Ono and Shozo Yamada : 成長ホルモン産生腺腫における14q32.3インプリンティング領域のmiRNA発現増加機構の解析, 成長科学協会研究年報, Vol.37, 177-181, Aug. 2014. (Tokushima University Institutional Repository) ● Metadata: 114136 (Tokushima University Institutional Repository: 114136)
5.	Tetsuo Ichikawa, Takafumi Noma, Keiko Miyoshi, Keisuke Nishigawa, Noriko Mizusawa, Miwa Matsuyama, Hiroshi Yoshimura and Maki Hosoki : 連携機能を活用した口腔からQOL向上を目指す研究報告書, 連携機能を活用した口腔からQOL向上を目指す研究報告書, 1-67, 2012.
6.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa, Zhi-Rong Qian and Shozo Yamada : 成長ホルモン産生腺腫および血清におけるmiRNAの解析, 成長科学協会研究年報, No.34, 209-215, Aug. 2011. (Tokushima University Institutional Repository) ● Metadata: 114135 (Tokushima University Institutional Repository: 114135)
7.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa, Zhi-Rong Qian, Toshiaki Sano and 山田正三 : 成長ホルモン産生腺腫におけるmiRNAの解析, 成長科学協会研究年報, Vol.33, 191-196, Jul. 2010. (Tokushima University Institutional Repository) ● Metadata: 114134 (Tokushima University Institutional Repository: 114134)
8.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa, Toshiaki Sano and Shozo Yamada : 成長ホルモン産生腺腫におけるp18INK4C遺伝子異常の解析, 成長科学協会研究年報, No.32, 243-247, Aug. 2009. (Summary) ヒトGH産生腺腫におけるp18INK4C遺伝子の関与を検討するために，腺腫におけるp18INK4C遺伝子の発現レベル，体細胞変異，メチル化異常を解析した．散発性GH・プロラクチン産生腺腫1例およびGH産生腺腫14例では，p18INK4C蛋白の発現を免疫組織化学で，p18INK4C遺伝子発現を定量的リアルタイムRT-PCR法で解析した．また，正常下垂体のmRNA量に比べて30 (Keyword) 免疫組織化学 CpG Island DNA変異分析 DNAメチル化プロモーター領域 RT-PCR法 SNPs Cyclin-Dependent Kinase Inhibitor p18 *下垂体腺腫-成長ホルモン産生(遺伝学,診断) ヒト成人(19~44) 中年(45~64) 男女 (Tokushima University Institutional Repository) ● Metadata: 114161 (Tokushima University Institutional Repository: 114161)
9.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa, Toshiaki Sano and 山田正三 : 成長ホルモン(GH)産生腺腫における癌抑制遺伝子異常の解析, 成長科学協会研究年報, No.31, 199-202, 2008. (Summary) 家族性成長ホルモン(GH)産生腺腫家系5家系を対象とてし，癌抑制遺伝子aryl hydrocarbon receptor-interating protein(AIP)異常の解析を行った．いずれの家系においてもカーニー複合体の症候はみられなかった．白血球からゲノムDNAを抽出し，AIP,MEN1,PRKAR1A,p27Kip1遺伝子の塩基配列を同定した．5家系において，API,MEN1,PRKAR1A,p27Kip1遺伝子の胚細胞変異はみられなかった．AIP遺伝子のプロモーター部位遺伝子では1家系においてC-270-269CG>AA及びC.911G>Aの変化がみられ，これは日本人対照78名にはみられなかった．家族性副甲状腺機能亢進症はMEN1の亜型の可能性があるため，9家系についてp27Kip1の遺伝子を解析したが，胚細胞変異はみられなかった．1家系においてc.165A>Gの一塩基多型がみられた．家族性GH産生腺腫発症にはAIP,MRN1,PRKAR1A,p27Kip1以外の遺伝子変化が関与している可能性が高いと考えられた． (Keyword) 血統癌抑制遺伝子多発性内分泌腫瘍1型 Cyclin-Dependent Kinase Inhibitor p27 下垂体腺腫-成長ホルモン産生(遺伝学) Aryl Hydrocarbon Receptor Nuclear Translocator PRKAR1A遺伝子ヒト (Tokushima University Institutional Repository) ● Metadata: 114160 (Tokushima University Institutional Repository: 114160)
10.	Katsuhiko Yoshimoto, Takeo Iwata, Noriko Mizusawa, Toshiaki Sano and 山田正三 : 成長ホルモン (GH) 産生腺腫におけるAIP遺伝子異常の解析, 成長科学協会研究年報, No.30, Jul. 2007. (Tokushima University Institutional Repository) ● Metadata: 114159 (Tokushima University Institutional Repository: 114159)

Patent:

1.	Noriko Mizusawa and Katsuhiko Yoshimoto : GLP-1の発現・分泌を指標としたスクリーニング系, 2008-075833 (Dec. 2007), .

Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)

ヒト抗肥満創薬を目指した多面的アプローチによる標的分子の探索と機能解析 (Project/Area Number: 22K06589 )
膵β細胞特異的Prss53の分子メカニズム (Project/Area Number: 21K11698 )
A strategy for the development of anti-obesity drugs related to D-dopachrome tautomerase. (Project/Area Number: 18K09520 )
下垂体腺腫におけるインプリント異常を含むDNAメチル化脱制御の解析 (Project/Area Number: 18K08481 )
miR-1290 promotes cell growth in NS-SV-AC, human submandibular gland cell line (Project/Area Number: 15K11042 )
Mechanisms of adipose tissue-specific expression and action of D-dopachrome tautomrase (Project/Area Number: 15K11040 )
Regulation of miRNAs located within the imprinted DLK1-DIO3 locus at 14q32 in pituitary adenomas (Project/Area Number: 15K09435 )
The elucidation of miRNAs in response to stress stimuli and its secretion into an oral cavity (Project/Area Number: 25670822 )
Salivary miRNA as new cell-to-cell communication molecules (Project/Area Number: 24592800 )
A study of molecular mechanisms by which D-dopachrome tautomerase improves insulin resistance in obesity (Project/Area Number: 24592799 )
Network of microRNA in pituitary adenomas (Project/Area Number: 24591365 )
Analysis of the salivatin function as incretin mimetics (Project/Area Number: 21592363 )
Functional analysis of parafibromin with activities of tumor suppressor and oncogene (Project/Area Number: 21591180 )
Role of the AIP gene in tumorigenesis of growth hormone-producing cells (Project/Area Number: 19591079 )
Function of parafibromin inhibiting parathyroid tumorigenesis (Project/Area Number: 17590963 )
Characterization of β cell-specific gene obtained by large cDNA sequencing. (Project/Area Number: 15590943 )
ヒトインスリン遺伝子上流のGG-BOXに結合する膵ラ氏島B細胞特異的因子の決定 (Project/Area Number: 12770639 )
Molecular basic research for obtaining genes specifying characteristics of pancreatic α and β cells. (Project/Area Number: 12671115 )
妊婦末梢血中の胎児細胞検出に関する研究-非侵襲的出生前診断法の確立- (Project/Area Number: 08877254 )
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Assistant Professor : Mizusawa, Noriko

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Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)