Tokushima University / Educator and Researcher Directory --- Bandou, Mika

Personal Web Page

https://researchmap.jp/tksperio (researchmap)

Field of Study

○	Medicine

Subject of Study

○

Book / Paper

Book:

1.	Yuji Inagaki, Jun-ichi Kido, Yasufumi Nishikawa, Rie Kido, Eijiro Sakamoto, Mika Bandou, Koji Naruishi, Toshihiko Nagata and Hiromichi Yumoto : Gan-Lu-Yin (Kanroin), Traditional Chinese Herbal Extracts, Reduces Osteoclast Differentiation In Vitro and Prevents Alveolar Bone Resorption in Rat Experimental Periodontitis, Jul. 2021.

Academic Paper (Judged Full Paper):

1.	Yuka Hiroshima, Rie Kido, Jun-ichi Kido, Mika Bandou, Kaya Yoshida, Akikazu Murakami and Yasuo Shinohara : Synthesis of secretory leukocyte protease inhibitor using cell-free protein synthesis system, Odontology, 2024. (Tokushima University Institutional Repository) ● Metadata: 119164 (Tokushima University Institutional Repository: 119164)
2.	Yuka Hiroshima, Jun-ichi Kido, Rie Kido, Kaya Yoshida, Mika Bandou, Kazuaki Kajimoto, Hiromichi Yumoto and Yasuo Shinohara : β-defensin 2 synthesized by a cell-free protein synthesis system and encapsulated in liposomes inhibits adhesion of Porphyromonas gingivalis to oral epithelial cells., Odontology, Vol.111, 830-838, 2023. (Tokushima University Institutional Repository) ● Metadata: 119198 (Link to Publication Site) ● Publication site (DOI): 10.1007/s10266-023-00789-x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36745267 ● Search Scopus @ Elsevier (PMID): 36745267 ● Search Scopus @ Elsevier (DOI): 10.1007/s10266-023-00789-x (Tokushima University Institutional Repository: 119198, DOI: 10.1007/s10266-023-00789-x, PubMed: 36745267)
3.	Ayuka Kawakami, Mika Bandou, Tomoe Takashi, Mizuki Sugiuchi, Mizusa Hyodo, Yuna Mishima, Masashi Kuroda, Hiroyasu Mori, Akio Kuroda, Hiromichi Yumoto, Munehide Matsuhisa, Hiroshi Sakaue and Rie Tsutsumi : Umami taste sensitivity is associated with food intake and oral environment in subjects with diabetes, The Journal of Medical Investigation : JMI, Vol.70, No.1.2, 241-250, 2023. (Summary) Dysgeusia is a serious problem in patients with diabetes because it often leads to overeating, which is associated with disease progression. This study aimed to investigate the association between taste sensitivity, eating habits, and the oral environment. In this cross-sectional study of 75 subjects with diabetes, gustatory function was assessed using the whole-mouth method, and lingual taste receptor gene expression was measured by real-time PCR. Food intake was evaluated using a food frequency questionnaire based on food groups. The oral environment was assessed using xerostomia and periodontal comprehensive examination. In total, 45.3%, 28.0%, and 18.7% of subjects showed lower umami taste sensitivity, low sweet taste sensitivity, and low salt taste sensitivity, respectively. Lower umami sensitivity correlated with lower estimated glomerular filtration rate and higher energy-source food intake. Subjects with diabetes with higher plaque control record showed significantly higher T1R3 gene expression than those with lower plaque control record. Reduced umami taste sensitivity is associated with decreased renal function and high energy food intake in diabetes. Subjects with diabetes with higher plaque control record showed significantly higher T1R3 gene expression, suggesting that the oral environment affects taste gene expression. J. Med. Invest. 70 : 241-250, February, 2023. (Keyword) Humans / Taste / Cross-Sectional Studies / Taste Perception / Diabetes Mellitus / Eating (Tokushima University Institutional Repository) ● Metadata: 118208 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.70.241 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37164729 ● Summary page in Scopus @ Elsevier: 2-s2.0-85158866092 (Tokushima University Institutional Repository: 118208, DOI: 10.2152/jmi.70.241, PubMed: 37164729, Elsevier: Scopus)
4.	Yuji Inagaki, Jun-ichi Kido, Yasufumi Nishikawa, Rie Kido, Eijiro Sakamoto, Mika Bandou, Koji Naruishi, Toshihiko Nagata and Hiromichi Yumoto : Gan-Lu-Yin (Kanroin), traditional Chinese herbal extracts, reduces osteoclast differentiation in vitro and prevents alveolar bone resorption in rat experimental periodontitis, Journal of Clinical Medicine, Vol.10, No.3, 386, 2021. (Summary) Gan-Lu-Yin (GLY), a traditional Chinese herbal medicine, shows therapeutic effects on periodontitis, but that mechanism is not well known. This study aims to clarify the precise mechanism by investigating the inhibitory effects of GLY extracts on osteoclastogenesis in vitro and on bone resorption in periodontitis in vivo. RAW264.7 cells are cultured with soluble receptor activator of nuclear factor-kappa B (sRANKL) and GLY extracts (0.01-1.0 mg/mL), and stained for tartrate-resistant acid phosphatase (TRAP) to evaluate osteoclast differentiation. Experimental periodontitis is induced by placing a nylon ligature around the second maxillary molar in rats, and rats are administered GLY extracts (60 mg/kg) daily for 20 days. Their maxillae are collected on day 4 and 20, and the levels of alveolar bone resorption and osteoclast differentiation are estimated using micro-computed tomography (CT) and histological analysis, respectively. In RAW264.7 cells, GLY extracts significantly inhibit sRANKL-induced osteoclast differentiation at a concentration of more than 0.05 mg/mL. In experimental periodontitis, administering GLY extracts significantly decreases the number of TRAP-positive osteoclasts in the alveolar bone on day 4, and significantly inhibits the ligature-induced bone resorption on day 20. These results show that GLY extracts suppress bone resorption by inhibiting osteoclast differentiation in experimental periodontitis, suggesting that GLY extracts are potentially useful for oral care in periodontitis. (Tokushima University Institutional Repository) ● Metadata: 116745 (Link to Publication Site) ● Publication site (DOI): 10.3390/jcm10030386 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33498415 ● Search Scopus @ Elsevier (PMID): 33498415 ● Search Scopus @ Elsevier (DOI): 10.3390/jcm10030386 (Tokushima University Institutional Repository: 116745, DOI: 10.3390/jcm10030386, PubMed: 33498415)
5.	Kohei Nonaka, Mika Bandou, Eijiro Sakamoto, Yuji Inagaki, Koji Naruishi, Hiromichi Yumoto and Jun-ichi Kido : 6-Shogaol inhibits advanced glycation end-products-induced IL-6 and ICAM-1 expression by regulating oxidative responses in human gingival fibroblasts, Molecules, Vol.24, No.20, e3705, 2019. (Summary) Advanced glycation end-products (AGEs) cause diabetes mellitus (DM) complications and accumulate more highly in periodontal tissues of patients with periodontitis and DM. AGEs aggravate periodontitis with DM by increasing the expression of inflammation-related factors in periodontal tissues. 6-Shogaol, a major compound in ginger, has anti-inflammatory and anti-oxidative activities. However, the influence of shogaol on DM-associated periodontitis is not well known. In this study, the effects of 6-shogaol on AGEs-induced oxidative and anti-oxidative responses, and IL-6 and ICAM-1 expression in human gingival fibroblasts (HGFs) were investigated. When HGFs were cultured with 6-shogaol and AGEs, the activities of reactive oxygen species (ROS) and antioxidant enzymes (heme oxygenase-1 [HO-1] and NAD(P)H quinone dehydrogenase 1 [NQO1]), and IL-6 and ICAM-1 expressions were investigated. RAGE expression and phosphorylation of MAPKs and NF-κB were examined by western blotting. 6-Shogaol significantly inhibited AGEs-induced ROS activity, and increased HO-1 and NQO1 levels compared with the AGEs-treated cells. The AGEs-stimulated expression levels of receptor of AGE (RAGE), IL-6 and ICAM-1 and the phosphorylation of p38, ERK and p65 were attenuated by 6-shogaol. These results suggested that 6-shogaol inhibits AGEs-induced inflammatory responses by regulating oxidative and anti-oxidative activities and may have protective effects on periodontitis with DM. (Tokushima University Institutional Repository) ● Metadata: 114673 (Link to Publication Site) ● Publication site (DOI): 10.3390/molecules24203705 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31619000 ● Summary page in Scopus @ Elsevier: 2-s2.0-85073474436 (Tokushima University Institutional Repository: 114673, DOI: 10.3390/molecules24203705, PubMed: 31619000, Elsevier: Scopus)
6.	Muneaki Hashimoto, Mika Bandou, Jun-ichi Kido, Kazumichi Yokota, Toshihiro Mita, Kazuaki Kajimoto and Masatoshi Kataoka : Nucleic acid purification from dried blood spot on FTA elute card provides template for polymerase chain reaction for highly sensitive Plasmodium detection, Parasitology International, Vol.73, 101941, 2019. (Summary) Polymerase chain reaction (PCR) is an essential diagnostic method for highly sensitive detection of Plasmodium-infected erythrocytes in patients with malaria. This study compared the performance of filter papers used for the preparation of dried blood spots (DBS) in detecting Plasmodium by PCR. Whole blood spiked with P. falciparum-infected erythrocytes to obtain samples with various levels of parasitemia were applied to Whatman 3MM Chr papers, FTA Cards, or FTA Elute Cards to prepare the DBS. DNA was purified from the DBS using a DNA purification kit and used as the template for nested PCR. In probit analysis, the estimated limit of detection (LoD) was 5.5 parasites/μL blood for Whatman 3MM Chr papers and FTA Cards and 1.6 parasites/μL blood for the FTA Elute Card. This result suggested that the DBS prepared on an FTA Elute Card yield the best template DNA for subsequent high-sensitivity PCR-based detection of P. falciparum-infected erythrocytes. This finding can help improve the accuracy of malarial diagnostic tests. (Keyword) DNA, Protozoan / Diagnostic Tests, Routine / Dried Blood Spot Testing / Humans / Limit of Detection / Malaria, Falciparum / Plasmodium falciparum / Polymerase Chain Reaction / RNA, Ribosomal, 18S (Link to Publication Site) ● Publication site (DOI): 10.1016/j.parint.2019.101941 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31442664 ● Search Scopus @ Elsevier (PMID): 31442664 ● Search Scopus @ Elsevier (DOI): 10.1016/j.parint.2019.101941 (DOI: 10.1016/j.parint.2019.101941, PubMed: 31442664)
7.	Kohei Nonaka, Yukari Kajiura, Mika Bandou, Eijiro Sakamoto, Yuji Inagaki, JH Lew, Koji Naruishi, Takahisa Ikuta, Kaya Yoshida, Tesuo Kobayashi, Hiromasa Yoshie, Toshihiko Nagata and Jun-ichi Kido : Advanced glycation end-products increase IL-6 and ICAM-1 expression via RAGE, MAPK and NF-kB pathways in human gingival fibroblasts, Journal of Periodontal Research, Vol.53, No.3, 334-344, 2018. (Summary) Diabetes mellitus (DM) is a risk factor for periodontal diseases and may exacerbate the progression of the pathogenesis of periodontitis. Advanced glycation end-products (AGEs) cause DM complications relative to levels of glycemic control and larger amounts accumulate in the periodontal tissues of patients with periodontitis and DM. In the present study, we investigated the effects of AGEs on the expression of inflammation-related factors in human gingival fibroblasts (HGFs) to elucidate the impact of AGEs on DM-associated periodontitis. HGFs were cultured with or without AGEs. Cell viability was examined, and RNA and protein fractions were isolated from AGE-treated cells. The expression of interleukin (IL)-6, intercellular adhesion molecule-1 (ICAM-1), and the receptor for AGE (RAGE) was investigated using reverse transcription-polymerase chain reaction, quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assay, and reactive oxygen species activity was measured using a kit with 2',7'-dichlorofluorescin diacetate. Human monocytic cells (THP-1) labeled with a fluorescent reagent were co-cultured with HGFs treated with AGEs and IL-6 siRNA, and the adhesive activity of THP-1 cells to HGFs was assessed. The expression of IL-6 and ICAM-1 was examined when HGFs were pretreated with recombinant human IL-6, the siRNAs of RAGE and IL-6, and inhibitors of MAPK and NF-κB, and then cultured with and without AGEs. The phosphorylation of MAPK and NF-κB was assessed using western blotting. AGEs increased the mRNA and protein expressions of RAGE, IL-6, ICAM-1 and reactive oxygen species activity in HGFs, and promoted the adhesion of THP-1 cells to HGFs, but had no effect on cell viability until 72 hours. Recombinant human IL-6 increased ICAM-1 expression in HGFs, while the siRNAs of RAGE and IL-6 inhibited AGE-induced IL6 and ICAM1 mRNA expression, and IL-6 siRNA depressed AGE-induced THP-1 cell adhesion. AGEs increased the phosphorylation of p38 and ERK MAPKs, p65 NF-κB and IκBα, while inhibitors of p38, ERK MAPKs and NF-κB significantly decreased AGE-induced IL-6 and ICAM-1 expression. AGEs increase IL-6 and ICAM-1 expression via the RAGE, MAPK and NF-κB pathways in HGFs and may exacerbate the progression of the pathogenesis of periodontal diseases. (Keyword) Antigens, Neoplasm / Diabetes Complications / Fibroblasts / Gingiva / Glycation End Products, Advanced / Humans / Intercellular Adhesion Molecule-1 / Interleukin-6 / MAP Kinase Signaling System / Mitogen-Activated Protein Kinase Kinases / Mitogen-Activated Protein Kinases / NF-kappa B / Periodontitis / Phosphorylation / Reactive Oxygen Species / THP-1 Cells (Tokushima University Institutional Repository) ● Metadata: 113617 (Link to Publication Site) ● Publication site (DOI): 10.1111/jre.12518 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29193068 ● Summary page in Scopus @ Elsevier: 2-s2.0-85036593558 (Tokushima University Institutional Repository: 113617, DOI: 10.1111/jre.12518, PubMed: 29193068, Elsevier: Scopus)
8.	Muneaki Hashimoto, Shouki Yatsushiro, Shohei Yamamura, Masato Tanaka, Hirokazu Sakamoto, Yusuke Ido, Kazuaki Kajimoto, Mika Bandou, Jun-ichi Kido and Masatoshi Kataoka : Hydrophilic-treated plastic plates for wide-range analysis of Giemsa-stained red blood cells and automated Plasmodium infection rate counting, Malaria Journal, Vol.16, No.1, 321, 2017. (Summary) Malaria is a red blood cell (RBC) infection caused by Plasmodium parasites. To determine RBC infection rate, which is essential for malaria study and diagnosis, microscopic evaluation of Giemsa-stained thin blood smears on glass slides ('Giemsa microscopy') has been performed as the accepted gold standard for over 100 years. However, only a small area of the blood smear provides a monolayer of RBCs suitable for determination of infection rate, which is one of the major reasons for the low parasite detection rate by Giemsa microscopy. In addition, because Giemsa microscopy is exacting and time-consuming, automated counting of infection rates is highly desirable. A method that allows for microscopic examination of Giemsa-stained cells spread in a monolayer on almost the whole surface of hydrophilic-treated cyclic olefin copolymer (COC) plates was established. Because wide-range Giemsa microscopy can be performed on a hydrophilic-treated plate, the method may enable more reliable diagnosis of malaria in patients with low parasitaemia burden. Furthermore, the number of RBCs and parasites stained with a fluorescent nuclear staining dye could be counted automatically with a software tool, without Giemsa staining. As a result, researchers studying malaria may calculate the infection rate easily, rapidly, and accurately even in low parasitaemia. Because the running cost of these methods is very low and they do not involve complicated techniques, the use of hydrophilic COC plates may contribute to improved and more accurate diagnosis and research of malaria. (Keyword) Automation / Azure Stains / blood / Cycloparaffins / Hydrophobic and Hydrophilic Interactions / Image Processing, Computer-Assisted / Malaria, Falciparum / Microscopy / Parasitemia / Plasmodium falciparum (Tokushima University Institutional Repository) ● Metadata: 113980 (Link to Publication Site) ● Publication site (DOI): 10.1186/s12936-017-1975-9 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28789644 ● Summary page in Scopus @ Elsevier: 2-s2.0-85027153631 (Tokushima University Institutional Repository: 113980, DOI: 10.1186/s12936-017-1975-9, PubMed: 28789644, Elsevier: Scopus)
9.	Chie Wada -Mihara, Koji Naruishi, Mika Bandou, Yasufumi Nishikawa, Lew Jung-Hwan, Eijiro Sakamoto, Takahisa Ikuta, Kaoru Kono, Yukari Kajiura, Mari Hashimoto, Yukiko Nakajima, Yuji Inagaki, Masami Ninomiya, Jun-ichi Kido and Toshihiko Nagata : Post clinical clerkship-OSCEを見据えた歯周病科での模擬OSCEの概要, Journal of Oral Health and Biosciences, Vol.29, No.2, 49-53, 2017. (Tokushima University Institutional Repository) ● Metadata: 111059 (Link to Publication Site) ● Publication site (DOI): 10.20738/johb.29.2_49 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.20738/johb.29.2_49 (Tokushima University Institutional Repository: 111059, DOI: 10.20738/johb.29.2_49)
10.	Koji Naruishi, Keiji Oishi, Yuuji Inagaki, Masumi Horibe, Mika Bandou, Masami Ninomiya, K Kawahara, J Minakuchi, S Kawashima, K Shima, Jun-ichi Kido and Toshihiko Nagata : Association between Periodontal Condition and Kidney Dysfunction in Japanese Adults: A Cross-Sectional Study, Clinical and Experimental Dental Research, Vol.2, No.2, 1-8, 2016. (Tokushima University Institutional Repository) ● Metadata: 115061 (Link to Publication Site) ● Publication site (DOI): 10.1002/cre2.39 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1002/cre2.39 (Tokushima University Institutional Repository: 115061, DOI: 10.1002/cre2.39)
11.	Yuka Hiroshima, Mika Bandou, Yuji Inagaki, Reiko Kido, Masatoshi Kataoka, Toshihiko Nagata and Jun-ichi Kido : Effect of Hangeshashinto on calprotectin expression in human oral epithelial cells., Odontology, Vol.104, No.2, 152-162, 2016. (Summary) Oral epithelial cells produce antimicrobial peptides (AMPs) to prevent microbial infection. Calprotectin (S100A8/S100A9) is one of these AMPs in oral epithelial cells, the expression of which is up-regulated by interleukin-1α (IL-1α). Hangeshashinto (HST) is a traditional Japanese herbal medicine that has anti-inflammatory effects. The purpose of this study was to investigate the effect of HST on the expression of calprotectin through the regulation of IL-1α in oral epithelial cells. Human oral epithelial cells (TR146) were cultured with HST in the presence or absence of anti-IL-1α antibody or IL-1 receptor antagonist, or with six major components of HST (3,4-dihydroxybenzaldehyde, baicalin, ginsenoside Rb1, glycyrrhizin, oleanolic acid and berberine). The expression of S100A8, S100A9, other AMPs and cytokine mRNAs was examined by RT-PCR and quantitative real-time PCR. Calprotectin expression and IL-1α secretion were investigated by ELISA. HST (6 μg/ml) increased the expression of S100A8/S100A9 mRNAs and calprotectin protein, and also up-regulated β-defensin 2 (DEFB4) and S100A7 expression. The expression of IL-1α mRNA and its protein was slightly but significantly increased by HST. A neutralizing antibody against IL-1α and IL-1 receptor antagonist inhibited HST-up-regulated S100A8/S100A9 mRNA expression. Although 3,4-dihydroxybenzaldehyde, baicalin and ginsenoside Rb1 as HST components increased S100A8/S100A9 expression, oleanolic acid and berberine decreased their expression. These results suggest that HST increases the expression of calprotectin, DEFB4 and S100A7 in oral epithelial cells. In response to HST, up-regulation of calprotectin expression may be partially induced via IL-1α. (Link to Publication Site) ● Publication site (DOI): 10.1007/s10266-015-0196-3 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25649126 ● Search Scopus @ Elsevier (PMID): 25649126 ● Search Scopus @ Elsevier (DOI): 10.1007/s10266-015-0196-3 (DOI: 10.1007/s10266-015-0196-3, PubMed: 25649126)
12.	Koji Naruishi, Yukari Kajiura, 西川泰史, Mika Bandou, Jun-ichi Kido and Toshihiko Nagata : Inhibitory Effects of Cryptotanshinone on Inflammation-related Molecules in Human Gingival Fibroblasts, The Japanese Journal of Conservative Dentistry, Vol.58, No.3, 212-218, 2015. (Summary) Purpose: Cryptotanshinone (CPT) isolated from the root of an Asian medicinal plant, Salvia miltiorrhiza bunge, acts as a potent anti-tumor or anti-inflammatory agent in vitro. However, the effects of CPT on the progression of periodontitis are still unknown. This study investigated the effects of CPT on the production of inflammation-related molecules in human gingival fibroblasts. Methods: Human gingival fibroblasts (HGFs), CRL-2014TM (ATCC), were used. Cytotoxicity of the cells by CPT was examined. Dead cells stained by trypan blue were counted and analyzed. Next, the levels of IL-6 and VEGF in IL-1β-treated cells with or without CPT were measured using ELISA kits. The productivity of cathepsin L in IL-1β-treated cells with or without CPT was examined using Western blotting. Results: The ratio of viable cell numbers was significantly decreased by 100 μmol/l CPT. Next, the increase of IL-6 and cathepsin L induced by IL-1β was significantly suppressed by the pretreatment of 10 μmol/l CPT in HGFs. On the other hand, productivity of VEGF induced by IL-1β was not changed by the pretreatment of 10 μmol/l CPT. Conclusion: CPT suppresses IL-1β-induced IL-6 and cathepsin L production in HGFs, and might regulate the progression of periodontitis. (Keyword) IL-1β / cryptotanshinone / human gingival fibroblasts / IL-1β / periodontal inflammation (Link to Publication Site) ● Publication site (DOI): 10.11471/shikahozon.58.212 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390001205520665472 ● Search Scopus @ Elsevier (DOI): 10.11471/shikahozon.58.212 (DOI: 10.11471/shikahozon.58.212, CiNii: 1390001205520665472)
13.	Jun-ichi Kido, Yukiko Bandou, Mika Bandou, Yukari Kajiura, Yuka Hiroshima, Yuji Inagaki, Hiromi Murata, Takahisa Ikuta, Reiko Kido, Koji Naruishi, Makoto Funaki and Toshihiko Nagata : YKL-40 level in gingival crevicular fluid from patients with periodontitis and type 2 diabetes, Oral Diseases, Vol.21, No.5, 667-673, 2015. (Summary) YKL-40 is a chitin-binding glycoprotein, the level of which increases in inflammatory diseases, diabetes mellitus (DM), cardiovascular diseases, and tumors. Gingival crevicular fluid (GCF) contains many proteins and markers of periodontitis. The purpose of this study was to investigate YKL-40 level in GCF from patients with periodontitis and DM and the association between YKL-40 level and chronic periodontitis (CP) or DM. The subjects were 121 patients with DM, CP, DM and periodontitis (DM-P), and healthy subjects (H). GCF was collected using paper strips after the sites for GCF collection were clinically evaluated for probing depth (PD), gingival index (GI), and bleeding on probing (BOP). YKL-40 in GCF was identified by Western blotting, and its level was determined by ELISA. YKL-40 was contained in GCF samples from H, DM, CP, and DM-P sites, and its levels (amount and concentration) in CP and DM-P were significantly higher than those in H and DM. GCF YKL-40 level significantly correlated with PD and GI, and its level in BOP-positive sites was significantly higher than that in BOP-negative ones. GCF YKL-40 level was elevated in periodontitis, but not DM. YKL-40 in GCF may be an inflammatory marker for periodontitis. (Link to Publication Site) ● Publication site (DOI): 10.1111/odi.12334 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25740558 ● Summary page in Scopus @ Elsevier: 2-s2.0-84930271794 (DOI: 10.1111/odi.12334, PubMed: 25740558, Elsevier: Scopus)
14.	Takahisa Ikuta, Yuji Inagaki, Kazuya Tanaka, Tsuyoshi Saito, Yukiko Nakajima, Mika Bandou, Jun-ichi Kido and Toshihiko Nagata : Gene polymorphism of β-defensin-1 is associated with susceptibility to periodontitis in Japanese., Odontology, Vol.103, No.1, 66-74, 2015. (Summary) Periodontitis is a multifactorial disease associated with genetic and environmental factors. Single-nucleotide polymorphisms (SNPs) are associated with susceptibility to common diseases such as diabetes and periodontitis. Although the oral cavity is exposed to various organisms, the conditions are well controlled by innate and acquired immune systems. Antimicrobial peptides (AMPs) play an important role in the innate immune system; however, the association of AMP-SNPs with periodontitis has not been fully elucidated. This study investigated the relationship between AMP-SNPs and periodontitis in Japanese. One hundred and five Japanese subjects were recruited, which included patients with aggressive, severe, moderate and mild periodontitis, and age-matched healthy controls. Genomic DNA was isolated from peripheral blood and genotypes of SNPs of β-defensin-1 and lactoferrin genes (DEFB1: rs1799946, rs1800972 and rs11362; and LTF: rs1126478) were investigated using the PCR-Invader assay. Protein level of AMPs in gingival crevicular fluid (GCF) was quantified by ELISA. Case-control studies revealed that the -44 CC genotype of DEFB1 (rs1800972) was associated with periodontitis (OR 2.51), particularly with severe chronic periodontitis (OR 4.15) and with combined severe and moderate chronic periodontitis (OR 4.04). No statistical differences were found in other genotypes. The β-defensin-1 concentrations in GCF were significantly lower in subjects with the -44 CC genotype of DEFB1 than in those without this genotype. No significant differences between GCF concentrations of AMPs and other genotypes were detected. The -44 CC genotype of the β-defensin-1 gene (DEFB1 rs1800972) may be associated with susceptibility to chronic periodontitis in Japanese. (Tokushima University Institutional Repository) ● Metadata: 106075 (Link to Publication Site) ● Publication site (DOI): 10.1007/s10266-013-0139-9 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24276427 ● Summary page in Scopus @ Elsevier: 2-s2.0-84887927465 (Tokushima University Institutional Repository: 106075, DOI: 10.1007/s10266-013-0139-9, PubMed: 24276427, Elsevier: Scopus)
15.	Yukari Kajiura, Mika Bandou, Yuji Inagaki, Toshihiko Nagata and Jun-ichi Kido : Glycated albumin and calprotectin levels in gingival crevicular fluid from patients with periodontitis and type 2 diabetes, Journal of Periodontology, Vol.85, No.12, 1667-1675, 2014. (Summary) Patients with diabetes mellitus (DM) have a high prevalence of periodontitis. Periodontitis in these patients is characterized by severe inflammation and tissue breakdown, and its diagnosis is important for cures of periodontitis and DM. The purpose of this study is to investigate the levels of glycated albumin (GA), a DM marker, and calprotectin, an inflammatory marker, in gingival crevicular fluid (GCF) from patients with periodontitis and DM (DM-P). The 78 participants in this study were patients with DM, chronic periodontitis (CP), DM-P, and healthy individuals (H). GCF and blood were collected, and GA and calprotectin in GCF were analyzed using Western blotting and enzyme-linked immunosorbent assay. Levels were compared among H, DM, CP, and DM-P groups. Blood GA and glycated hemoglobin (HbA1c) were measured, and the correlation among GCF GA and blood HbA1c or GA levels was investigated. Receiver operating characteristic (ROC) analysis for GCF GA to predict DM was performed. GA was identified in GCF, and its amount/concentration in GCF samples from DM and DM-P were significantly higher than those of non-DM groups (H and CP). Calprotectin amounts in GCF from CP and DM-P were significantly higher than in H and DM groups. GCF GA level was positively correlated with blood HbA1c and GA level. ROC analysis of GCF GA showed an optimal cutoff value to predict DM. GA showed a high level in GCF from patients with DM. Examination of GA and calprotectin in GCF may be useful for predicting DM-P. (Tokushima University Institutional Repository) ● Metadata: 109408 (Link to Publication Site) ● Publication site (DOI): 10.1902/jop.2014.140241 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25126693 ● Search Scopus @ Elsevier (PMID): 25126693 ● Search Scopus @ Elsevier (DOI): 10.1902/jop.2014.140241 (Tokushima University Institutional Repository: 109408, DOI: 10.1902/jop.2014.140241, PubMed: 25126693)
16.	Mika Bandou, Xianqiong Zou, Yuka Hiroshima, Masatoshi Kataoka, Karen F. Ross, Yasuo Shinohara, Toshihiko Nagata, Mark C. Herzberg and Jun-ichi Kido : Mechanism of interleukin-1α transcriptional regulation of S100A9 in a human epidermal keratinocyte cell line, Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms, Vol.1829, No.9, 954-962, 2013. (Summary) S100A9 is a calcium-binding protein and subunit of antimicrobial calprotectin complex (S100A8/A9). Produced by neutrophils, monocytes/macrophages and keratinocytes, S100A9 expression increases in response to inflammation. For example, IL-1α produced by epithelial cells acts autonomously on the same cells to induce the expression of S100A8/A9 and cellular differentiation. Whereas it is well known that IL-1α and members of the IL-10 family of cytokines upregulate S100A8 and S100A9 in several cell lineages, the pathway and mechanism of IL-1α-dependent transcriptional control of S100A9 in epithelial cells are not established. Modeled using human epidermal keratinocytes (HaCaT cells), IL-1α stimulated the phosphorylation of p38 MAPK and induced S100A9 expression, which was blocked by IL-1 receptor antagonist, RNAi suppression of p38, or a p38 MAPK inhibitor. Transcription of S100A9 in HaCaT cells depended on nucleotides -94 to -53 in the upstream promoter region, based upon the use of deletion constructs and luciferase reporter activity. Within the responsive promoter region, IL-1α increased the binding activity of CCAAT/enhancer binding protein β (C/EBPβ). Mutated C/EBPβ binding sequences or C/EBPβ-specific siRNA inhibited the S100A9 transcriptional response. Hence, IL-1α is strongly suggested to increase S100A9 expression in a human epidermal keratinocyte cell line by signaling through the IL-1 receptor and p38 MAPK, increasing C/EBPβ-dependent transcriptional activity. (Keyword) Base Sequence / Calgranulin B / Cell Line / DNA Primers / Epidermis / Humans / Interleukin-1alpha / Keratinocytes / Polymerase Chain Reaction / RNA Interference / Transcription, Genetic / p38 Mitogen-Activated Protein Kinases (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbagrm.2013.03.010 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23563247 ● Summary page in Scopus @ Elsevier: 2-s2.0-84880346974 (DOI: 10.1016/j.bbagrm.2013.03.010, PubMed: 23563247, Elsevier: Scopus)
17.	Kaori Abe, Y Hashimoto, S Yatsushiro, S Yamamura, Mika Bandou, Yuka Hiroshima, Jun-ichi Kido, M Tanaka, Yasuo Shinohara, Toshihiko Ooie, Yoshinobu Baba and Masatoshi Kataoka : Simultaneous immunoassay analysis of plasma IL-6 and TNF-α on a microchip., PLoS ONE, Vol.8, No.1, e53620, 2013. (Summary) Sandwich enzyme-linked immunosorbant assay (ELISA) using a 96-well plate is frequently employed for clinical diagnosis, but is time-and sample-consuming. To overcome these drawbacks, we performed a sandwich ELISA on a microchip. The microchip was made of cyclic olefin copolymer with 4 straight microchannels. For the construction of the sandwich ELISA for interleukin-6 (IL-6) or tumor necrosis factor-α (TNF-α), we used a piezoelectric inkjet printing system for the deposition and fixation of the 1st anti-IL-6 antibody or 1st anti-TNF-α antibody on the surface of the each microchannel. After the infusion of 2 µl of sample to the microchannel and a 20 min incubation, 2 µl of biotinylated 2nd antibody for either antigen was infused and a 10 min incubation. Then 2 µl of avidin-horseradish peroxidase was infused; and after a 5 min incubation, the substrate for peroxidase was infused, and the luminescence intensity was measured. Calibration curves were obtained between the concentration and luminescence intensity over the range of 0 to 32 pg/ml (IL-6: R(2) = 0.9994, TNF-α: R(2) = 0.9977), and the detection limit for each protein was 0.28 pg/ml and 0.46 pg/ml, respectively. Blood IL-6 and TNF-α concentrations of 5 subjects estimated from the microchip data were compared with results obtained by the conventional method, good correlations were observed between the methods according to linear regression analysis (IL-6: R(2) = 0.9954, TNF-α: R(2) = 0.9928). The reproducibility of the presented assay for the determination of the blood IL-6 and TNF-α concentration was comparable to that obtained with the 96-well plate. Simultaneous detection of blood IL-6 and TNF-α was possible by the deposition and fixation of each 1st antibody on the surface of a separate microchannel. This assay enabled us to determine simultaneously blood IL-6 and TNF-α with accuracy, satisfactory sensitivity, time saving ability, and low consumption of sample and reagents, and will be applicable to clinic diagnosis. (Keyword) Enzyme-Linked Immunosorbent Assay / Humans / Immunoassay / Interleukin-6 / Lab-On-A-Chip Devices / Luminescent Measurements / Reproducibility of Results / Tumor Necrosis Factor-alpha (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0053620 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23326472 ● Summary page in Scopus @ Elsevier: 2-s2.0-84872235277 (DOI: 10.1371/journal.pone.0053620, PubMed: 23326472, Elsevier: Scopus)
18.	Jun-ichi Kido, Kaori Abe, Shouki Yatsushiro, Mika Bandou, Yuka Hiroshima, Toshihiko Nagata, Toshihiko Ooie, Masato Tanaka and Masatoshi Kataoka : Determination of calprotectin in gingival crevicular fluid by immunoassay on a microchip, Clinical Biochemistry, Vol.45, No.15, 1239-1244, 2012. (Summary) Gingival crevicular fluid (GCF) contains calprotectin, which appears to be a useful biomarker for periodontal diseases because of its high level in GCF from periodontally diseased pockets. To determine calprotectin in GCF that has a very small volume, sandwich enzyme-linked immunosorbent assay (ELISA) on a microchip was performed and its utility was estimated. Anti-calprotectin primary antibody was discharged on a microchip using a piezoelectric inkjet printing system. Calprotectin standard and calprotectin in GCF samples from eleven subjects were determined by the ELISA method with the prepared microchip and their values were compared with those obtained by conventional ELISA. Using the ELISA on a microchip, a reasonable standard curve of calprotectin protein (1.56-100 ng/mL) was obtained. Calprotectin in GCF samples was quantified and showed reasonable values in accordance with the condition of periodontal diseases. The values determined by the microchip method and conventional ELISA showed a significant linear relationship (R(2)=0.981). Calprotectin in GCF was determined using the ELISA on a microchip with high efficiency and this ELISA method for calprotectin determination may become a useful method for diagnosing periodontal diseases. (Keyword) Aged / Antibodies, Immobilized / calibration / Enzyme-Linked Immunosorbent Assay / Female / Gingival Crevicular Fluid / Humans / Lab-On-A-Chip Devices / Leukocyte L1 Antigen Complex / Linear Models / Male / Microfluidic Analytical Techniques / Middle Aged / Periodontal Diseases / Reference Standards / Reproducibility of Results / Sensitivity and Specificity (Link to Publication Site) ● Publication site (DOI): 10.1016/j.clinbiochem.2012.05.009 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22609893 ● Search Scopus @ Elsevier (PMID): 22609893 ● Search Scopus @ Elsevier (DOI): 10.1016/j.clinbiochem.2012.05.009 (DOI: 10.1016/j.clinbiochem.2012.05.009, PubMed: 22609893)
19.	Yuka Hiroshima, Mika Bandou, Yuji Inagaki, Chie Wada -Mihara, Masatoshi Kataoka, Hiromi Murata, Yasuo Shinohara, Toshihiko Nagata and Jun-ichi Kido : Resistin in gingival crevicular fluid and induction of resistin release by Porphyromonas gingivalis lipopolysaccharide in human neutrophils, Journal of Periodontal Research, Vol.47, No.5, 554-562, 2012. (Summary) Resistin is an adipocytokine that induces insulin resistance and is predominantly expressed in adipocytes and peripheral blood mononuclear cells. Resistin expression increases in inflammatory diseases as well as diabetes mellitus, and is upregulated by bacterial pathogens and proinflammatory cytokines. The aim of this study was to identify resistin in human gingival crevicular fluid, to compare the resistin levels in gingival crevicular fluid between subjects with and without periodontitis and diabetes mellitus and to investigate the regulation of resistin release from human neutrophils by Porphyromonas gingivalis lipopolysaccharide (P-LPS). Gingival crevicular fluid samples were collected from patients with chronic periodontitis (n = 24), patients with diabetes mellitus-related periodontitis (n = 18) and healthy subjects (n = 21). Resistin in gingival crevicular fluid was determined using western blot analysis and an ELISA kit. The glycated hemoglobin (HbA(1c)) value was obtained from patients with diabetes mellitus-related periodontitis by a medical interview. Human neutrophils were cultured with P-LPS (0-1000 ng/mL), or incubated with inhibitors of actin or microtubule polymerization in the absence or presence of P-LPS. The medium and cellular fractions were used for determination of resistin by ELISA. The resistin level in gingival crevicular fluid from patients with periodontitis or diabetes mellitus-related periodontitis was significantly higher than that of healthy subjects. The resistin level in gingival crevicular fluid was correlated with gingival index score, but not blood HbA(1c) value. The P-LPS increased resistin release from human neutrophils, and its induction was decreased by actin polymerization inhibitors. We show, for the first time, the presence of resistin in gingival crevicular fluid. A high resistin level in gingival crevicular fluid samples from periodontitis patients may to some extent be related to P-LPS-induced resistin release from neutrophils. (Keyword) Actin Capping Proteins / Adult / Aged / Cell Culture Techniques / Chronic Periodontitis / Colchicine / Cytochalasin B / Cytochalasin D / Diabetes Complications / Female / Gingival Crevicular Fluid / Hemoglobin A, Glycosylated / Humans / Lipopolysaccharides / Male / Middle Aged / Neutrophils / Nocodazole / Nucleic Acid Synthesis Inhibitors / Periodontal Index / Periodontal Pocket / Periodontitis / Porphyromonas gingivalis / Resistin / Tubulin Modulators (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1600-0765.2011.01466.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22309231 ● Summary page in Scopus @ Elsevier: 2-s2.0-84865553635 (DOI: 10.1111/j.1600-0765.2011.01466.x, PubMed: 22309231, Elsevier: Scopus)
20.	Jun-ichi Kido, Mika Bandou, Yuka Hiroshima, Hiroyuki Iwasaka, Keisuke Yamada, Naoto Ohgami, Toshiyuki Namubu, Masatoshi Kataoka, Takenori Yamamoto, Yasuo Shinohara, Ikuko Sagawa and Toshihiko Nagata : Analysis of proteins in human gingival crevicular fluid by mass spectrometry, Journal of Periodontal Research, Vol.47, No.4, 488-499, 2012. (Summary) Gingival crevicular fluid is a bodily fluid transuded from periodontal tissues into the gingival crevice and periodontal pocket, and contains many species of components. Proteins in gingival crevicular fluid have been studied as markers for periodontal diseases. Mass spectrometric analysis is used for the analyses of proteins, lipids, saccharides and metals, and expected as an approach for disease diagnosis. For better analysis of the protein components in gingival crevicular fluid, we investigated proteins in gingival crevicular fluid samples from the healthy gingival crevice and periodontal pocket using mass spectrometry. Gingival crevicular fluid samples were collected from subjects who gave their informed consent and were periodontally healthy or had diseased pockets. These samples were electrophoretically separated, and each fraction on the gels was analysed by nano liquid chromatography coupled with tandem mass spectrometry. Antimicrobial peptides detected in gingival crevicular fluid were confirmed by western blotting. One hundred and four proteins were detected in gingival crevicular fluid samples from both healthy sites and sites of periodontitis; 64 proteins were contained only in gingival crevicular fluid from healthy sites and 63 proteins were observed only in gingival crevicular fluid from periodontitis sites. These proteins were blood-, cytoskeleton-, immunity-, inflammation- and lipid-related proteins and enzymes. Some proteins, including ceruloplasmin, glycogen phosphorylase, glutathione S-transferase, phosphoglycerate mutase, psoriasin, S100A11 and resistin, were identified for the first time in gingival crevicular fluid. Antimicrobial peptides, such as lactoferrin, α1-antitrypsin, lipocalin, S100A7, S100A8, S100A9 and cathelicidin, were observed by mass spectrometry and western blotting. Multiple protein components in gingival crevicular fluid were analysed at the same time using mass spectrometry, and this approach may be useful for the diagnosis of periodontal diseases. (Keyword) Adult / Aged / Antimicrobial Cationic Peptides / Blotting, Western / Case-Control Studies / Ceruloplasmin / Chromatography, Liquid / Electrophoresis, Polyacrylamide Gel / Female / Gingival Crevicular Fluid / Glutathione Transferase / Glycogen Phosphorylase / Humans / Male / Middle Aged / Periodontal Pocket / periodontitis / Phosphoglycerate Mutase / Proteins / Resistin / S100 Proteins / Tandem Mass Spectrometry (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1600-0765.2011.01458.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22220998 ● Search Scopus @ Elsevier (PMID): 22220998 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1600-0765.2011.01458.x (DOI: 10.1111/j.1600-0765.2011.01458.x, PubMed: 22220998)
21.	Jun-ichi Kido, Mami Hino, Mika Bandou and Yuka Hiroshima : Diagnosis of periodontal diseases by biomarkers, Electrical Engineering in Japan, Vol.179, No.1, 40-45, 2012. (Link to Publication Site) ● Publication site (DOI): 10.1002/eej.21150 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1002/eej.21150 (DOI: 10.1002/eej.21150)
22.	Yuka Hiroshima, Mika Bandou, Masatoshi Kataoka, Yuji Inagaki, Mark C. Herzberg, Karen F. Ross, Kazuo Hosoi, Toshihiko Nagata and Jun-ichi Kido : Regulation of antimicrobial peptide expression in human gingival keratinocytes by interleukin-1α, Archives of Oral Biology, Vol.56, No.8, 761-767, 2011. (Summary) In the oral cavity, mucosal keratinocytes resist bacterial infection, in part, by producing broad-spectrum antimicrobial peptides (AMPs) including defensin, adrenomedullin and calprotectin. Epidermal keratinocyte expression of many AMPs increases in response to interleukin-1α (IL-1α). IL-1α is produced by epidermal keratinocytes and regulates cell differentiation. To better understand innate immunity in the oral cavity, we sought to determine how IL-1α might regulate expression of AMPs by human gingival keratinocytes (HGKs) using DNA microarray and Western blot analyses. HGKs from three subjects expressed eleven AMPs, including S100A7, S100A8, S100A9, S100A12, secretory leucocyte protease inhibitor, lipocalin 2 (LCN2), cystatin C and β-defensin 2. Of the expressed AMPs, S100A7, S100A12 and LCN2 were up-regulated by IL-1α (inducible AMPs); the other AMPs were considered to be constitutive. Human gingival keratinocytes, therefore, express constitutive and IL-1α-inducible AMPs to provide a rapid and robust innate response to microbial infection. (Keyword) Acute-Phase Proteins / Adolescent / Adult / Anti-Infective Agents / Antimicrobial Cationic Peptides / Blotting, Western / Calgranulin A / Calgranulin B / Cell Culture Techniques / Cystatin C / Female / Gene Expression Regulation / Gingiva / Humans / Immunity, Innate / Interleukin-1alpha / Keratinocytes / Lipocalins / Male / Oligonucleotide Array Sequence Analysis / Proline-Rich Protein Domains / Proto-Oncogene Proteins / S100 Proteins / Secretory Leukocyte Peptidase Inhibitor / Serine Proteinase Inhibitors / Up-Regulation / Young Adult / beta-Defensins (Link to Publication Site) ● Publication site (DOI): 10.1016/j.archoralbio.2011.01.004 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21316034 ● Search Scopus @ Elsevier (PMID): 21316034 ● Search Scopus @ Elsevier (DOI): 10.1016/j.archoralbio.2011.01.004 (DOI: 10.1016/j.archoralbio.2011.01.004, PubMed: 21316034)
23.	Yuji Inagaki, Mika Bandou, 中島由紀子, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : Osmotic Stress Affects Calcium Deposition and Osteopontin Expression in Cultured Rat Dental Pulp Cells, The Japanese Journal of Conservative Dentistry, Vol.53, No.4, 367-375, 2010. (Summary) Osmotic stress is a stimulus caused by osmotic pressure, which is known to affect physiological functions in various tissues and cells. However, there is little information on the effect of osmotic stress on dental pulp tissues and cells. In this study, we investigated the relationship between osmotic stress and calcium deposition in cultured rat dental pulp cells. We also analyzed the effect of osmotic stress on the expression and phosphorylation of osteopontin (OPN), a multi-functional bone matrix protein, in the dental pulp cells. Both hypo- and hyper-osmotic stress affected cell-shape and -growth, and decreased calcium deposition in cultured rat dental pulp cells. Hypoosmotic stress increased OPN secretion and its protein ratio in the culture medium. Also, the secreted OPN was highly phosphorylated. On the other hand, hyper-osmotic stress decreased OPN secretion and its protein ratio and most of the OPN in the hypertoinc medium was dephosphorylated. Both hypo- and hyper-osmotic stress decreased calcium deposition in the cultured rat dental pulp cells. However, the mechanism of the inhibitory action seemed to be different in the two groups, because the amount and phosphorylation pattern of OPN were not similar between the hypo- and hyper-osmotic conditions. We concluded that osmotic stress affects calcium deposition in cultured rat dental pulp cells and that OPN expression and its phosphorylation may be a control factor of osmotic stress-associated mineralization. (Keyword) Osmotic stress / Dental pulp cell / Mineralization / osteopontin (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390001205520972544 (CiNii: 1390001205520972544)
24.	Yuka Hiroshima, Mika Bandou, Masatoshi Kataoka, Yasuo Shinohara, MC Herzberg, KF Ross, Yuji Inagaki, Toshihiko Nagata and Jun-ichi Kido : Shosaikoto increases calprotectin expression in human oral epithelial cells., Journal of Periodontal Research, Vol.45, No.1, 79-86, 2010. (Summary) BACKGROUND AND OBJECTIVE: Oral epithelial cells help to prevent against bacterial infection in the oral cavity by producing antimicrobial peptides (AMPs). A broad-spectrum AMP, calprotectin (a complex of S100A8 and S100A9 proteins), is expressed by oral epithelial cells and is up-regulated by interleukin-1alpha (IL-1alpha). Shosaikoto (SST) is a traditional Japanese herbal medicine that has immunomodulatory effects and is reported to enhance the levels of IL-1alpha in epithelial cells. The purpose of this study was to investigate the effect of SST on the expression of calprotectin and other AMPs through the regulation of IL-1alpha in oral epithelial cells. MATERIAL AND METHODS: Human oral epithelial cells (TR146) were cultured with SST (at concentrations ranging from 10 to 250 microg/mL) in the presence or absence of anti-IL-1alpha or IL-1 receptor antagonist. The expression of S100A8- and S100A9-specific mRNAs was examined by northern blotting. Calprotectin expression and IL-1alpha secretion were investigated by immunofluorescent staining or ELISA. The expression of other AMPs and IL-1alpha was analyzed by RT-PCR and by quantitative real-time PCR. RESULTS: Shosaikoto (25 microg/mL) significantly increased the expression of S100A8- and S100A9-specific mRNAs and calprotectin protein. Shosaikoto increased S100A7 expression, but had no effect on the expression of other AMPs. The expression of IL-1alpha-specific mRNA and its protein were slightly increased by SST. A neutralizing antibody against IL-1alpha or IL-1 receptor antagonist inhibited SST up-regulated S100A8/S100A9 mRNA expression. CONCLUSION: These results suggest that SST increases the expression of calprotectin and S100A7 in oral epithelial cells. In response to SST, up-regulation of calprotectin may be partially induced via IL-1alpha. (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1600-0765.2009.01203.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19602113 ● Search Scopus @ Elsevier (PMID): 19602113 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1600-0765.2009.01203.x (DOI: 10.1111/j.1600-0765.2009.01203.x, PubMed: 19602113)
25.	Mika Bandou, Yuka Hiroshima, Masatoshi Kataoka, MC Herzberg, KF Ross, Yasuo Shinohara, Takenori Yamamoto, Toshihiko Nagata and Jun-ichi Kido : Modulation of calprotectin in human keratinocytes by keratinocyte growth factor and interleukin-1alpha., Immunology and Cell Biology, Vol.88, No.3, 328-333, 2010. (Summary) Calprotectin is an antimicrobial complex composed of the S100A8 and S100A9 protein family subunits. Contributing to innate immunity, calprotectin expression is increased by interleukin-1alpha (IL-1alpha), which modulates keratinocyte differentiation. Keratinocyte growth factor (KGF) is produced by mesenchymal cells and has a mitogenic activity for epithelial cells. In this study, we investigated the effect of KGF on calprotectin expression in keratinocytes and modulation by IL-1alpha. Human keratinocytes were cultured with KGF in the presence or absence of a KGF receptor (KGFR) inhibitor or mitogen-activated protein kinase (MAPK) inhibitors. Calprotectin (S100A8/S100A9) expression was determined by northern blotting and enzyme-linked immunosorbent assay, respectively, whereas MAPK phosphorylation was analyzed by western blot analysis. KGF significantly decreased the expression of S100A8/S100A9-specific mRNAs and calprotectin protein. In the presence of KGF, KGFR inhibitor or extracellular-regulated kinase inhibitor restored KGF-downregulated expression of S100A8/S100A9. KGF increased IL-1alpha expression in keratinocytes, whereas IL-1alpha increased KGF expression in fibroblasts. Cocultured fibroblast and keratinocytes showed lower S100A8/S100A9 mRNA expression than keratinocytes alone in the presence or absence of IL-1alpha or KGF. These results suggest that fibroblast-derived KGF reduces or restricts calprotectin expression in keratinocytes, which supports our hypothesis that calprotectin expression in keratinocytes is modulated by factors associated with epithelial-mesenchymal interactions. (Link to Publication Site) ● Publication site (DOI): 10.1038/icb.2009.104 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20065999 ● Search Scopus @ Elsevier (PMID): 20065999 ● Search Scopus @ Elsevier (DOI): 10.1038/icb.2009.104 (DOI: 10.1038/icb.2009.104, PubMed: 20065999)
26.	Jun-ichi Kido, 日野真美, Mika Bandou and Yuka Hiroshima : バイオマーカーを用いた歯周病診断, IEEJ Transactions on Electronics, Information and Systems, Vol.129, No.2, 233-237, 2009. (Keyword) periodontal diseases / diagnosis / biomarker / microdevice / periodontal diseases / diagnosis / biomarker / microdevice (Link to Publication Site) ● Publication site (DOI): 10.1541/ieejeiss.129.233 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282679582732032 ● Search Scopus @ Elsevier (DOI): 10.1541/ieejeiss.129.233 (DOI: 10.1541/ieejeiss.129.233, CiNii: 1390282679582732032)
27.	Yuka Hiroshima, Yuji Inagaki, Mika Bandou, Jun-ichi Kido and Toshihiko Nagata : Long-term Observation of Marked Overfilling in Root Canal Therapy : A Report of Three Cases, The Japanese Journal of Conservative Dentistry, Vol.51, No.5, 485-492, 2008. (Summary) In endodontic therapy, overfilling of gutta-percha point in root canals sometimes occurs due to wrong measurement of working length and overextension of gutta-percha point. Although a slight overfilling to periapical tissues (within 2 mm past the apical foramen) is tolerable, marked overfilling should be checked by postoperative recheck radiographs and/or clinical symptoms. In this report, three clinical cases of marked overfilling are described and long-term radiographic observation (6-14 years) was continued. Overfilled gutta-percha points on the radiographic observation were 3.0 (case 1), 2.5 (case 2), and 3.5 mm (case 3) in the left maxillary molar of a 47-year-old woman, in the left mandibular molar of a 45-year-old woman, and in the left mandibular premolar of a 39-year-old woman, respectively. In case 1, an overfilled point was cut after 1.5 years and disappeared after 3.5 years, and then apical radiolucency was improved after 6 years. In case 2, overfilled points started to minimize after 3 years and disappeared after 14 years. In case 3, an overfilled point was minimized after 13 years accompanied with improvement of apical lesion. None of the cases showed any significant clinical symptoms after the overfilling. These observations are interesting to longitudinally evaluate the disappearance of overfilled gutta-percha and the improvement of apical lesion. (Keyword) Endodontic therapy / Overfilling / Radiographic diagnosis (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282680499131392 (CiNii: 1390282680499131392)
28.	Yuka Hiroshima, Mika Bandou, Masatoshi Kataoka, Toshihiko Nagata and Jun-ichi Kido : Regulation of calprotectin expression in human keratinocytes in vitro, Journal of the Japanese Association of Periodontology, Vol.49, No.3, 224-232, 2007. (Summary) Calprotectin, a heterodimeric complex of S100A8 and S100A9, is an antimicrobial peptide (AMP) expressed in healthy or inflamed epithelium and epidermis. The expression of calprotectin and other AMPs in keratinocytes is regulated by proinflammatory cytokines, bacterial products and keratinocyte differentiation modulators. Interleukin-1α (IL-1α), an autonomous cytokine in keratinocytes, induces keratinocyte differentiation and up-regulates calprotectin expression. Since keratinocyte differentiation is also specified<KG>by interactions with the basement membrane and connective tissue proteins, we sought to learn whether calprotectin expression is affected by extracellular matrix (ECM) proteins in the presence or absence of IL-1α. Human immortalized epidermal keratinocytes (HaCaT cells) were grown in vitro on different ECM substrates including type I collagen (Col I), type IV collagen (Col IV), fibronectin (FN) and laminin (LM) with or without IL-1α and were then cultured in basement membrane extract (Matrigel)-coated dishes or on a feeder layer of fibroblasts. Calprotectin expression in the cultured cells was investigated using immunohistochemical and northern blot analyses, and an enzyme-linked immunosorbent assay. The four ECM proteins (Col I, Col IV, FN and LM) had little effect on calprotectin expression. IL-1α significantly increased the expression of S100A8/ S100A9 mRNAs and calprotecin protein in the cells cultured on each of the ECM(Col I, Col IV, FN and LM)-coated dishes,but these ECM protein substrates did not show a further effect on calprotectin expression in the presence of IL-1α. On the other hand, Matrigel and the fibroblast-feeder layer slightly decreased the expression of S100A8/S100A9 mRNAs in HaCaT cells. These results suggest that calprotectin expression in keratinocytes is regulated by cytokines during epithelial-mesenchymal interactions.<KG>Nihon Shishubyo Gakkai Kaishi (J Jpn Periodontol) 49 : 224-232,2007. (Keyword) calprotectin / interleukin-1α / extracellular matrix / keratinocyte (Link to Publication Site) ● Publication site (DOI): 10.2329/perio.49.224 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282679388561152 ● Search Scopus @ Elsevier (DOI): 10.2329/perio.49.224 (DOI: 10.2329/perio.49.224, CiNii: 1390282679388561152)
29.	Mika Bandou, Yuka Hiroshima, Masatoshi Kataoka, Yasuo Shinohara, MC Herzberg, KF Ross, Toshihiko Nagata and Jun-ichi Kido : Interleukin-1alpha regulates antimicrobial peptide expression in human keratinocytes., Immunology and Cell Biology, Vol.85, No.7, 532-537, 2007. (Summary) Human epidermis and epithelium serve as physiologic barriers to protect against noxious and infectious agents. Contributing to the defense against infection, epithelial cells express antimicrobial peptides (AMPs). The expression of AMPs in keratinocytes is generally regulated directly by bacteria and indirectly by proinflammatory cytokines. Bacteria may also regulate AMP expression by inducing keratinocyte expression of the autonomous proinflammatory cytokine, interleukin-1alpha (IL-1alpha). To test the hypothesis that AMP expression may be regulated by cell autonomous cytokines, we investigated the effect of IL-1alpha on the expression of AMPs in human keratinocytes (HaCaT cells) by microarray, northern blot, reverse transcriptase (RT)-PCR and western blot analyses. IL-1alpha increased expression of mRNA in a dose- and time-dependent manner specific for lipocalin 2, S100A8, S100A9 and secretory leukocyte protease inhibitor (SLPI) more than twofold relative to nonstimulated cells (control), and slightly upregulated S100A7 and beta-defensin-2. Furthermore, the expression of lipocalin 2, S100A7, S100A8, S100A9 and SLPI proteins were upregulated by IL-1alpha. On the other hand, HaCaT cells expressed mRNA specific for other AMPs, including cystatin 3, adrenomedullin, RNase-7 and mucin 5, which were unaffected by IL-1alpha treatment. These results suggest that the autonomous keratinocyte cytokine, IL-1alpha, selectively upregulates the expression of AMPs which may modulate innate epithelial cell immunity in skin and mucosa. (Keyword) Immunity, Innate (Link to Publication Site) ● Publication site (DOI): 10.1038/sj.icb.7100078 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17549071 ● Search Scopus @ Elsevier (PMID): 17549071 ● Search Scopus @ Elsevier (DOI): 10.1038/sj.icb.7100078 (DOI: 10.1038/sj.icb.7100078, PubMed: 17549071)

Academic Paper (Unrefereed Paper):

1.	Jun-ichi Kido, Mika Bandou, Yuji Inagaki, 生田貴久, Yukari Kajiura, Yukiko Nakajima, Eijiro Sakamoto, Chie Wada -Mihara, Masami Ninomiya, 西川泰史, Jung-Hwan Lew, Koji Naruishi and Toshihiko Nagata : Diagnosis of Periodontal Diseases using Biomarkers in Gingival Crevicular Fluid, Journal of Oral Health and Biosciences, Vol.29, No.1, 13-20, 2016. (Summary) Periodontal diseases cause an inflammation and degradation of periodontal tissues and missing of teeth. The incidence rate of periodontal diseases is high in middle-aged and elderly people.A reasonable diagnosis of periodontal diseases is very important to keep teeth, however, conventional examinations of periodontal diseases is not necessarily exact and objective. Gingival crevicular fluid (GCF) is an exudate secreted from periodontal tissues and contains many components including proteolytic enzymes, inflammatory cytokines, blood-associated proteins, cellular and bacterial fragments. Because some proteins in GCF are related to inflammation, tissue degradation and bone metabolism, those proteins have been studying as a diagnostic marker of periodontal diseases. GCF is noninvasively collected using a sterile paper strip and biomarkers are determined using enzyme-linked immunosorbent assay (ELISA) and enzyme activity assay. We identified calprotectin, an inflammationrelated protein, in GCF and calprotectin level in GCF from periodontitis sites was significantly higher than that of healthy control. Calprotectin level in GCF was positively correlated to gingival index and other biomarkers and decreased by periodontal treatments. Resistin is an adipocytokine and its level increases in some inflammatory diseases. Resistin level in GCF from periodontitis sites was high compared to the level of healthy control samples. Procollagen type I C-terminal peptide (PICP) is a biomarker for bone metabolism and its level was high in GCF collected from periodontitis sites. These results suggested that calprotectin, resistin and PICP are useful biomarkers for periodontal diseases. On the other hand, we showed that glycated albumin (GA), a marker of diabetes mellitus (DM), was contained in GCF and GA level in GCF from DM patients was significantly higher than that of non-DM individuals. Components in GCF may be biomarkers of systemic diseases as well as periodontal diseases and their determination will be useful diagnostic examination of some diseases. Recently, we have been studying the determining system of GCF calprotectin, including microchip ELISA, surface plasmon resonance assay and immuno-chromatography assay. When GCF biomarkers are determined using the determining systems, we will simply, exactly and objectively diagnose periodontal diseases at our dental offices. (Keyword) 歯周病診断 / バイオマーカー / 歯肉溝滲出液 (Tokushima University Institutional Repository) ● Metadata: 109875 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050845763956844416 (Tokushima University Institutional Repository: 109875, CiNii: 1050845763956844416)

Review, Commentary:

1.	Jun-ichi Kido, Mika Bandou, E Sakamoto, Yukari Kajiura and Toshihiko Nagata : Effects of advanced glycation end-products on pathogenesis of diabetes-associated periodontitis, Journal of the Japanese Association of Periodontology, Vol.56, No.1, 17-24, 2014. (Keyword) 糖尿病関連歯周炎 / 最終糖化産物 / 歯周組織 (Link to Publication Site) ● Publication site (DOI): 10.2329/perio.56.17 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390001204414873472 ● Search Scopus @ Elsevier (DOI): 10.2329/perio.56.17 (DOI: 10.2329/perio.56.17, CiNii: 1390001204414873472)

Proceeding of International Conference:

1.	Yuka Hiroshima, Mika Bandou, Takahiro Hasegawa, Yuji Inagaki and Chie Wada -Mihara : Resistin release from neutrophils is induced by Porphyromonas gingivalis lipopolysaccharide., IADR (International Association of Dental Research) Barcelona, Spain, July 14-17, 2010,
2.	T Ikuta, Yukari Kajiura, Mika Bandou, Yuji Inagaki, Koji Naruishi, Jun-ichi Kido and Toshihiko Nagata : YKL-40 in gingival crevicular fluid from patients with periodontitis and diabetes., Euro Perio 2015, Jun. 2015.
3.	Yukari Kajiura, Mika Bandou, Jun-ichi Kido, Yuji Inagaki and Toshihiko Nagata : Determination of glycated albumin and calprotectin in gingival crevicular fluid from patients with periodontitis and diabetes., Euro Perio 2015, Jun. 2015.
4.	Yukari Kajiura, Mika Bandou, Yuji Inagaki, Hiromi Murata, Jun-ichi Kido and Toshihiko Nagata : Advanced glycation end-product increases oxidative stress in human gingival fibroblasts, 53th General Session of the Korean Academy of Periodontology Meeting, Seoul, Korea, Nov. 2013.
5.	Yukiko Nakajima, Jun-ichi Kido, Yuji Inagaki, Mika Bandou, Yuka Hiroshima, Hiromi Murata and Toshihiko Nagata : Effect of hypoxia on gene expression in human oral keratinocytes, 10th Asian Pacific Society of Periodontology Meeting, Nara, Sep. 2013.
6.	Jun-ichi Kido, Mika Bandou, Yuji Inagaki, Yuka Hiroshima, Hiromi Murata, Chie Wada -Mihara, 梶浦由加里, 生田貴久, 篠原宏貴, 橋本万里, Yukiko Nakajima, Yukiko Bandou, Makoto Funaki, Haruhiko Saito and Toshihiko Nagata : Diagnosis of diabetes-associated periodontitis using glycoalbumin and calprotectin in gingival crevicular fluid, 10th Asian Pacific Society of Periodontology Meeting, Nara, Sep. 2013.
7.	Toshihiko Nagata, Jun-ichi Kido, Mika Bandou, Yuka Hiroshima, Yuji Inagaki, Hiromi Murata, Chie Wada -Mihara, Mika Bandou and Makoto Funaki : Diagnosis of diabetes-associated periodontitis using biomarkers in gingival crevicular fluid, 91th General Session & Exhibition of the International Association for Dental Research. Seattle, USA, May 2013.
8.	Mika Bandou, Yukari Kajiura, Jun-ichi Kido, Yuji Inagaki, Masatoshi Kataoka and Toshihiko Nagata : Lipopolysaccharide induces oxidative stress and antioxidant responses in gingival fibroblasts, The 60th Annual Meeting of Japanese Association for Dental Research, Program and abstracts of papers, 79, Dec. 2012.
9.	Toshihiko Nagata, Jun-ichi Kido, Mika Bandou, Yuka Hiroshima, Yuji Inagaki, Masami Ninomiya, Chie Wada -Mihara, Hiromi Murata, Yukiko Bandou and Makoto Funaki : Diagnosis of diabetes-associated periodontitis by measuring biomarkers in gingival crevicular fluid, The 9th International Diabetes Federation Western Pacific Region Congress/ The 4th AASD Scientific Meeting, Nov. 2012.
10.	Yukiko Nakajima, Yuji Inagaki, Mika Bandou, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : Advanced glycation end-product increase calcification and inflammatory factors in cultured rat dental pulp cells, European Calcified Tissue Society, 39th Annual Congress Final programme, 73, Stockholm (Sweden), May 2012.
11.	Yuji Inagaki, Yukiko Nakajima, Mika Bandou, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : Relationship between pathologic calcification and osteopontin expression in dental pulp tissues of diabetic rats, European Calcified Tissue Society, 39th Annual Congress, Final Programme, 125, Stockholm (Sweden), May 2012.

Proceeding of Domestic Conference:

1.	枡富健二, Mika Bandou, Yuji Inagaki, Rie Kido, 植村勇太, 畑田祐佳里, Jun-ichi Kido and Hiromichi Yumoto : 糖尿病関連歯周炎高齢患者のオーラルフレイルリスクバイオマーカーの探索, 第66回春季日本歯周病学会学術大会(高松), May 2023.
2.	Yuji Inagaki, Mika Bandou, Takahisa Ikuta, Jun-ichi Kido and Hiromichi Yumoto : 侵襲性歯周炎(ステージIII, グレードC)に対して歯周基本治療と歯周外科治療を行い奏功した一症例, 第65回秋季日本歯周病学会学術大会(仙台), Sep. 2022.
3.	Mika Bandou, Yuji Inagaki and Hiromichi Yumoto : Report of two cases of root coverage with connective tissue graft for patients suffering from gingival reccesion -Consideration of sufficient and insufficient case-, 第65回秋季日本歯周病学会学術大会, Sep. 2022.
4.	Rie Kido, Eijiro Sakamoto, Yuka Hiroshima, Mika Bandou, Jun-ichi Kido, Takahisa Ikuta, Masami Ninomiya, Yuji Inagaki, Yasufumi Nishikawa, Yoritoki Tomotake, Koji Naruishi and Hiromichi Yumoto : イムノクロマト法を用いたカルプロテクチン測定による歯周病およびインプラント疾患の診断, 四国歯学会第59回例会, Mar. 2022.
5.	Rie Kido, Yuka Hiroshima, Takahisa Ikuta, Yuji Inagaki, Mika Bandou, Koji Naruishi, Jun-ichi Kido and Hiromichi Yumoto : 最終糖化産物による口腔上皮細胞の Lipocalin2 発現誘導は好中球の遊走性とサイトカイン発現を調節する, 第63回春季日本歯周病学会学術大会, May 2020.
6.	植村勇太, Masami Ninomiya, 和田明大, Rie Kido, 高木亮輔, 野中康平, 谷口裕哉, Takahisa Ikuta, Eijiro Sakamoto, Mika Bandou, Yuji Inagaki, Koji Naruishi, Jun-ichi Kido and Hiromichi Yumoto : 歯周病ならびに歯周組織再生療法に関する臨床研究について, 徳島県歯科医学大会・四国歯学会第56回例会, Feb. 2020.
7.	Kohei Nonaka, Mika Bandou, Jun-ichi Kido, Yuji Inagaki, Eijiro Sakamoto, Koji Naruishi and Hiromichi Yumoto : ショウガオールはヒト歯肉線維芽細胞においてAGEs誘導性の酸化ストレスを抑制する, 第62回秋季日本歯周病学会学術大会 (北九州), Oct. 2019.
8.	Nonaka Kohei, Mika Bandou, Jun-ichi Kido, Yuji Inagaki, Eijiro Sakamoto, Koji Naruishi and Hiromichi Yumoto : ショーガオールはヒト歯肉線維芽細胞におけるAGEs誘導性のIL-6およびICAM-1産生を抑制する, 第62回秋季日本歯周病学会学術大会, Oct. 2018.
9.	野中康平, Mika Bandou, Jun-ichi Kido, Yuji Inagaki, Eijiro Sakamoto, Koji Naruishi and Hiromichi Yumoto : 最終糖化産物はヒト歯肉線維芽細胞におけるIL-6とICAM-1の発現増加を介して単球との接着を誘導する, 第61回春季日本歯周病学会学術大会, Jun. 2018.
10.	Rie Kido, Eijiro Sakamoto, Mika Bandou, Yuji Inagaki, Masami Ninomiya, Chie Wada -Mihara, Takahisa Ikuta, Koji Naruishi, Toshihiko Nagata, Jun-ichi Kido and Hiromichi Yumoto : インプラント周囲溝滲出液中のカルプロテクチンとNTxを用いたインプラント疾患の診断, 第61回春季日本歯周病学会学術大会, Jun. 2018.
11.	Yuji Inagaki, Mika Bandou, 生田貴久 and Jun-ichi Kido : 歯肉退縮に対して異なる術式を用いて根面被覆を行った一症例, 日本歯周病学会60周年記念大会, Dec. 2017.
12.	Masami Ninomiya, Yuji Inagaki, Chie Wada -Mihara, Mika Bandou, Yukiko Nakajima, Eijiro Sakamoto, Ikuta Takahisa, Nishikawa Yasufumi, Jung-Hwan Lew, Rie Kido, Takagi Ryousuke, Nonaka Kouhei, Koji Naruishi, Jun-ichi Kido and Toshihiko Nagata : 新規歯周組織再生剤「リグロス歯科用液キット」の有効性, 四国歯学会第51回例会, Jun. 2017. (Keyword) periodontitis / fibroblast growth factor 2 / periodontal regeneration / Regroth
13.	Chie Wada -Mihara, Koji Naruishi, Mika Bandou, 西川泰史, Hwan Jung Lew, Eijiro Sakamoto, 生田貴久, 河野薫, Yukari Kajiura, 橋本万里, Yukiko Nakajima, Yuji Inagaki, Masami Ninomiya, Jun-ichi Kido and Toshihiko Nagata : アドバンスドOSCEを見据えた当科の模擬OSCEの概要, Shikoku Dental Research, Vol.29, No.2, 49-53, Jun. 2017.
14.	Yukari Kajiura, Mika Bandou, Jun-ichi Kido, Yuji Inagaki and Toshihiko Nagata : 歯肉溝滲出液を用いた糖尿病関連歯周炎の新規診断法の確立, 第23回日本歯科医学会総会, Oct. 2016.
15.	Mika Bandou, Yukari Kajiura, 野中康平, Eijiro Sakamoto, Koji Naruishi, Jun-ichi Kido and Toshihiko Nagata : 最終糖化産物はヒト歯肉線維芽細胞におけるIL-6およびICAM-1の発現を増加する, 第59回秋季日本歯周病学会学術大会, Oct. 2016.
16.	美原智恵, Koji Naruishi, Mika Bandou, 西川泰史, Jung-Hwan Lew, Eijiro Sakamoto, 生田貴久, 河野薫, Yukari Kajiura, 橋本万里, Yukiko Nakajima, Yuji Inagaki, Masami Ninomiya, Jun-ichi Kido and Toshihiko Nagata : アドバンスOSCEを見据えた当科の模擬OSCEの概要, 第49回四国歯学会例会, Jun. 2016.
17.	Jun-ichi Kido, Mika Bandou, Yukiko Nakajima, Yukari Kajiura, Yuji Inagaki, 生田貴久, Eijiro Sakamoto, Koji Naruishi and Toshihiko Nagata : ヒト口腔上皮細胞と歯肉線維芽細胞において低酸素環境が誘導する遺伝子発現の比較, 第143回日本歯科保存学会秋季学術大会, Nov. 2015.
18.	Yukari Kajiura, Jun-ichi Kido, Yukiko Nakajima, Mika Bandou, Yuji Inagaki, Koji Naruishi, Eijiro Sakamoto, Kaori Abe, Yuka Hiroshima and Toshihiko Nagata : 低酸素環境が誘導するヒト口腔上皮細胞における遺伝子発現の解析, 第58回秋季日本歯周病学会学術大会, Sep. 2015.
19.	Eijiro Sakamoto, Jun-ichi Kido, Yukari Kajiura, Mika Bandou, Yuji Inagaki, Koji Naruishi, 生田貴久 and Toshihiko Nagata : 最終糖化産物はヒト口腔上皮細胞の遺伝子発現を調節する, 第58回秋季日本歯周病学会学術大会, Sep. 2015.
20.	Koji Naruishi, Yukari Kajiura, 西川泰史, Mika Bandou, Jun-ichi Kido and Toshihiko Nagata : 培養歯肉線維芽細胞におけるクリプトタンシノンによる炎症関連分子の生産抑制効果, 第142回日本歯科保存学会春季学術大会, Jun. 2015.
21.	西川泰史, Koji Naruishi, Yukari Kajiura, Mika Bandou, Jun-ichi Kido and Toshihiko Nagata : カルプロテクチンがヒト歯肉線維芽細胞の炎症関連因子の発現に及ぼす影響, 第58回春季日本歯周病学会学術大会, May 2015.
22.	Mika Bandou, Yukari Kajiura, Yukiko Nakajima, Jun-ichi Kido, Yuji Inagaki, Hiromi Murata and Toshihiko Nagata : 最終糖化産物は口腔由来線維芽細胞・上皮細胞での炎症関連因子と酸化ストレス因子の発現に影響する, 第57回秋季日本歯周病学会学術大会, Oct. 2014.
23.	Yukari Kajiura, Yukiko Bandou, Jun-ichi Kido, Mika Bandou, Yuji Inagaki, Yukiko Nakajima, 生田貴久, Hiromi Murata, Yuka Hiroshima, Koji Naruishi and Toshihiko Nagata : 歯周病および糖尿病患者の歯肉溝滲出液中のYKL-40レベルの検討, 第57回秋季日本歯周病学会学術大会, Oct. 2014.
24.	Mika Bandou, Yuka Hiroshima, Yuji Inagaki, Jun-ichi Kido and Toshihiko Nagata : ヒト上皮細胞におけるInterleukin-1aによるS100A9遺伝子の転写調節, 第140回日本歯科保存学会春季学術大会, Jun. 2014.
25.	Jun-ichi Kido, Yukiko Nakajima, Mika Bandou, Yuji Inagaki and Toshihiko Nagata : 低酸素環境とP.gingivalis由来リポ多糖はヒト口腔上皮細胞での炎症関連因子および血管関連因子の発現を調節する, 第140回日本歯科保存学会春季学術大会, Jun. 2014.
26.	Yukari Kajiura, Mika Bandou, Jun-ichi Kido, Yuji Inagaki, 生田貴久, 橋本万里, 篠原宏貴, Masami Ninomiya, Hiromi Murata, Yukiko Nakajima, Satoshi Yoneda, 美原智恵, Yuka Hiroshima, Keiji Oishi and Toshihiko Nagata : 歯肉溝滲出液中のグリコアルブミンおよびカルプロテクチンを指標とした糖尿病関連歯周炎の診断, 第57回春季日本歯周病学会学術大会, May 2014.
27.	Yukiko Nakajima, Jun-ichi Kido, Mika Bandou, Yuji Inagaki and Toshihiko Nagata : Effect of hypoxia and P. gingivalis-lipopolysaccharide on the expression of inflammation-related molecules in human oral keratinocytes, 第57回春季日本歯周病学会学術大会, May 2014.
28.	Mika Bandou, Yukiko Nakajima, Yukari Kajiura, Jun-ichi Kido, Yuji Inagaki, Hiromi Murata and Toshihiko Nagata : 最終糖化産物は歯周組織細胞での炎症性関連因子と酸化ストレス因子の発現に影響する, 第57回日本糖尿病学会年次学術集会, May 2014.
29.	Yukari Kajiura, Yukiko Bandou, Jun-ichi Kido, Mika Bandou, Yuji Inagaki, Yukiko Nakajima, 生田貴久, Hiromi Murata, Yuka Hiroshima, Koji Naruishi and Toshihiko Nagata : 歯周病および糖尿病患者の歯肉溝滲出液中のYKL-40レベルの検討, 第57回日本歯周病学会秋期学術大会抄録集, May 2014.
30.	生田貴久, Yuji Inagaki, Yukiko Nakajima, Mika Bandou, Jun-ichi Kido and Toshihiko Nagata : 日本人歯周病患者を対象とした抗菌ペプチド遺伝子のSNPs解析と疾患感受性の検討, 第139回日本歯科保存学会秋季学術大会, Oct. 2013.
31.	Yukiko Nakajima, Jun-ichi Kido, Yuji Inagaki, Mika Bandou, Yuka Hiroshima, Hiromi Murata and Toshihiko Nagata : 低酸素環境がヒト口腔上皮細胞の各種遺伝子発現に及ぼす影響, 第56回秋季日本歯周病学会学術大会, Sep. 2013.
32.	梶浦由加里, Mika Bandou, Yuji Inagaki, Jun-ichi Kido and Toshihiko Nagata : 最終糖化産物が歯肉線維芽細胞における酸化ストレス反応に及ぼす影響, 第56回春季日本歯周病学会学術大会, Jun. 2013.
33.	Masami Ninomiya, Mika Bandou, Hiromi Murata, Takahisa Ikuta, Jun-ichi Kido and Toshihiko Nagata : A case report of comprehensive periodontal treatments for generalized aggressive periodontitis in two sisters, Journal of the Japanese Association of Periodontology, Vol.55, Jun. 2013. (Keyword) Aggressive periodontitis / family / Periodontal Treatment
34.	Jun-ichi Kido, Mika Bandou, Yukiko Bandou, Yuji Inagaki, Yuka Hiroshima, 梶浦由加里, Chie Wada -Mihara, Hiromi Murata, 生田貴久, 篠原宏貴, Makoto Funaki and Toshihiko Nagata : 糖尿病関連歯周炎の診断マーカーとしての歯肉溝滲出液中グリコアルブミンとカルプロテクチンの有用性, 第56回日本糖尿病学会, May 2013.
35.	Jun-ichi Kido, Mika Bandou, Yukiko Bandou, Yuji Inagaki, Yuka Hiroshima, 梶浦由加里, 美原智恵, Hiromi Murata, 生田貴久, 篠原宏貴, 橋本万里, Makoto Funaki, Haruhiko Saito and Toshihiko Nagata : --, 第56回日本糖尿病学会年次学術集会, May 2013.
36.	Jun-ichi Kido, Yuji Inagaki, Mika Bandou, Yukiko Bandou, Yuka Hiroshima, Hiromi Murata, Makoto Funaki, Haruhiko Saito and Toshihiko Nagata : 歯肉溝滲出液中のバイオマーカーを用いた糖尿病関連歯周炎の診断, 第55回日本糖尿病学会年次学術集会抄録集, 186, May 2012.
37.	Yuka Hiroshima, Mika Bandou, Masatoshi Kataoka, Jun-ichi Kido and Toshihiko Nagata : ヒト口腔上皮細胞のカルプロテクチン発現に及ぼす半夏瀉心湯の影響, 日本歯周病学会会誌第55回春季学術大会特別号, Vol.54, 131, May 2012.
38.	Kaori Abe, Mika Bandou, Yuka Hiroshima, Jun-ichi Kido and Masatoshi Kataoka : マイクロチップ基板を用いた血中サイトカインの迅速検出法の構築, 日本歯周病学会会誌第55回春季学術大会特別号, Vol.54, 114, May 2012.
39.	Mika Bandou, Jun-ichi Kido, Yuji Inagaki, Yuka Hiroshima, Hiromi Murata, Takahisa Ikuta, 篠原宏貴, 橋本万里, 山田由加里, Yukiko Bandou, Haruhiko Saito and Toshihiko Nagata : 糖尿病関連歯周炎の診断指標スクリーニングに向けた医科・歯科連携研究, 日本歯周病学会会誌第55回春季学術大会特別号, Vol.54, 112, May 2012.
40.	Jun-ichi Kido, Yuji Inagaki, Mika Bandou, Yuka Hiroshima, Hiromi Murata, Chie Wada -Mihara, Masumi Horibe, Satoshi Yoneda, Masami Ninomiya, Keiji Oishi, Eijiro Sakamoto, 中島由紀子, 生田貴久, 浅原洋士 and Toshihiko Nagata : バイオマーカーを用いた糖尿病関連歯周炎の診断研究, Journal of the Japanese Association for Dental Science, Vol.31, 86, Mar. 2012. (Keyword) *生物学的マーカー
41.	Jun-ichi Kido, Yuji Inagaki, Mika Bandou, Yuka Hiroshima, Hiromi Murata, Chie Wada -Mihara, Masumi Horibe, Satoshi Yoneda, Masami Ninomiya, Keiji Oishi, Eijiro Sakamoto, 中島由紀子, 生田貴久, 浅原洋士 and Toshihiko Nagata : バイオマーカーを用いた糖尿病関連歯周炎の診断研究, Journal of the Japanese Association for Dental Science, Vol.31, 86, Mar. 2012. (Keyword) *生物学的マーカー
42.	Jun-ichi Kido, Yuji Inagaki, Mika Bandou, Yuka Hiroshima, Hiromi Murata, Chie Wada -Mihara, Masumi Horibe, Satoshi Yoneda, Masami Ninomiya, Keiji Oishi, 坂本英次郎, 中島由紀子, 生田貴久, 浅原洋士 and Toshihiko Nagata : バイオマーカーを用いた糖尿病関連歯周炎の診断研究, Journal of the Japanese Association for Dental Science, Vol.31, 86, Mar. 2012. (Keyword) *生物学的マーカー
43.	Hiromi Murata, Jun-ichi Kido, Mika Bandou, Yuka Hiroshima, Yuji Inagaki and Toshihiko Nagata : 最終糖化産物はマクロファージ様細胞の炎症関連因子の発現を調節する, 日本歯科保存学会雑誌第135回秋季学術大会プログラム, 200, Oct. 2011.
44.	中島由紀子, 稲垣裕司, Mika Bandou, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : 最終糖化産物(AGEs)がラット培養歯髄細胞の石灰化物形成と抗菌ペプチド発現に及ぼす影響, 日本歯科保存学会雑誌第135回秋季学術大会プログラム, 46, Oct. 2011.
45.	Yukiko Bandou, Jun-ichi Kido, Yuka Hiroshima, Mika Bandou, Yuji Inagaki, Hiromi Murata, Yosuke Shikama, Makoto Funaki and Toshihiko Nagata : 歯肉溝滲出液中のNKL-40の分析, 日本歯周病学会会誌秋季特別号, Vol.53, 106, Sep. 2011.
46.	Jun-ichi Kido, Kaori Abe, Masatoshi Kataoka, Mika Bandou, Yuka Hiroshima, Yuji Inagaki and Toshihiko Nagata : マイクロチップELISA法による歯肉溝滲出液中のカルプロテクチン測定, 日本歯周病学会秋季特別号, Vol.53, 108, Sep. 2011.
47.	中島由紀子, Yuji Inagaki, Mika Bandou, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : ラット培養歯髄細胞における最終糖化産物(AGEs)の石灰化促進作用, 日本歯科保存学会雑誌第134回春季学術大会プログラム, 12, Jun. 2011.
48.	Mika Bandou, Yuji Inagaki, Jun-ichi Kido, Yuka Hiroshima, Masatoshi Kataoka, Hiromi Murata, Yukiko Bandou, Masami Ninomiya, Eijiro Sakamoto, 中島由紀子 and Toshihiko Nagata : 歯肉溝滲出液中のグリコアルブミン測定法の確立, 日本歯周病学会会誌春季特別号, Vol.53, 119, May 2011. (Keyword) periodontitis / diabetes mellitus / 歯肉溝滲出液 / グリコアルブミン
49.	Mika Bandou, Yuji Inagaki, Jun-ichi Kido, Yuka Hiroshima, Masatoshi Kataoka, Hiromi Murata, Yukiko Bandou, Masami Ninomiya, 坂本英次郎, 中島由紀子 and Toshihiko Nagata : 歯肉溝滲出液中のグリコアルブミン測定法の確立, 日本歯周病学会会誌春季特別号, Vol.53, 119, May 2011. (Keyword) periodontitis / diabetes mellitus / 歯肉溝滲出液 / グリコアルブミン
50.	Yuka Hiroshima, Mika Bandou, Jun-ichi Kido, Masatoshi Kataoka and Toshihiko Nagata : ヒト口腔上皮細胞におけるカルプロテクチン発現に及ぼす半夏瀉心湯の影響, 日本歯周病学会会誌春季特別号, Vol.53, 114, May 2011. (Keyword) periodontitis / 口腔上皮細胞 / 半夏瀉心湯 / カルプロテクチン
51.	Yukiko Nakajima, Yuji Inagaki, Mika Bandou, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : グルコースが糖尿病ラット由来歯髄細胞の石灰化物形成とオステオポンチン産生に及ぼす影響, 第133回日本歯科保存学会秋季学術大会(岐阜), Oct. 2010.
52.	Yuji Inagaki, Jun-ichi Kido, Mika Bandou, Yuka Hiroshima and Chie Wada -Mihara : 糖尿病関連歯周炎における歯肉溝浸出液中のバイオマーカーの分析, 第53回日本糖尿病学会, May 2010.
53.	Yuka Hiroshima, Mika Bandou, Jun-ichi Kido, Eijiro Sakamoto, 中島由紀子, Masatoshi Kataoka and Toshihiko Nagata : Porphyromonas gingivalis由来LPSはヒト好中球からのレジスチンの遊離を促進する, 第53回春季日本歯周病学会学術大会, Vol.52, 105, May 2010.
54.	Yuka Hiroshima, Mika Bandou, Jun-ichi Kido, 坂本英次郎, 中島由紀子, Masatoshi Kataoka and Toshihiko Nagata : Porphyromonas gingivalis由来LPSはヒト好中球からのレジスチンの遊離を促進する, 第53回春季日本歯周病学会学術大会, Vol.52, 105, May 2010.
55.	Jun-ichi Kido, Yuji Inagaki, Mika Bandou, Yuka Hiroshima, Masatoshi Kataoka, Chie Wada -Mihara, Masumi Horibe, Satoshi Yoneda, 坂本英次郎, 中島由紀子, Masami Ninomiya, Keiji Oishi, 淺原洋士 and Toshihiko Nagata : 歯肉溝浸出液中の糖尿病関連歯周炎バイオマーカーの検索, Journal of the Japanese Association of Periodontology, Vol.52, 97, May 2010.
56.	Yuji Inagaki, Jun-ichi Kido, Mika Bandou, Yuka Hiroshima, Masatoshi Kataoka, Chie Wada -Mihara, Masumi Horibe, Satoshi Yoneda, 坂本英次郎, 中島由紀子, Masami Ninomiya, Keiji Oishi, 淺原洋士 and Toshihiko Nagata : 糖尿病関連歯周炎における歯肉溝滲出液中のバイオマーカーの分析, Journal of the The Japan Diabetes Society, Vol.53, No.Suppl.1, S-145, Apr. 2010. (Keyword) 生物学的マーカー
57.	Yuka Hiroshima, Mika Bandou, Jun-ichi Kido, Yuji Inagaki, Chie Wada -Mihara, Keiji Oishi, Masatoshi Kataoka and Toshihiko Nagata : ヒト口腔上皮細胞における抗菌ペプチド遺伝子発現に及ぼす小柴胡湯の影響, 第131回日本歯科保存学会秋季学術大会, Oct. 2009.
58.	Yuji Inagaki, Mika Bandou, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : オスモティックストレスが歯髄細胞の硬組織形成能とオステオポンチン産生に及ぼす影響, 第131回日本歯科保存学会秋季学術大会, Oct. 2009.
59.	Mika Bandou, Yuka Hiroshima, Yuji Inagaki, Masatoshi Kataoka, Chie Wada -Mihara, Masumi Horibe, Satoshi Yoneda, Keiji Oishi, Masami Ninomiya, Javkhlan Purevjav, Jun-ichi Kido and Toshihiko Nagata : 糖尿病関連歯周炎における歯肉溝浸出液中バイオマーカーの分析, Journal of the Japanese Association of Periodontology, Vol.51, 101, Oct. 2009.
60.	Yuka Hiroshima, Mika Bandou, Jun-ichi Kido, Masatoshi Kataoka and Toshihiko Nagata : ヒト歯肉上皮細胞における抗菌ペプチド遺伝子発現のマイクロアレイ法による解析, 第52回秋季日本歯周病学会学術大会, Vol.51, 90, Oct. 2009.
61.	Jun-ichi Kido, Masatoshi Kataoka, 日野真美, Mika Bandou, Yuka Hiroshima and Toshihiko Nagata : 歯周病バイオマーカーのマイクロチップ基板を用いた測定と歯周病診断への応用, 第2回日本口腔検査学会, 28, Oct. 2009.
62.	Jun-ichi Kido, Masatoshi Kataoka, Mika Bandou, Yuka Hiroshima, Chie Wada -Mihara and Toshihiko Nagata : マイクロチップ基板を用いたカルプロテクチンの測定‐歯周病診断法への応用の可能性について‐, 第52回春季日本歯周病学会学術大会, Vol.51, 114, May 2009.

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

スクレロスチンを新規標的マーカーとした糖尿病関連歯周炎の非侵襲的診断法の開発 (Project/Area Number: 21K09874 )
高齢者糖尿病関連歯周炎患者のオーラルフレイルリスクバイオマーカーの探索 (Project/Area Number: 20K09957 )
Diagnosis of peri-implant diseases by cellular biomarkers and development of diagnostic device (Project/Area Number: 15K15767 )
Effect of advanced glycation end-products and inflammasome for pathogenesis of Diabetes mellitus-associated periodontitis (Project/Area Number: 15K11391 )
Investigation of diabetes-associated periodontitis pathogenesis from a point of relevance for advanced glycation end-product and redox regulation. (Project/Area Number: 24792333 )
ファイブロティックアクティビティから薬物性歯肉増殖症の発症リスクを診断する (Project/Area Number: 24593124 )
Effect of periodontopathic factors on osteoblastic differentiation of rat bone-marrow cells cultured under simulated microgravity (Project/Area Number: 23659979 )
Investigation of redox regulation by Keap-1 and Nrf2 system in periodontal tissue (Project/Area Number: 22792089 )
Analysis of association between gene polymorphisms of antimicrobial peptides and periodontitis among Japanese patients (Project/Area Number: 21592626 )
Development of the diagnostic method for periodontal diseases Using a microdevice to determine calprotectin (Project/Area Number: 21592625 )
Study of perlodontitis prevention viewed from robustness of periodontal tissues (Project/Area Number: 19592388 )
Search by Researcher Number (10510000)

Assistant Professor : Bandou, Mika

Research

Personal Web Page

Field of Study

Subject of Study

Book / Paper

Book:

Academic Paper (Judged Full Paper):

Academic Paper (Unrefereed Paper):

Review, Commentary:

Proceeding of International Conference:

Proceeding of Domestic Conference:

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