Tokushima University / Educator and Researcher Directory --- Hiroshima, Yuka

Personal Web Page

https://researchmap.jp/yuka-hiroshima (researchmap)

Field of Study

○	Periodontology

Subject of Study

○	歯周病と糖尿病に関する研究

Book / Paper

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.	Kayo Yoshida, Kaya Yoshida, Mariko Seyama, Yuka Hiroshima, Mana Mekata, Natsumi Fujiwara, Yasusei Kudo and Kazumi Ozaki : Porphyromonas gingivalis outer membrane vesicles in cerebral ventricles activate microglia in mice, Oral Diseases, Vol.29, No.8, 3688-3697, 2023. (Tokushima University Institutional Repository) ● Metadata: 118518 (Link to Publication Site) ● Publication site (DOI): 10.1111/odi.14413 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36266256 ● Search Scopus @ Elsevier (PMID): 36266256 ● Search Scopus @ Elsevier (DOI): 10.1111/odi.14413 (Tokushima University Institutional Repository: 118518, DOI: 10.1111/odi.14413, PubMed: 36266256)
3.	Jun-ichi Kido, Yuka Hiroshima, Rie Kido, Kaya Yoshida, Yuji Inagaki, Koji Naruishi, Kazuaki Kajimoto, Masatoshi Kataoka, Yasuo Shinohara and Hiromichi Yumoto : Lipocalin 2, synthesized using a cell-free protein synthesis system and encapsulated into liposomes, inhibits the adhesion of Porphyromonas gingivalis to human oral epithelial cells., Journal of Periodontal Research, Vol.58, No.2, 262-273, 2023. (Tokushima University Institutional Repository) ● Metadata: 119199 (Link to Publication Site) ● Publication site (DOI): 10.1111/jre.13088 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36579753 ● Search Scopus @ Elsevier (PMID): 36579753 ● Search Scopus @ Elsevier (DOI): 10.1111/jre.13088 (Tokushima University Institutional Repository: 119199, DOI: 10.1111/jre.13088, PubMed: 36579753)
4.	Hiroshi Ito, Yukihiro Numabe, Shuichi Hashimoto, Satoshi Sekino, Etsuko Murakashi, Hitomi Ishiguro, Daisuke Sasaki, Takashi Yaegashi, Hideki Takai, Masaru Mezawa, Yorimasa Ogata, Hisashi Watanabe, Yuichi Izumi, Jun-ichi Kido, Yuka Hiroshima and Toshihiko Nagata : Utility of a haemoglobin test of gingival crevicular fluid: A multicentre, observational study., Oral Diseases, 2023. (Link to Publication Site) ● Publication site (DOI): 10.1111/odi.14536 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36790046 ● Search Scopus @ Elsevier (PMID): 36790046 ● Search Scopus @ Elsevier (DOI): 10.1111/odi.14536 (DOI: 10.1111/odi.14536, PubMed: 36790046)
5.	Yasufumi Nishikawa, Yoritoki Tomotake, Hiromichi Kawano, Koji Naruishi, Jun-ichi Kido, Yuka Hiroshima, Akikazu Murakami, Tetsuo Ichikawa and Hiromichi Yumoto : Effects of Candidalysin Derived from Candida albicans on the Expression of Pro-Inflammatory Mediators in Human Gingival Fibroblasts, International Journal of Molecular Sciences, Vol.24, No.4, 3256, 2023. (Tokushima University Institutional Repository) ● Metadata: 118834 (Link to Publication Site) ● Publication site (DOI): 10.3390/ijms24043256 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36834667 ● Search Scopus @ Elsevier (PMID): 36834667 ● Search Scopus @ Elsevier (DOI): 10.3390/ijms24043256 (Tokushima University Institutional Repository: 118834, DOI: 10.3390/ijms24043256, PubMed: 36834667)
6.	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)
7.	Yuta Uemura, Yuka Hiroshima, Ayano Tada, Keiji Murakami, Kaya Yoshida, Yuji Inagaki, Tomomi Kuwahara, Akikazu Murakami, Hideki Fujii and Hiromichi Yumoto : Porphyromonas gingivalis Outer Membrane Vesicles Stimulate Gingival Epithelial Cells to Induce Pro-Inflammatory Cytokines via the MAPK and STING Pathways, Biomedicines, Vol.10, No.10, 2643, 2022. (Summary) () is a keystone pathogen associated with chronic periodontitis and produces outer membrane vesicles (OMVs) that contain lipopolysaccharide (LPS), gingipains, and pathogen-derived DNA and RNA. -OMVs are involved in the pathogenesis of periodontitis. -OMV-activated pathways that induce the production of the pro-inflammatory cytokines, interleukin (IL)-6, and IL-8 in the human gingival epithelial cell line, OBA-9, were investigated. The role of mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-κB in levels of -OMV-induced pro-inflammatory cytokines was investigated using Western blot analysis and specific pathway inhibitors. -OMVs induced IL-6 and IL-8 production via the extracellular signal-regulated kinase (Erk) 1/2, c-Jun N-terminal kinase (JNK), p38 MAPK, and NF-κB signaling pathways in OBA-9 cells. In addition, the stimulator of interferon genes (STING), an essential innate immune signaling molecule, was triggered by a cytosolic pathogen DNA. -OMV-induced IL-6 and IL-8 mRNA expression and production were significantly suppressed by STING-specific small interfering RNA. Taken together, these results demonstrated that -OMV-activated Erk1/2, JNK, p38 MAPK, STING, and NF-κB signaling pathways resulting in increased IL-6 and IL-8 expression in human gingival epithelial cells. These results suggest that -OMVs may play important roles in periodontitis exacerbation by stimulating various pathways. (Tokushima University Institutional Repository) ● Metadata: 117616 (Link to Publication Site) ● Publication site (DOI): 10.3390/biomedicines10102643 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36289904 ● Search Scopus @ Elsevier (PMID): 36289904 ● Search Scopus @ Elsevier (DOI): 10.3390/biomedicines10102643 (Tokushima University Institutional Repository: 117616, DOI: 10.3390/biomedicines10102643, PubMed: 36289904)
8.	Muhammad Reza Pahlevi, Keiji Murakami, Yuka Hiroshima, Akikazu Murakami and Hideki Fujii : pruR and PA0065 Genes Are Responsible for Decreasing Antibiotic Tolerance by Autoinducer Analog-1 (AIA-1) in Pseudomonas aeruginosa, Antibiotics, Vol.11, No.6, 773, 2022. (Tokushima University Institutional Repository) ● Metadata: 117279 (Link to Publication Site) ● Publication site (DOI): 10.3390/antibiotics11060773 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35740179 ● Search Scopus @ Elsevier (PMID): 35740179 ● Search Scopus @ Elsevier (DOI): 10.3390/antibiotics11060773 (Tokushima University Institutional Repository: 117279, DOI: 10.3390/antibiotics11060773, PubMed: 35740179)
9.	Mizuki Abe, Keiji Murakami, Yuka Hiroshima, Takashi Amoh, Mayu Sebe, Keiko Kataoka and Hideki Fujii : Autoinducer Analogs Can Provide Bactericidal Activity to Macrolides in Pseudomonas aeruginosa through Antibiotic Tolerance Reduction, Antibiotics, Vol.11, No.1, 2021. (Summary) Macrolide antibiotics are used in treating chronic biofilm infections despite their unsatisfactory antibacterial activity, because they display several special activities, such as modulation of the bacterial quorum sensing and immunomodulatory effects on the host. In this study, we investigated the effects of the newly synthesized quorum-sensing autoinducer analogs (AIA-1, -2) on the activity of azithromycin and clarithromycin against . In the killing assay of planktonic cells, AIA-1 and -2 enhanced the bactericidal ability of macrolides against PAO1; however, they did not affect the minimum inhibitory concentrations of macrolides. In addition, AIA-1 and -2 considerably improved the killing activity of azithromycin and clarithromycin in biofilm cells. The results indicated that AIA-1 and -2 could affect antibiotic tolerance. Moreover, the results of hydrocarbon adherence and cell membrane permeability assays suggested that AIA-1 and -2 changed bacterial cell surface hydrophobicity and accelerated the outer membrane permeability of the hydrophobic antibiotics such as azithromycin and clarithromycin. Our study demonstrated that the new combination therapy of macrolides and AIA-1 and -2 may improve the therapeutic efficacy of macrolides in the treatment of chronic biofilm infections. (Tokushima University Institutional Repository) ● Metadata: 117210 (Link to Publication Site) ● Publication site (DOI): 10.3390/antibiotics11010010 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35052885 ● Summary page in Scopus @ Elsevier: 2-s2.0-85121669540 (Tokushima University Institutional Repository: 117210, DOI: 10.3390/antibiotics11010010, PubMed: 35052885, Elsevier: Scopus)
10.	Rie Kido, Yuka Hiroshima, Jun-ichi Kido, Takahisa Ikuta, Eijiro Sakamoto, Yuji Inagaki, Koji Naruishi and Hiromichi Yumoto : Advanced glycation end-products increase lipocalin 2 expression in human oral epithelial cells., Journal of Periodontal Research, Vol.55, No.4, 539-550, 2020. (Tokushima University Institutional Repository) ● Metadata: 114681 (Link to Publication Site) ● Publication site (DOI): 10.1111/jre.12741 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32170733 ● Summary page in Scopus @ Elsevier: 2-s2.0-85081730917 (Tokushima University Institutional Repository: 114681, DOI: 10.1111/jre.12741, PubMed: 32170733, Elsevier: Scopus)
11.	Ryosuke Takagi, Eijiro Sakamoto, Jun-ichi Kido, Yuji Inagaki, Yuka Hiroshima, Koji Naruishi and Hiromichi Yumoto : S100A9 Increases IL-6 and RANKL Expressions through MAPKs and STAT3 Signaling Pathways in Osteocyte-Like Cells., BioMed Research International, Vol.2020, No.7149408, 2020. (Tokushima University Institutional Repository) ● Metadata: 114641 (Link to Publication Site) ● Publication site (DOI): 10.1155/2020/7149408 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32149126 ● Search Scopus @ Elsevier (PMID): 32149126 ● Search Scopus @ Elsevier (DOI): 10.1155/2020/7149408 (Tokushima University Institutional Repository: 114641, DOI: 10.1155/2020/7149408, PubMed: 32149126)
12.	Takenori Yamamoto, Mizune Ozono, Akira Watanabe, Kosuke Maeda, Atsushi Nara, Mei Hashida, Yusuke Ido, Yuka Hiroshima, Akiko Yamada, Hiroshi Terada and Yasuo Shinohara : Functional analysis of coiled-coil domains of MCU in mitochondrial calcium uptake, Biochimica et Biophysica Acta (BBA) - Bioenergetics, 148061, 2019. (Summary) The mitochondrial calcium uniporter (MCU) complex is a highly-selective calcium channel. This complex consists of MCU, mitochondrial calcium uptake proteins (MICUs), MCU regulator 1 (MCUR1), essential MCU regulator element (EMRE), etc. MCU, which is the pore-forming subunit, has 2 highly conserved coiled-coil domains (CC1 and CC2); however, their functional roles are unknown. The yeast expression system of mammalian MCU and EMRE enables precise reconstitution of the properties of the mammalian MCU complex in yeast mitochondria. Using the yeast expression system, we here showed that, when MCU mutant lacking CC1 or CC2 was expressed together with EMRE in yeast, their mitochondrial Ca-uptake function was lost. Additionally, point mutations in CC1 or CC2, which were expected to prevent the formation of the coiled coil, also disrupted the Ca-uptake function. Thus, it is essential for the Ca uptake function of MCU that the coiled-coil structure be formed in CC1 and CC2. The loss of function of those mutated MCUs was also observed in the mitochondria of a yeast strain lacking the yeast MCUR1 homolog. Also, in the D. discoideum MCU, which has EMRE-independent Ca-uptake function, the deletion of either CC1 or CC2 caused the loss of function. These results indicated that the critical functions of CC1 and CC2 were independent of other regulatory subunits such as MCUR1 and EMRE, suggesting that CC1 and CC2 might be essential for pore formation by MCUs themselves. Based on the tetrameric structure of MCU, we discussed the functional roles of the coiled-coil domains of MCU. (Keyword) calcium / ion channel / mitochondria / coiled-coil motif / yeast (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbabio.2019.148061 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31394096 ● Search Scopus @ Elsevier (PMID): 31394096 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbabio.2019.148061 (DOI: 10.1016/j.bbabio.2019.148061, PubMed: 31394096)
13.	Takenori Yamamoto, Moe Tsunoda, Mizune Ozono, Akira Watanabe, Kazumasa Kotake, Yuka Hiroshima, Akiko Yamada, Hiroshi Terada and Yasuo Shinohara : Polyethyleneimine renders mitochondrial membranes permeable by interacting with negatively charged phospholipids in them, Archives of Biochemistry and Biophysics, 2018. (Summary) Polyethyleneimines (PEIs) are used for transfection of cells with nucleic acids. Meanwhile, the interaction of PEI with mitochondria causes cytochrome c release prior to apoptosis; the mechanisms how PEI causes this permeabilization of mitochondrial membranes and the release of cytochrome c remain unclear. To clarify these mechanisms, we examined the effects of branched-type PEI and linear-type PEI, each of which was 25 kDa in size, on mitochondria. The permeabilization potency of mitochondrial membranes by branched PEI was stronger than that by linear PEI. The permeabilization by PEIs were insensitive to permeability-transition inhibitors, indicating that PEI-induced permeabilization was not attributed to permeability transition. Meanwhile, PEIs caused permeabilization of artificial lipid vesicles; again, the permeabilization potency of branched PEI was stronger than that of linear PEI. Such a difference in this potency was close to that in the case of isolated mitochondria, signifying that the PEI-induced permeabilization of mitochondrial membranes could be attributed to PEI's interaction with the phospholipid phase. Furthermore, this PEI-induced permeabilization of the lipid vesicles was observed only in the case of lipid vesicles including negatively charged phospholipids. These results indicate that PEIs interacted with negatively charged phospholipids in the mitochondrial membranes to directly lead to their permeabilization. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.abb.2018.06.003 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29886045 ● Search Scopus @ Elsevier (PMID): 29886045 ● Search Scopus @ Elsevier (DOI): 10.1016/j.abb.2018.06.003 (DOI: 10.1016/j.abb.2018.06.003, PubMed: 29886045)
14.	Satoshi Fujita, Masaki Suyama, Kenji Matsumoto, Atsushi Yamamoto, Takenori Yamamoto, Yuka Hiroshima, Takayuki Iwata, Arihiro Kano, Yasuo Shinohara and Mitsuru Shindo : Synthesis and evaluation of simplified functionalized bongkrekic acid analogs., Tetrahedron, Vol.74, No.9, 962-969, 2018. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.tet.2018.01.018 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-85041348582 (DOI: 10.1016/j.tet.2018.01.018, Elsevier: Scopus)
15.	Yuka Hiroshima, Takenori Yamamoto, Masahiro Watanabe, Yoshinobu Baba and Yasuo Shinohara : Effects of cold exposure on metabolites in brown adipose tissue of rats., Molecular Genetics and Metabolism Reports, Vol.15, 36-42, 2018. (Summary) Brown adipose tissue (BAT) plays an important role in regulation of energy expenditure while adapting to a cold environment. BAT thermogenesis depends on uncoupling protein 1 (UCP1), which is expressed in the inner mitochondrial membranes of BAT. Gene expression profiles induced by cold exposure in BAT have been studied, but the metabolomic biological pathway that contributes to the activation of thermogenesis in BAT remains unclear. In this study, we comprehensively compared the relative levels of metabolites between the BAT of rats kept at room temperature (22 °C) and of those exposed to a cold temperature (4 °C) for 48 h using capillary electrophoresis (CE) time-of-flight mass spectrometry (TOFMS) and liquid chromatography (LC)-TOFMS. We identified 218 metabolites (137 cations and 81 anions) by CE-TOFMS and detected 81 metabolites (47 positive and 34 negative) by LC-TOFMS in BAT. We found that cold exposure highly influenced the BAT metabolome. We showed that the cold environment lead to lower levels of glycolysis and gluconeogenesis intermediates and higher levels of the tricarboxylic acid (TCA) cycle metabolites, fatty acids, and acyl-carnitine metabolites than control conditions in the BAT of rats. These results indicate that glycolysis and β-oxidation of fatty acids in BAT are positive biological pathways that contribute to the activation of thermogenesis by cold exposure, thereby facilitating the generation of heat by UCP1. These data provide useful information for understanding the basal metabolic functions of BAT thermogenesis in rats in response to cold exposure. (Tokushima University Institutional Repository) ● Metadata: 115598 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ymgmr.2018.01.005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30023288 ● Search Scopus @ Elsevier (PMID): 30023288 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ymgmr.2018.01.005 (Tokushima University Institutional Repository: 115598, DOI: 10.1016/j.ymgmr.2018.01.005, PubMed: 30023288)
16.	Yuka Hiroshima, Eijiro Sakamoto, Kaya Yoshida, Kaori Abe, Koji Naruishi, Takenori Yamamoto, Yasuo Shinohara, Jun-ichi Kido and Carolyn L Geczy : Advanced glycation end-products and Porphyromonas gingivalis lipopolysaccharide increase calprotectin expression in human gingival epithelial cells., Journal of Cellular Biochemistry, Vol.119, No.2, 1591-1603, 2018. (Summary) Accumulation of advanced glycation end-products (AGEs) in periodontal tissues of patients with diabetes mellitus aggravates periodontitis, but the mechanisms are unknown. Calprotectin, a heterocomplex of S100A8 and S100A9 proteins, is a constitutive cytoplasmic component of healthy gingival epithelial cells. This study aimed at investigating the effects of AGE and Porphyromonas gingivalis lipopolysaccharide (PgLPS) on calprotectin expression in the human gingival epithelial cell line OBA-9. AGE and PgLPS increased the expression of S100A8 and S100A9 mRNAs, and AGE + PgLPS co-stimulation amplified their expression in OBA-9 cells. A higher concentration of calprotectin in cell lysates was also induced by stimulation with AGE and/or PgLPS. S100A8 was mainly translocated from the nucleus to the cytoplasm by AGE stimulation, while cytoplasmic localization of S100A9 was not altered following stimulation with AGE and/or PgLPS. Calprotectin was found in the cytoplasm of BSA-treated cells, but cytoplasmic and nuclear localization was observed following stimulation with AGE and/or PgLPS. AGE-induced S100A8, and S100A9 mRNA expression was partially suppressed by RAGE-specific siRNA. In contrast, PgLPS-induced S100A8 and S100A9 mRNA expression was strongly suppressed by TLR2-specific siRNA. Furthermore, the inhibition of p38, JNK MAPK, and NF-κB attenuated AGE- and PgLPS-induced S100A8 and S100A9 mRNA expression. Taken together, these results demonstrate that AGE acts in synergy with PgLPS to stimulate RAGE and TLR2 expression and activate p38, JNK MAPK, and NF-κB signaling pathways, resulting in increased activation of calprotectin (S100A8/S100A9) in human gingival epithelial cells. Our results suggest that calprotectin may be involved in the pathogenesis of diabetic periodontitis. This article is protected by copyright. All rights reserved. (Tokushima University Institutional Repository) ● Metadata: 119200 (Link to Publication Site) ● Publication site (DOI): 10.1002/jcb.26319 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28771806 ● Search Scopus @ Elsevier (PMID): 28771806 ● Search Scopus @ Elsevier (DOI): 10.1002/jcb.26319 (Tokushima University Institutional Repository: 119200, DOI: 10.1002/jcb.26319, PubMed: 28771806)
17.	Kaya Yoshida, Hirohiko Okamura, Yuka Hiroshima, Kaori Abe, Jun-ichi Kido, Yasuo Shinohara and Kazumi Ozaki : PKR induces the expression of NLRP3 by regulating the NF-κB pathway in Porphyromonas gingivalis-infected osteoblasts, Experimental Cell Research, Vol.354, No.1, 57-64, 2017. (Summary) The double-stranded RNA-dependent kinase (PKR), which is activated by double stranded RNA, induces inflammation by regulating NF-κB signaling. The NLR family pyrin domain-containing 3 (NLRP3) inflammasome also modulates inflammation in response to infection. Porphyromonas gingivalis (P.gingivalis) is an oral bacterium which is implicated in the pathogenesis of periodontal diseases. We previously reported that PKR is a key modulator of bone metabolism and inflammation in the periodontal tissue. PKR was also reported to induce inflammation in response to microbes by regulating the NLRP3 inflammasome, suggesting that PKR could affect inflammation along with NLRP3 in periodontal diseases. In this study, we investigated the effects of PKR on NLRP3 expression and NF-κB activity in P. gingivalis infected osteoblasts. We first constructed a SNAP26b-tagged P.gingivalis (SNAP-P. g.) and traced its internalization into the cell. SNAP-P. g. increased the activity of PKR and NF-κB and also induced NLRP3 expression in osteoblasts. Inhibition of NF-κB attenuated SNAP-P. g.-induced NLRP3 expression. The knockdown of PKR using shRNA decreased both the activity of NF-κB and the expression of NLRP3 induced by SNAP-P.g.. We therefore concluded that in osteoblasts, P. gingivalis activated PKR, which in turn increased NLRP3 expression by activating NF-κB. Our results suggest that PKR modulates inflammation by regulating the expression of the NLRP3 inflammasome through the NF-κB pathway in periodontal diseases. (Keyword) 3T3 Cells / Animals / Gene Expression Regulation / Humans / Inflammasomes / Inflammation / Mice / NF-kappa B / NLR Family, Pyrin Domain-Containing 3 Protein / Osteoblasts / Periodontal Pocket / Porphyromonas gingivalis / Receptors, G-Protein-Coupled / Signal Transduction / Transcription Factor RelA (Tokushima University Institutional Repository) ● Metadata: 111349 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.yexcr.2017.03.028 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28341446 ● Search Scopus @ Elsevier (PMID): 28341446 ● Search Scopus @ Elsevier (DOI): 10.1016/j.yexcr.2017.03.028 (Tokushima University Institutional Repository: 111349, DOI: 10.1016/j.yexcr.2017.03.028, PubMed: 28341446)
18.	Yuka Hiroshima, Kenneth Hsu, Nicodemus Tedla, Sze Wing Wong, Sharron Chow, Naomi Kawaguchi and Carolyn L Geczy : S100A8/A9 and S100A9 reduce acute lung injury., Immunology and Cell Biology, Vol.95, No.5, 461-472, 2017. (Summary) S100A8 and S100A9 are myeloid cell-derived proteins that are elevated in several types of inflammatory lung disorders. Pro- and anti-inflammatory properties are reported and these proteins are proposed to activate TLR4. S100A8 and S100A9 can function separately, likely through distinct receptors but a systematic comparison of their effects in vivo are limited. Here we assess inflammation in murine lung following S100A9 and S100A8/A9 inhalation. Unlike S100A8, S100A9 promoted mild neutrophil and lymphocyte influx, possibly mediated in part, by increased mast cell degranulation and selective upregulation of some chemokine genes, particularly CXCL-10. S100 proteins did not significantly induce proinflammatory mediators including TNF-, IL-1, IL-6 or serum amyloid A3 (SAA3). In contrast to S100A8, neither preparation induced S100A8 or IL-10 mRNA/protein in airway epithelial cells, or in tracheal epithelial cells in vitro. Like S100A8, S100A9 and S100A8/A9 reduced neutrophil influx in acute lung injury (ALI) provoked by LPS challenge but were somewhat less inhibitory, possibly because of differential effects on expression of some chemokines, IL-1, SAA3 and IL-10. Novel common pathways including increased induction of an NAD(+)-dependent protein deacetylase sirtuin-1 (SIRT1) that may reduce NF-B signalling, and increased STAT3 activation may reduce LPS activation. Results suggest a role for these proteins in normal homeostasis and protective mechanisms in the lung.Immunology and Cell Biology accepted article preview online, 11 January 2017. doi:10.1038/icb.2017.2. (Tokushima University Institutional Repository) ● Metadata: 115146 (Link to Publication Site) ● Publication site (DOI): 10.1038/icb.2017.2 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28074060 ● Search Scopus @ Elsevier (PMID): 28074060 ● Search Scopus @ Elsevier (DOI): 10.1038/icb.2017.2 (Tokushima University Institutional Repository: 115146, DOI: 10.1038/icb.2017.2, PubMed: 28074060)
19.	Hiroshi Ito, Yukihiro Numabe, Shuichi Hashimoto, Satoshi Sekino, Etsuko Murakashi, Hitomi Ishiguro, Daisuke Sasaki, Takashi Yaegashi, Hideki Takai, Masaru Mezawa, Yorimasa Ogata, Hisashi Watanabe, Satsuki Hagiwara, Yuichi Izumi, Yuka Hiroshima, Jun-ichi Kido, Toshihiko Nagata and Kazushi Kunimatsu : Correlation Between Gingival Crevicular Fluid Hemoglobin Content and Periodontal Clinical Parameters., Journal of Periodontology, Vol.87, No.11, 1314-1319, 2016. (Summary) Hb was observed in more than 60% of GCF samples in BOP(-) gingival sulci in both periodontally stable and periodontal-management-required groups. These results suggest inspection of Hb derived from microbleeding in gingival sulci may serve as an index for preclinical diagnosis. (Link to Publication Site) ● Publication site (DOI): 10.1902/jop.2016.160092 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27468797 ● Search Scopus @ Elsevier (PMID): 27468797 ● Search Scopus @ Elsevier (DOI): 10.1902/jop.2016.160092 (DOI: 10.1902/jop.2016.160092, PubMed: 27468797)
20.	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)
21.	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)
22.	Yuka Hiroshima, Linda Garthwaite, Kenneth Hsu, Hyouna Yoo, Sang-Ho Park, L Carolyn Geczy, K Rakesh Kumar and Cristan Herbert : ISU201 enhances the resolution of airway inflammation in a mouse model of an acute exacerbation of asthma., Mediators of Inflammation, Vol.2015, 405629, 2015. (Summary) Glucocorticoids are commonly used for treating asthma and its exacerbations but have well-recognised adverse effects and are not always effective. Few alternative treatments exist. Using a murine model of an acute exacerbation of asthma, we assessed the ability of ISU201, a novel protein drug, to suppress the inflammatory response when administered after induction of an exacerbation. Sensitised mice were chronically challenged with a low mass concentration of aerosolised ovalbumin, and then received a single moderate-level challenge to simulate an allergen-induced exacerbation. ISU201 was administered to mice 2 and 8 hours later, while pulmonary inflammation and expression of mRNA for chemokines and proinflammatory cytokines were assessed after 4, 12, and 24 hours. Relative to vehicle-treated controls, ISU201 suppressed accumulation of pulmonary neutrophils and eosinophils, while accelerating the decline in CXCL1, TNF-, and IL-6 in lavage fluid and lung tissue. ISU201 significantly reduced peak expression of mRNA for the chemokines Cxcl9 and Cxcl10, the adhesion molecules Icam1 and Vcam1, and the proinflammatory cytokines Il1b, Il12p40, and Csf1. The ability of ISU201 to promote resolution of inflammation suggests that it may have potential as an alternative to glucocorticoids in the management of asthma, including when administered after the onset of an acute exacerbation. (Link to Publication Site) ● Publication site (DOI): 10.1155/2015/405629 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25767333 ● Summary page in Scopus @ Elsevier: 2-s2.0-84924215816 (DOI: 10.1155/2015/405629, PubMed: 25767333, Elsevier: Scopus)
23.	Javkhlan Purevjav, Xu Guangfei, Chen Gang, Chenjuan Yao, Yuka Hiroshima, Hiroshi Yoshimura, Toshihiko Nagata and Kazuo Hosoi : Expression and LPS-Induced Elevation of Nod2 and Calprotectin in the Submandibular Gland of Wild-Type and TLR4-Knockout Male Mice, Journal of Research and Practice in Dentistry, Vol.2015, No.290259, 2015. (Link to Publication Site) ● Publication site (DOI): 10.5171/2015.290259 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.5171/2015.290259 (DOI: 10.5171/2015.290259)
24.	Hiroshi Ito, Yukihiro Numabe, Satoshi Sekino, Etsuko Murakashi, Hitomi Iguchi, Shuichi Hashimoto, Daisuke Sasaki, Takashi Yaegashi, Kazushi Kunimatsu, Hideki Takai, Masaru Mezawa, Yorimasa Ogata, Hisashi Watanabe, Satsuki Hagiwara, Yuichi Izumi, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : Evaluation of bleeding on probing and gingival crevicular fluid enzyme activity for detection of periodontally active sites during supportive periodontal therapy, Odontology, Vol.102, No.1, 50-56, 2014. (Summary) This study aimed to analyze the enzyme activity in gingival crevicular fluid (GCF) and its association with clinical parameters, especially bleeding on probing (BOP), and thus reconsider the significance and accuracy of recording BOP. A total of 184 patients who had entered supportive periodontal therapy were selected and GCF was collected from 401 sites before recording the clinical parameters, probing pocket depth (PPD), BOP, clinical attachment level, gingival index and plaque index. The enzyme activity of neutrophil elastase and aspartate aminotransferase and amount of protein in GCF were also analyzed. In the clinical parameters for biochemical data, amount of GCF showed the most correlation. A cut-off value for BOP and PPD were determined by the ROC curve and Youden index. Analysis was performed with all clinical parameters and biochemical data. Of the 401 sites, 51 were less than the cut-off value and were BOP-negative. On the other hand, 29 sites had values more than the cut-off value, with 14 BOP-negative sites and 15 BOP-positive sites. A conclusion is as follows: twenty-nine sites with values more than the cut-off value were diagnosed as sites requiring periodontal management, however, 14 of these were BOP-negative. These results suggest that combining other biochemical tests with examination of BOP and PPD may improve the validity of periodontal disease diagnosis. In future studies, it will be essential to find a marker that can precisely detect periodontal disease activity, and to develop a diagnostic tool for chair-side use. (Keyword) Aged / Female / Gingival Crevicular Fluid / Gingival Hemorrhage / Humans / Male / Middle Aged / Periodontal Pocket / periodontitis (Link to Publication Site) ● Publication site (DOI): 10.1007/s10266-012-0090-1 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23179356 ● Summary page in Scopus @ Elsevier: 2-s2.0-84892874741 (DOI: 10.1007/s10266-012-0090-1, PubMed: 23179356, Elsevier: Scopus)
25.	Yuka Hiroshima, Kenneth Hsu, Nicodemus Tedla, Ming Yuen Chung, Sharron Chow, Cristan Herbert and L Carolyn Geczy : S100A8 induces IL-10 and protects against acute lung injury., The Journal of Immunology, Vol.192, No.6, 2800-2811, 2014. (Summary) S100A8 is considered proinflammatory by activating TLR4 and/or the receptor for advanced glycation end products. The aim was to investigate inflammatory effects of S100A8 in murine lung. S100A8 was administered to BALB/c mice by nasal inhalation and genes induced over a time-course assessed. LPS was introduced intranasally either alone or 2 h after pretreatment of mice with intranasal application of S100A8 or dexamethasone. A Cys(42)-Ala(42) mutant S100A8 mutant was used to assess whether S100A8's effects were via pathways that were dependent on reactive oxygen species. S100A8 induced IL-10 mRNA, and expression was apparent only in airway epithelial cells. Importantly, it suppressed acute lung injury provoked by LPS inhalation by suppressing mast-cell activation and induction of mediators orchestrating leukocyte recruitment, possibly by reducing NF-B activation via an IB/Akt pathway and by downmodulating pathways generating oxidative stress. The Cys(42)-Ala(42) S100A8 mutant did not induce IL-10 and was less immunosuppressive, indicating modulation by scavenging oxidants. S100A8 inhibition of LPS-mediated injury was as potent, and outcomes were remarkably similar to immunosuppression by dexamethasone. We challenge the notion that S100A8 is an agonist for TLR4 or the receptor for advanced glycation end products. S100A8 induced IL-10 in vivo and initiates a feedback loop that attenuates acute lung injury. (Keyword) Acute Lung Injury / Anti-Inflammatory Agents (Link to Publication Site) ● Publication site (DOI): 10.4049/jimmunol.1302556 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24532576 ● Search Scopus @ Elsevier (PMID): 24532576 ● Search Scopus @ Elsevier (DOI): 10.4049/jimmunol.1302556 (DOI: 10.4049/jimmunol.1302556, PubMed: 24532576)
26.	L Carolyn Geczy, Ming Yuen Chung and Yuka Hiroshima : Calgranulins may contribute vascular protection in atherogenesis., Circulation Journal, Vol.78, No.2, 271-280, 2013. (Summary) S100A8, S100A9 and S100A12 are considered proinflammatory mediators of atherosclerosis. Known as calgranulins, they are major components of neutrophils and are upregulated in macrophages and foam cells. They influence leukocyte recruitment, and may propagate inflammation by binding TLR4 and/or receptor for advanced glycation endproducts (RAGE). However, the receptors for calgranulins remain an enigma; we have no evidence for TLR4 or RAGE activation by S100A8 or S100A12. Moreover, gene regulation studies suggest antiinflammatory functions for S100A8 and emerging reports indicate pleiotropic roles. Unlike S100A9, S100A8 effectively scavenges oxidants generated by the myeloperoxidase system in vivo, forming novel thiol modifications. S100A8 is also readily S-nitrosylated, stabilizing nitric oxide and transporting it to hemoglobin. S100A8-SNO reduces leukocyte transmigration in the vasculature. S-glutathionylation of S100A9 modifies its effects on leukocyte adhesion. Both S100A8 forms inhibit mast cell activation, at least partially by scavenging reactive oxygen species required for signaling. Conversely, S100A12 activates and sequesters mast cells. However S100A12 suppresses proinflammatory cytokine induction by SAA-activated monocytes and macrophages, and inhibits matrix metalloprotease activity. We propose that the abundance and types of cells expressing calgranulins in particular microenvironments, their relative concentrations and post-translational modifications may have distinct functional outcomes, including those that are protective, at different stages of atherogenesis. (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-13-1505 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24389598 ● Search Scopus @ Elsevier (PMID): 24389598 ● Search Scopus @ Elsevier (DOI): 10.1253/circj.CJ-13-1505 (DOI: 10.1253/circj.CJ-13-1505, PubMed: 24389598)
27.	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)
28.	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)
29.	Yukiko Nakajima, Yuji Inagaki, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : Advanced glycation end-products enhance calcification in cultured rat dental pulp cells, Journal of Endodontics, Vol.39, 873-878, 2013. (Summary) Amorphous calcification frequently appears in dental pulp tissues of diabetic patients; however, its pathologic process has not been fully elucidated. We previously found that pulp stones and thickened predentin occurred more frequently in diabetic rats. Recent findings demonstrated that accumulation of advanced glycation end-products (AGE) might be involved in vascular calcification complicated with diabetes. The aim of this study was to determine the effect of AGE on calcified nodule formation by rat dental pulp cells in culture. Rat dental pulp cells and gingival fibroblasts were independently cultured with 50 and 100 μg/mL AGE. Alkaline phosphatase activity and calcified nodule formation were measured. Expressions of receptor for AGE, osteopontin (OPN), and osteocalcin (OCN) mRNA were determined by quantitative real-time polymerase chain reaction. Protein levels of OPN and OCN secreted in culture medium were quantified by enzyme-linked immunosorbent assay. AGE (50 and 100 μg/mL) markedly increased both alkaline phosphatase activity and calcified nodule formation in dental pulp cells (P < .01), whereas it did not affect those in gingival fibroblasts. Real-time polymerase chain reaction analysis revealed that AGE increased mRNA expressions of receptor for AGE, OPN, and OCN in dental pulp cells (P < .05). Enzyme-linked immunosorbent assay analysis revealed that the protein levels of OPN and OCN produced by dental pulp cells were higher in AGE-treated than in untreated cells (P < .05). AGE enhanced the calcification potentials of rat dental pulp cells, suggesting that it may stimulate pathologic calcification of diabetic dental pulp tissues. (Keyword) Alkaline Phosphatase / Animals / Cell Culture Techniques / Cells, Cultured / Dental Pulp / Dental Pulp Calcification / Fibroblasts / Gingiva / Glycosylation End Products, Advanced / Male / Osteocalcin / Osteopontin / Rats / Rats, Wistar / Receptors, Immunologic / Time Factors (Link to Publication Site) ● Publication site (DOI): 10.1016/j.joen.2012.11.027 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23791254 ● Summary page in Scopus @ Elsevier: 2-s2.0-84879412695 (DOI: 10.1016/j.joen.2012.11.027, PubMed: 23791254, Elsevier: Scopus)
30.	Chie Wada -Mihara, 徳永格, Hiroyuki Seto, Eijiro Sakamoto, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : Topical injection of osteoprotegerin prevents alveolar bone loss in rat experimental periodontitis, Journal of the Japanese Association of Periodontology, Vol.54, No.2, 167-174, 2012. (Keyword) osteoprotegerin / experimental periodontitis / alveolar bone / osteoclast (Link to Publication Site) ● Publication site (DOI): 10.2329/perio.54.167 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282679391110400 ● Search Scopus @ Elsevier (DOI): 10.2329/perio.54.167 (DOI: 10.2329/perio.54.167, CiNii: 1390282679391110400)
31.	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)
32.	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)
33.	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)
34.	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)
35.	Purevjav Javkhlan, Yuka Hiroshima, Ahmad Azlina, Takahiro Hasegawa, Chenjuan Yao, Tetsuya Akamatsu, Jun-ichi Kido, Toshihiko Nagata and Kazuo Hosoi : Lipopolysaccharide-mediated induction of calprotectin in the submandibular and parotid glands of mice, Inflammation, Vol.34, No.6, 668-680, 2011. (Summary) S100A8 and S100A9 constitute a heterodimeric protein, calprotectin. The mRNAs of S100A8 and S100A9, being expressed at minimal levels in the submandibular and parotid glands (SMG and PG, respectively) of C3H/HeN mice, were induced strongly and transiently by lipopolysaccharide (LPS). Among the mRNAs of members of the S100 protein family examined, those of S100A8 and S100A9 were specifically induced by LPS in the salivary glands. The induction was assumed to be mediated via toll-like receptor 4 (TLR4), since their elevation was limited in C3H/HeJ mice, a TLR4-mutant strain. These proteins became expressed in the granular convoluted tubular cells and striated duct cells in the SMG, and in both acinar and duct cells in the PG (all in the cytoplasm). The salivary calprotectin level was not increased by LPS treatment, implying that elevated calprotectin was not secreted into the saliva and that they may function in microcellular environment of the salivary gland. (Keyword) Animals / Calgranulin A / Calgranulin B / Leukocyte L1 Antigen Complex / Lipopolysaccharides / Mice / Parotid Gland / RNA, Messenger / Salivary Glands / Submandibular Gland / Transcriptional Activation (Link to Publication Site) ● Publication site (DOI): 10.1007/s10753-010-9277-1 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21125321 ● Search Scopus @ Elsevier (PMID): 21125321 ● Search Scopus @ Elsevier (DOI): 10.1007/s10753-010-9277-1 (DOI: 10.1007/s10753-010-9277-1, PubMed: 21125321)
36.	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)
37.	Ahmad Azlina, Purevjav Javkhlan, Yuka Hiroshima, Takahiro Hasegawa, Chenjuan Yao, Tetsuya Akamatsu and Kazuo Hosoi : Roles of lysosomal proteolytic systems in AQP5 degradation in the submandibular gland of rats following chorda tympani parasympathetic denervation, American Journal of Physiology, Gastrointestinal and Liver Physiology, Vol.299, No.5, G1106-G1117, 2010. (Summary) Chorda tympani denervation (CTD) of rats was earlier shown to result in loss of submandibular gland (SMG) weight (at only 1 wk) and in continued reduction in aquaporin 5 (AQP5) protein expression (until 4 wk), without affecting its mRNA synthesis (Li X, Azlina A, Karabasil MR, Purwanti N, Hasegawa T, Yao C, Akamatsu T, Hosoi K. Am J Physiol Gastrointest Liver Physiol 295: G112-G123, 2008). The present study indicated that despite elevation of bax, a proapoptosis protein, by CTD, the operation also increased the level of bcl-2, an antiapoptosis protein, in the SMG. Terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL assay) showed no increase in the number of apoptotic cells in the SMG. CTD, however, induced strongly and transiently (at 1-3 days) the protein expression of LC3B-II, a marker protein of autophagosomes, suggesting that the reduction in the gland weight was due to onset of autophagy by CTD. Upon CTD, Lamp2, a lysosomal marker, gradually increased in amount, reaching a peak at the 14th day. Immunohistochemical analysis revealed an increase in the number of lysosome-like structures positive for both AQP5 and Lamp2 in the acinar cells of the SMG after CTD; similar changes were observed also for AQP5 and LC3Bs. These data suggest that AQP5 in the SMG entered autophagosomes and/or lysosomes for degradation upon CTD. In vitro AQP5-degrading activity was found in the SMG extracts, and such activity was shown to be increased by CTD. Inhibitor experiments implied cathepsins B and L to be candidate enzymes for this degradation under normal and CTD conditions, respectively. (Keyword) Animals / Apoptosis / Aquaporin 5 / Blotting, Western / Chorda Tympani Nerve / Immunohistochemistry / In Situ Nick-End Labeling / Lysosomal-Associated Membrane Protein 2 / Lysosomes / Male / Parasympathectomy / Proto-Oncogene Proteins c-bcl-2 / Rats / Rats, Sprague-Dawley / Submandibular Gland (Link to Publication Site) ● Publication site (DOI): 10.1152/ajpgi.00194.2010 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20689061 ● Search Scopus @ Elsevier (PMID): 20689061 ● Search Scopus @ Elsevier (DOI): 10.1152/ajpgi.00194.2010 (DOI: 10.1152/ajpgi.00194.2010, PubMed: 20689061)
38.	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)
39.	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)
40.	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)
41.	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)
42.	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)
43.	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)
44.	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)

Review, Commentary:

1.	Eijiro Sakamoto, Yuka Hiroshima, Jun-ichi Kido, Yasufumi Nishikawa, Koji Naruishi, Rie Kido and Hiromichi Yumoto : Various roles of calprotectin in periodontal disease and its possibility as a diagnostic marker for periodontal disease, Journal of the Japanese Association of Periodontology, Vol.62, No.4, 193-199, Dec. 2020. (Keyword) calprotectin / antimicrobial peptide / periodontal disease / DAMPs / diagnostic marker for periodontal disease (Link to Publication Site) ● Publication site (DOI): 10.2329/perio.62.193 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1391975831222787968 ● Search Scopus @ Elsevier (DOI): 10.2329/perio.62.193 (DOI: 10.2329/perio.62.193, CiNii: 1391975831222787968)

Proceeding of International Conference:

1.	E Sakamoto, Chie Wada -Mihara, K Tokunaga, H Seto and Yuka Hiroshima : Topical application of osteoprotegerin inhibits alveolar bone loss in rat experimental periodontitis, International Joint Symposium on Oral Science, Bali, Indonesia, Dec 17-19, 2010,
2.	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,
3.	Fenwick Jemma, Tedla Nicodemus, Raftery Mark, Zhong Ling, Yuka Hiroshima, Geczy Carolyn and Passam Freda : Investigating the role of platelet chemokines in the development of acute lung injury, Blood 2023, 123, Melbourne, Nov. 2023.
4.	Yuka Hiroshima, Eijiro Sakamoto, Kaori Abe, Kaya Yoshida, Koji Naruishi, Toshihiko Nagata, Yasuo Shinohara, Geczy Carolyn and Jun-ichi Kido : Advanced Glycation End-Products Increase Calprotectin in Human Gingival Epithelial Cells, The 95th General Session & Exhibition of the International Association for Dental Research (IADR), San Francisco, Mar. 2017.
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.	Yukiko Nakajima, Yuji Inagaki, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : AGE induces calcification and inflammatory factors in dental pulp tissues, 91th General Session & Exhibition of the International Accociation for Dental Research, Seattle, USA, May 2013.
9.	Yukiko Nakajima, Yuji Inagaki, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : AGE induces calcification- and inflammation-related factors in dental pulp cells, The 60th Annual Meeting of Japanese Association for Dental Research, Program and abstracts of papers, 92, Dec. 2012.
10.	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.
11.	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.
12.	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.
13.	Purevjav Javkhlan, Yuka Hiroshima, Azlina Ahmad, Takahiro Hasegawa, Chenjuan Yao, Tetsuya Akamatsu, Jun-ichi Kido, Toshihiko Nagata and Kazuo Hosoi : Induction of calprotectin mRNAs by lipopolysaccharide in the salivary gland of mice, The Journal of Medical Investigation : JMI, Vol.56, No.Suppl, 287-289, Tokushima, Dec. 2009. (Summary) Calprotectin is a major cytosolic calcium-binding protein of leukocytes which belongs to the S100 protein family. S100A8 and S100A9, major types of calprotectin are heterodimeric complexes being composed of light- and heavy-chain subunits. The calprotectin levels in the plasma, feces, synovial fluid, gingival crevicular fluid, dental calculus and saliva change when the host animal suffers from several inflammatory diseases. Members of Toll-like receptor (TLR) family are pattern-recognition receptors for lipopolysaccharide (LPS) and other pathogens. Here we examined if the biological role of TLR receptor is reflected to the calprotectin expression in the salivary gland. Time course study by using real-time RT-PCR detected higher levels of S100A8 and S100A9 mRNA at 1.5-3 h after injection of LPS in both the submandibular gland (SMG) and parotid gland (PG) of C3H/HeN mice but not in the same tissues of C3H/HeJ, a TLR-4 mutant strain, indicating that this induction is mediated via the TLR-4. These results indicate that, an inflammatory marker, calprotectin, is expressed in the mouse salivary gland and that LPS stimulated its synthesis. Calprotectin (S100A8/A9) showed minimum expression in all cellular segments in the SMG except excretory duct cells, which showed strong signal at the cytoplasm. LPS induced their expressions in the granular convoluted tubular cells and striated duct cells. In the PG, these proteins were expressed very weakly in both duct and acinar cells with a little stronger staining for the former cells. LPS injection induced calprotectin (S100A8/A9) in both duct and acinar cells especially in the former cells. (Keyword) Animals / Calgranulin A / Calgranulin B / Leukocyte L1 Antigen Complex / Lipopolysaccharides / Mice / Mice, Inbred C3H / Mice, Mutant Strains / Parotid Gland / RNA, Messenger / salivary glands / Submandibular Gland / Toll-Like Receptor 4 (Tokushima University Institutional Repository) ● Metadata: 111354 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.56.287 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20224205 ● Search Scopus @ Elsevier (PMID): 20224205 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.56.287 (Tokushima University Institutional Repository: 111354, DOI: 10.2152/jmi.56.287, PubMed: 20224205)

Proceeding of Domestic Conference:

1.	Rie Kido, Yuka Hiroshima, Jun-ichi Kido, Kaya Yoshida, Takahisa Ikuta and Hiromichi Yumoto : Antimicrobial activity of artificially synthesized secretory leukocyte protease inhibitor and its encapsulation into liposomes, 第66回春季日本歯周病学会学術大会, May 2023.
2.	Yuka Hiroshima : Porphyromonas gingivalis由来メンブレンベシクルが歯周組織に及ぼす影響, ダイバーシティ推進研究交流発表会オンライン2022, Mar. 2023.
3.	西松佳苗, 清水日向, 中村大輔, 植村勇太, Yuji Inagaki, Yuka Hiroshima, Jun-ichi Kido, Akikazu Murakami and Hiromichi Yumoto : Porphyromonas gingivalis由来OMVsは破骨細胞の分化と歯槽骨吸収に関与する, 四国歯学会第61回例会, Mar. 2023.
4.	仲村大輔, 植村勇太, Yuka Hiroshima, Keiji Murakami, Akikazu Murakami and Hiromichi Yumoto : Porphyromonas gingivalis 由来OMVsは破骨細胞の分化と歯槽骨吸収に関与する, 第75回日本細菌学会中国・四国支部総会(岡山・WEB), Oct. 2022.
5.	植村勇太, Yuji Inagaki, Yuka Hiroshima, 仲村大輔, Jun-ichi Kido and Hiromichi Yumoto : Porphyromonas gingivalis由来OMVs (Outer Membrane Vesicles)は破骨細胞の分化に関与する, 第65回秋季日本歯周病学会学術大会, Sep. 2022.
6.	Jun-ichi Kido, Yuka Hiroshima, Rie Kido, Kaya Yoshida, Yuji Inagaki, Koji Naruishi and Hiromichi Yumoto : 人工合成したβ-defensin 2によるPorphyromonas gingivalisの付着抑制およびリポソーム封入と口腔上皮細胞への送達, 四国歯学会第60回例会, Jun. 2022.
7.	Jun-ichi Kido, Yuka Hiroshima, Rie Kido, Kaya Yoshida, Yuji Inagaki, Koji Naruishi and Hiromichi Yumoto : 人工合成したbeta-defensin 2によるPorphyromonas gingivalisの付着抑制およびリポソーム封入と口腔上皮細胞への送達, 第65回春季日本歯周病学会学術大会, Jun. 2022.
8.	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.
9.	SATOH Tomomi, Yuka Hiroshima, Akikazu Murakami, Hideki Fujii, Akiko Sakurai, Keiko Kataoka and Keiji Murakami : カタラーゼをコードするkatA/katB遺伝子が及ぼす緑膿菌の抗菌薬抵抗性における影響, 第45回徳島県医学検査学会, Dec. 2021.
10.	Yuta Uemura, Yuka Hiroshima, 村上圭史, Yuji Inagaki, Hideki Fujii and Hiromichi Yumoto : Porphyromonas gingivalis OMVによる歯肉上皮細胞のサイトカイン産生機構, 四国歯学会第58回例会, Nov. 2021.
11.	Yuka Hiroshima, Rie Kido, Jun-ichi Kido, Yuji Inagaki, Koji Naruishi and Hiromichi Yumoto : 人工合成したLopocalin 2はPorphyromonas gingivalisの口腔上皮細胞への付着を抑制する, 第64回秋季日本歯周病学会学術大会, Oct. 2021.
12.	秋月皆人, 植村勇太, Keiji Murakami, Yuka Hiroshima, Hideki Fujii and Hiromichi Yumoto : 歯周病原細菌とその線毛TypeのPCRによる迅速検出システムの有効性の検討, 第74回日本細菌学会中国・四国支部総会, Oct. 2021.
13.	Yuta Uemura, Yuka Hiroshima, Keiji Murakami, 多田彩乃, Tomomi Kuwahara, Hideki Fujii and Hiromichi Yumoto : Porphyromonas gingivalis OMVによる歯肉上皮細胞のサイトカイン産生機構, 第74回日本細菌学会中国・四国支部総会, Oct. 2021.
14.	Yuta Uemura, Yuka Hiroshima, Keiji Murakami, Yuji Inagaki, Hiromichi Yumoto and Hideki Fujii : ヒト歯肉上皮細胞におけるPorphyromonas gingivalis由来メンブレンベシクルの炎症性サイトカイン産生誘導機構の解明, 第19回四国免疫フォーラム, Jun. 2021.
15.	Jun-ichi Kido, Yuka Hiroshima, Rie Kido, Kaya Yoshida, Yuji Inagaki, Koji Naruishi and Hiromichi Yumoto : リポソームに封入したリポカリン2の口腔上皮細胞への送達, 第64回春季日本歯周病学会学術大会, May 2021.
16.	Yuka Hiroshima, Yuta Uemura, Yuji Inagaki, Jun-ichi Kido and Hiromichi Yumoto : ヒト歯肉上皮細胞におけるPorphyromonas gingivalis由来メンブレンベシクルの炎症性サイトカイン産生誘導機構の解明, 第64回春季日本歯周病学会学術大会, May 2021.
17.	Yuka Hiroshima : Porphyromonas gingivalis由来メンブレンベシクルが歯周組織に及ぼす影響, ダイバーシティ推進研究交流発表会 2020, Feb. 2021.
18.	Yuta Uemura, Yuka Hiroshima, Yuji Inagaki and Hiromichi Yumoto : Porphyromonas gingivalis由来メンブレンベシクルがヒト歯肉上皮細胞に及ぼす影響, 日本歯科保存学会2020年度秋季学術大会(第153回), Nov. 2020.
19.	Yuta Uemura, Yuka Hiroshima, Keiji Murakami, 多田彩乃, Tomomi Kuwahara, Hideki Fujii and Hiromichi Yumoto : Porphyromonas gingivalis由来メンブレンベシクルがヒト歯肉上皮細胞に及ぼす影響, 第73回日本細菌学会中国・四国支部総会, 32, Oct. 2020.
20.	Pahlevi Reza Muhammad, Keiji Murakami, Yuta Kita, Rina Murata, Yuka Hiroshima and Hideki Fujii : Screening for the genes influenced by AIA-1 in Pseudomonas aeruginosa, 第73回日本細菌学会中国・四国支部総会, 31, Oct. 2020.
21.	AKIZUKI Minato, Keiji Murakami, Yuka Hiroshima, Hideki Fujii and Hiromichi Yumoto : MPCポリマーコーティングにおけるTi表面への歯周病原菌付着抑制効果の検討, 第73回日本細菌学会中国・四国支部総会, 30, Oct. 2020.
22.	Yuta Kita, Pahlevi Reza Muhammad, Rina Murata, Keiji Murakami, Yuka Hiroshima and Hideki Fujii : バイオフィルム形成緑膿菌におけるPA2384遺伝子の役割について, 第73回日本細菌学会中国・四国支部総会, 29, Oct. 2020.
23.	Rina Murata, Keiji Murakami, Yuka Hiroshima, Koichiro Tsuchiya, Keiko Kataoka and Hideki Fujii : 緑膿菌における抗菌薬添加によるスーパーオキシドの発生について, 第73回日本細菌学中国・四国支部総会, 22, Oct. 2020.
24.	Rie Kido, Jun-ichi Kido, Eijiro Sakamoto, Yasufumi Nishikawa, Yuka Hiroshima and Hiromichi Yumoto : イムノクロマト法を用いたカルプロテクチンの測定によるインプラント疾患の診断, 第63回秋季日本歯周病学会学術大会, Vol.62, 123, Oct. 2020.
25.	Jun-ichi Kido, Yuka Hiroshima, Rie Kido, Yuji Inagaki, Koji Naruishi and Hiromichi Yumoto : 無細胞蛋白質合成系を用いた抗菌ペプチドの合成とリポソーム封入, 日本歯科保存学会2020年度春季学術大会(第152回)(神戸), Jun. 2020.
26.	Yuka Hiroshima, Jun-ichi Kido, Rie Kido, Kaya Yoshida, Yuji Inagaki, Koji Naruishi and Hiromichi Yumoto : オーラルケアへの応用に関連するリポソームのデリバリー法の検討, 第63回春季日本歯周病学会学術大会, May 2020.
27.	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.
28.	村田梨菜, Keiji Murakami, Yuka Hiroshima, Keiko Kataoka and Hideki Fujii : 緑膿菌における抗菌薬添加による酸化ストレス反応について, 第93回日本細菌学会総会, Feb. 2020.
29.	岡本舞, Yuta Kita, Rina Murata, Pahlevi Reza Muhammad, Keiji Murakami, Yuka Hiroshima, Keiko Kataoka and Hideki Fujii : 緑膿菌におけるバイオフィルム形成菌の抗菌薬抵抗性について, 徳島県歯科医学大会, Feb. 2020.
30.	Rina Murata, Pahlevi Reza Muhammad, Keiji Murakami, Yuka Hiroshima, Keiko Kataoka and Hideki Fujii : 緑膿菌における抗菌薬添加と酸化ストレスについて, 徳島県歯科医学大会, Feb. 2020.
31.	喜田悠太, Keiji Murakami, Yuka Hiroshima and Hideki Fujii : 緑膿菌におけるバイオフィルム形成菌の抗菌薬抵抗性に関わる遺伝子について, 第72回日本細菌学会中国・四国支部総会, Nov. 2019.
32.	藤本望, 村田梨菜, Keiji Murakami, Yuka Hiroshima, Keiko Kataoka and Hideki Fujii : 亜硝酸イオンの口腔内における生理的意義について, 第72回日本細菌学会中国・四国支部総会, Nov. 2019.
33.	村田梨菜, 藤本望, Keiji Murakami, Yuka Hiroshima, Keiko Kataoka and Hideki Fujii : 緑膿菌における抗菌薬添加と酸化ストレスについて, 第72回日本細菌学会中国・四国支部総会, Nov. 2019.
34.	Yuka Hiroshima, Jun-ichi Kido, Rie Kido, Kaya Yoshida, Yuji Inagaki, Koji Naruishi and Hiromichi Yumoto : オーラルケアへの応用を目指した抗菌ペプチド合成とリポソーム封入, 第62回秋季日本歯周病学会学術大会, Oct. 2019.
35.	Keiji Murakami, 喜田悠太, 村田梨菜, Yuka Hiroshima, Keiko Kataoka and Hideki Fujii : 緑膿菌バイオフィルム形成菌の抗菌薬抵抗性に関わる遺伝子について, 第33回日本バイオフィルム学会学術集会, Jul. 2019.
36.	Rie Kido, Yuka Hiroshima, Takahisa Ikuta, Kaya Yoshida, Yuji Inagaki, Koji Naruishi, Kazumi Ozaki, Jun-ichi Kido and Hiromichi Yumoto : 最終糖化産物はヒト口腔上皮細胞のリポカリン2発現を増加する, 第62回春季日本歯周病学会学術大会, May 2019.
37.	Yuka Hiroshima : 生体抗菌ペプチドの動態と歯周病予防への応用の可能性, 第61回秋季日本歯周病学会学術大会, Oct. 2018.
38.	Takenori Yamamoto, Tsunoda Moe, Akira Watanabe, Mizune Ohzono, 井戸佑介, Yuka Hiroshima, Akiko Yamada, 寺田弘 and 篠原康雄 : ポリエチレンイミンがミトコンドリアからのシトクロムc漏出を誘起するメカニズム, 第40回生体膜と薬物の相互作用シンポジウム, Oct. 2018.
39.	Ryosuke Takagi, Eijiro Sakamoto, Yuji Inagaki, Yuka Hiroshima, Koji Naruishi, Jun-ichi Kido and Hiromichi Yumoto : カルプロテクチンはマウス骨細胞の炎症および骨代謝関連因子の発現を制御する, 第61回春季日本歯周病学会学術大会, Jun. 2018.
40.	Yuka Hiroshima, Takenori Yamamoto and Yasuo Shinohara : 最終糖化産物とPorphyromonas gingivalis由来LPSが誘導するヒト歯肉上皮細胞の遺伝子発現の解析, 第61回春季日本歯周病学会学術大会, Jun. 2018.
41.	大園瑞音, Takenori Yamamoto, 渡辺朗, Akiko Yamada, Yuka Hiroshima, Hiroshi Terada and Yasuo Shinohara : ミトコンドリアカルシウムユニポーター(MCU)の構造と機能の相関解析, 第9回日本生物物理学会中国四国支部大会, May 2017.
42.	谷口あい, Takenori Yamamoto, 井戸佑介, Yuka Hiroshima, Akiko Yamada and Yasuo Shinohara : クロナゼパムがマウスの遺伝子発現に及ぼす影響のマイクロアレイ解析, 日本薬学会年会, Mar. 2017.
43.	Takenori Yamamoto, 大園瑞音, 山越亮平, Akiko Yamada, Yuka Hiroshima, Hiroshi Terada and Yasuo Shinohara : 酵母発現系によるミトコンドリアカルシウムユニポーター(MCU)の構造機能解析, 日本薬学会年会, Mar. 2017.
44.	Takenori Yamamoto, 大園瑞音, 山越亮平, Akiko Yamada, Yuka Hiroshima, Hiroshi Terada and Yasuo Shinohara : 酵母再構成系を用いたミトコンドリアカルシウムユニポーターの構造機能解析, 第38回生体膜と薬物の相互作用シンポジウム, Nov. 2016.
45.	大和永奈, 山越亮平, Takenori Yamamoto, Yuka Hiroshima, 三芳秀人, Mitsuru Shindo, Hiroshi Terada and Yasuo Shinohara : ミトコンドリアのADP/ATP輸送体はボンクレキン酸とどのように相互作用しているのか, 第55回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2016.
46.	大園瑞音, Takenori Yamamoto, 山越亮平, Akiko Yamada, Yuka Hiroshima, Hiroshi Terada and Yasuo Shinohara : 酵母再構成系を用いたミトコンドリアカルシウムユニポーター(MCU)の構造機能解析, 第55回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2016.
47.	Yuka Hiroshima, Jun-ichi Kido, Eijiro Sakamoto, 阿部佳織, Kaya Yoshida, Toshihiko Nagata and Yasuo Shinohara : 最終糖化産物はヒト歯肉上皮細胞におけるS100A8およびS100A9発現を上昇する, 第59回秋季日本歯周病学会学術大会, Oct. 2016.
48.	Yuka Hiroshima, Jun-ichi Kido, Kaya Yoshida, Kaori Abe, Yasuo Shinohara and Toshihiko Nagata : Hypoxic condition down-regulates S100A8 expression in human oral epithelial cells, 第59回春季日本歯周病学会学術大会, May 2016.
49.	Kaya Yoshida, Natsumi Fujiwara, Yuka Hiroshima, Kaori Abe, Jun-ichi Kido and Kazumi Ozaki : Porphyhepatic cellsromonas gingivalis inhibits insulin signaling by regulating SOCS3 and IRS-1 in, 第59回春季日本歯周病学会学術大会, May 2016.
50.	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.
51.	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.
52.	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.
53.	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.
54.	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.
55.	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.
56.	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.
57.	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.
58.	伊藤弘, 沼部幸博, 関野愉, 村樫悦子, 井口一美, 戸円智幸, 橋本修一, 佐々木大輔, 八重柏隆, 國松和司, 高井英樹, 目澤優, 小方頼昌, 渡邊久, 萩原さつき, 和泉雄一, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : 歯肉溝滲出液(GCF)を用いた歯周病罹患部位の診断と治療効果のモニタリングの有用性 -歯周病迅速診断キット開発に向けて-(第六報), 日本歯科保存学雑誌第137回秋季学術大会講演抄録集, 65, Nov. 2012.
59.	中島由紀子, Yuji Inagaki, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : 最終糖化産物(AGE)はラット歯髄における石灰化物形成と炎症反応を進展させる, 日本歯科保存学雑誌第137回秋季学術大会講演抄録集, 97, Nov. 2012.
60.	伊藤弘, 関野愉, 村樫悦子, 井口一美, 橋本修一, 沼部幸博, 佐々木大輔, 八重柏隆, 國松和司, 高井英樹, 目澤優, 小方頼昌, 渡邊久, 萩原さつき, 和泉雄一, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : 歯肉溝滲出液(GCF)を用いた歯周病罹患部位の診断と治療効果のモニタリングの有用性-歯周病迅速診断キット開発に向けて-(第五報), 日本歯周病学会会誌第55回学術大会秋季特別号, Vol.54, 83, Sep. 2012.
61.	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.
62.	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.
63.	伊藤弘, 関野愉, 村樫悦子, 井口一美, 橋本修一, 沼部幸博, 佐々木大輔, 八重柏隆, 國松和司, 高井英樹, 目澤優, 小方頼昌, 渡辺久, 萩原さつき, 和泉雄一, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : 歯肉溝滲出液(GCF)を用いた歯周病罹患部位の診断と治療効果のモニタリングの有用性 -歯周病迅速診断キット開発に向けて-(第四報), 日本歯周病学会会誌第55回春季学術大会特別号, Vol.54, 126, May 2012.
64.	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.
65.	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.
66.	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
67.	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
68.	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
69.	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.
70.	伊藤弘, 沼部幸博, 関野愉, 村樫悦子, 井口一美, 戸円智幸, 橋本修一, 佐々木大輔, 八重柏隆, 國松和司, 高井英樹, 目澤優, 小方頼昌, 渡邊久, 萩原さつき, 和泉雄一, Yuka Hiroshima, Jun-ichi Kido and 永田俊彦 : 歯肉溝滲出液を用いた歯周病罹患部位の診断と治療効果のモニタリングの有用性-歯周病迅速診断キット開発に向けて-第三報, 日本歯科保存学会雑誌第135回秋季学術大会プロクラム, 124, Oct. 2011.
71.	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.
72.	伊藤弘, 沼部幸博, 関野愉, 村樫悦子, 井口一美, 橋本修一, 佐々木大輔, 八重柏隆, 國松和司, 高井英樹, 目澤優, 小方頼昌, 渡邊久, 萩原さつき, 和泉雄一, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : 歯肉溝滲出液(GCF)を用いた歯周病罹患部位の診断と治療効果のモニタリングの有用性-歯周病迅速診断キット開発に向けて- 第二報, 日本歯周病学会会誌秋季特別号, Vol.53, 107, Sep. 2011.
73.	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.
74.	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.
75.	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.
76.	美原智恵, Jun-ichi Kido, Satoshi Yoneda, Yuka Hiroshima, Hiroyuki Seto and Toshihiko Nagata : 上顎前歯の著しいフレアアウトを伴った薬物性歯肉増殖症の一症例, 日本歯周病学会会誌春季特別号, Vol.53, 139, May 2011. (Keyword) periodontitis / 薬物性歯肉増殖症
77.	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
78.	伊藤弘, 関野愉, 村樫悦子, 井口一美, 沼部幸博, 橋本修一, 佐々木大輔, 八重柏隆, 國松和司, 高井英樹, 目澤優, 小方頼昌, 渡邊久, 萩原さつき, 和泉雄一, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : 歯肉溝滲出液(GCF)を用いた歯周病罹患部位の診断と治療効果のモニタリングの有用性 -歯周病迅速診断キット開発に向けて- 第1報, 日本歯周病学会会誌春季特別号, Vol.53, 121, May 2011.
79.	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
80.	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
81.	Chie Wada -Mihara, Jun-ichi Kido, Satoshi Yoneda, Yuka Hiroshima, Hiroyuki Seto and Toshihiko Nagata : 上顎前歯の著しいフレアアウトを伴った薬物性歯肉増殖症患者の一症例, Journal of the Japanese Association of Periodontology, May 2011.
82.	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.
83.	坂本英次郎, Chie Wada -Mihara, 徳永格, 瀬戸浩行 and Yuka Hiroshima : ラット実験的歯周炎におけるオステオプロテジェリンの影響, 第53回秋季日本歯周病学会高松, Sep. 2010.
84.	Purevjav Javkhlan, Yuka Hiroshima, Ahmad Azlina, Takahiro Hasegawa, Chenjuan Yao, Tetsuya Akamatsu, Toshihiko Nagata and Kazuo Hosoi : Calprotectin expression in the mouse salivary gland: Induction by lipopolysaccharide, 第52回歯科基礎医学会(2010年9月20-22日), Sep. 2010.
85.	Yuka Hiroshima, Purevjav Javkhlan, Ahmad Azlina, Takahiro Hasegawa, Tetsuya Akamatsu and Kazuo Hosoi : 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52回歯科基礎医学会(2010年9月20-22日), Sep. 2010.
86.	Takahiro Hasegawa, Ahmad Azlina, Purevjav Javkhlan, Yuka Hiroshima, Chenjuan Yao, Tetsuya Akamatsu and Kazuo Hosoi : 唾液腺細胞におけるアクアポリン5リン酸化のシグナル伝達機構, 第52回歯科基礎医学会(2010年9月20-22日), Sep. 2010.
87.	Purevjav Javkhlan, Yuka Hiroshima, Ahmad Azlina, Takahiro Hasegawa, Chenjuan Yao, Tetsuya Akamatsu, Toshihiko Nagata and Kazuo Hosoi : Calprotectin expression in the mouse salivary gland: Induction by lipopolysaccharide, Journal of Oral Biosciences, Vol.52, No.supplement, 94, Sep. 2010.
88.	Yuka Hiroshima, Javkhlan Purevjav, Ahmad Azlina, Takahiro Hasegawa, Tetsuya Akamatsu and Kazuo Hosoi : 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, Journal of Oral Biosciences, Vol.52, No.supplement, 148, Sep. 2010.
89.	Takahiro Hasegawa, Ahmad Azlina, Javkhlan Purevjav, Yuka Hiroshima, Chenjuan Yao, Tetsuya Akamatsu and Kazuo Hosoi : 唾液腺細胞におけるアクアポリン5リン酸化のシグナル伝達機構, Journal of Oral Biosciences, Vol.52, No.supplement, 164, Sep. 2010.
90.	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.
91.	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.
92.	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.
93.	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.
94.	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
95.	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.
96.	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.
97.	Keiji Oishi, Yuka Hiroshima and Toshihiko Nagata : 著明な歯肉増殖を伴う慢性歯周炎患者の一症例, Journal of the Japanese Association of Periodontology, Vol.51, 106, Oct. 2009.
98.	Chie Wada -Mihara, 徳永格, 瀬戸浩行, 大場博史, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : ラット実験的歯周炎におけるオステオプロテジェリンの骨吸収と炎症におよぼす効果, 第52回秋季日本歯周病学会学術大会, Vol.51, 93, Oct. 2009.
99.	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.
100.	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.
101.	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.
102.	Javkhlan Purevjav, Yuka Hiroshima, Ahmad Azlina, Takahiro Hasegawa, Chenjuan Yao, Tetsuya Akamatsu, Toshihiko Nagata and Kazuo Hosoi : Calprotectin induction by lipopolysaccharide in the salivary gland of mice, 第51回歯科基礎医学会, Sep. 2009.
103.	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.

Et cetera, Workshop:

1.	Saho Yamanaka, Rina Murata, Keiji Murakami, Yuka Hiroshima, Hideki Fujii, Akiko Sakurai and Keiko Kataoka : 緑膿菌の抗菌薬抵抗性に関与する二成分制御系について, 第44回徳島県医学検査学会, Dec. 2020.
2.	Yuta Uemura, Yuka Hiroshima, Keiji Murakami, 多田彩乃, Tomomi Kuwahara, Hideki Fujii and Hiromichi Yumoto : Porphyromonas gingivalis由来メンブレンベシクルがヒト歯肉上皮細胞に及ぼす影響, 徳島大学研究クラスター Joint Meeting on Microbiology 2020, Nov. 2020.
3.	Pahlevi Reza Muhammad, Keiji Murakami, Yuta Kita, Rina Murata, Yuka Hiroshima and Hideki Fujii : Screening for the genes influenced by AIA-1 in Pseudomonas aeruginosa, 徳島大学研究クラスター Joint Meeting on Microbiology 2020, Nov. 2020.
4.	AKIZUKI Minato, Keiji Murakami, Yuka Hiroshima, Hideki Fujii and Hiromichi Yumoto : MPCポリマーコーティングにおけるTi表面への歯周病原菌付着抑制効果の検討, 徳島大学研究クラスター Joint Meeting on Microbiology 2020, Nov. 2020.
5.	Yuta Kita, Pahlevi Reza Muhammad, Rina Murata, Keiji Murakami, Yuka Hiroshima and Hideki Fujii : バイオフィルム形成緑膿菌におけるPA2384遺伝子の役割について, 徳島大学研究クラスター Joint Meeting on Microbiology 2020, Nov. 2020.
6.	Rina Murata, Keiji Murakami, Yuka Hiroshima, Koichiro Tsuchiya, Keiko Kataoka and Hideki Fujii : 緑膿菌における抗菌薬添加によるスーパーオキシドの発生について, 徳島大学研究クラスター Joint Meeting on Microbiology 2020, Nov. 2020.
7.	喜田悠太, Pahlevi Reza Muhammad, Keiji Murakami, Yuka Hiroshima and Hideki Fujii : 緑膿菌PA2384遺伝子の抗菌薬抵抗性への関与, 四国歯学会第55回例会, Sep. 2019.
8.	鹿庭美奈子, 喜田悠太, Keiji Murakami, Yuka Hiroshima, Takashi Amoh and Hideki Fujii : BNCのインフルエンザ感受性細胞への接着に関与する温度条件, 四国歯学会第54回例会, Mar. 2019.

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

The role of DNA of Periodontal bacterium OMVs in Alzheimer's diseases. (Project/Area Number: 23K09505 )
歯周医学における歯周病原細菌由来ベシクルの役割解明と歯周病重症化予防剤の開発 (Project/Area Number: 21K09896 )
Study of exosomes from cells in periodontal tissues with diabetes-associated periodontitis (Project/Area Number: 21K09895 )
バイオナノカプセルを用いた高齢者オーラルケアの基礎研究 (Project/Area Number: 20K09941 )
Investigation of molecular mechanism of S100A8 in diabetes-associated periodontitis (Project/Area Number: 17K17352 )
Basic study for oral care system using an artificial cell (Project/Area Number: 17H04418 )
Investigation of molecular mechanism of S100A8 in diabetes-associated periodontitis (Project/Area Number: 15H06451 )
レジスチンは唾液腺炎症のモジュレーターとなるか (Project/Area Number: 23792125 )
Search by Researcher Number (60545143)

Associate Professor : Hiroshima, Yuka

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