徳島大学 / 教育研究者総覧 --- 柳井亮二

個人のホームページ

https://researchmap.jp/7000023507 (researchmap)

https://orcid.org/0000-0002-0265-9760 (ORCID)

専門分野

○	ライフサイエンス (Life sciences) [眼科学 (Ophthalmology)]

研究テーマ

著書・論文

(著書・論文等の業績についてはhttps://researchmap.jp/7000023507 (researchmap)でも御覧頂けます．)

学術論文(審査論文):

1.	Ryoji Yanai, Hei Sho Uchi, Yukiko Kondo, Youichiro Fujitsu, Katsuyoshi Suzuki, Keiko Yoshimura, Naoki Kumagai, Mariko Egawa and Yoshinori Mitamura : The epidemiology of uveitis: comparison of its causes and visual outcomes between three-tiered medical facilities in Ube city, Scientific Reports, 15, 1, 8998, 2025. (要約) This study aimed to conduct a comparative epidemiological survey of uveitis across various healthcare settings and elucidate the clinical characteristics. We conducted a retrospective cross-sectional study in the Ube-City medical region in Yamaguchi prefecture and recruited 268 patients from a university hospital (151 patients), municipal hospitals (51 patients), and private eye clinics (58 patients). Medical records of patients newly diagnosed with uveitis between January 2018 and December 2019 in the institutes were included, reviewed, and compared. The main outcomes included the number of uveitis causes, treatment methods, and visual acuity. Panuveitis, which is associated with systemic diseases, such as Vogt-Koyanagi-Harada disease and sarcoidosis, was more prominent in university hospital patients. Conversely, anterior uveitis, including traumatic iritis, was prominently detected in general hospitals and private eye clinics. The best-corrected visual acuity improved to 1.0 (logMAR = 0); an improvement of 74%, 61%, and 54% was observed in private eye clinic, general hospital, and university hospital patients, respectively. This study identified differences in uveitis presentation and treatment across diverse clinical settings. The results of this study provide valuable data for differentiating the causes of uveitis at university hospitals, general hospitals, and private eye clinics. (キーワード) Community hospitals / Panuveitis / University hospital / Uveitis / Visual impairment (出版サイトへのリンク) ● Publication site (DOI): 10.1038/s41598-025-93223-x (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 40089526 ● Summary page in Scopus @ Elsevier: 2-s2.0-105000123177 (DOI: 10.1038/s41598-025-93223-x, PubMed: 40089526, Elsevier: Scopus)
2.	Ryoji Yanai, Sora Mizukami, Akihiko Sakamoto, Kenji Takemoto, Tetsuya Seto, Kazuya Uehara, Kiminori Yukata, Takashi Sakai, Keiko Iwaisako, Norihiko Takeda, Ryoji Yanai and Masataka Asagiri : Cell cycle checkpoint factor p15Ink4b is a novel regulator of osteoclast differentiation., Scientific Reports, 15, 1, 2025. (要約) Osteoclasts are specialized cells essential for bone resorption, a crucial process in bone remodeling, and dysregulation of osteoclastogenesis can lead to pathological bone loss such as osteoporosis and rheumatoid arthritis. Therefore, understanding the precise mechanisms governing osteoclast differentiation is crucial for developing effective therapies for skeletal diseases. In osteoclastogenesis, as well as other differentiated cells, it is well understood that cell cycle arrest is essential for terminal differentiation and is tightly regulated by CDK inhibitors such as Cip/Kip family and Ink4 family protein. In this manuscript, we identified p15Ink4b, a member of the Ink4 family, as a novel regulator of osteoclastogenesis by comprehensive single-cell RNA sequence data reanalyzing. Furthermore, histological analysis and in vitro osteoclast differentiation assay revealed that p15Ink4b functionally regulates osteoclastogenesis. Our findings may not only provide insights into the molecular mechanisms of osteoclast differentiation but also underscore the potential of harnessing cell cycle mechanisms to develop novel therapeutic strategies for bone diseases. (キーワード) Osteoclasts / Cell Differentiation / Animals / Mice / Osteogenesis / Cyclin-Dependent Kinase Inhibitor p15 / Cell Cycle Checkpoints / Humans / Mice, Inbred C57BL (出版サイトへのリンク) ● Publication site (DOI): 10.1038/s41598-025-89988-w (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 39979342 ● Search Scopus @ Elsevier (PMID): 39979342 ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-025-89988-w (DOI: 10.1038/s41598-025-89988-w, PubMed: 39979342)
3.	Tetsuya Seto, Kiminori Yukata, Shunya Tsuji, Yusuke Takeshima, Takeshi Honda, Akihiko Sakamoto, Kenji Takemoto, Hiroki Sakai, Mayu Matsuo, Yurika Sasaki, Mizuki Kaneda, Mikako Yoshimura, Atsushi Mihara, Kazuya Uehara, Aira Matsugaki, Takayoshi Nakano, Koji Harada, Yoshiro Tahara, Keiko Iwaisako, Ryoji Yanai, Norihiko Takeda, Takashi Sakai and Masataka Asagiri : Methylglyoxal compromises callus mineralization and impairs fracture healing through suppression of osteoblast terminal differentiation., Biochemical and Biophysical Research Communications, 747, 2025. (要約) Impaired fracture healing in diabetic patients leads to prolonged morbidity and increased healthcare costs. Methylglyoxal (MG), a reactive metabolite elevated in diabetes, is implicated in various complications, but its direct impact on bone healing remains unclear. Here, using a non-diabetic murine tibial fracture model, we demonstrate that MG directly impairs fracture healing. Micro-computed tomography revealed decreased volumetric bone mineral density in the callus, while callus volume remained unchanged, resulting in a brittle bone structure. This was accompanied by reduced expression of osteocalcin and bone sialoprotein, both critical for mineralization. Biomechanical analysis indicated that MG reduced the mechanical resilience of the fracture site without altering its elastic strength, suggesting that the impairment was not primarily due to the accumulation of advanced glycation end-products in the bone extracellular matrix. In vitro studies confirmed that non-cytotoxic concentrations of MG inhibited osteoblast maturation and mineralization. Transcriptomic analysis identified downregulation of Osterix, a key transcription factor for osteoblast maturation, without altering Runx2 levels, leading to decreased expression of key mineralization-related factors like osteocalcin. These findings align with clinical observations of reduced circulating osteocalcin levels in diabetic patients, suggesting that the detrimental effects of MG on osteoblasts may extend beyond bone metabolism. Our study highlights MG and MG-sensitive pathways as potential therapeutic targets for improving bone repair in individuals with diabetes and other conditions characterized by elevated MG levels. (キーワード) Animals / Pyruvaldehyde / Fracture Healing / Osteoblasts / Cell Differentiation / Calcification, Physiologic / Mice / Bony Callus / Mice, Inbred C57BL / Osteocalcin / Male / Sp7 Transcription Factor (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.bbrc.2025.151312 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 39799866 ● Search Scopus @ Elsevier (PMID): 39799866 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2025.151312 (DOI: 10.1016/j.bbrc.2025.151312, PubMed: 39799866)

国際会議:

1.	Ryoji Yanai and Yoshinori Mitamura : The influence of thick-type conventional soft contact lenses YOUSOFT ®, developing for the astigmatism correction on a rabbit corneal epithelium, ARVO2025, Apr. 2025.
2.	Ryoji Yanai, 三﨑裕子, Mariko Egawa, Masayuki Yamada and Yoshinori Mitamura : Two cases of Tatto-associated granulomatous uveitis, INFLAMMATIO 2024, Nov. 2024.
3.	Ryoji Yanai and Yoshinori Mitamura : The effects of the thick type of YOUSOFT contact lenses for aphakic hyperopia on a rabbit corneal epithelium, ISCLR Symposium, Aug. 2024.

国内講演発表:

1.	柳井亮二, 安永玄太, 辻竣也, 本田健, 岩田在博, 宮川英二, 吉田幸治, 岸本充弘, 酒井大樹, 藤瀬良弘, 朝霧成拳, 三田村佳典 : オメガ3脂肪酸を含有した鯨油摂取によるマウス脈絡膜新生血管の抑制効果, 第129回日本眼科学会総会, 2025年4月.
2.	Yoshinori Mitamura, MIki Akiko, Terasaki Hiroto, Chuji Shinichiro, sakaeda Yukinori, Seki Kyousuke, Ishigooka Gaku, Iwase Takeshi, Ohara Hiromi, Tsujinaka Hiroki, Fukuyama Hisashi, Abe yuuki and Ryoji Yanai : Six-month outcomes of faricimab treatment fou neovascular age-related macular degeneration, FujiRetina2025, Mar. 2025.
3.	Ryoji Yanai, Yasunaga Genta, Tsuji Shunya, Honda Takeshi, Iwata Arihiro, Miyagawa Eiji, Yoshida Koji, Kishimoto Mitsuhiro, Sakai Hiroki, Fujise Yoshihiro, Asagiri Masataka and Yoshinori Mitamura : Dietary intake of whale oil-containing ω-3 long-chain polyunsaturated fatty acids attenuates choroidal neovascularization in mice, FujiRetina2025, Mar. 2025.
4.	柳井亮二, 三田村佳典 : 強度乱視用高含水ソフトコンタクトレンズによる家兎角膜への安全性, 角膜カンファランス2025, 2025年2月.
5.	三﨑裕子, 柳井亮二, 江川麻理子, 山田将之, 三田村佳典 : Tattoo関連肉芽腫性ぶどう膜炎の2例, 第78回日本臨床眼科学会, 2024年11月.
6.	柳井亮二, 三﨑裕子, 山田将之, 江川麻理子, 三田村佳典 : Tattoo関連肉芽腫性ぶどう膜炎の2例, 第52回日本臨床免疫学学会総会, 2024年10月.

その他・研究会:

1.	柳井亮二, 猪本尚毅, 谷彰浩, 山田将之, 江川麻理子, 三田村佳典 : 徳島大学病院における自己免疫網膜症診断に対する診断と治療, 第84回徳島眼科集談会, 2024年12月.

科学研究費補助金 (KAKEN Grants Database @ NII.ac.jp)

鯨油由来の脂肪酸成分による免疫細胞誘導療法を目指した眼炎症抑制療法の開発 (研究課題/領域番号: 24K12808 )
破骨細胞の新たな調節メカニズム：炎症と細胞外マトリクスの相互作用の解明 (研究課題/領域番号: 24K12310 )
眼炎症疾患の患者を中心とした診療連携におけるぶどう膜炎診療システムの有用性 (研究課題/領域番号: 23K01903 )
知覚神経を介した眼特異的ゲートウェイ反射の解明と神経伝達物質による炎症再燃の抑制 (研究課題/領域番号: 21K09743 )
血液網膜バリアに着目したVEGFを標的としない加齢黄斑変性の治療法の開発 (研究課題/領域番号: 18K09449 )
結膜線維増殖反応における潜在的アレルギー炎症の関与 (研究課題/領域番号: 15K10870 )
CYP代謝産物による眼内慢性炎症疾患の制御メカニズムの解明と治療法の開発 (研究課題/領域番号: 15K10869 )
眼組織基底膜の糖化最終産物検出と生体内における糖化最終産物検出用臨床機器の開発 (研究課題/領域番号: 26670755 )
自然炎症制御を基軸とした網膜自己再生促進 (研究課題/領域番号: 26293373 )
環境酸素濃度の低下による角膜上皮バリアー機能の低下に対する修復機構の解明 (研究課題/領域番号: 22791663 )
環境酸素濃度に対する角膜構成細胞の増殖、細胞死、細胞機能に関する研究 (研究課題/領域番号: 20791256 )
角膜上皮創傷治癒過程における神経ガイダンス因子の機能解析 (研究課題/領域番号: 20592045 )
研究者番号（10346554）による検索

准教授 : 柳井亮二

研究活動

個人のホームページ

専門分野

研究テーマ

著書・論文

学術論文(審査論文):

国際会議:

国内講演発表:

その他・研究会:

科学研究費補助金 (KAKEN Grants Database @ NII.ac.jp)

准教授 : 柳井 亮二

研究活動

個人のホームページ

専門分野

研究テーマ

著書・論文

学術論文(審査論文):

国際会議:

国内講演発表:

その他・研究会:

科学研究費補助金 (KAKEN Grants Database @ NII.ac.jp)

准教授 : 柳井亮二