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犬の腫瘍における発現異常ノンコーディングスモールRNAの同定
Get PDFIn recent years, not only mRNA (messenger RNA) but also other small non-coding RNA have focused on molecular diagnosis and therapy in oncology fields. Especially in human medicine, many studies elucidate the ability and function of many microRNAs, which are small non-coding RNAs. However, there are still not many studies in the veterinary field. In my PhD study, I focused on the non-coding small RNA in canine oncology fields.
In the first chapter, I studied the dysregulated micro RNA in canine oral melanoma. At first, I performed the microarray-based miRNA profiling of canine malignant melanoma (CMM) tissue obtained from the oral cavity. Then, I also confirmed the differentially expressed microRNA by quantitative reverse transcription-PCR (qRT-PCR). An analysis of the microarray data revealed 17 dysregulated miRNAs; 5 were up-regulated, and 12 were down�regulated. qRT-PCR analysis was performed for 2 up-regulated (miR-204 and miR-383), 3 down-regulated (miR-122, miR-143, and miR-205) and 6 additional oncogenic miRNAs (oncomiRs; miR-16, miR-21, miR-29b, miR-92a, miR-125b and miR-222). The expression levels of seven of the miRNAs, miR�16, miR-21, miR-29b, miR-122, miR-125b, miR-204, and miR-383 were significantly up-regulated, while the expression of miR-205 was down- 2 regulated in CMM tissues compared with normal oral tissues. The microarray and qRT-PCR analyses validated the up-regulation of two potential oncomiRs, miR-204 and miR-383. I also constructed a protein interaction network and a miRNA–target regulatory interaction network using STRING and Cytoscape. In the proposed network, was a target for miR-383, and were targets for miR-204, and was a target for both. The miR-383 and miR-204 were potential oncomiRs that may be involved in regulating melanoma development by evading DNA repair and apoptosis.
In my second chapter, I focused on non-coding RNA other than microRNA, and I compared canine hepatocellular carcinomas (HCC) and hepatocellular adenomas (HCA). I elucidated the differential expression of Y RNA-derived fragments because Y RNA-derived fragments have yet to be investigated in canine HCC and HCA. I used qRT-PCR to determine Y RNA expression in clinical tissues, plasma, and plasma extracellular vesicles, and two HCC cell lines (95-1044 and AZACH). Y RNA was significantly decreased in tissue, plasma, and plasma extracellular vesicles for canine HCC versus canine HCA and healthy controls. Y RNA was decreased in 95-1044 and AZACH cells versus normal liver tissue and 3 in AZACH versus 95-1044 cells. In plasma samples, Y RNA levels were decreased in HCC versus HCA and Healthy controls and increased in HCA versus Healthy controls. Receiver operating characteristic analysis showed that Y RNA could be a promising biomarker for distinguishing HCC from HCA and healthy controls. Overall, the dysregulated expression of Y RNA can distinguish canine HCC from HCA. However, further research is necessary to elucidate the underlying Y RNA-related molecular mechanisms in hepatocellular neoplastic diseases. To the best of my knowledge, this is the first report on the relative expression of Y RNA in canine HCC and HCA.
In conclusion, I have demonstrated the up-regulation of potential oncomiRs, miR-16, miR-21, miR-29b, miR-122, miR-125b, miR-204 and miR�383 in CMM tissues. In particular, the strong up-regulation of miR-383 in CMM tissues compared with normal oral tissues identified by microarray screening was confirmed by qRT-PCR. I conclude that miR-383 and miR-204 may promote melanoma development by regulating the DNA repair/checkpoint and apoptosis. Then, I also demonstrated the Y RNA dysregulation in the cHCC. Especially to my knowledge, this is the first report on Y RNA in canine tumors. Interestingly, this ncRNA has distinctive characteristics and differentiates malignant tumors (HCC) from benign 4 tumors (HCA). The expression pattern of Y RNA is consistent across clinical samples and cell lines. Thus, Y RNA has promising potential for differentiating HCC from HCA. Further research is required to fully elucidate the role of Y RNA in the development and progression of canine HCC and HCA.In recent years, not only mRNA (messenger RNA) but also other small non-coding RNA have focused on molecular diagnosis and therapy in oncology fields. Especially in human medicine, many studies elucidate the ability and function of many microRNAs, which are small non-coding RNAs. However, there are still not many studies in the veterinary field. In my PhD study, I focused on the non-coding small RNA in canine oncology fields. In the first chapter, I studied the dysregulated micro RNA in canine oral melanoma. At first, I performed the microarray-based miRNA profiling of canine malignant melanoma (CMM) tissue obtained from the oral cavity. Then, I also confirmed the differentially expressed microRNA by quantitative reverse transcription-PCR (qRT-PCR). An analysis of the microarray data revealed 17 dysregulated miRNAs; 5 were up-regulated, and 12 were down�regulated. qRT-PCR analysis was performed for 2 up-regulated (miR-204 and miR-383), 3 down-regulated (miR-122, miR-143, and miR-205) and 6 additional oncogenic miRNAs (oncomiRs; miR-16, miR-21, miR-29b, miR-92a, miR-125b and miR-222). The expression levels of seven of the miRNAs, miR�16, miR-21, miR-29b, miR-122, miR-125b, miR-204, and miR-383 were significantly up-regulated, while the expression of miR-205 was down- 2 regulated in CMM tissues compared with normal oral tissues. The microarray and qRT-PCR analyses validated the up-regulation of two potential oncomiRs, miR-204 and miR-383. I also constructed a protein interaction network and a miRNA–target regulatory interaction network using STRING and Cytoscape. In the proposed network, was a target for miR-383, and were targets for miR-204, and was a target for both. The miR-383 and miR-204 were potential oncomiRs that may be involved in regulating melanoma development by evading DNA repair and apoptosis. In my second chapter, I focused on non-coding RNA other than microRNA, and I compared canine hepatocellular carcinomas (HCC) and hepatocellular adenomas (HCA). I elucidated the differential expression of Y RNA-derived fragments because Y RNA-derived fragments have yet to be investigated in canine HCC and HCA. I used qRT-PCR to determine Y RNA expression in clinical tissues, plasma, and plasma extracellular vesicles, and two HCC cell lines (95-1044 and AZACH). Y RNA was significantly decreased in tissue, plasma, and plasma extracellular vesicles for canine HCC versus canine HCA and healthy controls. Y RNA was decreased in 95-1044 and AZACH cells versus normal liver tissue and 3 in AZACH versus 95-1044 cells. In plasma samples, Y RNA levels were decreased in HCC versus HCA and Healthy controls and increased in HCA versus Healthy controls. Receiver operating characteristic analysis showed that Y RNA could be a promising biomarker for distinguishing HCC from HCA and healthy controls. Overall, the dysregulated expression of Y RNA can distinguish canine HCC from HCA. However, further research is necessary to elucidate the underlying Y RNA-related molecular mechanisms in hepatocellular neoplastic diseases. To the best of my knowledge, this is the first report on the relative expression of Y RNA in canine HCC and HCA. In conclusion, I have demonstrated the up-regulation of potential oncomiRs, miR-16, miR-21, miR-29b, miR-122, miR-125b, miR-204 and miR�383 in CMM tissues. In particular, the strong up-regulation of miR-383 in CMM tissues compared with normal oral tissues identified by microarray screening was confirmed by qRT-PCR. I conclude that miR-383 and miR-204 may promote melanoma development by regulating the DNA repair/checkpoint and apoptosis. Then, I also demonstrated the Y RNA dysregulation in the cHCC. Especially to my knowledge, this is the first report on Y RNA in canine tumors. Interestingly, this ncRNA has distinctive characteristics and differentiates malignant tumors (HCC) from benign 4 tumors (HCA). The expression pattern of Y RNA is consistent across clinical samples and cell lines. Thus, Y RNA has promising potential for differentiating HCC from HCA. Further research is required to fully elucidate the role of Y RNA in the development and progression of canine HCC and HCA.博士(獣医学)山口大学Yamaguchi Universit
Effect of defective calcium metabolism on otolith formation in zebrafish
Get PDFBenign paroxysmal positional vertigo (BPPV) is the most common vertigo disease and is more likely to occur in perimenopausal women, suggesting an association with osteoporosis. Since otoconia are primarily composed of calcium carbonate, abnormal calcium metabolism may lead to otoconia dislocation. However, the detailed mechanism is currently unknown. In this study, we investigated the effects of drugs (cadmium and dexamethasone) that cause abnormal calcium metabolism on otolith formation in zebrafish larvae. Here, otolith size was clearly reduced in the cadmium group, and the calcium content of the larvae was also markedly reduced. In contrast, in the dexamethasone group, which also had a lower calcium content than the control group, otolith size increased. Our results suggest that, as in bone, calcium metabolism influences the repeated dissolution and recrystallization of otoliths and maintains homeostasis in response to calcium concentrations in the endolymphatic fluid
慢性閉塞性肺疾患（ＣＯＰＤ）患者における座りがちな行動を検出するための日常生活動作における息切れ質問票（SOBDA-Q）の有用性
Get PDF博士(医学)山口大学Yamaguchi Universit
第130回山口大学医学会学術講演会並びに令和６年度評議員会・総会
Get PDF特別講演ⅠPenumbraを救う/石原秀行
特別講演Ⅱ（臨床）法医学に係る実務・教育・研究と今後の展望/髙瀬泉
中村賞受賞者講演 燥積層線維芽細胞シートは創傷治癒を促す再生医療において新たな扱いやすい被覆材である/松野祐太朗，柳原正志，上野耕司，斎藤寿郎，藏澄宏之，鈴木亮，桂春作，小賀厚憲，濱野公一
小西賞受賞者講演 左冠動脈主幹部分岐部病変に対するステント治療最適化に関する研究/岡村誉之，岩﨑清隆，藤村達大，宮崎要介，松山哲也，中田祐樹，兼行恵太，佐野元昭
学部学生演題No.１ 小野茶の抗菌作用と抗腫瘍作用についての研究/木村綾佑，伊東雅也，杉山尚平，泉本真志，原田耕志，三島克章
学部学生演題No.２ 完全自動化に向けたヒト腸内細菌叢に対するDNA抽出の比較/北野朝陽，北野宏明，浅井義之
学部学生演題No.３ Patau症候群における繊毛病発症機序の解明/小林大悟，板橋岳志，宮本達雄
学部学生演題No.４ 全身振動曝露した高齢者における心拍変動の性差および振動周波数特異性/和田直，ホセインマハブブ，長谷亮佑，山口奈津，原田規章，田邉剛
一般演題No.５ F-18-FDG集積を示す褐色脂肪組織/菅一能，河上康彦，清水文め，玉井義隆，中村敬子
一般演題No.６ 喘息の身体活動の多様性と胸部イメージングの意義/深津愛祐美，平野綱彦，岩本博志，土居恵子，村川慶多，村田順之，大谷俊人，川本数真，檜垣直子，天野芳宏，山根真由香，田辺直也，横山彰仁，礒部威，服部登，松永和人
一般演題No.７ 精巣腫瘤を契機に臨床的再発と診断し得た多発性骨髄腫の一例/能野翔太，山本薫，德永良洋，中邑幸伸，中林容子，太田康晴，湯尻俊昭
一般演題No.８ 直腸NETに対する内視鏡切除方法選択の検討/青山将司，浜辺功一，浜本果歩，大木美穂，児玉愛実，山本美音，吉松祐希，中村克彦，山本一太，山岡祐子，伊藤駿介，五嶋敦史，橋本真一，西川潤，高見太郎
一般演題No.９ 胃全摘+腹部食道切除術後の下縦隔リンパ節再発に対して5FU+シスプラチン+ニボルマブ併用療法が著効した食道胃接合部腺扁平上皮癌の一例/戒能秀直，須藤隆一郎，松本亮，西原聡志，藤井美緒，山下修，林雅太郎，藤井雅和，金田好和
一般演題No.10 ネフローゼ症候群におけるsoluble ST2測定の有用性の検討/橘高節明，岡田裕介，長谷川俊史
大学院成績優秀者講演No.11 入院期高齢心不全患者において栄養指標であるGeriatric Nutritional Risk Indexが退院１年後のアウトカムに与える影響/三浦正和，奥田真一，大野豊，中尾文昭，上山剛，山本健，池田安宏
大学院成績優秀者講演No.12 教師なし機械学習を用いた喘息症状サブタイプとその背景病態の同定/濱田和希，安部武志，早野崇英，村田順之，大石景士，平野綱彦，中津井雅彦，松永和人，浅井義之
大学院成績優秀者講演No.13 紫外線の歯周病菌バイオフィルムに対する殺菌効果について/米田翔磨，西川潤，田村優太，藤井智大，福田総一郎，柳井章江，清水勇輝，小林由紀，常岡英弘，野島順三，原田耕志，末廣寛，山﨑隆弘
大学院成績優秀者講演No.14 Jo-1抗体陽性筋炎では筋微小血管の補体依存性細胞傷害とTREM-1発現増強が誘導される/本田真也，清水文崇，佐藤亮太，水上洋一，渡邊健司，神田隆，中森雅之
大学院成績優秀者講演No.15 切迫早産治療におけるニフェジピンの薬物動態と妊娠延長効果・副作用との関連性の検討/田村美穂，村田晋，太田千絢，田中翔子，有近仁美，伯野大樹，岡田直人，牛島健太郎，辻泰弘，北原隆