請用此 Handle URI 來引用此文件：
http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/80373完整後設資料紀錄
| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 林立德(Li-Deh Lin) | |
| dc.contributor.author | Han-Wei Wang | en |
| dc.contributor.author | 王翰偉 | zh_TW |
| dc.date.accessioned | 2022-11-24T03:05:21Z | - |
| dc.date.available | 2021-08-31 | |
| dc.date.available | 2022-11-24T03:05:21Z | - |
| dc.date.copyright | 2021-08-31 | |
| dc.date.issued | 2021 | |
| dc.date.submitted | 2021-07-21 | |
| dc.identifier.citation | 1. Nair PN. Pathogenesis of apical periodontitis and the causes of endodontic failures. Crit Rev Oral Biol Med 2004;15(6):348-81. 2. Lin LM, Rosenberg PA. Repair and regeneration in endodontics. Int Endod J 2011;44(10):889-906. 3. Márton IJ, Kiss C. Overlapping protective and destructive regulatory pathways in apical periodontitis. J Endod 2014;40(2):155-63. 4. Segura-Egea JJ, Martín-González J, Cabanillas-Balsera D, Fouad AF, Velasco-Ortega E, López-López J. Association between diabetes and the prevalence of radiolucent periapical lesions in root-filled teeth: systematic review and meta-analysis. Clin Oral Investig 2016;20(6):1133-41. 5. Khalighinejad N, Aminoshariae MR, Aminoshariae A, Kulild JC, Mickel A, Fouad AF. Association between Systemic Diseases and Apical Periodontitis. J Endod 2016;42(10):1427-34. 6. Sasaki H, Hirai K, Martins CM, Furusho H, Battaglino R, Hashimoto K. Interrelationship Between Periapical Lesion and Systemic Metabolic Disorders. Curr Pharm Des 2016;22(15):2204-15. 7. Cabanillas-Balsera D, Martín-González J, Montero-Miralles P, Sánchez-Domínguez B, Jiménez-Sánchez MC, Segura-Egea JJ. Association between diabetes and nonretention of root filled teeth: a systematic review and meta-analysis. Int Endod J 2019;52(3):297-306. 8. Cotti E, Mezzena S, Schirru E, et al. Healing of Apical Periodontitis in Patients with Inflammatory Bowel Diseases and under Anti-tumor Necrosis Factor Alpha Therapy. J Endod 2018;44(12):1777-82. 9. Cotti E, Schirru E, Acquas E, Usai P. An overview on biologic medications and their possible role in apical periodontitis. J Endod 2014;40(12):1902-11. 10. Kawashima N, Okiji T, Kosaka T, Suda H. Kinetics of macrophages and lymphoid cells during the development of experimentally induced periapical lesions in rat molars: a quantitative immunohistochemical study. J Endod 1996;22(6):311-6. 11. Suzuki N, Okiji T, Suda H. Enhanced expression of activation-associated molecules on macrophages of heterogeneous populations in expanding periapical lesions in rat molars. Arch Oral Biol 1999;44(1):67-79. 12. Shi C, Pamer EG. Monocyte recruitment during infection and inflammation. Nat Rev Immunol 2011;11(11):762-74. 13. Kurihara T, Warr G, Loy J, Bravo R. Defects in macrophage recruitment and host defense in mice lacking the CCR2 chemokine receptor. J Exp Med 1997;186(10):1757-62. 14. Jia T, Serbina NV, Brandl K, et al. Additive roles for MCP-1 and MCP-3 in CCR2-mediated recruitment of inflammatory monocytes during Listeria monocytogenes infection. J Immunol 2008;180(10):6846-53. 15. Lin SK, Kok SH, Lee YL, et al. Simvastatin as a novel strategy to alleviate periapical lesions. J Endod 2009;35(5):657-62. 16. O'Neill LA, Pearce EJ. Immunometabolism governs dendritic cell and macrophage function. J Exp Med 2016;213(1):15-23. 17. Huang S, Rutkowsky JM, Snodgrass RG, et al. Saturated fatty acids activate TLR-mediated proinflammatory signaling pathways. J Lipid Res 2012;53(9):2002-13. 18. Karasawa T, Kawashima A, Usui-Kawanishi F, et al. Saturated Fatty Acids Undergo Intracellular Crystallization and Activate the NLRP3 Inflammasome in Macrophages. Arterioscler Thromb Vasc Biol 2018;38(4):744-56. 19. Carta G, Murru E, Banni S, Manca C. Palmitic Acid: Physiological Role, Metabolism and Nutritional Implications. Front Physiol 2017;8:902. 20. Shimano H, Sato R. SREBP-regulated lipid metabolism: convergent physiology - divergent pathophysiology. Nat Rev Endocrinol 2017;13(12):710-30. 21. Costales P, Castellano J, Revuelta-Lopez E, et al. Lipopolysaccharide downregulates CD91/low-density lipoprotein receptor-related protein 1 expression through SREBP-1 overexpression in human macrophages. Atherosclerosis 2013;227(1):79-88. 22. Matsushita K, Tajima T, Tomita K, Takada H, Nagaoka S, Torii M. Inflammatory cytokine production and specific antibody responses to lipopolysaccharide from endodontopathic black-pigmented bacteria in patients with multilesional periapical periodontitis. J Endod 1999;25(12):795-9. 23. Hong CY, Lin SK, Kok SH, et al. The role of lipopolysaccharide in infectious bone resorption of periapical lesion. J Oral Pathol Med 2004;33(3):162-9. 24. Kuda O, Pietka TA, Demianova Z, et al. Sulfo-N-succinimidyl oleate (SSO) inhibits fatty acid uptake and signaling for intracellular calcium via binding CD36 lysine 164: SSO also inhibits oxidized low density lipoprotein uptake by macrophages. J Biol Chem 2013;288(22):15547-55. 25. Li LC, Yang JL, Lee WC, et al. Palmitate aggravates proteinuria-induced cell death and inflammation via CD36-inflammasome axis in the proximal tubular cells of obese mice. Am J Physiol Renal Physiol 2018;315(6):F1720-F31. 26. Nathan C. Inducible nitric oxide synthase: what difference does it make? J Clin Invest 1997;100(10):2417-23. 27. Lin SK, Kok SH, Kuo MY, et al. Nitric oxide promotes infectious bone resorption by enhancing cytokine-stimulated interstitial collagenase synthesis in osteoblasts. J Bone Miner Res 2003;18(1):39-46. 28. Farhad AR, Razavi S, Jahadi S, Saatchi M. Use of aminoguanidine, a selective inducible nitric oxide synthase inhibitor, to evaluate the role of nitric oxide in periapical inflammation. J Oral Sci 2011;53(2):225-30. 29. Silva MJ, Sousa LM, Lara VP, et al. The role of iNOS and PHOX in periapical bone resorption. J Dent Res 2011;90(4):495-500. 30. 周千瑜. 藉由Metformin調節誘發性一氧化氮合成酶與一氧化氮合成減緩根尖病變進展. 國立臺灣大學/醫學院/臨床牙醫學研究所. Taiwan: National Taiwan University; 2019:46. 31. Foretz M, Guigas B, Bertrand L, Pollak M, Viollet B. Metformin: from mechanisms of action to therapies. Cell Metab 2014;20(6):953-66. 32. Park CS, Bang BR, Kwon HS, et al. Metformin reduces airway inflammation and remodeling via activation of AMP-activated protein kinase. Biochem Pharmacol 2012;84(12):1660-70. 33. Araújo AA, Pereira A, Medeiros C, et al. Effects of metformin on inflammation, oxidative stress, and bone loss in a rat model of periodontitis. PLoS One 2017;12(8):e0183506. 34. Liu L, Zhang C, Hu Y, Peng B. Protective effect of metformin on periapical lesions in rats by decreasing the ratio of receptor activator of nuclear factor kappa B ligand/osteoprotegerin. J Endod 2012;38(7):943-7. 35. Wang GS, Hoyte C. Review of Biguanide (Metformin) Toxicity. J Intensive Care Med 2019;34(11-12):863-76. 36. Nicolini AC, Grisa TA, Muniz F, Rösing CK, Cavagni J. Effect of adjuvant use of metformin on periodontal treatment: a systematic review and meta-analysis. Clin Oral Investig 2019;23(6):2659-66. 37. Lai EH, Yang CN, Lin SK, et al. Metformin Ameliorates Periapical Lesions through Suppression of Hypoxia-induced Apoptosis of Osteoblasts. J Endod 2018;44(12):1817-25. 38. Cassanta LTC, Rodrigues V, Violatti-Filho JR, et al. Modulation of Matrix Metalloproteinase 14, Tissue Inhibitor of Metalloproteinase 3, Tissue Inhibitor of Metalloproteinase 4, and Inducible Nitric Oxide Synthase in the Development of Periapical Lesions. J Endod 2017;43(7):1122-9. 39. Trifilieff A, Fujitani Y, Mentz F, Dugas B, Fuentes M, Bertrand C. Inducible nitric oxide synthase inhibitors suppress airway inflammation in mice through down-regulation of chemokine expression. J Immunol 2000;165(3):1526-33. 40. Kim SA, Choi HC. Metformin inhibits inflammatory response via AMPK-PTEN pathway in vascular smooth muscle cells. Biochem Biophys Res Commun 2012;425(4):866-72. 41. Wang HW, Lai EH, Yang CN, et al. Intracanal Metformin Promotes Healing of Apical Periodontitis via Suppressing Inducible Nitric Oxide Synthase Expression and Monocyte Recruitment. J Endod 2020;46(1):65-73. 42. Sundqvist G. Associations between microbial species in dental root canal infections. Oral Microbiol Immunol 1992;7(5):257-62. 43. Li Y, Lu Z, Zhang X, et al. Metabolic syndrome exacerbates inflammation and bone loss in periodontitis. J Dent Res 2015;94(2):362-70. 44. Shikama Y, Kudo Y, Ishimaru N, Funaki M. Possible Involvement of Palmitate in Pathogenesis of Periodontitis. J Cell Physiol 2015;230(12):2981-9. 45. Bettencourt IA, Powell JD. Targeting Metabolism as a Novel Therapeutic Approach to Autoimmunity, Inflammation, and Transplantation. J Immunol 2017;198(3):999-1005. 46. Namgaladze D, Brune B. Macrophage fatty acid oxidation and its roles in macrophage polarization and fatty acid-induced inflammation. Biochim Biophys Acta 2016;1861(11):1796-807. 47. Jones SF, Infante JR. Molecular Pathways: Fatty Acid Synthase. Clin Cancer Res 2015;21(24):5434-8. 48. Young KE, Flaherty S, Woodman KM, Sharma-Walia N, Reynolds JM. Fatty acid synthase regulates the pathogenicity of Th17 cells. J Leukoc Biol 2017;102(5):1229-35. 49. Carroll RG, Zaslona Z, Galvan-Pena S, et al. An unexpected link between fatty acid synthase and cholesterol synthesis in proinflammatory macrophage activation. J Biol Chem 2018;293(15):5509-21. 50. Lawler JF, Jr., Yin M, Diehl AM, Roberts E, Chatterjee S. Tumor necrosis factor-alpha stimulates the maturation of sterol regulatory element binding protein-1 in human hepatocytes through the action of neutral sphingomyelinase. J Biol Chem 1998;273(9):5053-9. 51. Gierens H, Nauck M, Roth M, et al. Interleukin-6 stimulates LDL receptor gene expression via activation of sterol-responsive and Sp1 binding elements. Arterioscler Thromb Vasc Biol 2000;20(7):1777-83. 52. Wang PL, Ohura K. Porphyromonas gingivalis lipopolysaccharide signaling in gingival fibroblasts-CD14 and Toll-like receptors. Crit Rev Oral Biol Med 2002;13(2):132-42. 53. Lee CJ, Lee SS, Chen SC, Ho FM, Lin WW. Oregonin inhibits lipopolysaccharide-induced iNOS gene transcription and upregulates HO-1 expression in macrophages and microglia. Br J Pharmacol 2005;146(3):378-88. 54. Chen C, Chen YH, Lin WW. Involvement of p38 mitogen-activated protein kinase in lipopolysaccharide-induced iNOS and COX-2 expression in J774 macrophages. Immunology 1999;97(1):124-9. 55. Łabuzek K, Liber S, Gabryel B, Okopień B. Metformin has adenosine-monophosphate activated protein kinase (AMPK)-independent effects on LPS-stimulated rat primary microglial cultures. Pharmacol Rep 2010;62(5):827-48. 56. Vaez H, Rameshrad M, Najafi M, Barar J, Barzegari A, Garjani A. Cardioprotective effect of metformin in lipopolysaccharide-induced sepsis via suppression of toll-like receptor 4 (TLR4) in heart. Eur J Pharmacol 2016;772:115-23. 57. Bogdan C. Nitric oxide and the immune response. Nat Immunol 2001;2(10):907-16. 58. Kobayashi Y. The regulatory role of nitric oxide in proinflammatory cytokine expression during the induction and resolution of inflammation. J Leukoc Biol 2010;88(6):1157-62. 59. Kodama K, Nishio Y, Sekine O, et al. Bidirectional regulation of monocyte chemoattractant protein-1 gene at distinct sites of its promoter by nitric oxide in vascular smooth muscle cells. Am J Physiol Cell Physiol 2005;289(3):C582-90. 60. Bambirra W, Jr., Maciel KF, Thebit MM, de Brito LC, Vieira LQ, Sobrinho AP. Assessment of Apical Expression of Alpha-2 Integrin, Heat Shock Protein, and Proinflammatory and Immunoregulatory Cytokines in Response to Endodontic Infection. J Endod 2015;41(7):1085-90. 61. Shi H, Kokoeva MV, Inouye K, Tzameli I, Yin H, Flier JS. TLR4 links innate immunity and fatty acid-induced insulin resistance. J Clin Invest 2006;116(11):3015-25. 62. Valdearcos M, Esquinas E, Meana C, et al. Lipin-2 reduces proinflammatory signaling induced by saturated fatty acids in macrophages. J Biol Chem 2012;287(14):10894-904. 63. Lancaster GI, Langley KG, Berglund NA, et al. Evidence that TLR4 Is Not a Receptor for Saturated Fatty Acids but Mediates Lipid-Induced Inflammation by Reprogramming Macrophage Metabolism. Cell Metab 2018;27(5):1096-110.e5. 64. Febbraio M, Hajjar DP, Silverstein RL. CD36: a class B scavenger receptor involved in angiogenesis, atherosclerosis, inflammation, and lipid metabolism. J Clin Invest 2001;108(6):785-91. 65. Stewart CR, Stuart LM, Wilkinson K, et al. CD36 ligands promote sterile inflammation through assembly of a Toll-like receptor 4 and 6 heterodimer. Nat Immunol 2010;11(2):155-61. 66. Lu Z, Li Y, Brinson CW, Kirkwood KL, Lopes-Virella MF, Huang Y. CD36 is upregulated in mice with periodontitis and metabolic syndrome and involved in macrophage gene upregulation by palmitate. Oral Dis 2017;23(2):210-8. 67. Li G, Robles S, Lu Z, et al. Upregulation of free fatty acid receptors in periodontal tissues of patients with metabolic syndrome and periodontitis. J Periodontal Res 2019;54(4):356-63. 68. Suvan JE, Finer N, D'Aiuto F. Periodontal complications with obesity. Periodontol 2000 2018;78(1):98-128. 69. Almeida A, Fagundes NCF, Maia LC, Lima RR. Is there an Association Between Periodontitis and Atherosclerosis in Adults? A Systematic Review. Curr Vasc Pharmacol 2018;16(6):569-82. 70. Kocher T, Konig J, Borgnakke WS, Pink C, Meisel P. Periodontal complications of hyperglycemia/diabetes mellitus: Epidemiologic complexity and clinical challenge. Periodontol 2000 2018;78(1):59-97. 71. Lamster IB, Pagan M. Periodontal disease and the metabolic syndrome. Int Dent J 2017;67(2):67-77. 72. Berlin-Broner Y, Febbraio M, Levin L. Association between apical periodontitis and cardiovascular diseases: a systematic review of the literature. Int Endod J 2017;50(9):847-59. 73. Lima SM, Grisi DC, Kogawa EM, et al. Diabetes mellitus and inflammatory pulpal and periapical disease: a review. Int Endod J 2013;46(8):700-9. 74. Glass CK, Olefsky JM. Inflammation and lipid signaling in the etiology of insulin resistance. Cell Metab 2012;15(5):635-45. 75. Schwendicke F, Göstemeyer G. Single-visit or multiple-visit root canal treatment: systematic review, meta-analysis and trial sequential analysis. BMJ Open 2017;7(2):e013115. 76. Martinho FC, Nascimento GG, Leite FR, Gomes AP, Freitas LF, Camões IC. Clinical influence of different intracanal medications on Th1-type and Th2-type cytokine responses in apical periodontitis. J Endod 2015;41(2):169-75. 77. Cotti E, Abramovitch K, Jensen J, et al. The Influence of Adalimumab on the Healing of Apical Periodontitis in Ferrets. J Endod 2017;43(11):1841-6. | |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/80373 | - |
| dc.description.abstract | "目的：研究棕櫚酸（palmitic acid，PA）與一氧化氮（NO）對於單核球/巨噬細胞的趨化性、以及根尖牙周炎的信息傳遞所造成的影響，並提出可能的治療方針。 方法：實驗使用J774與Mono-Mac-6等單核球/巨噬細胞（monocyte/macrophage）族系之細胞株。以西方點墨法分析固醇調節元件結合蛋白-1c（sterol regulatory element binding protein-1c，SREBP-1c），脂肪酸合酶（fatty acid synthase，FASN）以及誘導型一氧化氮合酶（inducible nitric oxide synthase，iNOS）的表現；以反相高效液相層析質譜儀測定PA含量；以small interfering RNA（siRNA）靜默SREBP-1c及FASN的表現；CC-趨化因子配體2（CC-chemokine ligand 2，CCL2）的分泌是以酶聯免疫吸附測定法（ELISA）量化；細胞趨化性則是以transwell細胞遷徙的方式量化；以測量培養液的亞硝酸鹽含量來量化產生的一氧化氮（NO）。以實驗誘發大鼠根尖牙周炎（induced apical periodontitis）模型來評估磺基-N-琥珀酰亞胺基油酸酯（sulfo-N-succinimidyl oleate，SSO）與二甲雙胍（N, N-dimethylbiguanide，藥品名metformin）抑制脂肪酸與iNOS，對於輔助根尖牙周炎治療所帶來的效益，再以根尖放射線造影（periapical x-ray）和微米電腦斷層攝影（micro-CT）評估病灶大小，以免疫組織化學染色評估monocyte/macrophage的數量與iNOS表現量。 結果：LPS刺激巨噬細胞的SREBP-1c成為活化態、增加FASN表現，並增強PA合成。靜默SREBP-1c可減弱脂多糖（lipopolysaccharide，LPS）強化的FASN表現。靜默FASN會抑制LPS增強的棕櫚酸合成。LPS和外源加入的棕櫚酸會提高CCL2和巨噬細胞的趨化性。抑制FASN表現可顯著減輕LPS增強的CCL2分泌。SSO可抑制LPS和PA增強的CCL2分泌和巨噬細胞趨化性。Metformin能抑制monocytes因LPS刺激產生的iNOS及NO，而且透過調節iNOS/NO路徑來抑制LPS增強的CCL2表現。在實驗誘發大鼠根尖牙周炎模型中，使用SSO治療以及根管內給予metformin，都能顯著抑制發炎擴展及monocyte/macrophage聚集。 結論：LPS/SREBP-1c/FASN/PA的訊息傳遞路徑會惡化細菌感染引起的根尖牙周組織破壞。控制脂肪酸的代謝與訊息傳遞有利於根尖牙周炎的治療。而在根管內使用metformin治療根尖牙周炎，其機制是抑制iNOS/NO的產生來減緩monocytes聚集與發炎反應。調控飽和脂肪酸與NO等代謝體的產生，對於根尖牙周炎的治療確實能發揮相當的助益。" | zh_TW |
| dc.description.provenance | Made available in DSpace on 2022-11-24T03:05:21Z (GMT). No. of bitstreams: 1 U0001-0806202103200700.pdf: 4501621 bytes, checksum: 8b59f58afafbd8630ff1d39d28536350 (MD5) Previous issue date: 2021 | en |
| dc.description.tableofcontents | 目錄 口試委員會審定書 I 誌謝 II 中文摘要 III Abstract （英文摘要） V 第一章 研究背景 1 第二章 研究目的 7 第三章 材料與方法 8 3.1 實驗細胞株培養與處理 8 3.1.1 小鼠macrophage細胞株J774 8 3.1.2 人類monocyte細胞株Mono-Mac-6 8 3.2 藥物製備 8 3.2.1 PA之製備 8 3.2.2 SSO之製備 9 3.2.3 Metformin之製備 9 3.2.4 硝普鈉 9 3.2.5 NG-甲基-L-精氨酸 9 3.3 蛋白質的萃取 9 3.4西方點墨法（Western blot） 10 3.5 SREBP-1c及FASN 基因靜默 12 3.6 細胞脂質萃取 12 3.7 反相高效液相層析質譜儀測定棕櫚酸 12 3.8 以酶聯免疫吸附測定法測定CCL2 13 3.9 細胞遷徙測定（Cell migration assay） 13 3.10 亞硝酸鹽測定（Nitrite assay） 13 3.11實驗誘發大鼠根尖牙周炎模型 14 3.11.1 以實驗誘發大鼠根尖牙周炎模型探討SSO抑制飽和脂肪酸對疾病治療產生的效益 14 3.11.2 以實驗誘發大鼠根尖牙周炎模型探討metformin抑制iNOS/NO對疾病治療產生的效益 15 3.12 放射線造影評估病灶大小 15 3.12.1 牙齒根尖放射線造影（periapical x-ray） 15 3.12.2 微米電腦斷層攝影（micro-CT）1 15 3.12.3 微米電腦斷層攝影（micro-CT）2 16 3.13 免疫組織化學染色（immunohistochemistry）與細胞計數 16 3.14 統計分析 17 第四章 結果 18 4.1 LPS刺激巨噬細胞表現成熟的SREBP-1c、FASN與合成棕櫚酸 18 4.2 LPS增強巨噬細胞趨化性和增加CCL2分泌是經由棕櫚酸合成量上升的作用 18 4.3 SSO抑制LPS和棕櫚酸刺激而增加的CCL2分泌和巨噬細胞趨化性 19 4.4 LPS會刺激monocytes表現iNOS和生成NO，而metformin可抑制LPS的效應 19 4.5 LPS透過iNOS/NO路徑來刺激monocytes分泌CCL2 19 4.6 Metformin可抑制因LPS刺激而分泌的CCL-2，而SNP減弱metformin的作用 20 4.7 SSO治療可減輕根尖牙周炎的骨質破壞和巨噬細胞的聚集 20 4.8 以根管內放置metformin的給藥方式可減低根尖牙周炎的骨吸收以及降低周圍組織的iNOS表現和monocytes聚集狀況 20 第五章 討論 22 第六章 結論 26 參考文獻 27 附錄 34 圖目錄 附圖一 4 附圖二 5 附圖三 6 圖一 34 圖二 35 圖三 36 圖四 37 圖五 38 圖六 39 圖七 40 圖八 41 圖九 42 圖十 43 圖十一 44 圖十二 45 表目錄 表一 46 | |
| dc.language.iso | zh-TW | |
| dc.subject | 二甲雙胍 | zh_TW |
| dc.subject | 根尖牙周炎 | zh_TW |
| dc.subject | 脂多糖 | zh_TW |
| dc.subject | 飽和脂肪酸 | zh_TW |
| dc.subject | 誘導型一氧化氮合酶 | zh_TW |
| dc.subject | 單核球／巨噬細胞 | zh_TW |
| dc.subject | 磺基-N-琥珀酰亞胺基油酸酯 | zh_TW |
| dc.subject | metformin | en |
| dc.subject | apical periodontitis | en |
| dc.subject | lipopolysaccharide | en |
| dc.subject | saturated fatty acid | en |
| dc.subject | inducible nitric oxide synthase | en |
| dc.subject | monocyte/macrophage | en |
| dc.subject | sulfo-N-succinimidyl oleate | en |
| dc.title | 以飽和脂肪酸與誘導型一氧化氮生合成的觀點探討代謝體的調控對於根尖牙周炎的治療潛能 | zh_TW |
| dc.title | To explore the treatment potential of modulating metabolisms of saturated fatty acid and inducible nitric oxide in apical periodontitis | en |
| dc.date.schoolyear | 109-2 | |
| dc.description.degree | 博士 | |
| dc.contributor.author-orcid | 0000-0003-3434-9094 | |
| dc.contributor.advisor-orcid | 林立德(0000-0002-6050-7394) | |
| dc.contributor.coadvisor | 林思洸(Sze-Kwan Lin) | |
| dc.contributor.coadvisor-orcid | 林思洸(0000-0002-7969-0280) | |
| dc.contributor.oralexamcommittee | 郭生興(Hsin-Tsai Liu), 洪志遠(Chih-Yang Tseng),孫家棟 | |
| dc.subject.keyword | 根尖牙周炎,脂多糖,飽和脂肪酸,誘導型一氧化氮合酶,單核球／巨噬細胞,磺基-N-琥珀酰亞胺基油酸酯,二甲雙胍, | zh_TW |
| dc.subject.keyword | apical periodontitis,lipopolysaccharide,saturated fatty acid,inducible nitric oxide synthase,monocyte/macrophage,sulfo-N-succinimidyl oleate,metformin, | en |
| dc.relation.page | 46 | |
| dc.identifier.doi | 10.6342/NTU202100970 | |
| dc.rights.note | 同意授權(限校園內公開) | |
| dc.date.accepted | 2021-07-22 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 臨床牙醫學研究所 | zh_TW |
| 顯示於系所單位： | 臨床牙醫學研究所 | |
文件中的檔案：
| 檔案 | 大小 | 格式 | |
|---|---|---|---|
| U0001-0806202103200700.pdf 授權僅限NTU校內IP使用（校園外請利用VPN校外連線服務） | 4.4 MB | Adobe PDF |
系統中的文件，除了特別指名其著作權條款之外，均受到著作權保護，並且保留所有的權利。