臺北榮民總醫院教學部於2019年6月20-21日舉辦國際醫學教育研討會,本次研討會的主題為「智慧醫院的醫學教育」,我們邀請來自各國專家學者們蒞臨演講與實務經驗分享,相信透過本活動,將對臨床教育規劃提出嶄新的思維,同時發展更加創新的內容,歡迎全國學術界及研究人員踴躍投稿。
一、徵稿內容範圍
1. 本會將邀請專家委員審閱,摘要稿件經委員評選錄取後,主辦單位將於2019年6月3日(星期一)通知錄取者,進行海報展示(Poster Exhibition)。
2. 海報展示規範:
摘要投稿經錄取者,擇優數名頒發獎狀及禮品,同時得免費參加6月21日整日Keynote Lecture (若為多人共同發表,以第一作者為限)。請投稿者仍先於報名期間進行報名,以利主辦單位統計參加人數。
五、聯絡方式
有任何問題歡迎諮詢本院教學部教師培育科傅小姐。
電話:(02)2875-7302
傳真:(02)2875-7305
Email:[email protected]
(本活動提供公務人員終身學習時數認證及本院教師培育科臨床教師教育訓練時數/教學計劃主持人進階課程教學能力3小時學分(6/20)、8小時學分(6/21),
衛生福利部西醫師、護理師/士、醫事檢驗師、醫事放射師及藥師之繼續教育積分申請中,其他醫事職類視報名情形申請相關繼續教育積分。)
範例
Original or Poster presentation格式
Tid1 in Head and Neck Cancer Tumorigenesis
Tid1頭頸癌化過程之角色
Jeng-Fan Lo
羅正汎
Institute of Oral Biology, National Yang-Ming University School of Dentistry, and Department of Dentistry, Taipei Veterans General Hospital, Taipei, Taiwan, ROC
國立陽明大學 牙醫學院 口腔生物研究所 及 台北榮民總醫院 口腔醫學部
Background: Tid1 is the human homologue of the Drosophila tumor suppressor Tid56, whose null mutation causes lethal tumorigenesis during the larval stage. The physiological function of Tid1 to mediate the tumorigenesis in various human cancer types has been reported. However, the molecular mechanism by which Tid1 involves in carcinogenesis in human head and neck squamous cell carcinoma (HNSCC) remains poorly understood. Herein, we investigated the clinical significance of Tid1 expression in HNSCC and its role in tumorigenesis.
Methods: To determine the expression patterns of Tid1 in HNSCC, the biopsies of 47 HNSCC cancerous tissues were examined by immunohistochemistry analysis. To evaluate the physiological function of Tid1 in human oral cancer cells, HNSCC cells overexpressing Tid1 were generated and the cell proliferation, cell motility, cell invasion, anchorage-independent growth of those cell, and in vivo tumorigenicity were examined. To verify the molecular mechanism of Tid1 involving in HNSCC, the EGFR molecular pathway of Tid1-expressing cells were examined.
Results: We showed that ectopically overexpression of Tid1 negatively regulated cell proliferation, anchorage-independent growth, cell motility, cell invasion, and tumorigenicity of oral cancer cells. Low Tid1 expression is associated with increased cancer recurrence and tumor status, but reduced patient survival in HNSCC patients. In addition, Tid1 attenuates EGFR activity and blocks the activation of AKT in HNSCC cells.
Conclusion: We demonstrate that Tid1 functions as a tumor suppressor in human HNSCC. Furthermore, molecular mechanism mediated by Tid1 might be a potential therapeutic target for HNSCC therapy.
一、徵稿內容範圍
- 沉浸醫學(AR、VR)
- 新科技輔助醫學教育(3D列印)
- AI 對醫學教育的影響
- AI 在醫學教育的應用
- 線上教學
- 智慧醫療下人文教育
- 全人醫療
- 其他符合本次研討會主題之內容
- 請使用Microsoft Office Word 2003或以上版本繕打(須能與Office 2003相容)。
- 語言:題目、作者姓名及服務單位為中英文並列,內文一律請以英文書寫。
- 字型:Times New Roman及標楷體。
- 大小:題目14級字、服務單位10級字並斜體、作者姓名及摘要內容12級字。
- 摘要內容:Original or Poster Presentation請依四段繕打,分別為背景(Background)、方法(Method)、結果(Results)、結論(Conclusion);Review or Invited Speech則不須分成四段繕打。以上皆不需加附註(References)、圖表(Figures and Tables)及關鍵詞(Keywords)。
- 版面配置:中等邊界。
- 對齊方式:題目、服務單位及作者姓名皆靠左對齊,摘要內容左右對齊。
- 字數:約250至350字,以不超過一頁A4為限。
- 作者姓名後面請勿加上職稱。
- 相關投稿格式及內容,請參考以下範例,欲投稿者煩請自行下載修改。收件後若有格式不符處,主辦單位將自行修改,並不會更動內文。
- 投稿方式:請將Word檔寄至fdc@vghtpe.gov.tw 傅小姐,恕不接受紙本稿件,來信投稿時,請務必註明聯絡人之姓名、電話及電子郵件。
- 投稿期限:即日起至2019年5月20日(星期一)晚上12點止。
1. 本會將邀請專家委員審閱,摘要稿件經委員評選錄取後,主辦單位將於2019年6月3日(星期一)通知錄取者,進行海報展示(Poster Exhibition)。
2. 海報展示規範:
- 海報請務必事先準備,應由作者自行製作並親自張貼,請勿將海報郵寄至本院。
- 海報規格:115cm(高)*90cm(寬)。
- 海報張貼及移除時間:
- 張貼時間:2019年6月21日(星期五)上午08:00至09:00
- 移除時間:2019年6月21日(星期五)下午16:00至17:00
- 海報張貼地點:致德樓一樓會議室外。
摘要投稿經錄取者,擇優數名頒發獎狀及禮品,同時得免費參加6月21日整日Keynote Lecture (若為多人共同發表,以第一作者為限)。請投稿者仍先於報名期間進行報名,以利主辦單位統計參加人數。
五、聯絡方式
有任何問題歡迎諮詢本院教學部教師培育科傅小姐。
電話:(02)2875-7302
傳真:(02)2875-7305
Email:[email protected]
(本活動提供公務人員終身學習時數認證及本院教師培育科臨床教師教育訓練時數/教學計劃主持人進階課程教學能力3小時學分(6/20)、8小時學分(6/21),
衛生福利部西醫師、護理師/士、醫事檢驗師、醫事放射師及藥師之繼續教育積分申請中,其他醫事職類視報名情形申請相關繼續教育積分。)
範例
Original or Poster presentation格式
Tid1 in Head and Neck Cancer Tumorigenesis
Tid1頭頸癌化過程之角色
Jeng-Fan Lo
羅正汎
Institute of Oral Biology, National Yang-Ming University School of Dentistry, and Department of Dentistry, Taipei Veterans General Hospital, Taipei, Taiwan, ROC
國立陽明大學 牙醫學院 口腔生物研究所 及 台北榮民總醫院 口腔醫學部
Background: Tid1 is the human homologue of the Drosophila tumor suppressor Tid56, whose null mutation causes lethal tumorigenesis during the larval stage. The physiological function of Tid1 to mediate the tumorigenesis in various human cancer types has been reported. However, the molecular mechanism by which Tid1 involves in carcinogenesis in human head and neck squamous cell carcinoma (HNSCC) remains poorly understood. Herein, we investigated the clinical significance of Tid1 expression in HNSCC and its role in tumorigenesis.
Methods: To determine the expression patterns of Tid1 in HNSCC, the biopsies of 47 HNSCC cancerous tissues were examined by immunohistochemistry analysis. To evaluate the physiological function of Tid1 in human oral cancer cells, HNSCC cells overexpressing Tid1 were generated and the cell proliferation, cell motility, cell invasion, anchorage-independent growth of those cell, and in vivo tumorigenicity were examined. To verify the molecular mechanism of Tid1 involving in HNSCC, the EGFR molecular pathway of Tid1-expressing cells were examined.
Results: We showed that ectopically overexpression of Tid1 negatively regulated cell proliferation, anchorage-independent growth, cell motility, cell invasion, and tumorigenicity of oral cancer cells. Low Tid1 expression is associated with increased cancer recurrence and tumor status, but reduced patient survival in HNSCC patients. In addition, Tid1 attenuates EGFR activity and blocks the activation of AKT in HNSCC cells.
Conclusion: We demonstrate that Tid1 functions as a tumor suppressor in human HNSCC. Furthermore, molecular mechanism mediated by Tid1 might be a potential therapeutic target for HNSCC therapy.
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