Precision Medicine Notes

中山醫學大學高教深耕計畫教育課程暨研討會
精準醫學新境界 New Frontier of Precision Medicine
【研討會】第十屆臨床醫學研究所聯合教學研究研討會
The 10th Annual Symposium of Graduate Institutes of
Clinical Medicine in Taiwan: New Frontier of Precision Medicine
地點:中山醫學大學正心樓
日期: 108 年 7 月 27 日
指導單位∕ 教育部
主辦單位∕ 中山醫學大學/中山醫學大學附設醫院
承辦單位∕ 中山醫學大學醫學研究所/附設醫院精準醫學中心
協辦單位∕ 長庚大學臨床醫學研究所台北醫學大學臨床醫學研究所
中國醫藥大學臨床醫學研究所台灣大學臨床醫學研究所
成功大學臨床醫學研究所高雄醫學大學臨床醫學研究所
國防大學醫學院醫學科學研究所陽明大學臨床醫學研究所
慈濟大學醫學科學研究所台灣精準醫學學會
107120052
目錄
一、議程表…………………………………………………………………. 1
二、演講者簡介……………………………………………………………. 3
大會演講石瑜教授……………………………………………………………… 3
課程李英雄教授…………………………………………………………… 4
林克亮副教授………………………………………………………………………6
三、大會演講 (0211 教室)……………………………………………………7

演講者：Yu Shyr, Ph.D. 石瑜教授
Professor of Biostatistics, Biomedical Informatics, and Health
Policy Vanderbilt University Medical Center USA
題目：Big Data, Smart Data, and Actionable Data:
Shaping the Future of Precision Medicine and Healthcare
四、課程大綱 (0212 教室)……………………………………………….. 8
1. 主講者：林克亮副教授/題目：A 10-Year-Ground Sword for
Precision Medicine 精準醫學十年磨劍……………………………………… 8
2. 主講者：李英雄教授/題目：Dramatic Advances in Precision
Medicine Based on Megadata-Driven Artificial Intelligence
基於大數據驅動人工智慧精準醫學之戲劇性進展………………………… 9
3. 主講者：李英雄教授/題目：New Frontier of Precision Medicine
at the Chung-Shan Medical University
精準醫學新境界在中山醫學大學……………………………………………. 10
4. 主講者：李英雄教授/題目：A Fine Perspective of Precision
Medicine in Taiwan 台灣精準醫學一幅美好的遠景………………………… 11
5. 主講者：林克亮副教授/題目：Building the Framework of Health
Care in Precision Medicine Ecosystem
建立精準醫療生態系統之健康照護架構……………………………………. 12
I
五、研討會 (0211 教室) 演講摘要………………………………….…….. 13

主持人：中國醫藥大學馬文隆副教授報告人：鍾瑋敏指導老師：馬文隆 13
主持人：長庚大學蕭長春副教授報告人：傅宏鈞指導老師：康宏佑 14
主持人：成功大學沈延盛所長報告人：侯雅琴指導老師：沈延盛 16
主持人：慈濟大學蔡榮坤所長報告人：陳家輝指導老師：洪智煌
17
主持人：臺北醫學大學陳冠州所長報告人:高治圻指導老師:吳麥斯/張偉嶠
18
主持人：臺灣大學楊偉勛所長報告人：吳振吉副教授 19
主持人：陽明大學王錦鈿所長報告人：李雅婷指導老師：牛道明 20
主持人：國防醫學院黃坤崙所長報告人：陳杭港指導老師：王智弘
21
主持人：國防醫學院黃坤崙所長報告人：陳鉞忠指導老師：蔡建松
22
主持人：高雄醫學大學黃阿梅教授報告人：陳昭儒指導老師：劉于鵬
23
主持人：中山醫學大學陳進典所長報告人：李欣樺指導老師：林志立
24
六、研討會壁報展示摘要…………………………..………………………. 25
1. A 組 (0221 教室)……………………………………..…………………………… 25
A1 吳博銘/Po Ming Wu 成功大學/臨床醫學研究所……………………………… 25
A2 徐千玉/Chien-Yu Hsu 國立成功大學/臨床醫學研究所……………………... 26
A3 翁尚楣/Shang-Mei Weng 國立成功大學/臨床醫學研究所…………………… 27
A4 吳淨眉/Ching Mei Wu 中國醫藥大學/生物醫學研究所………………………. 28
A5 吳世偉/Shih-Wei Wu 國防醫學院/醫學科學研究所…………………………... 29
A6 林樂天/Le-Tien Lin 國防醫學院/醫學科學研究所……………………………. 30
A7 陳杭港/Hang-Kang Chen 國防醫學院/醫學科學研究所……………………… 31
A8 曾元生/Yuan-sheng Tzeng 國防醫學院/醫學科學研究所…………………….. 32
A9 蕭鎮源/Chen-Yuan Hsiao 國防醫學院/醫學科學研究所……………………… 33
A10 鄭文勝/Wen-Sheng Cheng 國防醫學院/醫學科學研究所……………………. 34
2. B 組 (0222 教室)………………………………………………………………… 35
B1 邵愛寧/Ai-Ning Shao 成功大學/臨床醫學研究所……………………………... 35
B2 鄭婉婷/Woan Ting Tay 國立成功大學/臨床醫學研究所……………………….. 36
B3 許芸溱/ Yun-Chen Hsu中國醫藥大學/ 生物醫學研究所……………………… 37
B4 鄭朝鴻/Chao-Hung Cheng 中國醫藥大學/公共衛生學系/性荷爾蒙中心….. 38
B5 呂家菡/Jia-Han Lu 中國醫藥大學/生物醫學研究所…………………………... 39
B6 張庭瑄/Ting-Hsuan Chang 中國醫藥大學/生物醫學研究所…………………... 40
II
B7 黃伯仁/中國醫藥大學/臨床醫學研究所…………………………………….. 41
B8 黃建中/Chien-Chung Huang 中國醫藥大學/臨床醫學研究所………………... 42
B9 林讓均/Jang-Chun Lin 台北醫學大學/臨床醫學研究所………………………. 43
B10 鮑淑怡/Shu-I Pao 國防醫學院/醫學科學研究所……………………………… 44
B11 陳易廷/Yi-Ting Chen 國防醫學院/醫學科學研究所…………………………. 45
B12 蔡宗訓/Tsung-Hsun Tsai 中國醫藥大學臨床醫學研究所……………………. 46
B13 王振宏/Chen-Hung Wang 中國醫藥大學/臨床醫學研究所…………………. 47
3. C 組 (0223 教室)………………………………………………………………… 48
C1 呂維勛/ Wei-Hsun Lu 成功大學/臨床醫學研究所…………………………….. 48
C2 陳文榮/中山醫學大學/醫學研究所…………………………………………….. 49
C3 鍾馨瑤/Hsin-Yao Chung 中國醫藥大學/生物醫學研究所…………………….. 50
C4 張耀文/Yaw-Wen Chang 國防醫學院/醫學科學研究所……………………….. 51
C5 鍾新華/Hsin-Hua Chung 國防醫學院/醫學科學研究所……………………….. 52
C6 曾博郁/Po-Yu Tseng 陽明大學/醫學研究所……………………………………. 53
C7 林尚宏/Shang-Hung Lin 長庚大學/醫學研究所……………………………….. 54
C8 何筱莉/Hsiao-Li Ho 中山醫學大學/醫學研究所………………………………. 55
C9 吳悌暉/Ti-Hui Wu 國防醫學院/醫學科學研究所……………………………… 56
七、所長、主持教授簡歷………………………………………………… 57
中國醫藥大學藍先元所長………………………………………………………... 57
長庚大學蕭長春教授……………………………………………………………... 58
成功大學沈延盛所長……………………………………………………………... 59
慈濟大學蔡榮坤所長……………………………………………………………. 60
臺北醫學大學陳冠州所長………………………………………………………... 61
臺灣大學楊偉勛所長……………………………………………………………... 62
陽明大學王錦鈿所長……………………………………………………………... 63
國防醫學院黃坤崙所長…………………………………………………………... 64
高雄醫學大學吳明蒼所長………………………………………………………... 65
中山醫學大學陳進典所長………………………………………………………... 66
III
一、議程表
正心樓 2 樓 0211 教室
08:00 - 08:40 報到
08:45 - 09:00 長官開幕致詞
Yu Shyr, Ph.D. 石瑜教授
Professor of Biostatistics, Biomedical Informatics, and Health Policy
09:00 - 09:40 Vanderbilt University Medical Center USA
題目：Big Data, Smart Data, and Actionable Data:
Shaping the Future of Precision Medicine and Healthcare
09:40 - 10:00 交流時間(Coffee Break)
時間/教室正心樓 2 樓 0211 教室正心樓 2 樓 0212 教室
主持人：中國醫藥大學馬文隆副教授主講者：林克亮老師
報告人：鍾瑋敏指導老師：馬文隆
10:00 - 10:30 題目：The Translational Research of Androgen 題目：A 10-Year-Ground
Receptor in Ovarian Cancer Stemness and Sword for Precision Medicine
Chemoresistance 精準醫學十年磨劍
主持人：長庚大學蕭長春副教授
報告人：傅宏鈞醫師指導老師：康宏佑
10:30 - 11:00
題目：SKP2 and P16INK4A Modulate Stemess
and Radioresistance of cervical cancer
主持人：成功大學沈延盛教授主講者：李英雄教授
報告人：侯雅琴指導老師：沈延盛
11:00 - 11:30
題目：Dissecting the genetic and molecular 題目：Dramatic Advances in
alterations in pancreatic cancer progression Precision Medicine Based on
主持人：慈濟大學蔡榮坤所長 Megadata-Driven Artificial
報告人：陳家輝指導老師：洪智煌 Intelligence
11:30 - 12:00 題目：Neuroprotective Effects of Collagen- 基於大數據驅動人工智慧精準
Glycosaminoglycan Matrix Implantation following 醫學之戲劇性進展
Surgical Brain Injury
12:00 - 12:10 團體合照
海報評審/午餐:
12:10 - 13:20 邀請各校與會教授擔任海報評審委員分派在 3 午餐
間教室進行簡短的口頭報告 (8 min) 和評分
1
主持人：臺北醫學大學陳冠州所長主講者：李英雄教授

報告人：高治圻指導老師：吳麥斯/張偉嶠題目：New Frontier of
13:30 - 14:00
題目：Association of genetic polymorphism and Precision Medicine at the
chronic kidney disease related complications Chung-Shan Mdical University
主持人：臺灣大學楊偉勛所長精準醫學新境界在中山醫學大
14:00 - 14:30 報告人：吳振吉學
題目：兒童聽損之精準醫療
主持人：陽明大學王錦鈿所長主講者：李英雄教授
報告人：李雅婷指導老師：牛道明題目：A Fine Perspective of
14:30 - 15:00 題目：Development of a Gene Therapy for Fabry Precision Medicine in Taiwan
Disease Using Adeno-Associated Viral Vector 台灣精準醫學一幅美好的遠景
Mediated Gene Transfer
主持人：國防醫學院黃坤崙所長
報告人：陳杭港指導老師：王智弘
題目：Insonation of Systemically Delivered
15:00 - 15:30
Cisplatin-Loaded Microbubbles Significantly
Attenuates Nephrotoxicity of Chemotherapy in
Experimental Models of Head and Neck Cancer
15:30 - 15:40 交流時間(Coffee Break)
主持人：高雄醫學大學吳明蒼所長
報告人：陳昭儒指導老師：劉子鵬
15:40 - 16:10
題目：Characterization of lung cancer stem cells at
different EMT status
主持人：國防醫學院黃坤崙所長主講者：林克亮副教授
題目：Building the Framework
報告人：陳鉞忠指導老師：蔡建松
of Health Care in Precision
題目：Downstream Molecular Signals Of P2Y12 Medicine Ecosystem
Receptor Signaling In Patients Receiving Dual 建立精準醫療生態系統之健康
16:10 – 16:40 照護架構
Antiplatelet Therapy-Biphasic Effect Of AR-C On
The PLCβ-1 Pathway In-vitro Maybe A Possible
Mechanism Of High On-Treatment Platelet
Reactivity
主持人：中山醫學大學陳進典所長
報告人：李欣樺指導老師：林志立
16:40 - 17:10
題目：miR-302 : implication for age-related
diseases
17:10 - 17:20 頒獎
17:20 - 17:40 下屆主辦系所所長閉幕致詞
2
二、演講者簡介
Professor of Biostatistics, Biomedical
Informatics, and Health Policy
Professor Yu Shyr
石瑜教授
現職 Current Position
Chairman, Department of Biostatistics
Director, Vanderbilt Center for Quantitative Sciences
Director, Vanderbilt Technologies for Advanced Genomics Analysis and
Research Design
Harold L. Moses Chair in Cancer Research
學歷 Education
Doctor of Philosophy, University of Michigan, Ann Arbor, Biostatistics
Master of Science, Michigan State University, Statistics
經歷 Positions and Employment

Director, Center for Quantitative Sciences Vanderbilt University
Medical Center
Associate Editor, Associate Editor for Statistics JAMA Oncology
Voting member, United States Food and Drug Administration
Director, Vanderbilt Technologies for Advanced Genomics Analysis and
Research Design, Vanderbilt University Medical Center
3
中山醫學大學醫學研究所
講座教授
Professor Ying-Shiung Lee

李英雄教授
中山醫學大學醫學研究所講座教授
中山醫大附設醫院執行長
學歷 Education
國立台灣大學醫學院醫學系
台灣
台大醫學院附設醫院住院醫師 / 總醫師 / 心臟科研究員 / 講師
台北醫學院兼任副教授 /兼任教授
中原大學兼任副教授
長庚大學醫學院教授 / 臨床醫學研究所所長 /醫學院院長
長庚紀念醫院心內科主任 / 副院長 / 中醫體系執行長
佛教慈濟綜合醫院新店院區院長
中國醫藥大學研發長 / 健康照護學院院長 /副校長
中國醫藥大學附設醫院醫研部主任 / 顧問
中國科學院北京電子顯微鏡室客座研究員
北京大學客座教授
北京醫科大學 (現為北京大學醫學部) 客座教授
中國醫科大學客座教授
4
福建醫科大學客座教授
上海醫科大學 (現為復旦大學醫學院) 客座教授
揚州大學客座教授
成都中醫藥大學客座教授
內蒙古醫學院客座教授
廈門大學醫學院兼任教授
5
中山醫學大學
醫學檢驗暨生物技術學系
Keh-Liang Lin, Ph.D.

林克亮副教授
中山醫學大學醫學檢驗暨生物技術學系副教授
台灣精準醫學學會副秘書長
教育部退撫儲金監理會委員
學歷 Education
國立臺灣大學醫學院微生物學研究所博士
國立臺灣大學醫學院微生物學研究所碩士
私立台北醫學大學醫事技術學系學士
Western Australia Research Institute for Child Health 博士研究
中山醫學大學醫學檢驗暨生物技術學系系主任
中山醫學大學醫學視光學系創系主任
中山醫學大學推廣教育中心主任
中山醫學大學附設醫院檢驗科主任
中山醫學大學附設醫院濫用藥物檢驗中心主任
6
三、大會演講
演講者：Yu Shyr, Ph.D. 石瑜教授
Professor of Biostatistics, Biomedical Informatics, and Health Policy Vanderbilt

University Medical Center USA
演講題目：Big Data, Smart Data, and Actionable Data: Shaping the Future of Precision
Medicine and Healthcare
演講摘要：
The key concepts of precision medicine are prevention and treatment strategies that take
individual molecular profile and clinical information into account. Single-cell next-
generation sequencing technologies (NGS), liquid biopsy for circulating tumor DNA
(ctDNA) analysis, microbiomics, radiomics, and other types of high-throughput assays
have exploded in popularity in recent years, thanks to their ability to produce an
enormous volume of data quickly and at relatively low cost. The emergence of these big
data has advanced the goals of precision medicine; however, across the entire continuum
of big data capture and utilization, many more challenges lie ahead—from analysis of
high-throughput biomarkers to maximum exploitation of the electronic health record
(EHR), to the ultimate goal of clinical guidance based on a patient’s genome.
In recent years, almost all top biomedical journals have published major findings using
advanced data science technologies, including complex statistical modeling, machine
learning, and AI. Interpreting these results for patients and applying them for clinical
guidance, however, remain significant challenges.
In this presentation, I will offer some perspectives on the changing landscape for
precision medicine, including the road map for choosing between statistical modeling
and machine learning; the concept of treating unstructured text as quantitative data; the
need for physicians to adapt their mindset around the explosive growth in information
technology; machine learning; and the AI revolution. These areas present great
opportunities for medical researchers to strengthen their role in precision medicine. I
will finish up with some thoughts about future medical developments, including how to
design and conduct pivotal trials, pragmatic trials, and real-world evidence studies in
the precision medicine era.
7
四、課程大綱 (0212 教室)
主講者：林克亮副教授
課程題目：A 10-Year-Ground Sword for Precision Medicine 精準醫學十年磨劍

課程摘要：『Precision Medicine』精準醫學一詞，是 2009 年哈佛大學商學院教授 Clayton
Christensen 在新書「The Innovator’s Prescription」中提出的，而真正揭開序幕是到西元 2011 年
由美國國家研究委員會(the US National Research Council)提出的概念(Concept)，隨後美國歐巴
馬總統任內提出『3+1』的大型醫學研究計畫: (1). 2013 年腦科學研究計畫(Brain Initiative)、(2).
2015 年精準醫學啟動計畫(Precision Medicine Initiative) 、(3).2016 年癌症探月計畫(Cancer
Moonshot Initiative)，以及(4). 2016 年五月卸任前半年追加人類微生物基因體計畫(Human
Microbiome Project, HMP)，除了宣示美國舉全國之力的探月精神針對進行相關精準醫學相關研
究，這四大計畫環環相扣，縝密布局，企圖對人類生命健康構建全面性解決(Total solution)或系
統性解決(Systems solution)之道。英國國家創新局隨後也宣布成立精準醫學彈射計劃(Precision
Medicine Catapult)。中國政府提出『健康中國』戰略計畫，將精準醫學納入國家『十三五』大
健康、大衛生及大醫學計畫，提出『精細管理, 精準醫學』。世界各國政府頃全力投入資源與參
與主導，中、美、英三國領袖人物的加持驅動下，引導產、官學研界紛紛搖旗吶喊，推波助瀾，
更以組國家隊態勢加入國際間精準醫學的競賽，未來 10-15 年內那一國家會勝出？再請拭目以
待，相信無論哪一個國家領先，全世界都將受益。台灣也在 2016 年 11 月 26 日由行政院相關
單位發布全力推動「利基型的精準醫學」，將建立四大系統，包括健康監測記錄系統、快速即
時檢測系統(精準診斷需求)，用藥確效檢測系統及疾病風險評估系統(回饋治療策略)，統整產、
學、研界的研發能量，推動精準醫療產業的發展，引領醫學更上一層樓。要達成精準醫學終極
的目標，個人基因變異及其所有的體學(Multi-Omics)的分析，人所處環境健康(Environmental
health)、營養狀況及與生活型態(Life style)產生的大數據(Big data)，這十年發展，精準醫學結合
萬物聯網(Internet of Everything, IOE)及人工智慧(Artificial Intelligence, AI)，建立所謂的 AIoE
醫學平台，提高疾病風險評估的準確性，達到系統中醫學(Systems Chinese Medicine)之天人合
一及上醫醫未病的預防醫學(Preventive medicine)與預測醫學(Predictive medicine)之精準醫學健
康 4.0 新境界。
8
主講者：李英雄教授
課程題目：Dramatic Advances in Precision Medicine Based on Megadata-Driven
Artificial Intelligence 基於大數據驅動人工智慧精準醫學之戲劇性進展

課程摘要：電腦科學(Computer Science)的突破性進展及數位(字)技術(Digital Technology)的革命
性創新使得龐大的數據/資料之收集、儲存、追蹤、觀察、分析、辨識、確證及預測都能依照一
定的程序按部就班如期完成，達致預期的目標。大數據(Big Data)幾乎無所不包侵襲各個學門/
領域及各行各業，當然生技醫藥領域亦無法倖免，已成為現今科學火紅炙熱的一門顯學，只要
掌握大數據，以及數據的演算分析法，就將在 21 世紀的大數據時代勝出，居引領主導時局的
角色，當今的世界已經邁入大數據年代是無庸置疑的事實了。
近年來，人工智慧(能)的蓬勃發展是奠基於大數據的強力支撐及電腦演算法(Algorithms)的
不斷精進，尤其是機器學習演算法(Machine-Learning algorithm)/深度學習演算法(Deep-Learning
algorithm)的成功研發問世，使得許多不可能變成可能，在指定的特殊任務之執行力，人工智慧
幾乎已超越人類，就以臨床醫學的診斷與治療及藥學的藥物探索研發而論，醫藥學界的專家都
自嘆不如。因此，人工智慧介入醫學領域的轉譯應用必能促使臨床實證更精確有效，達到真正
的個人(性)化醫療(Personalized medicine)，並驅動《精準醫學》無限的拓展延伸邁入新境界，朝
向新紀元奮發前進，創造新的里程碑。至於製藥與生技企業正如火如荼建構先進高端的人工智
慧平台從事藥物與產品之研發，不僅可有效縮短整個製程，而且亦能大幅節省成本，更重要的
是提升企業的執行效率，改善陳舊的結構，促使創新轉型永續經營。
總之，大數據奠基人工智慧正舖天蓋地無孔不入侵襲醫藥生技領域的各個層面，引起革命
性的轉變，驅使《精準醫學與藥學》早日實現，諸君拭目以待吧！
9
課程題目：New Frontier of Precision Medicine at the Chung-Shan Medical University
精準醫學新境界在中山醫學大學
課程摘要：西元 2015 年，美國「National Research Council」倡導《Toward Precision Medicine
(邁向精準醫學)》之宗旨/目標與使命/任務，簡述如下：
1. 宗旨/目標：Building Knowledge Network (建構知識網)
2. 使命/任務：
(1) For Biochemical Researches (生物醫學研究)
(2) For a New Taxonomy of Diseases (疾病的新分類)
由此簡潔的詞句不言而喻《精準醫學》的整體理念是為生物醫學研究暨疾病的新分類必須
建構知識網才能落實完成。隨後，National Research Council 轄下成立「Precision Medicine
Committee (精準醫學委員會)」來推動《Creating Information Commons(創造資訊庶民)》，其目
的在於將精準醫學的相關資訊向社會大眾做廣泛的宣導，藉以共享知識網絡帶來的效益。
本校基於美國 National Research Council」提倡《精準醫學》的宏觀理念作出即時明確的共

鳴回響，順應時勢，求新求變，遂於西元 2016 年起開始著手建構精準醫學相關的知識網，至
西元 2019 年，陸續完成字數總共逾百萬字的五本中文版精準醫學系列教科書，是目前舉世獨
一無二的精準醫學經典著作。
這五本精準醫學集大成的橫空出世，頓使中山醫學大學的醫學教育站在時代的前沿，引領
台灣醫學界朝向「破壞式創新醫學(Innovative Destruction of Medicine)」作徹底的轉型，開創醫
學的新紀元，企盼台灣的醫界同道精誠團結來共襄盛舉，早日達成目標。
10
課程題目：A Fine Perspective of Precision Medicine in Taiwan 台灣精準醫學一幅美
好的遠景
課程摘要：西元 2015 年，美國總統 Barack Obama 啟動《Precision Medicine Initiative》的計畫
是關鍵性的臨門一腳，驅動全球的生技醫藥界人士紛紛響應共襄盛舉，台灣醫學界理所當然不
會缺席，甚至立即採取行動，於西元 2015 年 8 月成立《台灣精準醫學學會》
，除了推動美國倡
導的精準醫學之理念外，更是不遺餘力落實精準醫學，接地氣、本土化、創立新模式，如建立
精準醫學次專科醫師暨諮詢師的認證制度就是最好的佐證。
《台灣精準醫學學會》是台灣精準醫學邁向美好遠景之寄託與依歸，身負任重道遠的偉大
使命，其任務不同於傳統常規的專科醫學學會，除了舉辦例行性的學術會議與活動外，最重要
的職責是緊密無縫地鍵結台灣生技醫藥產業界從事科技的創新研發與產品製造行銷，提供國際
市場的需求，對全球的經濟發展作出貢獻。值得重視在此一提的是台灣精準醫學學會正積極促
進產、學、研界全面性共同合作來推動精準醫學的理念成為 21 世紀大健康暨生技醫藥產業的
新商業/營運模式(New Business Model)，全體遵循所制定的準則章程，同心協力集思廣益為台
灣醫學教育及生技醫藥產業之轉型戮力以赴，並為改善專業人士的培育訓練而不辭辛苦，唯有
如此，台灣精準醫學的未來發展才有美好的遠景，衷心企盼同道精誠團結，共同完成新時代賦
予精準醫學的崇高使命。
近年來，本人朝思暮想，面臨 21 世紀知識爆炸的時代，精準醫學大數據正逐漸沉浸健康/醫療
照護的機構，包括行政機關、公司行號、醫療院所等無一倖免，可是不論是從事醫療/健康服務
的提供者及肩負行政管理的職員對精準醫學大數據之基本知識與分析能力都亟需加強教育與
培訓，因此本人意欲策畫《精準醫學大數據管理分析師》的培育課程，藉以未雨綢繆，儲備人
才以應未來醫學轉型之所需。中山醫學大學與台灣精準醫學學會共同合作設計《精準互聯系統
醫學(Precision Communications Medicine)》的多元跨域整合學程(如下圖)，將於西元 2020 年，
世人稱為《The Year of Good Vision (好的憧憬年)》期間，擇日正式開班講授作育英才，揚帆啟
航之日希望志同道合之士撥冗蒞臨指教是盼。
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主講者：林克亮副教授
課程題目：Building the Framework of Health Care in Precision Medicine Ecosystem
建立精準醫療生態系統之健康照護架構
課程摘要：『Precision Medicine』在基礎學術領域翻譯為『精準醫學』，若在臨床實務(Clinical
practice)則將之稱為為『精準醫療』
。在二十一世紀轉譯醫學(Translation Medicine)的概念，精準
醫學或精準醫療基礎學術與臨床實務，應要追朔至西元 1985 年首先推動基因體計畫的科學家
之一的 Dr. Leroy Hood，在 2000 年最早建立系統生物學研究所(Institute of Systems Biology)，
提出 4P 醫學『4P Medicine, Preventive Medicine, Predictive Medicine, Personalized Medicine &
Participatory Medicine 』，精準醫學(Precision medicine)早先由 Clayton Christensen 在 2009 年
新書中率先提出，隨後美國國家研究委會於 2011 年提出朝向精準醫學(Toward precision
medicine)的概念，主要推動建構生物醫學研究及疾病新分類的知識網絡(Knowledge network)，
隨後美國歐巴馬總統在 2015 年元月提出精準醫學啟動計畫(Precision Medicine Initiative)，帶動
全世界推動發展精準醫學的潮流；我們台灣精準醫學學會也在當年也就是 2015 年籌備立案成
立，去年九月台衛生福利部也公告『特定醫療技術檢驗檢查檢驗醫療儀器施行或使用管理辦法』
簡稱特管辦法發布實施，相信會更有安全保障的加速台灣精準醫學相關領域的發展。21 世紀
醫療是健康的世紀，在生物醫學科技的大幅發展下，實施「精準醫學」已經是水到渠成，結合
基礎科技發展與臨床實務及產業需求，台灣精準醫學學會跨業跨界規劃及推動『精準醫學專科
醫師』及『精準醫學諮詢師』的認證制度值得肯定，結合臨床醫師、藥師、醫檢師、護理師及
生物科技界人才，建立完善台灣精準醫學生態系統之臨床照護團隊，引進最新正確生物科技來
提升台灣臨床精準醫學醫療品質，也將深耕至高級中學學生及普羅庶民大眾，期盼醫療與教育
結合，善盡醫學大學社會責任；並致力於推廣我們中山醫學大學李英雄教授倡導的精準醫學
10Ps (6Ps+ 4Ps)整合醫學教育架構概念，其中臨床實務端之『6Ps』
：包括 1.預防醫學(Preventive
Medicine), 2. 預測醫學(Predictive Medicine), 3. 先制醫學(Pre-emptive Medicine), 4. 精準醫學
(Precision Medicine), 5. 個人化醫學 (Personalized Medicine )& 6. 參與醫學 Participatory
Medicine 』。學校基礎教育端之『4Ps』：包括 1. 熱情(Passion), 2. 專業(Prpfession), 3. 製造者
(Producer)及 4. 出版者(Publisher), 培育出態度熱情具跨業跨界多專業領域學生，並能創新創意
的發表文章及腳踏實地擔當臨床實務工作，使精準醫學概念進入李英雄教授最近提出的精準互
聯系統醫學(Precision Communications Medicine)的新境界，建構完整精準醫學健康照護之醫療
生態系統。
12
五、研討會 (0211 教室)
演講摘要
學校系所: 中國醫藥大學
演講人姓名: 鍾瑋敏 / Wei-Min Chung
現職: 臨床醫學研究所博士班學生
電子信箱: qqrice68@yahoo.com.tw
指導老師姓名: 馬文隆 / Wen-Lung Ma
演講題目(英文):
The Translational Research of Androgen Receptor in Ovarian Cancer Stemness and
Chemoresistance
演講摘要(英文):
Ovarian cancer (OVCA) arise from three cellular origin, including surface epithelial cells, germ cells,
and stromal cells. The most lethal OVCA is epithelial onarian cancer (EOC) which can be divided into
four histological subtypes, including serous carcinoma (SC, ~75 ), mucinous carcinoma (MC, ~3 ),
endometrioid carcinoma (EC, ~10 ) and clear cell carcinoma (CCC, ~10 ). Cancer stem/progenitor
cells (CSPCs) are considered cancer promoter for their capacity of unlimited self-renewal and drug
resistance. Androgen receptor (AR) belongs to nuclear receptor superfamily, which activation through
biunding with androgens. AR has been suggested to play role in OVCA development. In the thesis, an
ligand-independent AR function to enriches CSPCs (e.g., CD133+) via facilitated self-renewal in
ovarian teratocarcinoma cells (OVTC, germ cell tumors) was demonstrated. Moreover, an OVTC
promoter roles of onco-miR (miR-21) had been associated with AR expression. The miR-21 itself is
essential for promoting cell growth through sustaining CSPCs. On the other hand, the pathological
roles of AR in SC-EOC was characterized. The AR and ABCG2 were colaterally expressed in SC-
EOC lesions. The AR expression is linked to SC-EOC of taxel treatment modality to poor prognosis.
Palitaxel treatment could turn on AR tranactivation function in vitro, of which explained the paclitaxol
resistence in molecular aspect. The mechanistic dissection has delineated a paclitaxol-AR/AhR (aryl-
hydrocarbon receptor)-ABCG2 regulatory axis in SC-EOC cells. For the translational approach, the
ASC-J9 (AR degradation enhancer) treatment could resensitize paclitaxel-resistance SC-EOC in vitro
and in vivo. Therefore, the utilization of ASC-J9 for OVCA therapy is vivid in the future. In conclusion,
this thesis summarized the roles of AR play in OVCA disease development in cellular and molecular
levels. This thesis illustrated the mode-of-action for ASC-J9 pharmaceutical development.
13
學校系所: 長庚大學醫學院臨床醫學研究所

演講人姓名: 傅宏鈞 / Hung-Chun Fu
現職: 長庚醫療財團法人高雄長庚紀念醫院婦產部
電子信箱: allen133@cgmh.org.tw
指導老師姓名: 康宏佑 / Hong-Yo Kang (蕭長春副教授代，Chang-Chun Hsiao)
SKP2 and P16INK4A Modulate Stemness and Radioresistance of cervical cancer
Cervical carcinoma is the third common malignancy in women worldwide. Radiation therapy (RT)
with or without cisplatin-containing chemotherapy is the most commonly used treatment modality in
patients with advanced cervical cancer. Loco-regional recurrences are frequently found in patients.
The recurrent cervical cancer cell had higher radioresistance. The prognosis and response to irradiation
were quite different in patients with a similar status of cervical cancer receiving RT or concurrent
chemoradiotherapy (CCRT). Clearly, there remains a need for a better understanding of the molecular
events involved the responses of cervical cancer to RT. We try to get a breakthrough in new therapeutic
targets and new biomarkers to predict the prognosis of the patients. We aim to identify a molecular
marker predicting the response of cervical cancer to radiotherapy.
In the literature review, we found the radioresistance of cell was different at the different phase of cell-
cycle (G1-S-G2-M). The cells in the S phase are the most radioresistant. S-phase kinase-associated
protein 2 (SKP2) and cyclin-dependent kinase inhibitor 2A (CDKN2A, P16INK4A) are tow important
proteins during G1-S phase of cell-cycle. SKP2 promotes cells into S-phase. In contrast to SKP2,
P16INK4A decelerates the cell's progression from G1 phase to S phase. We suspected SKP2 and P16INK4A
maight play an important role in radioresistant cervical cancer.
SKP2 is an E3 ubiquitin ligase and a part of SKP1-Cul1-F-box (SCF) complexes. It has important roles
in the ubiquitination of proteins involved in the cell cycle and also marks various other cellular proteins
for destruction. Previous studies showed overexpression of SKP2 was frequent in human cancer
progression and metastasis, and evidence suggested that SKP2 plays a protooncogenic role both in
vitro and in vivo. It is still unclear whether SKP2 is a prognostic factor of cervical cancer treated with
radiotherapy. We try to further study to answer the question.
P16INK4A is encoded by the CDKN2A gene and is thought to be a tumor suppressor. P16 INK4A is
important in cell-cycle regulation by decelerating the progression of cycle from G1 to S phase. We
used P16INK4A as a biomarker for cervical carcinogenesis. It is still unclear whether P16 INK4A is a
prognostic factor for cervical cancer receiving radiotherapy. We tried to investigate the expression and
clinical significance of P16INK4A in cervical cancer.
14
We included the patients (n = 149) with cervical cancer who had undergone radiotherapy from 2004
to 2006. Tumor samples were collected to examine the association between the expression of SKP2
and prognosis in cervical cancer. We found higher expression of SKP2 associated with recurrence
(HRs: 2.52, p < 0.001), death (HRs: 2.01, p < 0.001) and higher locoregional recurrence rate (HRs:
3.76, p < 0.001). Cervical cancer cell lines with higher expression of SKP2 showed higher colony
formation, cell survival rate and fewer DNA damages after irradiation.
And, we proved the prognosis of the cervical cancer with higher expression of P16 INK4A were better.
In cell model, we knocked down expression of P16INK4A in HeLa and C33A cells and found they were
more radioresistant and chemoresistat. P16INK4A is not only the gatekeeper of G1-S cell phase, but also
an important factor of senescence of general or stem cells. Our data showed depletion of P16INK4A
caused higher expression of sex determining region Y-box 2 (SOX2) and Aldehyde dehydrogenase 1
family, member A1 (ALDH1A1) in cervical cancer cells. And, higher self-renew ability was observed.
So, we hypothesized
P16INK4A inhibits stemness of cervical cancer cells and promotes radiosensitivity. In our clinical data
showed the patients cervical whose cancer samples with lower P16 INK4A and higher stem cell markers
(SOX2 and ALDH1A1) had poorer prognosis and higher recurrent rate.
Our data suggest that high SKP2 and P16INK4A expression markers predict poor prognostic outcomes
and are a promising target in patients with cervical cancer.
Key words: cervical cancer, SKP2, P16INK4A, radiotherapy, cancer stem cells
15
學校系所: 國立成功大學臨床醫學研究所
演講人姓名: 侯雅琴 / Ya-Chin Hou
現職: 博士後研究員
電子信箱: yachi2016@yahoo.com.tw
指導老師姓名: 沈延盛所長 / Yan-Shen Shan
Dissecting the genetic and molecular alterations in pancreatic cancer progression
Pancreatic cancer (PC) is one of the most deadly cancers and the overall survival
improved only minimally over the past 40 years. Nearly all diagnosed patients ultimately succumb to
the disease is attributable to its characteristics of clinically silent in early stage, high incidence of local
invasion, distant metastasis, and resistance to radiotherapy and most systemic chemotherapies,
suggesting that understanding etiology in PC patients may lead to the development of intervention
strategies to alleviate or treat this disease. Genetic analysis or molecular profiling of PC yielded
insights related to altered signaling pathways; however, those events that occur during tumorigenesis
in the same patients, particularly in Asian populations, remain unknown. Here we collected pancreatic
tumors of 65 patients annotated with clinical outcome and etiological features for whole exome
sequencing and oncomine comprehensive cancer panel assay. Tissue microarrays consisting of the
same samples were constructed for molecular profiling to identify biomarkers for PC diagnosis and
prognosis. We observed four major driver genes in pancreatic carcinogenesis, such as KRAS, TP53,
SMAD4, and CDKN2A mutations in 91%, 95%, 46%, and 91% of the samples, respectively. G12
mutations comprise 90% of all KRAS mutations. We also compared significantly mutated genes (p <
0.05) according to survival status of patients and identified 63 mutated genes that involve numerous
pathways including regulation of cell proliferation, cell death, cell communication, intracellular signal
transduction, protein modification and metabolic process, and immune system. Moreover, the presence
of cancer stem cells, tumor infiltrating cells, and the expression of immunosuppressive markers were
determined by a quantitative immunostaining approach. These data showed that the combination of
CD8+ T cells infiltration and PD-L1 expression is well-suited as an indicator for classifying PC tumors
and predicting clinical outcomes. Low CD8+ T cell infiltration and high PD-L1 expression are
correlated with the level of CD44+/CD133+ CSCs. Our study highlights an interaction among CD8+ T
cells infiltration, PD-L1 expression, and CD44+/CD133+ CSCs existence, which contributes to PC
progression and immune evasion. These findings offer the potential factors for prognostic evaluation
of PC and help in designing promising immune-based therapeutic strategies.
16
學校系所: 慈濟大學醫學科學研究所
演講人姓名: 陳家輝 / Jia-Hui Chen
現職: 台北慈濟醫院一般外科主治醫師
電子信箱: procto77@gmail.com
指導老師姓名: 洪智煌 / Chih-Huang Hung
Neuroprotective Effects of Collagen-Glycosaminoglycan Matrix Implantation following
Surgical Brain Injury
Neurological deficits following neurosurgical procedures are inevitable; however, there are still
no effective clinical treatments. Earlier reports revealed that collagen-glycosaminoglycan (CG) matrix
implantation promotes angiogenesis, neurogenesis, and functional recovery following surgical brain
injury (SBI). Our study was conducted to further examine the potential neuroprotective effects of
collagen-glycosaminoglycan (CG) matrix implantation following neurosurgery. CG implantation
was performed in the lesion cavity created by surgical trauma. The Sprague-Dawley rat model of SBI
was used as established in the previous study by the author. The rats were divided into three groups as
follows: (1) sham (SHAM), (2) surgery-induced lesion cavity (L), and (3) CG matrix implantation
following surgery-induced lesion cavity (L+CG). Proinflammatory (tumor necrosis factor-alpha (TNF-
α), interleukin-6 (IL-6), and NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells))
and anti-inflammatory (IL-10 and granulocyte-macrophage colony-stimulating factor (GMCSF))
cytokine expression was evaluated by enzyme-linked immunosorbent assays. Microglial activation
was evaluated by immunohistochemistry, and the neuroprotective effect of CG matrix implantation
was evaluated by an immunohistochemical study of microglia ED-1 and IBA-1 (activated microglia)
and myeloperoxidase (MPO) and by the analysis of IL-6, IL-10, TNF-α, NF-κB, and GMCSF cytokine
levels. Apoptosis was also assessed using a TUNEL assay. The results showed that CG matrix
implantation following surgically induced lesions significantly decreased the density of ED-1, IBA-1,
and MPO (activated microglia). The tissue concentration of proinflammatory cytokines, such as TNF-
α, IL-6, and NF-κB was significantly decreased. Conversely, the anti-inflammatory cytokines GMCSF
and IL-10 were significantly increased. Implantation of the CG matrix following SBI has
neuroprotective effects, including the suppression of microglial activation and the production of
inflammatory-related cytokines.
17
學校系所: 臺北醫學大學臨床醫學研究所
演講人姓名: 高治圻 / Kao Chih-Chin
現職: 台北醫學大學附設醫院腎臟內科醫師
電子信箱: 121008@h.tmu.edu.tw
指導老師姓名: 吳麥斯 / Wu Mai-Szu
張偉嶠 / Chang Wei-Chiao
Association of genetic polymorphism and chronic kidney disease related complications
Chronic kidney disease patients have a high risk of cardiovascular diseases. Many risk factors have
been reported, such as diabetes, hypertension, chronic inflammation, anemia and erythropoietin
resistance. However, these traditional risk factors do not fully explain the excess cardiovascular risk
and erythropoietin resistance in these patients. Therefore, we aimed to investigate the association of
genetic variants (in candidate genes) and interested phenotypes (cardiovascular complications and
erythropoietin resistance). In our study, we enrolled 190 chronic kidney disease patients who received
chronic dialysis for at least 3 months at Taipei Medical University Hospital. We collected
demographics, clinical laboratory data, and interested outcomes. The tagged SNPs (single nucleotide
polymorphisms) of candidate genes were selected and genotyping was performed using the TaqMan
Allelic Discrimination Assay (Applied Biosystems, Foster City, CA). Analysis showed EDN1
rs4714384 (CC/TC vs. TT) polymorphism was associated with an increased risk of a CV event. Further
functional exploration showed that it was a quantitative trait locus which may significantly alter gene
expression in the tibial artery. In the study of erythropoietin resistance, we found STIM1 rs1561876 G
allele, ORAI1 rs6486795 GG and rs7135617 AA associated with risk of erythropoietin resistance.
These findings may become meaningful biomarker in the clinical practice. Further validation studies
are required to confirm the roles of genetic variants in the phenotypes of these patients.
Key words: chronic kidney disease, erythropoietin resistance, genetic polymorphism
18
學校系所: 臺大醫學院臨床醫學研究所
演講人姓名: 吳振吉 / Chen-Chi Wu
現職: 合聘教授
電子信箱: chenchiwu@ntuh.gow.tw
Precision medicine of pediatric hearing impairment
Sensorineural hearing impairment (SNHI) in children is a common clinical entity, and is an
etiologically heterogeneous condition caused by a plethora of genetic and/or environmental factors.
My team and I have been dedicated to the early detection, diagnosis, and management of pediatric
SNHI over the past 15 years. Our previous and current work includes clinical genetic studies,
translational studies, and basic animal studies, covering a wide but continuous range of research
interests in this field.
1. Clinical genetic studies
To date, we have established a large SNHI cohort in Taiwan, composed of >3000 families with
>6000 patients. We have screened pathogenic variants of common deafness genes, including GJB2,
SLC26A4 and mitochondrial 12S rRNA gene, in all the families. We have clarified the
epidemiological data of these common deafness genes in the Taiwanese population. Recently, we
initiated an international collaborative project to perform genetic examination in ~200 Mongolian
families with SNHI. Our results unraveled a unique genetic profile in Mongolian patients as
compared to other European and Asian populations.
From 2013, we started to establish novel diagnostic platforms using the next-generation
sequencing (NGS) technology. We have been upgrading our NGS-based platform continuously, and
currently, we can use it to screen ~200 known deafness genes simultaneously. We also selected 27
predominant deafness genes in the Chinese patients, and commercialized a NGS-based diagnostic
panel for the patients with affordable price. To date, we have subjected >300 families to our NGS-
based diagnostic platform for genetic testing. Our results revealed that NGS-based platforms could
significantly improve the diagnostic yield and enable us to achieve genetic diagnosis in both
multiplex and simplex families.
2. Translational studies
Precise genetic diagnoses facilitate genetic counseling in the SNHI families and enable
personalized medicine in the affected patients. Our studies over the past years confirmed the utility
of genetic examination for deafness in predicting the disease course (e.g. the progression/severity
of SNHI) and the treatment outcome (e.g. the outcome with cochlear implants [CIs]). In our recent
longitudinal studies which incorporated newborn genetic and CMV screenings into the newborn
hearing screening protocol, we demonstrated that the incorporation of these screening tests could
be useful in identifying hearing-impaired children at an earlier age.
3. Basic animal studies
To explore the pathophysiology and potential therapeutic strategies, we have generated several
strains of cell-lines, as well as knock-in mouse models harboring deafness mutations of interest. We
have established platforms to assess the audiovestibular phenotypes, inner ear morphology, and
auditory electrophysiology in the mouse models. Recently, we started to investigate the feasibility
of gene therapy. Our preliminary findings revealed that Anc80-mediated gene therapy was able to
improve hearing and restore balance function in mice with defected Pjvk gene, a deafness gene
related to unfavorable CI outcomes. Our results indicate that gene therapy is likely to become a
treatment option for pediatric SNHI, as well as a possible armamentarium that can augment the
function of CIs.
19
學校系所:陽明大學臨床醫學研究所
演講人姓名: 李雅婷 / Lee, Ya-Ting
現職: 碩二學生
電子信箱: angellee112233@gmail.com
指導老師姓名: 牛道明 / Niu, Dau-Ming
Development of a Gene Therapy for Fabry Disease Using Adeno-Associated Viral Vector
Mediated Gene Transfer
Fabry disease (FD) is an X-linked lysosomal storage disease, which is caused by genetic
mutations on human GLA gene that encoded alpha-galactosidase A enzyme. The incidence of FD was
around 1 in 50,000 worldwide, but relatively higher at approximately 1 per 1,471 in Taiwan due to a
special mutation in the 4th intron (IVS4+919 G>A). The biological function of GLA is involved in the
breakdown of globotriaosylceramide (Gb3) in lysosome. Lack of GLA enzyme activity resulted in
accumulation of Gb3 and caused life-threatening diseases such as stroke, cardiac, and renal failure.
The enzyme replacement therapy (ERT) with recombinant human GLA (rhGLA) is the most common
therapy for FD. However, ERT has several disadvantages, such as short half-life of protein drug,
limited efficacy for patients with renal failure, and extremely expensive. Therefore, development of a
new therapeutic strategy for FD is highly demanded. The gene therapy using adeno-associated virus
(AAV) vectors may be a promising therapeutic approach. Previous researches took advantage of AAV1,
AAV2, AAV8 to express the therapeutic GLA gene in Fabry mice. However, the increasing of enzyme
activity in kidney was not observed. In this study, we try to use AAV9, which affords a higher level of
heart transduction and transgene expression than AAV8, to treat the Gla knockout (Gla−/y) mice. We
developed AAV9 viral vector encoding GLA and applied to Gla−/y mice to validate the therapeutic
efficacy. The GLA enzyme activity was significantly higher in plasma, liver, heart and kidney of Fabry
mice after treated with AAV9-GLA than those treated with AAV8-GLA. We had also determined that
α-Gal A activity can sustain for at least 3 months. Further more, we had found out that both AAV8 and
AAV9 groups showed low immunogenicity in Fabry mice. Moreover, AAV9 group ameliorated
proteinuria when compared to untreat groups. Taken together, our data demonstrated the therapeutic
potential of AAV9 vector–mediated GLA gene therapy for Fabry disease.
20
學校系所: 國防醫學院醫學科學研究所
演講人姓名: 陳杭港 / Hang-Kang Chen
現職: 國軍台中總醫院王智弘院長實驗室博士後研究員
電子信箱: hwalongchen@yahoo.com.tw
指導老師姓名: 王智弘 / Chih-Hung Wang
Insonation of Systemically Delivered Cisplatin-Loaded Microbubbles Significantly
Attenuates Nephrotoxicity of Chemotherapy in Experimental Models of Head and Neck
Cancer
The use of cisplatin (CDDP), the most common chemotherapy drug for head and neck
cancer, is limited by its undesirable side effects, especially nephrotoxicity. We investigated ultrasound
microbubbles (USMB) as a tool to increase the local intra-tumoral CDDP level while decreasing
systemic CDDP cytotoxicity. We allowed CDDP to interact with human serum albumin and then
sonicated the resulting CDDP-albumin complex to generate CDDP-loaded MBs (CDDP-MBs). We
then established a head-and-neck tumor-bearing mouse model by implanting FaDu-fLuc/GFP cells
into severe combined immunodeficiency mice and used IVIS® bioluminescence imaging to determine
the tumor xenograft formation and size. Twice weekly (until Day 33), we administered CDDP only,
CDDP + MBs + US, CDDP-MBs, or CDDP-MBs + US intravenously by tail-vein injection. The US
treatment was administered at the tumor site immediately after injection. The in vivo systemic
distribution of CDDP indicated that the kidney was the most vulnerable organ, followed by the liver,
and then the inner ear. However, CDDP uptake into the kidney and liver was significantly decreased
in both the CDDP-MBs and CDDP-MBs + US groups, suggesting that MB binding significantly
reduced the systemic toxicity of CDDP. The CDDP-MBs + US treatment reduced the tumor size as
effectively as conventional CDDP-only chemotherapy. Therefore, the combination of CDDP-MBs
with ultrasound is effective and significantly attenuates CDDP-associated nephrotoxicity, indicating a
promising clinical potential for this approach.
Keywords: ultrasound; microbubble; cisplatin; nephrotoxicity; head and neck cancer; chemotherapy
21
學校系所: 國防醫學院醫學科學研究所
演講人姓名: 陳鉞忠 / Yueh-Chung Chen
現職: 臺北市立聯合醫院心臟內科部主任
電子信箱:chenyuehchung.tw@yahoo.com.tw
指導老師姓名: 蔡建松 Chien-Sung Tsai
演講題目: Downstream Molecular Signals Of P2Y12 Receptor Signaling In Patients Receiving
Dual Antiplatelet Therapy-Biphasic Effect Of AR-C On The PLCβ-1 Pathway In-vitro Maybe A
Possible Mechanism Of High On-Treatment Platelet Reactivity.
演講摘要:
Clopidogrel is a P2Y12 inhibitor used in dual antiplatelet therapy (DAPT) to inhibit platelet
activation and aggregation. High on-treatment platelet reactivity (HOTPR) after clopidogrel treatment
is correlated with stent thrombosis, and has been attributed to genetic variations in the CYP2C19 gene.
However, although Taiwanese patients exhibit HOTPR, they have a relative lower subacute stent
thrombosis rate compared to Caucasians, suggesting that HOTPR could be mediated via mechanisms
other than liver cytochrome activity. In this study, we developed an ex-vivo system to investigate the
role of P2Y12 signaling on HOTPR in patients with different reactivities to DAPT. In hypo-reactive
patients, expression of p-SYK, p-VASP, p-GSK, p-AKT, Rap1b, and P2Y12 proteins were significantly
higher in the ADP, ADP+PGE1, ADP+aggrastat, and ADP+PGE1+aggrastat samples compared to
control samples. Expression of PLCβ1 and p-PKC proteins were significantly higher in the ADP, and
ADP+PGE1 compared to the other groups; expression of Rap 1b was higher in the
ADP+PGE1+aggrastat group compared to the other groups. AR-C, exerted a non-proportional effect
in downstream signaling from the PLCβ-1 pathway in hypo-reactive samples. P-VASP was
upregulated by AR-C in a dose-dependent manner. MRS 2279, a P2Y1 inhibitor, exerted an inhibitory
effect on the Gβγ-regulated PLCβ-1 pathway but not the Gαi pathway, and significantly inhibited
P2Y12 receptor activity. Our data suggested that P2Y12 signaling could play a role in HOTPR
independent of CYP2C19 activity. Activation of the P2Y12 Gα1 receptor was shown to stimulate
platelet activation by cAMP-dependent as well as cAMP independent mechanisms. The GTP-bound
Gα subunit and the Gβγ subunits subsequently interact with their respective downstream effectors to
propagate their signaling pathways. Activation of phospholipase C β (PLCβ) by Gα or Gβγ has been
shown to play an important role in ADP-induced platelet activation by increasing cytosolic Ca2+
concentrations and promoting integrin activation via a Rap1-mediated pathway. An interesting finding
from this study was the biphasic effect of AR-C on the PLCβ-1 pathway during P2Y12 signaling in-
vitro. Treating hypo-reactive samples with increasing doses of AR-C, a potent P2Y12 receptor
inhibitor, resulted in a non-proportional effect in downstream signaling from the PLCβ-1 pathway,
suggesting that this could be possibly connected to clinical hypo-reactivity, and that it was independent
of CY2C19 activity.
22
學校系所: 高雄醫學大學醫學研究所臨床組

演講人姓名: (中文) 陳昭儒 (英文) Chao-Ju Chen
現職: 高雄醫學大學附設醫院檢驗醫學部主治醫師
電子信箱: chaoju.chen@gmail.com
指導老師姓名: (中文) 劉于鵬 (英文) Yu-Peng Liu
演講題目(英文): Characterization of lung cancer stem cells at different EMT status

Cancer cells with mesenchymal attributes potentially display chemoresistance. Cancer stem
cells (CSCs), which are intrinsically resistant to most chemotherapy agents, exhibit considerable
phenotypic heterogeneity in their epithelial versus mesenchymal states. However, the drug response
of CSCs in the epithelial and mesenchymal states has not been completely investigated. In this study,
we found that epithelial-type (E-cadherinhigh/CD133high) CSCs displayed a higher sphere formation
ability and chemoresistance than mesenchymal-type (E-cadherinlowCD133high) CSCs. Gene expression
profiling of the CSC and non-CSC subpopulations with distinct epithelial-to-mesenchymal transition
(EMT) states showed that MyoD family inhibitor domain-containing (MDFIC) was selectively
upregulated in epithelial-type CSCs. Knockdown of MDFIC sensitized epithelial-type CSCs to
chemotherapy agents. Ectopic expression of MDFIC increased the chemoresistance of mesenchymal-
type CSCs. In a tissue microarray, high MDFIC expression was associated with poor prognosis of non-
small cell lung cancer (NSCLC) patients. A mechanistic study showed that the MDFIC p32 isoform,
which is located in the cytoplasm, interacted with the destruction complex, Axin/GSK-3 / -catenin.
This interaction stabilized -catenin by inhibiting -catenin phosphorylation at S33/37 and increased
the nuclear translocation and transcriptional activity of -catenin. Knockdown of -catenin decreased
MDFIC-enhanced chemoresistance. These results suggested that the upregulation of MDFIC enhanced
the chemoresistance of epithelial-type CSCs by elevating -catenin activity. Thus, targeting MDFIC-
regulated -catenin signaling of epithelial-type CSCs may be a potential strategy to overcome
chemoresistance in NSCLC.
23
學校系所：中山醫學大學醫學研究所
演講人姓名：李欣樺 / Hsin-Hua Li
現職：博士後研究員
電子信箱：vivid529@hotmail.com
指導老師姓名：黃建寧 / Chien-Ning Huang
林志立 / Chih-Li Lin
演講題目(英文)：miR-302 cluster : implication for age-relative diseases
演講摘要(英文)：
Aging is a progressive loss of physiological integrity, leading to impaired function and increased
vulnerability to death. Multiple aging theories have been proposed, including chronic inflammation,
oxidative stress, and cellular senescence. However, the exact mechanism underlying aging is still
unclear. the miR-302 miRNA cluster was recently demonstrated to play an important role for regulating
the pluripotency and reprogramming process of embryonic stem cells (ESC) and induced pluripotent
stem cells (iPSCs). Functional studies have also identified that miR-302 drives self-renewal by
regulating the balance between oxidative stress and apoptosis. Therefore, miR-302 is capable of
stimulating self-renewal and pluripotency through modulating specific intracellular signaling.
Interestingly, studies showed that the decreased expression of miR-302 induced by various age-relative
diseases such as non-alcoholic fatty liver disease (NAFLD), type 2 diabetes (T2D), and Alzheimer’s
disease (AD). Both oxidative stress and mitochondrial dysfunction play a strong role in the
pathogenesis of these diseases. In particular, upregulation of miR-302 is able to alleviate oxidative
stress, suggesting miR-302 may exert potential benefits in anti-aging processes. However, the
underlying mechanisms of miR-302 and aging are still largely unclear. In the present study, we
demonstrated that free fatty acids (FFA) mixture-induced lipotoxicity contributes to lipid droplet
formation, oxidative stress, mitochondria dysfunction and senescence, and decreased the endogenous
level of miR-302. Conversely, overexpression of miR-302 not only attenuated FFA-induced
lipotoxicity in hepatic cells, but also prevented glucolipotoxicity-induced dysfunction and apoptosis
in β-cells. Moreover, we also found that miR-302 can protect against Aβ-induced neurotoxicity in
neuronal cells. In conclusion, our study suggests that miR-302 may serve as a potential target for
developing novel therapeutic strategies and drug targets in aging-related diseases.
24
六、研討會壁報展示摘要
A 組
編號 : A1
題目: A possible biomarker in neonatal hypoxic-ischemic encephalopathy with
inflammation sensitization
作者: 吳博銘
Purpose: Neonatal hypoxic–ischemic encephalopathy (HIE) is the most common cause of
encephalopathy in infancy. Therapeutic hypothermia is the current standard therapy for neonatal
HIE, especially for moderate and severe HIE. The decision of hypothermia depended on HIE
severity and should be made within 6 hours after birth. Inflammation may also has impacts on HIE
severity. We would like to find reliable biomarkers to correlate HI severity with or without
inflammation in the experimental animals.
Experimental Design: We will establish animal models with different severity of HIE and add
lipopolysaccharide to enhance inflammation. Hypothermia will be performed on these models.
Possible biomarkers in serum will be tested.
Results: In this study, we had established an animal HIE model with different severity and adding
lipopolysaccharide (LPS) would further worsen brain injury by measuring infarct volume and
functional analysis. Hypothermia could reduce either mild or severe HI brain damage and also
reduce inflammation-sensitized HI brain damage. Serum OPN is downregulated in HI group but is
enhanced in inflammation- sensitized HI group. Serum Glial fibrillary acidic protein (GFAP) mildly
elevated in HI group but apparently elevated in inflammation- sensitized HI group.
Conclusions: Combination of those two markers may help to distinguish HI group from
inflammation-sensitized HI group.
25
編號 : A2
題目: The role of Transthyretin in Alzheimer's disease
作者: 徐千玉
Transthyretin (TTR) is a transport protein distributed in the serum and cerebrospinal fluid (CSF).
Previous studies have shown that TTR may act as a chaperone to potential bind with β-amyloid (Aβ)
and reduce the level of Aβ peptide in vitro, but the detailed mechanism remain elusive. Thus, we intend
to investigate whether TTR can improve the Aβ clearance and attenuate cognitive deficits in a
transgenic mouse model of AD. We established a transgenic mouse model of TTR-overexpressed AD
mice and found that TTR could restore cognition impairment of AD mice and reduce Aβ level in the
brain. Meanwhile, TTR overexpression also reduced active neuro-immune cells in the brain. In
conclusion, in the present study, we demonstrate that TTR attenuated the AD pathology in vivo.
26
編號 : A3
題目: Identification of exosomal proteins in promoting lung cancer metastasis
作者: 翁尚楣
Propose:
Lung cancer is one of common cancer with high mortality nowadays. Cancer metastasis is responsible
for over 95% cancer-related death. However, the mechanism of exosomal protein-mediated metastasis
is unclear. Studies reported that exosomal cargo such as mRNA, proteins, and DNA can regulate the
tumour cell function and initiate the metastasis. In our previous results, we found that low-invasive
lung adenocarcinoma CL1-0 cells, which received the exosome secreted from highly-invasive lung
adenocarcinoma CL1-5 cells, enhanced the mobility. Here, we hypothesize that CL1-5 cells release
the exosomal protein transferring to CL1-0 cells and then promote the aggressiveness of CL1-0 cells.
Experimental Design:
To investigate that CL1-5 promote tumor progression of CL1-0 in vivo, we subcutaneously co-injected
the CL1-0-GFP-luciferase (CL1-0-GL) with CL1-0-RFP or CL1-5-RFP into NOD-SCID mice
separately. The CL1-0-GL tumor growth and distant metastasis were detected by luminescent. Next,
to examine the migration ability of CL1-0 after received the exosomes derived from CL1-5 cells, the
wound healing assay was used to check the migration ability of CL1-0 which were co-cultured with
CL1-5 cells in the transwell. We also observed whether exosomes labeled by GFP-CD9 fusion protein
secreted from CL1-5 transited through the size-limited transwell and were received by CL1-0.
Moreover, the exosomal proteins derived from CL1-0 and CL1-5 were identified by LC-MS/MS. The
expression of those proteins in cells and exosomes were confirmed by Western blotting. The role of
those proteins on cell motility will be studied by the wound healing assay and short hairpin RNA
(shRNA) knocking down the expression of those proteins.
Result: CL1-5-RFP promoted CL1-0-GL cells more aggressive in vivo. Exosomes from CL1-5 were
received by CL1-0 and regulated the migration ability in the transwell system. Furthermore, we
identified Ephrin receptor A2 (EPHA2) and EH domain-containing protein1 (EHD1) that associated
with cell migration. Protein expression levels of EPHA2 and EHD1 were higher in cells and exosomes
of CL1-5 compared to CL1-0. Conclusion In this study, high invasive lung cancer cells can transfer
exosomal proteins to promote metastasis of low invasive lung cancer cells. Keywords: Lung cancer,
metastasis, exosome
27
編號 : A4
題目: The effects of cocaine-induced behavioral sensitization on microglia’s

number and morphology.
作者: 吳淨眉
Cocaine causes persistent behavioral changes presumably by inducing long-term cellular/molecular
changes in the brain. In comparison to neurons, microglia in the brain can easily change in cellular
number and morphology. The aim of this study is to investigate the behavioral effect of cocaine in
mice and asked whether cocaine had an effect on microglia number and morphology. Male mice (B6,
8 weeks) were used in this study, and they were habituated by 3 days prior to cocaine treatment.
Thereafter, twenty four mice were randomly divided into 3 groups to receive daily i.p. injections of
either: saline, 10mg/kg cocaine, or 15mg/kg cocaine, for 5 days. During 5 days of treatment, we found
that groups injected 10mg/kg and 15mg/kg cocaine increased locomotion in mice, whether it has
significance in group of 15mg/kg cocaine. After that, we fed the mice normally and did not do any
treatment until the 21th day. On the 21 day, we gave all mice the last injection of cocaine and found
that 10mg/kg of cocaine is enough to cause the expression. The results demonstrated that cocaine can
cause addiction. After the behavioral experiment, we took out the tissues and used the brain slices for
Iba-1 staining. We observed hippocampus and found that in cocaine 15mg/kg, it can increase the
expression of Iba1 on microglia and decrease ramification. We demonstrate cocaine sensitization can
affect microglia in shapes and numbers.
28
編號 : A5
題目: Polarization of alveolar macrophage in model of diet induced obese mice

with ventilator induced lung injury
作者: 吳世偉
Purpose: The role of obesity in ventilator induced lung injury (VILI) is still not clear. Alveolar
macrophages are key initiators in the pathogenesis of acute lung injury; and M1 macrophage,
classically activated macrophages, secrets pro-inflammatory cytokines and initially predominate the
process of lung injury. High-fat feeding had been proposed to protects mice from VILI. In this abstract,
we tried to exam the influence of obesity in VILI and elucidate the polarization of alveolar
macrophages.
Materials and methods: High fat diet‐induced obesity (HD) and lean C57Bl/6 mice (CD) at aged 10-
12 weeks were mechanically ventilated for 6 hours, using lower(LV) or higher(HV) tidal volumes
without PEEP. Healthy non-ventilated mice served as normal control(CV). Bronchoalveolar lavage
fluid(BALF),Serum and lung tissue were collected for cytokine assay, histology and flow cytometry
analysis.
Results: Obese mice have fewer amount of M1-polarized macrophages and less proportion of M1-
sepctrum shift with VILI. Obese mice have significant decline in concentration of BALF protein and
cytokines such as IL-6,IL-1b, which is compared with lean mice in VILI. Lung histology also shows
that obese mice have less inflammatory cell infiltration and interstitial edema.
Conclusion: Our results revealed that obese mice have less severity of ventilator induced lung injury.
In contrast to previous concept, at least in lung, obesity has less linkage to M1 polarization, which
probably explained less lung injury in our diet induced obese mice model. Further studies are needed
to elucidate such relationship and possible mechanism.
29
編號 : A6
題目: Protective effects of hypercapnic acidosis on Ischemia–reperfusion-

induced retinal injury
作者: 林樂天
Ischemia–reperfusion (I/R) injury is associated with numerous retinal diseases, such as diabetic
retinopathy, acute glaucoma, and other vascular retinopathies. Hypercapnic acidosis (HCA) has a
protective effect on lung, myocardial, and central nervous system ischemic injury models. However,
no study has evaluated its protective effects in an experimental retinal I/R injury model. In this study,
retinal I/R injury was induced in Sprague Dawley rats by elevating the intraocular pressure to 110
mmHg for 60 minutes. HCA was induced before and after the injury. After 24 hours, the terminal dUTP
nick end labeling assay was performed. Moreover, the ratios of cleaved caspase-3/total caspase-3,
phosphorylated IκB/IκB, and phosphorylated p38 were measured through Western blotting. After 7
days, the rats’ aqueous humor was analyzed. In addition, electroretinography and retinal thickness
measurement were performed in the rats. Moreover, the retinal neural cell line RGC-5 was exposed to
500 µM H2O2 for 24 hours to induce a sustained oxidative stress in vitro. The effects of HCA were
evaluated by comparing oxidative stress, MAPK signals, NF-κB signals, survival rates, and apoptosis
rates in the RGC-5 cells before and after H2O2 exposure. We further investigated whether the potent
I/R-protective heat shock protein (HSP) 32 contribute to in vitro and in vivo protective effects of HCA.
Our results indicated that HCA has protective effects against retinal I/R injury both in vivo and in vitro,
at multiple levels, including antiapoptotic, anti-inflammatory, antioxidative, and functional retinal cell
protection. Further research clarifying the role of HCA in retinal I/R injury prevention and treatment
is warranted.
30
編號 : A7
題目: Insonation of Systemically Delivered Cisplatin-Loaded Microbubbles

Significantly Attenuates Nephrotoxicity of Chemotherapy in Experimental
Models of Head and Neck Cancer
作者: 陳杭港
The use of cisplatin (CDDP), the most common chemotherapy drug for head and neck cancer, is limited
by its undesirable side effects, especially nephrotoxicity. We investigated ultrasound microbubbles
(USMB) as a tool to increase the local intra-tumoral CDDP level while decreasing systemic CDDP
cytotoxicity. We allowed CDDP to interact with human serum albumin and then sonicated the resulting
CDDP-albumin complex to generate CDDP-loaded MBs (CDDP-MBs). We then established a head-
and-neck tumor-bearing mouse model by implanting FaDu-fLuc/GFP cells into severe combined
immunodeficiency mice and used IVIS® bioluminescence imaging to determine the tumor xenograft
formation and size. Twice weekly (until Day 33), we administered CDDP only, CDDP + MBs + US,
CDDP-MBs, or CDDP-MBs + US intravenously by tail-vein injection. The US treatment was
administered at the tumor site immediately after injection. The in vivo systemic distribution of CDDP
indicated that the kidney was the most vulnerable organ, followed by the liver, and then the inner ear.
However, CDDP uptake into the kidney and liver was significantly decreased in both the CDDP-MBs
and CDDP-MBs + US groups, suggesting that MB binding significantly reduced the systemic toxicity
of CDDP. The CDDP-MBs + US treatment reduced the tumor size as effectively as conventional
CDDP-only chemotherapy. Therefore, the combination of CDDP-MBs with ultrasound is effective and
significantly attenuates CDDP-associated nephrotoxicity, indicating a promising clinical potential for
this approach.
31
編號 : A8
題目: Effect of Hypercapnic Acidosis on T cells After Skin Allografts
作者: 曾元生
Purpose: Evidence reveals that hypercapnic acidosis (HCA) modulates immune responses. However,
the effect of HCA on allogenic skin graft rejection is unknown. We examined whether HCA might
improve skin graft survival in a mouse model of skin transplantation. Materials and methods: A major
histocompatibility-complex-incompatible BALB/c to C57BL/6 mouse skin transplantation model was
used. Animals were divided into sham control, air, and HCA groups. Mice in the HCA group were
exposed daily to 5% CO2 in air for 1 h. Skin grafts were harvested for histologic analyses. The lymph
node cells and splenocytes were stained with fluorescence-conjugated mAbs against CD4, CD8, and
Foxp3. Results: Skin allograft survival in mice treated with HCA was significantly longer than that
observed in air group. CD4+CD8+ T cells at day 3 was decreased in spleen and lymph node in HCA
group. Further, the FOXP3+CD4+ Treg cells was increased in lymph node in HCA group. Conclusion:
Hypercapnic acidosis (HCA) significantly prolonged the survival of incompatible skin allografts in
mice by suppressed the immune responses of alloreactive T cells of skin allografts. This suggests a
therapeutic potential of HCA in treating allograft rejection after solid organ transplantation.
32
編號 : A9
題目: The Curative Effect about Human Umbilical Cord of Wharton’s Jelly
Mesenchymal Stem Cells to Treat Myocardial Infarction Rats Model
作者: 蕭鎮源
Myocardial infarction (MI) is a fatal disease that is increasing in incidence. The worst sequelae of MI
include myocardial fibrosis and deterioration of pumping function that can lead to irreversible heart
failure. We try to set the MI rats model and examine the effect of transplantation WJ-MSCs. Human
mesenchymal stem cells derived from the Wharton's jelly of umbilical cord (WJ-MSCs) are the lack
of HLA-DR, low expression of MHC class I molecules and also lack CD80 and CD86 proteins. These
cells do not elicit acute rejection and are suitable for allogeneic transplantation. WJ-MSCs, similarly
to embryonic stem cells, have distinct capacity for self-renewal while maintaining their multi-potency
and could be induced to differentiate into cardiomyocytes in vitro and muscle cell in vivo. Thereafter,
we supposed WJ-MSCs are good resource for repaired the injured heart after myocardium
infarction.The rats were intubated and ventilated with a mechanical ventilator. Electrocardiography
(ECG) electrodes were applied, and recorded. A 2-cm para-sternal incision was made over the chest
wall. The heart was explored and the LAD was ligated with 8-O Prolene. ST elevation was thought to
indicate a successful model MI. Normal saline, undifferentiated human WJ-MSCs (1.6 × 106) or TGF-
β2–stimulated human WJ-MSCs (1.6 × 106) were injected directly into the myocardium around the
site of ligation.Electrocardiograph, echocardiogram, serum cardiac Troponin I level, Masson’s
Trichrome staining, immunohistochemistry were used to analyze the therapeutic effects.Cardiac
troponin I (c-TnI) was significant increasing in the LAD ligated animals after 6 hour later, indicating
that the rats experienced acute myocardial infarction with severe myocardial damage. In addition, the
serum c-TnI level was significantly lower in both the MSC and TGF-β2 groups than in controls. Thus,
the transplanted MSCs appear to reverse cardiac damage after LAD ligation. Examined the cardiac
function by 2D, M-mode cardiac echography every two weeks. The LV end-systolic dimension and
LV end-distolic dimension were also examined to calculate the ejection fraction (EF) and fractional
shortening (FS). The EF in the MI group showed 72.6 ± 5% at day 14 after operation and 51.9 ± 6.6%
at day 28 after operation. In the sham groups, the EF showed 92.4 ± 0.7% and 91.7 ± 0.9% respectively.
In the undifferentiated WJ-MSCs transplanted group, the EF showed 89 ± 1.2% and 88.2 ± 2.3%
respectively; and in the transplanted TGF-β2 treated WJ-MSCs group, the EF showed 93.5 ± 1% and
94.1 ± 1.2% respectively. Transplantation of either undifferentiated or TGF-β2 stimulated WJ-MSCs
improved left ventricular function after MI. The effects were most marked using undifferentiated WJ-
MSCs. These results indicate WJ-MSCs as a potential stem cell source for use in myocardial infarct
therapy.
33
編號 : A10
題目: Evaluation for Rho kinase inhibitor applied in glaucoma filtering surgery
作者: 鄭文勝
Glaucoma is a leading cause of irreversible blindness in the world and presents as a disease with optic
nerve atrophy, in which apoptosis of retinal ganglion cells is found pathologically. It is a disease of
multifactorial etiology with a characteristics of retinal nerve fiber layer defects and visual field loss
clinically. Increased intraocular pressure (IOP) is a major risk factor to glaucoma development and
progression, which is caused by imbalance of aqueous humor productions and outflow. Filtering
surgeries are the most popular manipulation in glaucoma surgical treatments. One of the major factors
resulting in failure of the procedures is scleral or subconjunctival scarring. In the past, 5-fluorouracil
and mitomycin-C have been used as adjunctive agents, but the effect and safety of these agents are not
satisfied. In previous report, a Rho kinase inhibitor, Y-27632, had been reported to be benefits in
improving glaucoma filtering surgery. However, the kinase of Y-27632 is not very selective to Rho
kinase. A new Rho kinase inhibitor, AR-12286, showed more specific inhibitory effect on Rho kinase.
In this study, we applied AR-12286 on the trabeculectomized eyes in rabbits. The eyes with AR-12286
showed longer period of lowering IOP and less fibrotic response.
34
B 組
編號 : B1
題目: Metabolic Signatures of Renal Epithelial and Mesenchymal Cells
作者: 邵愛寧
Purpose:
Around 10% of the population worldwide is affected by chronic kidney disease (CKD), and the number
is growing every year. The need for treatment and improvement becomes an important issue. CKD
often results in kidney fibrosis, which is characterized by loss of renal cells and their replacement by
extracellular matrix (ECM). Epithelial-to-mesenchymal transition (EMT) induced by transforming
growth factor beta (TGFβ) family in renal tubular cells has been proposed as one of the models for
kidney fibrosis. Recent studies show that kidney fibrosis is accompanied by metabolic reprogramming,
altering the energy source from oxidative phosphorylation to glycolysis. However, whether metabolic
reprogramming is causative for kidney functional loss remains unknown. Modulation of glycolysis has
been shown to affect cancer cell EMT, suggesting that cancer EMT can be regulated by modulating
metabolic reprogramming. However, very few studies address the relationship between metabolic
reprogramming and EMT in kidney fibrosis. Therefore, we attempt to study the interaction between
metabolic reprogramming and renal EMT. Our preliminary results showed that TGFβ treatment
downregulated epithelial markers (E-cadherin) and upregulated mesenchymal markers (N-cadherin
and Fibronectin) in proximal tubular cells. This is accompanied by increased glycolytic flux, reflected
by medium acidification, and increased glucose consumption and lactate production. Therefore, we
hypothesize that modulation of metabolic reprogramming reverses renal cell EMT and kidney fibrosis.
Experimental Design:
We treated TGFβ to induce EMT in HK-2 human proximal tubular cells (PTCs). EMT marker proteins
were determined by immunoblotting. Metabolite levels were analyzed by liquid chromatography–mass
spectrometry (LC-MS). Glycolytic flux of PTCs was examined by a Seahorse XF24 analyzer.
Conclusions:
1. TGFβ treatment resulted in expression of EMT marker with increased glycolytic flux and decreased
TCA cycle PPP.
2. Lactate dehydrogenase inhibition showed reversal of TGFβ-induced upregulation of mesenchymal
markers, with partially attenuation of TGFβ-induced downregulation of metabolites for TCA cycle and
PPP.
35
編號 : B2
題目: Investigation of potential cardiotoxicity of anti-PD-1 immune checkpoint

inhibitor
作者: 鄭婉婷
In recent year, the emerging of immune therapies with immune checkpoint inhibitors (ICIs) have
resulted in significant improvement of cancer patients’ clinical outcome with traditionally poor
prognosis. ICIs target immune checkpoints such as cytotoxic T-lymphocyte associated antigen (CTLA-
4), programmed cell death protein-1 (PD-1), or programmed cell death ligand-1 (PD-L1) have been
investigated as a novel mechanism to enhance the immune system and combat or prevent cancer cells
evade immune surveillance. Unfortunately, immune-related-adverse events (irAEs) had been reported
after patients received ICIs. Cardiotoxicity can be resulted by off-target effects of these treatments on
the heart. There were increasing clinical reports showing several fatal heart-relevant adverse cases
such as pericarditis, cardiomyopathy, heart failure and myocarditis after ICIs treatment. Intriguingly,
previous basic researches demonstrated PD-1 serves as a protective mechanism to prevent T-cell
mediated cardiomyocytes damage because of mice with PD-1 deficiency manifest autoimmune dilated
cardiomyopathy and results in fatal myocarditis. However, there is limited evidence on the role and
detailed pathway of anti-PD-1 treatment-mediated cardiac inflammation, thus, there is an unmet need
to understand the effects and mechanism of cardiotoxicities associated with anti-PD-1 treatment for
future side effects prevention and to increase outcome and life quality of cancer patients.
36
編號 : B3
題目: Study of the Roles of K-RAS Mutation-Related Lipid Metabolism in

Pancreatic Cancer Gemcitabine Sensitivity
作者: 許芸溱
Purpose: Pancreatic ductal adenocarcinoma (PDAC) is know for its poor prognosis, resulting from
resistance to chemotherapy. Its driver mutation K-RAS signaling reprograms cancer cell metabolism
where cancer cells exhibit increased lipid biosynthesis. Studying on mutant K-RAS-mediated lipid
metabolism may provide treatment options. To uncover possible lipid pathways in PDAC, we analyzed
differentially expressed lipid genes and microRNA in K-RAS mutant pancreatic samples in the TCGA
database. TCGA analysis showed negative correlation between PLA2G16 and miR-139-5p expression,
which suggested the negative regulation that hasn’t been proved. Besides, PLA2G16 participates in
cancer progression in several cancers, however its roles have never been discussed in PDAC.
Methods: PLA2G16 and miR-139-5p expression were detected by QPCR in PDAC cell lines. PDAC
cell lines ASPC1 and CFPAC were manipulated to knockdown PLA2G16 by lentiviral deliver system.
To assess influence of PLA2G16 on PDAC progression, functional assays (colony formation, wound
healing assay, gemcitabine cytotoxic efficacy) were applied. LDL from metabolic syndrome (MetS), a
known contributor of gemcitabine resistance in PDAC, was treated in ASPC1 cells to validate the
interaction with PLA2G16. The miRNA-target interaction was measured by western blot and QPCR
in miR-139-5p mimic transfected ASPC1 cells.
Results: In PDAC cells, knocked down PLA2G16 enhanced gemcitabine cytotoxic activity, but was
irrelevant to cell migration/invasion, and basal cell growth. Also, MetS LDL treatment caused an
increase in PLA2G16 protein expression. The result of mimic miR-139-5p transfection in ASPC1 cells
showed that PLA2G16 expressions couldn’t be altered by miR139-5p.
Conclusion: This study revealed that PLA2G16 was upregulated in K-RAS mutant PDAC and it
regulated gemcitabine sensitivity in ASPC1 cells. Therefore, PLA2G16 could be a potential
therapeutic target for gemcitabine resistance PDAC.
Keyword: pancreatic ductal adenocarcinoma (PDAC), gemcitabine resistance, PLA2G16, miR-139-
5p
37
編號 : B4
題目: Study of the roles of Lipid Droplet- Related Lipidome Reprogramming in

Cisplatin Sensitivity
作者: 鄭朝鴻
Purpose: 脂滴是一種動態型胞器，其功能是將脂肪酸轉成中性脂質並儲存。根據文獻表示：癌
細胞中具有較普通細胞多的脂滴表達，同時也與癌細胞的化療耐藥性有顯著的相關性。而鉑類
藥物為癌症臨床治療的第一線化療藥物，在臨床治療上已被證實易使癌細胞產生抗藥性現象和
復發的機率。其治療的對象中，上皮性卵巢癌因其腫瘤組織學型態的不同，對鉑類化療藥也具
有不同的抗性和復發率。過去的研究中表示不同組織學型態的卵巢癌其 LDL-R 的表達也不同，
LDL-R 介導 LPC 的改變進一步使癌細胞具有不同的抗藥性表現。為了揭示脂滴在 LDL-R 介導
的脂質中對抗藥性的作用，我們使用 ICP-MS 分析了脂滴中鉑的表現，發現脂滴攜帶鉑類藥物
的表現與 LDL-R 的表達呈現正相關。
Methods: Fig.1 在 EOCs 細胞系中通過西方墨點法檢測 LDL-R 的表達。依照組織學型態的不

同，通過 lentiviral delivery system 將 EOCs 細胞系中 SKOV3 over expression LDL-R；MDAH2774
和 TOV21G knock down LDL-R。使用 Cisplatin 處理 knock down LDL-R 細胞系用以驗證 LDL-
R 下游介導的脂質 LPC 對抗藥性的表現。為了瞭解重編輯細胞內脂質對抗藥性的影響，使用
微脂體技術將目標脂質 LPC 包覆鉑類藥物製成新型製劑 liposome-LPC-cisplatin(LLC)，處理
over expression LDL-R。Fig.2 使用密度梯度離心法分離細胞中的脂滴，並使用 ICP-MS 分析其
鉑含量
Results:在 EOCs 細胞系中，knock down LDL-R 之細胞株能明顯改善卵巢癌細胞對 Cisplatin 的

抗藥性；而在 over expression LDL-R 之細胞株中能增加癌細胞對 Cisplatin 的抗藥性，然而使用
LLC 藥物後卻能改善 over expression LDL-R 之細胞株的抗藥性。而在 ICP-MS 分析脂滴內鉑含
量的表現中，脂滴內鉑含量的表達與 LDL-R 的表現呈正相關。
Conclusion: 本研究藉由重編輯細胞內脂質的表達，表達了脂質對抗藥性的作用，並進一步驗
證支持 LDL-R 的表達對化療抗藥性的影響。同時，LDL-R 的表達支持脂滴對癌細胞化療抗藥
性的輔助作用，進一步表示了 LDL-R、LPC 以及脂滴在化療耐藥性中扮演的角色。
38
編號 : B5
題目: Ganoderma lucidum suppress the expression of EZH2 in triple-negative

breast cancer
作者: 呂家菡
Breast cancer (BC) is most attack rate cancer in women, which was mammary gland cell abnormal
growth generated. In the last decade, the therapeutic can treat different subtype breast cancer chose
distinct therapy. In BC, the triple-negative breast cancer (TNBC) not only had more aggressive and
worse prognosis also more side effect than other subtype in treatment. Based on the TNBC didn't
expressed ER, PR and Her2 receptor, the treatment was limit to chemotherapy. Therefor we would like
a kind of drug which could reduce side effect or enhance ability of kill cancer. In Asia, the Chinese
tradition herb Ganoderma has been used to treat disease for centuries. Ganoderma is composed of
Fruiting body, Mycelium and Spore. G. lucidum has been known the efficacy, which inhibition the
proliferation and cell cycle through signaling pathway in multiple cancer cell. Enhancer of zeste
homolog 2 (EZH2) was associated with DNA methyltransferases also relative with cancer progression,
patient survival and in multiple cancer were overexpression. To investigate whether G. lucidum has an
effect EZH2 in triple-negative breast cancer (TNBC) and may be used as an adjuvant therapy in
treatment. In this experiment we used Fruiting bod of Ganoderma lucidum (G. lucidum). MDA-MB-
231 and BT-549 of triple-negative breast cancer were treated with G. lucidum and measured the
viability in MTT assay, Caspase-3 activity and detection the protein expression change used Western
blot. In this study display that G. lucidum could decrease the TNBC survival, specifically BT-549 cell.
And the Caspase-3 was activity in treated G. lucidum compare to control. Then, G. lucidum were
reduced EZH2 expression in BT-549 cell. In contrast, these proteins weren't affected by G. lucidum in
MDA-MB-231. Keyword: Ganoderma lucidum, EZH2, triple-negative breast cancer
39
編號 : B6
題目 : Pipoxolan inhibits LPS-induced inflammation via suppressing MAPK

pathways in murine RAW264.7 cells
作者: 張庭瑄
Purpose: Pipoxolan (pipo), a relaxant of smooth muscle, has been reported to exhibit anti-cancer effect;
however, its anti-inflammatory effects have not yet been examined. In this study, we evaluate the
suppressive effect of Pipo on the MAPK pathway in LPS-induced RAW 264.7 macrophages. Materials
and methods: The cell viability and the inflammatory cytokine NO were evaluated by MTT and NO
assay respectively. On the other hand, PGE2 and IL-6 were examined by ELISA assay. To elucidate
pro-inflammatory factors of INOS and COX-2, NF-κB, and phosphorylation of MAPKs were
examined by Western blotting analysis. Results: The results reveal that Pipo indeed decreased
inflammatory cytokines of NO and IL-6 release. Compared with control group, Pipo prominently
suppressed LPS-induced NF-κB p65 and p50 expression. Pipo decreased phosphorylation of IKB and
MAPKs. Moreover, the effect of Pipo also present in Carrageenan-induced edema study Conclusion:
This study provides evidence that Pipo suppressed the phosphorylation of IKB and MAPK signaling
pathways, and inhibited the production of major pro-inflammatory molecules
40
編號 : B7
題目: Curcumin Promotes Connexin 43 degradation and Temozolomid-induced

apoptosis in Glioblastoma cells
作者: 黃伯仁
Glioblastoma (GBM) is the most commonly occurring tumor in the cerebral hemispheres. Currently,
temozolomide (TMZ), an alkylating agent that induces DNA strand breaks, is considered the frontline
chemotherapeutic agent for GBM. Despite its frontline status, GBM patients commonly exhibit
resistance to TMZ treatment. We have recently established and characterized TMZ-resistant human
glioma cells. The aim of this study is to investigate whether curcumin modulates cell apoptosis through
the alternation of the connexin 43 (Cx43) protein level in TMZ-resistant GBM. Overexpression of
Cx43, but not ATP-binding cassette transporters (ABC transporters), was observed (approximately
2.2-fold) in TMZ-resistant GBM cells compared to the Cx43 levels in parental GBM cells.
Furthermore, at a concentration of 10μM, curcumin significantly reduced Cx43 protein expression by
about 40%. In addition, curcumin did not affect the expression of other connexins like Cx26 or
epithelial-to-mesenchymal transition (EMT) proteins such as β-catenin or αE-catenin. Curcumin
treatment led to an increase in TMZ-induced cell apoptosis from 4% to 8%. Importantly, it did not
affect the mRNA expression level of Cx43. Concomitant treatment with the translation inhibitor
cycloheximide (CHX) exerted additional effects on Cx43 degradation. Treatment with the autophagy
inhibitor 3-MA (methyladenine) did not affect the curcumin-induced Cx43 degradation. Interestingly,
treatment with the proteasome inhibitor MG132 (carbobenzoxy-Leu-Leu-leucinal) significantly
negated the curcumin-induced Cx43 degradation, which suggests that curcumin- induced Cx43
degradation occurs through the ubiquitin-proteasome pathway.
41
編號 : B8
題目: Adiponectin promotes VEGF expression in rheumatoid arthritis synovial

fibroblasts and induces endothelial progenitor cell angiogenesis through inhibition
of miR-106a-5p
作者: 黃建中
Rheumatoid arthritis (RA) is a worldwide common rheumatic disease and is characterized by
progressive symmetric polyarthritis which, without adequate treatment, would lead to bony erosions
and joints deformity. Angiogenesis is one of the pivotal pathogenic mechanisms in RA and angiogenic
process results in recruitment of more leukocytes into the synovium to promote proinflammatory
cytokines and destructive proteases production. Adiponectin is a circulating hormone mainly secreted
by adipocytes and growing studies indicate that increased adiponectin levels in both serum and
synovial fluid are associated with RA disease activity. Proinflammatory property of adiponectin in RA
has been elucidated, but the angiogenic effect of adiponectin in RA has not been well understood. Thus,
the aim of this study is to investigate the mechanism of adiponectin in RA angiogenesis. By using
MH7A cells, the RA synovial fibroblast cell line, we found that adiponectin dose- and time-
dependently enhances vascular endothelial growth factor (VEGF) expression. This would promote
endothelial progenitor cells tube formation and migration activities. We proved these angiogenic
reactions are through the MEK/ERK signaling pathway and downregulation of microRNA-106a-5p
(miR-106a-5p) not only in vitro but also in vivo experiments with utility of chick chorioallantoic
membrane and Matrigel plug assay. Rather than adiponectin receptor 2 (AdipoR2), it is via adiponectin
receptor 1 (AdipoR1) that adiponectin exerts angiogenic function in RA. In collagen-induced arthritis
mouse model, we demonstrated that inhibition of adiponectin expression could significantly ameliorate
paw swelling and bone erosions. Taken together, our results indicate that adiponectin stimulates
VEGF-dependent EPCs tube formation and migration in RA synovial fibroblasts. These angiogenic
effects are mediated through the MEK/ERK signaling pathway, as well as miR-106a-5p
downregulation by connecting to the AdipoR1. The anti-angiogenic strategy by targeting adiponectin
might be beneficial as an add-on therapy with current standard treatments of RA. This deserves further
clinical studies.
42
編號 : B9
題目: Musashi-1 Enhances Glioblastoma Migration by Promoting ICAM1

Translation
作者: 林讓均
Purpose: Glioblastoma multiforme (GBM) is a lethal brain tumor with a mean survival rate of 1 year.
One major reason for therapeutic failure is that GBM cells that can infiltrate the healthy brain possess
tumor properties of stemness & invasion. Musashi-1 (MSI1), a neural stem cell marker, plays an
important role in the maintenance of stem cell state, and tumorigenesis in GBM. In human glioma,
irradiation significantly elevated intercellular adhesion molecule-1 (ICAM1) levels and then increased
tumor invasion. The crucial role of MSI1/ICAM1 association in invasion of GBM has as the hypothesis.
Materials and Methods: These phenomena are likely due to MSI1 upregulation, which occurred
simultaneously with higher expression of ICAM1 in GBM cells. MSI1 knockdown effectively
suppressed ICAM1 expression and blocked motility and invasion in GBM cells, while overexpressing
ICAM1 reversed these effects.
Results: Cell track assays show that MSI1 knockdown significantly reduces cell motility, whereas
MSI1 overexpression can promote cell motility. Taken together, MSI1 may manipulate cell invasion
and motility in vitro. To find specific MSI downstream migration genes, we obtained 5 genes from the
microarray results, including ICAM1, IL8, POSTN, PRDM1, & SP1. The flow cytometry revealed the
populations of 5 genetic proteins. ICAM1 (39.1±3.53)% is significantly upregulated by MSI1
overexpression. The mRNA expression of ICAM1 is downregulated in the GBM with MSI1
knockdown. MSI1 regulates invasion ability via ICAM1. Significantly, MSI1 does not directly interact
with the ICAM1 protein but interacts with its mRNA suggests that MSI1 contributes to a regulatory
mechanism via RNA-binding activity and protects or facilitates ICAM1-translation of GBM in the
presence of mRNA. MSI1 can stabilize ICAM1 mRNA, which likely contributes to ICAM1
expression. Finally, MSI1 and ICAM-1 were coexpressed at high levels in GBM tissues with the lowest
survival rate .
Conclusion: The MSI1/ICAM1 pathway plays an important role in oncogenic resistance, including
increasing tumor invasion.
43
編號 : B10
題目: Effect of microgravity on the mesenchymal stem cell characteristics of

limbal fibroblasts
作者: 鮑淑怡
Purpose: Mesenchymal stem cells (MSCs) are important for regenerative medicine. Limbal fibroblasts
(LFs), present in the corneal limbus, have been shown to possess MSC characteristics, and can
differentiate into other cell types. The current study sought to investigate the effect of microgravity on
the proliferation and differentiation of LFs, and identify culture conditions to obtain a high proportion
of LFs possessing MSC characteristics.
Materials and methods: A rotary cell culture system was used to generate microgravity. Cellular
proliferation and MSC marker (CD14, CD45, CD90, CD105, and SSEA4) expression were evaluated
by WST-1 test and flow cytometry, respectively. Differentiation of LFs into adipocytes, osteocytes,
and chondrocytes was examined. The effects of LF-conditioned medium on limbal stem cell
differentiation were assessed.
Results: The cellular proliferation rates under microgravity were significantly lower than those under
normal gravity (0.44 vs. 0.18 at 24 h, and 0.70 vs. 0.44 at 48 h, both P 0.004). Higher proportions of
cells expressed CD90 (95.33% vs 81.69%), CD105 (95.32% vs 87.96%), and SSEA4 (68.26% vs
26.13%) under microgravity than under normal gravity. The differentiation potential of LFs was more
prominent under microgravity. The LF-conditioned medium attenuated the differentiation of limbal
corneal epithelial stem cells.
Conclusion: Under microgravity, LFs showed a higher proportion of MSC characteristics and were
easily induced into different linage cells. Culture in a microgravity environment may allow harvesting
a greater number of MSC-like LFs for stem cell therapy in ocular surface reconstruction.
44
編號 : B11
題目: The Synergy between Palmitate and IL-26 for Metabolic Production Is
Dependent on the MyD88/NFκB and MAPK Pathway
作者: 陳易廷
Purpose: We hypothesize that high levels of saturated fatty acid in obese rheumatic patients may
exacerbate the progression of disease due to the synergetic effects.
Materials and methods: Cultured primary human chondrocytes and synovial cells were stimulated with
0.5 mM FFA (palmitate) for 24 h to induce inflammatory production. After treatment, cell lysates were
prepared and immunoblotted for COX-2, IL-6, and MMP-1. To determine the activation of synergizes
signaling pathway, cell lysed were prepared and immunoblotted for MAPK/ERK signaling pathway.
Results: Our preliminary studies reveal that palmitate has synergetic with IL-26 to induce
inflammatory cytokines on chondrocytes and synoviocytes in a palmitate dose-dependent manner,
which enhance the almost 5-folds expression of COX-2, IL-6 and MMP-1 compared with palmitate
and IL-26 only. The synergize effect via the TLR4/MAPK/ERK signaling cascade.
Conclusion: Obesity is associated with rheumatoid arthritis but obesity may result in RA progression
is still unclear. Therefore, we treated high levels palmitate to mimic obesity and treated IL-26 to mimic
RA on chondrocytes and synoviocytes. The data observed that palmitate and IL-26 might synergy
inflammation via the TLR4/MAPK or TLR4/NF-κΒ signaling cascade.
45
編號 : B12
題目: RNA‐binding protein, human antigen R regulates hypoxia‐induced

autophagy by targeting ATG7/ATG16L1 expressions and autophagosome
formation
作者: 蔡宗訓
Autophagy, a prosurvival mechanism offers a protective role during acute kidney injury.We show novel
findings on the functional role of RNA binding protein, HuR during hypoxia‐induced autophagy in
renal proximal tubular cells‐2 (HK‐2). HK‐2 cells showed upregulated expressions of HuR and
autophagy‐related proteins such as autophagy related 7 (ATG7), autophagy related 16 like 1
(ATG16L1), and LC3II under hypoxia. Increased autophagosome formation was visualized as LC3
puncta in hypoxic cells. Further, short hairpin‐RNA‐mediated loss of HuR function in HK‐2 cells
significantly decreased ATG7 and ATG16L1 protein expressions. Bioinformatics prediction revealed
HuR motif binding on the coding region of ATG7 and AU‐rich element at 3 ′ UTR ATG16L1
messnger RNA(mRNA). The RNA immunoprecipitation study showed that HuR was predominantly
associated with ATG7 and ATG16L1 mRNAs under hypoxia. In addition, HuR enhanced
autophagosome formation by regulating LC3II expressions. These results show that HuR regulates
ATG7 and ATG16L1 expressions and thereby mediate autophagy in HK‐2 cells. Importantly, HuR
knockdown cells underwent apoptosis during hypoxia as observed through the terminal
deoxynucleotidyl transferase dUTP nick end labeling assay.Collectively, these findings show the
crucial role of HuR under hypoxia by regulating autophagy and suppressing apoptosis in renal tubular
cells.
46
編號 : B13
題目: A novel desensitization site A384P of glycine receptor alpha 1 subunit

linked to human hyperekplexia
作者: 王振宏
Hyperekplexia, which is an inherited neuronal disorder characterized by exaggerated startle responses
with unexpected sensory stimuli, is caused by the dysfunction of glycinergic inhibitory transmission.
From analysis of newly identified human hyperekplexia mutations in glycine receptor (GlyR) α1
subunit, we found that a missense mutation α1A384P showed substantially enhanced desensitization
without obvious alteration in agonist sensitivities, protein expression, or agonist induced maximum
responses when expressed in HEK293T cells. In comparison, another human hyperekplexia mutation
a1P250T, which was previously reported to relate to desensitization, caused strong reduction of
maximum currents in addition to altered desensitization. The mutation-caused desensitization was
partially reversed by co-expression of the β subunit in α1P250T -containing GlyRs, whereas the
reduced maximum currents in α1P250T were even aggravated by β co-expression. In comparison,
a1A384P and a1A384Pβ GlyRs showed similar extent of enhancement in desensitization and
indistinguishable maximum currents. These results were further confirmed by overexpression of
α1P250T or α1A384P in primary cultures of cortical neurons. These observations suggest that, unlike
α1P250T that causes reduced channel conductance, enhanced desensitization is the major functional
deficit in α1A384Pβ and is highly associated with pathogenesis of hyperekplexia. Furthermore,
combining the electrophysiological results and the data from structural analysis, we suggest that
α1P250, which is located at the beginning of the transmembrane domain TM2, directly controls the
channel pore constriction and thereby its mutation affects both channel gating and desensitization.
α1A384P is located at the end of the intracellular M3-M4 linker, possibly interacting with adjacent
residues on TM3 or the M1-M2 linker to influence channel desensitization. These results indicate that
A384 is a new site in controlling the desensitization state of GlyR α1. In summary, our present results
demonstrate a novel desensitization site on GlyR α1 and suggest a strong link between GlyRs
desensitization and human hyperekplexia
47
C 組
編號 : C1
題目 : Volume and functional changes of the remnant pancreatic tissue after

pancreatectomy: Does the pancreas regenerate?
作者: 呂維勛
Background/Objectives: The improvement of survival after pancreatectomy had promoted the
consideration of long-term metabolic consequences. Unlike the well-documented liver regeneration
after partial hepatectomy, pancreatic regeneration after pancreatectomy is still controversial. Herein,
our aims of the study are to determine the volume change of the remnant pancreas and the functional
changes in glucose metabolism. Methods: This study included the patients from Jan. 2009 to Dec. 2017
undergoing partial pancreatectomy, including distal pancreatectomy (DP) and
pancreaticoduodenectomy (PD) for a variety of disease. During follow-up, the endocrine function was
assessed according to the level of serum glucose, HbA1C, C-peptide. The pancreas volume was
determined via abdominal CT scan which was routinely assessed before the operation and at 3 months,
1 year and 2 years postoperatively. Results: Of 135 patients, 90 patients underwent PD and 45 patients
underwent DP. The remnant pancreas in the PD group had an atrophic change. The mean ratio of the
remnant pancreas compared with initial residual pancreas at 3 months, 1 and 2 years after
pancreatectomy were 80.79%, 68.67%, and 65.34% respectively (p<0.001). In contrast, the remnant
pancreas in most of the DP patients are slightly hypertrophic, the mean ratio of the remnant pancreas
at 3 months, 1 and 2 years postoperatively were 106.25%, 106.62% and 110.43% (p=0.019). The DP
patients had a higher incidence of new-onset diabetes than the PD patients, although the difference
was not statistically significant (33.3% vs. 22.7%, p=0.115). Also, 29.2% of the PD patients with
preoperative DM had resolved after PD. However, neither the pancreas volume nor C-peptide level
showed a significant relation to postoperative new-onset DM. Our result also showed no significant
correlation between the C-peptide level and remnant pancreas volume. The C-peptide level dropped
significantly after partial pancreatectomy in both groups (p<0.001) and the impact on C-peptide level
was more severe in the DP group. Postoperative C-peptide level restored partially in both groups
(β±SE= 16.33±5.03, p= 0.001) regardless of the volume change and PD group had a greater restoration
capacity of C-peptide secretion (β±SE= 13.26±5.50, p= 0.016). Conclusions: The remnant pancreas
tissue atrophied in the PD patients but hypertrophied in DP patients. The function of β-Cell would be
partially restored after partial pancreatectomy and the distal portion of the pancreas in the PD group
had a greater restoration capacity of β-Cell.
48
編號 : C2
題目: Opposing Trends in Incidence/Mortality Rates and Ratios for Testicular

Cancer Based on Health Care Disparity
作者: 陳文榮
The mortality-to-incidence ratio (MIR) is associated with the clinical outcomes of different types of
cancer as well as the ranking of health care systems. However, the association between MIRs for
testicular cancer and health care disparities, including differences in expenditures and health system
rankings, has not yet been reported. We used the Spearman's rank correlation coefficient (CC) to
analyze the correlation between testicular cancer MIRs and both total expenditures on health/gross
domestic product (e/GDP) and World Health Organization (WHO) health system rankings. After
screening the data for quality and missing information, 57 countries were chosen for analysis.
Generally, developed countries and regions had relatively high rates of incidence/mortality but with a
favorable MIR. Among continents, Europe had the highest incidence rates, whereas the highest MIRs
were in Africa. Globally, favorable testicular cancer MIRs were observed in countries with both a high
e/GDP and good WHO ranking (CC = -0.568, p < 0.001 and CC = 0.655, p < 0.001, respectively). In
conclusion, the MIR for testicular cancer varies in countries and regions based on both total health
expenditures and health care system ranking which might serve as an indicator for health disparity.
49
編號 : C3
題目: A Next-Generation Sequencing-Based Platform for Quantitative Detection

of Hepatitis B Virus Pre-S Mutants in Plasma Predicts Hepatocellular Carcinoma
Recurrence
作者: 鍾馨瑤
Hepatocellular carcinoma (HCC) is a leading cause of cancer-related death worldwide. Despite
curative resection, high recurrence of HCC remains a big threat, leading to poor patient outcome.
Chronic hepatitis B virus (HBV) infection is a major risk factor for HCC development. HBV pre-S
mutants, which harbor deletions over pre-S1 and pre-S2 gene segments of large surface antigen, have
been demonstrated to dysregulate multiple signaling pathways leading to HCC formation and have
been implicated in HCC recurrence. Therefore, in this study, we developed a platform, based on the
next-generation sequencing (NGS), for quantitative detection of pre-S mutants in plasma of HBV-
related HCC patients and evaluated their prognostic values in HCC recurrence. Compared to the
current TA cloning-based analysis, the NGS-based analysis could detect pre-S deletion in plasma
quantitatively, and the detection rate was significantly more sensitive. We demonstrated that the
presence of deletion spanning pre-S2 gene segment and the high percentage of pre-S2 plus pre-S1+pre-
S2 deletion, either alone or in combination, was significantly and independently associated with poor
recurrence-free survival and had greater prognostic performance than other factors in predicting HCC
recurrence. In conclusion, our data suggest that the NGS-based quantitative detection of pre-S mutants
in plasma represents a promising approach for identifying patients at high risk for HBV-related HCC
recurrence after surgical resection in a noninvasive manner.
50
編號 : C4
題目: Roles and Functions of Medical Students within the Longitudinal

Relationship with Patients: From the Patient Perspective
作者: 張耀文
Background
One of the primary goals of undergraduate medical education is to prepare the graduates who exhibit
the attitude and ability of patient-centered care. The foundation of patient care is the ongoing
partnership between patient and health provider. However, the relationship between patient and
medical student is short and fragmented in the framework of discipline-based rotational clinical
training. The principles of longitudinal integrated clerkship (LIC) are continuity of care, curriculum,
and supervision. This study explored the patients’ perspectives of the LIC students’ roles and functions
in the base of continuity of care. Summary of work
Patients who were cared longitudinally by the LIC medical students were invited to participate. The
data was collected by a trained research assistant with a semi-structured interview in person or over
the telephone. The researchers thematically analyzed the transcribed verbatim using a general
inductive approach to identify themes in patient’s descriptions of their experiences interacting with
medical students.
Summary of results
The results of the analysis revealed three significant roles of students in the longitudinal integrated
clerkship: friends of the profession, caretakers, and learners. The major interactions between patients
and students identified in this study were students’ comforting and consulting. Patients felt warmness
from students’ comforting. Through communication apps of handheld devices, patients felt much
easier to access health advises. With support from attendings, patients recognized the student’s
assistive roles in care. And patients and students learned simultaneously during the processes of
consultation: patients got health education or care and students learned communication skills and
experience of care. Interviewed patients had high satisfaction with this program.
Discussion and conclusions
The LIC students could establish a longitudinal relationship with patients. This link was not like the
disease treatment relationship between attendings and patients. From the patient’s perspective, the
roles of medical students were more like learners and friends of the medical profession. Therefore,
what the patients expected the students learned from this relationship were empathy and doctor-patient
communication, not only medical knowledge and skills.
51
編號 : C5
題目: LMX1A Hypermethylation Is a Prognostic Marker in Early-stage

Colorectal Cancer
作者: 鍾新華
Colorectal cancer (CRC) is one of the leading causes of cancer incidence and mortality in the world.
Clinical outcomes of CRC patients are different because of the complexity of colorectal carcinogenesis.
Potential prognostic biomarkers are required for guiding therapies and improving treatment outcomes.
Previously, we have showed that LMX1A methylation could be as biomarkers in many cancers and
LMX1A functioned as tumor suppressor in cervical cancer. However, the role of LMX1A gene in CRC
remains unclear. This study aimed to investigate the methylation frequency of LMX1A gene and the
potential value of LMX1A promoter methylation in CRC. We used methylation-specific PCR (MSP)
and quantitative methylation-specific PCR (Q-MSP) to determine the methylation level of LMX1A in
CRC cell lines and tissues. We also performed statistical analyses to elucidate the association between
LMX1A methylation and clinical characteristics. The results of MSP showed that LMX1A was fully
methylated in the 5 CRC cell lines. In addition, the quantitative analysis of LMX1A methylation in
these 5 CRC cell lines showed a consistent data with the gel-based results. Furthermore, our Q-MSP
data showed that methylation level of LMX1A was significantly increased in CRC tissues as compared
with the adjacent non-tumor tissues (n = 151) (P < 0.0001). Moreover, our data further revealed that
stage I and II CRC patients with LMX1A methylation had a poorer 5-year overall survival (P = 0.0108)
and disease-free survival (P = 0.0468). In summary, our results showed that LMX1A is
hypermethylated in CRC and LMX1A hypermethylation is a novel prognostic marker in early-stage
CRC.
52
編號 : C6
題目: Application of artificial intelligence approach for the prediction of acute

kidney injury in patients following cardiac surgery
作者: 曾博郁
Purpose: Acute kidney injury (AKI) is an important complication of the cardiac surgeries and is
associated with a poor prognosis. A model that accurately estimates a patient's risk for AKI after
cardiac surgery can optimize clinical decision-making and postoperative treatment strategies to
minimize the risk for AKI. Several risk models have been developed to predict postoperative AKI after
cardiac surgery. However, there is less study analyzing clinical big data with the application of machine
learning to predict AKI after cardiac surgery.
Materials and Methods: We retrospectively enrolled the patients undergoing cardiac surgery in Far
East Memorial Hospital from August 2016 to August 2018. The primary outcome was the development
AKI defined according to KDIGO (Kidney Disease Improving Global Outcome) criteria. The variables
used for analysis including demographic characteristics, clinical condition, preoperative biochemistry
data, preoperative medication and intraoperative variables including time-series hemodynamic
features. The following machine learning methods were used: logistic regression, support vector
machine (SVM), random forest (RF) and extreme gradient boosting (Xgboost) and ensemble
(RF+Xgboost). Performance of these techniques was evaluated by the area under the receiver-
operating characteristic curve (AUC). We utilized SHAP values to explain the prediction model.
Results: A total of 671cases including 250(37.3%) patients received coronary artery bypass (CABG),
347(51.7%) patients received valve replacement surgery and 74(11%) patient accepted combined
surgery. AKI developed in 163(24.3%) patients during the first postoperative week. The best
performance regarding AUC was achieved by the ensemble model to predict the AKI of all stages
(0.84, 95% confidence interval (CI) 0.78–0.90). Simple decision tree was illustrated on Figure 2. The
top 3 important features in importance matrix plot of RF were intraoperative urine output, packed RBC
transfused during surgery and preoperative level of hemoglobin. The SHAP values explained the
positive or negative impact of the most important features attribute to the RF.
Conclusion: Artificial intelligence approach with machine learning method may predict AKI after
cardiac surgery and may be applied to evaluate surgical risk.
53
編號 : C7
題目: MiR-146a-5p Expression in Peripheral CD14+ Monocytes from Patients

with Psoriatic Arthritis Induces Osteoclast Activation, Bone Resorption, and
Correlates with Clinical Response
作者: 林尚宏
In psoriatic arthritis (PsA), progressive bone destruction is mediated by monocyte-derived osteoclasts.
MicroRNAs (miRNAs) regulate many pathophysiological processes; however, their function in PsA
patient monocytes has not been examined. This study aims to address whether specific miRNAs in
CD14+ monocytes and monocyte-derived osteoclasts cause active osteoclastogenesis in PsA patients.
Candidate miRNAs related to monocyte activation (miR-146a-5p, miR-146b-5p and miR-155-5p)
were measured in circulatory CD14+ monocytes collected from 34 PsA patients, 17 psoriasis without
arthritis (PsO) patients, and 34 normal controls (NCs). CD14+ monocytes were cultured with media
containing TNF-α and RANKL to differentiate into osteoclasts. Osteoclast differentiation and bone
resorption were measured by TRAP immunostaining and dentin slice resorption, respectively. The
results showed that the miR-146a-5p expression was higher in PsA patient-derived CD14+ monocytes
compared to PsO and NCs. Activation and bone resorption were selectively enhanced in osteoclasts
from PsA patients, but both were abrogated by RNA interference against miR-146a-5p. More
importantly, after clinical improvement using biologics, the increased miR-146a-5p expression in
CD14+ monocytes from PsA patients was selectively abolished, and associated with blood CRP level.
Our findings indicate that miR-146a-5p expression in CD14+ monocytes derived from PsA patients
correlates with clinical efficacy, and induction of osteoclast activation and bone resorption
54
編號 : C8
題目: The Investigation of glycylglycerin-bound miR-302 attenuates Aβ-induced

neurotoxicity through restoration of neuronal insulin signaling and autophagy
activity
作者: 何筱莉
Many studies have shown an association between impaired CNS insulin signaling and Alzheimer’s
Disease (AD), suggesting that insulin resistance might play an important role in the pathogenesis of
brain diseases. Up to the present, using a virus to conduct gene therapy is an important avenue to
treatment of a large number of diseases both heritable and acquired, but numerous problems and risks
exist that prevent using viral vectors. In this study, we demonstrated F6 (a mixture of glycylglycerin
and miR-302) directly enters into neuronal cells to provide neuroprotection through restoring impaired
insulin signaling. In our results, we showed that F6 activated Akt signaling, which subsequently
stimulated Nanog expression to suppress Aβ-induced insulin resistance. In addition, we also found that
F6 stimulates autophagy through regulating AMPK/Sirt1 signaling to alleviate Aβ-induced
mitochondria dysfunction and oxidative stress. Overall, the restored insulin signaling and decreased
autophagy activity may be associated with F6-mediated aging delaying. Based on our findings, F6 may
provide neuroprotection through restoration of impaired insulin signaling, promotion of autophagy
activity and attenuation of aging processes.
55
編號 : C9
題目: LMX1A inhibits tumorigenesis of lung cancer
作者: 吳悌暉
Purpose: LMX1A is hypermethylated and functions as a tumor suppressor in cervical cancer, ovarian
cancer, and gastric cancer. But its rule in lung cancer is unclear. The aim of this study is to evaluate
the rule of LMX1A in lung cancer.
Materials and Methods: We analyzed the function of LMX1A by examining cell lines, animal models
and human lung cancer tissues.
Results: The LMX1A was hypermethylated in lung cancer patients and some of the lung cancer cell
lines. Methylation status was corelated with LMX1A expression in some of the lung cancer cell lines.
The expression of LMX1A inhibited H1299 lung cancer cell proliferation, migration, invasion in vitro,
as well as tumorigenicity in a xenotransplantation mouse model.
Conclusion: The present study demonstrated, for the first time, that LMX1A is a tumor suppressor of
lung cancer. The mechanisms of LMX1A in tumorigenicity in lung cancer warrant further investigation.
56
七、所長、主持教授簡歷
姓名(中文) 藍先元姓名(英文) HSIEN-YUAN LANE
工作單位中國醫藥大學系所生物醫學研究所
職稱所長/教授
電子信箱 hylane@gmail.com
個人網址 http://webap.cmu.edu.tw/TchEportfolio/index_1/lanehy
Ph.D., Graduate Institute of Life Sciences, National
最高學歷 Defense Medical Center (Taiwan)
M.D, Taipei Medical University (Taiwan)
2006-2008: Adjunct Research Fellow, Institute of Biomedical Sciences,
Academia Sinica
2007-present: Director, Department of Psychiatry, CMU and Hospital
經歷 2009-present: Distinguished Professor, Director, Graduate Institute of
Clinical Medical Science, CMU
2016-present: Distinguished Professor, Director, Graduate Institute of
Biomedical Sciences, CMU
Neuropsychopharmacology
專長 Cognitive neuroscience
Precision medicine
代表性研究成果論文:
Sarcosine or D-serine add-on treatment for acute exacerbation of schizophrenia: a randomized,

double-blind, placebo-controlled study. Lane HY, Chang YC, Liu YC, Chiu CC, Tsai GE. Arch Gen
Psychiatry. 2005 Nov;62(11):1196-204.
Inhibition of glycine transporter-I as a novel mechanism for the treatment of depression. Huang CC,
Wei IH, Huang CL, Chen KT, Tsai MH, Tsai P, Tun R, Huang KH, Chang YC, Lane HY*, Tsai GE.
Biol Psychiatry. 2013 Nov 15;74(10):734-41.
Add-on treatment of benzoate for schizophrenia: a randomized, double-blind, placebo-controlled trial
of D-amino acid oxidase inhibitor. Lane HY, Lin CH, Green MF, Hellemann G, Huang CC, Chen
PW, Tun R, Chang YC, Tsai GE. JAMA Psychiatry. 2013 Dec;70(12):1267-75.
Benzoate, a D-amino acid oxidase inhibitor, for the treatment of early-phase Alzheimer disease: a
randomized, double-blind, placebo-controlled trial. Lin CH, Chen PK, Chou LJ, Chang YC, Chen
YS, Tsai GE, Lane HY*. Biol Psychiatry. 2014 May; 75(9):678-85.
Distinctively higher plasma G72 protein levels in patients with schizophrenia than in healthy
individuals. Lin CH, Chang HT, Chen YJ, Lin CH, Huang CH, Tun R, Tsai, G, Lane HY*. Mol
Psychiatry. 2014 June 19(6):636-7.
Sodium benzoate, a D-amino acid oxidase inhibitor, added to clozapine for the treatment of
schizophrenia: a randomized, double-blind, placebo-controlled trial. Lin CH, Lin CH, Chang YC,
Huang YJ, Chen PW, Yang HT, Lane HY*. Biol Psychiatry. 2018 Sep 15;84(6):422-432.
57
姓名(中姓名(英
蕭長春 Chang-Chun Hsiao
文) 文)
工作單位長庚大學系所臨床醫學研究所
職稱副教授
電子信箱 cchsiao@mail.cgu.edu.tw
個人網址 http://gicm.cgu.edu.tw/files/11-1042-164.php
University of Minnesota, Biomedical Engineering, 博士

最高學歷
長庚大學高雄分部副教授
經歷
基因體醫學、基因甲基化
專長癌症科學
體外震波與治療應用
1.Y-C Chen, T-W Chen, M-C Su, C-J Chen, K-D Chen, C-W Liou, P. Tang, T-Y Wang, J-C Chang, C-C Wang,
H-C Lin, C-H Chin, K-T Huang, M-C Lin, Chang-Chun Hsiao*. (2016, Apr). Whole Genome DNA
Methylation Analysis of Obstructive Sleep Apnea: IL1R2/ NPR2/ AR/ SP140 Methylation and Clinical
Phenotype. Sleep, 39(4):743–755. (SCI, 24/192 (12%), Clinical Neurology).本人為通訊作者.
2. S-H Lin, J-C Ho, S-C Li, J-F Chen, Chang-Chun Hsiao * and C-H Lee (2019, Jan). MiR-146a-5p Expression
in Peripheral CD14+ Monocytes from Patients with Psoriatic Arthritis Induces Osteoclast Activation, Bone
Resorption, and Correlates with Clinical Response. Journal of Clinical Medicine, 8(1): 1-12. (SCI, 15/155 =
9%, Medicine, General & Internal). 本人為通訊作者
3.S-F Jian*, Chang-Chun Hsiao*, S-Y Chen, C-C Weng, T. Kuo, D-C Wu, W-C Hung, and K-H Cheng (2014,
Apr). Utilization of Liquid Chromatography Mass Spectrometry Analyses to Identify LKB1-APC Interaction in
Modulating Wnt/β-Catenin Pathway of Lung Cancer Cells. Molecular Cancer Research, 12(4):622-35. (SCI,
44/211 (20 %), ONCOLOGY). NSC 101-2314-B-110-001-MY2. *本人為第一作者.
4. K-L Wu, Y-C Chiu, C-C Yao, C-E Tsai, M-L Hu, C-M Kuo, W-C Tai, S-K Chuah, Chang-Chun Hsiao*
(2019, Apr). Effect of extracorporeal low-energy shockwave on diabetic gastroparesis in a rat model. Journal of
Gastroenterology and Hepatology, 34(4) 720-727. (SCI, 27/80, Gastroenterology and Hepatology). 本人為通
訊作者.
5. M-T Kuo, P-C Fang, H-J Yu, T-L Chao, C-C Chien, S-L Tseng, Y-H Lai, Chang-Chun Hsiao*, T.C. Chang
(2016, Apr). A Multiplex Dot Hybridization Assay for detection and Differentiation of Acanthamoeba and
Herpes Keratitis. INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE, 57:2158–2163. (SCI, 7/57
(12%), OPHTHALMOLOGY). 本人為通訊作者.
58
Yan-Shen Shan
姓名(中文) 沈延盛姓名(英文)
(Also name Yen-Sheng Shen)
工作單位國立成功大學系所臨床醫學研究所
職稱特聘教授兼任所長
電子信箱 ysshan@mail.ncku.edu.tw
個人網址 https://researchoutput.ncku.edu.tw/zh/persons/yan-shen-shan
Visiting Scholar of University of Pennsylvenia, USA
最高學歷
Ph.D., Clinical Medicine, National Cheng Kung University
2019.08- Dean, College of Medicine, National Cheng Kung University
2017.08- Chief, Institute of Clinical Medicine, National Cheng Kung University
經歷 2016.08- Distinguished Professor, Institute of Clinical Medicine, National Cheng Kung
University and Director, Department of Clinical Medical Research, National Cheng Kung
University Hospital
Gastrointestinal Medicine: Surgical Oncology, Traumatology, Surgical nutrition and
infection
專長 Cancer biology (tumor microenvironment)
Regeneration medicine (liver and pancreas regeneration)
1. Ya-Chin Hou, Ying-Jui Chao, Min-Hua Hsieh, Hui-Ling Tung, Hao-Chen Wang, Yan-Shen
Shan*. Low CD8+ T cell infiltration and high PD-L1 expression are associated with level of
CD44+/CD133+ cancer stem cells and predict an unfavorable prognosis in pancreatic cancer.
Cancers. 2019 Apr 15; 11(4). pii: 541; doi:10.3390/cancers11040541.
2. Ya-Chin Hou, Chih-Jung Wang, Ying-Jui Chao, Hao-Yun Chen, Hao-Chen Wang, Hui-Ling Tung,
Jung-Ting Lin and Yan-Shen Shan*. Elevated serum Interleukin-8 level correlates with cancer-
related cachexia and sarcopenia: an indicator for pancreatic cancer outcomes. J. Clin. Med. 2018
Dec 1; 7(12). pii:502. doi: 10.3390/jcm7120502.
3. Hao-Chen Wang, Chin-Wang Chen, Chia-Lung Yang, I-Min Tsai, Ya-Chin Hou, Chang-Jung
Chen, Yan-Shen Shan*. Tumor-associated macrophages promote epigenetic silencing of gelsolin
through DNA methyltransferase 1 in gastric cancer cells. Cancer Immunol Res. 2017, Oct; 5(10):
885-897.
4. Hao-Chen Wang, Tzu-Ying Li, Ying-Jui Chao, Ya-Chin Hou, Yuan-Shuo Hsueh, Kai-Hsi Hsu,
Yan-Shen Shan*. KIT exon 11 codons 557-558 deletion mutation promotes liver metastasis
through the CXCL12/CXCR4 axis in gastrointestinal stromal tumors. Clin Cancer Res. 2016 Jul
15; 22(14):3477-87.
5. Andrea Wang-Gillam, Chung-Pin Li, György Bodoky, Andrew Dean, Yan-Shen Shan, Gayle
Jameson, Teresa Macarulla, Kyung-Hun Lee, David Cunningham, Jean F. Blanc, Richard Hubner,
C.-F. Chiu, Gilberto Schwartsmann, Jens Siveke, Fadi Braiteh, Victor Moyo, Bruce Belanger,
Navreet Dhindsa, Eliel Bayever, Daniel D. Von Hoff, Li-Tzong Chen; NAPOLI-1 Study Group.
Nanoliposomal irinotecan with fluorouracil and folinic acid in metastatic pancreatic cancer after
previous gemcitabine-based therapy (NAPOLI-1): a global, randomised, open-label, phase 3 trial.
Lancet 2016,Feb 6; 387(10018):545-557.
6. Ming-Chen Yang, Hao-Chen Wang, Ya-Chin Hou, Hui-Ling Tung, Tai-Jan Chiu, Yan-Shen
Shan*. Blockade of autophagy reduces pancreatic cancer stem cell activity and potentiates the
tumoricidal effect of gemcitabine. Mol. Cancer. 2015 Oct 12; 14:179.
59
姓名(中文) 蔡榮坤姓名(英文) RONG-KUNG TSAI

工作單位慈濟大學系所醫學科學研究所
職稱醫學科學研究所所長
電子信箱 rktsai@tzuchi.com.tw
個人網址 http://www.gims.tcu.edu.tw/?page_id=522
高雄醫學大學醫學研究所博士
最高學歷
慈濟大學醫學科學研究所教授兼所長
經歷佛教慈濟醫療財團法人花蓮慈濟醫院眼科研究中心主任
佛教慈濟醫療財團法人花蓮慈濟醫院眼科教授兼主任
電氣生理學、動物實驗模式、眼科分子生物學、神經再生
專長
1. Kishan Kapupara, Tzu-Lun Huang, Yao-Tseng Wen, Shun-Ping Huang, RongKung Tsai* (2019,
Apr). Optic nerve head width and retinal nerve fiber layer changes are proper indexes for validating the
successful induction of experimental anterior ischemic optic neuropathy. EXPERIMENTAL EYE
RESEARCH , 181,105-111
2. Rupendra Shrestha , Yao-Tseng Wen , Dah-Ching Ding and Rong-Kung Tsai (2019, Jan). Aberrant
hiPSCs-Derived from Human Keratinocytes Differentiates into 3D Retinal Organoids that Acquire
Mature Photoreceptors. Cells, 8(1), 36,1- 23.
3. Kapupara K, Wen YT, Tsai RK and Huang SP (2017, Nov). Soluble P-selectin promotes retinal
ganglion cell survival through activation of Nrf2 signaling after ischemia injury. Cell Death Dis,
16;8(11):e3172
4. Huang TL, Wen YT, Chang CH, Chang SW, Lin KH , and Tsai RK* (2017, Mar).Early
Methylprednisolone Treatment Can Stabilize the Blood-Optic Nerve Barrier in a Rat Model of Anterior
Ischemic Optic Neuropathy (rAION).Investigative Ophthalmology & Visual Science, 58(3),1628-
1636.
60
姓名(中文) 陳冠州姓名(英文) Chen Kuan Chou

工作單位台北醫學大學系所臨床醫學研究所
職稱所長
電子信箱 kuanchou@tmu.edu.tw
個人網址 https://www.shh.org.tw/page/TeamDocDetail.aspx?deptCode=08&docCode=08141
臺北醫學大學醫學研究所博士
最高學歷
雙和醫院泌尿科主任(現職)
經歷臺北醫學大學醫學系泌尿學科部定專任教授
亞洲太平洋攝護腺學會執行會員
攝護腺癌
專長泌尿科學
分子保健劑協同臨床醫療整合研究
＊
1. Peng CC, Chen CY, Chen CR, Chen CJ, Shen KH, Chen KC, Peng RY. Renal Damaging
Effect Elicited by Bicalutamide Therapy Uncovered Multiple Action Mechanisms As
Evidenced by the Cell Model. Sci Rep. 2019 Mar 4;9(1):3392. (corresponding author)
＊
2. Lin YC, Wu MS, Lin YF, Chen CR, Chen CY, Chen CJ, Shen CC, Chen KC, Peng CC.
Nifedipine Modulates Renal Lipogenesis via the AMPK-SREBP Transcriptional
Pathway. Int J Mol Sci. 2019 Mar 29;20(7). pii: E1570. (corresponding author)
3. Tian YS#, Chen KC#, Zulkefli ND, Maner RS, Hsieh CL. Evaluation of the Inhibitory Effects of Genipin
on the Fluoxetine-Induced Invasive and Metastatic Model in Human HepG2 Cells. Molecules. 2018 Dec
14;23(12).(equal first author).
4. Lin YC, Lai YJ, Lin YC, Peng CC, Chen KC, Chuang MT, Wu MS, Chang TH. Effect of weight loss on the
estimated glomerular filtration rates of obese patients at risk of chronic kidney disease: the RIGOR-TMU
study. J Cachexia Sarcopenia Muscle. 2019 Apr 2. doi: 10.1002/jcsm.12423.
5. Sung SY, Chang JL, Chen KC, Yeh SD, Liu YR, Su YH, Hsueh CY, Chung LW, Hsieh CL. Co-Targeting
Prostate Cancer Epithelium and Bone Stroma by Human Osteonectin-Promoter-Mediated Suicide Gene Therapy
Effectively Inhibits Androgen-Independent Prostate Cancer Growth. PLoS One. 2016, 7;11(4):e0153350.
61
姓名(中文) 楊偉勛姓名(英文) Wei-Shiung Yang

工作單位臺大醫學院系所臨床醫學研究所
職稱教授兼所長
電子信箱 wsyang@ntu.edu.tw
個人網址
美國華盛頓大學遺傳學博士
最高學歷
1. 臺大醫學院臨床醫學研究所暨醫學系內科教授
經歷 2. 臺大醫院醫學研究部規劃訓練組組長
3. 臺大醫院內科部內分泌新陳代謝科主治醫師
內分泌學
專長新陳代謝學
遺傳學
1. Pei‐Lung Chen, Shyang‐Rong Shih, Pei‐Wen Wang, Ying‐Chao Lin, Chen‐Chung Chu, Jung‐Hsin Lin,
Szu‐Chi Chen, Ching‐Chung Chang, Tien‐Shang Huang, Keh Sung Tsai1, Fen‐Yu Tseng, Chih‐Yuan
Wang, Jin‐Ying Lu, Wei‐Yih Chiu, Chien‐Ching Chang, Yu‐Hsuan Chen, Yuan‐Tsong Chen, Cathy
Shen‐Jang Fann*, Wei‐Shiung Yang* and Tien‐Chun Chang*. Genetic determinants of anti‐thyroid
drug‐induced agranulocytosis by human leukocyte antigen genotyping and genome‐wide association
study. Nat Commun. 2015 Jul 7;6:7633.
2. Wang YT, Tseng PH, Chen CL, Han DS, Chi YC, Tseng FY, Yang WS. Cardiovascular Diabetology.
Human serum RNase-L level is inversely associated with metabolic syndrome and age. 16(1):46.2017
Apr 11.
3. Chiang, J. K. Chen, C. L. Tseng, F. Y. Chi, Y. C. Huang, K. C. Yang, W. S.* Higher blood aldosterone
level in metabolic syndrome is independently related to adiposity and fasting plasma glucose.
Cardiovasc Diabetol. 2015 Jan 13;14(1):3.
62
姓名(中文) 王錦鈿姓名(英文) Wang, Chin-Tien

工作單位陽明大學系所臨床醫學研究所
電子信箱 chintien@ym.edu.tw
個人網址 https://icm.ym.edu.tw/files/13-1235-12352.php
美國奧勒岡大學哲學博士(微免)
最高學歷
陽明大學臨床醫學研究所教授
經歷臺北榮民總醫院醫學研究部研究員
分子病毒、反轉錄病毒、愛滋病毒
專長
1. Ting-Wei Guo, Fu-Hsien Yu, Kuo-Jung Huang and Chin-Tien Wang*. 2016. p6gag domain
confers in cis HIV-1 Gag-Pol assembly and release capability. J. Gen. Virol. 97: 209–219.
2. Fu-Hsien Yu, Kuo-Jung Huang and Chin-Tien Wang* 2017. C-terminal HIV-1 transframe
p6* tetra-peptide blocks enhanced Gag cleavage incurred by leucine zipper replacement
of a deleted p6* domain. J. Virol. 91(10): e00103-17.
3. Fu-Hsien Yu and Chin-Tien Wang* 2018. HIV-1 protease with leucine zipper fused at N-terminus
exhibits enhanced linker amino acid-dependent activity. Retrovirology15:32
https://doi.org/10.1186/s12977-018-0413-6
63
姓名(中文) 黃坤崙姓名(英文) KUN-LUN HUANG

工作單位國防醫學院系所醫學科學研究所
電子信箱 kun@ndmctsgh.edu.tw
PhD, University of Hawaii

最高學歷
MD, National Defense Medical Center
Executive Dean, National Defense Medical Center, 2015 –2017
經歷 Director, Tri-Service General Hospital, Critical Care Medicine, 2015 -2016

Director, National Defense Medical Center, Graduate Institute of Aerospace and Undersea
Medicine, 2009-2014
Diving medicine
專長 Critical care medicine
Chest medicine
1. Wu SY, Wu CP, Kang BH, Li MH, Chu SJ, Huang KL*. (2012) Hypercapnic acidosis attenuates
reperfusion injury in isolated and perfused rat lungs. Crit Care Med 40(2):553-559.
2. Huang KL*. (2013) Decompression sickness acclimatization. (Review) Adapt Med 5:49-54.
3. Tang SE, Wu CP, Wu SY, Peng CK, Perng WC, Kang BH, Chu SJ, Huang KL*. (2014)
Stanniocalcin-1 ameliorates lipopolysaccharide-induced pulmonary oxidative stress, inflammation,
and apoptosis in mice. Free Radical Biol Med 71C:321-331.
4. Wu SY, Tang SE, Ko FC, Wu GC, Huang KL*, Chu SJ. (2015) Valproic Acid Attenuates Acute
Lung Injury Induced by Ischemia–Reperfusion in Rats. Anesthesiology 122:1327-1337.
5. Lin HJ, Wu CP, Peng CK, Lin SH, Uchida S, Yang SS, Huang KL*. (2015) WNK4 mediates alveolar
fluid regulation in hyperoxia-induced lung injury. Crit Care Med 43:e412-419.
6. Shen CH, Peng CK, Chou YC, Pan KT, Chang SC, Chang SY, Huang KL*. (2015) Predicting
duration of mechanical ventilation in patients with carbon monoxide poisoning: a retrospective
study. J Crit Care. 30:19-24.
7. Lan CC, Peng CK, Tang SE, Wu SY, Huang KL*, Wu CP*. (2016) Anti-vascular endothelial growth
factor antibody suppresses ERK and NF-κB activation in ischemia-reperfusion lung injury. PLoS
ONE 11(8):e0159922.
8. Lan CC, Peng CK, Tang SE, Lin HJ, Yang SS, Wu CP*, Huang KL*. (2017) Inhibition of Na-K-Cl
cotransporter isoform 1 reduces lung injury induced by ischemia-reperfusion. J Thorac Cardiovasc
Surg 153: 206-215.
9. Liao WI, Wu SY, Wu GC, Pao HP, Tang SE, Huang KL*, Chu SJ*. (2017) Ac2-26, an Annexin A1
Peptide, Attenuates Ischemia-Reperfusion-Induced Acute Lung Injury. Int J Mol Sci 18(8):1771.
10. Hung CM, Peng CK, Wu CP, Huang KL*. (2018) Bumetanide attenuates acute lung injury by
suppressing macrophage activation. Biochem Pharmacol 156:60-67.
11. Shen CH, Lin JY, Chang YL, Wu SY, Peng CK, Wu CP, Huang KL*. (2018) Inhibition of NKCC1
modulates alveolar fluid clearance and inflammation in ischemia-reperfusion lung injury via
TRAF6-mediated pathway. Front Immunol 9:2049.
64
姓名(中文) 吳明蒼姓名(英文) Ming-Tsang Wu

工作單位高雄醫學大學系所臨床醫學研究所
職稱教授/所長
電子信箱 960021@cc.kmuh.org.tw
美國哈佛大學公共衛生學院博士
最高學歷
中山醫學院醫學士
高雄醫學大學附設醫院社區醫學部部長
經歷高雄醫學大學職業安全衛生研究所所長
小港醫院環境職業醫療中心主任
分子流行病學
專長公共衛生學
環境暨職業醫學
1. Wu CF, Chen HM, Sun CW, Chen ML, Hsieh CJ, Wang SL,* Wu MT*: Cohort profile: Taiwan
Maternal and Infant Cohort Study (TMICS) of phthalate exposure and health risk assessment. Int J
Epidemiol 2018 Apr 30. doi: 10.1093/ije/dyy067.
2. Lin PID, Wu CF, Kou HS, Huang TY, Shiea J, Wu MT*: Soap and the removal of di-(2-
ethylhexyl)phthalate from hands: N-of-1 and Crossover Designs. Sci Reports 2017 Mar
28;7(1):454.
3. Tsai HJ, Wu CF, Tsai YC, Huang PC, Chen ML, Wang SL, Chen BH, Chen CC, Wu WC, Hsu PS,
Hsiung C*, Wu MT*: Intake of phthalate-tainted foods and serum thyroid hormones in Taiwanese
children and adolescents. Sci Reports 2016 Jul 29;6:30589.
4. Tsai HJ, Chen BH (co-first author), Wu CF, Wang SL, Huang PC, Tsai YC, Chen ML, Ho CK,
Hsiung CA*, Wu MT*: Intake of phthalate-tainted foods and microalbuminuria in children: the
2011 Taiwan food scandal. Environ Int 2016 Apr-May;89-90:129-37.
5. Wu MT, Lin PC, Pan CH, Peng CY. Risk assessment of personal exposure to polycyclic aromatic
hydrocarbons and aldehydes in three commercial cooking workplaces. Sci Rep. 2019 Feb
7;9(1):1661. doi: 10.1038/s41598-018-38082-5.
65
姓名(中文) 陳進典姓名(英文) Gin-Den Chen

工作單位中山醫學大學系所醫學研究所
電子信箱 gdchentw@hotmail
個人網址
台灣大學公共衛生學院健康政策與管理研究所博士
最高學歷
中山醫學大學醫學系
中山醫學大學附設醫院總院醫研部副院長
經歷中山醫學大學附設醫院總院醫管部副院長
骨盆鬆弛與尿失禁
專長骨盆臟器神經學
婦科腫瘤
1. Ginden Chen, Wan-Lin Chiang, Bih-Ching Shu, Yueliang Guo, Shu-Ti Chiou, Tung-liang Chiang.
Associations of caesarean delivery and the occurrence of neurodevelopmental disorders, asthma or
obesity in childhood based on Taiwan birth cohort study. BMJ Open. 2017 Sep 27;7(9):e017086.
doi: 10.1136/bmjopen-2017-017086.
2. Chen SL, Ng SC, Huang YH, Chen GD. Are patients with bladder oversensitivity different from
those with urodynamically proven detrusor overactivity in female overactive bladder syndrome? J
Chin Med Assoc. 2017 Jul 27. pii: S1726-4901(17)30145-4. doi: 10.1016/j.jcma.2017.03.009.
3. Ng SC, Chen GD. Obliterative LeFort colpocleisis for pelvic organ prolapse in elderly women aged
70 years and over. Taiwan J Obstet Gynecol. 2016 Feb;55(1):68-71.
4. Soo-Cheen NG, Suh-Woan Hu, Gin-Den Chen. A community-based epidemiological survey of
overactive bladder and voiding dysfunction in female Taiwanese residents aged 40 years and above.
Taiwan J Obstet Gynecol. 2017 Dec;56(6):811-814.
66
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中山醫學大學高教深耕計畫教育課程暨研討會

精準醫學新境界 New Frontier of Precision Medicine

Clinical Medicine in Taiwan: New Frontier of Precision Medicine

三、大會演講 (0211 教室)……………………………………………………7

五、研討會 (0211 教室) 演講摘要………………………………….…….. 13

主持人：臺北醫學大學 陳冠州所長 主講者：李英雄教授

Professor of Biostatistics, Biomedical

Informatics, and Health Policy

經歷 Positions and Employment

Professor Ying-Shiung Lee

Keh-Liang Lin, Ph.D.

經歷 Positions and Employment

演講者：Yu Shyr, Ph.D. 石瑜教授

Professor of Biostatistics, Biomedical Informatics, and Health Policy Vanderbilt

四、課程大綱 (0212 教室)

課程題目：A 10-Year-Ground Sword for Precision Medicine 精準醫學十年磨劍

課程題目：Dramatic Advances in Precision Medicine Based on Megadata-Driven

Artificial Intelligence 基於大數據驅動人工智慧精準醫學之戲劇性進展

課程題目：New Frontier of Precision Medicine at the Chung-Shan Medical University

本校基於美國 National Research Council」提倡《精準醫學》的宏觀理念作出即時明確的共

課程題目：A Fine Perspective of Precision Medicine in Taiwan 台灣精準醫學一幅美

課程題目：Building the Framework of Health Care in Precision Medicine Ecosystem

五、研討會 (0211 教室)

學校系所: 長庚大學 醫學院臨床醫學研究所

Key words: chronic kidney disease, erythropoietin resistance, genetic polymorphism

Possible Mechanism Of High On-Treatment Platelet Reactivity.

學校系所: 高雄醫學大學 醫學研究所 臨床組

演講題目(英文): Characterization of lung cancer stem cells at different EMT status

題目: A possible biomarker in neonatal hypoxic-ischemic encephalopathy with

題目: The role of Transthyretin in Alzheimer's disease

題目: Identification of exosomal proteins in promoting lung cancer metastasis

題目: The effects of cocaine-induced behavioral sensitization on microglia’s

題目: Polarization of alveolar macrophage in model of diet induced obese mice

題目: Protective effects of hypercapnic acidosis on Ischemia–reperfusion-

題目: Insonation of Systemically Delivered Cisplatin-Loaded Microbubbles

題目: Effect of Hypercapnic Acidosis on T cells After Skin Allografts

題目: Metabolic Signatures of Renal Epithelial and Mesenchymal Cells

題目: Investigation of potential cardiotoxicity of anti-PD-1 immune checkpoint

題目: Study of the Roles of K-RAS Mutation-Related Lipid Metabolism in

題目: Study of the roles of Lipid Droplet- Related Lipidome Reprogramming in

Methods: Fig.1 在 EOCs 細胞系中通過西方墨點法檢測 LDL-R 的表達。依照組織學型態的不

Results:在 EOCs 細胞系中，knock down LDL-R 之細胞株能明顯改善卵巢癌細胞對 Cisplatin 的

題目: Ganoderma lucidum suppress the expression of EZH2 in triple-negative

題 目 : Pipoxolan inhibits LPS-induced inflammation via suppressing MAPK

題目: Curcumin Promotes Connexin 43 degradation and Temozolomid-induced

題目: Adiponectin promotes VEGF expression in rheumatoid arthritis synovial

題目: Musashi-1 Enhances Glioblastoma Migration by Promoting ICAM1

題目: Effect of microgravity on the mesenchymal stem cell characteristics of

Dependent on the MyD88/NFκB and MAPK Pathway

題目: RNA‐binding protein, human antigen R regulates hypoxia‐induced

題目: A novel desensitization site A384P of glycine receptor alpha 1 subunit

題 目 : Volume and functional changes of the remnant pancreatic tissue after

題目: Opposing Trends in Incidence/Mortality Rates and Ratios for Testicular

題目: A Next-Generation Sequencing-Based Platform for Quantitative Detection

題目: Roles and Functions of Medical Students within the Longitudinal

題目: LMX1A Hypermethylation Is a Prognostic Marker in Early-stage

題目: Application of artificial intelligence approach for the prediction of acute

題目: MiR-146a-5p Expression in Peripheral CD14+ Monocytes from Patients

題目: The Investigation of glycylglycerin-bound miR-302 attenuates Aβ-induced

題目: LMX1A inhibits tumorigenesis of lung cancer

Sarcosine or D-serine add-on treatment for acute exacerbation of schizophrenia: a randomized,

University of Minnesota, Biomedical Engineering, 博士

長庚大學 高雄分部 副教授

姓名(中文) 蔡榮坤 姓名(英文) RONG-KUNG TSAI

主持人：臺北醫學大學陳冠州所長主講者：李英雄教授

學校系所: 長庚大學醫學院臨床醫學研究所

學校系所: 高雄醫學大學醫學研究所臨床組

題目 : Pipoxolan inhibits LPS-induced inflammation via suppressing MAPK

題目 : Volume and functional changes of the remnant pancreatic tissue after

長庚大學高雄分部副教授

姓名(中文) 蔡榮坤姓名(英文) RONG-KUNG TSAI

姓名(中文) 陳冠州姓名(英文) Chen Kuan Chou

姓名(中文) 楊偉勛姓名(英文) Wei-Shiung Yang

姓名(中文) 王錦鈿姓名(英文) Wang, Chin-Tien

姓名(中文) 黃坤崙姓名(英文) KUN-LUN HUANG

姓名(中文) 吳明蒼姓名(英文) Ming-Tsang Wu

姓名(中文) 陳進典姓名(英文) Gin-Den Chen