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臺北醫學大學 轉譯醫學博士學位學程 李友專、蕭宏昇、吳駿翃所指導 祁力行的 以全基因轉錄組和蛋白質體分析來鑑定驗證頭頸部鱗狀上皮細胞癌的生物標記 （2021），提出Im@TMU關鍵因素是什麼，來自於基因轉錄組、蛋白質體、頭頸部鱗狀上皮細胞癌、生物標記、科斯-基因模式、全人照護、正念止觀、存活分析、頸部淋巴節、深度學習、質譜儀、口腔顎面外科、法醫學、應用程式介面、醫學資訊學、口腔癌、檳榔、考古病理學。
而第二篇論文臺北醫學大學 代謝與肥胖科學研究所碩士班 陳揚卿、黃士懿所指導 Shirley Priscilla Gunawan的 慢性睡眠剝奪改變人類和動物的青春期時間 （2021），提出因為有 puberty、sleep deprivation、inflammation、oxidative stress、gut dysbiosis的重點而找出了 Im@TMU的解答。
以全基因轉錄組和蛋白質體分析來鑑定驗證頭頸部鱗狀上皮細胞癌的生物標記
為了解決Im@TMU 的問題，作者祁力行 這樣論述：
頭頸部鱗狀上皮細胞癌(以下稱為 HNSCC) 在全球都是重要的健康問題之一。手術、放射、以及化學治療目前是HNSCC 患者的標準治療。病患的存活必須仰賴: 1)足夠(大)的手術切緣、病理報告指引的放射治療，2)系統性治療(標靶、免疫療法)的「生物標記」，以及3)全人癌症照護(顧及靈性須求、身體照護、心理支持，與社會支援)。HNSCC癌症存活分析在傳統上，是利用組織中基因表現量的差異(DEGs)，以臨床資訊搭配蛋白質體的數據，來找尋生物標記。而採用HNSCC全基因表現量、結合存活分析的方法，則首見於2021年發表的「pvalueTex」。本文介紹質譜法分析HNSCC，以及pvalueTex的處
理流程，包括數據檢索、前製處理、特徵選擇、「無段式」閾值分析、Kaplan--Meier存活分析，和Cox比例風險模型。我們依此發現，HNSCC的獨立預後因子為: 生物標記（TMSB4X、CAMK2N1、CALML5 和FCGBP）、腫瘤大小，以及手術切緣狀態。由總存活期 (OS) 、無復發存活期(RFS)較差的的患者檢體中，可以發現大量表現的TMSB4X蛋白。實驗中發現，若抑制HNSCC細胞株中的TMSB4X，其細胞增殖速率會減少，且降低小鼠的頸部淋巴結轉移，證明TMSB4X與HNSCC的頸部轉移有高度相關。至於CAMK2N1、CALML5和FCGBP基因的表現量，則與患者的總存活期(OS)
密切相關。我們必須推廣全人癌症照護的觀念，強調靈性、精神、情感、身體和社會關係層面，對癌症患者存活的重要影響。全人癌症照護結合有效的生物標記，終將成為真正量身定製的個人化治療。
慢性睡眠剝奪改變人類和動物的青春期時間
為了解決Im@TMU 的問題，作者Shirley Priscilla Gunawan 這樣論述：
Sleep deprivation (SD) has become a secular trend in adolescents that causes adverse health outcomes. A growing evidence shows that SD may contribute in precocious puberty. However, to date, the exact mechanisms of how sleep deprivation results in early sexual maturation remain unclear. Therefore,
we aim to investigate further about the correlation between SD and pubertal timing, and clarify the mechanisms. A total of 459 boys and 959 girls with a mean age of 11.71 ± 1.78-year-old and 9.72 ± 1.77-year-old, respectively, were included in this study. The results showed that SD led to early sexu
al maturation through obesity as the mediator, especially in girls. Subsequently, we investigated using experimental animals to explore the underlying mechanisms. Sprague-Dawley juvenile rats were exposed to 4 weeks of chronic sleep deprivation (CSD). Food and water were provided ad libitum. and the
y were sacrificed when they were 7-weeks-old. The vaginal opening and balanopreputial observation were performed every morning throughout the study to determine the pubertal onset in female and male rats, respectively. A vaginal smear was performed daily on female rats to assess the estrous cycles.
The animal study depicted different results as they had lower body weight which eventually led to delayed puberty. In addition, SD caused elevated levels of oxidative stress and systemic inflammation, lower short-chained fatty acids, and gut dysbiosis which also affected the pubertal timing. Taken t
ogether, this study shows how sleep deprivation differently affects the pubertal timing in humans and animals.