走在汽車革命的路上論文書籍站
國立東華大學 生命科學系 翁慶豐所指導 THIYAGARAJAN VARDHARAKAN的 以電腦模擬、體外、體內與奈米吸附篩選及印證天然化合物 （2014），提出KONI 1130關鍵因素是什麼，來自於粘著斑激酶、絲狀偽足、上皮間質轉化、抗腫瘤、長夜暗羅。
而第二篇論文輔仁大學 食品科學系 陳政雄所指導 林承萱的 金屬爪蓋墊片鄰苯二甲酸酯轉移之影響因子探討 （2011），提出因為有 鄰苯二甲酸酯類、塑化劑、金屬瓶蓋墊片、聚氯乙烯、迴歸分析的重點而找出了 KONI 1130的解答。
以電腦模擬、體外、體內與奈米吸附篩選及印證天然化合物
為了解決KONI 1130 的問題，作者THIYAGARAJAN VARDHARAKAN 這樣論述：
Focal adhesion kinase (FAK) is a nonreceptor protein tyrosine has been overexpressed in many types of tumors and plays an important role in number of cell signaling pathways including cell migration, proliferation, viability, and cell survival. This study was aimed to identify the novel and specifi
c inhibitors from natural compounds via molecular docking of FAK (Y397) and investigate the underlying mechanism of action. The 3D structure of the FAK (PDB ID: 2AL6) was used for docking 107 Natural compounds. Based on their high affinity and energy interaction, top two compounds Antroquinonol from
Antrodia camphorata and 16-hydroxy-cleroda-3,13-dien-16,15-olide (HCD) from Polyalthia longifolia were selected and further validated with C6 Glioma and N18 Neuroblastoma cell lines. Protein (2AL6) - ligands interaction analysis indicated that H-bond with residues Arg 86 and Arg 125. These compoun
ds showed a potential effect on cell viability by MTT assay; in contrast cell cycle analysis showed cell arrest in subG1 and G0-G1 phase, respectively and further induction of apoptosis was confirmed by TUNEL assay. Atomic Force Microscopy data depicted that the formation of filopodia on intracellu
lar surface decreased in treated cells as compared to the control. In addition, both compounds inhibited the activity of MMP 2 and 9 using Zymography. The protein levels of FAK, pFAK, Rac1 and cdc 42 were decreased, which are the key regulators for the formation of filopodia and cell migration. Fur
ther, both the compounds regulate the expression of epithelial mesenchymal transition (EMT) proteins. HCD and antroquinonol induce the autophagy through ROS mechanism. Further, HCD conjugated with Cu-MSN showed a controlled drug release and reduced the tumor growth of glioma. Taken together, this st
udy suggests that Antroquinonol and 16-hydroxy-cleroda-3,13-dine-16,15-olide could be a potential inhibitor of FAK for anti-tumorigenesis and anti-metastasis.
金屬爪蓋墊片鄰苯二甲酸酯轉移之影響因子探討
為了解決KONI 1130 的問題，作者林承萱 這樣論述：
鄰苯二甲酸酯類為一種內分泌干擾化學物質，具致突變及致癌性，常用於一些塑膠材質，但從食品包材轉移至食品時，則會造成人體危害。本研究目的主要探討影響金屬爪蓋內墊片於儲藏期間之鄰苯二甲酸酯類塑化劑轉移的因素。研究藉由水性 (三種酸鹼值) 與油性 (橄欖油模擬液) 接觸金屬爪蓋墊片，於冷藏、室溫及模擬運輸之高溫進行儲藏試驗三個月，模擬液經溶劑萃取鄰苯二甲酸酯再以固相萃取純化，並利用 HPLC 鑑定與定量。另以 FTIR-ATR 分析金屬爪蓋塗層及墊片材質。結果顯示以HPLC分析11種鄰苯二甲酸酯類化合物的偵測極限範圍為 0.1-0.5 ppm。水性模擬液經儲藏12週皆無鄰苯二甲酸酯之檢出，顯示酸鹼值
及溫度不影響水模擬液中鄰苯二甲酸酯類釋出。油性模擬液與墊片於高溫及長時間接觸會造成其中鄰苯二甲酸酯轉移，以鄰苯二甲酸二-[2-乙基己基]酯 (Di-2-ethylhexyl phthalate) 及鄰苯二甲酸二異壬酯 (Diisononyl phthalate) 為主要檢出化合物。FTIR-ATR 分析發現金屬爪蓋塗層無 -C=O 官能基，而聚氯乙烯材質之墊片則有此官能基，推測為鄰苯二甲酸酯來源。利用迴歸分析鄰苯二甲酸酯之轉移方程式，食品極性、儲藏溫度及時間為主要影響因子使鄰苯二甲酸酯從聚氯乙烯墊片轉移至食品中。藉由控制包材中鄰苯二甲酸酯含量、溫度及儲藏時間可降低塑化劑之轉移程度。