Interacting的問題，透過圖書和論文來找解法和答案更準確安心。 我們找到下列包括價格和評價等資訊懶人包

Philosophy of Religion Around the World: Critical Perspectives and Approaches

為了解決Interacting的問題，作者 這樣論述：

Much philosophical thinking about religion in the Anglophone world has been hampered by the constraints of Eurocentrism, colonialism and orientalism. Addressing such limitations head-on, this exciting collection develops models for exploring global diversity in order to bring philosophical studie

s of religion into the globalized 21st century. Drawing on a wide range of critical theories and methodologies, and incorporating ethnographic, feminist, computational, New Animist and cognitive science approaches, an international team of contributors outline the methods and aims of global philosop

hy of religion. From considering the importance of orality in African worldviews to interacting with Native American perspectives on the cosmos and investigating contemplative studies in Hinduism, each chapter demonstrates how expertise in different methods can be applied to various geographical reg

ions, building constructive options for philosophical reflections on religion. Diversifying Philosophy of Religion raises important questions regarding who speaks for and represents religious traditions, setting the agenda for a truly inclusive philosophy of religion that facilitates multiple standp

oints.

Interacting進入發燒排行的影片

布里斯洛中間體自由基反應機制之理論研究

為了解決Interacting的問題，作者謝明修 這樣論述：

含氮雜環卡賓（N-heterocyclic carbene）催化之化學反應中，布里斯洛中間體（Breslow intermediate）扮演重要的催化角色。布里斯洛中間體能以親核基（nucleophile）或自由基（radical）之形式參與反應。本論文探討布里斯洛中間體之自由基特性及形成機制（mechanism），其自由基可從氫自由基轉移或直接氧化形成。安息香縮合反應（benzoin condensation）中，布里斯洛中間體將氫原子轉移至苯甲醛（benzaldehyde）以形成自由基，此自由基可結合形成安息香產物，或排除反應之副產物，使其重新進入催化反應。唯此路徑之反應能障高於傳統非自

由基路徑。此研究亦探討四種布里斯洛中間體之不同電子組態的位能面。其中烯醇鹽（enolate）形式能產生偶極束縛態（dipole-bound state），此為產生自由基之新路徑；拉電子基（electron-withdrawing group）以及立體障礙基（bulky groups）可穩定基態。另外，我們亦研究布里斯洛中間體之碎片化（fragmentation）與重組（rearrangement）。布里斯洛中間體之催化反應可能因其碳氮鍵斷裂而中止，形成碎片。我們證實其反應中可以形成自由基，亦可形成離子。反應趨向之路徑與布里斯洛中間體之羥基的質子化型態有關。碎片化反應亦可視為轉酮醇酶（tran

sketolase）中之噻胺（thiamin）催化反應中之副反應；此研究證實轉酮醇酶透過限制布里斯洛中間體之結構與質子化型態，使其碳氮鍵斷裂需更高之反應能量，進而抑制此副反應。

Floating World to Modern World: The Japanese Print in Transition

為了解決Interacting的問題，作者Paget, Rhiannon 這樣論述：

A stunning introduction to the history of Japanese printmaking, with highlights from the de Young museum’s vast collectionIn 1868, Japan underwent a dramatic transformation following the overthrow of the shogun by supporters of Emperor Meiji, marking the end of feudal military rule and ushering i

n a new era of government that promoted modernizing the country and interacting with other nations. Japanese print culture, which had flourished for more than a century with the production of color woodcuts (the so-called ukiyo-e, or ＂floating world＂ images), also changed course during the Meiji er

a (1868-1912), as societal changes and the once-isolationist country’s new global engagement provided a wealth of new subjects for artists to capture. Featuring selections from the renowned Achenbach Foundation for Graphic Arts’ permanent collection, Japanese Prints in Transition: From the Floating

World to the Modern World documents the shift from delicately colored ukiyo-e depictions of actors, courtesans, and scenic views to brightly colored images of Western architecture, modern military warfare, technology (railroad trains, steam-powered ships, telegraph lines), and Victorian fashions and

customs.

探討CPT1C在類基底型乳癌中調控上皮-間質轉型及腫瘤幹細胞特性所扮演的角色

為了解決Interacting的問題，作者王慶弘 這樣論述：

代謝途徑重整是腫瘤的重要特徵之一，腫瘤細胞可藉由調控自身的代謝偏好而有利其在代謝壓力的情況下存活，並維持高速增生。有研究更進一步指出乳癌細胞傾向於透過調控脂肪酸氧化代謝的效率限制酶CPT1C來增加脂肪酸氧化的活性，進而促進細胞增生，甚至維持腫瘤幹細胞特性及產生抗藥性。因此，本研究旨在釐清類基底型乳癌是否透過調節CPT1C影響細胞脂肪酸氧化代謝的活性，進而誘發上皮-間質細胞轉型及腫瘤幹細胞特性。我們的先導結果指出，透過TCGA數據資料庫分析，CPT1C表現量在類基底型乳癌患者中高於其他乳癌類型，並在具有淋巴結轉移或遠端轉移的患者中具有較高的表現量;而在類基底型乳癌患者中，擁有較高CPT1C表現

量的族群同時存活率也較差。此外，在類基底型乳癌患者中，相較於其他CPT1同功酶(CPT1A、CPT1B)， 唯有CPT1C的表現量和存活率呈現負相關。接著，正常類基底型人類乳腺上皮細胞中過度表現CPT1C會增加脂肪酸氧化代謝活性，同時也誘導上皮-間質細胞轉型、細胞遷移、侵襲，並且提升腫瘤幹細胞特性；反之，利用微小干擾RNA抑制類基底型乳癌細胞株的CPT1C表現則可降低腫瘤的發展。以上結果顯示CPT1C確實在類基底型乳癌細胞的高度上皮-間質細胞轉型及癌幹性中扮演不可或缺的角色，未來我將繼續探討調控CPT1C的分子機制及利用動物實驗進行驗證。我們的研究不僅對於新穎療法的開發有很大的幫助，也釐清現行

生酮飲食療法用於類基底型乳癌的謬誤。關鍵詞: 脂肪酸氧化、CPT1C、類基底型乳癌、上皮-間質細胞轉型、腫瘤幹細胞特性