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(R)Evolution

為了解決Confirm with的問題，作者 這樣論述：

They tried to kill the ugliness but they only made it stronger.The icecaps melted and the water consumed the shorelines but New York City still stands. All four boroughs prosper thousands of feet over the old metropolis hastily protected by walls. Proper citizens live above in a beautiful, protec

tive dome on concrete stilts and criminals serve life below in the polluted, walled ghost of a city.Richard Smith, a street-sweeper, enjoyed life in NYC with his wife until their deformed, life-supported child is medically terminated at birth by the government, pulling Richard’s soul into darkness.W

hen he receives a distressing message from a group known as Right-To-Life, Richard sinks lower. His child and many others may be alive and living with the criminals below in old New York. He needs to find his son and there is only one way possible to confirm if it’s true.What he finds may be more th

an what society above can fathom.A tense, wild ride of a sci-fi dystopian novel from the author of the Blunt Force Kharma series.

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社會住宅智慧綠建築導入資訊模型之研究

為了解決Confirm with的問題，作者洪國桓 這樣論述：

建築資訊模型(Building Information Modeling, BIM)是目前營建業界中，最熱門的技術，而BIM技術是一個在數位虛擬空間中可事先模擬營建工程專案中協助建築生命週期各項作業及可能情境中以利運用視覺化管理模式，達成事先解決問題，為工程作業中之新技術、新方法；然而BIM技術的發展還存在許多問題，主要是因為建築專案工程個案的獨特性、參與者眾多複雜與建築生命週期長等特質，造成設計與施工階段產生了許多不符預期的成果，對營運維護階段影響鉅大。本研究主要係依據文獻分析法、問卷調查法以及專家訪談法，調查相關文獻彙整分析國內公共工程運用BIM技術現況，以及國內各機關及廠商目前採用BI

M技術之情形，透過問卷方式確認題綱後與專家訪談彙整，且分析針對有關影響社會住宅智慧綠建築導入建築資訊模型之執行成效並研擬改善對策，藉以提升營建專案整體效率以及效益之價值。

Toward a Critical Theory of Nature: Capital, Ecology, and Dialectics

為了解決Confirm with的問題，作者Cassegård, Carl 這樣論述：

Challenging the normalization of a capitalist reality in which environmental destruction and catastrophe have become ’second nature’, Towards a Critical Theory of Nature offers a bold new theoretical understanding of the current crisis via the work of the Frankfurt School. Focusing on key notions

of dialectics, natural history, and materialism, a critical theory of nature is outlined in favor of a more traditional Marxist theory of nature, albeit one which still builds on core Marxist concepts to confirm humanity’s central place in manufacturing environmental misery. Pre-eminent thinkers of

the Frankfurt school, including, Georg Lukács, Ernst Bloch, Theodor Adorno, and Alfred Schmidt, are highlighted for their potential to diagnose the interpenetration of capitalism and nature in a way that neither absolutizes nor obliterates the boundary between the social and natural. Further theore

tical claims and practical consequences of a critical theory of nature challenge other contemporary theoretical approaches like eco-Marxism, social constructivism and new materialism, to situate it as the only approach with genuinely radical potential. The possibility of utopian idealism for underst

anding and responding to the current climate crisis is carefully measured against the dangers of false hope in setting out realistic goals for change. Environmental change in turn is seen through the prism of recent cultural currents and movements, situating the power of a critical theory of nature

in relation to understandings of the Anthropocene; concepts of apocalypse, and postapocalypse. This book culminates in a powerful tool for an anti-capitalist critique of society’s painfully extractive relationship to a deceptively abstracted natural world.

潛藏危機：Musashi-1固有無序區域介導與神經退行性疾病相關蛋白之異常聚集

為了解決Confirm with的問題，作者杜岱芸 這樣論述：

蛋白質病變(proteopathy)是退行性疾病的常見原因，通過錯誤折疊的蛋白質異常聚集形成類澱粉沉積症(amyloidogenesis)，從而導致破壞組織內的穩態。尤其是，近期研究表明細胞內具有固有無序區域 (intrinsically disordered regions)的蛋白容易進行液-液相分離(liquid-liquid phase separation)，從而在細胞中組裝蛋白質凝聚層(coacervates)。在本研究中，我們假設具有固有無序區域的蛋白質受環境壓力影響，促進異常折疊甚至形成聚集體，這將進一步形成澱粉樣斑塊(amyloid plaques)並在組織內堆積，導致蛋白質

病變。我們主要探討不僅是RNA結合蛋白、也是幹性基因的Musashi-1，是否與具有豐富IDR的Musashi-1 C-末端區域相互作用以進行液-液相分離，最終形成澱粉樣原纖維(amyloid fibrils)。為了確認哪些序列更易於形成澱粉樣蛋白，因此對Musashi-1的C-末端進行了序列連續刪除來取得不同長度的片段。我們的研究結果表明Musashi-1 C-末端面對不同pH值和鹽濃度會影響液-液相分離狀態，包含改變蛋白質相分離的出現時間、形狀和大小，隨著時間的推移，Musashi-1 C-末端也可以形成澱粉樣蛋白原纖維。而當在氧化壓力下，它會在細胞內誘導組裝應激顆粒與不可逆的聚集體的形成

，另一方面，當細胞同時表達Musashi-1 C-末端和內源性TDP-43，Musashi-1 C-末端誘導TDP-43從細胞核錯誤定位到細胞質。此外，Musashi-1 C-末端促進磷酸化和泛素化TDP-43。總結來說，我們提出了關於Musashi-1與神經退行性疾病相關蛋白相互作用導致異常聚集的新見解，這些發現有助於提供解決退行性疾病的新思路。