Eclipse是目前最被普遍使用的開發環境與工具整合平台。已經有很多的軟體工具被建置或整合至其中；並且有越來越多的工具開發者嘗試將他們的工具以所謂外掛程式的方式整合至此平台。但是，由於Eclipse是一套新式且複雜的平台，大多數工具開發者並不知如何將其工具封裝為Eclipse外掛程式，而且學習Eclipse外掛程式開發也需冗長過程。基於此種因素，我們構想出一套可外掛軟體(Pluggable Software)的規範，對一般命令列工具的輸入、執行和輸出等部份提出限制條件。只要工具開發者建構的工具程式符合可外掛軟體的規範，就能利用我們提供的輔助工具，幫助工具開發者迅速將其工具整合到Eclipse平台。 / Eclipse is a development environment and tool integration platform which is currently widely used. There has been many software tools built in the form of plug-ins and integrated into this platform, and more and more tool developers are trying to integrate their tools into this platform. But, since Eclipse is a relatively new and complicated system, most tool developers do not know how to develop Eclipse plug-ins, and it is a steep learning curve to get familiar with Eclipse plug-in development. Therefore, we propose the definition of pluggable softwares, which are general command line tools but must satisfy special restrictions imposed on their input, execution and output for ease of integration. As long as the tool developer can build a tool conforming to our definition, the aiding tool we provide can help the developer rapidly integrate his tool into the platform.

推薦系統為網站提升使用者滿意度、減少使用者所花費的時間並且替網站提供方提升銷售，是現在網站中不可或缺的要素，而推薦系統的研究集中在娛樂項目，學術研究論文推薦系統的研究有限。若能給予有價值的相關文獻，提供協助，無疑是加速進步的速度。 在過去的研究中，為了達到個人化目的所使用的方法，都有不可避免或未解決的缺點，2002年美國研究圖書館協會提出布達佩斯開放獲取計劃(Budapest Open Access Initiative)，不要求使用者註冊帳號與支付款項就能取得研究論文全文，這樣的做法使期刊走向開放的風氣開始盛行，時至今日，開放獲取對學術期刊網站帶來重大的影響。在這樣的時空背景之下，本研究提出一個適用於學術論文之推薦機制，以FP-Growth演算法與協同過濾做為推薦方法的基礎，消弭過去研究之缺點，並具個人化推薦的優點，經實驗驗證後，證實本研究所提出的推薦架構具有良好的成效。 / Recommendation system is used in many field like movie, music, electric commerce and library. It’s not only save customers’ time but also raise organizations’ efficient. Recommended system is an essential element in a website. Some methods have been developed for recommended system, but they are primarily focused on content or collaboration-based mechanisms. For academic research, it is very important that relevant literature can be provided to researchers when they conduct literature review. Previous research indicates that there are inevitable or unsolved shortcomings in existing methods such as cold starts. Association of Research Libraries purpose “Budapest Open Access Initiative” that is advocate open access concept. Open access means that users can get full paper without register and pay fee. It’s a major impact to academic journal website. In this space-time background, we propose a hybrid recommendation mechanism that takes into consideration the nature of recommendation academic papers to mitigate the shortcomings of existing methods.

承保責任啟動(trigger of coverage)是開啟保險人履行契約義務的觸發機制，目的在於確定保險人的責任範圍，依照契約給付義務。有鑑於責任保險本質之特殊性，責任保險承保責任啟動值得進一步探討與研究。 美國曾歷經大量的石棉及環境污染訴訟，保險人必須承擔不確定連續性曝險之損害造成的長尾責任，使其財務規劃不易，故保險人以限制承保責任啟動之方式，限縮承保範圍。在司法實務上因此發展許多相關理論，對於保單條款之適用方式及適法性做出解釋。 我國尚未對於責任保險承保責任啟動機制及其衍生的問題深入分析，關於承保責任啟動之規範定位不明。惟實務保單條款已有針對責任保險保單作出承保責任啟動方式之約定，其約定之合法性及妥適性為何，均有檢討之必要。 本文以介紹美國責任保險承保責任啟動，保險契約當事人如何運用此機制為主軸，藉由美國法之經驗，探討我國如何定位此制度，實務上保單條款出現之相關問題如何解決，在現有的法制下應如何解釋與補充，提出建議與理由，希冀能對我國責任保險理論之建構有所貢獻。

STAT1是一個轉錄因子，在細胞生理功能中是非常重要的訊息傳遞者，在免疫系統具有抗病毒的角色，但是目前為止對於STAT1在中樞神經系統所扮演的角色仍不清楚。爲證實STAT1的表現與空間記憶的形成有關聯，我們將大白鼠分成兩組，一組為有訓練的組別，另一組則為無訓練的組別分別進行水迷津試驗，試驗完畢後取出大鼠的海馬迴CA1區域組織進行即時定量聚合酶連鎖反應與西方墨點法分析。結果顯示，經過水迷津訓練的刺激下，STAT1 mRNA與蛋白質分別減少約34 %及40 %，而STAT2 mRNA及蛋白質的表現則不受空間學習的影響。爲了進ㄧ步探討STAT1在空間學習記憶過程中所扮演的角色，實驗利用STAT1 siRNA轉染至海馬迴CA1區域抑制STAT1的表現，發現降低STAT1表現會促進大白鼠在水迷津試驗的學習能力，實驗同時也轉染STAT2 siRNA至CA1區域，結果顯示STAT2不參與大白鼠空間記憶的形成。本實驗室先前發現降低laminin β1表現量會促進大白鼠的空間學習記憶 (unpublished observation, 附錄二)，此外laminin β1基因啟動子上具有STAT1結合序列：interferon-γ activated site (GAS)。因此，實驗利用PC12細胞進行laminin β1報導基因分析，結果顯示STAT1會促進 laminin β1啟動子的轉錄活性。而爲了進一步探討在STAT1影響空間學習與記憶歷程中與laminin β1的關聯性，實驗利用STAT1 siRNA抑制大白鼠海馬迴CA1區STAT1的表現並促進空間學習與記憶的同時，發現laminin β1 mRNA及蛋白質表現量都受到STAT siRNA的抑制，而轉染野生型STAT1-Flag質體則會增加laminin β1 mRNA及蛋白質的表現量，顯示STAT1正向調控laminin β1的表現。本篇論文提出海馬迴CA1區域的STAT1參與動物空間學習與記憶的形成，其中可能與STAT1正向調控laminin β1的表現有關。 / STAT1 is a signal transducer and transcription factor in the cell. Several reports have indicated that STAT1 plays a critical role in immune response against virus infection in animals. However, the role of STAT1 in the central nervous system is still unclear. In the present study, we aimed to examine the role of STAT1 involved in spatial memory formation in rat and the possible downstream gene that STAT1 regulates. Rats were randomly divided into the trained group and the non-trained group. Animals were subjected to water maze learning according to the previous behavioral paradigm. Their hippocampus CA1 tissues were dissected out for STAT1 mRNA level and protein level determination. Results indicated that spatial training markedly decreased STAT1 mRNA level and protein level in the CA1 area, but this change was not found for STAT2 mRNA and protein expression. To further confirm the role of STAT1 involved in spatial learning and memory, animals were transfected with STAT1 siRNA in the CA1 area. Results showed that STAT1 siRNA transfection significantly facilitated water maze performance, whereas their water maze performance under STAT2 siRNA transfection was not altered. Previous studies from our laboratory have demonstrated that laminin β1 impairs spatial memory formation in rat (unpublished observation). In addition, promoter analysis indicates that the laminin β1 promoter region contains two GAS elements, which is the STAT1/STAT1 and STAT1/STAT3 binding site. Results from luciferase reporter assay revealed that transfection of STAT1 siRNA decreased laminin β1 promoter activity, whereas transfection of STAT1 wild-type plasmid increased laminin β1 promoter activity. To further study the relationship between STAT1 and laminin β1 in spatial memory formation, we used STAT1 siRNA to knockdown STAT1 expression and these animals were subjected to spatial training. We then determined their laminin β1 expression. Results showed that the laminin β1 mRNA level and protein level were both significantly decreased by STAT1 siRNA transfection. Besides, STAT1 wild-type plasmid transfection increased laminin β1 mRNA level and protein level in the CA1 area associated with spatial memory impairment. These results together suggest that STAT1 negatively regulates spatial memory formation. Further, STAT1 may impair spatial memory formation through increased laminin β1 expression.