1,720,965 research outputs found
The effect of BisGMA on cyclooxygenase-2 expression, PGE2 production and cytotoxicity via reactive oxygen species- and MEK/ERK-dependent and -independent pathways
No full textCopyright © 2009 Elsevier Ltd All rights reserved.Mei-Chi Chang, Li-Deh Lin, Chiu-Po Chan, Hsiao-Hua Chang, Lin-I. Chen, Hsueh-Jen Lin, Hung-Wei Yeh, Wan-Yu Tseng, Po-Shuen Lin, Chiu-Chun Lin and Jiiang-Huei Jenghttp://www.elsevier.com/wps/find/journaldescription.cws_home/30392/description#descriptio
Maintenance Cost of Elevated Expressway-A Case Study of Jianguo Expressway and Xinsheng Expressway in Taipei City
No full text橋梁於生命週期規劃設計與營造階段，往往著重在機能、成本、進度、品質等議題面向，而忽略後續營運維護階段中維護經濟性之規劃或管理，導致可觀之營運維護成本陸續產生。國內橋齡逐漸老化，伴隨而來的是的龐大的維護修繕成本，而政府財政日漸拮据，管理單位對橋梁之維護規劃難度也日益升高，短絀的預算加上對橋梁全生命週期成本管理的錯誤觀念，已直接導致國內橋梁加速劣化，現存橋梁維護成本的妥善利用已成為目前橋梁管理單位研究的重大課題之一。
臺灣因地形關係，大部分陸上交通需仰賴橋梁做為連結各區域之交通聯繫，對於少數偏遠之鄉、鎮及部落而言，僅能靠橋梁維持對外交通之聯結，因此橋梁成為經濟發展不可或缺的重要公共建設；建造於市區內的高架快速道路橋梁，則提供車輛迅速到達目的地的功能，使都市交通得以順暢，減輕都市化造成之交通負荷量；然而，橋梁容易因地震、豪雨等天災侵襲，以及車輛超載等外部因素導致橋梁損壞，可能釀成用路人傷亡及交通中斷等災害；因此本研究以臺北市「建國高架橋」與「新生高架橋」為研究對象，蒐集彙整民國85至99年維護修繕成本資料進行研究，探討高架快速道路橋梁各構件於維護修繕支出比例與內容，並歸納出橋梁維護作業上之關鍵維護項目，評估後提出相關研擬對策，提供橋梁管理機關在有限的維修經費狀況下執行預算編列及維護管理規劃之參考。During bridges life-cycle design and construction stage, emphasis are often on function, cost, schedule, and quality, but this ignores plan or management of protecting economy in the stage of following operation and maintenance, and this leads to successive production of considerable cost of operation and maintenance. Bridge ages in Taiwan gradually become old, what follows is huge amount of maintenance cost. However, government finance becomes tight, difficulty in maintenance and design of bridges by management unit raises day by day. Short budget plus wrong concept of bridge life-cycle cost management have directly caused bridges in Taiwan accelerate deterioration. Well use of current bridge maintenance cost has become one of the major topics of bridge management unit researches.
Most of the on-land traffics in Taiwan need to depend on bridges to connect various local areas due to the terrain. For few far counties, towns and tribes, they can only depend on bridges supporting communication with outside traffics. Therefore, bridges become indispensable important public construction; the elevated expressway bridges built inside cities provide vehicles with the function of arriving destination rapidly, this makes city traffic unhindered, reducing the traffic load caused by urbanization; however, bridges easily get damaged by earthquakes, torrential rains and other natural disasters, and by overload of vehicles and other external factors, and this could cause passer-by casualties, traffic interruption and other disasters; hence this research use Taipei “Jianguo Expressway” and “Xinsheng Expressway” as research objects, collecting maintenance cost between year 85 to year 99 to research. Investigating elevated expressway bridges each component’s ratio and content in maintenance cost, and induces key maintenance items on bridges maintenance operations, propose related plan after evaluation, provide bridges management department with executing budget plan under limited maintenance fee, and with reference of maintenance management plan
Dickkopf 3 (Dkk3) regulates the expression of zebrafish myf5 promoter via phosphorylated p38a-dependent Smad4 stability
No full textMyf5 是肌肉發育 (myogenesis) 調控因子MRFs (myogenic regulatory factors) 的一員，對於肌肉的特化及分化都具有重要的功能。在斑馬魚myf5 intron I 中含有一個 microRNA，命名為miR-In300，它能夠結合dickkopf 3 (dkk3) 3’UTR並抑制其轉錄作用，進而負調控 myf5 表達影響肌肉發育。但 Dkk3 是一種分泌性蛋白質，它是藉由何種調控路徑來影響 myf5 的表達尚不清楚。在本實驗中我們發現抑制 Dkk3 會造成磷酸化的p38a蛋白質下降；注射 p38a 專一轉譯抑制劑 (morpholino, MO) knockdown p38a 的表現後，發現胚胎體節形狀不正常，且 myf5 mRNA表達較少，這些表型和注射dkk3-MO 的胚胎類似，且利用dominant-negative form 的p38a 競爭也得到相同的結果。利用 p38 inhibitor (SB203580) 抑制 p38 磷酸化阻斷MAPK pathway亦會造成myf5下降。當注射p38a-MO到帶有 myf5上游 80kb 啟動子驅動 GFP 的斑馬魚轉殖品系Tg(myf5(80K):GFP) 之胚胎後，會造成myf5啟動子驅動GFP的表現能力下降。若額外添加 p38a mRNA就可以挽救因注射p38a-MO所造成綠螢光表現下降的缺陷，但若額外添加磷酸化位點突變的 p38a mRNA則無法達到挽救的效果。這些結果證明 p38a 是經由磷酸化作用來調控 myf5啟動子的活性。另一方面，加入dominant-negative form 的Smad2及Smad3a 後，胚胎體節發育不正常且 myf5 表現下降，這和注射dkk3-MO及p38a-MO的胚胎有類似的表型。利用 luciferase assay 及注射 smad2/3a/3b/4 mRNA 到Tg(myf5(80K):GFP) 轉殖品系的胚胎，發現過量表現 Smad2 及Smad3a 會增強myf5 啟動子的活性；更進一步地，利用Chromatin immunoprecipitation assay 證實 Smad3a 可直接結合到 myf5 啟動子上，藉由 Smad2/3a complex 開啟 myf5 的啟動子。而當抑制 Dkk3 或 p38a 時，Smad4 蛋白質表現會下降而Smad3蛋白質量不改變；且過量表現 smad4 mRNA可以挽救 dkk3-MO 造成 myf5 下降的情形。綜合上述證據，我們總結 Dkk3 藉由調控 p38a 的磷酸化來維持 Smad4 蛋白質穩定性，進而使 Smad4 能與 Smad2/3a 形成complex 來開啟斑馬魚 myf5 的啟動子。Myf5, one of the myogenic regulatory factors, plays roles in the specification and differentiation of muscular cells during myogenesis. An intronic microRNA, miR-In300, located within zebrafish myf5 intron I, has been reported to silence myf5 through targeting dkk3. However, the detailed molecular mechanism underlying how the secreted Dkk3 controls the myf5 expression is totally unknown. In this study, we found that knockdown of dkk3 reduced the protein level of the phosphorylated p38a. Injection of p38a-specific morphorlino (MO), which inhibits the translation of p38a mRNA, resulted that the malformed somites and the reduced myf5 transcripts, which photocopied the defects induced by injection of dkk3-MO. These phenotypes were also observed in the embryos injected with the dominant-negative form of p38a. Blocking the MAPK pathway through interfering the phosphorylation of p38 by introducing SB203580 caused the down-regulation of myf5 expression. Furthermore, the GFP fluorescent signal was dramatically decreased when we injected p38a-MO into the embryos derived from transgenic line Tg(myf5(80K):GFP), in which the GFP was driven by myf5 promoter. This p38a-MO-induced defects were rescued by co-injection with p38a mRNA, but were not rescued with the mutated p38a mRNA containing a mutation at phosphorylation domain. This line of evidences suggested that the phosphorylation of p38a is required for activating of myf5 promoter activity. Moreover, the defective phenotypes induced by injection the dominant-negative form of either Smad2 or Smad3 were as same as those of embryos injected with either dkk3- or p38a-MO. Using luciferase assay and injection of samd2/3a/4 mRNA in the embryos derived from Tg(myf5(80K):GFP), we found that overexpression of Smad2 and Smad3a did enhance the myf5 promoter activity. Furthermore, we proved that Smad3a directly bound at the upstream regulatory region of myf5 using chromatin immunoprecipitation assay. Interestingly, knockdown of either dkk3 or p38a resulted in the decrease of Smad4 protein level, but did not change the Smad3 protein level. Injection of smad4 mRNA enabled embryos to rescue the down-regulation of myf5 in the dkk3-MO-injected embryos. Taken together, we concluded that Dkk3 regulates the phosphorylation of p38a to maintain the stability of Smad4 protein, which, in turn, to allow the complex of Smad2/3a/4 to activate the zebrafish myf5 promoter activity.中文摘要 ------------------------------------------------------ 1文摘要 ------------------------------------------------------ 2獻回顧 ------------------------------------------------------ 4言 ----------------------------------------------------------- 15驗材料與方法 -------------------------------------------- 17果 ----------------------------------------------------------- 29論 ----------------------------------------------------------- 42結 ----------------------------------------------------------- 53考文獻 ----------------------------------------------------- 54表 ----------------------------------------------------------- 75錄 ----------------------------------------------------------- 9
dickkopf-3-related Gene Regulates the Expression of Zebrafish myf5 Gene through Phosphorylated p38a-dependent Smad4 Activity
No full textNovel intronic microRNA represses zebrafish myf5 promoter activity through silencing dickkopf-3 gene
No full textParallel infection of Japanese encephalitis virus and Wolbachia within the cells of mosquito salivary glands
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Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Variations on the Author
Full text link“Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship
Appropriate Similarity Measures for Author Cocitation Analysis
Full text linkWe provide a number of new insights into the methodological discussion about author cocitation analysis. We first argue that the use of the Pearson correlation for measuring the similarity between authors’ cocitation profiles is not very satisfactory. We then discuss what kind of similarity measures may be used as an alternative to the Pearson correlation. We consider three similarity measures in particular. One is the well-known cosine. The other two similarity measures have not been used before in the bibliometric literature. Finally, we show by means of an example that our findings have a high practical relevance.information science;Pearson correlation;cosine;similarity measure;author cocitation analysis
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