preserves中文的問題，透過圖書和論文來找解法和答案更準確安心。 我們找到下列問答集和資訊懶人包

讓世界看見臺灣

為了解決preserves中文的問題，作者莊博欽CharlesChuang,余慈雅JulieYu 這樣論述：

　　全球新肺炎流行肆虐，台灣成功防疫成為全世界最安全的地方！   　　台灣防疫的成功實力能夠幫助世界各國，除了介紹台灣醫療環境的健保制度，如何守護全民健康的觀念，得以成功防疫新冠肺炎之外，同時更介紹台灣的科技、傳統文化、人文藝術、美食、觀光的豐富資源……歡迎世界各國人士將台灣列入觀光旅遊的選擇之地，讓全世界能夠真正的看見台灣。   　　在文化語言的交流與學習上，推動全球華文學習繁體漢字才是正統，唯有台灣才是繁體中文的世界教育中心，本書以中、英文對照的內容撰述，將文字的翻譯融入其中，亦是一種中、英文學習溝通的最佳教材與工具。   　　As the new coro

navirus (COVID-19) rages the world, Taiwan has become the safest place in the world due to its success in epidemic prevention!   　　Taiwan's success in epidemic prevention proves it has the ability to help countries around the world, and Taiwan Can Help!  This book introduces Taiwan's medical env

ironment, the National Health Insurance System and the measures taken to protect the health of the people, which are all key elements that helped in the fight of the new coronavirus (COVID-19) prevention. At the same time, the introduction of the technology, traditional culture, humanities and arts,

food, and the rich resources in tourism in Taiwan are included, welcoming people from all over the world to visit and see the real Taiwan.    　　In terms of cultural and language exchange and learning, it is orthodox to promote the learning of traditional Chinese characters, and Taiwan is the so

le world education center for traditional Chinese. This book is written in both Chinese and English, and by integrating the translation of the text into the book, it is one of the best teaching materials and tools for Chinese and English learning and communication.

preserves中文進入發燒排行的影片

探討在神經退化性疾病中調控核醣核酸結合蛋白MBNL2表現之機轉

為了解決preserves中文的問題，作者王李馨 這樣論述：

中文摘要 iAbstract iiContents iiiIntroduction 1Myotonic dystrophy type 1 (DM1) 1Cerebral involvement of adult-onset DM1 2Genetic basis of DM1 4Molecular mechanism in DM1 4Mouse models of DM1 with expression of CUG repeats 6RNA-binding protein: Muscleblind-like (MBNL) family

8MBNL1 and MBNL2 knockout mice 9Calcium-dependent cysteine protease: Calpain 11Calpain-1 and -2 11Calpain-1 and -2 deficient mice 12Calpain-1 and -2 in neurodegeneration 13Alzheimer’s disease (AD) 14Disease stages of AD 14Clinical presentations of AD 15Brain atrophy of AD

15Two pathological hallmarks of AD 16The aims of the study 20Materials and methods 211. Animals 212. Primary hippocampal neuron culture, drug treatment, virus infection and transfection 213. Cell culture and transient transfection 234. Total protein extraction and sub

cellular fractionation 245. Immunoprecipitation (IP) 256. Immunoblotting analysis 257. RNA preparation, RT-PCR and splicing analysis 268. Immunofluorescence staining and immunohistochemistry 279. Quantification of fluorescent images of brain sections 2910. Quantif

ication of fluorescent images of neurons 3011. Antibodies 3012. Plasmids 3113. Statistical analysis 31Results 331. Characterize the role of MBNL2 in neuronal maturation1.1. MBNL2 is expressed postnatally and increased as neuronal maturation 331.2. MBNL2 expression

is required for promoting adult pattern of RNA processingand neuronal differentiation 342. Determine how neurodegenerative conditions reduce MBNL2 expression2.1. Glutamate-induced excitotoxicity reduces MBNL2 protein expression viaNMDAR activation 352.2. NMDAR-mediated Calpain-2 acti

vation causes MBNL2 protein degradation 362.3. Calcium-dependent nuclear translocation of CAPN2 is associated with reducedMBNL2 expression 382.4. Dysregulated calcium homeostasis reduces MBNL2 expression 392.5. Enhanced nuclear translocation of CAPN2 occurs in the EpA960/CamKII-Cre

brain 402.6. Enhanced nuclear translocation of CAPN2 in neurodegeneration recapitulates thefetal developmental pattern 413. Explore the possibility of the reduced MBNL2 expression associated re-induced fetalpattern of RNA processing as a common feature among neurodegenerative disorders3.

1. Enhanced nuclear translocation of CAPN2, reduced MBNL2 expression and associated aberrant MBNL2-regulated alternative splicing in the degenerative brains of AD 41Discussion 44Perspective 48References 49List of figuresFigure 1. MBNL2 is expressed postnatally and increased with bra

in maturation 64Figure 2. MBNL2 is expressed in the more differentiated cells during hippocampusmaturation 65Figure 3. MBNL2 is expressed ubiquitously in the adult mouse brain 66Figure 4. MBNL2 is expressed in the neurons, oligodendrocytes and astrocytes 67Figure 5. The knockdown

efficiency of MBNL2 shRNAs in cultured neurons 68Figure 6. The alternative splicing and polyadenylation of MBNL2 targets show a fetal to adult transition during neuronal differentiation 70Figure 7. MBNL2 depletion disrupts the developmental RNA processing transition in cultured neurons

71Figure 8. MBNL2 depletion impairs dendrite maturation in cultured neurons 72Figure 9. Glutamate treatment induces excitotoxicity in mature cultured neurons showing condensed nucleus 74Figure 10. Glutamate-induced excitotoxicity reduces MBNL2 protein level in mature cultured neurons 75

Figure 11. Glutamate reduces MBNL2 level via NMDAR activation in cultured neurons 77Figure 12. NMDAR-mediated MBNL2 reduction is calcium dependent 78Figure 13. The alternative splicing and polyadenylation of MBNL2 targets are disrupted in neurons treated with glutamate or NMDA 79Figure 14.

MBNL2 mRNA level is unchanged in cultured neurons treated with glutamate or NMDA 81Figure 15. MBNL2 protein is stable in the neurons 82Figure 16. NMDAR signaling-mediated MBNL2 reduction requires calpain activity incultured neurons 83Figure 17. Protein expression of CAPN1 and CAPN2 are alte

red in NMDA-treatedneurons 84Figure 18. MBNL2 binds to both CAPN1 and CAPN22 in HEK293 cells 85Figure 19. Knockdown efficiency of CAPN1 or CAPN2 shRNAs in neurons 86Figure 20. NMDAR-mediated calpain-2 activation causes MBNL2 degradation inneurons 87Figure 21. Depletion of CAPN2 preserves

MBNL2-regulated alternative splicing andpolyadenylation in neurons upon NMDA treatment 88Figure 22. CAPN2 is predominantly expressed in the cytoplasm of mature neurons 90Figure 23. NMDA treatment induces the nuclear translocation of CAPN2 in neurons 91Figure 24. NMDAR-mediated MBNL2 reduct

ion requires calpain-2 expression in thenucleus and cytoplasm of neurons 92Figure 25. NMDA-induced nuclear translocation of CAPN2 requires calcium 93Figure 26. Nuclear translocation of CAPN2 involves in MBNL2 degradation 94Figure 27. Dysregulated calcium homeostasis induces the nuclear tran

slocation of CAPN2 and reduced MBNL2 expression in neurons 95Figure 28. CAPN2 depletion preserves MBNL2 expression in the neurons with dysregulated calcium homeostasis 96Figure 29. Effect of CAPN2 depletion on the RNA processing pattern of MBNL2 targets in A23187-treated neurons 97Figure 30

. CAPN2 nuclear translocation is occurred in the EpA960/CaMKII-Cre mouse brains 98Figure 31. Nuclear-to-cytoplasmic distribution of CAPN2 during neuronal differentiation 99Figure 32. Nuclear translocation of CAPN2 occurs in the APP/PS1 and THY-Tau22brains 100Figure 33. Reduced MBNL2 express

ion in the APP/PS1 and THY-Tau22 brains 101Figure 34. Aberrant MBNL2-regulated alternative splicing in the APP/PS1 and THY-Tau22 brains 102

The Divine Comedy: Inferno

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為了解決preserves中文的問題，作者Dante Alighieri/ Musa, Mark 這樣論述：

　　義大利最偉大的詩人但丁與莎士比亞、哥德並稱西歐文學史上的三個世界級天才。艾略特讚譽但丁《神曲》只有莎士比亞全部劇作堪與比擬。香港嶺南大學翻譯系主任黃國彬耗二十餘年完成三韻體《神曲》中文全譯本及詳盡注釋，並收錄多雷插畫136幅，及地獄、煉獄、天堂結構圖等，共計146幅圖。文圖並茂，印刷裝訂精美。 　　但丁歷時十餘年完成《神曲》，長達一萬四千二百三十三行的古典長詩，全書分為《地獄篇》、《煉獄篇》、《天堂篇》三部分，主要故事為：但丁在黑林裡迷路，危急時獲維吉爾之助，跟隨他穿過地獄和煉獄，後來獲貝緹麗彩親自領導遊歷天堂，最後得見上帝一面。是魔幻、新奇、恐怖、驚險、智慧的奇境之旅。 　　神曲——

地獄篇 　　旅人但丁在黑林裡迷路，因聖母瑪利亞、拉結、貝緹麗彩之助而獲古羅馬詩人維吉爾搭救，隨維吉爾進入地獄，目睹各種受刑的陰魂，包括背判上帝的撒旦。 　　*本書中譯本由九歌出版 　　An acclaimed translation of Dante Alighieri's The Divine Comedy Volume 1: Inferno that retains all the style, power and meaning of the original, this Penguin Classics edition is translated from the Italian

with an introduction by Mark Musa. 　　This vigorous translation of Inferno preserves Dante's simple, natural style, and captures the swift movement of the original Italian verse. Mark Musa's blank verse rendition of the poet's journey through the circles of hell recreates for the modern reader the

rich meanings that Dante's poem had for his contemporaries. Musa's introduction and commentaries on each of the cantos brilliantly illuminate the text. 　　Dante Alighieri (1265-1321), scion of a Florentine family, mastered in the art of lyric poetry at an early age. His first major work is La Vita N

uova (1292) an exercise in sonnet form constructed as a tribute to Beatrice Portinari, the great love of his life. It is believed that The Divine Comedy - comprised of three canticles, Inferno, Purgatorio, and Paradiso - was written between 1308 and 1320. 　　If you enjoyed the Inferno you might like

Giovanni Boccaccio's Decameron, also available in Penguin Classics. 　　'Musa operates on the principle that a translator's first duty is to render the original text as exactly as possible without compromising the literary quality of the work ... [This is] the best English-language version of the In

ferno currently available' 作者簡介 但丁．阿利格耶里（Dante Alighieri） 　　1265年5月底在翡冷翠（Firenze）出生，為 長子。1277年娶傑瑪．迪馬涅托．多納提（Gemma di Manetto Donati），生二子、一女。但丁流放後，一直想重返翡冷翠，卻沒有成功，這個遭遇對他打擊很大，深夜在作品中深夜描寫流放之苦。1321年9月在拉溫 納（Ravenna）去世。但丁是義大利偉大的詩人、文學家，他和莎士比亞、塞萬提斯、歌德、托爾斯泰都屬於世界級的一流文學大師。但丁作品有：《新生》 (Vita Nuova)、《詩歌集》(Rime)、

《筵席》(Convivio)、《俗語論》(De vulgari eloquentia)、《帝制論》(Monarchia)、《書信集》(Epistole)、《牧歌集》(Egloghe)、《水土探究》 (Questio de aqua et terra)、《神曲》(La Divina Commedia)。《神曲》分三篇：《地獄篇》(Inferno)、《煉獄篇》(Purgatorio)、《天堂篇》(Paradiso)。 　 　Dante Alighieri was born in Florence in 1265 and belonged to a noble but impoverished f

amily. His life was divided by political duties and poetry, the most of famous of which was inspired by his meeting with Bice Portinari, whom he called Beatrice,including La Vita Nuova and The Divine Comedy. He died in Ravenna in 1321. 　　Mark Musa is Distinguished Professor of French and Italian at

the Center for Italian Studies, Indiana University.

解析下視丘投射至海馬回突觸中共同傳遞麩胺酸及-氨基丁酸的功能意義

為了解決preserves中文的問題，作者伊木夏 這樣論述：

中文摘要海馬回為負責認知及情緒功能的關鍵腦區。齒狀回為海馬回次核區中的第一個訊號處理器其會接受來自大腦皮質及皮質下核區傳來的訊號。其中，大腦皮質至海馬回路徑會在記憶獲得及提取時傳遞記憶相關的訊息；然而，來自皮質下的訊號參與了調控皮質及海馬回間的訊息溝通。下視丘乳頭上核藉由共同釋放兩種截然不同的快速神經傳遞物質，也就是麩胺酸及-氨基丁酸，來實質上的支配齒狀回活性，因而能協助空間定位及空間記憶的形成。然而乳頭上核中神經元是藉由何種突觸機制來調控齒狀回活性及其突觸可塑性尚未被釐清。齒狀回由興奮性的顆粒細胞及抑制性的中間神經元所組成。在這本論文中，我用光遺傳學、電生理及藥理學的方法，證明來自乳頭上

核的訊號會透過不同的突觸機制差異性地調控齒狀回中不同種細胞的活性。選擇性活化乳頭上核會在所有的突觸後神經元產生突觸興奮及突觸抑制作用，然而這兩種作用的比例是會依突觸後細胞種類的不同而改變的。具體來說，樹突抑制型中間神經元主要接收突觸興奮作用，然而體抑制型中間神經元及顆粒細胞則主要接收突觸抑制訊號。雖然單獨活化乳頭上核並不足以興奮顆粒細胞，但是在有興奮性驅動力的情況下，活化乳頭上核可使顆粒細胞產生動作電位的時間更精準並縮短其產生動作電位所需的時間。此外，在有皮質訊號輸入時活化乳頭上核會增加顆粒細胞動作電位的產生，進而促使皮質到顆粒細胞突觸間的長期增強作用。總結來說，這些發現顯示了乳頭上核共同傳遞

的麩胺酸及-氨基丁酸對於維持齒狀回中興奮/抑制的動態平衡是有貢獻的，並且能透過提升皮質到顆粒細胞突觸間的長期增強作用來幫助記憶的編碼。