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How tall how high di的問題，我們搜遍了碩博士論文和台灣出版的書籍，推薦Dacy, Matthew D.,Fallon, Jackie寫的 Taking Flight: The Peregrine Falcons of Mayo Clinic: A Coloring + Activity Book / Celebrating the World’’s Fastest Animal 和Long, Ethan的 Horse & Buggy Plant a Seed都 可以從中找到所需的評價。
這兩本書分別來自 和所出版 。
國立臺北科技大學 環境工程與管理研究所 胡憲倫所指導 許素雅的 整合設計策略和工具以實現ICT和電子產品的永續生產與消費： 學術與工業界的實施 （2021），提出How tall how high di關鍵因素是什麼，來自於永續設計、生命週期思考、工業設計、永續生產與消費、系統創新、ICT和電子產業。
而第二篇論文臺北醫學大學 新藥研發產業博士學位學程 黃偉展、許凱程所指導 曾惠如的 開發小分子藥物用於治療中樞神經系統疾病 （2020），提出因為有 中樞神經系統疾病、阿滋海默氏症、神經膠質母細胞瘤、多發性硬化症的重點而找出了 How tall how high di的解答。
Taking Flight: The Peregrine Falcons of Mayo Clinic: A Coloring + Activity Book / Celebrating the World’’s Fastest Animal
為了解決How tall how high di 的問題，作者Dacy, Matthew D.,Fallon, Jackie 這樣論述：
Your creativity will soar through coloring and other activities as you discover how the peregrine falcon is a force of nature -- and healing -- at Mayo Clinic.Since 1987, a nest box atop the tall buildings at Mayo Clinic in Rochester, Minnesota, has been home to generations of peregrine falcons.
Established to help save the endangered species, the Mayo Clinic Peregrine Falcon Program allows patients, staff and falcon fans around the world to watch -- in person or online -- as the falcons raise their young. Through these majestic creatures, we see that nature can be a vital part of the heali
ng process and a reminder of the wonder of daily life. Wildlife lovers of all ages can meet the falcons and learn about the earth’s fastest animal through fun activities and surprising facts. Inspiring stories, original illustrations, color photographs and a stunning four-color centerfold depicting
a chick’s development also bring the peregrines of Mayo Clinic to life. Printed on high quality paper ready to enhance with crayons, pencils, markers, or watercolors, each coloring page is perforated for easy removal and display. Taking Flight: The Peregrine Falcons of Mayo Clinic is more than a co
loring book -- it’s a tribute to the resilience of the birds who inspired it.
整合設計策略和工具以實現ICT和電子產品的永續生產與消費： 學術與工業界的實施
為了解決How tall how high di 的問題，作者許素雅 這樣論述：
今日全球許多公司已有永續發展產品的意識。永續消費與生產強調盡可能減少自然資源消耗、有毒材料的使用、排放廢物和污染物，延續服務與產品的生命週期。由於設計師掌握大部分產品成本與生命週期，因此設計納入永續性致關重要。過去幾十年，生命週期思維和循環經濟設計為商業組織、工業部門廣泛使用的設計策略，此外，學著也提出許多永續性設計的策略和工具，但卻缺少被產品設計師和開發人員實踐與應用。本研究目的包括（1）了解目前永續產品設計開發所應用的設計策略、挑戰、機會，（2）提出循環經濟對於永續產品服務和商業模式，（3）將創新技術整合產品服務設計，增進社會永續性。 本研究為應用混合方法，包括行動研究、系統文獻回顧、設
計思維研究和專家訪談，訪談學術界和工業界開發 ICT 和電子產品及相關服務的設計的專家。本研究共分為四個階段，第一階段為透過觀察泰國的永續設計課程，了解目前應用生命週期思維來設計家用電器和消費性電子產品所面臨的挑戰和機遇； 第二階段為探討台灣 ICT 電子產業如何透過永續設計擴大公司業務。；第三階段透過學術性文獻與灰色文獻系統性的回顧，從全球ICT電子產業中四種實施場景，彙整出11 項循環設計要素；第四階段為提出如何透過多樣化的設計思考工具來實踐嶄新且永續的商業模式與服務設計，藉此解決台灣高齡化社會問題。本論文包含七種永續設計方法與四階段的研究。 研究結果顯示，社會永續性設計仍然被多數ICT
電子產業忽視， 因此本研究認為，永續設計的策略與工具應納入社會科技系統中，其中包括社會創新，運用金字塔底部設計、整體仿生學和過渡設計，此獨特的設計方法將可提供學界與產業界專業人士使用。此外，本研究認為學術界和工業界需要緊密合作來實踐永續的系統創新。
Horse & Buggy Plant a Seed
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為了解決How tall how high di 的問題，作者Long, Ethan 這樣論述：
How long does it take for a seed to grow? Horse and Buggy can't wait to find out in this hilarious story about waiting from Geisel medalist Ethan Long.Is it ready yet? What about now? Horse is so excited for the seed he planted to grow, he can't help asking Buggy a million questions. But with a litt
le sunshine, water, and patience, Horse and Buggy are in for a surprise when their tiny seed grows into. . .a gigantic watermelon Ethan Long delivers a perfect punchline for emergent readers in this latest Horse & Buggy. An I Like to Read(R) book. The award-winning I Like to Read(R) series focuses
on guided reading levels A through G, based upon Fountas and Pinnell standards. Acclaimed author-illustrators--including winners of Caldecott, Theodor Seuss Geisel, and Coretta Scott King honors--create original, high quality illustrations that support comprehension of simple text and are fun for ki
ds to read with parents, teachers, or on their own Ethan Long is an artist and animator who has written and illustrated dozens of children’s books. His accolades include a Theodor Seuss Geisel Medal for Up, Tall, and High! and a daytime Emmy nomination for Tasty Time with Ze Frank.
開發小分子藥物用於治療中樞神經系統疾病
為了解決How tall how high di 的問題，作者曾惠如 這樣論述：
Table of Contents摘要 1Abstract 2I Protein disulfide isomerase-4 inhibitors against glioblastoma: design, synthesis and biological evaluation 3A. Introduction 41. Introduction of glioblastoma 42. Introduction of protein disulfide isomerase 83. Relationship between PDI and cancer 144. Res
earch object and design 16B. Result and Discussion 201. Chemistry 202. Biological evaluation and docking analysis 25C. Conclusion 34II Acridine-based histone deacetylase inhibitors as multitarget agents against Alzheimer’s disease: synthesis and biological evaluation 35A. Introduction 3
61. Introduction of Alzheimer’s disease 362. Current therapeutic options and benefit of multitarget agents 383. Introduction of histone deacetylase 394. Relationship between HDAC and AD 415. Introduction of beta amyloid and its relationship with AD 436. Introduction of acetylcholinesteras
e and its relationship with AD 467. Research purpose and design 48B. Result and Discussion 501. Chemistry 502. Biological evaluation and docking analysis 53C. Conclusion 72III Sobrerol derivatives against autoimmune neurologic disease: synthesis and biological evaluation 73A. Introduct
ion 741. Introduction of multiple sclerosis 742. Current therapeutic options and unmet medical need 773. Introduction of interleukin-6 804. Relationship between interleukin-6 and multiple sclerosis 835. Research purpose and design 85B. Result and Discussion 861. Chemistry 862. Biolog
ical evaluation 87C. Conclusion 91Experimental Section 92I. Machine and material 921. General machines and methods: 922. Materials and solvents purchased from: 923. Purification and dehydration of solvent: 95II. Chemistry synthetic routes and physical properties 96A. Protein disulfide
isomerase-4 inhibitors against glioblastoma: design, synthesis and biological evaluation 96B. Acridine-based histone deacetylase inhibitors as multitarget agents against Alzheimer’s disease: synthesis and biological evaluation 128C. Sobrerol derivatives against autoimmune neurologic disease: sy
nthesis and biological evaluation 137III. Method of biological assay 146A. Protein disulfide isomerase-4 inhibitors against glioblastoma: design, synthesis and biological evaluation 146B. Acridine-based histone deacetylase inhibitors as multitarget agents against Alzheimer’s disease: synthesis
and biological evaluation 148C. Sobrerol derivatives against autoimmune neurologic disease: synthesis and biological evaluation 154Reference 155Supplementary Figures 176List of TablesTable 1. The human PDI family. 10Table 2. IC50 value for the inhibition against PDIA4 by compounds 5b-c 25Tab
le 3. IC50 value for the inhibition against PDIA4 by compounds 11a-c 28Table 4. IC50 value for the inhibition against PDIA4 by compounds 23a-v 29Table 5. Cytotoxicity of PDIA4 inhibitors in glioblastoma cell line, U-87 MG 31Table 6. PAMPA-BBB results of compound 23v and reference compounds 32Tab
le 7. Four stages of Alzheimer’s disease as well as related symptoms. 37Table 8. The human HDAC family. Classes, HDACs, subcellular localization, and structures of HDAC isoforms. 40Table 9. IC50 value (μM) of compounds 31a-d against HDACs. 53Table 10. IC50 value (μM) of compounds 36a-h against HD
ACs 55Table 11. Inhibitory activities of compounds 31a, and 36a-h against Aβ1-42 oligomerization 57Table 12. IC50 value (μM) of compounds 31a, and 36a-h against AChE 58Table 13. IC50 value (μM) of compounds 31a, and 36b against HDAC1, -2, and -3. 59Table 14. EC50 value for increasing acetylation
of histone H3 and tubulin by quantification of western blot. 66Table 15. Metabolic stability of compounds 31a, 36b, and testosterone 69Table 16. BBB permeability evaluation of compounds 31a, and 36b using MDR1-MDCK permeability model 70Table 17. Clinical used disease-modifying therapies of MS 7
8Table 18. Classification of immune-related cytokines. 80Table 19. Cytokines and their functions. 82Table 20. IC50 of sobrerol derivatives in inhibiting IL-6 expression. 89List of FiguresFigure 1. WHO 2016 classification of diffuse gliomas 5Figure 2. FDA approved anti-glioma agents in chemothera
py 7Figure 3. Illustration of disulfide bonds formation and redox reactions involving PDI. 8Figure 4. Schematic overview of PDI structure. 9Figure 5. Schematic overview of relationship between ER stress, UPR, and PDI in cancer cell. 15Figure 6. Chemical structure of reported PDI inhibitors. 17F
igure 7. Flowchart of the process for lead-compound identification. 18Figure 8. Design of potent PDIA4 inhibitors. 19Figure 9. Molecular docking and interaction analysis of compounds 5b and 5c.. 27Figure 10. Molecular docking and interaction analysis of compound 23v. 30Figure 11. Anticancer acti
vities of compound 23v in human glioblastoma U-87 MG xenograft mouse model 33Figure 12. FDA approved drugs in treating AD patients. 38Figure 13. Tau incorporate with HDAC6 to form pathological tau beading. 42Figure 14. Molecular mechanisms of Aβ-oligomers synaptotoxicity 43Figure 15. Graphic ill
ustration of amyloid precursor protein (APP) metabolism 44Figure 16. Graphic illustration of biological action of acetylcholine. 47Figure 17. Reported anti-AD agents with acridine-related structures. 48Figure 18. Reported HDAC inhibitor. 49Figure 19. Design of a novel series of multi-target drug
s for AD treatment. 49Figure 20. Illustration of inhibiting assay of Aβ1-42 oligomerization. 56Figure 21. Illustration of inhibiting assay of Aβ1-42 oligomerization. 56Figure 22. Validation of docking protocol 60Figure 23. Docking pose and interaction of compounds 31a and 36b 61Figure 24. Docki
ng pose and interaction of compound 31a in HDAC6 and HDAC7. 62Figure 25. Docking poses and interactions of compounds 31a and 36b 64Figure 26. Western blot analysis of compounds 31a and 36b in murine neuroblastoma N2a cells 65Figure 27. Graphic illustration of cell viability of compounds 31a and 3
6b 66Figure 28. Enhancement of primary rat hippocampal neurite outgrowth by compounds 31a and 36b 67Figure 29. Quantification of lengths and numbers of primary rat hippocampal neurite branching 68Figure 30. Nesting behavior of APP/PS1 mice treated with compounds 31a and 36b 71Figure 31. Cost of
multiple sclerosis and according economic burden 74Figure 32. Graphic illustration of four categories of multiple sclerosis. 76Figure 33. examples of disease-modifying agents of multiple sclerosis. 79Figure 34. Biological function of interleukin-6 in inflammation, immune, and disease 81Figure 35
. Potential roles of IL-6 in autoimmune neurological disease 84Figure 36. Design strategy of IL-6 secretion inhibitors. 85Figure 37. Bar figure illustration of inhibitory activity of sobrerol derivatives against IL-6 expression 87Figure 38. Structure-activity relationship of sobrerol derivatives.
88Figure 39. Bar figure illustration of cytotoxicity of sobrerol derivatives 90List of SchemesScheme 1. Synthetic route of compounds 5a-c. 21Scheme 2. Synthetic route of compounds 11a-c. 22Scheme 3. Synthetic route of compound 19. 23Scheme 4. Synthetic route of compounds 23a-v. 24Scheme 5. Sy
nthetic route of compounds 31a-d. 50Scheme 6. Synthetic route of compounds 36a-h. 52Scheme 7. Synthetic rout of compounds 38a-r. 86Scheme 8. Synthetic rout of compounds 39. 86