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單一醫學中心之心臟移植免疫用藥與併發症研究

為了解決sl63 amg價格的問題，作者林宜璋 這樣論述：

本論文內容分成三個部分。第一部分為進行我國器官移植患者使用抗排斥藥的健保醫療費用之分析；第二部分是心臟移植術後之乳酸中毒併發症研究；第三部分為不同器官保存液對心臟移植後心肌保護之影響。第一部分研究：我們收集在 2011 年間台灣健保資料庫醫療服務數據，其中包含 377 名心臟、1,693 名腎臟及 1,412 名肝臟移植患者，以評估其醫療保健服務的利用率。經過為期一年的追蹤，結果顯示使用tacrolimus患者與使用cyclosporine的接受移植患者相比較，其全年門診次數（40.7 vs. 38.6），門診費用（10,383 vs. 8,155 美元）及總費用（12,516 vs. 10

,372 美元）皆顯著增加。此外，接受tacrolimus治療的心臟移植患者之住院費用較cyclosporine的患者高1.7倍。第二部分研究：因高乳酸血症可能在心臟手術後早期發生，且與其預後相關。我們回溯性地檢視與分析自2006–2013年間，來自單一個醫學中心的心臟移植醫療病歷紀錄，分析發現58名連續性的心臟移植接受者中，有12名患者於進入加護病房後，其血中乳酸濃度皆高於可偵測高值（> 15 mmol/L），高峰時間為術後1.9 ± 2.0小時，全手術期的最高乳酸值為3.1 mmol/L，而多數患者（11/12）的術後乳酸值，在術後27.5 ± 12.8小時回到 < 4 mmol/L，並顯

示10名患者的拔管時間有延後趨勢（P < .01）。患者血糖濃度顯著地由術前的 148.9 ± 45.2 mg/dL，升至乳酸濃度高峰時為 375.7 ± 96.9 mg/dL（P < .01）。第三部分研究：本研究目的是比較使用一次劑量 Bretschneider's histidine–tryptophan–ketoglutarate（HTK）溶液和使用重複劑量冷血停搏液（cold blood cardioplegia，CBC）保存捐贈者心臟時，心肌細胞保護作用的功效。我們納入 67 名於 2002–2012 年間，在單一個醫學中心接受心臟移植的患者資料。回溯性統計學結果顯示使用HTK與C

BC兩組之間的心臟移植術後的心臟酵素、血液動力學數據、加護病房住院天數及 30 天內死亡率，均無顯著差異性。然而，HTK 組的體外循環使用時間顯示有較短的傾向（P = .091），且HTK組的術後強心指數較高（P < .001），體外循環使用時間也較短（P = .02）。本研究主要結論為：(1) 使用tacrolimus作為免疫抑制療法的接受移植患者在所有醫療保健服務中的醫療費用支出均顯著高於使用cyclosporine治療的接受移植患者；(2) 嚴重乳酸血症經常在心臟移植手術後早期發生，且多數在 30 小時內恢復；但造成術後拔管時間延後；(3) 一次劑量的HTK溶液能夠有效地降低體外循環使用

時間，用以保存捐贈者心臟，而其與重複劑量的CBC溶液相較，具有同等的心肌細胞保護作用。

Identification of active agents inducing ossification and novel biomarkers associated with osteoporosis

為了解決sl63 amg價格的問題，作者Zuha Imtiyaz 這樣論述：

TABLE OF CONTENTSABSTRACT ixLIST OF ABBREVIATIONS xi1. INTRODUCTION 11.1 Bone and bone remodeling 11.2 Osteoporosis 61.2.1 Disease epidemiology 71.2.2 Current drugs used for osteoporosis and their mode of action 91.3 Biomarkers of bone formation 121.3.1 SNPs as biomarkers 161.4 Relation of

FTCDNL1 gene with osteoporosis 191.5 Herbs with medicinal value for bone formation 20RATIONALE 25AIM 262. MATERIALS AND METHODS 272.1 Reagents and chemicals used 272.2 Extraction and isolation 292.2.1 Turpinia formosana Nakai. 292.2.2 Euonymus spraguei Hayata. 292.3 Cell culture 302.3.1 H

uman osteoblast (HOb) cells 302.3.2 Human osteosarcoma (MG-63) cells 302.3.3 Cell culture of RAW 264.7 cells and differentiated osteoclasts 312.4 MTT assay for cell viability assay 312.5 ALP activity assay 312.6 Mineralization assay 322.7 RNA isolation and reverse transcription 322.8 Real-tim

e quantitative PCR analysis 332.9 Estrogen receptor expression assay 352.10 Plasmid DNA purification 352.11 DNA transfection 362.12 siRNA transfection 362.13 Western blot 372.14 Immunofluorescence 372.15 Statistical Analysis 383. RESULTS 393.1 Elucidating osteogenic potential of compounds i

solated from Turpinia formosana Nakai 393.1.1 Isolated compounds from Turpinia formosana 393.1.2. Cytotoxicity of compounds isolated from T. formosana in HOb cells 413.1.3 Effect of isolated compounds on ALP activity in HOb cells 433.1.4 Effect of isolated compounds on mineralization in HOb cell

s 453.1.5 Effect of isolated compounds on estrogen receptor expression in HOb cells 473.1.6 Effect of isolated compounds on the genetic markers of bone formation in HOb cells 493.2. Isolated compounds from Euonymus spraguei mediate of osteogenesis through multiple pathways 523.2.1 Effect of vari

ous extractants for E. spraguei on cell viability, ALP activity and mineralization in HOb cells 523.2.2 Compounds isolated from ES 563.2.3 Effect of syringin (8) and (-)-epicatechin (9) on the viability of HOb cells 573.2.4 Effect of syrngin (8) and (-)-epicatechin (9) on ALP activity in HOb cell

s 583.2.5 Effect of syrngin (8) and (-)-epicatechin (9) on mineralization in HOb cells 603.2.6 Effect of syrngin (8) and (-)-epicatechin (9) on Estrogen receptor (ER) expression 623.2.7 Effect of syringin (8) and (-)-epicatechin (9) on the mRNA expression levels of bone remodelling-related genes

633.2.8 Effect of syringin (8) and (-)-epicatechin (9) on BMP-2 pathway 663.2.9 Effect of syringin (8) and (-)-epicatechin (9) on RANKL/OPG 693.2.10 Effect of syringin (8) and (-)-epicatechin (9) on autophagy 713.2.11 Effect of syringin (8) and (-)-epicatechin (9) on OPN expression 733.2.12 Eff

ect of syringin (8) and (-)-epicatechin (9) on the viability of RANKL-induced osteoclasts 753.3. Elucidating the association between FTCDNL1 on bone formation and its role in osteoporosis onset 773.3.1 Transfection of FTCDNL1 into MG-63 cells 773.3.2 Effect of FCTDNL1 overexpression on bone forma

tion-related genes 793.3.3 Effect of FTCDNL1 knockdown on cell viability of MG63 cells 833.3.4 Effect of FTCDNL1 knockdown on ALP activity in MG63 cells 844. DISCUSSION 854.1. Elucidating osteogenic potential of compounds isolated from Turpinia formosana 874.2 Isolated compounds from Euonymus

spraguei mediate of osteogenesis through multiple pathways 904.3. Elucidating the association between FTCDNL1 on bone formation and its role in osteoporosis onset 945. CONCLUSION 96LIST OF PUBLICATIONS 97BIBLIOGRAPHY 98 LIST OF FIGURESFig 1. Types of cells found within the bone tissue 1Fig 2.

Interplay between osteoblasts and osteoclasts 3Fig 3. Involvement of various cells at different stages of bone remodelling 4Fig 4. Static and dynamic changes in bone 7Fig 5. Growth rate of osteoporosis, estimated number of osteoporotic fracture worldwide by 2050 9Fig 6. Mechanism of action of th

e current drugs for osteoporosis. 11Fig 7. Role of various biomarkers at various stages of bone formation 14Fig 8. Signalling cascade of BMP-2 pathway. 16Fig 9. Display of the importance of a SNP and its significance in the phenotype 17Fig 10. Pictorial representation of aim of the study. 26Fig

11. Structures of the isolated compounds elucidated using various spectroscopic techniques. 40Fig 12. Cytotoxic effect of compounds isolated from T.formosna. 41Fig 13. Induction of ALP activity by 1, 2, 3 and 6. 43Fig 14. Mineral deposition by 1, 2, 3 and 6. 46Fig 15. Expression of ERs affected

by 1, 2, 3, and 6. 48Fig 16. 1 elevates mRNA expression of bone formation-related genes. 50Fig 17. Pictorial summary of underlying mechanism for osteogenesis by 1. 51Fig 18. Solvent test for extraction of E. spraguei (ES). 54Fig 19. Structure of compounds isolated from ES. 56Fig 20. Cell viabi

lity of HOb cells on 8 and 9 treatments. 57Fig 21. Induction of ALP activity by 8 and 9. 58Fig 22. Mineral deposition by 8 and 9.. 61Fig 23. Influence of 8 and 9 on ER expression. 62Fig 24. Expression of bone formation-related genes after 8 and 9 treatments.. 65Fig 25. 8 and 9 mediates their ef

fect via BMP-2 signalling pathway. 67Fig 26. Attenuation of RANKL/OPG ratio by 8 and 9. 69Fig 27. Modulation of autophagy by 8 and 9. 72Fig 28. Induction of OPN by 8 and 9. 74Fig 29. Cytotoxic effect of 8 and 9 on osteoclasts. 75Fig 30. Pictorial summary of osteogenesis induced by 8 and 9. 76F

ig 31. Transient transfection of FCTDNL1 in MG63 cells. 78Fig 32. mRNA expression levels of bone formation related biomarkers after FTCDNL1 overexpression. 81Fig 33. FTCDNL1 knockdown does not affect viability of MG63 cells. 83Fig 34. ALP activity of MG63 cells after FTCDNL1 knockdown. 84Fig 35.

Mechanism of 8 and 9 in RANK-RANKL interaction 92Fig 36. Role of autophagy in bone formation. 93Fig 37. Pictorial representation of osteogenesis with FTCDNL1 and future prospects. 95LIST OF TABLESTable 1. Primer and probe combination used for real-time PCR 34Table 2. Primer sequences used for r

eal-time PCR 35Table 3. Sequences of siRNA used for FTCDNL1 knockdown 37Table 4. Phytochemical as therapeutic agents and their plant source 85