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應用液相層析質譜儀為主的代謝體學研究方式於葡萄糖六磷酸去氫酶缺乏紅血球的氧化還原訊息及基安-巴瑞症候群的臨床診斷

為了解決S11 JG 推薦的問題，作者唐湘瑜 這樣論述：

指導教授推薦書論文口試委員審定書致謝……………………………………………………………………iii中文摘要………………………………………………………………ivAbstract……………………………………………………………viTable of content………………………………………………viiiList of tables…………………………………………………xList of figures…………………………………………………xiList of Abbreviations………………………………………xivChapter 1 General introduction ..........

...1Metabolomics background .....................1Glucose-6-phosphate dehydrogenase deficiency in red blood cells....4Demyelinating diseases …………6Dissertation Overview.........7Chapter 2 Futile metabolic struggle of glucose 6-phosphate dehydrogenase-deficient red blood cells upon oxidant challenge.

.......8Introduction..........8Materials and methods........11Results..............18Discussion...........28Chapter 3 Alterations of plasma levels of metabolic profiles are associated with Guillain-Barre syndrome..........37Introduction............37Materials and methods..........42Results.........

...................51Discussion........................ 56Chapter 4 Overall discussion and conclusion......63References..........66Tables...............88Figures..............100Appendix.............128List of tablesTable 1. List of identified compounds in RBC metabolic profile…….…88Table 2. Spearm

an rank correlation matrix between metabolites and RBC elongation index that were significant (p < 0.05). ...................... 90Table 3. Basal demographics of GBS patients, MSc patients and controls ..................................................................................................

.. 91Table 4. Levels of plasma antioxidant, MDA, and MPO in GBS andcontrol group............................................................................... 92Table 5. Association with γ- tocopherol and δ-tocopherol by Pearson rank correlation coefficient (n = 22) ................................

................... 93Table 6. List of amino acids or amines that were significantly changedbetween GBS and control group ................................................. 94Table 7. List of acylcarnitines that were significantly changed betweenGBS and control group .................................

.............................. 95Table 8. List of lysophosphatidylcholines that were significantly changed between GBS and control group ................................................. 96Table 9. List of phosphatidylcholines that were significantly changedbetween GBS and control group ............

..................................... 97Table 10. List of sphingomyelins that were significantly changed betweenGBS and control group…………………..…………….…..…..99List of figuresFigure 1. The applications of metabolomics and the number ofpublications indexed related to metabolomics…….………….100Figure 2. Meta

bolomics workflow for targeted and untargetedanalysis……………………………………………….……….101Figure 3. G6PD activity and PCR-RFLP assay for the G6PD variant. .. 102Figure 4. Enhanced susceptibility of G6PD-deficient RBCs toDIA-induced oxidative damage.. .............................................. 103Figure 5.

Osmotic deformability profile of RBCs under variousincubation conditions .............................................................. 104Figure 6. Base peak chromatograms (BPC) from extracts of control RBCsand G6PD deficient RBCs with or without diamide treatment ..................................

............................................................... .105Figure 7. Changes in metabolome of G6PD-deficient and control RBCsupon DIA challenge. ................................................................. 106Figure 8. Differential effect of DIA on GSH metabolic pathways innormal and G

6PD-deficient RBCs. . ........................................ 107Figure 9. Association between the glutamine/glutamate ratio and theelongation index in G6PD deficient RBCs upon DIAchallenge……………………………………………..……….108Figure 10. Differential effect of DIA on purine metabolic pathways innormal and G6PD

-deficient RBCs. ......................................... .109Figure 11. Effect of ATP in RBC deformability.. ................................... 110Figure 12. Measurement of glycolytic and pentose phosphate pathwaymetabolites in RBCs upon DIA treatment.. .............................. 111Figure 13

. Activation of AMPK in DIA-treated G6PD-deficient RBCs.. .................................................................................................. 112Figure 14. Effect of AMPK inhibitor in deformability of diamide-treatedRBCs.. ..............................................................

......................... 113Figure 15. Inactivation of pyruvate kinase in DIA-treated G6PD-deficientRBCs.. ....................................................................................... 114Figure 16. A schematic diagram illustrating how DIA differentially affectsmetabolism in normal and G6

PD-deficient RBCs.. ................. 115Figure 17. Changes in global metabolome of GBS and control group.. 117Figure 18. Flow chart of data statistics in untargeted metabolic profile. 118Figure 19. Significantly different metabolites of lipids between GBS andcontrol.. ..............................

....................................................... 119Figure 20. Significantly different metabolites between GBS and control .. .................................................................................................. 120Figure 21. Targeted metabolomics profiles in GBS, control, and MS

cgroups.. ..................................................................................... 121Figure 22. Significantly lower levels of amino acids (or amines) in GBScompared to control and MSc group. ....................................... 122Figure 23. Significantly lower levels of acylcarniti

nes in GBS comparedto control and MSc group.... ..................................................... 123Figure 24. Significantly lower levels of lysophosphatidylcholines in GBScompared to control and MSc group .. ..................................... 124Figure 25. Significantly lower levels of sphi

ngomyelins in GBS comparedto control and MSc group... ...................................................... 125Figure 26. Lower levels of steroids in GBS compared with control group.. .............................................................................126Figure 27. Significantly lower leve

ls of lipophilic metabolites in GBS... .............................................................................. 127