Option sweep 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整理懶人包

利用聲化學合成法製備奈米複合材料修飾電極用於呋喃妥因與維生素B2的電化學檢測

為了解決Option sweep 中文的問題，作者洪偉森 這樣論述：

第一部分 本篇利用沉澱法合成釩酸釩奈米顆粒，再利用超聲處理方法摻入GNSs，得到SmVO4-GNSs(SmVG)奈米複合材料，並用於對生物流體樣品中檢測呋喃妥因(NFT)。通過XRD技術與FT-IR進行結構與功能分析，結果顯示所製備SmVO4具有純度。拉曼光譜和FESEM確認GNSs具有SmVO4成分並透過XPS進行鑑定元素的存在。SmVO4-GNSs修飾電極對NFT表現出較低的還原電位以達到最大還原電流響應，Epc= -0.37 V，且應用於實際生物樣品中具良好回收率，靈敏度和檢測下限分別計算出為 0.875 µA mM-1cm-2 和 0.0087 µM，是一種應用於檢測NFT的良

好電極材料。第二部分 本篇使用水熱法合成了Ru@Co(OH)F複合材料，與 GCN 超聲混合以製備奈米複合材料電極改性劑，並應用於電化學測定維生素B2，借助XPS、FTIR進行表徵，結果顯示高結晶性質及出更高的比表面積，有助於改善電化學性能催化劑。由於其優異的電化學性能Ru–Co3P2和GCN之間的活性表面積及其協同作用，具有出色的電化學特性，其中包括了良好的線性範圍為0.062µM至3468.75µM，優秀的奈莫爾檢測限:6 nM和高度靈敏:1.277µAµM‑1 cm‑2等優勢，是作為測定環境中維生素B2含量之良好材料。

先天免疫及日夜節律改變對感覺神經性聽力障礙之影響

為了解決Option sweep 中文的問題，作者楊昭輝 這樣論述：

Table of Contents指導教授推薦書………………………………………………………口試委員會審定書……………………………………………………致 謝……. iii中文摘要… ivAbstract…. viTable of Contents viiiDirectory of Figures xiiiDirectory of Tables xvAbbreviations xviCHAPTER I. INTRODUCTION 11.1 Background 11.1.1 Sensorineural hearing loss (SNHL)

11.1.2 The factors which influence the severity of SNHL 11.1.3 The mechanisms in the cochlea behind SNHL 21.1.4 Innate immunity and Toll-like receptors (TLRs) in the cochlea in response to external stimuli 31.1.5 The impact of innate immunity alteration on SNHL 41.1.6 Circadian clock i

n the cochlea 51.1.7 Circadian regulation in SNHL 71.2 Study aims and hypotheses 81.2.1 Investigation of the TLR signaling in SSNHL 81.2.2 Investigation of the circadian clock in SSNHL 91.2.3 Investigation of the impact of innate immunity activation on aminoglycoside ototoxicity 91

.2.4 Investigation of the impact of circadian clockdysregulation on noise-induced hearing loss 9CHAPTER II. MATERIALS AND METHODS 112.1 Clinical experiments: mRNA expression of TLRs and circadian clock genes in patients with SSNHL 112.1.1 Subjects 112.1.2 Real-time quantitative reverse t

ranscriptase-polymerasechain reaction (qRT-PCR) analysis 122.1.3 Immunocytochemical (ICC) studies 132.1.4 Flow cytometry 132.1.5 Statistical Analysis 142.2 Animal experiments I: activation of cochlear TLR7 and TLR9 signaling pathway during chronic kanamycin treatment 142.2.1 Animals

142.2.2 Treatment with Gardiquimod, CpG ODN and KM 152.2.3 qRT-PCR assay of mRNA expression 152.2.4 Assessment of auditory brainstem response (ABR) and distortion product otoacoustic emission (DPOAE) 162.2.5 Surface preparation of the cochlear sensory epithelium 172.2.6 Immunocytochemi

stry for outer hair cell (OHC) counts 172.2.7 Immunohistochemistry for cryosections 182.2.8 Statistical analysis 192.3 Animal experiments II: dysregulation of cochlear circadianclock genes during acoustic trauma 192.3.1 Animals 192.3.2 Control and alteration of the LD cycle 192.3.3

Noise exposure 202.3.4 Assessment of ABR and DPOAE 202.3.5 qRT-PCR assay of mRNA expression 212.3.6 Surface preparation of the cochlear sensory epithelium 222.3.7 Immunocytochemistry for outer hair cell (OHC) counts 222.3.8 Immunocytochemistry for synaptic ribbon counts and 4-hydroxy

nonenal (4-HNE) 232.3.9 Immunohistochemistry for cryosections 242.3.10 Statistical analysis 25CHAPTER III. RESULTS 263.1 Innate immunity responses in patients with SSNHL 263.1.1 Differential expression of TLR and downstream genes in leukocytes between SSNHL patients and controls 26

3.1.2 Expression of innate immunity genes in SSNHL patients according to age and existence of DM 263.1.3 Expression of TLR genes between the SSNHL patients with PTA > 90 dB and PTA  90 dB 273.1.4 ICC staining for TLR2 273.1.5 Percentage of CD14+ monocytes expressing TLR2 inSSNHL patients a

nd controls using flow cytometry 273.2 Circadian clock in patients with SSNHL 283.2.1 Sleep questionnaires of patients with SSNHL 283.2.2 Expression of circadian clock genes in patients withSSNHL and controls using qRT-PCR 293.2.3 Correlations of circadian clock gene expression withheari

ng severity or vertigo in SSNHL 293.2.4 Expression of circadian clock genes in PB leukocytes of SSNHL patients with and without sleep disturbance 303.3 Impact of cochlear TLR alterations on aminoglycosideototoxicity 303.3.1 Increased Tlr7 and Tlr9 gene expression in the cochlea after chroni

c KM treatment 303.3.2 Subcutaneous Gardiquimod and CpG ODN increasedcochlear Tlr7 and Tlr9 signaling genes 313.3.3 Gardiquimod and CpG ODN did not affect baseline auditory thresholds in CBA/CaJ mice 313.3.4 Simultaneous treatment of CpG ODN and KM elevated the ABR threshold shifts and incr

eased outer hair cell loss. 323.3.5 Simultaneous treatment of CpG ODN and KM increased cochlear Tlr9 signaling genes and cytokines 333.3.6 CpG ODN increased macrophages infiltration into thecochlea 333.4 The impact of cochlear circadian dysregulation onnoise-induced hearing loss 343.4.1

Circadian oscillation was present in the cochlea 343.4.2 Constant light (LL) dysregulated cochlear circadianoscillation 343.4.3 LL did not affect baseline auditory thresholds andneural response amplitudes 353.4.4 LL did not affect low-intensity noise-induced temporary threshold shift (TTS)

and ABR wave I amplitudes changes 353.4.5 LL augmented high-intensity noise-induced permanent threshold shift (PTS) and outer hair cell (OHC) loss 363.4.6 LL increased high-intensity noise-induced reduction ofsynaptic ribbons 373.4.7 LL increased high-intensity noise-induced 4-HNE in OHCs

383.4.8 LL increased high-intensity noise-induced mRNAexpression of Tlr4 and proinflammatory cytokines 38CHAPTER IV. DISCUSSION 404.1 Increased TLR expression in SSNHL and TLR2 expression is associated with hearing severity 404.2 Decreased circadian clock gene expression in SSNHL 434.3

Activation of Tlr9 by CpG ODN exacerbated aminoglycoside ototoxicity and increased cochlear proinflammatory cytokines 464.4 Circadian dysregulation by constant light exacerbatednoise-induced hearing loss and increased oxidativestress in OHCs 494.5 Conclusion 54CHAPTER V. FUTURE PERSPECTIVE

S 55FIGURES… 56Tables…… 80REFERENCE 87APPENDIX 105IRB Approval 106Approval of animal study 111Research Projects 116Bibliography 117口試委員審查意見回覆 118Directory of FiguresFigure 1. Expression of Toll-like receptors (TLRs) in sudden sensorineural hearing loss (SSNHL) patients

and normal controls 57Figure 2. Immunocytochemical (ICC) staining of peripheralblood (PB) leukocytes. 58Figure 3. Flow cytometry to access the TLR2 expression. 59Figure 4. Real-time quantitative polymerase chain reaction (RT-PCR)and ICC staining for the expression levels of circadianclock g

enes. 60Figure 5. Severity of hearing loss, vertigo and circadian clock gene expression in patients with SSNHL. 61Figure 6. Expression of circadian clock genes in SSNHL patientswith and without insomnia. 62Figure 7. Cochlear Tlr mRNA expression after KM treatment. 63Figure 8. mRNA expres

sion of Tlr7, Tlr9 and downstreamingcytokines after Gardiquimod or CpG ODN treatment. 64Figure 9. Timeline of auditory brainstem response (ABR)measurement. 65Figure 10. ABR thresholds of mice treated with Gardiquimod orCpG ODN. 66Figure 11. The effect of CpG ODN in ABR thresholds andouter h

air cells (OHCs) during KM treatment. 67Figure 12. mRNA Expression of Tlr9 and downstreamingcytokines after KM and CpG ODN treatment. 68Figure 13. Representative images of IL-6 immunostaining over the cochlea. 69Figure 14. Iba+ macrophages in the cochlea. 70Figure 15. Relative transcript

profiles of circadian clock genes in the cochlea 71Figure 17. The ABR thresholds and wave I amplitudes in the LD and constant light (LL) groups. 73Figure 18. Timeline of experiments for testing the ABR. 74Figure 19. The ABR threshold shifts, wave I amplitudes and synaptic ribbon counts in

the LD and LL groups after 92-dB noise exposure. 75Figure 20. The ABR threshold shifts, OHC cell counts, and DPOAE2F1-F2 amplitudes in the LD and LL groups after 106-dB noise exposure. 76Figure 21. Synaptic ribbon counts in the LD and LL groups after106-dB noise exposure. 77Figure 22. 4-hyd

roxynonenal (4-HNE) immunolabeling in cochlear surface preparations in the LD and LL groups after106-dB noise exposure. 78Figure 23. Relative expression of Tlr4 and proinflammatorycytokines in the LD and LL groups after 106-dB noise exposure. 79Directory of TablesTable 1. Characteristics of su

dden sensorineural hearingloss (SSNHL) patients and controls in innate immunitystudy 81Table 2. The expression levels of the innate immunity genes in SSNHL patients and controls determined by real-time quantitative polymerase chain reaction (qRT-PCR) 82Table 3. The expression levels of the inn

ate immunity genes inSSNHL patients without diabetes mellitus and controls determined by qRT-PCR 83Table 4. Characteristics of SSNHL patients and control incircadian clock study 84Table 5. Insomnia Sleep Questionnaire (ISQ) 85Table 6. p-value of F test to detect the circadian rhythmicity of

mRNA transcripts of circadian clock genes in the cochlea by CircWave software 86