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通過金屬奈米粒子放大的表面電漿共振感測器適體以實現的高靈敏度及高選擇度的帕金森氏α-突触核蛋白生物标志物檢測

為了解決fg-908 ptt的問題，作者黃強恩 這樣論述：

Recommendation Letter from the Thesis AdvisorThesis Oral Defense Committee CertificationPreface or Acknowledgments iiiChinese Abstract viEnglish Abstract viiTable of Contents ixList of Figures xiiList

of Tables xvi1 Introduction 11.1 Background and scope of problem 11.2 Objective of research and methodologies 41.3 Outline of the thesis 52 Background Overview 72.1 Parkinson’s disease and the role

of α-syn in neurodegenerative disorder 92.1.1 Parkinson’s disease: from the observation into the standardize clinical rating diagnosis 92.1.2 α-syn as a genetic protein for Parkinson’s disease 122.1.3 The role of α-syn in neuroinflammation and spread of PDpathology

162.1.4 α-syn in peripheral blood for routine test of PD 172.2 SPR biosensors for Parkinson’s clinical diagnosis 232.2.1 General principle of surface plasmon resonance 232.2.2 Maxwell derivation for dispersion relationship 242.2.3 Resonance condition of SPR biosensor

322.2.4 SPR biosensor performance 322.2.5 Application of SPR biosensor for detecting α-syn proteins . 352.2.6 Sensitivity of SPR: Limitation and enhancement strategy 362.3 The role of nanoparticle in developing ultrasensitive of SPR biosensors 382.3.1 Nanoparticles as a sensi

tivity enhancement in SPR biosensors 382.3.2 Magnetic nanoparticle 392.3.3 Gold nanoparticle 432.4 Reduction non-specific binding (NSB) in SPR sensor surface 492.4.1 NSB in SPR sensor surface 492.4.2 Blocking method for reducing NSB in sensor surfa

ce 512.4.3 Chemical modification on sensor surface for reducing NSBin sensor surface 522.5 Aptamer for developing a selective SPR biosensor 532.5.1 Nucleic acid aptamer 532.5.2 Applications of aptamer on biosensors 562.5.3 Aptamer for recognizing α-

syn in PD clinical applications 583 Experimental Design and Methodology 623.1 SPR sensor platform configuration 633.1.1 Experimental set-up 633.1.2 Trapezoid prism 643.1.3 OLED light source with BEF and DBEF films 643.1.4 Fabrication o

f Au film sensor chip 653.2 Analytical chemistry sample preparation 673.2.1 Preparation α-syn sample in PBST buffer and diluted serumsamples 673.2.2 Clinical sample preparation 673.2.3 Aptamer and antibody preparation 683.2.4 AuNPs and

MNPs preparation 683.3 SPR experimental procedure 693.3.1 Normalization of SPR signal 693.3.2 Surface modification of Au film 703.3.3 SPR measurement of the α-syn sample using AuNPs 713.3.4 SPR measurement of the α-syn sample using MNPs 723.3.

5 SPR measurement of clinical samples 734 Optimization of SPR experimental parameter toward NSB effect on serumsamples 754.1 Optimization of SAMs monolayer 764.2 Selectivity test toward un-specific protein 794.3 Effect of blocking agents on seru

m samples 815 Effect of nanoparticles on SPR sensitivity for the detection of α-syn . 845.1 Metal nanoparticle enhanced SPR sensitivity 855.2 Detection of α-syn by using metal nanoparticles 876 Serum sample measurements 906.1 Detection of α-syn in artific

ial human serum samples 916.2 Clinical sample measurements 926.3 Regeneration recoverability and shelf-life stability of sensor chips 946.3.1 Regeneration recoverability test 956.3.2 Shelf-life stability test of the fabricated sensor chips 977 Summary, conclusions

, and future works 997.1 Summary and conclusions 997.2 On going works: Investigating the mechanism of α-syn in the pathogenesis of PD based on animal model 101Bibliography 103List of Figures2.1 Milestone of first generation PD research

from 1817 into 1967 92.2 Phsyiologic and pathogenic of α-syn to in aggregration of PD. (a)DNA sequence for SNCA of the PCR product used for mutationdetection [1]. (b) Schematic representation of α-syn aggregrationprocess [2], which can be described by (c) compartmentalized αsyn residing on the v

esical lysosome membrane [3]. (d) The role ofextracellular α-syn in neuroinflammation, neurotoxicity, and spreadof pathology [4] 132.3 Summary of acknowledge biosensing method used for quantifyingα-syn in clinical blood samples (reference from Tab. 2.1) 222.4 Schematic descripti

on of SPR sensing platform 242.5 Schematic of a planar waveguide between medium dielectric andmetal, with refraction light penetrate through the both of mediumbased on Snell’s law 262.6 (a) Dispersion relation of Kretschmann configuration for excitingSP wave. (b) Reflectan

ce profil of SPR due to the photon lightabsorption 322.7 Schematic of SPR structures based on MNP as a sensitivity enhancement: (a) labeling, (b) cluster nanoparticles, and (c) separationenrichment method. Inset figure shows separation and enrichmentof target protein based on an

tibody-immobilized MNPs. The target protein inside the complex buffer was incubated with antibodycoated MNPs. Then, the target protein binded with MNPs wasseparated with other un-specific proteins by using external magnet.By removing the complex solutions, the aggregates target proteinwith MNPs were

reconstituted with a clean buffer to provide a cleansolution with minimize un-specific proteins 402.8 (a)Schematic of coupling effect between AuNPs and Au films toamplify SPR electric field [5, 6]. Within the evanescent wave, theelectron oscillation on AuNPs can pile up charge on the Au fil

m andmake Au film has an image field of AuNPs. The charge transferfrom Au film to AuNPs depends on (b) nanoparticle size [7, 8], (c)gap distance between AuNPs and Au film [9], and (d) nanoparticledistribution [10] 442.9 Schematic of specific and non-specific binding in a SPR sen

sor surface. 502.10 SELEX process for producing an aptamer with adaptive recognitionto the specific cell target with high affinity and specificity than theconventional antibody [11–13] 542.11 Increasing number of publications reporting aptasensors-based onSPR biosensing in analytical me

asurement. The reports listed wasobtained from SCOPUS search engines with ”SPR” and ”aptasensors” as a key-word search 572.12 F5R1 and F5R2 aptamer for the receptor agent on α-syn antigen,with SELEX process was used to form oligonucleotide sequence withhigh affinity and high specific

target binding [14] 603.1 Schematic design of SPR biosensing platform used for α-syn quantification 633.2 Fabrication flow and structure of the Au sensor chip functionalizedself-assembled monolayers (SAMs) 663.3 Distribution of the NHS/EDC-raw signal as a

normalization buffer.Inset figure: raw SPR signal from the output of spectrometer withpurple arrow indicate the signal for NHS/EDC 693.4 SPR sensogram for (a) sensing surface modification process and (b)different sensor surface blocking, which involved 0.1 M ethanolamine(ETH) and 2% bovine

serum albumin (BSA) 713.5 SPR sensogram for the detection of α-syn (a) in PBST buffer and(b) 1:1000 dilution human serum samples 723.6 Real-time SPR response for 1 pg/mL α-syn detection in PBST bufferusing labeling mAB-MNPs 733.7 Real time monitoring of SPR respon

se in clinical serum measurements. 744.1 (a) SPR response for adsorption of NHS/EDC-esters (upper panel),covalent bonding of SA at a concentration 200 µg mL−1 and to nonspecific proteins from human AB male serum with dilution 1:1000(bottom panel) at variations in the alkanethiol mixture. (b) Schemat

icnon-specific and specific binding on SPR sensing surface with variations alkanethiol mixtures 77xiii4.2 Selectivity test of SPR biosensing involving aptamers and antibody.(a) Schematic illustration of un-specific protein interference. (b)SPR sensogram for three control test involvin

g (1) blank test, (2)unspecific protein with actin, BSA, and IgG with concentration100 µg/mL, and (3) α-syn target control with concentration 0.1 fg/mL. 804.3 (a) SPR signal for ETH and BSA blocking toward human AB maleserum with various dilution factors. (b) SPR sensorgram and (c)schematic illustra

tion for ETH and BSA blocking mechanism 825.1 Metal nanoparticle enhanced SPR sensitivity. (a) The SPR spectrum with and without metal nanoparticles. (b) Sensitivity enhancement of SPR biosensing in various distribution of AuNPs.Inset figure shows the effect of MNPs concentration toward SPRsen

sitivity. (c) FESEM image for AuNPs for 30 mins, 50 mins, and70 mins 865.2 Limit of detection (LOD) SPR biosensing with and without nanoparticles. Error bars is obtained from three replicated measurement.LOD was calculated based on Eq. 2.52 886.1 Calibration curve f

or detecting α-syn in diluted human serum witherror bars indicated standard deviation from three replicated measurements. LoD was calculated from Eq. 2.52 926.2 Preliminary evaluation of the SPR biosensors incorporated directAuNPs-F5R1 aptamers, adopting optimal experimental parametersof cl

inical sample measurements. Whisker box of (a) SPR responseand (b) concentration of α-syn on between HC group and the PD(PD), provided by one-way ANOVA method. Homogeneity variancewith Turkey tests indicated the p-value is smaller than the thresholdsignificant level (p = 0.05), which is implied a si

gnificant differencebetween HC populations and PD populations. (c) Level of α-syn inplasma and serum from the acknowledge platforms 936.3 Regeneration recoverability test of the AuNPs-F5R1 aptamers-BSA.(a) SPR sensorgram and (b) SPR signal for repeated detection of100 ag/mL α-syn in spiked

human serum with dilution 1:1000 on achip regenerated after each measurement. A PBST buffer solutionwas flowed into the flow cell before and after the α-syn serum samplewas injected onto the chip surface, to establish the baseline signal.A Glycerin pH 2.0 solution was used to remove α-syn and un-spe

cificserum protein from the surface 966.4 (A) Repeatability of the the AuNPs-F5R1 aptamers-BSA sensor indetection of 100 ag/mL α-syn in spiked human serum with dilution1:1000 with different condition storage: (red color) in 4 °C and (bluecolor) in room temperature. The reflectivity resp

onse of the samesensor chip measured in 1 days and 30 days of detection of α-synserum samples after storage in (b) 4 °C and (c) room temperature 977.1 SPR sensorgram for the detection of α-syn in mice serum samples.The error bars was obtained from three replicated measurements 101List of Tables2

.1 Summary of the methods of quantification of α-syn in clinical bloodsamples involving plasma and serum 182.2 SPR immunosensors incorporating AuNPs 474.1 Performance factor of SAMs mixture variations 784.2 Sensitivity of SPR biosensing to detect PD serum with various

dilution factor after optimizing specificity parameters 835.1 Comparison between label-free and labelling method by using metalnanoparticles 89

探討胃酸分泌抑制劑對上消化道疾病患者罹患肝細胞癌風險性的影響

為了解決fg-908 ptt的問題，作者徐奐嫣 這樣論述：

研究背景胃酸分泌抑制劑（acid-suppressive agents）質子幫浦抑制劑（proton pump inhibitors, PPIs）與第二型組織胺受體拮抗劑（histamine 2 receptor antagonists, H2RAs）對罹患肝細胞癌（hepatocellular carcinoma, HCC）風險性的影響尚不明確。有些相關機轉顯示：胃酸分泌抑制劑可能影響罹患肝細胞癌的風險；而胃酸分泌抑制劑主要用於上消化道疾病（upper gastrointestinal diseases, UGIDs）的治療。本研究旨在探討：使用胃酸分泌抑制劑對上消化道疾病患者罹患肝細胞癌

風險性的影響。研究方法本研究為具有人口代表性的（population-based）回溯性（retrospective）世代研究（cohort study），以臺灣全民健康保險研究資料庫（National Health Insurance Research Database, NHIRD）的2000年100萬人承保抽樣歸人檔（Longitudinal Health Insurance Database 2000, LHID 2000）作為資料來源，納入2001年到2005年新診斷為UGIDs的患者，並排除年齡 ≤ 18歲者，再選取：有使用胃酸分泌抑制劑（H2RAs、PPIs）者（實驗組別一）與無

使用胃酸分泌抑制劑者（實驗組別二）。將「第一次有UGIDs診斷的日期」定義為：診斷日期；將「第一次有任何一種PPIs或H2RAs紀錄的日期」定義為：指標日期。另外，自LHID 2000之中篩選出2001-2005年間從未被診斷為UGIDs的病人，並排除「第一次有任何一種PPIs或H2RAs紀錄的日期後365天內，使用胃酸分泌抑制劑高於90天」者，即：無UGIDs且無固定使用胃酸分泌抑制劑的病人。再從中隨機抽樣並依性別、年齡及指標年（index year）與組別二以1:1比例進行配對（指標年：與組別二之診斷日期相同的年份），作為對照組別（comparison group）。所有組別皆持續追蹤六年

，統計分析其罹患肝細胞癌的風險。不同組別間罹患肝細胞癌風險性的比較，使用Cox比例危險模式（Cox proportional hazard model）來估計。研究結果在上消化道疾病患者當中，有使用胃酸分泌抑制劑者（實驗組別一）與無使用胃酸分泌抑制劑者（實驗組別二）相比，罹患肝細胞癌的風險性顯著增加，其校正後危險比（adjusted hazard ratio, HR）1.53，95% 信賴區間（confidence interval, CI）1.32-1.76；而且，胃酸分泌抑制劑之使用劑量對後續罹患肝細胞癌風險的影響，有顯著上升的趨勢（P < 0.01）。此外，有UGIDs且無使用胃酸分泌抑

制劑者（實驗組別二）與無UGIDs且無固定使用胃酸分泌抑制劑者（對照組別）相比，其罹患肝細胞癌的風險也顯著增加（校正後危險比1.94，95% 信賴區間1.59-2.36）。結論胃酸分泌抑制劑（PPIs、H2RAs）之使用會增加上消化道疾病患者罹患肝細胞癌的風險；而且，胃酸分泌抑制劑的影響具有劑量效應。另外，上消化道疾病本身也會增加罹患肝細胞癌的風險。不過，這些結果仍需要進一步的研究來驗證。