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The Construction and Its Development of Concepts of Neo-Confucianism: A Study of Ch'en Ch'un’s Pei-hsi tzu-i
No full text朱熹是南宋最重要的理學大師，身為朱熹晚年所收的門人之一，陳淳生平兩次從學朱熹，最後他成為直承朱熹學說的高弟。在朱熹的門人之中，陳淳從事的是建立一套朱熹性理之學的字義觀念，這些性理觀念時有爭議，而陳淳試圖給予更清楚明確的解釋。
朱子學派在南宋影響廣大，陳淳於其間具有傳播朱熹學說的重要地位。他不僅是發展朱熹性理思想，並且衛護師說，經由講授朱學、排擊陸學，陳淳闡發了朱熹的教育思想，諸如「推究道理根原」、「下學上達」、「道問學」等重要的論學觀點。
在朱熹性理思想內容方面，諸如「理氣不離，不分先後」，「心有體有用，心統性情」，「鬼神只是陰陽二氣之屈伸往來」等觀念，陳淳有所繼承亦有所發展，本論文將詳述他在建立朱熹性理字義觀念方面的貢獻。
儒學教育在宋元時期得到了高度的發展，在諸家學派之中，朱子學派居於主流地位。朱熹門人後學繼承師說，藉由小學教育傳播性理思想，而陳淳的《北溪字義》即為其中的典型教材，後世學者極為看重陳淳此書，視之為「初學性理」的入門書。日後，無論是私學或官學，均受到陳淳此書的影響。程朱理學官學化、成為科舉程式之後，闡述性理思想的場屋用書日益增多，汗牛充棟，陳淳的《北溪字義》一書創立了性理之書的論述模式與書寫體例，實具有開其先河之功。Chu Hsi was the important Neo-Congfucianism Master of the Southern Song Dynasty. As one of the students of old age Chu Hsi, Ch’en Ch’un only saw Chu Hsi personally twice in his life, but he finally had inherited in a direct line from his teacher. Among Chu Hsi’s disciples, Ch’en Ch’un wrote his dictionary or glossary in order to give a clear explanation of the disputed points about the terminology of Chu Hsi’s philosophy.
On account of Chu Hsi’s influence, His school prevailed in Sounthern Song Dynasty. Ch’en Ch’un, Chu Hsi’s successors played an important role in it. He not only developed his teacher’s thoughts, but also safeguarded it. He gave lectures and defended against such philosophers as Lu Chiu-yuan disciples, so he promoted Chu Hsi’s educational thoughts such as “Seek the original reason推究道理根原”, “My studies lie low, and my penetration rises high下學上達”, “Pursuing scholarship of Neo-Confucianism道問學”.
Ch’en Ch’un has brought forth quite a few innovations in concepts of Chu Hsi’s philosophy. From his series of theses “Principle and material force flock together, and hard to say which precedes”, “Hsing性is the principle of hsin心; Ch’ing情is the function of the hsin心; Hsin心is the director of ch’ing情and hsing性“, “Yin陰and yang陽are just the fluctuations of ch’i氣; one advance, one contraction, one dispersion, and one extension.” This paper expounds the explaining and amplying to Chu Hsi’s thought and the chief characteristics of Neo-Confucian of Ch’en Ch’un’s. Moreover, it brings to light his great contributions to terminology in the field of. Chu Hsi’s philosophy.
Confucian education had undergone high development period in Song and Yuan Dynasties. Chu Hsi school education was the most representative and developed than any other schools. Chu Hsi’s disciples transmited their teacher’s hsing-li-hsueh through primary education. A typical teaching material was Ch’en Ch’un’s Pei-hsi tzu-i. His work gained profound attention at that time and was commonly called “Hsing-li Beginners guide”. To diferrent degree, both private and official educationion Ming and Ching Dynasties was impacted by Ch'en Ch'un's work. Since Chu Hsi school’s Neo-Confucian became the imperial examination, more and more examinations books of hsing-li were published. Obviously, Ch'en Ch'un's Pei-hsi tzu-i pioneer discussed model and writing style for hsing-li-hsueh性理學.第一章 序論 1
第一節 陳淳與《北溪字義》 2
一、陳淳的學思歷程 2
二、《北溪字義》的內容和性質 5
第二節 性理之學的形成及發展 7
一、「性理」二字的涵義 7
二、性理之學與性理之書 9
第三節 從性理之學論陳淳《北溪字義》的定位 14
一、《北溪字義》近年研究成果綜述 14
二、本論文研究方法 21
第二章 《北溪字義》的思想背景 24
第一節 朱熹對陳淳論學的影響 24
一、凡字義須推究道理根原 24
二、先作下學工夫而後上達天理 30
三、窮理須走向道問學一路 35
第二節 陳淳講學與衛護師門 38
一、陳淳的為學方法及其對科舉的態度 38
二、陳淳衛護師說及其對陸學的態度 47
第三章 《北溪字義》的學術特色 53
第一節 對朱熹思想的繼承及發展 53
一、理氣先後問題 53
二、心之體用關係 59
三、陰陽鬼神之說 65
第二節 辨析性理字義的方法 73
一、字義的相對關係 74
二、字義的分屬關係 80
三、字義的脈絡關係 84
第四章 《北溪字義》的學術影響 89
第一節 《北溪字義》與宋元小學教育的關係 89
第二節 《北溪字義》對明清性理之學的影響 99
第五章 結論 113
參考書目 11
The effect of GABAB and alpha-2 Adrenergic Receptor on membrane excitability in Noradrenergic Neurons of A7 Catecholamine Cell Group in Rats
No full text大鼠A7核區兒茶胺酚細胞群是由一群分泌正腎上腺素之神經元所組成，其軸突投射到脊髓背角並參與痛覺的調控。然而，型態上的分析顯示在A7核區中也有神經傳導物質釋放的軸突結構-膨體，推測在A7局部會有正腎上腺素的分泌進行自我調控。為了驗證這個假設，我們取腦幹之腦薄片，利用全細胞膜電位記錄的方式去探討正腎上腺素對A7核區正腎上腺素神經元神經細胞興奮性之影響。10 uM正腎上腺素會抑制A7正腎上腺素神經元之自主放電並造成細胞膜電位之過極化，並可被正腎上腺素alpha-2受器阻斷劑所阻斷。將膜電位箝制在-70mV，給予正腎上腺素會引發一個向外的電流，其反轉電位在-97 mV並有向內整流的性質，顯示活化alpha-2受器可能去開啟G蛋白偶合向內整流鉀離子通道(GIRK)。此外，正腎上腺素引發之電流可被G蛋白偶合向內整流鉀離子通道之阻斷劑-鋇離子以及Tertiapin-Q所阻斷。然而，以alpha-2受器阻斷劑阻斷正腎上腺素作用，並不會造成神經細胞動作電位產生的頻率增加，顯示在A7核區內生性的正腎上腺素抑制神經元的情況並不顯著。綜合以上結果，活化A7正腎上腺素alpha-2受器會開啟GIRK通道去抑制神經元之興奮性，但神經元透過釋放正腎上腺素去調控自我的興奮性的負回饋機制並不顯著。此之外，A7的兒茶胺酚神經元受到持續的GABA中間神經元的抑制。另外也有型態上的證據顯示，A7神經細胞表現大量的GABAB受器。GABAB 受器被廣泛的發現會去開啟GIRK通道。GIRK會影響神經細胞的膜電位及興奮性。因此我們推測，內生性的GABA 可能持續活化GABAB受器，造成細胞神經興奮性的抑制。Baclofen是GABAB 受器的促效劑，會抑制A7正腎上腺素神經元之自主放電並造成細胞膜電位之過極化。將膜電位箝制在-70mV，給予Baclofen會引發一個向外的電流，其反轉電位在-105 mV並有向內整流的性質，顯示活化GABAB受器可能去開啟G蛋白偶合向內整流鉀離子通道(GIRK)。此外，Baclofen引發之電流可被G蛋白偶合向內整流鉀離子通道之阻斷劑-鋇離子以及Tertiapin-Q所阻斷。電刺激A7神經元的周邊的組織，可引發出GABAB的電流，顯示在A7神經元上的GABAB受器會受到突觸釋放的GABA所活化。另外，當我們給予GABAB受器的阻斷劑，會造成神經細胞動作電位放射的頻率上升，顯示，A7神經元會受到持續的GABA的抑制，這個抑制是透過GABAB受器所造成的。合以上結果，在腦幹A7核區之兒茶胺酚細胞正腎上腺素alpha-2受體與GABAB受體會開啟GIRK通道，並調控細胞的神經興奮性。The A7 catecholamine cell group consists of noradrenergic (NAergic) neurons that project axonal terminals to the dorsal horn of the spinal cord. Morphological analysis revealed that there are also axonal varicosities in A7 area, suggesting a possibility of autoregulation in NAergic neurons in A7 area. To test this, we firstly examined whether NE is able to affect the neuronal excitability of A7 NAergic neurons via whole-cell patch recording in brainstem slices. Bath application of 10 uM NE resulted in suppression of spontaneous spiking and membrane hyperpolarization in A7 neurons, which is blocked by alpha-2 receptor antagonist. Under voltage-clamp, application of NE produced an outward current (INE). The INE has reversal potential of -97mV and property of inward rectification, showing that hyperpolarization by alpha-2 adrenoceptors were caused by opening of G-protein-coupled inwardly rectifying potassium (GIRK) channels. This is further confirmed by the results that INE was blocked by Barium and Tertiapin-Q, the two blockers of GIRK channel. However, under resting or exiting conditions, application of alpha-2 adrenoceptors antagonist did not increase the firing rate. Theses results suggest that activation of alpha-2 adrenoceptors suppressed neuronal excitability of NAergic neurons by opening GIRK. However, feedback mechanism mediated by alpha-2 receptor targeting on GIRK channels was not prominent in A7 NAergic neurons.A7 catecholamine cell group have been proposed to receive tonic GABAergic inhibition from local interneurons. The GIRK channels play an important role in determining resting membrane potential (Vm) and regulation of neuronal excitability, and are well known to be activated by metabotropic GABAB receptor in brain. Since NAergic neurons express high level of GABAB receptor, the effect of GABAB receptor on NAErgic neurons and the possible relationship to GIRK channel in A7 area are tested here. Bath application of 10 uM baclofen caused suppression of spontaneous firing and hyperpolarization of Vm in A7 neurons. This effect was blocked by CGP 54626, a specific GABAB receptor antagonist. Under voltage-clamp recording, application of baclofen produced an outward current (Ibaclofen). The Ibaclofen has reversal potential of -105mV and property of inward rectification, showing that hyperpolarization by GABAB receptor was caused by opening of GIRK channels. This is further confirmed by results that Ibaclofen was blocked by Barium and Tertaipin Q, the two bockers of GIRK channel. On the other hand, GABAB-mediatd current can be evoked in A7 neurons, suggesting that the GABAB receptor can be activated by the synaptic released GABA. Firing rates of NAergic neurons significantly increased in bath appilication of GABAB antagonist CGP54626, suggesting that there was endogenous GABA tonic suppressing the neuron. Taken together, these results suggest that NAergic neurons are subjective to tonic inhibition by GABAB receptors, which open GIRK channels and regulate excitability in A7 area.o sum up, alpha-2 adrenoceptor and GABAB receptor opens GIRK channel and regulates the excitability of A7 NAergic neruons.口試委員會審定書謝…………………………………………………………....i文摘要…………………………………………..iii文要…………………………………………………. ……….vntroduction ………………………………………...…………..1 The ascending pain pathway and descending pain pathway………….1 The role of A7 catecholamine cell group in descending modulation of pain………....2 Autoregulation of NAergic neurons………...............4 Adrenoceptors and cellular mechanism…………………………5ABAB receptor and cellular mechanism……………….…….6 protein-coupled inwardly rectifying K+ channel…………..6bjective…………………………………...………….…8aterials and methods…………………………………..10reparation of brain stem slices…………………..10isualization of neurons in A7 and Electrophysiology………10ata analysis…………………………………………………...12rugs………………………………………………………………...13illing recorded neurons with biocytin and histology….13mmunohistochemistry for double labeling……………….14esults……………………………………………………….....16ocalization of A7 cell group and axon terminals in the local A7 area…16E hyperpolarized A7 catecholamine cell group and decreased input resistance…17-2 adrenergic antagonist, Rauwolscine, blocked the effect evoked by NE…18pening of GIRK channel by NE………………………21xpression of GIRK1 on NAergic neurons in A7 cell group…22he ambient NE on NAergic neurons of A7 cell group………22ther potent function of a-2 adrenocpor on NAergic neurons in A7 area…23aclofen hyperpolarized A7 catecholamine cell group and decreased input resistance…………………………….24ABABB receptor antagonist, CGP54626, blocked the effect evoked by baclofen….26pening of GIRK channel by baclofen………………....27he tonic GABAB receptor-rmediated inhibition on NAergic neurons of A7 cell group…………………………………....28vocation of GABAB receptor-mediated postsynaptic current…29nteraction between GABAB receptor and a-2 adrenoceptor ………29isscusion………………………………………………...31drenoceptors subtypes of NAergic neurons in A7 area……31ntegration of signals by GIRK channel…………….......32unctional roles of a-2 adrenoceptor in A7 NAergic neurons………………………34onic inhibition of GABA on NAergic neurons in A7 area………37eferences……………………………………………......40igures………………………………………………4
Investigation of Physics of Vascularity Index Using Canine Renal Model
No full text本文研究血液灌流指數VI（Vascularity Index）其所代表血液動力學之意義，主要利用非侵襲性超音波(Echo)系統與侵襲性血流血壓量測系統，以犬隻腎臟為平台，量測其血液灌流量特徵，採用實驗室開發之醫學影像處理軟體分析超音波影像，以探討VI與壓力波和流量波之相關性。
實驗對象為年齡9個月至5歲，重量為14至25公斤之健康犬隻，量測部位為左邊腎臟，非侵襲性實驗總共進行11隻狗的實驗，同時擷取腎臟血管及腹腔大動脈影像資料，針對當中取樣頻率較高的4隻狗將腎臟血管分成葉間動脈（上游）、弓狀動脈（中游）、末稍小動脈（下游）三個部分，並對此三個部分的VI波形，與腹腔大動脈的變形波及流量波進行比對，由比對結果得下游週邊血管統計分析上的相關性高於上、中游血管，VI與變形波迴歸分析的判定係數（ ）分別有0.9371、0.9755、0.8962、0.9037的相關性。藥物實驗總共進行3隻狗的實驗，針對2組較佳的資料資料分析，結果得給藥後平均血壓有下降的趨勢，由86 ± 1 mmHg下降至70 ± 2、72 ± 2、72 ± 1 mmHg，由於Dopamine所影響的是腎臟的血流，以致於給藥後的VI和給藥前腹腔大動脈變形波之間的相關性降低。This study aimed at investigating the physical meaning of VI（Vascularity Index）, using color duplex ultrasound. The renal hemodynamics of canine was used as the testing platform for the quantification of VI using a medical imaging analysis software developed in house. The dynamics power Doppler VI were compared with the pressure waveform and flow waveform measured upstream at the abdominal aorta.
Eleven health dogs aged from nine mouths to five years old, weighted 14- 25 Kg were used in this study. Ultrasonic scanning was focused on the left renal of each dog non-invasively. Both the Doppler spectrum of the renal blood flow and the M-mode image of the abdominal aorta were recorded. Among the test cases, four dogs were selected to differentiate the renal blood vessels at various sections of the kidney; namely interlobar artery（top）、 arcuate artery（middle）、arteriole（below）. Comparing the VI waveforms that obtained from various renal sections with the aortic diameter deformation waveform (which is considered as an alternative pressure waveform) we find the VI waveform from arteriole has a higher correlation statistically than the interlobar artery and the arcuate artery. The corresponding regression analysis were about 0.9371、0.9755、0.8962、0.9037 for these renal VI and the pressure waveform. Dopamine was also used to control the renal blood flow of canine without much alteration of physiological conditions. The blood pressure changed slightly from 86 ± 1 mmHg to 70 ± 2, 72 ± 2 and 72 ± 1 mmHg. Because of the Dopamine affected the renal blood vessels, the regression coefficient between the VI waveform and pressure waveform decreased due to the pharmaceutical action.誌 謝……………….……………………………………………I
中文摘要………………………………………………………………II
英文摘要…………………………………………………………… III
內文目錄………………………………………………………………IV
圖表目錄………………………………………………………………VI
第一章 緒論……………………………………………………… 1
1-1前言………………………………………………………… 1
1-2文獻回顧…………………………………………………… 3
1-3 研究背景與動機…………………………………………… 6
1-4 論文架構…………………………………………………… 7
第二章 研究原理………………………………………………… 10
2-1超音波量測系統………………………………………… 10
2-1-1超音波基本原理……………………………………… 11
2-1-2 超音波顯示模式………………….…………………… 11
2-2腎臟生理學……………………………………………… 13
2-3血液灌流量指數…….…………………………………15
2-3-1 VI…………………..………….…………………… 15
2-3-2 DFVI…………………..…………………………… 16
第三章 研究方法及設備………………….……………………… 19
3-1 實驗方法簡述……………………………………… 19
3-2 實驗設備…………………………………………… 19
3-3 實驗動物…………………………………………… 21
3-4 實驗流程…………………………………………… 21
3-4-1 前置作業…………………………….………… 21
3-4-2 非侵襲性動物實驗………………….………… 21
3-4-3 侵襲性動物實………………………….……… 22
3-4-4 非侵襲性動物實驗(Dopamine藥物實驗).. 23
3-5資料處理與分析……………………………………… 24
3-5-1資料收集……………………………………… 24
3-5-2資料分析…………………………….………… 24
第四章 結果與討論…………………………………………… 33
4-1 波形分析……………………………………………… 33
4-1-1 腎臟血流的壓力、流量波形分析……………… 33
4-1-2 VI、DFVI波形分析………………………… 36
4-1-3 Correlation Map的應用…………….…… 38
4-2 不同部位VI、DFVI波形和腹腔大動脈血管之變形波、流速波
的比對………………………………….………………… 42
4-2-1 葉間動脈（上游）VI、DFVI波形和腹腔大動脈血管之
變形波、流速波的比對……………………….……… 46
4-2-2 弓狀動脈（中游）VI、DFVI波形和腹腔大動脈血管之
變形波、流速波的比對………………..……… 55
4-2-3 末稍小動脈（下游）VI、DFVI波形和腹腔大動脈血管之
變形波、流速波的比對……………………… 64
4-3 Dopamine藥物給予的影響…………………………… 73
4-4 VI、DFVI波形和變形波、流速波波形的相似性… 77
4-5 討論…………………………………………………… 81
4-5-1 壓力波與變形波比對之探討……………………..81
4-5-2 Correlation Map說明………………………… 81
4-5-3 Dopamine藥物實驗之探討………..…………….82
4-5-4 實驗討論…………………………………………… 83
第五章 結論…………………………………………………… 85
5-1 結論………………………………………………… 85
5-2 未來展望…………………………………………… 86
參考文獻………………………………………………………… 8
Application of the Empirical Mode Decomposition in the Impact-Echo Method
No full text本研究之主旨為探討希爾伯–黃轉換(Hilbert–Huang Transform) 與其它訊號處理方法之差異，並將之應用於敲擊回音試驗，評估其可行性，最後提出定位裂縫的新訊號處理程序，使頻譜更清晰、峰值更明顯，且裂縫尖峰易判讀。
希爾伯–黃轉換為一非線性且非穩態之時間–頻率域訊號處理方法。在此轉換中，訊號首先以經驗模態分解法做自適性的分解，自動地產生構成此訊號的分量，稱為本質模態函數(Intrinsic Mode Function)，再利用希爾伯轉換求得每個本質模態函數的即時頻率與即時振幅，最後在時間–頻率軸所構成之二維圖譜上繪製即時振幅之等高線圖，即為希爾伯頻譜。透過希爾伯頻譜，便可更進一步解析隱含於訊號中的物理意義。
本研究嘗試以希爾伯–黃轉換分析敲擊回音訊號，發現其希爾伯頻譜上為一條上下振盪的明亮軌跡，難以辨識主頻，也無法據以偵測混凝土試體內部缺陷位置。然而配合短時傅利葉轉換或小波轉換，可觀察到各本質模態函數的時間–頻率分布特徵，即可判斷出各本質模態函數所對應之物理意義。其中雜訊能量最小，其時頻圖沿時間軸或頻率軸都無明顯變化；表面波能量消散最快；內部缺陷回音訊號能量消散次之，在缺陷深度所對應之頻率會出現明顯的峰值；模態振動能量最大，但消散最慢，在對應之自然頻率也會出現峰值。一旦定出代表內部缺陷回音訊號之本質模態函數，便可對此函數進行傅利葉轉換，並找出內部缺陷之頻率尖峰。經過數值模擬與模型試驗，可發現本文所提出之訊號處理程序所得到之頻譜與原始訊號相比，干擾更少、峰值更明顯，且不受模態振動之影響。第一章 前言 1
1-1 研究動機 1
1-2文獻回顧 2
1-3 研究內容 3
第二章 敲擊回音法 6
2-1 應力波傳行為 6
2-2 敲擊回音法 8
2-3 敲擊回音試驗參數 11
2-3-1 敲擊源 11
2-3-2 總取樣時間 14
2-3-3 取樣時距 15
2-4 敲擊回音法算例 16
第三章 訊號處理方法 23
3-1 傅利葉轉換 23
3-2 短時傅利葉轉換 25
3-3 小波轉換 26
3-4 希爾伯–黃轉換 30
3-4-1 希爾伯轉換 30
3-4-1.1 基本定義 31
3-4-1.2 相位平移系統 32
3-4-1.3 希爾伯轉換的性質 34
3-4-1.4 解析訊號 37
3-4-1.5 即時頻率 42
3-4-2 經驗模態分解法 49
3-4-2.1 本質模態函數 49
3-4-2.2 經驗模態分解法 51
3-4-2.3 相關性檢測與跨零點檢測 58
3-4-3 希爾伯頻譜與邊際頻譜 61
3-5 數值算例 64
3-5-1 諧波訊號 64
3-5-2 暫態訊號與內在調頻訊號 67
3-5-3 高斯雜訊 74
3-6 敲擊回音訊號分析方法 76
第四章 數值模型 105
4-1 有限元素分析軟體簡介 106
4-2 有限元素分析步驟 107
4-2-1 幾何模型建立 107
4-2-2 網格劃分 108
4-2-3 元素定義 109
4-2-4 負載與束制 111
4-2-5 求解 112
4-2-6結果分析 113
4-3 數值模型訊號分析 113
4-3-1 數值模型一 113
4-3-2 數值模型二 120
4-4 小結 123
第五章 模型試驗 141
5-1 模型試體 141
5-2 實驗設備 142
5-3 測點佈置 143
5-4 實驗參數 144
5-5 模型試驗訊號分析 145
5-5-1 模型試驗一 146
5-5-2 模型試驗二 156
5-6 小結 160
第六章 結論與展望 187
參考文獻 19
Study of Histoplasma-Induced Macrophage Apoptosis
No full text組織胞漿菌是一種寄生在巨噬細胞內之病原性胞內寄生真菌。在受到感染的寄主當中，噬細胞不只是胞漿菌之目的細胞，亦為清除感染之作用細胞並且能夠提供抗原給抗原呈獻細胞。在實驗室之前的研究當中發現到噬細胞在吞入活胞漿菌之後會進行細胞凋亡。樹突狀細胞即可由吞噬死亡之噬細胞當中獲得胞漿菌之抗原，交叉呈獻抗原已活化CD8 T細胞。因此，胞漿菌引發之噬細胞凋亡對於CD8 T 細胞之活化非常地重要。然而，真菌和噬細胞間的交互作用如何引發噬細胞的細胞凋亡仍是一個待解決的課題。本研究的主題當中，就是界定引發噬細胞凋亡的分子。
我首先發現到誘發型一氧化氮合成酵素會在噬細胞感染胞漿菌之後被引發。然而，細胞凋亡率在誘發型一氧化氮合成酵素基因缺陷之噬細胞當中並未降低，而若將噬細胞以活性氧之消除劑N-acetyl- cysteine處理，細胞凋亡率同樣沒有降低的現象，顯示活性氮化物以及活性氧化物皆不參與在噬細胞的凋亡當中。有趣的是，在噬細胞吞入活胞漿菌之後亦會產生腫瘤壞死因子-Histoplasma is a facultative intracellular pathogen of the macrophage. In the infected host, macrophage serves not only as a target cell and an effector cell but also as an antigen donor. Work from our laboratory has shown that macrophages undergo apoptosis after taking up viable Histoplasma yeasts. The dendritic cells take up Histoplasma antigen from dying macrophages cross-prime CD8 T cells. Thus, Histoplasma-induced macrophage apoptosis is important to the activation of CD8 T cells in an infected host. However, it remains to be clarified how the fungus-host cell interaction causes macrophage apoptosis. The focus of the present study was to delineate the molecule(s) that is involved in inducing macrophage apoptosis.
First, I found that inducible nitric oxide synthase (iNOS) was upregulated in macrophages after infection by Histoplasma. However, the apoptosis rate was not reduced in iNOS-deficient macrophages nor in macrophages treated with N-acetyl-cysteine, a reactive oxygen species scavenger, demonstrating neither reactive nitrogen nor oxygen intermediates is involved in macrophage apoptosis. Interestingly, TNF-a production was high in macrophages after uptake of viable Histoplasma. To investigate whether TNF-a is involved in inducing macrophage apoptosis, macrophages from TNF-a-/-, TNFR1-/-, TNFR2-/- and TNFR1-/-R2-/- mice were used. The results showed that in macrophages deficient in TNF-a, TNFR1, TNFR2 or TNFR1R2, the rate of Histoplasma-induced apoptosis was dramatically reduced. Both caspase-8 and pan-caspase inhibitors also significantly reduced macrophage apoptosis. The results of this study demonstrated that production of TNF-a, which through the TNF receptor-transduced signals mediates Histoplasma-induced macrophage apoptosis.Table of Content
Abstract i
Abstract (Chinese) iii
Chapter I. Introduction
Part 1 Histoplasma and host defense 1
Part 2 Pathogen-induced apoptosis 2
Part 3 Cross-presentation 4
Part 4 Rationale to study Histoplasma-induced macrophage
apoptosis 5
Chapter II. Materials and Methods
Part 1 Experimental procedures
1.1 Mice 6
1.2 Fungus and infection 6
1.3 Culture of primary resident peritoneal macrophage 6
1.4 Total RNA isolation and reverse transcription 7
1.5 Quantitative real-time PCR 8
1.6 TNF-a ELISA assay 8
1.7 Determination of hypoploid cells 9
1.8 TUNEL staining for detection of apoptosis 9
Part 2. Experimental materials
2.1 Complete RPMI-1640 medium 10
2.2 Enriched BHI medium 11
2.3 1X Hank’s balanced solution (HBSS) 11
2.4 Hypotonic DNA staining buffer 11
2.5 10X PBS buffer 11
2.6 ELISA buffer 12
2.7 General materials 12
2.8 Immunological reagents 13
2.9 Sequences primers 14
2.10 Instruments 14
Chapter III. Results
Part 1. Histoplasma and macrophage apoptosis
1.1 Macrophages undergo apoptosis after engulfing viable Histoplasma yeast cells 16
Part 2. Histoplasma-induced TNF-a production is the cause of macrophage apoptosis
2.1 Inducible nitric oxide synthase is not involved in Histoplasma-induced macrophage apoptosis 17
2.2 Reactive oxygen species is not involved in Histoplasma-induced macrophage apoptosis 17
2.3 Histoplasma-induced macrophage apoptosis is TNF-a dependent 18
2.4 Signals transduced by both TNFR1 and TNFR2 are important in the induction of apoptosis 19
Part 3. Caspase activation in Histoplasma-induced macrophage apoptosis
3.1 Histoplasma-induced macrophage apoptosis is caspase-dependent 20
Chapter IV. Discussion
Part 1. Molecules involved in the Histoplasma-induced macrophage apoptosis. 22
Part 2. Signaling pathways of TNFR1 and TNFR2 that lead to apoptosis. 24
Reference 26
Figures
Figure 1. Macrophages undergo apoptosis after ingesting viable Histoplasma yeast cells 32
Figure 2. Histoplasma-induced macrophage apoptosis is not mediated by inducible nitric oxide. 34
Figure 3 Inhibition of ROS production does not reduce Histoplasma-induced macrophage apoptosis.. 36
Figure 4. TNF-a is produced by peritoneal macrophages after engulfing viable Histoplasma. 38
Figure 5. Viable Histoplasma-induced cell death is reduced in the absence of TNF-a 40
Figure 6. Histoplasma-induced macrophage apoptosis is mediated by TNF receptor-transduced signal. 42
Figure 7. Signals transduced by TNFR1 as well as TNFR2 are important in the induction of apoptosis. 44
Figure 8. TNFR1 or TNFR2 macrophages produce same levels of TNF-a as wild type 46
Figure 9.Histoplasma-induced macrophage apoptosis is caspase- dependent. 48
Figure10. Histoplasma-induced macrophage apoptosis is through capsase-8. 5
Effective Node Location Assignment and Connectivity Maintenance for Mobile Video Surveillance Service on Wireless Ad Hoc Networks
No full text本論文發展一個更快速並且適合實作於晶片的演算法來求解行動視訊偵搜服務網路視訊涵蓋連結建立的問題，當目標物在網路取像涵蓋範圍外時，可快速的建立一條視訊連結來涵蓋目標物，以便將目標物的影像傳送給影像需求端。本論文利用呂文彥2008對於行動視訊偵搜服務網路所建構的初始涵蓋視訊連結數學模型(Initial Coverage and Connection Problem, ICCP)為基礎，以設計快速、質佳、且有潛力實作於晶片上為目標，發展一套ICCP問題的求解方法。
此外無線網路傳輸通道品質不穩定的情形，在呂文彥的研究中僅假設無線網路環境中沒有干擾且任務節點的電池能量階可以應付任務的需求。但實際在執行任務中，或因節點的能量會下降導致封包訊號的傳輸強度減弱，或因傳輸頻道環敬因素而影響視訊影像傳輸的品質。因此發展一套機制當傳輸通道品質不穩定時保持視訊連結完整也是一個重要的問題。
對於ICCP涵蓋視訊連結問題求解的方法，本論文以貪婪法則(Greedy Heuristic)和分支界定法(Branch-and-Bound)為基礎建立二階段貪婪分之界定法(Two Stage Greedy Branch-and-bound Solution Algorithm, TSGBA)來求解。首先透過貪婪式的步驟建構一條取向傳輸路徑，將此路徑指派節點移動的距離作為一個上限值，以減少後續分支界定法所需搜尋的路徑組合。接著再以深度優先搜尋(Depth first search)分支界定法搜尋其他可能的路徑組合。在搜尋的過程當中若某部分的任務節點移動距離已經超過了所設定的上限，便不再往下繼續搜尋以減少求解所花費的時間。分析TSGBA演算法得知其平均複雜度雖仍為指數型成長，但透過一開始所設定的上限，在大多數情況可以有效排除掉許多不可能的路徑組合，進而降低整體求解的時間。透過隨機產生30組網路節點的測試顯示，TSGBA在CPU 為Intel [email protected]、記憶體2G的電腦上可在短時間內(10秒/10個網路節點)得到一組品質佳(平均與最佳解誤差5%)的指派結果。故雖然此演算法的複雜度為指數成長，但透過啟發式步驟定義出的上限可以有效縮短實際的計算時間，因此此演算法仍然具有製作於晶片上的潛力。
另外針對傳輸通道品質不穩定的情形，本論文也提出一套保持連線機制，包括: (1)週期性的感測任務節點剩餘能量以及封包接收訊號強度、(2)針對節點電池能量與接收封包強度兩項指標分別定義兩層臨界點以決定機制啟動時機、(3)利用TSGBA求解演算法重新求解涵蓋視訊連結問題找尋替代路徑。透過此機制可減少連線因傳輸通道品質不佳而中斷的機率。
本論文且將TSGBA進行實作。實作的環境延用了呂文彥2008在應用層中使用VB.NET 2003TM 所實作的視訊偵蒐系統 (包括自身廣播系統以及指揮機制) ，接著以Visual Basic程式語言將TSGBA求解演算法實作成模組並且整合到視訊偵蒐系統軟體架構的應用層中，來實現自動化求解規劃節點移動位置建立涵蓋視訊連結的功能。This thesis develops a rapid and suitable for VLSI implementation algorithm to solve the connection establishment problem of a mobile video surveillance system. When the target is out of the coverage, this algorithm can establish a video connection to cover the target quickly and stream the target’s image to the requesting node. Base on the mathematical model, Initial and Coverage Connection Problem (ICCP), established by Wun-Yan Lyu 2008, we design a solution algorithm to solve this problem for the purpose of fast, good quality and has the potential to implement.
For the unstable transmission quality in wireless networks, the research of 呂文彥 does not address much. He assumes that there is no interference within the network and battery energy of each node can meet requirements of missions. Nevertheless, the real situation is that the energy of the node would decrease continuously to attenuate the transmission strength of packets and then affect qualities of videos. Thus, to develop the mechanism to maintain the completeness of video connection when the quality of transmission channel is not great is also an vital issue.
Based on the Greedy Heuristic and the Branch-and-Bound methodology, this thesis first, by the heuristic step, sets the upper bound of the moving distance of the assigned node to reduce the path combinations that the second part of the algorithm needs to search. Next, the thesis utilizes the Depth First Search of the Branch and Bound methodology to find the shortest path and then designs the Two Stage Greedy Branch and bound Algorithm (TSGBA), which is adapted to be embedded in chips, for solving the ICCP. TSGBA can obtain an assignment result with good quality (averagely 5% inaccuracy to optimal solutions) in a short time period (10seconds/ 10 nodes within networks.)
This thesis also addresses the mechanism for maintaining connections for the issues of unstable transmission channel quality. The main concepts are: (1) the periodic inspection of residual energy in mission nodes and packet receiving strength (2) the definitions of the critical points in two layers for battery energies of nodes and packet receiving strength to identify the activation time (3) The exploitation of the TSGBA to re-solve ICCP for finding substitutive paths. This mechanism would re-assign the locations of nodes to avoid the break off of connections, when the transmission quality is lower than some level in the mission.
As for the implementation, this thesis inherits the interfaces of Wun-Yan Lyu 2008 (the self broadcast system and the commanding mechanism) that were developed via VB.NET 2003TM in the application layer. Using Visual Basic programming language to implement TSGBA as an object and integrate it in the interfaces, this thesis can achieve the automatic solution findings of node location assignments for establishing video coverage connections without optimization tool suites
Design and Implementation of a Sigma-Delta Modulated Fractional-N Frequency Synthesizer
No full text在今日的射頻前級電路中，本地震盪器是一個不可或缺的要件，而設計一個兼具快速的鎖定速度、低相低雜訊和高頻率解析度的頻率合成器也成為一個挑戰。本論文探討MASH的三角積分調變器對於頻率合成器輸出相位雜訊的影響，另外由積體電路實現一個整合性的除小數頻率合成器，並使用MASH 1-1-1 三角積分調變器作為除頻數之調變，一方面藉由打亂除頻器的模數得到較好雜訊抑制，另一方面將雜訊推至較高頻的頻率，而能被鎖相迴路所澸除。此頻率合成器使用0.18μm Mixed-signal 1P6M CMOS製程，可操作於4GHz，模擬的相位雜訊在1MHz處為-115dBc/Hz，並在600MHz的跳頻間距下可達到小於30μm的鎖定時間。Nowadays, local oscillator is an essential component of the RF front-end. And the design for a frequency synthesizer with agile settling speed, low phase noise and high frequency resolution has become a challenge. The thesis discusses the influence of the MASH Sigma-Delta Modulator (SDM) to the synthesizer output phase noise. The integrated fractional-N frequency synthesizer is implemented with MASH 1-1-1 SDM. On one hand, better fractional and reference spurious suppression is achieved by randomizing the modulus of frequency dividers; on the other hand, the spurious noise is push to higher frequency and will be further filtered out by the PLL. The frequency synthesizer is operated over 4GHz. The simulated phase noise is -115dBc/Hz at 1MHz offset, and the settling time is less than 30μs at 600MHz frequency jumping.ABSTRACT…………………………………………………………………v
LIST OF FIGURE……………………………………………………… xi
LIST OF TABLES……………………………………………………… xv
CHAPTER 1 INTRODUCTION………………………………………………1
1.1 Motivatio………………………………………………………… 1
1.2 Various Types of Frequency Synthesizer Architectures…2
1.2.1 Digital Synthesizer………………………………………… 2
1.2.2 Direct Synthesizer……………………………………………3
1.2.3 PLL-Based Synthesizer……………………………………… 3
1.2.4 Fractional-N Synthesizer……………………………………5
1.3 Fractional-N Synthesis in Various CommunicationSystems8
1.4 Thesis Organization…………………………………………… 9
CHAPTER 2 THE BASICS OF FREQUENCY SYNTHESIZER………………11
2.1 General Considerations……………………………………… 11
2.1.1 Phase Noise……………………………………………………12
2.1.2 Spurs……………………………………………………………13
2.2 Phase Locked Loop(PLL) Fundamentals………………………14
2.2.1 Voltage Controlled Oscillator(VCO)…………………… 15
2.2.2 Phase Frequency Detector(PFD)……………………………16
2.2.3 Charge Pump(CP)………………………………………………19
2.2.4 Loop Filter……………………………………………………21
2.3 Phase Noise Performance Analysis………………………… 23
2.3.1 Noise at Input……………………………………………… 23
2.3.2 Noise of VCO………………………………………………… 25
2.4 Charge-Pump PLL Design……………………………………… 26
2.4.1 Second-Order PLL…………………………………………… 26
2.4.2 Third-Order PLL………………………………………………29
2.4.3 Fourth-Order PLL…………………………………………… 32
CHAPTER 3 SYBTHESIZER ARCHITECTURE BEHAVIORAL SIMULATION 35
3.1 Design Specification………………………………………… 35
3.2 Synthesizer Architecture…………………………………… 36
3.3 Behavioral Simulation…………………………………………36
3.3.1 Integer-N PLL Model…………………………………………38
3.3.2 Dual-Controlled Integer-N PLL Model……………………40
3.3.3 Fractional-N PLL Model…………………………………… 42
CHAPTER 4 DESIGN OF FREQUENCY SYNTHESIZER……………………47
4.1 PLL Building Blocks……………………………………………47
4.1.1 Phase Frequency Detector(PFD)……………………………47
4.1.2 Charge Pump(CP)………………………………………………49
4.1.3 Loop Filter(LF)………………………………………………50
4.1.4 Voltage Controlled Oscillator(VCO)…………………… 53
4.1.5 Multi-Modulus Divider(MMD)……………………………… 55
4.2 Sigma-Delta Modulator…………………………………………57
4.2.1 Modulator Topology………………………………………… 58
4.2.2 Implementation of Pipelined MASH 1-1-1 Modulator… 60
CHAPTER 5 SIMULATION AND MEASUREMENT RESULTS……………… 65
5.1 Mixed Signal Design Flow…………………………………… 65
5.2 Simulation Tools……………………………………………… 67
5.3 Simulation Results…………………………………………… 67
5.3.1 Simulation Results of PFD and Charge Pump……………68
5.3.2 Simulation Results of VCO…………………………………71
5.3.3 Simulation Results of MMD…………………………………73
5.3.4 Simulation Results of MASH 1-1-1 SDM………………… 74
5.3.5 Closed-Loop Simulation ……………………………………76
Reference………………………………………………………………8
Spectral Sidelobe Property of MC-CDMA and OFCDM Signals and Its Applications
No full text本篇論文探討多載波分碼多重存取及正交頻率分碼多工信號之頻譜旁波特性。在此討論中，頻域展頻碼所具備的快速旁波衰減特性可確保信號頻譜旁波隨著頻率快速衰減。給定頻域展頻碼的長度，信號頻譜旁波衰減速率有一個與碼長有關的上限。將碼字適當地排列，所有正交可變展頻因子碼與正交互補格雷碼造成的信號頻譜旁波衰減速率可完全由其引數來描述。藉由此描述，可建立針對頻譜旁波抑制的正交可變展頻因子碼與正交互補格雷碼之碼字選取機制，而所有多相位碼所造成的頻譜旁波衰減特性則完全相同。最後，本篇論文亦提出一種針對頻譜旁波抑制的正交可變展頻因子碼樹管理策略，此策略同時可以解決展頻碼阻塞的問題。In this thesis, the spectral sidelobe properties of MC-CDMA and OFCDM signals are investigated. Particularly, a general fast-sidelobe-decaying property of the frequency-domain spreading codes is observed to provide small power spectral sidelobes. Given the length of the frequency-domain spreading code, a limitation on the resulted sidelobe-decaying rate is also obtained. It is shown that, by proper arrangements, the spectral sidelobe properties of MC-CDMA or OFCDM signals with (frequency-domain spreading) OVSF and OCG codes can be completely described by their code indices. According to this description, new assigning principles for (frequency-domain spreading) OVSF and OCG codes subject to spectral sidelobe suppression are proposed. Also, all polyphase codes are shown to yield the same spectral sidelobe property. Furthermore, a new code tree management strategy for OVSF code is proposed aiming to maximize the sidelobe-decaying rate of the overall transmitted MC-CDMA or OFCDM signal, and in the meanwhile to eliminate the code-blocking problem completely.Abstract .......... iontents .......... iiist of Figures .......... ivist of Tables .......... vi Introduction .......... 1.1 Combining CDMA and OFDM .......... 1.2 Spreading Code Assignment .......... 4.3 Motivation .......... 7 Signal Models and Spectral Characteristics .......... 9.1 Signal Models .......... 9.2 Fast-Sidelobe-Decaying Property .......... 14.3 Limitation on Sidelobe-Decaying Order .......... 16 Sidelobe-Decaying Orders of Orthogonal Spreading Codes .......... 18.1 Overview of Orthogonal Spreading Codes .......... 18.2 Sidelobe-Decaying Orders of OVSF Codes .......... 22.3 Sidelobe-Decaying Orders of OCG Codes .......... 26.4 Sidelobe-Decaying Orders of Polyphase Codes .......... 31 Numerical Results and Applications .......... 37.1 Fractional Out-of-Band Power Characteristics .......... 37.2 Code Assignment With a Fixed Spreading Factor .......... 40.3 OVSF Code Tree Management .......... 44 Conclusion .......... 49ibliography .......... 51ppendix .......... 5
An antinociceptive role for substance P in acid-induced chronic muscle pain
No full text[[sponsorship]]生物醫學科學研究所[[note]]已出版;[SCI];有審查制度;具代表性[[note]]http://gateway.isiknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=Drexel&SrcApp=hagerty_opac&KeyRecord=0027-8424&DestApp=JCR&RQ=IF_CAT_BOXPLOT[[note]]http://gateway.isiknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=RID&SrcApp=RID&DestLinkType=FullRecord&DestApp=ALL_WOS&KeyUT=00029895020000
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