No description available.

No description available.

No description available.

Du, Juan. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 110-134). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

孫黎. / 本論文於1997年10月呈交. / 論文(碩士) -- 香港中文大學硏究院工商管理學部, 1998. / 參考文獻: leaves 138-147. / 中英文摘要. / Sun Li. / 摘要 --- p.1 / Chapter 壹 --- 緖言 --- p.3 / Chapter 貳 --- 文獻評論 --- p.8 / Chapter 一、 --- 循環論 --- p.8 / Chapter 二、 --- 衝突論 --- p.11 / Chapter 三、 --- 生態論 --- p.12 / Chapter 四、 --- 制度論 --- p.13 / Chapter 參 --- 交易成本理論框架 --- p.14 / Chapter 一、 --- 市場學中的交易成本理論 --- p.14 / Chapter 二、 --- 甚麼是交易成本 --- p.16 / Chapter 三、 --- 交易成本理論的假設 --- p.18 / Chapter 四、 --- 決定治理結構的因素 --- p.20 / Chapter 五、 --- 渠道治理結構的形式 --- p.23 / Chapter 肆 --- 制度演化分析框架 --- p.32 / Chapter 一、 --- 甚麼是市場 --- p.32 / Chapter 二、 --- 制度的內涵 --- p.33 / Chapter 三、 --- 制度與渠道演變的軌跡 --- p.35 / Chapter 四、 --- 制度演變與學習適應 --- p.40 / Chapter 五、 --- 制度演變的模型 --- p.43 / Chapter 六、 --- 作爲適應性機制的渠道 --- p.46 / Chapter 伍 --- 中國市場渠道分析框架 --- p.50 / Chapter 一、 --- 美國市場渠道的變革史 --- p.51 / Chapter 二、 --- 中國渠道結構的演變 --- p.52 / Chapter 陸 --- 實証分析 --- p.72 / Chapter 一、 --- 機會主義與制度分析 --- p.73 / Chapter 二、 --- 層級體系的分權化演變 --- p.88 / Chapter 三、 --- 計算機市場渠道分析 --- p.97 / Chapter 四、 --- 批發市場的興起 --- p.107 / Chapter 五、 --- 國有商業企業的發展 --- p.116 / Chapter 染 --- 結論與建議 --- p.130 / Chapter 一、 --- 總結 --- p.130 / Chapter 二、 --- 理論應用與發展 --- p.131 / Chapter 三、 --- 政策與策略管理的建議 --- p.133 / Chapter 四、 --- 硏究限制 --- p.136 / Chapter 捌 --- 參考文獻 --- p.138 / 附錄中英專有名詞翻譯對照 --- p.148

Kwan Hiu Yee. / "June 2006." / 2+ in the title is superscript. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2006. / Includes bibliographical references (p. 131-150). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstracts in English and Chinese.

Thesis (Ph. D.)--Ohio State University, 2006. / Title from first page of PDF file. Includes bibliographical references (p. 213-226).

Neuropathic pain is a complex clinical syndrome characterized by increased sensitivity to thermal and/or mechanical stimuli that may or may not be accompanied by the phenomenon of spontaneous or aberrant pain sensations. <p>Over the past decade, the mechanisms underlying the behavioral manifestations of inflammatory neuropathic pain have become more clearly elucidated. These include the involvement of: 1) transient receptor potential vanilloid receptor 1 (TRPV1) in the generation of thermal hyperalgesia; 2) acid sensing ion channel 3 (ASIC3) in some aspects of the development/maintenance of mechanical hypersensitivity; 3) the tetrodotoxin resistant sodium channels Nav1.8 and Nav1.9 in both hyperalgesia and spontaneous pain; and 4) activation of the MAP Kinases p38 and ERK1/2 in the regulation of expression of the aforementioned molecules.<p>Interestingly, it is the pro-inflammatory neurotrophin nerve growth factor (NGF) that is the common link between all of these mediators of neuropathic pain. Increased availability of NGF under conditions of inflammation has been shown to drive increased expression/upregulation of TRPV1, ASIC3, Nav1.8 and Nav1.9, as well as phospho-p38 and phospho-ERK1/2.<p>Evidence presented here continues to support a role for neurotrophin-3 (NT-3) in antagonizing the effects of increased NGF on trkA signaling, neuropathic pain behaviors and some of the molecules associated with the generation of such behaviors.<p>More specifically, the work culminating in this thesis demonstrates a novel role for NT-3 in negative modulation of TRPV1, ASIC3, Nav1.8 and Nav1.9, as well as phospho-p38 expression in response to the chronic constriction injury model of neuropathic pain. Finally, initial insights into how this negative regulation of these nociceptive markers might occur is elucidated in studies demonstrating that NT-3 differentially affects levels of the key signaling molecule phospho-ERK in trkA-positive versus trkC-positive neurons in naïve dorsal root ganglia (DRG).

This thesis looks at the problem of designing a coding strategy for interference channels with rate-limited transmitter cooperation. We first consider a simple communication model in which the classic two-user Gaussian interference channel is augmented by rate-limited conferencing links between the transmitters. The main contribution is a partial zero-forcing precoding strategy based on a shared-private rate splitting scheme at the transmitter, in which each transmitter communicates part of its message to the other transmitter, and subsequently partially pre-subtracts the interfering signal using a zero-forcing precoder. We extend the proposed strategy to a class of multiuser interference channels, and outline a distributed algorithm to compute the precoder coefficients. The partial zero-forcing precoding strategy is shown to be particularly effective in certain high SNR/INR regimes, and simulation results for a multicell system highlight the cooperation gain due to the proposed strategy.

This thesis looks at the problem of designing a coding strategy for interference channels with rate-limited transmitter cooperation. We first consider a simple communication model in which the classic two-user Gaussian interference channel is augmented by rate-limited conferencing links between the transmitters. The main contribution is a partial zero-forcing precoding strategy based on a shared-private rate splitting scheme at the transmitter, in which each transmitter communicates part of its message to the other transmitter, and subsequently partially pre-subtracts the interfering signal using a zero-forcing precoder. We extend the proposed strategy to a class of multiuser interference channels, and outline a distributed algorithm to compute the precoder coefficients. The partial zero-forcing precoding strategy is shown to be particularly effective in certain high SNR/INR regimes, and simulation results for a multicell system highlight the cooperation gain due to the proposed strategy.