Le thème général de cette thèse est relié à la performance des industries laitière et avicole canadienne sous la pression de libéralisation du commerce agroalimentaire. Le premier essai analyse la libéralisation des échanges dans l'industrie laitière canadienne à partir d'un modèle d'équilibre spatial. Le modèle théorique maximise une fonction objective, qui est définie comme étant la somme des surplus des intervenants dans le secteur laitier canadien, sous les contraintes d'allocation des ressources. Quatre scénarios de libéralisation sont étudiés. Les résultats dépendent fortement de la relation entre amélioration de l'accès au marché et quota de mise en marché (QMM). Les résultats associés à un compromis potentiel dans le cadre du Cycle de Doha indiquent que la libéralisation des échanges entraînerait un gain net pour l'industrie laitière canadienne. Le deuxième essai étend l'analyse précédente en introduisant une structure oligopolistique sur les marchés des produits laitiers et un monopole discriminant sur le marché du lait à la ferme. Deux scénarios de libéralisation sont étudiés et correspondent aux deux limites du spectre des présentes négociations dans le cadre du cycle de Doha. Les résultats montrent que le gain total de l'industrie laitière suite à la libéralisation pourrait atteindre 1028,6 millions$. Le troisième essai évalue les réformes dans la tarification du poulet vivant au Canada en utilisant un modèle linéaire-quadratique des inventaires. En 2003, une nouvelle tarification du poulet vivant a été introduite au Canada pour remplacer le processus de négociation entre les producteurs et les entreprises de transformation. Le modèle dérive les équations de production et des ventes des transformateurs. Ces dernières sont utilisées pour estimer les paramètres structuraux liés aux coûts de production, d'inventaire et d'ajustement dans le secteur de la transformation. Les paramètres estimés sont par la suite utilisés pour simuler les impacts de la nouvelle tarification sur la décision de production dans l'industrie et sur le bien-être des producteurs. Les simulations montrent que la nouvelle tarification avantage les producteurs dans la mesure où leurs préférences impliquent une aversion significative au risque.

Various molecular pathways in the brain shape our understanding of good and bad, as well as our motivation to seek and avoid such stimuli. This work evolves around how systemic inflammation causes aversion; and why general unpleasant states such as sickness, stress, pain and nausea are encoded by our brain as undesirable; and contrary to these questions, how drugs of abuse can subjugate the motivational neurocircuitry of the brain. A common feature of these various disease states is involvement of the motivational neurocircuitry - from mesolimbic to striatonigral pathways. Having an intact motivational system is what helps us evade negative outcomes and approach natural positive reinforcers, which is essential for our survival. During disease-states the motivational neurocircuitry may be overthrown by the molecular mechanisms that originally were meant to aid us. In study I, to investigate how inflammation is perceived as aversive, we used a behavioral test based on Pavlovian place conditioning with the aversive inflammatory stimulus E. coli lipopolysaccharide (LPS). Using a combination of cell-type specific gene deletions, pharmacology, and chemogenetics, we uncovered that systemic inflammation triggered aversion by MyD88-dependent activation of the brain endothelium followed by COX1-mediated cerebral prostaglandin E2 (PGE2) synthesis. Moreover, we showed that inflammation-induced PGE2 targeted EP1 receptors on striatal dopamine D1 receptor–expressing neurons and that this signaling sequence induced aversion through GABA-mediated inhibition of dopaminergic cells. Finally, inflammation-induced aversion was not an indirect consequence of fever or anorexia but constituted an independent inflammatory symptom triggered by a unique molecular mechanism. Collectively, these findings demonstrate that PGE2-mediated modulation of the dopaminergic circuitry is a key mechanism underlying inflammation-induced aversion. In study II, we investigate the role of peripheral IFN-γ in LPS induced conditioned place aversion by employing a strategy based on global and cell-type specific gene deletions, combined with measures of gene-expression. LPS induced IFN-ɣ expression in the blood, and deletion of IFN-ɣ or its receptor prevented conditioned place aversion (CPA) to LPS. LPS increased the expression of chemokine Cxcl10 in the striatum of normal mice. This induction was absent in mice lacking IFN-ɣ receptors or Myd88 in blood brain barrier endothelial cells. Furthermore, inflammation-induced aversion was blocked in mice lacking Cxcl10 or its receptor Cxcr3. Finally, mice with a selective deletion of the IFN-ɣ receptor in brain endothelial cells did not develop inflammation-induced aversion. Collectively, these findings demonstrate that circulating IFN-ɣ binding to receptors on brain endothelial cells which induces Cxcl10, is a central link in the signaling chain eliciting inflammation-induced aversion. In study III, we explored the role of melanocortin 4 receptors (MC4Rs) in aversive processing using genetically modified mice in CPA to various stimuli. In normal mice, robust aversions were induced by systemic inflammation, nausea, pain and kappa opioid receptor-induced dysphoria. In sharp contrast, mice lacking MC4Rs displayed preference towards most of the aversive stimuli, but were indifferent to pain. The unusual flip from aversion to reward in mice lacking MC4Rs was dopamine-dependent and associated with a change from decreased to increased activity of the dopamine system. The responses to aversive stimuli were normalized when MC4Rs were re-expressed on dopamine D1 receptor-expressing cells or in the striatum of mice otherwise lacking MC4Rs. Furthermore, activation of arcuate nucleus proopiomelanocortin neurons projecting to the ventral striatum increased the activity of striatal neurons in a MC4R-dependent manner and elicited aversion. Our findings demonstrate that melanocortin signaling through striatal MC4Rs is critical for assigning negative motivational valence to harmful stimuli. The neurotransmitter acetylcholine has been implied in reward learning and drug addiction. However, the role of cholinergic receptor subtypes in such processes remains elusive. In study IV we investigated the function of muscarinic M4Rs on dopamine D1R expressing neurons and acetylcholinergic neurons, using transgenic mice in various reward-enforced behaviors and in a “waiting”-impulsivity test. Mice lacking M4-receptors from D1-receptor expressing neurons exhibited an escalated reward seeking phenotype towards cocaine and natural reward, in Pavlovian conditioning and an operant self-administration task, respectively. In addition, the M4-D1RCre mice showed impaired waiting impulsivity in the 5-choice-serial-reaction-time-task. On the contrary, mice without M4Rs in acetylcholinergic neurons were unable to learn positive reinforcement to natural reward and cocaine, in an operant runway paradigm and in Pavlovian conditioning.  Immediate early gene expression mirrored the behavioral findings arising from M4R-D1R knockout, as cocaine induced cFos and FosB was significantly increased in the forebrain of M4-D1RCre mice, whereas it remained normal in the M4R-ChatCre mice. Our study illustrates that muscarinic M4Rs on specific neural populations, either cholinergic or D1R-expressing, are pivotal for learning processes related to both natural reward and drugs of abuse, with opposing functionality.

已實現投資報酬率與無風險利率之差、被稱為超額報酬，而股票的預期報酬率超過無風險利率的部份則為股票風險溢酬，是許多資產評價模型的重要依據，例如資本資產定價模型。有不同的理論架構解釋說明風險溢酬值，例如；股票風險溢酬的迷思、短期損失的憎惡、生還存留因素和回歸與偏離平均值等等。 研究台灣股市的超額報酬與股票風險溢酬，有助投資大眾和企業理性面對股市的預期報酬和風險，對台股才有合理的期望報酬值。分析1967年迄2003年的台灣金融市場，計算過去37年長期的幾何平均年報酬率，以臺灣證券交易所發行量加權股價指數為台股市場報酬率，已實現台股實質年報酬率為6.71%。無風險報酬率使用第一銀行的一年期定期存款利率，實質台幣存款年利率為3.07%，消費者物價指數年增率則為4.80%。以年資料計算的台股實質超額報酬，算術和幾何值分別為12.48%和3.63%(年)，計算月資料算術平均和幾何平均值分別為0.77%和0.25%(月)。過去37年長期的台股超額報酬現象未較歐美市場的情況更加明顯，也比一般市場的預期報酬率低。 因資料取得的限制、台股的理論超額報酬方面，1991年迄2003年的近十三年來，經固定股利成長模式和盈餘成長模式的兩種計算方式，台股的實質超額報酬分別為 0.6%和-4.3%，此時期台股的投資報酬率比起台幣存款並不突出、且是低超額報酬。同期的已實現的實質超額報酬值；算術平均1.69%和幾何平均-3.35%。評估目前台股風險溢酬，將十分接近過去37年長期歷史資料得到的超額報酬數值，算術年均值為12.48%(年)和0.77%(月)，幾何平均分別為3.63%(年)和0.25%(月)，低風險溢酬是當前台灣股票市場的一般現象。 / The difference between the observed historical investment return and the risk-free interest rate is the excess return. The equity risk premium, ERP is the expected rate of return on the aggregate stock market in excess of the rate of risk-free security. ERP is one of important factor of many asset-pricing models, including Capital Asset Pricing Model, CAPM. There were many theories and factors to explain the equity risk premium; equity premium puzzle, myopic loss aversion, survivorship bias, mean reversion & aversion and etc. Studying the value of Taiwan equity excess return and risk premium is fundamental for investors and institutions evaluating the expected market investment return and risk. Analyzing the data from year 1967 to 2003 for thirty-seven years long holding period, Taiwan Stock Exchange Capitalization Weighted Stock Index as Taiwan stock market return, the realized real return was 6.71%. One-year bank time deposit rate as NT dollars risk-free asset rate and real interest rate was 3.07% and consumer price index, CPI annual growth rate was 4.80%. The historical real yearly excess return was 12.45% for arithmetic mean and 3.63% geometric mean; the historical real monthly excess return was 0.77% for arithmetic mean and 0.25% geometric mean. Taiwan realized equity excess returns were not higher than the returns in the developed countries and were also lower than the market's expectation. Due to the limits of available data, the theoretical equity excess returns that were calculated on two theoretical models; Constant Growth Dividend Discount Model (dividend yield model) and earnings yield model were 0.6% and -4.3% from year 1991 to year 2003. Comparing the same period of historical realized excess returns of 1.69% for arithmetic mean and -3.35% geometric mean, Taiwan stock market returns were not spectacular. The current equity risk premium of Taiwan stock market is low and should be near the level of the long historical realized equity excess return.