Although the U.S. houses five percent of the world's population, we have the highest incarceration numbers on earth, with more than two million people behind bars. The penal institution has neither deterred crime nor effectively rehabilitated the criminal. Prisons are overcrowded, understaffed, and have funding issues, yet the system prevails. If a business was spending billions of dollars, yet failing at its stated mission, investors would pull their funds and the business would fold. For a massive failing system to persist uninterrupted it must be fulfilling some need. What prison does is punish millions of bodies. Since this is what the system succeeds at, this is the need it must be fulfilling. I argue that this need is exacerbated by institutions that promote body aversion and activate in us a latent tendency for the flawed sinful body to be chastised. Reformists have made efforts at changing the system, and former political prisoner, Angela Davis, has called for the system to be abolished. I argue that before reform or abolition can be successful, there must be a change in perception of the human body. This study delves into how our collective need to punish bodies is illustrated in ancient rituals of sacrifice, which evolved into torture in the public square, before the penal institution took root. Myriad institutions take their toll on our perceptions of the body, and corporations exploit prisoners for free labor in a land where slavery is supposedly outlawed.

No description available.

La thèse étudie l'impact de l'excès de confiance des banquiers sur le jugement, l'évaluation et la décision d'investissement (de crédit). Dans le but d'approfondir les recherches opposant experts et novices, nous avons répliqué notre étude sur des étudiants. Aux côtés des mesures et des analyses de l'excès de confiance, nous avons étudié l'attitude face au risque.Une étude qualitative a d'abord été menée, par entretiens semi-directifs avec des chargés d'affaires professionnels et directeurs d'agence. Nous avons observé des marques de surconfiance grâce à l'analyse lexicale quantitative et qualitative mais aucun lien de type cause à effet avec la décision n'a pu être établi.Ce travail a été complété par une expérimentation mesurant les différentes formes des concepts comportementaux et testant leurs impacts lors de jugement, évaluation et investissement dans des entreprises. Les résultats montrent un excès de confiance et une aversion au risque généralisés, sans différences significatives à ce stade entre les deux populations, mais de fortes disparités dans le processus d'étude des investissements et dans la prise de décision. Les étudiants ont tendance à former une impression immédiate sur les entreprises puis ils réviseront ce jugement lors de l'investissement. Les banquiers sont influencés dans leur choix d'investissement par les conclusions issues de la phase d'évaluation et leur niveau d'excès de confiance. / This work analyzes bankers' overconfidence in the granting process. Empirical and experimental work provides evidences that experts' judgment and students' judgment could differ. We have replicated our study on students and measure overconfidence and attitudes toward risk.In a first qualitative study, we analyze the bankers' overconfidence thanks to the interviews we made. We highlight their overconfidence; however we could not find any link such as cause/effect with their decisions.We extend our work with an experimentation with bankers and students. After measuring different forms of overconfidence and attitudes toward risk, we have tested the impact of overconfidence on a assets' study. Each participant had to judge, evaluate and decide to invest in different assets. The first results show that no differences can be made between bankers and students on the overconfidence and attitudes toward risk. Nevertheless, in the assets' study, students tend to form a global preference and revise their judgment during their investment (intervention of the risk aversion). On the opposite, bankers are influenced by the overconfidence bias and the evaluation stage when they form their investment choices.

Le système de l’immunité innée cérébrale module le fonctionnement du cerveau et les processus comportementaux tout au long de la vie d'un individu. Parmi les différents protagonistes de ce système de l'immunité innée cérébrale, les cellules gliales jouent un rôle majeur notamment en régulant la synthèse de facteurs inflammatoires tels que les cytokines. Ces dernières, outre leur rôle dans la coordination de l'action des différents partenaires cellulaires de ce système, modifient l'activité neuronale. Lors d'un épisode inflammatoire, le système de l'immunité innée s'active et l'ensemble des signaux mis en place par les processus immunitaires est regroupé sous le terme de neuroinflammation. Plus particulièrement, les cytokines proinflammatoires et l’ATP libérés dans ce cadre ont été décrits comme étant capables de moduler la plasticité synaptique d'une part et les capacités d’apprentissages et de mémorisation d'autre part. Cependant, la compréhension de l’impact d’un épisode inflammatoire sur le système nerveux central et les capacités d’apprentissage n’est pas totale. Une cible potentielle de ces facteurs est le système de neurotransmission glutamatergique. En effet, les facteurs proinflammatoires peuvent augmenter ou diminuer l’expression ou l’activité de certaines sous-unités des récepteurs glutamatergiques. Mon objectif a été de déterminer dans quelle mesure la transmission glutamatergique est altérée en condition neuroinflammatoire et comment cela pouvait induire des altérations des capacités d’apprentissage chez le rongeur. Pour cela nous avons choisi comme tâche comportementale l’aversion gustative conditionnée, dont les mécanismes moléculaires nécessaire à sa mise en place sont connus et reposent sur la transmission glutamatergique dans une structure corticale particulière chez les rongeurs: le cortex insulaire. Notre étude visait à déterminer les mécanismes cellulaires et moléculaires par lesquels une inflammation localisée à ce cortex peut induire des modifications comportementales et biochimiques. Nous avons pu montrer que l’infusion de lipopolysaccharide, un puissant agent inflammatoire, dans le cortex insulaire induisait une augmentation de l'aversion conditionnée. Ceci était corrélé à une augmentation d’expression des récepteurs AMPA au glutamate dans cette structure, plus particulièrement dans le compartiment synaptique. Nous avons également pu montrer que l’infusion de LPS dans le cortex insulaire induisait la synthèse et la libération de cytokines proinflammatoires localement, sans stimuler le système de l’immunité périphérique. Même si ces cytokines sont connues comme étant des agents modulateurs de la neurotransmission glutamatergique, leur infusion dans le cortex insulaire n’a pas reproduit dans notre cas les effets de l’infusion du LPS. Par contre, nous avons montré que l’ATP était impliqué dans les effets du LPS sur l’apprentissage aversif, puisque le blocage des récepteurs purinergiques dans le cortex insulaire a permis de reverser les effets du LPS sur l’acquisition de l’aversion gustative. En conclusion, nos résultats suggèrent qu'une inflammation localisée dans le cortex insulaire conduit à la libération et à l'action d’ATP sur les cellules gliales et/ou neuronales, aboutissant à une hausse de l’acquisition de l’aversion gustative conditionnée. / The cerebral innate immune system is activated under pathophysiological conditions and can consequently modulate brain functioning and cognitive processes. This modulation is exerted by signals produced by immune-like processes grouped under the term of neuroinflammation and involving neuro-glial communication within the brain. In particular, proinflammatory cytokines and ATP, all produced during this immune system activation have been directly linked to modulation of synaptic plasticity and/or learning and memory functions in animals models. However, the cellular mechanisms by which neuroinflammation modulates neural plasticity and cognitive processes are still unclear. One candidate is the glutamatergic system. Indeed, pro-inflammatory factors can increase or decrease glutamatergic receptors expression and/or activity. Our study was dedicated at deciphering to what extent glutamatergic transmission is altered under neuroinflammation and how this may lead to learning and memory alteration. To this aim, we used the conditioned taste aversion, a task highly dependent on glutamatergic transmission into the insular cortex. Indeed, blockade of NMDA or AMPA receptors in this cortical area before acquisition greatly impairs conditioned taste aversion. The aim of our study was thus to investigate the behavioral and cellular impact of an inflammation restricted to the insular cortex on glutamatergic receptors expression and CTA memory formation. Here we show that a cortical inflammation, induced by LPS infusion into the insular cortex, prior to CTA acquisition enhances the aversion strength presumably through LPS-induced increase of glutamatergic AMPA, but not NMDA, receptor expression/trafficking at the insular synapses. Moreover, we show that ATP release, but not pro-inflammatory cytokines, is responsible for LPS-induced CTA enhancement. In conclusion we propose that inflammation restricted to the insular cortex enhances CTA acquisition through an ATP-dependent mechanism presumably involving an increase of glutamatergic AMPA receptor expression at the neuronal synapses.

Kahneman and Tversky (1979) first demonstrated that when individuals decide whether or not to accept a gamble, potential losses receive more weight than possible gains in the decision. This phenomenon is referred to as loss aversion. We investigated how loss aversion in risky financial decisions is influenced by sudden changes to wealth, employing both behavioral and neurobiological measures. We implemented an fMRI experimental paradigm, based on that employed by Tom et al. (2007). There are two treatments, called RANDOM and CONTINGENT. In RANDOM, the baseline setting, the changes to wealth, referred to as wealth shocks in economics, are independent of the actual choices participants make. Under CONTINGENT, we induce the belief that the changes in income are a consequence of subjects' own decisions. The magnitudes and sequence of the shocks to wealth are identical between the CONTINGENT and RANDOM treatments. We investigated whether more loss aversion existed in one treatment than another. The behavioral results showed significantly greater loss aversion in CONTINGENT compared to RANDOM after a negative wealth shock. No differences were observed in the response to positive shocks. The fMRI results revealed a neural loss aversion network, comprising the bilateral striatum, amygdala and dorsal anterior cingulate cortex that was common to the CONTINGENT and RANDOM tasks. However, the ventral prefrontal cortex, primary somatosensory cortex and superior occipital cortex, showed greater activation in response to a negative change in wealth due to individual's own decisions than when the change was exogenous. These results indicate that striatum activation correlates with loss aversion independently of the source of the shock, and that the ventral prefrontal cortex (vPFC) codes the experimental manipulation of agency in one's actions influencing loss aversion.

Cette thèse porte sur les conséquences de l’aversion à l’ambiguïté dans des contextes dynamiques en économie. En particulier, elle s’intéresse aux conséquences de l’aversion à l’ambiguïté dans les décisions d’investissement irréversibles, ainsi que dans un problème d’aléa moral dynamique, modélisé en temps continu. Le premier chapitre propose une revue de la littérature traitant de l’aversion à l’ambiguïté en contexte dynamique. Nous y passons en revue les modèles existants ainsi que leurs applications en économie et en finance. Le second chapitre s’intéresse aux décisions d’investissement irréversible d’un monopole et de firmes en compétition parfaite, en présence d’ambiguïté à propos de la volatilité du processus stochastique gouvernant la demande. Cette notion particulière d’ambiguïté nécessite de mobiliser les outils récents de la théorie des espérances non linéaires. On y montre qu’en présence d’aversion à l’ambiguïté, la stratégie optimale d’un monopole implique d’investir plus rapidement que dans un marché en concurrence parfaite. Le troisième chapitre s’appuie sur les résultats du second chapitre pour traiter le cas d’une concurrence imparfaite entre deux firmes. Le quatrième chapitre traite d’un problème d’aléa moral dynamique en temps continu et on y introduit la notion plus classique d’ambiguïté à propos de la dérive du processus gouvernant l’incertitude. On y montre que sous certaines restrictions semblables au cas standard, le contrat optimal est linéaire par rapport à la production finale. Ce résultat nous permet ensuite de discuter l’effet de l’aversion à l’ambiguïté sur les incitations et l’utilisation de l’information. / This thesis focuses on the consequences of ambiguity aversion in dynamic contexts in economics. In particular, we focus on the consequences of ambiguity aversion in irreversible investment problems, and in dynamic moral hazard problems in continuous-time. The first chapter reviews the literature on ambiguity in dynamic contexts, and reviews existing models as well as their applications in economics and finance. The second chapter deals with irreversible investment in the monopoly case and under perfect competition, under ambiguous volatility. The notion of ambiguous volatility requires the use of recent tools in non linear expectation theory. We show that the optimal entry strategy of a monopoly under ambiguous volatility implies investing sooner than the perfectly competitive equilibrium under volatility ambiguity. The third chapter builds on the results of the second chapter and treats a special case of imperfect competition. The last chapter deals with a dynamic principal-agent problem under moral in continuous-time, in which agents perceive ambiguity about the drift of the relevant process. We show that under certain conditions, the optimal contract is linear in final output. We then use this result to discuss the effect of ambiguity aversion on the incentive power of the optimal contract and the informativeness principle.

Dans le cadre de ce mémoire, nous proposons d’étudier l’effet de deux biais sur les investisseurs aux marchés financiers. Plus particulièrement, nous tentons de déterminer si, conformément à la théorie, l’aversion à la perte entraîne des préférences pour de longs horizons d’investissement et de faibles niveaux de rétroaction, et si l’aversion à l’ambiguïté engendre pour sa part des préférences contraires. Les données expérimentales montrent que l’effet de l’aversion à la perte sur les préférences est minime. Toutefois, l’aversion à l’ambiguïté aurait un effet manifeste sur celles-ci, menant les participants à préférer de courts horizons d’investissement, ainsi qu’une grande fréquence de rétroaction. Ces préférences peuvent vraisemblablement être expliquées par le désir des participants de mettre à jour plus rapidement leurs anticipations afin de sortir du contexte d’ambiguïté dans lequel ils se trouvent.

Theoretical models predict that ambiguity is an asset pricing factor in addition to risk, however few of them have been tested in the real market. This thesis tests one of the hypotheses that, investors’ propensity to invest in stocks is reduced when ambiguity in the marketplace increases. The hypothesis is tested by using equity fund flows and households’ equity holding as measurements of the market participation, and using dispersion in analysts’ forecasts about aggregate returns as measurement of ambiguity. The results confirm this hypothesis, since the increases in ambiguity are significantly and negatively related to equity fund flows, as well as the likelihood that the average household invests in equities. Moreover, the results also find that the fund flows in non-dividend paying stocks are more sensitive to the changes in ambiguity, and investors transfer capital from the equity market into more liquid asset classes during high-ambiguity periods. In addition, this thesis also tests whether there is heterogeneity in individuals’ ambiguity aversion, and examines the psychological roots of ambiguity aversion. FNE theory explains ambiguity aversion as the result of fearing negative evaluation from others. It predicts that married households are more ambiguity averse; while households with higher income and education, or households that are more mature, are less ambiguity averse. On the other hand, self-evaluation theory explains ambiguity aversion as the result of minimizing anticipated regret. It predicts that households that are more optimistic, or have less income, are less ambiguity averse; while households that have negative market experience, or have higher income, are more ambiguity averse. The results show that married households, or households with high income / negative market experience, are more ambiguity averse; and households that are more optimistic / more mature, are less ambiguity averse. Therefore, both theories have successful predictions, suggesting that the ambiguity aversion is the combined result of the two motivations.

The present study was designed to evaluate the efficacy of utilizing an avoidance conditioning paradigm in EMG biofeedback training and to compare this method to the standard biofeedback training paradigm. Frontalis EMG levels of 20 college students were monitored during non-stress and stress conditions. Half then received standard EMG biofeedback training. The other half received biofeedback with contingent aversive stimulation. Both groups received training to a relaxation criterion of 3 microvolts for 100 seconds or, for a maximum of two 20 minute sessions. Subjects were then monitored again during non-stress and stress conditions. Both groups obtained significant EMG reductions due to training with no significant differences between them. Standard biofeedback training required less time for subjects to achieve the relaxation criterion than did biofeedback with a shock-avoidance contingency. Possible applications of avoidance contingent biofeedback were suggested.

Background: Parkinson's disease (PD) is a chronic, progressive, neurodegenerative disorder with currently no known cure. PD has a significant impact on quality of life of the patients, as well as, the caregivers and family members. It is the second most common cause of chronic neurological disability in US and Europe. According to National Parkinson's Foundation, there are almost 1 million patients in the Unites States and 50,000 to 60,000 new cases of PD are diagnosed each year. The total number of cases of PD is predicted to double by 2030. The annual cost associated with this disease is estimated to be $10.8 billion in the United States, including the cost of treatment and the cost of the disability. Although it is primarily thought of as a movement-disorder and is clinically diagnosed based on motor symptoms, non-motor symptoms such as cognitive and emotional deficits are thought to precede the clinical diagnosis by almost 20 years. By the time of clinical diagnosis, there is 80% loss in the dopamine content in the striatum and 50% degeneration of the substantia nigra dopamine cells. The research presented in this thesis was an attempt to develop an animal model of PD in its pre-motor stages. Such a model would allow us to develop pre-clinical markers for PD, and facilitate the development and testing of potential treatment strategies for the non-motor symptoms of the disorder. Specific Aims: There were five specific aims for this research: * The first specific aim dealt with development of a rat model of PD with slow, progressive onset of motor deficits, determination of timeline for future studies, and quantification the dopamine depletion in this model at a pre-motor stage. * The second and the third specific aims focused on testing for emotional (aversion) deficits and cognitive (executive functioning) deficits in this rat model at the 3 week timepoint determined during specific aim 1. * The fourth specific aim was to determine the brain network changes associated with the behavioral changes observed our rat model using resting state connectivity as a measure. * The fifth and the final specific aim was to test sodium butyrate, a drug from the histone deacetylase inhibitor family, as a potential treatment option for cognitive deficits in PD. Results: The 6-hydroxy dopamine based stepwise striatal lesion model of pre-motor PD, developed during this research, exhibits delayed onset of Parkinsonian gait like symptoms by week 4 after the lesions. At 3 weeks post lesion (3WKPD), the rats exhibit 27% reduction in striatal dopamine and 23%reduction in substantia nigra dopamine cells, with lack of any apparent motor deficits. The 3WKPD rats also exhibited changes in aversion. The fMRI study with the aversive scent pointed towards possible amygdala dysfunction sub-serving the aversion deficits. The executive function deficits tested using a rat analog of the Wisconsin card sorting test, divulged an extra-dimensional set shifting deficit in the 3WKPD rats similar to those reported in PD patients. The resting state connectivity study indicated significant changes in the 3WKPD rats compared to age matched controls. We observed increased overall connectivity of the motor cortex and increased CPu connectivity with prefrontal cortex, cingulate cortex, and hypothalamus in the 3WKPD rats compared to the controls. These observations parallel the observations in unmedicated early-stage PD patients. We also observed negative correlation between amygdala and prefrontal cortex as reported in humans. This negative correlation was lost in 3WKPD rats. Sodium butyrate treatment, tested in the cognitive deficit study, was able to ameliorate the extra-dimensional set shifting deficit observed in this model. This treatment also improved the attentional set formation. Conclusion: Taken together, our observations indicate that, the model of pre-motor stage PD developed during this research is a very high face validity rat model of late Braak stage 2 or early Braak stage 3 PD. Sodium butyrate was able to alleviate the cognitive deficits observed in our rat model. Hence, along with the prior reports of anti-depressant and neuroprotective effects of this drug, our results point towards a possible treatment strategy for the non-motor deficits of PD.