Pendrina é um transportador de ânions inserido na membrana apical de células foliculares. Estudos subseqüentes demonstraram que a proteína pode mediar o efluxo apical do iodeto nos tirócitos. Sendo o iodo fundamental para a síntese de hormônios tiroidianos foi objetivo deste estudo avaliar o efeito da administração aguda de iodo na expressão do mRNA da proteína pendrina, em curtos períodos de tempo (30min à 24h).Ratos Wistar foram divididos em: controle e iodo, que receberam injeção de salina ou NaI, sendo decapitados após 30, 1 e 24h dessa administração.O RNA da tiróide foi extraído para a análise da expressão do mRNA da Pendrina por Real Time PCR e Northern Blot. Para o estudo in vitro utilizou-se a linhagem celular de tiróide de rato PCCl3, que foi tratada ou não com 10-3M de NaI. As células permaneceram sob tratamento por 30´, 1 e 24h, quando então o RNA foi extraído para análise da expressão por Real Time PCR.Houve aumento significativo do mRNA da Pendrina em todos os grupos, indicando que mecanismos foram desencadeados visando o efluxo do iodeto da célula. / Pendrin is a chloride/iodide exchange located at the apical membrane of thyrocytes. Mutations in its gene lead to a defect in iodide organification. This suggested that pendrin could function as an apical iodide transporter in this cells. Since iodine is essential for thyroid hormone synthesis, this study attempted to investigate that possibility by evaluating whether the acute iodide administration, from 30min up to 24h, could regulate the Pendrin mRNA expression. Rats received NaI or saline, and were sacrificed 30´, 1 and 24h later.Thyroid total RNA was extracted and Pendrin mRNA content was evaluated by Northern Blotting and Real-Time PCR. For in vitro study,PCCl3 rat thyroid cells were cultured and treated or no with 103M NaI. After 30´, 1 and 24h, the cells were harvested and total RNA was extracted. The mRNA content was evaluated by Real-Time PCR. The mRNA increased in all groups of study, indicating that excess of iodide leads to an activation of Pendrin gene transcription and as consequence increased efflux of this element.

Pendrina é um transportador de iodo na tiróide, codificada pelo gene PDS.Sabendo-se que o iodo é fundamental para a síntese de T3 e T4 foi objetivo avaliar o efeito do iodo na expressão gênica, atividade e promotor da pendrina. Foram utilizados ratos Wistar, que receberam injeção de salina ou 2mg de NaI. Após 30, 1, 24 e 48h as tiróides foram removidas para análise do mRNA e proteína, por PCR em Tempo Real e Western Blot. Ainda, utilizou-se celulas PCCl3, que foram tratadas ou não com 10-3M de NaI. Após 30, 1, 24 e 48h o RNA/proteína foram isolados.Determinou-se o efluxo pela medição do125I presente no meio de cultura. Para analisar a atividade do promotor, ele foi inserido no vetor pGL3-básico.Nossos resultados mostram que houve aumento do mRNA da pendrina em resposta ao iodo em todos os tempos estudados, porém não houve aumento da atividade promotora.A expressão da proteína pendrina, bem como taxa do efluxo de iodeto, aumentou nos tempos mais longos de tratamento.Esses dados apontam um importante papel de pendrina para o fenômeno de autoregulação da tiróide. / Pendrin is an iodide transporter in thyroid, encoded by the PDS gene. Since iodide is essential for the synthesis of T3 and T4, this study aimed to evaluate the iodine effect on pendrin gene expression and on the activity of its promoter. Male rats received an injection of saline or 2mg of NaI. After 30, 1, 24 and 48h the thyroids were removed for mRNA and protein analysis by Real Time PCR and Western Blot. Moreover, PCCl3 cells were treated or not with 10-3M NaI. After 30, 1, 24 and 48h the RNA/protein were isolated. The efflux was determined by measure of 125I in the culture medium. For the promoter analysis, it was inserted in pGL3-basic plasmid. The results indicated that the pendrin mRNA amount increased after iodide treatment. However, the promoter activity was unchanged. The protein expression and iodide efflux increased only after 24h of treatment. These data suggest an important role of pendrin for the autoregulation of the thyroid.

Die Dissertation diskutiert die kantische Metaphysik des Geistes anhand der in der Kritik der reinen Vernunft und den aus dem Nachlass veröffentlichten Vorlesungen zur Metaphysik geleisteten Auseinandersetzung mit der rationalen Psychologie seiner Vorgänger, insbesondere Baumgarten und Wolff. Es wird dafür argumentiert, dass Kant die Meinungen seiner Vorgänger nicht uneingeschränkt zurückweist, sondern die Vorstellung der Seele als Substanz in seine Diskussion der Personalität, mentaler Kräfte, der Möglichkeit einer Körper-Seele Interaktion sowie der Willensfreiheit teilweise beibehält. Ein Verdienst dieser Interpretation ist es, die Kontinuität zwischen Kants vorkritischer Position und seiner kritischen Philosophie aufzuzeigen. Darüber hinaus soll aber auch auf eine wichtige Funktion der kantischen Metaphysik des Geistes für seine praktische Philosophie hingewiesen werden. / This dissertation considers Kant’s discussions of the metaphysics of mind in his critical encounter with the rational psychology of Baumgarten, Wolff, and others in the Critique of Pure Reason and his lectures on metaphysics. In contrast with prevailing interpretations, I argue that Kant does not offer a straightforward rejection of his predecessors but that he retains some commitments to the substantial view of the self and modifies others within the framework of transcendental idealism to provide accounts of the nature of personhood, mental powers, the possibility of mind-body interaction, and the possibility of freedom of the will. This interpretation of Kant reveals continuity between Kant’s pre-critical and critical positions on the metaphysics of mind and points forward to a role for aspects of Kant’s metaphysics of mind in his practical philosophy.

Pendrina é um transportador de iodo na tiróide, codificada pelo gene PDS.Sabendo-se que o iodo é fundamental para a síntese de T3 e T4 foi objetivo avaliar o efeito do iodo na expressão gênica, atividade e promotor da pendrina. Foram utilizados ratos Wistar, que receberam injeção de salina ou 2mg de NaI. Após 30, 1, 24 e 48h as tiróides foram removidas para análise do mRNA e proteína, por PCR em Tempo Real e Western Blot. Ainda, utilizou-se celulas PCCl3, que foram tratadas ou não com 10-3M de NaI. Após 30, 1, 24 e 48h o RNA/proteína foram isolados.Determinou-se o efluxo pela medição do125I presente no meio de cultura. Para analisar a atividade do promotor, ele foi inserido no vetor pGL3-básico.Nossos resultados mostram que houve aumento do mRNA da pendrina em resposta ao iodo em todos os tempos estudados, porém não houve aumento da atividade promotora.A expressão da proteína pendrina, bem como taxa do efluxo de iodeto, aumentou nos tempos mais longos de tratamento.Esses dados apontam um importante papel de pendrina para o fenômeno de autoregulação da tiróide. / Pendrin is an iodide transporter in thyroid, encoded by the PDS gene. Since iodide is essential for the synthesis of T3 and T4, this study aimed to evaluate the iodine effect on pendrin gene expression and on the activity of its promoter. Male rats received an injection of saline or 2mg of NaI. After 30, 1, 24 and 48h the thyroids were removed for mRNA and protein analysis by Real Time PCR and Western Blot. Moreover, PCCl3 cells were treated or not with 10-3M NaI. After 30, 1, 24 and 48h the RNA/protein were isolated. The efflux was determined by measure of 125I in the culture medium. For the promoter analysis, it was inserted in pGL3-basic plasmid. The results indicated that the pendrin mRNA amount increased after iodide treatment. However, the promoter activity was unchanged. The protein expression and iodide efflux increased only after 24h of treatment. These data suggest an important role of pendrin for the autoregulation of the thyroid.

Pendrina é um transportador de ânions inserido na membrana apical de células foliculares. Estudos subseqüentes demonstraram que a proteína pode mediar o efluxo apical do iodeto nos tirócitos. Sendo o iodo fundamental para a síntese de hormônios tiroidianos foi objetivo deste estudo avaliar o efeito da administração aguda de iodo na expressão do mRNA da proteína pendrina, em curtos períodos de tempo (30min à 24h).Ratos Wistar foram divididos em: controle e iodo, que receberam injeção de salina ou NaI, sendo decapitados após 30, 1 e 24h dessa administração.O RNA da tiróide foi extraído para a análise da expressão do mRNA da Pendrina por Real Time PCR e Northern Blot. Para o estudo in vitro utilizou-se a linhagem celular de tiróide de rato PCCl3, que foi tratada ou não com 10-3M de NaI. As células permaneceram sob tratamento por 30´, 1 e 24h, quando então o RNA foi extraído para análise da expressão por Real Time PCR.Houve aumento significativo do mRNA da Pendrina em todos os grupos, indicando que mecanismos foram desencadeados visando o efluxo do iodeto da célula. / Pendrin is a chloride/iodide exchange located at the apical membrane of thyrocytes. Mutations in its gene lead to a defect in iodide organification. This suggested that pendrin could function as an apical iodide transporter in this cells. Since iodine is essential for thyroid hormone synthesis, this study attempted to investigate that possibility by evaluating whether the acute iodide administration, from 30min up to 24h, could regulate the Pendrin mRNA expression. Rats received NaI or saline, and were sacrificed 30´, 1 and 24h later.Thyroid total RNA was extracted and Pendrin mRNA content was evaluated by Northern Blotting and Real-Time PCR. For in vitro study,PCCl3 rat thyroid cells were cultured and treated or no with 103M NaI. After 30´, 1 and 24h, the cells were harvested and total RNA was extracted. The mRNA content was evaluated by Real-Time PCR. The mRNA increased in all groups of study, indicating that excess of iodide leads to an activation of Pendrin gene transcription and as consequence increased efflux of this element.

A l’issue d’un accident nucléaire, les produits de fission de l’uranium tel les iodes radioactifs sont dispersés dans l’environnement. L’homme est susceptible d’être exposé à ces éléments majoritairement via l’inhalation d’air et/ ou l’ingestion d’aliments contaminés. L’iode 131 est connu pour être responsable de l’augmentation de l’incidence du cancer de la thyroïde. Une des contremesures pour prévenir cette pathologie est l’ingestion de dose unique de comprimés d’iodure de potassium (KI) à fin de saturer la glande thyroïde par de l’iode stable et d’éviter ainsi l’accumulation de l’iode radioactif. Les scénarios de rejets réitérés d’iodes radioactifs lors des deux accidents majeurs Tchernobyl et Fukushima ont mis en évidence les limites de cette mesure, des prises répétées de KI pour protéger dans le temps les populations s’avèrent nécessaires. Dans la littérature on dispose de peu de données clinique et préclinique sur la prise répétée d’iode stable, quant à son usage ça n’a pas été décrit. La doctrine iode ainsi que l’autorisation de mise sur le marché (AMM) du KI envisage seulement la prise unique à renouveler exceptionnellement chez la population adulte. L’iode est connu pour être un élément clé de la fonction thyroïdienne, on jouant un double rôle à la fois de substrat de régulateur de la thyroïde. Si sa présence est indispensable à la formation des hormones thyroïdienne, son excès exerce un effet inhibiteur transitoire de cette synthèse connu sous le nom de l’effet Wolff-Chaikoff. Les hormones thyroïdiennes jouent un rôle majeur dans le développement et la fonction de presque tous les organes du corps (cerveau, cœur, os...), la moindre variation de leurs niveau peut impacter l’homéostasie du corps. Ainsi, il est difficile d’appliquer la prise répétée du KI en absence connaissances biologiques et toxicologiques. Pour combler ses lacunes et proposer une solution de prophylaxie répétée en cas d’exposition réitérée, le programme de recherche français PRIODAC : PRophylaxie répétée par l’IODe stable en situation ACcidentelle (ANR/RSNR), dont fait partie cette thèse vise à exploiter les modalités d’administration répétées du KI chez toutes les tranches d’âge (in utero, adulte et âgé), et d’évaluer la toxicologie de la prise répétée de KI sur les grandes fonctions physiologiques de l’organisme. Trois modèles de rats Wistar ont fait l’objet de ce travail de thèse : le modèle de référence rat adulte (âgé de 3 mois), le modèle à risque, organisme en développement (exposé durant la gestation) et un autre modèle à risque le rat âgé (âgé de 12 mois), ces trois modèles ont reçus 8 prise consécutive de KI 1mg/kg/24h. Les effets biologiques de ce traitement pendant 8 jours ont été évalués à long-terme (30 jours post-prophylaxie). Concernant, le modèle de référence ont n’a pas observé d’impact néfaste à long-terme de la prise répétée du KI (Lebsir, Cohen et al. 2018; Lebsir, Manens et al. 2018) par contre sur les modèles à risque plusieurs effets à long-terme ont été mis en évidence. Chez la progéniture exposée in utero, la coordination motrice ainsi que l’expression de quelques gènes clés du cerveau ont été négativement modifiées par le traitement. Chez le rat âgé la biochimie clinique, l’expression de quelques gènes clés de la fonction cardiovasculaire ainsi que le système rénine-angiotensine-aldostérone ont été significativement impacté par le traitement. En conclusion, les résultats obtenus montrent l’innocuité sur le plan toxicologique du KI administré à 1mg/kg toutes les 24h pendant 8 jours chez le modèle adulte et la nocuité de ce schéma prophylactique chez les modèles à risque in utero et âgé. Ces résultats ont été communiquées à la pharmacie centrale des armées (producteur et détentrice de l’AMM) afin de servir de données d’entrée pour des études de bonne pratique de laboratoire notamment pour le modèle adulte et également, afin de contribuées à l’évolution de la doctrine de l’iode en terme de radioprotection. / Following nuclear accidents, uranium fission products such as radioactive iodines are released into the environment. Humans are likely to be exposed to these elements mainly through inhalation of air and / or ingestion of contaminated food. Iodine 131 is known to be responsible for increasing the incidence of thyroid cancer. One of the available countermeasures is the ingestion of a single dose of potassium iodide (KI) tablets to saturate the thyroid gland with stable iodine and thus prevent the uptake of the radioactive isotope.Repeated releases of radioactive iodine during the two major accidents Chernobyl and Fukushima have highlighted the weaknesses of this measure, repeated intake of KI maybe necessary. In the literature there is little clinical and preclinical data on the repeated intake of stable iodine, regarding its use it has not been described. The iodine doctrine as well as the Marketing Authorization (MA) of the KI considers only the single taking, to renew exceptionally in the adult population. Iodine is known to be a key component of thyroid function, playing a dual role as both a substrate and a regulator of the thyroid. If its presence is essential for the synthesis of thyroid hormones, its excess exerts a transient inhibitory effect on this synthesis known as the Wolff-Chaikoff effect. Thyroid hormones affect the development and function of almost all organs of the body (brain, heart, bone ...), the slightest variation in their level can impact the homeostasis of the body. Hence, the toughness of applying repeated KI intake in the absence of biological and toxicological data. To fill this gap and find a solution in the event of repeated exposure, the French research program PRIODAC: repeated potassium iodide prophylaxis in accidental situation (ANR / RSNR), of which this thesis is part, aims to define the modalities of repeated administration of KI in all age groups (in utero, adult and elderly), and evaluate the biological consequences on the the body’s major physiological functions. Three models of Wistar rats were used in this work: the reference model adult rat (3 months), the first sensitive model offspring (exposed during gestation) and another sensitive model the older rat (12 months ), these three models received 8 consecutive intake of KI 1mg / kg / 24h. And the effects were assessed at long-term (30 days post-prophylaxis). On the reference model, there was no long-term adverse impact of repeated KI intake (Lebsir, Cohen et al. 2018; Lebsir, Manens et al. 2018). On the other hand, sensitive models reveal several long-term effects; the offspring exhibited impaired motor coordination and variation of the expression of some key brain genes. And in the elderly rat urinary biochemistry, expression of some key genes of the cardiovascular function, as well as the renin-angiotensin-aldosterone system were significantly impacted by the treatment. In conclusion, the results obtained show the toxicological safety of KI administered at 1 mg / kg every 24 hours for 8 days in the adult model, and the harm of this prophylactic scheme in sensitive models in utero and elderly. These results were sent to the French central pharmacy of armies and will serve as input data for good laboratory practice studies that eventually will contribute to the evolution of the iodine doctrine and KI MA.

L’iode est un composant essentiel aux hormones thyroïdiennes. Les cellules thyroïdiennes captent l’iode circulant et le concentrent vers le colloïde. Il est alors incorporé à la thyroglobuline, protéine précurseur des hormones, par un mécanisme d’organification. La capacité de captation de l’iode par la thyroïde est finement régulée notamment par la « Thyroid Stimulating Hormone » (TSH) mais aussi l’iode circulant. En effet, en cas d’une élévation de l’iode circulant, la thyroïde déclenche un mécanisme d’autorégulation appelée l’effet Wolff-Chaikoff. Ce phénomène se traduit par une limitation transitoire de production des hormones thyroïdiennes qui s’accompagne notamment d’une diminution de l’expression du NIS (Natrium Iodide Symporter), la protéine responsable du transport actif de l’iode dans la thyroïde. Dans cette étude, des approches omiques globales ont été mises à profit pour étudier cette régulation dans le contexte de l’administration d’un produit iodé et de souris invalidées pour un gène codant pour un transporteur de monocarboxylate exprimé dans la thyroïde. Dans la première partie, l’effet des agents de contraste iodés (ICA), couramment utilisés en imagerie médicale, a été étudié. L’administration de ces agents entraine une réduction de la captation de l’iode souvent expliquée par un effet Wolff-Chaikoff associé à un potentiel relargage d’iode. Par une approche de protéomique quantitative global, le protéome de thyroïde de souris, après administration d’ICA, a été comparé au protéome en conditions d’excès d’iode. Après un traitement des données et une analyse bioinformatique, nos résultats mettent en évidence l’existence de peu de mécanismes en commun induits par l’iode et les ICA mais cependant de plus importantes variations d’expression de protéines sont déclenchées uniquement par les ICA. Cette étude est en accord avec une durée plus importante de l’inhibition de la fonction après une administration d’ICA comparée à celle de l’iode stable. Dans la deuxième partie, le rôle de SLC5A8 dans la fonction thyroïdienne et les mécanismes sous-jacents à l’effet Wolff-Chaikoff ont été étudiés chez des souris invalidées pour le gène Slc5a8 (Solute carrier family 5 number 8) et des souris non mutées. SLC5A8 est une protéine membranaire identifiée au laboratoire et exprimée dans la membrane apicale du thyrocyte. Cette protéine catalyse un transport de monocarboxylate dans différents organes mais son rôle dans la thyroïde demeure non élucidé. L’invalidation n’entraine pas d’effet majeur sur la fonction thyroïdienne. En mettant à profit une approche multiomique comparative, combinant la transcriptomique, la protéomique et la métabolomique, les effets de cette invalidation et/ou de la régulation par l’iode de la thyroïde ont été explorés. Le traitement des data révèle de nombreuses voies activées dans les différentes conditions avec des mécanismes de compensation de l’effet de l’invalidation par l’administration d’iode. Les résultats indiquent que la perte de fonction de SLC5A8 affecte l’organification et/ou maturation de la thyroglobuline, le contrôle du stress oxydatif et de l’iode libre dans la thyroïde. / Iodine is an essential component of thyroid hormones. Thyroid cells capture the circulating iodine and concentrate it in the colloid. Then, it is incorporated into the thyroglobulin, the hormone precursor protein, by an organification mechanism. The iodine uptake capacity by the thyroid is finely regulated, not only by the Thyroid Stimulating Hormone (TSH) but also by circulating iodine. Indeed, in case of high circulating iodine, the thyroid actives a self-regulating mechanism called the Wolff-Chaikoff effect. This phenomenon results in a transient limitation of thyroid hormone production which is accompanied by a decrease in the expression of NIS (Natrium Iodide Symporter), the protein that is responsible for the active transport of iodine in the thyroid. In this study, global omics approaches were used to study this regulation in the context of the administration of an iodized product and mice invalidated for a gene coding a monocarboxylate transporter expressed in the thyroid. In the first part, the effect of iodinated contrast media (ICM), commonly used in medical imaging, has been studied. The administration of these agents leads to a reduction in the uptake of iodine often explained by a Wolff-Chaikoff effect associated with an iodine release potential. Through an overall quantitative proteomic approach, the mouse thyroid proteome, after administration of ICM, was compared to the proteome under conditions of excess iodine. In the second part, the role of SLC5A8 in thyroid function and the mechanisms underlying the Wolff-Chaikoff effect were studied in mice invalidated for the Slc5a8 gene (Solute carrier family 5 number 8) and wild type mice. SLC5A8 is a membrane protein identified in the laboratory and expressed in the thyrocyte apical membrane. This protein catalyzes the monocarboxylates transport in different organs but its role in the thyroid remains unsolved. Invalidation does not have a major effect on thyroid function. By using a comparative multiomic approach which combines transcriptomics, proteomics and metabolomics, the effects of this invalidation and / or regulation by iodine in the thyroid have been explored. Data processing reveals many pathways activated under different conditions with mechanisms to compensate for the effect of invalidation by the administration of iodine. The results indicate that the loss of SLC5A8 function affects the organization and / or maturation of thyroglobulin, the control of oxidative stress and of free iodine in the thyroid.

Zwei Drucke von Willy Wolff, ein Porträt dieses Künstlers von Max Uhlig sowie eine Zeichnung von Curt Querner aus dem Besitz Wolff's wurden der SLUB von Frau Gerda Dudeck geschenkt, die von 1970 bis zum Tod Willy Wolff's 1985 mit dem Künstler zusammenlebte und die dadurch zur besten Kennerin seines Werkes wurde....

Submitted by Geandra Rodrigues (geandrar@gmail.com) on 2018-01-25T14:03:25Z No. of bitstreams: 0 / Approved for entry into archive by Adriana Oliveira (adriana.oliveira@ufjf.edu.br) on 2018-01-26T10:55:34Z (GMT) No. of bitstreams: 0 / Made available in DSpace on 2018-01-26T10:55:34Z (GMT). No. of bitstreams: 0 Previous issue date: 2017-03-24 / CNPq - Conselho Nacional de Desenvolvimento Científico e Tecnológico / O entendimento atual do papel desempenhado pela psicologia do filósofo alemão Christian Wolff (1679-1754) na história da psicologia é problemático, e isto em razão da persistência de algumas questões gerais a seu respeito tanto na historiografia da psicologia quanto na Wolff scholarship. Estas questões são: 1- Qual é a relação entre os escritos psicológicos alemães e latinos de Wolff? 2- Em que consiste a separação wolffiana entre psicologia empírica e racional? 3- Wolff adota uma perspectiva monista ou dualista em sua psicologia? Visando ao avanço do conhecimento a respeito da psicologia de Wolff, e de seu papel na história da psicologia, o presente estudo busca responder a estas questões, lançando mão de três hipóteses: (1) os escritos psicológicos de Wolff constituem uma unidade; (2) o sistema psicológico de Wolff constitui uma unidade; (3) monismo e dualismo constituem uma unidade na psicologia de Wolff. Após a explicação detalhada na Introdução do problema e dos procedimentos do estudo, nos Capítulos 1 e 2 é desenvolvida uma análise histórico-filosófica dos principais escritos psicológicos alemães e latinos de Wolff. Contrastando os dados desta análise com diversas teses da literatura secundária, no Capítulo 3 é realizada a avaliação das hipóteses. Na Conclusão, são retomadas as questões iniciais do estudo, e estimado o seu valor para a historiografia da psicologia e para a Wolff scholarship. / The current understanding of the role played by the psychology of German philosopher Christian Wolff (1679-1754) in the history of psychology is problematic. And the main reason is that, both in the historiography of psychology and in Wolff scholarship, some general questions remain unanswered: 1- What kind of relationship is there between Wolff‟s German and Latin psychological writings? 2- What does the Wolffian separation between empirical and rational psychology consist in? 3- Which perspective does Wolff adopt in his psychology: monist or dualist? Our study intends to answer these questions, and to contribute to the improvement of the available knowledge about Wolff‟s psychology and the role played by it in the history of psychology. Three hypotheses are presented here as possible answers: (1) Wolff‟s psychological writings form an unity; (2) Wolff‟s psychological system is an unity; (3) Wolff establishes an unity between monism and dualism in his psychology. After a thorough explanation of the research problems and procedures in the Introduction, Chapters 1 and 2 display a historical and philosophical analysis of Wolff‟s German and Latin main psychological writings. Chapter 3 contains the evaluation of the hypotheses, which is developed by means of the confrontation of the results from chapters 1 and 2 with several theses from the secondary literature. The Conclusion addresses once more those questions presented at the Introduction, and finishes with some general considerations regarding the value of this study to the historiography of psychology and to Wolff scholarship.

Tesis para optar al grado de Magister en Filosofía mención Axiología y Filosofía Política / Años atrás la opinión pública vio como un grupo de jóvenes arrojaba un arma incendiaria contra el palacio La Moneda (símbolo del Estado en Chile). Dicho grupo se auto identificaba como “Movimiento Anarquista” y predicaban más o menos lo mismo que el movimiento anarquista español (o CNT) que luchó en contra de la dictadura franquista; me refiero a un rechazo a la autoridad del Estado. También, desde hace algunos años, vemos como otro grupo le exige al Estado lo mismo que aquel grupo de jóvenes. Ahora, eso sí, no se trata de jóvenes protestando; se trata de gente algo mayor identificados con los altos poderes económicos del país que, con corbatas y ternos exigen algo similar: un Estado que no se entrometa es sus acciones. Pero ¿Qué tienen en común estos grupos tan disímiles? ¿Por qué culpan al Estado de sus males? ¿Qué hace el Estado en su contra? ¿Será que al menos, en esencia, comparten ideas similares? La primera respuesta que a cualquiera que se le viene a la cabeza sobre estos cuestionamientos es que claramente este rechazo de la autoridad del Estado tiene algo que ver con nuestra Libertad. Pareciese, según lo creen algunos, que el gran problema que ven en el Estado es que éste intefiere con nuestra Libertad y con nuestras decisiones; pareciese que el Estado les ata las manos y no les deja actuar a sus anchas. De este modo, si es que aceptásemos que estas respuestas instintivas tienen algo de verdad, deberíamos aceptar también que, por lo menos en apariciencia, estos grupos sostienen que el Estado necesariamente viola Libertades. ¿No sería más sensato ver al Estado como institución política que trata de promover nuestra Libertad? En esta tesis trataremos de mostrar las soluciones teóricas que estas posiciones han dado a estas interrogantes junto con tratar de resolver la cuestión de si estas posturas sotienen una semejanza significativa. Para esto, nuestra primera labor será posicionar filosóficamente lo que representan estas posturas. Respecto a las posiciones Anarquistas, no hay ningún problema ya que dicha postura tiene una vasta defensa teórica representada por un largo historial de pensadores. Respecto a los grupos que exigen más libertad al Estado y que representan a altos poderes económicos del país es algo más complejo, filosóficamente hablando. Es fácil encontrar un correlato teórico en términos económicos (se les suele llamar capitalistas, libre cambistas, liberales, etc.), no obstante en términos filosóficos no es tan claro a quién representan. Descartamos a los liberales (principalmente a los de corte ralwsiano) ya que sus posiciones no representan una confrontación directa entre las Libertades y el Estado. Creemos que la posición filosófica que más se ajusta a dicha descripción son los Libertarios ya que estos serían quienes extreman el rasgo de la libertad en su argumentación que incluso se acentúa cuando hablamos sobre derechos de propiedad.