No description available.

The purpose of the study is to investigate the Western Sahara policy within the Swedish Parliament and Government, as well as how the policy has changed since. The study will help to get a broader understanding of how Sweden's foreign policy works and how the various international relations are covered. The theory of the study encompasses small state pragmatism as well as neutrality policy from Sweden's perspective. Sweden's policy on Western Sahara has changed in line with the aforementioned time periods: cold war, relaxation and terrorism. These periods of time have put in concrete work there you get an understanding of how the policies and Sweden have adapted during the different periods.

Doctor en Bioquímica / Las enfermedades cardiovasculares corresponden a la principal causa de muerte. En un corazón normal, insulina promueve incorporación de glucosa y su utilización estimulando la glicolisis, y estimulando la síntesis de proteínas. Por otro lado, durante isquemia/reperfusión, insulina promueve cardioprotección. Sin embargo, todos los estudios se han enfocado en estudiar el rol de insulina durante la reperfusión; por lo tanto, los efectos de esta hormona son desconocidos durante la isquemia. Además, antecedentes sugieren que el factor transcripcional NF-κB podría ser protector durante isquemia. NF-κB, controla una variedad de procesos antiapoptóticos, inflamatorios y de adhesión celular, entre otros. Una proteína controlada tanto por insulina como por NF-κB, en células endoteliales, es VCAM-1. Esta proteína es importante para el desarrollo del corazón y la diferenciación muscular. Por lo tanto, se estudiaron el rol de NF-κB y VCAM-1 y su regulación por insulina en el cardiomiocito isquémico. Para probar esto, cardiomiocitos neonatos fueron sometidos a isquemia simulada (IS) por 8 horas en ausencia o presencia de insulina 10 nM en combinación de diferentes tratamientos (inhibición de AKT mediante AKTi VIII, inhibición de NF-κB por BAY 11-7082 y reducción de VCAM-1 por siRNA). Los efectos protectores de insulina fueron evaluados mediante conteo celular, actividad LDH presente en el medio, fragmentación del DNA. Insulina protegió frente a isquemia, disminuyendo la necrosis y apoptosis durante IS. La presencia de los inhibidores AKTi VIII y BAY 11-7082 redujeron los efectos protectores de insulina. El silenciamiento de VCAM-1 también inhibió los efectos protectores de insulina en IS. Además, el silenciamiento de VCAM-1 resultó en aumento en la activación de AKT durante IS y menos respuesta frente la presencia de insulina. Estos resultados sugieren que insulina reduce la necrosis de los cardiomiocitos a través de la activación de AKT y NF-κB. Más aún, VCAM-1 estaría regulando este rol protector de insulina durante IS a través de la regulación de AKT. Estos hallazgos aportan a clarificar el rol protector de insulina durante isquemia, y su posible utilización durante cirugías y trasplante de corazón. Finalmente, estos resultados dejan a la luz un nuevo rol de VCAM-1 en la señalización de insulina y apoyan la idea que activación de AKT no siempre es sinónimo de cardioprotección / In Chile and worldwide cardiovascular diseases are the major causes of death. In the normal heart, insulin promotes glucose uptake and its utilization via glycolysis, regulates long-chain fatty acid uptake and protein synthesis. On the other hand, during ischemia/reperfusion, insulin promotes cardioprotection. Nevertheless, all studies have focused on insulin effects during reperfusion. Moreover, the transcription factor NF-κB seems to be protective against ischemia. VCAM-1 is a protein regulated by both insulin and NF-κB. Therefore, we explored the cardioprotective action of insulin and the role of AKT, NF-κB and VCAM-1 on the protective role of this hormone during ischemia. To test this, cultured neonatal rat cardiomyocytes were exposed to simulated ischemia by 8 hours in the absence or presence of insulin in combination with different treatments (AKT inhibition by AKTi VIII, NF-κB inhibition by BAY 11-7082 and VCAM-1 reduction by siRNA transfection). Cytoprotective effects of insulin were measured by cell count, LDH release and DNA. We found that insulin protected against simulated ischemia. Moreover, insulin protected cardiomyocytes from simulated ischemia by reducing necrotic cell death. Protective effects of insulin were dependent of AKT and NFκB. Additionally, silence of VCAM-1 inhibited insulin protection against simulated ischemia. We found that VCAM-1 silencing resulted in an AKT overactivation and less insulin response. These results show that insulin reduces ischemia-induced cardiomyocyte necrosis through an AKT and NF-κB dependent mechanism. Moreover, VCAM-1 regulates this protective role of insulin during ischemia. These novel findings clarify the role of insulin during ischemia and propose a new function of VCAM-1 as an insulin signaling regulator / Conicyt, Fondap, Fondecyt, Nemesis

The UN doctrine for Peacekeeping operations is based on three fundamental principles for obtaining legitimacy for military operations. The purpose of this thesis is to investigate the change in the UN Security Council's view of legitimacy and the use of force in the context of the UN Peacekeeping Operation in Mali between 2013 -2016, and how this has been demonstrated in the robust mandate authorized by the UN Security Council. Using Fairclough´s Critical Discourse Analysis Model, together with the resolutions and debates from the Security Council that constitutes the MINUSMA mandate and is the basis for this analysis. The analytical results identify two significant changes in the Security Council's view regarding legitimacy and methods, including the use of force applied in the field to defend the integrity of the mandate. Firstly, the view of legitimacy changes from extending support to host-nation authorities, to instead supporting the implementation of the peace agreements. Secondly, the Security Council's view on the use of legitimate force switches from defensive operations to preventive measures. This study fills a research gap on robust mandates, and how the UN's highest decision-making body is evolving its view on legitimacy in peacekeeping operations.

This diploma thesis deals with security in the hospital enviroment. The work creates a new evacuation plan for large-monoblock Hospital for adults in FN Motol. Evacuation plan covers all activities of the announcement of evacuation after the removal of the last patient from the hospital. For developed evacuation plan at workcompiled four simulation models in SIMUL8. With these models, theevacuation plan and tested models provide a quantitative value, according to which it can better prepare for possible evacuation. This thesis has fulfilled its purpose -- was created functional evacuation plan, and simulation models provide additional information as to which should be ensured smoother running of the evacuation.

2003 invaderade USA tillsammans med ett antal av dess allierade Irak. Invasionen genomfördes utan mandat från FN:s säkerhetsråd. Uppsatsen handlar om hur USA och Bushadministrationen motiverade den invasionen och om hur FN:s och FN-stadgans regelverk reglerar internationell våldsanvändning.Syfte med uppsatsen är att se hur Bushadministrationens motiveringar förhåller sig till FN-stadgan och till den tillhörande resolutioner.Detta har gjorts genom en kvalitativ textanalys där tal och officiella dokument analyserats. Som teoretisk grund har realismen använts. Realismen har även använts som en förklaringsmodell för varför USA handlade som de gjorde.Resultatet i uppsatsen visar att USA:s invasion av Irak 2003 ej var förenlig med FN-stadgan och till den tillhörande resolutioner. Men tydliga kopplingar mellan USA:s aggerande och Realismen kan identifieras.

This study explores how constructivism's view of we and them have affected Belgium and France in the 1994 genocide in Rwanda, as well as how their actions with a starting point in soldairty affected UN's actions during the genocide in Rwanda. With a qualitative text analysis and a constructivist reading, official documents from the UN are analysed. The analysis shows that Belgium, France and the UN based on a constructivist reading, act because the feeling of we and them, which results in Belgium recalling their troops in Rwanda as well as their cooperation with France in the humanitarian rescue of foreign citizen which were based in Rwanda in the start of the genocide. The humanitarian rescue as well as the recalling of troops, could with a starting point in constructivism, explain that they acted from a we point of view and that they saw the citizens of Rwanda as them, which they did not feel solidarity to. With no solidarity, they did not act as if Rwanda and the UN, France and Belgium represented a we with a similar identity. The study also discusses the complexity in trying to explain different causes and reasons to someone's behaviour and that the research question itself is complex and could be explained in many perspectives. But in the conclusion the study answer the research question, that a perspective with the feeling of we and them could explain why France, Belgium and the UN acted in that way in the geoncide in Rwanda.

No description available.

This master thesis is addressing an issue of information system used in The University Hospital Brno. The current system and its environment is evaluated using analysis SWOT, HOS2009 and other observations. Based on the results the work elaborates the idea of an unified information system and its feasibility in practice.

Memoria para optar al Título Profesional de Químico Farmacéutico / Resolvina D1 y Resolvina E1 inhiben la activación de AKT, ERK1/2 y NF-kB dependiente de LPS y previenen la expresión de ICAM-1 y VCAM-1 en fibroblastos cardíacos Los fibroblastos cardiacos (FC) son células que tienen como función regular la matriz extracelular (MEC), pueden responder a estímulos endógenos o exógenos que alteren la homeostasis del sistema, y en caso de injuria, pueden proliferar y migrar hacia el sitio de daño. Uno de los agentes proinflamatorios más estudiados y utilizados es el lipopolisacárido (LPS) bacteriano, éste desencadena la respuesta inflamatoria activando las vías de señalización Akt, ERK1/2 y NF-κB, que conducen a la expresión de citoquinas proinflamatorias y factores de crecimiento los que, a su vez, aumentan la expresión de proteínas de adhesión como ICAM-1, VCAM-1, E-selectina, L-selectina, entre otras; permitiendo que células del sistema inmune viajen desde la circulación sanguínea hasta el sitio de injuria, para cicatrizar la herida. La inflamación puede ser terminada activamente por mediadores proresolutivos. Unos de estos mediadores son la Resolvina (Rv) D1 y E1. La RvD1 proviene del ácido docosahexaenoico y la RvE1 del ácido eicosapentaenoico. Estas se biosintetizan durante la inflamación y se les ha asociado propiedades antiinflamatorias, limitando la infiltración de neutrófilos, estimulando la fagocitosis de los macrófagos y reduciendo el nivel de dolor inflamatorio y fibrosis. Sin embargo, no existe evidencia de los efectos que podría tener en FC. El objetivo de este trabajo fue evaluar los efectos de RvD1 y RvE1 en FC, para así estudiar las acciones que tendría en un contexto inflamatorio inducido por LPS, evaluando la actividad en las vías de señalización Akt, ERK1/2 y NF-κB y sobre la expresión de las proteínas de adhesión ICAM-1 y VCAM-1. 12 Los resultados obtenidos muestran que RvD1 presenta una significativa disminución de la activación de Akt y ERK1/2, no así de NF-κB. RvE1 disminuye significativamente la activación de ERK1/2, sin embargo, no presenta cambios significativos respecto al control en la fosforilación de Akt y NF-κB. Además, se demostró que en FC estimulados con LPS y pretratados con RvD1, disminuyó la activación de las vías Akt, ERK1/2 y NF- κB respecto a LPS, y consecuentemente disminuyó la expresión de VCAM-1, pero no de ICAM-1. Por otro lado, RvE1 disminuyó significativamente la activación de Akt, no así la activación de ERK1/2 y NF-κB estimuladas por LPS. Además, disminuyó la expresión de ICAM-1 estimulado por LPS, pero no de VCAM-1. En conclusión, nuestros resultados sugieren que tanto RvD1 como RvE1 poseen propiedades resolutivas en un modelo de inflamación en FC, lo cual posibilitaría su uso como nuevas herramientas terapéuticas en enfermedades cardiacas / Resolvin D1 and Resolvin E1 inhibit AKT, ERK1/2 and NF-kB activation LPSdependent and prevent ICAM-1 and VCAM-1 expression in cardiac fibroblasts Cardiac fibroblasts (CF) are cells that regulate the extracellular matrix (ECM), they can respond to endogenous or exogenous stimuli that alter the homeostasis of the system, and in case of cardiac tissue injury, they can proliferate and migrate to the site of damage. One of the most studied and used proinflammatory agents is bacterial lipopolysaccharide (LPS), it triggers the inflammatory response activating the signaling pathways Akt, ERK1/2 and NF-κB, which lead to the expression of proinflammatory cytokines and growth factors that increase the expression of adhesion proteins such as ICAM-1, VCAM- 1. E-selectin, L-selectin, among others. These effects of LPS favor to the cells of the immune system extravasate to the site of injury to degrade the microorganism and heal the wound. Inflammation can be actively terminated by proresolving mediators, such as RvD1 and RvE1. RvD1 derived from docosahexaenoic acid and RvE1 from eicosapentaenoic acid. These are biosynthesized during inflammation and have been associated with anti- inflammatory properties, limiting the infiltration of neutrophils, stimulating the phagocytic activity of macrophages and reducing the level of inflammatory pain and fibrosis. However, there is no evidence respect of the effects it could have on FC. In this study, we investigated the role of RvD1 and RvE1 in FC, to study the actions that would have in an inflammatory context induced by LPS, evaluating the activity in the signaling pathways Akt, ERK1/2 and NF-κB and the expression of adhesion proteins ICAM-1 and VCAM-1. 14 The results show that RvD1 exert a significant decrease of Akt and ERK1/2 activity, but not NF-κB; RvE1 significantly decreases the activation of ERK1/2, however, it does not present significant effect in regard to the control in the phosphorylation of Akt and NF-κB. In addition, the pretreatment with RvD1, has decreased the activation of the Akt, ERK1/2 and NF-κB pathways respect to LPS, and consequently decreased the expression of VCAM-1, but not ICAM-1. On the other hand, RvE1 has significantly decreased the activation of Akt stimulated by LPS, but not of ERK1/2 nor NF-κB. Additionally, the expression of ICAM-1 stimulated by LPS has decreased, but not of VCAM-1. In conclusion, our results suggest that RvD1 and RvE1 have resolutive properties in an inflammatory model in CF, which would make possible its use as new therapeutic tool in cardiac diseases / Proyecto Fondecyt N° 1170425