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Confidentiel. Résumé non fourni. / Confidentiel. Résumé non fourni

Syftet med uppsatsen är att fördjupa kunskapen om Yoko Shimomuras musikaliska kännetecken och hur hon gestaltar, urskiljer samt sammankopplar karaktärer i instrumental spelmusik, med särskilt fokus på några av spelserien Kingdom Hearts (2002-2020) bosskampssituationer. Detta görs genom analyser av sex bosskampsteman centrerat kring olika versioner av spelseriens centrala antagonist Xehanort. Versioner som inte enbart byter namn och utseende genom spelserien, utan även klonats, rest i tiden, kroppsligt besatt andra karaktärer eller som delats upp i två eller fler versioner av en och samma karaktär. Uppsatsen ämnar även att pröva och utforska Shimomuras kompositionstekniker i en egen musikalisk gestaltning, för att på så vis illustrera hur uppsatsens resultat praktiskt kan tillämpas och vara användbara för framtida kompositörer av spelmusik. Genom en egenutvecklad audiovisuell analysmodell visar resultaten på hur Shimomura använder sig av karaktärs-specifika ledmotiv, ackompanjemang och instrumenteringar för att identifiera de olika karaktärerna. Hon återanvänder även delar av ledmotiv eller andra rytmiska mönster och ackompanjemang i de olika bosskampstemana för att tydliggöra för karaktärernas relationer. Den musikaliska gestaltningen tillför även en audiell aspekt till uppsatsens resultat och ämnar att representera ett exempel på hur de teoretiska resultaten kan användas praktiskt.

Why do local populations regard peacekeepers from certain countries as friendly, and from others not? This study delves into the cultural proximity and cultural awareness of peacekeepers, suggesting it as one factor that influences public perceptions on the peacekeepers and the mission as a whole. I argue that a closer cultural proximity of peacekeepers to the mission country correlates positively with a more favorable public perception on the mission. The working mechanism behind the relationship is based on the theory of winning hearts and minds. Aiming for empirical validation, this hypothesis undergoes examination by using a structured focused comparison between the Malian cities of Gao and Timbuktu. In addition, I complement the study with the method of process tracing, using own data collected through expert interviews with 10 individuals who gained field experience in MINUSMA. The results of the structured focused comparison yield unexpected results: The evidence does not align with the hypothesis due to a lack of variation in the peacekeepers‘ cultural proximity between the cases. However, the tracing of the causal mechanism proves invaluable. It finds support for certain parts of the theorized mechanism while inviting for further exploration on additional intervening factors that reshape or complement the causal chain.

For the past decade and even earlier, globalization has been a popular buzzword in academia and has provoked a number of intellectual discussions concerning its nature and effects. In these discussions concepts such as cultural imperialism, cultural homogenization, and indigenization appear which are perceived by-products of globalization in many cases. While some debate the moral implications of globalization and these related phenomena few prefer to take a more neutral stance and simply investigate the objects that are born from the combination two distinct cultural traditions. My research investigates the cultural flow between the United States and Japan which can be considered 'cultural sharing'. In this context, globalization is a phenomenon that can happen on equal footing and can support the exchange of distinct cultural ideas as a beneficial and voluntary process. In the last century, both Japan and the United States have borrowed cultural items from one another and localized them. The step after borrowing and localization occurs when parties from each country work together with the intent of creating a joint project. Kingdom Hearts stands as a prime example of this because the Japanese company Square and the American company Disney collaborated in order to create a product which represents a hybridization of both cultures.

Thesis (PhD)--University of Stellenbosch, 2011. / ENGLISH ABSTRACT: The Mechanism of -adrenergic preconditioning ( -PC) Ischaemic preconditioning (IPC), a potent endogenous protective intervention against myocardial ischaemia, is induced by exposure of the heart to repetitive short episodes of ischaemia and reperfusion. The protective effects of this phenomenon have been demonstrated to be mediated by release of autocoids such as adenosine, opioids and bradykinin. Release of endogenous catecholamines and activation of the beta-adrenergic receptors (b-AR) have also been shown to be involved in ischaemic preconditioning. However, the exact mechanism whereby activation of the - adrenergic signal transduction pathway leads to cardioprotection, is still unknown. In view of the above, the aims of the present study were to evaluate: (i) the respective roles of the 1-, 2- and 3-AR receptors as well as the contribution of Gi protein and PKA to -adrenergic preconditioning, (ii) the role of the prosurvival kinases, PKB/Akt and ERK 44/p42 MAPKinase in -drenergic preconditioning, (iii) whether b-AR stimulation protect via ischaemia and the formation of adenosine; the respective roles of the A1-, A2-, A3-adenosine receptors as well as the involvement of the PI3-K/PKB/Akt and ERKp44/p42 signal transduction pathways, in the cardioprotective phenomemon of -adrenergic preconditioning and (iv) the contribution of the mitochondrial KATP channels (mKATP), reactive oxygen species and NO to the mechanism of -AR-induced cardioprotection. Methods: Isolated perfused rat hearts were subjected to 35 min regional ischaemia (RI) and reperfusion. Infarct size (IS) was determined using tetrazolium staining (TTC) and data were analyzed with ANOVA. Hearts were preconditioned with 5 min isoproterenol 0.1 μM ( 1/ 2-AR agonist), or formoterol 1 nM ( 2-AR agonist) or BRL 37344 1 μM ( 3-AR agonist) followed by 5 min reperfusion. The roles of the 1-, 2- and 3-ARs as well as NO were explored by using the selective antagonists CGP-20712A (300 nM), ICI -18551 (50 nM), SR59230A (100 nM) and NOS inhibitors L-NAME (50 μM) or LNNA (50 μM) respectively. Involvement of ROS and the mK+ ATP channels was studied by administration of N-acetyl cysteine (NAC, 300 μM) and the mitK+ ATP iv channel blocker 5-HD (100 μM) during the triggering phase. The role of PKA and PI3-K/Akt was investigated by the administration of the blockers Rp-8-CPT-cAMPs (16 μM) and wortmannin (100 nM) respectively, prior to RI or at the onset of reperfusion. Pertussis toxin (PTX), 30 μg kg-1 was administered i.p., 48 h prior to experimentation. The role of adenosine and the adenosine A1, A3, A2A and A2B receptors was studied by using adenosine deaminase and the selective antagonists DPCPX (1 μM), MRS 1191(1 μM), ZM241385 (1 μM) and MRS1754 (1 μM). Activation of PKB/Akt and ERKp44/p42 was determined by Western blot. Results: Infarct sizes of hearts preconditioned with isoproterenol of formoterol were significantly smaller compared to those of non-preconditioned hearts. This was associated with an improvement in postischaemic mechanical performance. However the 3-AR agonist BRL37344 could not reduce infarct size. The 1- and 2-AR blockers CGP-20712A and ICI-118551 completely abolished the isoproterenol-induced reduction in infarct size and improvement in mechanical recovery, while the 3-AR blocker was without effect. Both Rp-8-CPT-cAMPs and wortmannin significantly increased infarct size when administered before 1/ 2-AR preconditioning or at the onset of reperfusion while it reduced mechanical recovery during reperfusion. PTX pretreatment had no significant effect on the reduction in infarct size induced by 1/ 2-AR or 2-AR preconditioning, however it reduced mechanical recovery in the latter. The NOS inhibitors had no effect on the reduction in infarct size induced by 1/ 2-AR preconditioning, but depressed mechanical function during reperfusion. The significant reduction in infarct size by 1/ 2-PC, was associated with activation of ERKp44/p42 and PKB/Akt during the triggering phase, as well as during reperfusion. DPCPX (A1-AdoR antagonist) had no effect on the 1/ 2-PC-induced reduced infarct size or ERK p44/p42 and PKB activation. A2A-AdoR, but not A2b-AdoR, blockade during the trigger phase abolished the reduction in infarct size of 1/ 2-PC. Both antagonists significantly reduced ERK and PKB activation in the trigger phase. In addition, when applied at the onset of reperfusion they significantly reduced ERK p44 / v p42 MAPK and PKB/Akt activation to an even greater extent. MRS-1191 (A3-AdoR antagonist) blocked 1/ 2-PC when applied prior to index ischaemia or when added during early reperfusion, significantly inhibiting both ERK p44 and PKB activation. Cardioprotection of 1/ 2-PC was abolished by inhibition of ROS generation with NAC in the triggering phase as well as at the start of reperfusion. However, the mitoK+ ATP channel blocker 5- HD was without effect. Conclusions: Protection afforded by an acute transient stimulation of the -ARs, depends on the activation of both 1-AR and 2-ARs but not the 3-AR. PKA as well as PI3-K activation prior to sustained ischemia and at the onset of reperfusion were essential for cardioprotection. With functional recovery as endpoint, it appears that NO is involved in 1/ 2-AR preconditioning, while the Gi protein may play a role in 2-AR preconditioning. The production of endogenous adenosine induced by transient b1/b2 stimulation of the isolated rat heart is involved in b−AR preconditioning. Cardioprotection was shown not to be dependent on the A1AdoR while activation of the A3-AdoR occurs during both the triggering and mediation phases. Both the adenosine A2A and, to a lesser extent, the adenosine A2B receptors participate in the triggering phase of b1/b2-PC. Generation of ROS during the triggering and reperfusion phases is involved in eliciting protection, but no role for the mKATP channels could be demonstrated. Finally, activation of the RISK pathway (PKB/Akt and ERKp44/p42) during the triggering phase is a prerequisite for protection. In addition, cardioprotection by b-AR is characterized by activation of the RISK pathway during reperfusion. / AFRIKAANSE OPSOMMING: Iskemiese prekondisionering (IPC) is ‘n kragtige endogene beskerming teen miokardiale iskemie, wat deur blootstelling van die hart aan kort opeenvolgende episodes van iskemie en herperfusie, ontlok word. Hierdie beskerming word medieer deur vrystelling van outakoïede soos adenosine, opioïede en bradikinien. Vrystelling van endogene katekolamiene en aktivering van die betaadrenerge reseptore (b-AR) is bewys om ook by hierdie proses betrokke te wees. Die presiese meganismes waardeur aktivering van die -adrenerge seintransduksiepad tot miokardiale beskerming lei, is nog onbekend. In die lig van bogenoemde, was die doel van die huidige studie om die volgende te evalueer: (i) die onderskeie rolle van die b1-, b2- en b3-AR sowel as die bydrae van die Gi proteïen en PKA in b- adrenerge prekondisionering, (ii) of b-AR stimulasie beskerming ontlok via iskemie en vorming van adenosien, die onderskeie rolle van die A1-, A2-, A3-adenosien reseptore (AdoRs) sowel as die PI3- K/PKB/Akt en ERKp44/p42 seintransduksie paaie, (iv) die mitochondriale KATP (mKATP) kanale, vry suurstof radikale en NO in b−AR prekondisionering. Metodes: Geïsoleerde, geperfuseerde rotharte is aan 35 minute streeksiskemie en herperfusie onderwerp. Infarktgrootte (IS) is deur die tetrazolium (TTC)-kleuringsmetode bepaal. Data is met behulp van ANOVA analiseer. Harte is geprekondisioneer vir 5 min met isoproterenol 0.1 μM ( 1/ 2-AR agonist), of formoterol 1 nM ( 2-AR agonist) of BRL 37344 1 μM ( 3-AR agonist), gevolg deur 5 min herperfusie, voor streeksiskemie. Die belang van die 1-, 2- en 3-ARs sowel as NO is ondersoek, deur onderskeidelik gebruik te maak van selektiewe antagoniste nl CGP- 20712A (300 nM), ICI -18551 (50 nM), SR59230A (100 nM) en NOS inhibitore L-NAME (50μM) of LNNA (50μM). Die rol van die mK+ ATP kanale en ROS is bepaal deur die toediening van die mK+ ATP kanaal blokker 5-HD (100 μM) en die vrye-radikaal opruimer, N-asetiel cysteine (NAC, 300 μM). Die belang van PKA en PI3-K/Akt is bepaal deur toediening van die PKA blokker Rp-8- CPT-cAMPs (16μM) en wortmannin (100nM) respektiewelik. Pertussis toxin (PTX), 30 μg kg-1 is i.p toegedien, 48 uur voor eksperimentasie. vii Die rol van adenosien en die adenosien A1, A2A, A2B en A3 reseptore is bestudeer, deur gebruik te maak van adenosien deaminase en die selektiewe antagoniste DPCPX (1 μM), MRS 1191(1 μM), ZM241385 (1 μM) and MRS1754 (1 μM),repektiewelik. Die middels is deurgaans toegedien tydens die prekondisioneringsprotokol (“snellerfase”) of tydens vroeë herperfusie. Aktivering van PKB/Akt en ERK p44/p42 is deur Western blot analise bepaal. Resultate: Infarktgrootte van harte wat geprekondisioneer is met of isoproterenol ( 1/ 2-PC) of formoterol ( 2-PC), was beduidend kleiner as díe van ongeprekondisioneerde harte. Dit is geassosieer met ‘n toename in postiskemiese meganiese herstel. Die 3-AR agonis BRL37344 ( 3- PC) het egter geen effek op infarktgrootte gehad nie. Die selektiewe 1- en 2-AR blokkers CGP- 20712A en ICI-118551 het die afname in infarktgrootte heeltemal opgehef, asook die verbetering in meganiese herstel tydens herperfusie terwyl die 3-AR blokker geen effek getoon het nie. Beide Rp- 8-CPT-cAMPs en wortmannin het infarktgrootte beduidend vergroot en meganiese herstel beduidend verlaag, wanneer dit net voor 1/ 2-prekondisionering of tydens die begin van herperfusie toegedien is. PTX voorafbehandeling het geen beduidende effek op die vermindering van infarktgrootte (geïnduseer deur 1/ 2-PC of 2-PC) gehad nie. Meganiese herstel is egter verminder in die geval van 2-PC. Die NOS inhibitore het geen effek op die vermindering in infarktgrootte geïnduseer deur b1/b2 gehad nie, maar het ook meganiese herstel onderdruk. Die beduidende afname in infarktgrootte deur b1/b2 prekondisionering is gekenmerk deur aktivering van ERKp42/p44 en PKB/Akt tydens die snellerfase. Soortgelyke aktivering van hierdie kinases is ook tydens herperfusie van b-AR geprekondisioneerde harte waargeneem. DPCPX (A1-AdoR antagonis) het geen effek op die infarkt-verminderde effek van 1/ 2- prekondisionering of op ERK p44/p42 en PKB aktivering gehad nie. A2A-AdoR, maar nie A2b – AdoR, blokkade tydens die snellerfase, het die effek van b-AR prekondisionering op infarktgroottee opgehef. Beide antagoniste het die aktivering van ERKp42/p44 en PKB/Akt tydens die snellerfase onderdruk. Wanneer toegedien tydens herperfusie, het dit die aktivering van hierdie kinases tot ‘n groter mate onderdruk. MRS-1191 (A3-AdoR antagonis) het infarktgrootte beduidend verhoog en 1/ 2-prekondisionering geblokkeer, beide wanneer dit voor indeks-iskemie toegedien is of tydens vroeë herperfusie, tesame met inhibisie van PKB en ERK p44/p44 aktivering. viii Die kardiobeskerming van 1/ 2-prekondisionering is opgehef deur middel van opruiming van vry suurstof radikale deur NAC in die snellerfase sowel as aan die begin van herperfusie. Die mK+ ATP kanaal blokker 5-HD het geen effek op b-AR prekondisionering gehad nie. Gevolgtrekking: Kardiobeskerming teweeggebring deur ‘n kort periode van stimulasie van die - ARs, is afhanklik van die aktivering van beide 1-AR en 2-ARs, maar nie 3-AR nie. PKA sowel as PI3-K aktivering, net voor volgehoue iskemie en tydens vroeë herperfusie, is aangedui om noodsaaklik vir 1/ 2-AR prekondisionering te wees. Waar funksionele herstel as eindpunt gebruik is, blyk dit dat NO wel betrokke is by 1/ 2-AR prekondisionering, terwyl die Gi protein ‘n rol mag speel in 2-AR prekondisionering. Vorming van endogene adenosien tydens b-adrenerge stimulasie is betrokke by b-AR prekondisionering. Hierdie beskerming is nie van die A1-AdoR afhanklik nie, maar aktivering van die A3-AdoR is nodig tydens beide die sneller en herperfusie fases. Beide die A2A-AdoR, en tot ‘n mindere mate die A2B–AdoR, is ook betrokke by die snellerfase. Vorming van vry suurstof radikale is nodig vir b-AR prekondisionering, nterwyl die mKATP kanale nie betrokke is nie. Ten slotte, aktivering van die RISK seintransduksiepad (ERKp42/p44 en PKB/Akt) tydens die snellerfase is ‘n voorvereiste vir die ontlokking van beskerming. Daarbenewens word b-AR prekondisionering gekarakteriseer deur aktivering van hierdie pad tydens herperfusie. / South African Medical Research Council / University of Stellenbosch

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317 pathologisch-anatomische Befundberichte über die Morphologie des Myokards, der Koronararterien, der Aorta und der Pulmonalarterien von Herzen, die in der Homograftbank des Deutschen Herzzentrums Berlin in den Jahren 1996 bis 1998 für eine potentielle Klappenspende (Aorten- und Pulmonalklappen) seziert worden waren, wurden ausgewertet. 178 dieser Herzen stammten von Herztransplantatempfängern und zeigten naturgemäß schwere pathologische Veränderungen. Sechs Herzen stammten von Leichen. 133 Herzen waren hirntoten Menschen entnommen worden. Ursprünglich hatte bei vielen dieser 133 Spenderherzen die Absicht bestanden, sie für die Transplantation zu verwenden, was aus verschiedenen Gründen nicht möglich war. Ziel der retrospektiven Studie war die Erfassung der morphologischen Situation der Organe, wobei der Schwerpunkt auf der Gruppe der Spenderherzen lag. / This work contains an analysis of 317 records with a detailed description of the morphology of myocardium, coronary arteries, aortas and pulmonary arteries of hearts dissected for the purpose of harvesting the aortic and pulmonary valves as allografts in the Heart Valve Bank of the German Heart Institute, Berlin, from 1996 through 1998. 178 hearts stemmed from patients who recieved heart transplants. Naturally these organs revealed severe pathologic findings. Cadaveric organs (non beating hearts) amounted to six. 133 hearts were taken from brain dead human beings. Many of these 133 donor organs were originally considered to be potentially usable for transplantation, but were discarded for various reasons. The objective of this retrospective study was to ascertain the morphologic state of the hearts with special focus on the 133 donor hearts.

The traditional history educational methods mainly consists of and are focused on memory, reading, repetition and writing skills, however this paper aims to give an overview of research regarding “Game-based learning”, it’s uses in education of history, and if it can be used as a way to complement the traditional education and give history teachers the tools to make their teaching more diverse. Useful materials were found in the databases: EBSCO, IEEE Xplore och Science Direct. Each of the 3 practical and 3 informational studies has been carefully selected by their subject relevance and the quality of the study’s gathering, use and compilation of data. The results in this overview are both positive and negative. The studies found on the subject show that the students not only learn historical facts when using game-based learning but also become very engaged in the lesson and achieve a deeper historical perspective where they can understand the historical events in the historical context and relate to people of that point in time. However, the drawbacks are that some students have been reported to have missed some facts altogether, and that would have been avoided in traditional education (Erhel & Jamet, 2013). Another drawback that has been noted is that Game Based learning is incredibly time consuming and if it is not used correctly it risks creating a dilemma for the history teacher where the teacher has to choose Game-based learning or traditional education of history (Watson & Mong & Harris, 2010). But if it is used correctly, studies have also shown that they can be combined (Erhel & Jamet, 2013; Kuran & Tozoglu & Tavernari, 2018).