abstract: Why and when do political actors use violence? This project answers these questions by exploring the dynamics of the interactions between state authorities and political dissidents. Both the state and the dissidents face the dilemma of using violence to achieve their political goals. While structural factors influence state violence and dissident violence, I contend that we need to examine how the dynamics of the state-dissident interactions shape these actors’ political behavior. This project first asks if nonviolent methods of resistance are effective--and perhaps even more successful than violent methods--why do opposition movements ever resort to violence? I argue that the efficacy of nonviolent resistance changes over time. When the likelihood of demobilization increases, dissident movements doubt the effectiveness of nonviolent resistance and weigh violence as an alternative tactic. The first chapter of this dissertation shows that the failure in expanding the size of a movement over several periods provides increases the risk of demobilization, and so dissident violence. I also argue while the expansion of the movement decreases the risk of dissident violence, a sudden and large expansion in the size of the movement overburdens its monitoring and sanctioning capacities, which raises the risk of dissident violence. These arguments are supported empirically using two different datasets. In the second theoretical part of this project, I examine the effects of foreign interventions on the dynamics of state repression and dissident violence. I find that the diplomatic statements and efforts such as disapproving state behavior, asking for political reform, and threatening to impose economic sanctions and to deploy military forces either did not have a significant effect, or increased state repression and decreased state concession during the Arab Spring. Finally, the last part of this project contributes to the literature on the formal modeling of dissent-repression by developing a recursive model of political violence dynamics. In addition to addressing several drawbacks in the literature, this model endogenizes the mobilization and demobilization of the movement and explains how these changes affect dissident violence. Due to the complexity of the developed mathematical model, I use a computational model to find the optimal outcomes. This computational model also can be used for simulating the state’s and the dissidents’ behavior under different scenarios. / Dissertation/Thesis / Doctoral Dissertation Political Science 2018

Introdução: Resistência aos antirretrovirais pode limitar opções de tratamento, principalmente em pacientes com acúmulo de falhas terapêuticas, o que pode comprometer resultados clínicos. Objetivos: caracterizar o perfil de mutações na transcriptase reversa e protease do HIV-1 de pacientes em falha ao tratamento. Secundariamente, avaliar associação entre mutações e número de falhas terapêuticas, associação entre mutações e subtipos do HIV-1 e apresentar a evolução temporal da prevalência dos subtipos do HIV-1, no estado do Pará, ao Norte do Brasil. Método: Estudo transversal, no qual se avaliam genotipagens, entre janeiro de 2004 a dezembro de 2013, com dados obtidos de formulário de solicitação do exame padronizado pela RENAGENO e de impressos dos resultados, ambos arquivados em quatro serviços de atendimento especializados. Foram incluídos os testes realizados por laboratório da RENAGENO, em maiores de 18 anos, e o primeiro exame daqueles que o realizaram em mais de um momento, totalizando 377 amostras. As mutações são descritas de acordo com o banco de dados de resistência do HIV da Universidade de Stanford (http://hivdb.stanford.edu), estimam-se suas prevalências e avaliam-se mutações de resistência de acordo com o número de falhas no momento da genotipagem, bem como diferenças de mutações entre subtipos B e não-B do HIV-1. Resultados: A mutação M184V foi a mais prevalente (80,1%), seguida da K130N (40,6%) e TAM. Em pacientes multiexperimentados previamente à genotipagem, resistência a ZDV, d4T e TDF foi associada às mutações M41L, D67N, V118I, L210W, K219Q e T69D; bem como resistência a todos os IP/r associou-se às mutações principais M46I, V82A, L90M, I54V, I84V, M46L e L76V. O subtipo B é o predominante no Pará (90,7%) e diferenças de prevalência de mutações entre subtipos ocorreram entre as mutações L63P e A71T versus subtipo B, enquanto as mutações L76V, M36I, K20R, L10V, L89M e F53L associaram-se ao subtipo não-B. Conclusão: A seleção de mutações de resistência do HIV-1 relacionada aos antirretrovirais é similar ao descrito em literatura. O acúmulo de falhas ao tratamento favorece a emergência de mutações, o que reforça o monitoramento de falha virológica, seguida de genotipagem para minimizar o impacto de resistência. Estudos adicionais de epidemiologia molecular são necessários para avaliar melhor a questão da prevalência de subtipos de HIV-1 no estado e possíveis associações com mutações de resistência do HIV-1. / Introduction: Resistance to antiretroviral treatment can limit treatment options, especially in patients with accumulation of therapeutic failures, which may compromise clinical outcomes. Objectives: characterizing the profile of mutations in the protease and reverse transcriptase of HIV-1 patients in the treatment failure. Secondarily to evaluate the association between mutations and the number of treatment failures, association between mutations and subtypes of HIV-1 and present the temporal evolution of the prevalence of subtypes of HIV-1 in the state of Pará in northern Brazil. Method: cross-sectional study in which genotyping is evaluated between January, 2004 and December, 2013 with data obtained from the standardized application form for the examination RENAGENO and printed the results, both filed in four specialty care services. We included those by laboratory RENAGENO in 18 years and the first examination in those who underwent more than one time, totaling 377 samples. Mutations are described according to the database of HIV resistance at Stanford University (http://hivdb.stanford.edu), estimated their prevalence and resistance is evaluated according to the number of failures at the time of genotyping as well as differences between mutations and subtype B and non-B HIV-1. Results: The M184V mutation was the most prevalent (80.1%), followed by K130N (40.6%) and TAM. In patients who received at least three treatments prior to genotyping, resistance to ZDV, d4T and TDF was associated with mutations M41L, D67N, V118I, L210W, K219Q and T69D; well as resistance to all PI / r was associated with the major mutations M46I, V82A, L90M, I54V, I84V M46L and L76V. HIV-1 subtype B was the most prevalent (90.7%) and there were differences between subtypes B versus mutations: L63P and A71T were more frequent in the subtype B, whereas mutations L76V, K20R, L10V, L89M and F53L were in non-B subtypes. Conclusion: The selection of resistance mutations in HIV-1 related to antiretroviral is similar to that described in the literature. The accumulation of failures to treatment favors the emergence of mutations, reinforcing the monitoring and evaluation of virologic failure by genotyping to minimize the impact resistance. Additional molecular epidemiological studies are needed to better assess the issue of prevalence of subtypes of HIV-1 in the state and possible associations with resistance mutations in HIV-1.

Introdução: Resistência aos antirretrovirais pode limitar opções de tratamento, principalmente em pacientes com acúmulo de falhas terapêuticas, o que pode comprometer resultados clínicos. Objetivos: caracterizar o perfil de mutações na transcriptase reversa e protease do HIV-1 de pacientes em falha ao tratamento. Secundariamente, avaliar associação entre mutações e número de falhas terapêuticas, associação entre mutações e subtipos do HIV-1 e apresentar a evolução temporal da prevalência dos subtipos do HIV-1, no estado do Pará, ao Norte do Brasil. Método: Estudo transversal, no qual se avaliam genotipagens, entre janeiro de 2004 a dezembro de 2013, com dados obtidos de formulário de solicitação do exame padronizado pela RENAGENO e de impressos dos resultados, ambos arquivados em quatro serviços de atendimento especializados. Foram incluídos os testes realizados por laboratório da RENAGENO, em maiores de 18 anos, e o primeiro exame daqueles que o realizaram em mais de um momento, totalizando 377 amostras. As mutações são descritas de acordo com o banco de dados de resistência do HIV da Universidade de Stanford (http://hivdb.stanford.edu), estimam-se suas prevalências e avaliam-se mutações de resistência de acordo com o número de falhas no momento da genotipagem, bem como diferenças de mutações entre subtipos B e não-B do HIV-1. Resultados: A mutação M184V foi a mais prevalente (80,1%), seguida da K130N (40,6%) e TAM. Em pacientes multiexperimentados previamente à genotipagem, resistência a ZDV, d4T e TDF foi associada às mutações M41L, D67N, V118I, L210W, K219Q e T69D; bem como resistência a todos os IP/r associou-se às mutações principais M46I, V82A, L90M, I54V, I84V, M46L e L76V. O subtipo B é o predominante no Pará (90,7%) e diferenças de prevalência de mutações entre subtipos ocorreram entre as mutações L63P e A71T versus subtipo B, enquanto as mutações L76V, M36I, K20R, L10V, L89M e F53L associaram-se ao subtipo não-B. Conclusão: A seleção de mutações de resistência do HIV-1 relacionada aos antirretrovirais é similar ao descrito em literatura. O acúmulo de falhas ao tratamento favorece a emergência de mutações, o que reforça o monitoramento de falha virológica, seguida de genotipagem para minimizar o impacto de resistência. Estudos adicionais de epidemiologia molecular são necessários para avaliar melhor a questão da prevalência de subtipos de HIV-1 no estado e possíveis associações com mutações de resistência do HIV-1. / Introduction: Resistance to antiretroviral treatment can limit treatment options, especially in patients with accumulation of therapeutic failures, which may compromise clinical outcomes. Objectives: characterizing the profile of mutations in the protease and reverse transcriptase of HIV-1 patients in the treatment failure. Secondarily to evaluate the association between mutations and the number of treatment failures, association between mutations and subtypes of HIV-1 and present the temporal evolution of the prevalence of subtypes of HIV-1 in the state of Pará in northern Brazil. Method: cross-sectional study in which genotyping is evaluated between January, 2004 and December, 2013 with data obtained from the standardized application form for the examination RENAGENO and printed the results, both filed in four specialty care services. We included those by laboratory RENAGENO in 18 years and the first examination in those who underwent more than one time, totaling 377 samples. Mutations are described according to the database of HIV resistance at Stanford University (http://hivdb.stanford.edu), estimated their prevalence and resistance is evaluated according to the number of failures at the time of genotyping as well as differences between mutations and subtype B and non-B HIV-1. Results: The M184V mutation was the most prevalent (80.1%), followed by K130N (40.6%) and TAM. In patients who received at least three treatments prior to genotyping, resistance to ZDV, d4T and TDF was associated with mutations M41L, D67N, V118I, L210W, K219Q and T69D; well as resistance to all PI / r was associated with the major mutations M46I, V82A, L90M, I54V, I84V M46L and L76V. HIV-1 subtype B was the most prevalent (90.7%) and there were differences between subtypes B versus mutations: L63P and A71T were more frequent in the subtype B, whereas mutations L76V, K20R, L10V, L89M and F53L were in non-B subtypes. Conclusion: The selection of resistance mutations in HIV-1 related to antiretroviral is similar to that described in the literature. The accumulation of failures to treatment favors the emergence of mutations, reinforcing the monitoring and evaluation of virologic failure by genotyping to minimize the impact resistance. Additional molecular epidemiological studies are needed to better assess the issue of prevalence of subtypes of HIV-1 in the state and possible associations with resistance mutations in HIV-1.

Many materials are made up of small crystals, or grains. Grain boundaries are the interfaces between two grains and affect the flow of heat through the material. These interfaces serve to interfere with the energy carriers by scattering or disrupting them. Because of the negative effect these interfaces have on these energy carriers, they inhibit heat flow and act as thermal resistors. The thermal boundary resistance between two grains of the same material is sometimes referred to as the Kapitza resistance, although this term is also used to describe the thermal resistance between solid/solid interfaces of different materials or solid/liquid interfaces. A better understanding of the heat transport process on a micro-scale is especially relevant to nuclear energy applications. Nuclear fuels are polycrystalline materials that experience large heat differences over small distances. An improved understanding of these grain boundaries and the role they play in transferring heat can help better predict nuclear fuel performance and improve nuclear reactor efficiency and safety. The study of the thermal resistance across crystal interfaces and their potential influence on nuclear fuels is a topic that has received relatively little attention. While the thermal resistance across a single grain boundary is rather small, the total resistance generated from many grain boundaries can have a big impact on the material. Smaller grains mean there are more interfaces, which will result in a lower overall thermal conductivity. For this study, Kapitza resistance across individual grain boundaries was measured using a laser-based measurement technique. The sample material was Cerium Oxide. It was used because of its similar properties to Uranium Oxide, which is a popular material used in nuclear fuel. The average interfacial thermal resistance measured at room temperature in this thesis study was 9.88∙10-9 �2�/�. The average measured value fit in an accepted range from other results found in similar studies.

Soybean mosaic virus (SMV) and peanut mottle virus (PMV) are potyviruses that can cause serious yield reductions in soybean [Glycine max (L.) Merr.]. Virus resistant soybean cultivars have been released with alleles at the Rsv1 and Rpv1 locus that confer resistance to SMV and PMV, respectively. A high-resolution map-based cloning approach was undertaken to isolate Rsv1 and Rpv1 from soybean, with hopes of providing insight into this host-pathogen relationship. A mapping population of 1,056 F2 individuals was constructed from the cross of the resistant cultivar PI 96983 (Rsv1 and Rpv1) by the susceptible cultivar Lee 68 (rsv1 and rpv1). Ninety-one of the 1,056 F2 individuals had a cross-over (recombination) in the chromosomal region between microsatellite, or simple sequence repeat (SSR) marker loci Hsp176 and Sat120, and these 91 recombinant lines (RLs) were selected for further genetic analysis. Genotypes of Rsv1 and Rpv1 for the 91 RLs were obtained by inoculating their F2:3 progeny with SMV-G1 and PMV-P1, respectively. The 91 RLs also were used for mapping one random amplified polymorphic DNA (RAPD), five SSR, and 21 restriction fragment length polymorphism (RFLP) markers. Included in these RFLP markers were seven resistance gene candidate (RGC) and five resistance gene candidate flanking (RGCF) markers. RGC probes encode a protein with homology to previously cloned plant disease resistance genes, and RGCF probes are sequences obtained from the flanking regions of candidate disease resistance genes. The resultant high-resolution map consisted of 41 marker loci detected by 27 molecular markers. Rsv1 and Rpv1 cosegregated with one or more RFLP bands detected by RGCF probes: GG27-1a, 3gG2SP, and/or T3G. Analyses of the disease reaction and molecular marker data from seven RLs suggested that the map position of Rsv1 should be at a locus different from that designated by the linkage analysis software, Mapmaker 3.0. Compared to the other 89 RLs, a high percentage (>34%) of F3 plants grown from four of these seven RLs gave a necrotic reaction when inoculated with SMV-G1. From this evidence, we believed that another locus independent of Rsv1 was involved in PI 96983's response to SMV-G1. The two loci conferring resistance to SMV-G1 were designated Rsv1a and Rsv1b. / Master of Science

The aim of this study was to explore the role of feedback in managing resistance to organisational change. A general systems theoretical model of individual resistance to change was developed. It describes the origin, function and outcomes of individual resistance to planned organisational change. The role of feedback within this process was identified as a central one and feedback was therefore identified as an important point of leverage in managing resistance to change. The survey feedback approach was adopted in a retail organisation undergoing significant change. Staff were asked to respond to a survey on their experience of the change. Results were analysed and then fed back to them during group discussions. The process was repeated. It was concluded that the survey feedback approach significantly contributed to a reduction in resistance to change and that both survey feedback approach and the model of individual resistance to change merit further investigation. / Industrial Psychology / M.A. (Industrial Psychology)

The aim of this study was to explore the role of feedback in managing resistance to organisational change. A general systems theoretical model of individual resistance to change was developed. It describes the origin, function and outcomes of individual resistance to planned organisational change. The role of feedback within this process was identified as a central one and feedback was therefore identified as an important point of leverage in managing resistance to change. The survey feedback approach was adopted in a retail organisation undergoing significant change. Staff were asked to respond to a survey on their experience of the change. Results were analysed and then fed back to them during group discussions. The process was repeated. It was concluded that the survey feedback approach significantly contributed to a reduction in resistance to change and that both survey feedback approach and the model of individual resistance to change merit further investigation. / Industrial Psychology / M.A. (Industrial Psychology)

Master of Science / Department of Biomedical Science / H. Morgan Scott / The modern phenomenon of increasing prevalence of antibiotic resistance in clinically relevant bacteria threatens humanity’s ability to use antibiotics to treat infection in both humans and animals. Despite the marked complexity of bacterial evolution, there is tremendous importance in unfolding the process by which antibiotic resistance genes emerge, disperse, and persist in the natural world. This thesis investigates certain aspects of this process in two experimental studies that differ primarily by scale but also by methodology. The first study examined the long-term annual prevalence of ceftiofur and tetracycline resistance in Canadian beef cattle from 2002 to 2011 at both phenotypic and genotypic levels. Ceftiofur was present at a very low prevalence (<4%) that did not statistically increase over the decade (p<0.05). Relative proportions of tetracycline genes tet(A), tet(B), and tet(C) also did not significantly change over the observation period. However, it was surprising that almost 20% of isolates recovered from nonselective agar harbored tet(C) given that current literature generally indicates that tet(C) is significantly less prevalent than tet(A) or tet(B). The usage of historical samples in addition to parallel selective plating using agar supplemented with antibiotics provided insight into systemic bias present in common microbial approaches. Long-term sample freezing significantly diminished the recoverability of E. coli over time. Additionally the usage of selective MacConkey agar containing tetracycline biased the proportions of tetracycline genes to over-represent the tet(B) gene in commensal E. coli compared to nonselective MacConkey agar. The second study attempted to explain the short-term selection effects of antibiotic treatment on the overall ecological fitness of commensal E. coli using bacterial growth parameters estimated from spectrophotometric growth curves as a simple surrogate of general fitness. Treating cattle with either tetracycline or ceftiofur was found to not only select in favor of tetracycline resistant bacteria, but also increased the overall fitness among the tetracycline resistant population. However, growth curves were unable able to explain why transiently selected resistant bacteria were eventually replaced by susceptible bacteria once the selection pressure was removed.

The rate at which bacterial pathogens are becoming resistant to antibiotics is quite alarming, and therefore much attention has been focussed on this area. The mechanism whereby the bacterial cells acquire resistance is studied in order to determine how this process works as well as to determine if any future resistance mechanisms can be circumvented. In this study three different genera and the antibiotics that are resistant to them were used, namely, penicillin resistant Streptococcus, vancomycin resistant Enterococcus and methicillin resistant Staphylococcus. The results prove that the active sites SXXK, SXN and KT(S) G in the penicillin resistance Streptococcus plays a major role in resistance. It is seen in this study that the SXXK active site is found in all the resistant and most of the intermediate strains, therefore proving to be an important component of the cell wall resistance. It was subsequently noticed the greater the number of mutations found in the sequences the higher the resistance. Three dimensional structures showed the actives sites and their binding pockets. The results also show the change in conformation with a mutation in the active site. The results also proved that the Penicillin Binding Protein (PBP) genes essential for resistance are PBP Ia, PBP 2b and PBP 2x. The results obtained, for the vancomycin resistance in Enterococcus study, proved that the VanC and VanE cluster are very much alike and VanE could have evolved from VanC. There is also close similarity between the different ligase genes. The VanX 3D structure shows the position of the critical amino acids responsible for the breakdown of the D-Ala-D-Ala precursors, and the VanA ligase 3D structure shows the amino acids responsible the ligation of the D-Ala-D-Lac precursors. The analysis performed on the methicillin resistance in Staphylococcus study showed that the genes used to confer resistance are very similar between different strains as well as different species. / Thesis (M.Sc.)-University of KwaZulu-Natal, Pietermaritzburg, 2005.

To improve understanding of the effectiveness of host resistance against Leptosphaeria spp., three aspects of effectiveness of resistance were investigated. With focus on the major Rlm-mediated resistance against L. maculans, changes in effectiveness of Rlm7-mediated resistance to prevent initiation of disease epidemics at the leaf spot stage were investigated in winter oilseed rape field experiments at five sites in the UK over the period with the cropping seasons 2009/2010 - 2013/2014. L. maculans isolates virulent against Rlm7 were identified in the UK. This may be associated with observed changes in lesion phenotypes on the Rlm7 cultivars in field conditions. However, despite increased severity of phoma leaf spotting on Rlm7 cultivars, there was no associated increase in phoma stem canker severity at the end of the cropping seasons. The effectiveness of winter oilseed rape cultivars for control of phoma stem canker (caused by L. maculans or L. biglobosa) was affected by the coexistence of the two Leptosphaeria species in oilseed rape crops. Weather conditions influenced ascospore release of both species and favoured L. biglobosa ascospore release in 2011, resulting in subsequent increased L. biglobosa phoma leaf spotting and stem canker severity. However, coexistence of Leptosphaeria spp. on oilseed rape crops was affected by the cultivar resistance against L. maculans. CE experiments showed that there were interactions between the two Leptosphaeria spp. in planta. Their coexistence on B. napus was influenced by the different host responses that they trigger during host colonisation. Effects of increased temperature on effectiveness of resistance against L. maculans and on severity of symptoms by Leptosphaeria spp. on B. napus were investigated. Increased temperature affected both Rlm4- and Rlm7-mediated resistance, when assessed by phenotypic and molecular techniques. Increased temperature was associated with increased symptom severity, for both L. maculans and L. biglobosa lesions on plants. Cultivar quantitative resistance background increased effectiveness of resistance against phoma stem canker pathogens at increased temperature and should be deployed in in strategies for adaptation to climate change to avoid increased phoma stem canker epidemics in the future.