NATO's experience of supporting security sector reform in the Western Balkans (1995-2015)

© Cranfield University, 2017This thesis has considered the theoretical and practical underpinning of SSR and NATO's role in its application within two countries of the Western Balkans. It began by reviewing the extant literature on SSR and then analysed NATO's evolution and how it developed its role in assisting countries with reform of their security sectors in the aftermath of the Cold War. Unlike organisations such as the UN and EU, NATO does not have a formal policy and conceptual framework for Security Sector Reform (SSR) but uses a range of interlocking programmes that have evolved over time. The thesis examined critically NATO's interventions in both Bosnia-Herzegovina and Kosovo and how that role transformed from being a security provider to one of advising and mentoring on reform of the security sectors. A comparative analysis was then conducted of the cross-case data presented in the two case studies. The research has reinforced the reality that different actors with different agendas will inevitably complicate an already challenging situation in postconflict and post-authoritarian countries. It became evident that national agendas within the North Atlantic Council also influenced the Alliance's ability to support SSR in the two countries studied. Through a combination of both primary and secondary research the study has established that NATO still managed to add considerable value to these reform processes and has the potential for doing so in the future in other countries. There were limitations to its approach and these have been highlighted. At times NATO's contextual understanding of the situation on the ground was weak and its use of political soft power to encourage the reforms in the countries studied was eclectic but, ultimately, it has had a measure of success in its endeavours. The research has generated a framework of factors for NATO to use when considering current and potential SSR engagements. As NATO becomes more deeply involved in projecting stability through SSR support after a decade of war fighting, this list of factors could have international significance

Evolutionary prisoner's dilemma game on a square lattice

A simplified prisoner's game is studied on a square lattice when the players interacting with their neighbors can follow only two strategies: to cooperate (C) or to defect (D) unconditionally. The players updated in a random sequence have a chance to adopt one of the neighboring strategies with a probability depending on the payoff difference. Using Monte Carlo simulations and dynamical cluster techniques we study the density $c$ of cooperators in the stationary state. This system exhibits a continuous transition between the two absorbing state when varying the value of temptation to defect. In the limits $c \to 0$ and 1 we have observed critical transitions belonging to the universality class of directed percolation.Comment: 6 pages including 6 figure

Series expansions of the percolation probability on the directed triangular lattice

We have derived long series expansions of the percolation probability for site, bond and site-bond percolation on the directed triangular lattice. For the bond problem we have extended the series from order 12 to 51 and for the site problem from order 12 to 35. For the site-bond problem, which has not been studied before, we have derived the series to order 32. Our estimates of the critical exponent $\beta$ are in full agreement with results for similar problems on the square lattice, confirming expectations of universality. For the critical probability and exponent we find in the site case: $q_c = 0.4043528 \pm 0.0000010$ and $\beta = 0.27645 \pm 0.00010$; in the bond case: $q_c = 0.52198\pm 0.00001$ and $\beta = 0.2769\pm 0.0010$; and in the site-bond case: $q_c = 0.264173 \pm 0.000003$ and $\beta = 0.2766 \pm 0.0003$. In addition we have obtained accurate estimates for the critical amplitudes. In all cases we find that the leading correction to scaling term is analytic, i.e., the confluent exponent $\Delta = 1$.Comment: 26 pages, LaTeX. To appear in J. Phys.

Vortex dynamics in a three-state model under cyclic dominance

The evolution of domain structure is investigated in a two-dimensional voter model with three states under cyclic dominance. The study focus on the dynamics of vortices, defined by the points where three states (domains) meet. We can distinguish vortices and antivortices which walk randomly and annihilate each other. The domain wall motion can create vortex-antivortex pairs at a rate which is increased by the spiral formation due to the cyclic dominance. This mechanism is contrasted with a branching annihilating random walk (BARW) in a particle antiparticle system with density dependent pair creation rate. Numerical estimates for the critical indices of the vortex density ($\beta=0.29(4)$) and of its fluctuation ($\gamma=0.34(6)$) improve an earlier Monte Carlo study [Tainaka and Itoh, Europhys. Lett. 15, 399 (1991)] of the three-state cyclic voter model in two dimensions.Comment: 5 pages, 6 figures, to appear in PR

Modification of an aggressive model of Alport Syndrome reveals early differences in disease pathogenesis due to genetic background

The link between mutations in collagen genes and the development of Alport Syndrome has been clearly established and a number of animal models, including knock-out mouse lines, have been developed that mirror disease observed in patients. However, it is clear from both patients and animal models that the progression of disease can vary greatly and can be modifed genetically. We have identifed a point mutation in Col4a4 in mice where disease is modifed by strain background, providing further evidence of the genetic modifcation of disease symptoms. Our results indicate that C57BL/6J is a protective background and postpones end stage renal failure from 7 weeks, as seen on a C3H background, to several months. We have identifed early diferences in disease progression, including expression of podocyte-specifc genes and podocyte morphology. In C57BL/6J mice podocyte efacement is delayed, prolonging normal renal function. The slower disease progression has allowed us to begin dissecting the pathogenesis of murine Alport Syndrome in detail. We fnd that there is evidence of diferential gene expression during disease on the two genetic backgrounds, and that disease diverges by 4 weeks of age. We also show that an infammatory response with increasing MCP-1 and KIM-1 levels precedes loss of renal function

Anomalous Behavior of the Contact Process with Aging

The effect of power-law aging on a contact process is studied by simulation and using a mean-field approach. We find that the system may approach its stationary state in a nontrivial, nonmonotonous way. For the particular value of the aging exponent, $\alpha=1$, we observe a rich set of behaviors: depending on the process parameters, the relaxation to the stationary state proceeds as $1/\ln t$ or via a power law with a nonuniversal exponent. Simulation results suggest that for $0<\alpha<1$, the absorbing-state phase transition is in the universality class of directed percolation.Comment: 4 pages revtex (twocolumn, psfig), 3 figure

Series expansions of the percolation probability for directed square and honeycomb lattices

We have derived long series expansions of the percolation probability for site and bond percolation on directed square and honeycomb lattices. For the square bond problem we have extended the series from 41 terms to 54, for the square site problem from 16 terms to 37, and for the honeycomb bond problem from 13 terms to 36. Analysis of the series clearly shows that the critical exponent $\beta$ is the same for all the problems confirming expectations of universality. For the critical probability and exponent we find in the square bond case, $q_c = 0.3552994\pm 0.0000010$, $\beta = 0.27643\pm 0.00010$, in the square site case $q_c = 0.294515 \pm 0.000005$, $\beta = 0.2763 \pm 0.0003$, and in the honeycomb bond case $q_c = 0.177143 \pm 0.000002$, $\beta = 0.2763 \pm 0.0002$. In addition we have obtained accurate estimates for the critical amplitudes. In all cases we find that the leading correction to scaling term is analytic, i.e., the confluent exponent $\Delta = 1$.Comment: LaTex with epsf, 26 pages, 2 figures and 2 tables in Postscript format included (uufiled). LaTeX version of tables also included for the benefit of those without access to PS printers (note that the tables should be printed in landscape mode). Accepted by J. Phys.

Critical behaviour of a surface reaction model with infinitely many absorbing states

In a recent letter [J. Phys. A26, L801 (1993)], Yaldram et al. studied the critical behaviour of a simple lattice gas model of the CO-NO catalytic reaction. The model exhibits a second order nonequilibrium phase transition from an active state into one out of infinitely many absorbing states. Estimates for the critical exponent $\beta$ suggested that the model belongs to a new universality class. The results reported in this article contradict this notion, as estimates for various critical exponents show that the model belongs to the universality class of directed percolation.Comment: 10p+5fig, LaTeX+fig in uuencoded P

Predicting GP visits: A multinomial logistic regression investigating GP visits amongst a cohort of UK patients living with Myalgic encephalomyelitis

Background Myalgic Encephalomyelitis (ME) is a chronic condition whose status within medicine is the subject of on-going debate. Some medical professionals regard it as a contentious illness. Others report a lack of confidence with diagnosis and management of the condition. The genesis of this paper was a complaint, made by an ME patient, about their treatment by a general practitioner. In response to the complaint, Healthwatch Trafford ran a patient experience-gathering project. Method Data was collected from 476 participants (411 women and 65 men), living with ME from across the UK. Multinomial logistic regression investigated the predictive utility of length of time with ME; geographic location (i.e. Manchester vs. rest of UK); trust in GP; whether the patient had received a formal diagnosis; time taken to diagnosis; and gender. The outcome variable was number of GP visits per year. Results All variables, with the exception of whether the patient had received a formal diagnosis, were significant predictors. Conclusions Relationships between ME patients and their GPs are discussed and argued to be key to the effective delivery of care to this patient cohort. Identifying potential barriers to doctor patient interactions in the context of ME is crucial

Tissue Proteome of 2-Hydroxyacyl-CoA Lyase Deficient Mice Reveals Peroxisome Proliferation and Activation of ω-Oxidation

Peroxisomal fatty acid α-oxidation is an essential pathway for the degradation of β-carbon methylated fatty acids such as phytanic acid. One enzyme in this pathway is 2-hydroxyacyl CoA lyase (HACL1), which is responsible for the cleavage of 2-hydroxyphytanoyl-CoA into pristanal and formyl-CoA. Hacl1 deficient mice do not present with a severe phenotype, unlike mice deficient in other α-oxidation enzymes such as phytanoyl-CoA hydroxylase deficiency (Refsum disease) in which neuropathy and ataxia are present. Tissues from wild-type and Hacl1−/− mice fed a high phytol diet were obtained for proteomic and lipidomic analysis. There was no phenotype observed in these mice. Liver, brain, and kidney tissues underwent trypsin digestion for untargeted proteomic liquid chromatography-mass spectrometry analysis, while liver tissues also underwent fatty acid hydrolysis, extraction, and derivatisation for fatty acid gas chromatography-mass spectrometry analysis. The liver fatty acid profile demonstrated an accumulation of phytanic and 2-hydroxyphytanic acid in the Hacl1−/− liver and significant decrease in heptadecanoic acid. The liver proteome showed a significant decrease in the abundance of Hacl1 and a significant increase in the abundance of proteins involved in PPAR signalling, peroxisome proliferation, and omega oxidation, particularly Cyp4a10 and Cyp4a14. In addition, the pathway associated with arachidonic acid metabolism was affected; Cyp2c55 was upregulated and Cyp4f14 and Cyp2b9 were downregulated. The kidney proteome revealed fewer significantly upregulated peroxisomal proteins and the brain proteome was not significantly different in Hacl1−/− mice. This study demonstrates the powerful insight brought by proteomic and metabolomic profiling of Hacl1−/− mice in better understanding disease mechanism in fatty acid α-oxidation disorders