VictorJuiz/thesis huggingface dataset:
Magnetic distortion calibration for the LHCb Ring Imaging Cherenkov (RICH) Detector, and the search for CP violation in D*+ -&gt; D0(K-K+)pi+ decays

The asymmetry under simultaneous charge and parity transformation (CP violation) has driven the understanding of electroweak interactions since its discovery in the kaon system. CP violation was subsequently discovered in the B system. Charmed mesons form the only heavy neutral meson system in which CP violation has yet to be observed unambiguously.
A Study of indirect CP violation in D mesons through the determination of the parameter Aγ is presented using a data sample of pp collisions, corresponding to an integrated luminosity of 37.7 pb-1, collected with the LHCb detector and recorded at the centre-of-mass energy if 7 TeV at the LHC. The parameter Aγ is the asymmetry of the effective lifetimes measured in decays of D0 and anti-D0 mesons to the CP eigenstates K&plus;K-. Aγ is sensitive to both the CP violation parameters &verbar;q/p&verbar; and φ. Fits to the data sample yield Aγ(KK) = (0.39 ± 0.55 ± 0.24)%, where the first uncertainty is statistical and the second systematic. This result is consistent with no CP violation.
Critical for this analysis is the particle identification provided by the LHCb Ring Imaging Cherenkov (RICH) system. To ensure good performance, a proper calibration of the RICH photon detectors response is necessary. A system for the calibration of the magnetic distortion induced by the LHCb dipole magnet on the photon detector is described. The system currently provides the calibration parameters used in the LHCb event reconstruction software and allows for a significant improvement in the overall particle identification performance.
The dynamics of transnational alliances in Africa, 1990–2010: governments, rebel groups, and power politics

The Second Congo War (1998–2003) is widely considered the deadliest conflict since World War II, yet it has received little attention by International Relations theorists. A closer look reveals that both this war and its precursor, the First Congo War (1996–7), were neither simply intra-state nor just inter-state conflicts; their central feature were transnational alliances between neighboring governments and Congolese rebel groups. In fact, with one exception, every episode of internal war in sub-Saharan Africa from 1990 to 2010 involved external support to the rebel side from at least one African government.
In order to explain both the origins and the dynamics of transnational alliances, this dissertation develops a three-step theory. It explains why governments of weak states support foreign rebel groups, why they choose some groups from a specific country as alliance partners but not others, and why some of these allies subsequently behave uncooperatively towards their foreign sponsors, leading to the breakdown of alliances and the formation of new ones. The theory draws on both the rational choice literature and the realist school of thought. It also adapts insights from principal-agent theory. Overall, the three-step theory presents transnational alliances as the continuation of domestic politics by other means: both governments and rebel groups use them as an instrument in their own domestic struggle for power.
Drawing on a wide range of sources, including over one hundred interviews – almost all of them conducted in the Democratic Republic of Congo, Rwanda, and Uganda – the dissertation uses process tracing to apply the theory to seventeen transnational alliances from the Congo Wars and their aftermath. It also tests the theory’s first step more widely in a cross-case analysis of forty-two African weak state dyads. Together, this multi-method approach demonstrates both the internal and the external validity of the theory.
Pricing exotic options using improved strong convergence

Today, better numerical approximations are required for multi-dimensional SDEs to improve on the poor performance of the standard Monte Carlo integration. With this aim in mind, the material in the thesis is divided into two main categories, stochastic calculus and mathematical finance. In the former, we introduce a new scheme or discrete time approximation based on an idea of Paul Malliavin where, for some conditions, a better strong convergence order is obtained than the standard Milstein scheme without the expensive simulation of the Lévy Area. We demonstrate when the conditions of the 2−Dimensional problem permit this and give an exact solution for the orthogonal transformation (θ Scheme or Orthogonal Milstein Scheme). Our applications are focused on continuous time diffusion models for the volatility and variance with their discrete time approximations (ARV). Two theorems that measure with confidence the order of strong and weak convergence of schemes without an exact solution or expectation of the system are formally proved and tested with numerical examples. In addition, some methods for simulating the double integrals or Lévy Area in the Milstein approximation are introduced. For mathematical finance, we review evidence of non-constant volatility and consider the implications for option pricing using stochastic volatility models. A general stochastic volatility model that represents most of the stochastic volatility models that are outlined in the literature is proposed. This was necessary in order to both study and understand the option price properties. The analytic closed-form solution for a European/Digital option for both the Square Root Model and the 3/2 Model are given. We present the Multilevel Monte Carlo path simulation method which is a powerful tool for pricing exotic options. An improved/updated version of the ML-MC algorithm using multi-schemes and a non-zero starting level is introduced. To link the contents of the thesis, we present a wide variety of pricing exotic option examples where considerable computational savings are demonstrated using the new θ Scheme and the improved Multischeme Multilevel Monte Carlo method (MSL-MC). The computational cost to achieve an accuracy of O(e) is reduced from O(e−3) to O(e−2) for some applications.
Genome-wide analysis of selection in insects, mammals and fungi

Characterising and understanding factors that affect the rate of molecular evolution in proteins has played a major part in the development of evolutionary theory. The early analyses of amino acid substitutions stimulated the development of the neutral theory of molecular evolution, which later evolved into the nearly neutral theory. More recent work has lead to a better understanding of the role selection plays at the molecular level, but there is still limited understanding of how higher levels of protein organisation affect the way natural selection acts.
The investigation of this question is the central aim of this thesis, which is addressed via the analysis of selective pressures in secondary protein structures in insects, mammals and fungi. The analyses for the first two groups were conducted using publically available datasets. To conduct the analyses in fungi, genome sequence data from the fungal genus Microbotryum (sequenced in our laboratory) was assembled and annotated, resulting in the development of a number of bioinformatics tools which are described here. The fungal, insect and mammalian datasets were interrogated with regard to a number of structural features, such as protein secondary structure, position of a site with regard to adaptively evolving sites, hydropathy and solvent-accessibility. These features were correlated with the signals of positive and purifying selection detected using phylogenetic maximum likelihood and Bayesian approaches.
I conclude that all of the factors examined can have an effect on the rate of molecular evolution. In particular, disordered and hydrophilic regions of the protein are found to experience fewer physiochemical constraints and contain a higher proportion of adaptively evolving sites. It is also revealed that positively selected residues are ‘clustered’ together spatially, and these trends persist in the three taxa. Finally, I show that this variation in adaptive evolution is a result of both selective events and physiochemical constraint.
The identification and analysis of molecular biomarkers in the p53 tumour suppressor pathway that affect cancer progression in humans

The tumour suppressor p53 is at the centre of the signalling pathway that controls cellular processes crucial in tumourogenesis, cancer progression and tumour clearance. Alterations in the p53 pathway that lead to cancer progression can be good candidates for molecular biomarkers that would assist in the identification of patients with different prognoses, but also serve as good predictors of appropriate targeted therapies.
Patient cohorts and cancer cell panels are utilised to seek associations with the attenuation of the p53 pathway and cancer progression. Firstly, the alternatively spliced transcript of the p53 inhibitor HDMX, which is frequently found in tumours with poor prognosis, is studied. The high ratio of the alternatively spliced HDMX-S transcript over the full-length HDMX-FL transcript (HDMX-S/FL) is demonstrated to associate with p53 pathway attenuation in cancer cells and breast carcinomas, and with faster metastatic progression of osteosarcoma and breast cancer patients. Secondly, inherited polymorphism in the HDMX gene is investigated and demonstrated as a unique and highly reproducible eQTL, which identifies patients with different prognoses for metastatic disease in breast cancer and melanoma cohorts. Lastly, a screening approach to identify novel inherited polymorphisms in the p53 pathway genes that associate with metastatic progression of melanoma is developed and implemented, and subsequently in silico and in vitro functional analyses are performed to investigate a mechanism behind the FOXO3 SNP, identified as the strongest candidate, whereby the experimental evidence demonstrate that the causal SNP in the FOXO3 haplotype is controlled by the GATA3 transcription factor.
Together, the work presented in this thesis provides strong support for the role of the p53 pathway in the metastatic progression of cancer, and suggests that molecular biomarkers that can detect changes in the activity of p53 pathway genes could offer a robust set of biomarkers for cancer progression applicable to different types of cancer.
The gene structure and the polymorphism of the human complement component C4

1. The DNA sequence of the human complement C4A gene from a cosmid clone Cos 3A3 was determined and the complete exon-intron structure elucidated. The 5' flanking region of the C4 gene contains three TATA sequences and a transcriptional enhancer core sequence, which are >200 nucleotides (nt) and 60-70 nt upstream from the CAP site, respectively. The gene consists of 42 exons coding for a precursor protein of 1745 residues. The first exon codes for a 51 nt 5' untranslated sequence, a leader peptide of 19 residues, and the N-terminus of the β chain. The β-α and the α-γ chain junctions are encoded by exons 17 and 34, respectively. The anaphylatoxin C4a and the thiolester site are encoded by phase 1-1 symmetrical exons. Most of the amino acids encoded at the splice junctions are polar or charged. Between exons 10 and 11 is a 6-7 kb intron that is flanked by direct long terminal repeats and may be absent in some C4 genes located at the second C4 locus. The last exon codes for the C-terminus of the γ chain and a 140 bp 3' untranslated sequence. The intergenic region between the C4 gene and its neighbouring 21-hydroxylase (210Hase) gene is ~3028 bp.
2. Eighteen polymorphic amino acids on C4 have been identified through genomic DNA, cDNA and protein sequencing. Fourteen of them are located on the* chain (C4a: 2 changes; C4d: 12 changes). The rest are scattered on the β and the γ chains. There are potential size variations by one residue on the β chain, and by a tripeptide that contains a sulphation site on the α chain.
3. Four common and rare C4 alleles have been cloned from individuals whose C4 proteins were chemically and serologically characterised. Analysis of the sequences at the C4d regions has allowed the identification of the C4A/C4B isotypic residues at positions 1101-6: C4A has the sequence PCPVLD, while C4B has the sequence LSPVIH. Presumably these isotypic residues are the cause of the class-specific, differential chemical reactivates. Moreover, the probable locations for the two Eodgers (Kg) and the six Chido (Ch) antigenic determinants were deduced. The C4B isotypic residues may be involved in the expression of the Ch2 and the Ch4 epitopes, while the C4A isotypic residues may not be related to either of the Eg determinants.
4. Definitive restriction fragment length polymorphisms (RFLPs) representing the exact locations responsible for the isotypicity between C4A and C4B, and for their generally associated Rg1 and Ch1 antigenic determinants, have been designed. In combination with the Taq I polymorphic patterns specific for the C4 and for the 210Hase gene loci, it has been shown that the null allele of the HLA haplotype B44 DR6 C4A 3 C4B QO is not a C4B allele, but probably encodes another C4A 3 allotype at the second C4 locus.
The sea officers: gentility and professionalism in the Royal Navy, 1775-1815

This thesis argues that British naval officers provide a useful category of analysis for social and cultural historians. While previous scholarship has largely ignored naval officers or treated them as equivalent, socially and professionally, to army officers or the traditional professions, the present study argues that the nature of service at sea presented challenges to officers' social status. Drawing on thousands of recently-digitized sources, as well as extensive archival materials, it explores the formation of naval officers' social identity, the forces that shaped their careers, and the changing landscape of social status at the end of the eighteenth century. The demands of life at sea placed naval officers in a liminal social space. Their claims to gentility were contingent and contested. They needed to be proficient in practical as well as theoretical skills. At the same time, officers were expected to be gentlemen. How officers shaped, and were shaped by, the changing definitions of that term provides the framework for the thesis.
It makes three central contributions to the fields of British social and naval history. First, it emphasizes the continuing significance of social status boundaries in Georgian Britain. The existing literature misconstrues the chronology of the changing nature of gentility and misunderstands the relationship of naval officers to issues of gentility and professionalism. Second, it recalibrates our understanding of the nature and mechanisms of patronage networks. Social backgrounds made relatively insignificant contributions to shaping officers' careers; patrons used a much wider range of criteria when selecting clients. Finally, it questions the traditional separation of naval history from social and cultural history. The Navy and naval officers were central to British life at the end of the eighteenth century and cannot be effectively analysed separately. The Navy was both socially unique and uniquely important to Britain during the crisis of the Wars with Revolutionary and Napoleonic France.
ENU mouse mutant with a hypomorphic mutation in DNA ligase IV

This thesis describes the generation, mapping, and characterisation of a mutant mouse strain derived from a genome-wide ENU mutagenesis programme in collaboration between Australian National University and Oxford University funded by the Wellcome Trust. Starting with the identification of the growth retardation and immunodeficiency phenotype in the G3 progeny of one mutagenised mouse, we mapped the mutation to the DNA Ligase IV (LigIV) gene. The enzyme is the final component of the nonhomologous end joining (NHEJ) pathway of DNA double strand break repair, which is involved in maintenance of genomic stability and in VDJ rearrangement of lymphocyte receptor genes. The mutation is a single base change that results in a Y288C amino acid substitution near the active site of the LigIV enzyme. The mutation causes an over 20- fold reduction in the LigIV enzymatic activity in vivo, partly though its effect on protein stability and expression levels.
This mouse strain is the first viable animal model of LigIV deficiency, and therefore this work contributes to our understanding of the pathology of the human LigIV syndrome. Here we provide a detailed characterisation of the strain, addressing a number of questions about the physiological pathways in which LigIV activity is limiting. Lymphocyte development is impaired in the mutants and peripheral lymphocyte numbers are reduced nearly 100-fold, but a population of B1 cells develops in the peritoneal cavity. In addition to impaired VDJ rearrangement, lymphocyte survival in peripheral lymphoid organs is also affected by the mutation and this may contribute to the lymphopenia. We also demonstrate that LigIV is required for normal immunoglobulin class switching. Furthermore, the mutant bone marrow is deficient in reconstituting haematopoiesis in irradiated recipients and we observe an age-dependent decline in the stem and progenitor cell population in the bone marrow of the mutant mice, suggesting that LigIV activity may also be limiting in the maintenance and function of haematopoietic stem cells. In addition, the mutant mice are highly predisposed to haematopoietic malignancies.
This demonstrates how ENU mutagenesis can be used to create hypomorphic alleles of genes essential for survival, contributing to our understanding of the function of mammalian genes and creating animal models of human genetic diseases.
The earthquake cycle of the Manyi Fault, Tibet

This thesis focuses on the Manyi Fault in Northern Tibet which experienced a Mw 7.6 earthquake in 1997. The remoteness of the area limits the feasibility of measurements in the field, however the climate makes it ideal to study by remote sensing, specifically Interferometric Synthetic Aperture Radar (InSAR). The mechanics of the earthquake have been well documented however there are still numerous questions about the other stages of the earthquake cycle (postseismic and interseismic) across the fault. Previous studies of the postseismic motion across the Manyi Fault using four years of ERS SAR data show the deformation can be explained by either viscoelastic relaxation of a Standard Linear Solid body with a viscosity of 4x1018 Pa s or afterslip. We use the ERS timeseries and ratemaps formed from a network of ENVISAT SAR scenes from 2003-2010 to analyse the postseismic deformation. We create a series of afterslip models based on rate-and-state frictional laws, along with series of viscoelastic models with various rheologies (Maxwell and Burgers). Our results show that an afterslip model fits the data slightly better than a Burgers rheology but not within resolvable errors. A range of afterslip models fit the data well, with frictional parameters ranging from 8x10-4 to 2x10-3 and a preseismic slip rate of 8 to 20 mm/yr. The best-fitting Burgers rheology has a Kelvin element viscosity of 4x1018 Pa s and Maxwell element viscosity of 6x1019 Pa s. We analyse the interseismic InSAR signal observed before the 1997 earthquake using ERS data from 1992-1997 to find that the Manyi Fault was accumulating strain at 3+/-2 mm/yr. We also find the seismic locking depth was 22+/-15 km which correlates with the maximum depth of slip during the earthquake. We show there is no significant deformation across the fault to the north of the Manyi Fault which may be an extension to the Kunlun fault. We discuss an analytical 2D thin viscous channel model from literature that has been shown to match the data in this thesis. We show that, once errors are properly accounted for, their model cannot explain both the post and preseismic datasets.

Keywords: postseismic
rheology
afterslip
tectonics
viscoelastic
earthquakes
Manyi
Tibet
Advisor: Parsons, B
Fronto-temporal connections in schizophrenia and bipolar disorder

Schizophrenia and bipolar disorder are chronic and devastating disorders affecting 1% of the population worldwide. They have the same prevalence in both sexes, although it is well accepted that schizophrenic men present an earlier age of onset, higher prevalence of negative symptoms and poorer prognosis. With the advent of neuroimaging techniques such as computed tomography scans and magnetic resonance imaging (MRI), it has been possible to discover brain abnormalities in these disorders. The vast majority of the studies have focused on the grey matter of the brain; however, since 1994, diffusion-weighted images (DWI) allow us to detect white matter abnormalities (Le Bihan et al). This study aims to analyse white matter connections between the frontal and temporal lobes in healthy controls, schizophrenic and bipolar patients.
30 schizophrenic, 21 bipolar patients and 35 healthy controls were matched for age. Probabilistic tractography, the state-of-the-art technique, was used for tracing the uncinate and arcuate fasciculus and the cingulum bundle. Grey matter and white standard space masks were used for tracing these bundles and compared in terms of which were more consistent and reliable for diffusion tensor imaging (DTI) measurements.
Major psychosis showed a greater reduction of factional anisotropy (FA) than controls in the arcuate fasciculus bilaterally and a trend for decreased FA in the uncinate fasciculus bilaterally. No FA, mean diffusivity (MD) or Volume differences were found in the cingulum bundle.
Schizophrenic and bipolar patients showed an FA reduction in the arcuate and uncinate fasciculus compared to controls. Asymmetries were present in patients and controls for the FA, MD and Volume. No sex differences were found in patients or controls.
White matter masks are preferred for analysing FA and MD and grey matter masks for the Volume of a whole tract.

Keywords: cingulum bundle
uncinate fasciculus
arcuate fasciculus
schizophrenia
diffusion tensor imaging
bipolar disorder
Advisor: Mackay, C