VictorJuiz/thesis huggingface dataset:
Multi-agent exploration of indoor environments under limited communication constraints
Keywords: Robotics
Multi-Agent Systems

This thesis considers cooperation strategies for teams of agents autonomously exploring an unknown indoor environment under limited communication constraints. The primary application considered is Urban Search-and-Rescue, although other applications are possible, such as surveying hazardous areas. We focus on developing cooperation strategies that enable periodic communication between the exploring agents and the base station (human operators). Such strategies involve an inherent trade-off between allocating team resources towards facilitating communication and increasing the speed of exploration.
We propose two classes of approaches to address this problem: using opportunistic rendezvous to guide the team behaviour, and explicitly arranging rendezvous between agents. In the opportunistic approach, the allocation of team resources between exploration and communication can be indicated with a single numerical parameter between 0 and 1 -- the return ratio -- which leads to complex emergent cooperative behaviour. We show that in some operating environments agents can benefit from explicitly arranging rendezvous. We propose a novel definition of a rendezvous location as a tuple of points and show how such locations can be generated so that the topology of the environment and the communication ranges of agents can be exploited. We show how such rendezvous locations can be used to both improve the speed of exploration and to improve team connectivity by allowing relays to contribute to the overall exploration.
We evaluate these approaches extensively in simulation and discuss their applicability in search-and-rescue scenarios.
Bounds on computation from physical principles
Keywords: Generalised probabilistic theories
Quantum computation

The advent of quantum computing has challenged classical conceptions of which problems are efficiently solvable in our physical world. This raises the general question of what broad relationships exist between physical principles and computation. The current thesis explores this question within the operationally-defined framework of generalised probabilistic theories. In particular, we investigate the limits on computational power imposed by simple physical principles. At present, the best known upper bound on the power of quantum computers is that BQP is contained in AWPP, where AWPP is a classical complexity class contained in PP. We define a circuit-based model of computation in the above mentioned operational framework and show that in theories where local measurements suffice for tomography, efficient computations are also contained in AWPP. Moreover, we explicitly construct a theory in which the class of efficiently solvable problems exactly equals AWPP, showing this containment to be tight. We also investigate how simple physical principles bound the power of computational paradigms which combine computation and communication in a non-trivial fashion, such as interactive proof systems. Additionally, we show how some of the essential components of computational algorithms arise from certain natural physical principles. We use these results to investigate the relationship between interference behaviour and computational power, demonstrating that non-trivial interference behaviour is a general resource for post-classical computation. We then investigate whether post-quantum interference is a resource for post-quantum computation. Sorkin has defined a hierarchy of possible post-quantum interference behaviours where, informally, the order in the hierarchy corresponds to the number of paths that have an irreducible interaction in a multi-slit experiment. In quantum theory, at most pairs of paths can ever interact in a fundamental way. We consider how Grover's speed-up depends on the order of interference in a theory, and show that, surprisingly, the quadratic lower bound holds regardless of the order of interference.
Resolution of proteotoxic stress in the endoplasmic reticulum by ubiquitin ligase complexes
Keywords: protein degradation
proteotoxic stress
Hrd1
endoplasmic reticulum
E3 ubiquitin ligase

The eukaryotic endoplasmic reticulum (ER) is a multifunctional organelle, primarily responsible for the folding and maturation of secretory proteins, as well as lipid metabolism, calcium homeostasis, ubiquitin-dependent signalling and cell fate decisions. ER-associated degradation (ERAD) oversees protein folding and delivers misfolded proteins for degradation by the proteasome via ubiquitin conjugation mediated by RING-type E3 ubiquitin ligases. An intact ERAD is crucial to cellular homeostasis, as unresolved protein imbalances cause ER stress that ultimately lead to apoptosis. The human ER accommodates at least 25 E3s, however our understanding is mostly limited to Hrd1 and AMFR/gp78, both of which have a defined function in ERAD. To understand the contribution of ER E3s to cellular and organelle homeostasis, this study used mass spectrometry of purified E3 complexes to identify cofactors and build interaction networks of ER-resident E3s. These findings will form the foundation for investigating the biological roles of these ubiquitin ligases. Transcriptional analysis highlighted the centrality of Hrd1 among all ER-resident E3s in response to protein misfolding in the ER. Additionally, the contribution of individual Hrd1 complex components to resolving proteotoxic stress was assessed using a misfolded antibody subunit (IgM heavy chain), rather than conventional pharmacological treatments. The ERAD components essential for substrate degradation and survival under proteotoxic stress were identified, highlighting the pivotal role of Hrd1, its cofactor SEL1L and the Derlin family members. Finally, it was demonstrated that autophagy induction in response to proteasome inhibition is key to relieve the burden of protein misfolding in the ER, as it sustained the survival of cells defective for ERAD. Importantly, this study proposes a potential involvement of Hrd1 in signalling from the ER to autophagy, suggesting potential crosstalk between the ERAD and autophagic pathways.
Markers of synovial inflammation in cohorts at risk of knee osteoarthritis
Keywords: biomarkers
knee osteoarthrits

Background and objectives. Knee osteoarthritis (KOA) is a leading cause of disability in the developed world. Additionally, it is possibly linked with premature mortality. Low-grade inflammation is associated with a high risk of non-traumatic KOA incidence but also with metabolic syndrome. Knee injury is a major risk factor for KOA and is associated with an inflammatory response. Heterogeneity of both the symptoms and progression makes early identification of individuals at risk difficult. The aim of this thesis was to examine the diagnostic value of selected biomarkers to identify microscopic synovitis, examine their predictive value for KOA development and any association with excess premature mortality.
Methods. Four serum biomarkers, COMP, resistin, C3M and CRPM, all linked with both knee pain and synovial or systemic inflammation, were selected and an additional sonographic marker was tested. Data from two cohorts has been utilised for the purpose of this thesis: the Oxford Knee Injury Cohort, a prospective study of NHS patients with recent ACL and/or meniscal injuries, and the Chingford women’s study, a community-based prospective cohort with over 23 years of follow-up.
Results. Cross-sectionally, sonographic markers correspond well with microscopically defined post-traumatic synovitis. Two biomarkers, COMP and resistin, were associated with development of incident radiographic KOA (RKOA), while two others, C3M and CRPM, predicted development of painful RKOA independently to age and BMI. High C3M levels and presence of painful RKOA were associated with premature mortality. Knee pain alone, especially in presence of RKOA was an independent predictor of mortality, but RKOA without pain was not.
Conclusion. These results support the use of the studied biomarkers in complex predictive models for development of KOA and associated premature mortality. Taking the competing risk of death into account is an important consideration in this field
Functional characterisation of multiple sclerosis-­associated single nucleotide polymorphisms in the Eomesodermin region
Keywords: Eomesodermin
MAIT cells
Multiple sclerosis

Multiple sclerosis (MS) is a common inflammatory neurological disease affecting young adults, causing significant disability and increased mortality. Genome wide association studies (GWAS) have uncovered over 100 single nucleotide polymorphisms (SNPs) associated with MS susceptibility, most of which lie outside transcribed DNA and therefore do not have obvious consequences. SNPs in two such non-coding DNA segments upstream of the EOMES gene, encoding Eomesodermin (Eomes) have been consistently associated with MS, as well as with the two other autoimmune diseases rheumatoid arthritis (RA) and ankylosing spondylitis (AS). Eomes has been shown to be important for embryonic and neural development, as well as in the immune system, the latter of which was the focus of this investigation.
The association of genetic polymorphisms in the EOMES region with MS was interrogated using computational methods. Imputation analysis enabled detection of new variants, which aligned with regions of epigenetic significance and possible regions of DNA-interaction, implying an effect on regulation of gene expression.
Subsequently, Eomes expression was characterised in peripheral blood cell populations, with the highest expression detected in natural killer cells and effector/memory T cell subsets, including MAIT cells, an innate-like lymphocyte population. To investigate potential genotype dependent changes in Eomes expression and the effect on downstream pathways, studies were performed using samples from healthy donors prospectively genotyped for the two MS associated loci. Despite observing significant differences in expression between genotype groups in a pilot study, findings in a larger cohort did not reach the threshold for significance. Finally, the presence of MAIT cells was investigated in the context of MS and these cells were detected in MS lesions.
Collectively, in this D.Phil project I have illustrated potential ways in which the functional relevance of disease-associated SNPs in non-coding regions can be studied. This has been thoroughly investigated through computational studies, analysis of gene expression in peripheral blood cells, and in genotype-dependent studies of both expression and downstream function.
Modelling preferences in economics
Keywords: Knightian uncertainty
duality
auction
Catastrophes
competitive equilibrium
indivisible goods
product-mix auction
Incomplete preferences
Social cost of carbon
convex geometry
complements
Policy choice
tropical geometry
substitutes
Climate change

This thesis considers the economics of preferences in two different contexts.
First it examines damages from climate change. I argue that our ignorance of the welfare implications of higher levels of warming, as well as scientific uncertainty in precisely what might trigger these scenarios, imply that our tastes and beliefs are incomplete (in the sense of Galaabaatar and Karni, 2013). That is, there are many 'plausible' ways to evaluate a given scenario.
In Chapter 1, then, I develop this theory, and use it to formally separate climate impacts into three sorts: those understood well, those understood badly, and those representing the worst possible scenario. I provide a generalisation of the 'dismal theorem' of Weitzman (2009a), and address the question of policy choice: prices versus quantities (cf. Weitzman, 1974).
Chapter 2 is an example of the analysis propounded in Chapter 1. I explore the sensitivity of the social cost of carbon to assumed damages from 4C warming, to the assumed extent of CO2 emissions, and to the modelling of the climate and carbon cycles. The analysis shows that differing prior assumptions can alter our evaluation of policy by orders of magnitude.
The second part of this thesis regards preferences for indivisible goods. In Chapter 3, which is joint work with Paul Klemperer, I introduce to this field the 'tropical hypersurface', being those prices at which an agent's demand changes. Simple geometric features of this set tell us the precise trade-offs that interest the agent. Thus we develop a new taxonomy of valuations, demandtypes′;familiar¬ionssuchas⊂stitutesandcomp≤mentsareexamp≤s.F∈ally,weprovidea≠cessaryandsufficientconditiononthesedemand types' for existence of competitive equilibrium, which implies several existing results, as well as new and quite different examples.
Socio-political identity in Chosŏn Korea during the Japanese and Manchu invasions 1567-1637: Barbarians at the gates
Keywords: nationalism
Manchu invasions
socio-political identity
Imjin War

This thesis explores social and political identities in Chosŏn Korea between the years 1567 and 1637, particularly during the Imjin War (1592-1598) and the Manchu Invasions (1627 and 1636-1637). During the Imjin War, the Japanese caused widespread destruction over the entire Korean peninsula and the Ming army entered the country. The Later Jin briefly invaded in 1627 and launched a large scale invasion in 1636. The Manchus overran Chosŏn’s feeble defenses and forced Chosŏn to become a vassal state of the Qing Empire.
Scholars are at odds over the form of socio-political identity during this period of foreign invasion. Some claim these wars created the 'Korean nation' for the first time, while others contend that no such socio-political concepts could have existed before the twentieth century. However, researchers often use the same philosophical approaches and merely select aspects of certain theorists' frameworks that best support their arguments. Both the theories and historian's methodologies are limited in their explanation of socio-political identity of the premodern Korean past and even more so for the time of the Imjin and Manchu Invasions.
My research attempts to solve these theoretical problems by creating a 'fusion of horizons' between past and modern concepts of socio-political identity in order to explore the political and cultural environments of the Chosŏn people before and during the wars (bildung). This is achieved firstly by relying on official government histories and individually written diaries that, together, create a more complete picture of former socio-political identity. Secondly, I propose understanding Chosŏn by looking at the definitions of the king, state, people, culture, history, and foreign world using their own definitions from their own times.
Contingent capital: a theoretical and empirical analysis
Keywords: Basel
monitoring
contingent convertible
market discipline
Contingent capital

This thesis is about the design of contingent capital (CoCos) to induce monitoring and to therefore reduce the expected size of taxpayer funded bailouts. CoCos are debt instruments that either convert into debt or are written down when a bank approaches distress—based on a reduction in the bank's capital.
The thesis begins with a moral hazard model that provides a stylised illustration of the circumstances where either shareholders or CoCo investors can be induced to monitor. It predicts that shareholders will monitor if conversion reduces their claim to zero and CoCo investors will monitor if conversion reduces the value of their claim below what they paid when the CoCo was issued. It then assess different elements of the model—including the social cost that gives rise to the need for bailouts, the usual mechanisms to reduce the need for bailouts, and the bank specific insolvency regime adopted in the European Union.
The focus then turns to monitoring incentives induced by CoCos. It discusses triggers and advocates higher minimum trigger levels. It then defines monitoring in the context of CoCos, assesses the extent to which monitoring is undertaken in CoCo markets, and makes recommendations about how incentives to monitor might be strengthened.
Identification and characterisation of the haematopoietic stem/progenitor cells at risk for leukaemia development following radiation exposure
Keywords: Acute myeloid leukaemia
Radiation
Nod-scid gamma
Haematopoietic stem cell

A variety of epidemiological studies have provided support for an increased leukaemia incidence following exposure to both high and low dose radiation. There is a close histopathological similarity between human and murine acute myeloid leukaemia with mouse models of the disease being most often used. We report here, for the first time, that allogeneic haematopoietic stem cells can compete for niches in the nonmyeloablated NSG bone marrow compartment and that the nonmyeloablated NSG bone marrow microenvironment is capable of supporting allogeneic long-term HSC engraftment and differentiation. Using this NSG transplantation model, we then provided evidence of a reduced contribution of low dose irradiated HSCs towards longterm haematopoiesis. We further report on the generation and characterisation of a novel Chr2MDRmCh mouse model where a construct positioned in the minimal deleted region following radiation exposure carries the fluorescent protein mCherry, which is expressed under control of the ubiquitous Rosa26 promoter. Crossing these mice with Sfpi1GFP mice allowed the early detection of an expanding haematopoietic clone which had lost mCherry fluorescence following radiation exposure (and so also the chromosome 2 homologue carrying the fluorescent construct and the Sfpi1 gene). Finally, we report on a gender-dependent leukaemic progression and characterisation where 3 Gy irradiated male mice only present with acute myeloid leukemia and irradiated female mice mainly develop leukaemia with a lymphoid phenotype. In conclusion, the work in this thesis postulates data obtained from two novel mouse models and which could help to further identify key molecular mechanisms involved in leukaemia initiation and development.
Carry-over and consequences of social connections amongst wild birds
Keywords: Social Relationships
Animal Behaviour
Scrounging
Social Structure
Social Networks
Ornithology
Evolution
Social Information
Ecology
Great tits
Blue tits
Information transmission
Paridae
Spatial Structure
Zoology
Biology

Ecological factors are known to influence the spatial distribution of individuals, which in turn governs social structure. However, social interactions can have important individual- and population-level consequences and may shape various ecological processes (Chapter 1). In this thesis, I examine the factors shaping social networks amongst wild birds (Paridae). I demonstrate that these social connections are biologically important, and influence numerous processes, including spatial structure itself.
First, I demonstrate that both the spatial occurrence and dynamic social decisions of individuals underpin the non-random composition of foraging flocks (Chapter 2). Reciprocally, I show that the spatial arrangement of individuals’ breeding locations is predicted by the previous winter's social network, as birds breed nearer to, and share territory boundaries with, those they held the strongest connections to (Chapter 3).
I then use experiments to directly assess the consequences of social structure. I show that birds exhibit compensatory shifts in their social network position upon removal of their flock mates (Chapter 4). Following this, I introduce a novel experimental system that automatically controls which individuals could feed together. These externally-imposed foraging constraints cause social segregation at non-experimental food patches (Chapter 5), which also carries over into breeding site prospecting (Chapter 5). I show that social information transmission, regarding the location of novel food patches, also changes to correspond to the experimentally imposed social network structure (Chapter 6). Furthermore, social foraging associations are found to influence social learning, as birds appear to prioritise learning from those who provide relevant information on a regular basis. Finally, I demonstrate that birds choose to forgo maximising their own food intake to sustain their relationships (Chapter 7). Through prioritising their pair-bond over their own preferences, this also changes the social composition of foraging flocks, indicating how a single relationship can govern wider social network position. Additionally, I show how social relationships can influence individual behavioural plasticity and the learning of foraging strategies.
This thesis thus contributes to elucidating the relationship between spatial structure and social networks within wild populations. It also demonstrates how social systems respond to external changes, and the direct causal implications of this for shaping spatial structure, information flow and individuals' social and foraging strategies. Together, these findings form a foundation for expanding our understanding of the ecological and evolutionary implications of social networks and the mechanisms underpinning this (Chapter 8).
Mechanisms of long-term presynaptic plasticity at Schaffer-collateral synapses
Keywords: calcium imaging
long-term depression
transmitter release
long-term potentiation
NMDA receptors
synaptic plasticity
L-type voltage-gated calcium channels
nitric oxide
hippocampus

Synaptic plasticity is thought to be integral to learning and memory. The two most common forms of plasticity are long-term potentiation (LTP) and long-term depression (LTD), both of which can be supported either by presynaptic changes in transmitter release probability (Pr), or by postsynaptic changes in AMPA receptor number. It is generally thought that the induction of LTP and LTD at Schaffer-collateral synapses in the hippocampus depends on the activation of NMDA receptors (GluN). Recent studies, however, have demonstrated that both increases and decreases in Pr can be induced under blockade of postsynaptic GluN receptors, suggesting that the activation of postsynaptic GluN receptors by glutamate is only a strict requirement for postsynaptic plasticity. In this thesis, I therefore re-examined the role of glutamate in presynaptic plasticity. I used single synapse imaging along with electrophysiological and pharmacological techniques to independently manipulate and monitor the levels of glutamatergic signalling during synaptic activity. I discovered that glutamate is inhibitory and unnecessary for the induction of LTP at the presynaptic locus. My findings support a novel model of presynaptic plasticity in which the net activity-dependent changes in Pr at an active presynaptic terminal is jointly determined by two opposing processes that can be simultaneously active: 1) postsynaptic depolarization, which, via the activation of L-type voltage-gated Ca2+ channels, increases Pr by driving the synthesis and release of nitric oxide from neuronal dendrites and 2) glutamate release, which through the activation of presynaptic GluN receptors, decreases Pr. Computationally, this model suggests that plasticity functions to reduce prediction-errors that arise during synaptic activity, and, thereby offers a biologically plausible mechanism by which neuronal networks may optimize learning at the level of single synapses.