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    32151 research outputs found

    A character theoretic formula for base size

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    Funding: Research of Coen del Valle is supported by the Natural Sciences and Engineering Research Council of Canada (NSERC), [funding reference number PGSD-577816-2023], as well as a University of St Andrews School of Mathematics and Statistics Scholarship.A base for a permutation group G acting on a set Ω is a sequence B of points of Ω such that the pointwise stabiliser GB is trivial. The base size of G is the size of a smallest base for G. We derive a character theoretic formula for the base size of a class of groups admitting a certain kind of irreducible character. Moreover, we prove a formula for enumerating the non-equivalent bases for G of size l ∈ ℕ. As a consequence of our results, we present a very short, entirely algebraic proof of the formula of Mecenero and Spiga for the base size of the symmetric group Sn acting on the k-element subsets of {1, 2, 3,...,n}. Our methods also provide a formula for the base size of many product type permutation groups.Peer reviewe

    A short computation of the Rouquier dimension for a cycle of projective lines

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    Funding: The second author was supported by EPSRC Grant EP/V049097/1 (Lagrangians from Algebra and Combinatorics).Given a dg category , we introduce a new class of objects (weakly product bimodules) in op ⊗ generalizing product bimodules. We show that the minimal generation time of the diagonal by weakly product bimodules provides an upper bound for the Rouquier dimension of . As an application, we give a purely algebro-geometric proof of a result of Burban and Drozd that the Rouquier dimension of the derived category of coherent sheaves on an n-cycle of projective lines is one. Our approach explicitly gives the generator realizing the minimal generation time.Peer reviewe

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    Progressive evolution of Streptococcus equi from Streptococcus equi subsp. zooepidemicus and adaption to equine hosts

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    Funding: This project and work performed by H.J.W. was funded by the PetPlan Charitable Trust (S19-741-780). J.D. is funded by Shandong Provincial Modern Agricultural Industry Technology System (SDAIT-27-05), the Agricultural Seed Projects of Key Research and Development Plan of Shandong Province (2023LZGCQY020), the Natural Science Foundation of Shandong Province (ZR2020MC182) and Shandong Provincial Youth Innovation and Technology Support Program (2019KJF018). N.L. is funded by the European Research Council (grant number 804744). Work undertaken by SES was kindly funded by the Horse Trust (G4017 and G2019).Streptococcus equi subsp. equi causes the equine respiratory disease 'strangles', which is highly contagious, debilitating and costly to the equine industry. S. equi emerged from the ancestral Streptococcus equi subsp. zooepidemicus and continues to evolve and disseminate globally. Previous work has shown that there was a global population replacement around the beginning of the twentieth century, obscuring the early genetic events in this emergence. Here, we have used large-scale genomic analysis of S. equi and its ancestor S. zooepidemicus to identify evolutionary events, leading to the successful expansion of S. equi. One thousand two hundred one whole-genome sequences of S. equi were recovered from clinical samples or from data available in public databases. Seventy-four whole-genome sequences representative of the diversity of S. zooepidemicus were used to compare the gene content and examine the evolutionary emergence of S. equi. A dated Bayesian phylogeny was constructed, and ancestral state reconstruction was used to determine the order and timing of gene gain and loss events between the different species and between different S. equi lineages. Additionally, a newly developed framework was used to investigate the fitness of different S. equi lineages. We identified a novel S. equi lineage, comprising isolates from donkeys in Chinese farms, which diverged nearly 300 years ago, after the emergence of S. equi from S. zooepidemicus, but before the global sweep. Ancestral state reconstruction demonstrated that phage-encoded virulence factors slaA, seeL and seeM were acquired by the global S. equi after the divergence of the basal donkey lineage. We identified the equibactin locus in both S. equi populations, but not S. zooepidemicus, reinforcing its role as a key S. equi virulence mechanism involved in its initial emergence. Evidence of a further population sweep beginning in the early 2000s was detected in the UK. This clade now accounts for more than 80% of identified UK cases since 2016. Several sub-lineages demonstrated increased fitness, within which we identified the acquisition of a new, fifth prophage containing additional toxin genes. We definitively show that acquisition of the equibactin locus was a major determinant in S. equi becoming an equid-exclusive pathogen, but that other virulence factors were fixed by the population sweep at the beginning of the twentieth century. Evidence of a secondary population sweep in the UK and acquisition of further advantageous genes implies that S. equi is continuing to adapt, and therefore, continued investigations are required to determine further risks to the equine industry.Peer reviewe

    Lying to our children

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    Most parents lie to their children. They do it for fun, as a method of behaviour control, and to protect children from what they consider to be dangerous truths. At the same time, most parents bring their children up with the message that honesty is a virtue and that lying is usually wrong. How should our practice and our preaching be reconciled? In this paper, I examine the ethics of parental lies. Most philosophers who have written on the ethics of deception have focused on deception of and by autonomous adults. I therefore begin by surveying this literature. Contemporary philosophers have given three types of reason to explain what makes lying wrong (when it is wrong): negative consequences, breaches of trust, and interference with autonomy. I briefly analyze what constitutes a breach of trust and identify four factors that affect how bad a breach is. I then explicate how lying can constitute a wrongful interference with autonomy. A long-running debate concerns whether lying is ethically different than other forms of deception. I argue—briefly—that we do not need to resolve this debate in order to evaluate parental deception. Armed with a framework for what makes lying to autonomous adults wrongful, I turn to the special case of parental lying. Since the parent-child relationship is typically very close, lying to one’s child is a relatively serious breach of trust. This is exacerbated in the case of serious lies that implicate the parent-child relationship or the child’s identity. On the other hand, at least for young children, concerns about autonomy are less significant than for autonomous adults. I close by applying my analysis, along with data on the consequences of parental deception, to different types of parental lie. I argue that lying to one’s child is more rarely justified than is commonly thought, and delineate the circumstances in which it can be justified.Peer reviewe

    Blocking the exit : Research ethics and bureaucratic writing practices

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    I argue that the standard model of research ethics pushes the ethnographer of bureaucracies to the cautious, concise and compliant textual practices styles of the bureaucracy itself. Given the methodological importance of writing to ethnography, this matters. To make the argument, I draw on my experience of my decision to embargo my PhD thesis, an ethnography of an international donor agency. I show how the key gatekeeper to my research sought to translate concepts from research ethics (consent, avoidance of harm) into insisting on writing and stylistic practices familiar to his organisation (scope of work, risk), in order to constrain future academic publications. These dilemmas played out in the text of the thesis, its styles, forms and arguments. In studying up, the ethical demands of writing present challenges to the text and its methodological significance. I suggest that navigating these methodological challenges demand strategies that also start with the text.Peer reviewe

    The refugee political in the age of imperial crisis, decolonization, and cold war, 1930s–1950s

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    Funding: This research was funded in whole or in part by the Austrian Science Fund (FWF) under Project No. I-5444 G; Grant-DOI: 10.55776/I5444.The three decades spanning the 1930s, '40s, and '50s witnessed the birth of the modern global state system, characterized by a protracted and tortuous transition from a world of empires to a world of nation-states. The demise of Nazi, British, and Japanese empires emancipated millions of people across the world. However, as old empires dissolved, new post-imperial states continued older colonial-origin forms of ethno-religious discrimination and ruling-class dominance, or invented novel hierarchies. Hence, this epoch was marked by catastrophic outbursts of racial violence, sectarian war, and genocide. If majoritarian nation-states were the privileged offspring of this transformation, then refugees were the unwanted issue. The national citizen and the refugee were co-created. Against their forced displacement and subalternization, refugees re-politicized their selves. We define this as ‘the refugee political’: refugees constructing themselves as political beings and building wide-ranging alliances – with churches, politicians, and entrepreneurs; with peasants, industrial workers, and feminists. They became ‘subaltern internationalists’, linking the Dachen Islands to the United States, and maritime Southeast Asia to India; connecting central European Jews to Australian women, or impoverished Indians to Soviet and Chinese communists. They created new forms of ‘refugee polis’ – political communities which were simultaneously local and daringly transnational.Peer reviewe

    A bacterial network of T3SS effectors counteracts host pro-inflammatory responses and cell death to promote infection

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    Funding: HWY is a recipient of the NUS Yong Loo Lin School of Medicine Postgraduate Research Scholarship. This work was supported by grants from the National University Health System(NUHSRO/2020/117/STARTUP/04) and Ministry of Education (MOE-T2EP30123-0006) to KWC.Innate immune signalling and cell death pathways are highly interconnected processes involving receptor-interacting protein kinases (RIPKs) as mediators of potent anti-microbial responses. However, these processes are often antagonised by bacterial type III secretion system (T3SS) effectors, and the cellular mechanisms by which the host retaliates are not completely understood. Here, we demonstrate that during Citrobacter rodentium infection, murine macrophages and colonic epithelial cells exhibit RIPK1 kinase-dependent caspase-8 activation to counteract NleE effector-mediated suppression of pro-inflammatory signalling. While C. rodentium injects into the host cells a second effector, NleB, to block caspase-8 signalling, macrophages respond by triggering RIPK3-mediated necroptosis, whereupon a third T3SS effector, EspL, acts to inactivate necroptosis. We further show that NleB and EspL collaborate to suppress caspase-8 and NLRP3 inflammasome activation in macrophages. Our findings suggest that C. rodentium has evolved to express a complex network of effectors as an adaptation to the importance of cell death for anti-bacterial defence in the host-pathogen arms race.Peer reviewe

    Insights into new mechanosensitive behaviors of G protein-coupled receptors

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    Funding: PA gratefully acknowledges support from the Leverhulme Trust (RL-2022-015), and from the UKRI BBSRC (BB/X019047/1).G protein-coupled receptors (GPCRs) represent a diverse and vital family of membrane proteins that mediate intracellular signaling in response to extracellular stimuli, playing critical roles in physiology and disease. Traditionally recognized as chemical signal transducers, GPCRs have recently been implicated in mechanotransduction, the process of converting mechanical stimuli into cellular responses. This review explores the emerging role of GPCRs in sensing and responding to mechanical forces, with a particular focus on the cardiovascular system. Cardiovascular homeostasis is heavily influenced by mechanical forces such as shear stress, cyclic stretch, and pressure, which are central to both normal physiology and the pathogenesis of diseases such as hypertension and atherosclerosis. GPCRs, including the angiotensin II type 1 receptor (AT1R) and the β2-adrenergic receptor (β2-AR), have demonstrated the ability to integrate mechanical and chemical signals, potentially through conformational changes and/or modulation of lipid interactions, leading to biased signaling. Recent studies highlight the dual activation mechanisms of GPCRs, with β2-AR now serving as a key example of how mechanical and ligand-dependent pathways contribute to cardiovascular regulation. This review synthesizes current knowledge of GPCR mechanosensitivity, emphasizing its implications for cardiovascular health and disease, and explores advancements in methodologies poised to further unravel the mechanistic intricacies of these receptors.Peer reviewe

    Dramatics as analogical engagement : Balthasar and performance studies in dialogue

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    This thesis maintains that analogy constitutes the fundamental principle of Balthasar’s approach to dramatics, and explores its potential contribution to performance studies. It seeks to demonstrate the relevance and applicability of his approach to dramatics, rather than merely employing theatrical and performance studies to advance or construct theological doctrines. In dialogue with performance studies, this thesis examines Balthasar’s idea of analogy and assesses its applicability through textual analysis. Chapter One establishes the groundwork for this dialogue by introducing performance studies, exploring its alignment with Balthasar’s dramatic, and analyzing the significance of analogy. Chapter Two defines Balthasar’s concept of analogy and offers a critically constructive analysis by addressing its limitations and examining his analogical view of dramatic soteriology. The next two chapters elaborate on the foundational notion of drama as enactive representation, and situate the discussion within Balthasar’s framework of dramatic soteriology. Chapter Three observes the complexity and pervasiveness of representation, and examines how these aspects are accommodated within the dramatic soteriology. Chapter Four delves deeper into the nature of enactment and its liminality, with special attention to the importance of death in the Balthasar’s dramatic. Finally, Chapter Five demonstrates the adaptability of Balthasar’s analogical approach through a reading of a second-century text, the Acts of John—the only Gnostic work he critiques in the Theo-Drama. This analysis provides a rigorous test case for assessing the soundness of his approach and its broader applicability within the field of performance studies."This work was supported by the Indonesia Endowment Fund for Education (Lembaga Pengelola Dana Pendidikan) [202207220610853]."--Fundin

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