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University of Oxford

Country: United Kingdom

University of Oxford

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6,753 Projects, page 1 of 1,351
  • Funder: UKRI Project Code: 2733065

    Here, "reference" is construed as the relation between a linguistic expression and a "referent". The latter is understood as an image in the speaker's mind, which can represent either a real or an abstract entity. Full noun phrases (proper and common names) and reduced noun phrases (pronouns and zero forms) constitute the main "referential devices" in a language. In most cases, the choice between them depends on how much a referent is "activated" in the speaker's mind: the higher the degree of activation, the higher the possibility that a reduced noun phrase will be used. There have been numerous suggestions regarding the factors, which determine the degree of a referent's activation (Kibrik 2011: 390-393). While other scholars considered these factors separately, Kibrik (2011: 60-61) suggested that the degree of activation is determined by all of them collectively and can be measured quantitatively with his cognitive multi-factorial (CMF, henceforth) method. I will apply the CMF approach to several diachronic stages of the Japanese language. The CMF approach has been previously applied to Contemporary Japanese by Efimova (2006). While her study has achieved a breakthrough in the field, it still suffers from a serious limitation. Efimova uses the x2 test for her statistical analysis which only allows to establish a correlation between two parameters: in her case, between each activation factor and a referential device. In other words, this statistical method is not adequate to her multi-factorial analysis, since it cannot reflect the interaction between activation factors. In my research, the multinomial (polytomous) logistic regression will be used. Key research questions: 1) Have the strategies of referential choice in Japanese written narratives changed diachronically? 2) If so, what are the morphosyntactic mechanics of this change? 3) Which of the activation factors affect referential choice in different epochs and genres? 4) Has the use of 3rd person pronouns and passivisation (instead of topicalisation) actually become more extensive in Modern Japanese under the influence of European languages (Li 2000)? The theoretical significance of the proposed research is two-fold. Firstly, to my knowledge, no investigation of referential choice at any synchronic stage of pre-Modern Japanese has been conducted before. Meanwhile, a study like this might shed new light on some issues, concerning the use of null elements and pronouns. Secondly, the proposed research will contribute to the general theory of discourse linguistics, since there has been no extensive study on the diachrony of referential structure in any given language. The only attempt in this direction has been undertaken by Song (2021), who applied "referential density" tests to three stages of the English language (Old, Middle, and Modern) and demonstrated that the stable increase of "referential density" (number of overt arguments over the number of predicates) reflects major changes in argument structure, valency, and transitivity. I will also apply the "referential density" tests to different stages of Japanese as well. As for practical significance, the findings of this research will be useful in solving the perennial problems of machine translation such as the resolution of zero elements and pronoun reference.

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  • Funder: UKRI Project Code: 2108281

    A hallmark of human cognition is the ability to learn and execute multiple tasks in succession ("continual" learning). Psychologists and Neuroscientists have investigated how executive functions control switching between tasks. However, in these studies (1) subjects were usually provided with full instructions a priori and (2) stimuli were highly simplified. In contrast, in the real world, (1) visual information is high-dimensional, (2) optimal stimulus-response contingencies need to be detected without instructions via trial and error and (3) the brain is challenged to represent task-sets in a way that avoids interference with future learning and enables flexible reuse of neural codes in similar environments. The neural basis of this continual learning, however, remains enigmatic. Notably, in Machine Learning, even state-of-the art algorithms fail to continuously acquire structured, protected and reusable representations of the world. The aim of the proposed DPhil is to investigate the computational mechanisms and neural representations underlying continual learning via the following three experiments: Experiment 1: Neural Correlates of Continual Task Learning. I investigate if sequential in contrast to interleaved learning facilitates the emergence of multiple compressed representations of task-sets in human PFC that are protected against interference. Experiment 2: Rule Transfer for Continual Task Performance. How does the brain reuse abstract knowledge in novel situations that are partially related to previous experience? Experiment 3: Unsupervised Structure Learning for Categorisation. Does low-level sensory learning of the statistical structure of our environment serve as scaffold for later task learning?

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  • Funder: UKRI Project Code: PP/E002900/1
    Funder Contribution: 224,340 GBP

    See joint LC-ABD document of support.

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  • Funder: UKRI Project Code: MR/T002107/1
    Funder Contribution: 771,800 GBP

    Diabetes affects >425 million people worldwide and accounts for one death every 6 seconds. In the UK, ~3.7 million people currently have the disease (90% have type 2 diabetes) and a further 1 million are undiagnosed. Diabetes increases the risk of heart disease, stroke, kidney disease and blindness, and reduces life expectancy by up to 10 years. It also consumes about 10% of the UK's direct healthcare costs. If we are to ameliorate the severe socio-economic impact of diabetes, and to develop new and better therapies, it is essential to have a clearer understanding of the underlying molecular mechanisms involved. The overall aim of this proposal is to generate this knowledge and to identify new pathways and targets for therapeutic drug development. Type 2 diabetes is characterised by a chronically elevated level of blood sugar (chronic hyperglycaemia), which results from insufficient secretion of the hormone insulin from the beta-cells of the pancreas. The hyperglycaemia fuels diabetes progression by further reducing beta-cell function and mass. We aim to understand how chronic hyperglycaemia impairs beta-cell function and mass, so speeding beta-cell decline. Such fundamental knowledge is currently lacking but has the potential to transform therapy, facilitating the development of novel drugs targeted at improving insulin secretion and preserving beta-cell function. It is well established that glucose (sugar) must be metabolised in order to stimulate insulin secretion. Work from several laboratories, including our own, has previously shown that this is because a glucose metabolite known as ATP, regulates the activity of a tiny pore in the beta-cell membrane known as the KATP channel. When this pore is open, insulin is not released. An acute rise in blood glucose leads to ATP generation, KATP channel closure and insulin release. However, studies suggest that chronic elevation of blood glucose adversely affects beta-cell metabolism, leading to a failure of ATP generation and KATP channel closure. Consequently, insulin secretion is prevented. Our recent studies indicate this is because hyperglycaemia causes marked changes in the expression of metabolic genes. Why this happens is unknown. We now aim to understand precisely how chronic hyperglycaemia, like that which occurs in diabetes, leads to changes in beta-cell metabolism, gene and protein expression, and ATP production. Understanding how hyperglycaemia impairs beta-cell function and mass in diabetes will provide novel insights into how its deleterious effects can be prevented and/or reversed, and identification of the pathways involved should help pinpoint specific targets for therapeutic drug development.

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  • Funder: UKRI Project Code: MR/K011480/1
    Funder Contribution: 394,933 GBP

    Endometriosis is a common women's health problem characterised by the presence of deposits resembling endometrium (lining of the uterus) on ectopic sites in the pelvis, causing chronic inflammation, severe pelvic pain and reduced fertility. Family studies indicate that the disease can be inherited. In a recent study comparing genetic information from 5,675 women with endometriosis and 9,331 controls, we found a genetic variant on chromosome 7 associated with moderate-severe endometriosis. In an independent study involving 190,803 individuals, the same genetic region was found to be associated with fat distribution (waist-hip ratio). The signal is located between genes, and it is unclear how the variant - or those in its vicinity - act on transcription of DNA and ultimately on the development of endometriosis or differences in fat distribution. We are collecting endometriotic tissue, endometrium, subcutaneous abdominal fat and blood from women undergoing a laparoscopy for symptoms of endometriosis, or for tubal sterilisation. Using these samples, we will investigate whether DNA transcription in the region of interest is different between women with moderate-severe endometriosis and controls, and between tissues. We will also explore all known genetic variants in the region, and investigate how these affect transcription levels. Implicated variants will be investigated for association with endometriosis risk, and waist-hip ratio, in up to 10,936 women. The proposed work will provide crucial information on gene regulation in the implicated region and its effect on clinical phenotypes, information required for the translation of the genome-wide association findings into clinical meaningful results that can inform the development of new (non-invasive) diagnostic methods and identification of novel drug targets.

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