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Results

Open Access Awards 2017/18 30 Sep 2018

Not available

Amount: £58,344
Funder: The Wellcome Trust
Recipient: University of Exeter

Decolonising madness? Transcultural psychiatry, international order and the birth of a global psyche 07 Mar 2018

Are mental illnesses and the core concepts in the psychiatric toolkit universal and identical across cultures, ethnic groups and 'civilisations'? This research will offer the first substantial historical analysis of the roots of the current global mental health movement and transcultural psychiatry. It challenges the idea that the concept of a global psyche is a recent development, and aims to demonstrate that it emerged in the aftermath of WWII and during decolonisation, when Western psychiatry endeavored to leave behind its colonial legacies, and lay the foundation for a new union of Western and non-Western concepts of mental illness and healing. In this period, leading psychiatrists across the globe set about identifying and debating the universal psychological characteristics and psychopathological mechanisms shared among all cultures. My research will explore this psychiatric, social and cultural search for a new definition of 'common humanity', and analyse the core medical-historical forces behind it. The International Pilot Study of Schizophrenia will serve as a case study. The project will involve the scoping of archives in Europe, Africa, Asia and the US, the employment of four research assistants, organisation of an international conference, and the creation of a network of researchers and practitioners in global psychiatry.

Amount: £28,155
Funder: The Wellcome Trust
Recipient: University of Exeter

University of Southampton MSc Global Health 11 Jul 2018

In an increasingly interdependent world, complex health problems require solutions that transcend geographic boundaries and draw on international and multidisciplinary collaboration to develop innovative responses. The MSc in Global Health within the School of Social Science at Southampton University is a multi-disciplinary programme designed to equip students with the necessary skills to understand and respond to global health challenges. Taught by research-active academic experts from multidisciplinary backgrounds, it includes core modules which provide students with a comprehensive understanding of key issues and concepts in transnational health. In addition the course has a strong quantitative component, which provides students with a robust understanding of statistical and epidemiological methods. A further feature is that students are able to choose from a range of optional modules offered by the Schools of Social Science (which includes social statistics, demography and gerontology), Geography and Law, as well as the Faculties of Medicine and Health Sciences in order to tailor their programme to meet their specific needs and interest. While not exclusively designed for those planning a research career, a significant proportion of former students have successfully chosen or continued on this path and currently work for academic institutions or research departments within governmental bodies.

Amount: £84,405
Funder: The Wellcome Trust
Recipient: University of Southampton

Role of Inhibitor of Kappa B Kinase Epsilon in Sex-dependent Differences in Metaflammation 19 Apr 2017

With the failure in curbing the global obesity epidemic, there is an urgent need to develop therapies to treat obesity-associated metabolic diseases. This requires a better understanding of the molecular mechanisms that not only promote, but also prevent metabolic disease development. Although, chronic low-grade inflammation ("metaflammation") is an important causative factor in metabolic diseases, the anti-inflammatory effects of estrogens may provide important insights into disease prevention. Indeed, pre-menopausal women are protected from obesity-linked metabolic diseases. Previously, I have identified immunometabolic proteins, e.g. IKBKE, that limit metabolic stress-induced inflammation and these are influenced by sex. However, it remains unclear whether, and how, estrogens alter innate immune sensitivity to metabolic stress. This project will address this and test the hypothesis that both estrogen- and IKBKE-dependent pathways function in a common signalling network to regulate energy balance and metaflammation. I will investigate, invitro and invivo, the synergies that exist between estrogen- and IKBKE-depended actions in metaflammation. Ultimately, the knowledge gained may support the notion that estrogens and IKBKE are key in raising the threshold for metabolic stress-induced inflammation. This may identify novel therapeutic targets to treat obesity-linked metabolic diseases and shed light on the immunometabolic changes that accompany menopause in all ageing women.

Amount: £589,119
Funder: The Wellcome Trust
Recipient: University of Southampton

What are the molecular mechanisms regulating neuronal sensitivity to BDNF? 31 May 2018

Neurotrophins and their receptors play a key role in the maintenance and remodelling of the nervous system, and defects in trophic signalling are associated with mental illness as well as neurodegeneration. To date, the cellular mechanisms regulating neurotrophin receptor bioavailability are not fully understood. Here we focus on BDNF and its receptor, TrkB, which are widely expressed throughout the central nervous system. This project will investigate the role of two novel potential TrkB regulators that recently emerged from our screens. Candidates will be expressed in HEK-TrkB cells and primary cortical mouse neurons, and (i) TrkB receptor expression levels and (ii) downstream signalling events will be investigated using both Western blotting and immunofluorescence techniques. These experiments will address whether the candidates modulate TrkB availability and activity. A better understanding of the cellular mechanisms underlying TrkB regulation may highlight potential therapeutic targets to counteract TrkB degradation and restore sensitivity of vulnerable cells to the beneficial actions of BDNF.

Amount: £0
Funder: The Wellcome Trust
Recipient: University of Southampton

Postgraduate Medical Humanities Conference 2016 30 Apr 2016

Following on from the success of preceding Postgraduate Medical Humanities Conferences in 2014 and 2015, this interdisciplinary conference aims to reflect the broad and vibrant research of the medical humanities by bringing together postgraduate researchers from a number of different disciplines from institutions across the UK and abroad. The conference will enable students at all stages of their postgraduate career to exchange ideas and share their work in a welcoming and stimulating environment, providing the opportunity to discuss their research with scholars working from a range of perspectives. Delegates have been invited to submit abstracts for a twenty-minute paper or sixty-minute workshop on any subject relating to health, illness, sex, and medicine. Panels will be supplemented by two keynote speeches, a roundtable discussion about engagement and impact, and a related performance that will be open to both delegates and the wider community. There will be a conference meal on the first evening of the conference, and a networking event on the second evening of the conference. We hope that the conference will promote interdisciplinary approaches and collaboration. We also hope to provoke lively debate about the intersection of medical practice and medical humanities.

Amount: £3,100
Funder: The Wellcome Trust
Recipient: University of Exeter

30 Years of ChildLine 31 Dec 2015

October 2016 will mark the 30th anniversary of the charity, ChildLine. We propose a witness seminar, supported by ChildLine/NSPCC, bringing together ChildLine’s founders and staff, counsellors, journalists and policymakers to reflect upon the charity’s foundation and ongoing contribution to children’s services. This is a timely event. The Independent Inquiry into Child Sexual Abuse (July 2015-) is stressing the need to centre the experiences of victims and survivors in the investigations. Terse debate about the role of the voluntary sector in the provision of childcare and child protection has been highlighted by the recent closure of Kids Company. The ‘Wellcome Witness seminars’ have demonstrated the rewards of using oral history to extend existing records about developments in recent medical science and practice. Our event will build on this model to create resources about the history of present-day issues surrounding children’s health and wellbeing. Our key goals are to open conversations between charity and healthcare practitioners, policymakers, academics and journalists/broadcasters about these subjects, with outputs that can be applied to inform policy. We will disseminate findings through an archived audio recording and transcription of the event, academic articles and policy briefs. We will also develop networking platforms for future engagement between participants.

Amount: £4,570
Funder: The Wellcome Trust
Recipient: University of Southampton

Biochemical examination of metabo-synaptic coupling in a model of early cognitive decline 01 Apr 2016

Recently, interest has grown regarding the role of amyloid beta (Abeta) in impairing synaptic function in the early stages of Alzheimer’s disease (AD). These specialised areas of cell-to-cell communication play a vital role in memory formation but also represent a significant metabolic burden to neuronal cells. Notably, dysfunction in two key neurotransmitter subtypes (acetylcholine and glutamate) occurs early on in AD progression and these are the target of two classes of drugs to treat AD (cholinesterase inhibitors and memantine respectively). Additionally, functional brain imaging has shown that impaired use of glucose (the predominant fuel source for neurotransmitter production in the brain) is an early and potentially causative change occurring in AD pathophysiology. However, our understanding of how this coupling of metabolism and synapse activity becomes dysfunctional remains limited. To address this, the protein expression and activity of key pathways involved in both glucose metabolism and neurotransmitter release/recycling will be assessed in AD-relevant brain regions (cortex and hippocampus) following acute Abeta overexpression using Western blotting and enzyme-linked immunosorbent assays (ELISAs). Assessment of these changes will highlight where in these pathways becomes dysfunctional first, providing novel targets for early, potentially disease-modifying treatments.

Amount: £1,500
Funder: The Wellcome Trust
Recipient: University of Southampton

The effect of systemic bacterial infection on the onset and progression of disease in an animal model of Alzheimers's disease. 01 Apr 2016

Tg2576 mice will be used as a model of human Alzheimer’s disease (AD). These transgenic mice are genetically modified to overexpress a mutant form of the amyloid precursor protein (APP). APP develops into beta amyloid protein which is a major component of plaques that form in the brain of AD patients. Brain tissue has already been collected at 12, 16 or 20 months. At each stage of the disease mice have been treated with saline or an attenuated strain of Salmonella typhimurium to investigate the hypothesis that systemic bacterial infections modifies plaque formation through promoting neuroinflammation. The ability of microglia and macrophages to phagocytose and proliferate will be investigated. This will help establish if the innate immune response to the infection is causing the increasing amyloid plaque deposition and neuronal loss that causes the onset and/or progression of AD. Antibodies will be used to stain microglial cells (via binding to MHCII, FcRI and CD11b).The antibodies iNOS and Ki67 will be used to analyse the microglia’s ability to perform phagocytosis and proliferating respectively. As well as this, antibodies SMI-32 and NeuN will be used to establish whether damage or swelling has occurred to neurons as a result of the pathogen.

Amount: £2,000
Funder: The Wellcome Trust
Recipient: University of Southampton

tRNA Methylation as an Antibacterial Target 01 Apr 2016

In response to the continued evolution of bacterial resistance to antibiotics, the discovery and exploitation of novel bacterial target mechanisms, such as essential enzymes, is increasingly important to feed novel candidates into the antibiotic discovery pipeline. tRNA m(1)G37 methyltransferase (TrmD), catalyses the post-transcriptional methylation of guanine 37 in specific bacterial tRNAs, which is an essential step. Deletion mutants for this enzyme in both gram negative and gram positive bacteria causes an increase in translational errors, decelerated growth and cell death. Substantial structural differences have been identified between TrmD and the human equivalent (Trm5), strongly suggesting the development of highly selective inhibitors for TrmD should be possible, thus reducing the probability of off-target toxicity. Current TrmD inhibitors show promising in vitro potency (micromolar range), but their low activity against cultured bacteria is proposed to arise from poor bacterial uptake of the compounds (inefficient crossing of the bacterial cell wall). Our objective is to design, prepare and biologically evaluate a small library of novel TrmD inhibitors. These compounds will feature a range of modifications selected to enhance bacterial cell uptake. The activity of these compounds will be measured by comparing in vitro potency with activity in bacterial cultures.

Amount: £2,000
Funder: The Wellcome Trust
Recipient: University of Southampton

Investigation into the effect of desialylation on Galectin-9 interaction with tumour cell surfaces. 01 Apr 2016

Galectin-9 is known to possess immunomodulatory properties both inside and external to the cell, inducing both pro and anti-inflammatory responses. It was originally proposed as an eosinophil chemoattractant. Recently, the group I wish to work with have shown that galectin-9 induces apoptosis of specific T-cells and has therapeutic potential in targeting specific chemotherapy-resistant tumour cells. Galectin-9-carbohydrate lattices can be formed at the cell surface as a result of galectin-9 crosslinking with glycoconjugates and gangliosides. Many of the immunomodulatory functions of galectin-9 involves initial binding to membrane glycoproteins and glycolipids, leading to cytoskeleton-dependent actions such as apical polarization, apoptosis and autophagy. However, the mechanisms by which galectin-9-induced changes in cytoskeleton dynamics are poorly understood. In this study we will determine the effect of extracellular-galectin-9 treatment on ovarian and colon cancer cells, pre- and post-treatment with sialidase. Alteration of the surface glycosylation pattern on malignant cells potentially affects tumour immunity by directly influencing interactions with lectins on their surface. Therefore we will quantify a) galectin-9 binding; b) F-actin changes and c) apoptotic status of tumour cells, pre- and post-treatment with sialidase. These studies will provide insight into the structure-functional interaction between galectin-tumours to help understand the biological functions of galectin-9.

Amount: £2,000
Funder: The Wellcome Trust
Recipient: University of Exeter

Institutional Strategic Support Fund Phase2 FY2014/16 27 Oct 2014

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Amount: £1,000,000
Funder: The Wellcome Trust
Recipient: University of Exeter

The Cross-Disciplinary Invention of Sexuality: Sexual Science Beyond the Medical, 1890-1940. 20 Jan 2015

This project represents a fundamental rethinking of the emergence of the scientific study of human sexuality in the c19th and reconsiders how modern understandings of sexuality were constructed. We critique the hitherto dominant assumption that 'sexology' existed as a clearly understood and primarily medical field of knowledge. We present a new account of the rise of a cross-disciplinary 'sexual science' driven by dissatisfaction with exclusively medical approaches. From the 1890s, medical docto rs argued that a properly scientific understanding of sexuality required input from additional areas of knowledge (e.g. anthropology, sociology, history, literature). This project offers the first full investigation of the conceptual and cultural factors driving the evolution of a cross-disciplinary sexual science: the desire to understand the global variety of sexual behaviour; an interest in historical and cultural variation; and a new focus on the 'normal' and 'healthy' alongside the 'path ological' and 'abnormal'. We examine the ways in which these studies challenged biological explanations of sexuality, raising questions about the 'nature/nurture' divide, and brought imperially-shaped debates about race, the primitive, civilization and degeneration into the heart of sexual science. Thus the project sheds new light on the evolution of a range of categories that are central to understandings of human behaviour in the modern world. Interdisciplinary collaborations will produce m onographs, journal issues and edited collections. A stakeholder-led engagement programme will raise broader questions about the relation between medical and non-medical forms of knowledge in the past and present to address contemporary challenges surrounding sexual health and wellbeing.

Amount: £425,352
Funder: The Wellcome Trust
Recipient: University of Exeter

Health Law and Bioethics at the Frontiers of Innovation Postgraduate Bioethics Conference. 14 Jul 2014

The Postgraduate Bioethics Conference (PGBC) is an annual conference aimed at doctoral researchers in applied ethics broadly conceived. Over the past seven years, often with the support of the Wellcome Trust, PGBC has become established as the leading environment for doctoral candidates whose work involves bioethics to network and present their work. The theme of PGBC 2014 is Health Law and Bioethics at the Frontiers of Innovation and it will take place on 4-5 September at the University of So uthampton. There will be keynote speeches by Professor John Bryant, Professor Bobbie Farsides, Professor John Harris and Professor Jonathan Montgomery. With a focus on training and career development, we will also run two workshops. Bioethics in Practice will be led and organised by Professor Montgomery. Publishing in Bioethics , will involve a panel of editors from leading bioethics journals. Confirmed speakers are Professor Ruth Chadwick (Bioethics), Dr John Coggon (Health Care Analysis), P rofessor David Hughes (Sociology of Health and Illness) and Dr Sara Fovargue (Medical Law Review). We expect over 50 participants, of whom 24 will present a paper. The participants are likely to be mostly UK and Ireland-based doctoral researchers. Please see the website for further details: www.postgradbioethics.com.

Amount: £6,289
Funder: The Wellcome Trust
Recipient: University of Southampton

Third European Advanced Seminar in Philosophy of Life Sciences. 31 Mar 2014

This is the third of a series of biennial meetings of senior scholars and research students from six major research centres in the philosophy of the life sciences and medicine across Europe. These six centres provide the core funding for this meeting. The present application is a request for additional support to be able to host two international senior speakers and offer a scholarship to one deserving PhD student. The aims of this series are: (1) to acquaint young researchers with recent trends in their own and neighbouring disciplines and allow them to network in an early stage of their career; (2) to facilitate exchange of young researchers among the institutions involved and potentially enhance the institutional research scope; and (3) to create a platform for more senior scientists to develop new programs and projects on a European level.

Amount: £2,825
Funder: The Wellcome Trust
Recipient: University of Exeter

Identification of novel subtype of monogenic diabetes by excluding Type 1 diabetes using a polygenic risk score 19 Nov 2015

Background: Finding the genetic aetiology of monogenic diabetes has had profound scientific and clinical implications. Currently, novel subtypes of monogenic diabetes are identified by studying patients who have a clinical phenotype of known subtypes of monogenic diabetes but lack mutations in the known genes. This approach is biased: lacking ability to identify previously undescribed phenotypes. In non-obese children, Type 1 diabetes (T1D) is the only alternative diagnosis to monogenic diabetes . Therefore potential novel monogenic subtypes can be found by excluding T1D by presence of autoantibodies, but this approach is limited as autoantibodies are absent in 10-20% of T1D patients. Preliminary Data: I showed a T1D-genetic risk score (T1D-GRS), based on T1D associated common genetic variants, in the neonatal period(<6months) identifies individuals with monogenic diabetes by robustly excluding T1D. Key goals: I will genotype the T1D-GS in large cohorts of slim patients with childhood -onset diabetes from the UK (n=5000), and Turkey (n=700) to identify patients in whom T1D is highly unlikely (T1D-GS <1st centile of T1D) so monogenic diabetes highly likely. I will perform whole-genome-sequencing on these patients to find novel genetic aetiologies. I will perform detailed phenotyping of the individuals with confirmed novel genetic aetiologies to understand the associated biology.

Amount: £415,179
Funder: The Wellcome Trust
Recipient: University of Exeter

Vacation Scholarships 2017 - University of Southampton 16 Jun 2017

Vacation Scholarships 2017 - University of Southampton

Amount: £11,500
Funder: The Wellcome Trust
Recipient: University of Southampton

Use of a Drosophila model to study circadian control of metabolic health. 27 Apr 2017

Internal daily timekeeping systems known as circadian clocks are used by all types of organisms to regulate their metabolism. For example, the clock-controlled scheduling of food intake and use affects health and longevity in both mammals and insects. Time-restricted or nutrient-restricted feeding improves the health of both mice and fruit flies (Panda, Science 2016). The period gene, which plays a key role in the circadian clocks of animals, provides a link between daily timekeeping and metabolic health. Flies lacking the period gene store less glycogen and triglycerides in spite of ingesting more food and are, therefore, more sensitive to starvation. I propose to test where and how the period gene provides this metabolic function. In particular, I will ask whether its role in starvation resistance is due to its control of sleep/wake rhythms or its function in periperhal clocks of metabolic tissues such as the fat body. Moreover, Dr Wijnen's laboratory recently showed that the period gene is induced at colder temperatures (Goda et al., Proc Biosci 2014) and I will test whether period-mediated starvation resistance is found preferentially at colder temperatures.

Amount: £0
Funder: The Wellcome Trust
Recipient: University of Southampton

Controlling phosphodiesterase activity in biofilm dispersal 27 Apr 2017

Biofilm formation and dispersal are controlled by the secondary messenger bis-(3’-5’) cyclic dimeric guanosine monophosphate (c-di-GMP); high levels are associated with biofilm formation, while a reduction induces dispersal. The enzymes catalysing formation of c-di-GMP are diguanylate cyclases, while phosphodiesterases catalyse the breakdown of c-di-GMP. Structural studies of the EAL type phosphodiesterases were observed in the host laboratory in the presence of substrate c-di-GMP, suggesting that these structures would require further steps to attain full catalytic activity. The host laboratory have recently demonstrated that dimerization and active site formation as well as formation of three metal binding sites are distinct activation steps required to tune the enzymatic activity of phosphodiesterases (Scientific Reports 2017). The proposed project deals with the motility regulator protein, MorA, and the mucoid alginate regulator, MucR, from Pseudomonas aeruginosa. Both proteins have dual activity as diguanylate cyclase and phosphodiesterase. Interestingly, the two linked catalytic domains influence each other's activity; different levels of activity are observed for the phosphodiesterases when comparing isolated domains with the linked conformation. The objective of the project is to purify these proteins and determine their catalytic activities, comparing the isolated domains, mixtures of the individual domains, and the cyclase-phosphodiesterase domains in linked conformation.

Amount: £0
Funder: The Wellcome Trust
Recipient: University of Southampton

The impact of systemic inflammation on the brain. 27 Apr 2017

Brain tissue from adult mice has already been collected, with a control group treated with saline and another treated with an attenuated strain of Salmonella typhimurium, triggering a systemic immune response including production of pro-inflammatory mediators that communicate with the brain triggering neuroinflammation and neuronal dysfunction. Selected groups of mice have been treated with two different inhibitors that block the activity of the cytokine IL-1beta, in order to investigate if this pro-inflammatory cytokine plays a direct role in neuroinflammation during systemic infection. In this project we will compare a small molecule with a biologic, both targeting cytokines, but via different mechanisms. The brain tissue will be examined using antibodies to stain activation markers of microglial cells (CD11b, FcRI, MHCII) and activation markers of cerebral endothelial cells (VCAM, ICAM, MHCII). Synaptic activation markers, from both the pre- and post-synaptic membranes, will be investigated by isolated mRNA from hippocampal enriched tissue. This investigation into phenotypic changes in microglial, cerebral endothelial cells and BBB function will be used to determine if the inhibition of IL-1beta is beneficial in reducing neuroinflammation as a result of systemic infection. This could later be applied to AD models, taking into consideration behavioural changes.

Amount: £0
Funder: The Wellcome Trust
Recipient: University of Southampton