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Results

Investigation of epithelial differentiation in a mouse wound model 31 May 2018

Lipoxygenase (LOX) enzymes are expressed by infiltrating immune cells and are involved in innate immune and inflammatory response, all of which are fundamental processes in wound healing. The overarching aims of this larger body of work is to evaluate the role of 12/15-LOX in the cellular orchestration of wound healing using a murine model. We have induced full thickness (4mm) wounds in wildtype and 12/15-LOX knockout mice, then measured wound closure rates and harvested skin tissue at various time points post wounding and conducted histological evaluation of skin sections. Our initial data has found that in 12/15-LOX knockout skin there is enhanced fibroblast expansion, and a reduced infiltration of macrophages, both of which might be beneficial in chronic wound states where failure in fibroblast proliferation and an overt inflammatory state occur. However chronic wounds also displays deficits in wound re-epithelialisation and given that 12/15-LOX products can inhibit epidermal hyperplasia (by modulating cyclin/CDK signalling), we believe that KO mice might also display an enhanced re-epithelialisation phenotype. Therefore, to test this hypothesis we will explore the rate of re-epithelialisation and the cytokeratin profile of epithelial keratinocytes in KO and wildtype mice at various time points post wounding.

Amount: £0
Funder: The Wellcome Trust
Recipient: Cardiff University

How curiosity enhances hippocampus-dependent memory 06 Jun 2018

In today’s world, it is most desirable to optimize cognitive capacities, such as learning, across the lifespan. One fundamental, yet poorly understood, method is via a person’s intrinsic curiosity. Despite the ubiquity and importance of curiosity in everyday life, we have a very limited appreciation of the exact neural mechanisms of curiosity-enhanced learning. Because initial curiosity studies have relied on the passive encoding of material, one fundamental aspect of curiosity – active exploration to acquire further knowledge – remains to be investigated. I, therefore, propose a new virtual reality paradigm to characterize the neural mechanisms of how active curiosity enhances memory. Across three principal approaches, I will ask how separate stages of memory (orientation vs. initial learning vs. different modes of consolidation) contribute to curiosity-related memory enhancements and why curiosity-based learning might vary between healthy individuals. I will uncover whole-brain mechanisms and ‘zoom in’ on specific curiosity- and memory-related brain structures using complementary state-of-the-art measures and analyses. Combining such approaches is vital if we are to understand how curiosity enhances memory, but may also aid crucial translation of laboratory-based findings on learning and memory to real-world issues (e.g., influence on educational policies and implications for cognitive resilience in the elderly).

Amount: £959,155
Funder: The Wellcome Trust
Recipient: Cardiff University

Identifying the pathogenic triggers of CD8 T-cells in multiple sclerosis . 13 Nov 2014

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS), affecting 2.5 million individuals worldwide. Treatments are available, but are complicated by side effects and variable response profiles. There is an urgent need to define the pathogenesis of MS and design novel therapeutics. There is evidence that CD8 T-cells play a major role in the pathogenesis of MS. Studies also suggest a role for herpes viruses in MS, however, it remains unclear what triggers di sease. My preliminary data demonstrates that CSF resident T-cells have an antigen-driven phenotype. T-cell receptor (TCR) usage in the CSF resident CD8 T-cell repertoire is highly skewed with a restricted number of dominant TCRs. I hypothesize that a viral infection, such as EBV, triggers CD8 T-cells, which subsequently target and damage host cells. Here, I intend to identify the pathogenic triggers of dominant CSF-resident T-cells, thereby elucidating the aetiology of this debilitating disease. Specific aims: 1. To perform an in-depth phenotypic analysis of T-cell populations in the CSF of MS patients. 2. To identify dominant CSF resident TCRs in MS patients. 3. To define the pathogenic triggers of dominant CSF-resident TCRs.

Amount: £173,892
Funder: The Wellcome Trust
Recipient: Cardiff University

The role of innate immune regulation in viral pathogenesis and the development of anti-viral T cell memory 11 Jul 2017

Immune mechanisms that regulate antiviral immune responses determine whether the host can control pathogen replication and virus-induced immunopathology. The pathogenic human cytomegalovirus (HCMV) establishes chronicity and induces inflammation-associated pathologies. Cytomegalovirus (CMV) also induces the largest known expansion of T cells, and thus represents an important tool for identifying mechanisms inducing robust T cell immunity. CMV may also be exploited as an attenuated vaccine vector. Using a CMV model of viral pathogenesis, I identified that immune regulation during initial infection determines the extent of virus-induced inflammation and development of long-lived virus-specific immunity. The key goals of this proposal are: Identify innate immune components that mediate viral pathogenesis and understand how they are controlled Test whether innate immune pathways can be a) safely targeted therapeutically to treat viral disease and/or b) used to predict genetic risk of CMV pathogenesis Identify the early immunological events that promote CMV-specific T cell memory development, and elucidate whether regulatory pathways controlling these factors can be harnessed to enhance virus-driven memory T cell formation induced by attenuated viral vectors This research will determine whether innate immune activation can be exploited to: 1) safely treat viral pathogenesis and/or 2) enhance virus-induced T cell memory responses.

Amount: £1,942,612
Funder: The Wellcome Trust
Recipient: Cardiff University

Integrative Neuroscience. 14 Jul 2014

Not available

Amount: £149,985
Funder: The Wellcome Trust
Recipient: Cardiff University

Control of homeostasis and inflammation by the macrophage metabolome. 07 Apr 2014

Macrophages are a heterogeneous population of immune sentinels who shape the physiology of most tissues; this fundamental role often contributes to the pathogenesis of inflammatory disorders such as rheumatoid arthritis and cancer. Recently, marked heterogeneity in tissue-resident macrophage origins has been observed, with many having prenatal rather than adult bone marrow origins. Little is currently known about how the functions of these distinct macrophage populations are controlled. However, I have observed that the phenotype of tissue-resident macrophages can be directed through tissue-specific transcription factors, which control modulators of macrophage function including metabolic regulators. I have identified extensive regulation of metabolic enzymes during an inflammatory response with a clear disparity between bone marrow-derived and tissue-resident macrophages. These enzymes have the potential to direct distinct macrophage functions through both control of the metabolome an d direct interactions with key transcription factors. I hypothesise that precise regulation of metabolic enzymes is critical for specific macrophage function. The objectives are: i) characterise the metabolomes of distinct macrophage subsets during inflammation; ii) determine functional consequences of metabolic modulation; and iii) investigate specific functions of select metabolic regulators in inflammation in-vivo. Understanding how metabolic regulation controls cell function could lead to no vel therapeutic approaches to inflammatory diseases.

Amount: £250,000
Funder: The Wellcome Trust
Recipient: Cardiff University

The immunopathogenesis of Epstein-Barr virus-associated malignancies. 26 Nov 2012

Epstein-Barr virus (EBV) infects >90% of the human population and is associated with a broad spectrum of diseases, including an array of distinct malignancies. Indeed, EBV was first isolated from a Burkitt lymphoma tumour specimen almost 50 years ago and represents the prototype human oncogenic virus. The global burden of EBV-associated malignancies is startling, with approximately 200,000 new cases reported annually. At present, however, there are no commercially available vaccines, no effectiv e antiviral drugs and no virus-targeted therapeutics to prevent or treat these devastating malignancies. The research questions in this proposal reflect the pressing need for rational intervention in the EBV-associated oncogenic process, collectively aiming to identify pathways to prevention and cure. Novel immunotechnological approaches will be developed to profile EBV-specific T-cell immunity and reveal the immunological lesions that underlie the failure of immune surveillance in otherwise imm unocompetent individuals. These tools will also be used to monitor a poxvirus-vectored vaccine that aims to generate EBV-derived latent antigen-specific T-cell responses to correct the immune deficit and effectively target transformed B-cells. Further, novel bispecific high affinity T-cell receptor-based reagents will be developed to redirect T-cell immunity against established EBV-associated malignancies. Successful delivery and application of these cutting edge immunotechnologies and immunothe rapeutic strategies will have direct translational implications for human health.

Amount: £2,065,190
Funder: The Wellcome Trust
Recipient: Cardiff University

Excitatory-inhibitory balance in adolescents at high genetic risk of mental disorder: a study of cortical gamma oscillations and GABA concentrations in 22q11.2 deletion syndrome. 26 Jun 2013

Neurodevelopmental disorders such as schizophrenia, autism and ADHD share clinical features, environmental risk factors and show familial co-aggregation. Recent genetic findings suggest that both common and rare genetic variants confer susceptibility across this spectrum of disorders, suggesting common pathogenic mechanisms. Cortical excitatory-inhibitory imbalance is proposed as one potential mechanism for the increased risk of mental disorder across traditional diagnostic boundaries. Marker s of disturbance in this balance include gamma oscillations (measured by magnetoencephalography, MEG) and GABA concentrations (measured by MRS). These markers have been shown to be abnormal in idiopathic schizophrenia, autism and ADHD. The 22q11.2 deletion is one of the strongest known genetic risk factors for mental disorder. I propose to use MEG and MRS to investigate cortical gamma oscillations and GABA concentrations in a sample of adolescents with 22q11.2 deletion syndrome and a sample o f unaffected siblings. I will conduct between-group analyses to determine whether the 22q11.2 deletion is associated with abnormal gamma oscillatory activity and GABA concentrations in the cortex. I will also investigate the relationship between gamma oscillations, GABA concentrations and psychopathology in 22q11.2DS. To my knowledge, this will be the first study of gamma oscillations and GABA concentrations in this high-risk group.

Amount: £307,019
Funder: The Wellcome Trust
Recipient: Cardiff University

The role of journal press releases in shaping biomedical news reporting. 15 Jul 2013

Public understanding of science and health is an important issue in society. Whether the topic is climate change, GM foods, or vaccines, each requires informed public engagement to arrive at democratic and ethically responsible solutions. Our project aims to uncover the causes of misreporting of health-related science, with implications for improving the interaction between scientists, the media, and the public. Despite years of debate about the (mis)representation of science in the media, th ere remains little hard evidence to indicate when, where and why problems arise. Our previous research has been among the first to address this issue, suggesting that university press releases (PRs) are a source of misreporting. The proposed study will investigate an even more crucial, but hitherto ignored, link between science and the media: PRs issued by major academic journals. Understanding the origin of misreporting is crucial for three reasons. First, occasional gross failure in the sc ience-media relationship, such as in the MMR scandal, causes demonstrable harm and death. Second, the cumulative effect of smaller-scale misrepresentation damages society by jeopardising public education and eroding trust in science. Finally, knowing origins of misreporting would allow for development of corrective guidelines that improve practices in PR formulation.

Amount: £4,990
Funder: The Wellcome Trust
Recipient: Cardiff University

Institutional Strategic Support Fund 2011/12. 20 Dec 2011

The Trust’s major directions for use of this Fund are as follows: 1. To assist the Institution in developing its research strategy across College’s and Schools 2. To encourage new inter-departmental synergies, cross-disciplinary collaborations, and inter-institutional initiatives 3. To add value to existing Wellcome Trust investments in the Institution. Strengthening Biomedical and Clinical SciencesCardiff University will build on successes of the first ISSF Award, widening the portfolio to encompass all the priority research areas in the College of Biomedical and Life Sciences (CBLS). We will build new links with relevant research in computing, physical sciences, humanities and social sciences and consolidate ties with partner Universities in the South West. CBLS, which includes all the Health-related Schools in the University, has recently completed a comprehensive review of its research portfolio and identified five Themes around which investment will be focused: Immunology, Infection & Inflammation; Mind, Brain & Neuroscience; Cancer; Public Health & Integrative Biosystems. The ISSF Award will impact in all these areas. Previous ISSF success 2013The Award, with matched funding, supported new academic appointments, seven project grants, thirty-one seedcorn grants and eight mobility awards. Infrastructure was supported through substantial spend on new equipment. Public engagement was supported through contributions to high profile local events and stand-alone meetings.

Amount: £750,000
Funder: The Wellcome Trust
Recipient: Cardiff University

Tractometry. 04 Oct 2011

Not available

Amount: £1,788,305
Funder: The Wellcome Trust
Recipient: Cardiff University

Using machine learning algorithms to analyse complex genetic data in sub-phenotypes of psychiatric disorders. 25 Jun 2012

The main objective for my PhD will be to apply machine learning methods and algorithms to complex genetic data in an attempt to identify features that characterise different sub­ phenotypes in psychiatric disorders. This will not only look for the contribution of individual genes, but also at possible biological gene-gene interactions and functional pathways. The use of non-parametric machine learning techniques will allow us to go beyond classical statistical (parametric) methods and search for more complex underlying patterns in the data.

Amount: £150,112
Funder: The Wellcome Trust
Recipient: Cardiff University

Modulating hippocampal neurogenesis to restore learning and memory in mesial temporal lobe epilepsy. 25 Jun 2012

Learning and memory dysfunction is the commonest neuropsychological effect of mesial temporal lobe epilepsy (mTLE). Because the underlying neurobiology is poorly understood, there are no pharmacological strategies to restore learningand memory function. Neurogenesis in the adult dentate gyrus is important for allocentric hippocampal learning, is impaired in chronic mTLE due to chronic neuroinflammation, and we have recently shown thatrestoring neurogenesis in animal models returns allocentric learning to normal. Using 30 cultures of sclerotic hippocampus from epilepsy surgery patients we also show that this antineurogenic effect is Q£!1!y mediated via IL-1beta release. Cytokines released into the stem cell microenvironment from astrocytes, neurons and microglia are key modulators of neurogenesis under normal and neuroinflammatory states and are also primed by the complement system. Status epilepticus induced epigenetic modification of hippocampal neural stem cells also appears to play a role bothin normal and in chronically altered neurogenesis in mTLE. Our objectives are to examine the role of cytokines, the complement system andepigenetic modification in generating and maintaining the anti-neurogenic niche in animal models and human mTLE, and whether these affect hippocampal learning, in order to identify drug targets for treating cognitive impairment in human mTLE.

Amount: £150,112
Funder: The Wellcome Trust
Recipient: Cardiff University

MIND - Modelling and imaging using non-gaussian diffusion. 28 May 2012

A clinical diffusion-weighted sequence (b-value=1000 s/mm2) is generally sensitive to water molecules hindered in the extra-cellular/extra-axonal space. When stronger b-values are applied, restrictions and long-range spatial/temporal correlations lead to a failure of the Gaussian approximation. My project will fully characterize water dynamics in brain tissue outside the Gaussian regime, to gain microstructural insights and overcome the low specificity of DT-MRI. I will achieve this by expanding my work on three different non-Gaussian approaches: (1) anomalous diffusion imaging (ADI) which models the diffusion-weighted signal as a stretched-exponential function, linking the exponent to local tissue heterogeneity; (2) the composite hindered and restricted model of diffusion (CHARMED) which models diffusion in white matter using both extra-axonal and intra-axonal compartments; and (3) diffusion kurtosis imaging (DKI) which quantifies the deviation of a generic probability distribution fr om a Gaussian. Long experimental times and lack of clear links with underlying histology currently preclude wider deployment and translation of these methods. My goals are clear: (i) to fully characterize the link between ADI/CHARMED/DKI and tissue microstructure in the animal model; (ii) to develop and optimize a protocol to assay key and complementary microstructural parameters; and (iii) to demonstrate the clinical feasibility and utility of this new approach.

Amount: £250,000
Funder: The Wellcome Trust
Recipient: Cardiff University

Institutional Strategic Support Fund Phase2 FY2014/16 27 Oct 2014

The Trust’s major directions for use of this Fund are as follows: 1. To assist the Institution in developing its research strategy across College’s and Schools 2. To encourage new inter-departmental synergies, cross-disciplinary collaborations, and inter-institutional initiatives 3. To add value to existing Wellcome Trust investments in the Institution. Strengthening Biomedical and Clinical SciencesCardiff University will build on successes of the first ISSF Award, widening the portfolio to encompass all the priority research areas in the College of Biomedical and Life Sciences (CBLS). We will build new links with relevant research in computing, physical sciences, humanities and social sciences and consolidate ties with partner Universities in the South West. CBLS, which includes all the Health-related Schools in the University, has recently completed a comprehensive review of its research portfolio and identified five Themes around which investment will be focused: Immunology, Infection & Inflammation; Mind, Brain & Neuroscience; Cancer; Public Health & Integrative Biosystems. The ISSF Award will impact in all these areas. Previous ISSF success 2013The Award, with matched funding, supported new academic appointments, seven project grants, thirty-one seedcorn grants and eight mobility awards. Infrastructure was supported through substantial spend on new equipment. Public engagement was supported through contributions to high profile local events and stand-alone meetings.

Amount: £1,500,000
Funder: The Wellcome Trust
Recipient: Cardiff University

Open access award 2015/16. 21 Sep 2015

Not available

Amount: £72,725
Funder: The Wellcome Trust
Recipient: Cardiff University

Cardiff, Integrative Neuroscience. 29 May 2015

Not available

Amount: £150,321
Funder: The Wellcome Trust
Recipient: Cardiff University

Open access award. 20 Sep 2011

Not available

Amount: £75,000
Funder: The Wellcome Trust
Recipient: Cardiff University

Integrative Neuroscience. 31 Aug 2011

Please provide a summary of your proposed research, including key goals (no more than 200 words) The close relationship between neuronal activity and subsequent changes in vessel tone, thus cerebral blood flow, is termed neurovascular coupling (NVC). This coupling mechanism is not yet fully understood. In Multiple Sclerosis (MS), a chronic autoimmune inflammatory disease, hypoperfusion and impaired cerebrovascular reactivity are seen, both components of NVC. Our primary aim is to examine the effect of inflammation on NVC and how decoupling may contribute to tissue damage. MS individuals will be compared with matched controls, and blood biomarkers relating to vascular function will be measured. Another aim is to advance methodologies measuring NVC, studied previously at CUBRIC. In response to a visual task, gamma oscillations using MEG (magnetoencephalography) were regressed against BOLD/ASL (Blood Oxygen Level Dependent contrast/Arterial Spin Labelling) responses, measuring neuronal activity and blood flow, respectively. Regression coefficients define an empirical measure of NVC, with good repeatability. This project will optimise a motor task with these methods, assessing NVC in another functional domain relevant to MS. Many neuroimaging techniques are based on NVC; an increased knowledge of NVC pathways will provide insight into their signals. This research will deepen understanding of the role of NVC in brain pathologies, particularly MS, and potentially inform therapeutic directions.

Amount: £146,543
Funder: The Wellcome Trust
Recipient: Cardiff University

Investigating retrieval control mechanisms. 31 Aug 2011

This PhD project is designed to understand the reasons for memory problems in people suffering from schizophrenia. It is likely that these memory problems are at least in part due to failures of memory control processes: that is, failures in processes involved in strategically regulating how information is encoded and retrieved. In pursuing this question event-related potential (ERP), functional magnetic resonance imaging (fMRI) and behavioural measures will be employed. ERPs have been shown to index several different kinds of retrieval control processes. Similarly, fMRI measures have been shown to be particularly sensitive to encoding operations. Together, such methods are extremely well-suited to investigations of this type. The overall goal of the project is to understand how memory control operates in people suffering from schizophrenia, and how failures of encoding and retrieval control contribute to their memory problems. This will be accomplished in the following ways: - Identifying robust ERP,fMRI and behavioural markers of encoding and retrieval control operations - Observing how these vary according to schizotypy ratings. - Investigating the effects of intervention/training on memory control processes.

Amount: £146,543
Funder: The Wellcome Trust
Recipient: Cardiff University