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Recipients:
6th East Paddington Brownie Guide Unit
University College London
Currency:
GBP
Amounts:
£0 - £500
£500 - £1,000
Award Year:
2018

Results

Quantitative evaluation of gene dosage effects in the Ras/ERK and PI3K/mTOR pathways on metastatic transformation of oesophageal cancer 02 Nov 2018

<p>Distant metastases account for ~90% of cancer-related deaths, but our understanding of the determinants of this process is limited. I propose to elucidate early genomic mechanisms that enable cells to acquire a metastatic phenotype, with focus on allelic imbalance resulting from copy number changes and the underlying genomic instability. I have previously characterized the implications of genomic amplifications of receptor tyrosine kinases and downstream pathways (MAPK/ERK/PI3K) in the progression of oesophageal adenocarcinoma, a cancer with frequent metastases and prevalent genomic instability. Recent studies have highlighted similar gene dosage effects in KRAS promoting metastasis in pancreatic cancer, and a more general role for genomic instability in accelerating metastatic spread.</p> <p>This study proposes to explore the involvement of such alterations in local invasion in oesophageal adenocarcinoma using whole-genome and RNA sequencing data from primary tumours of this type. I aim to: (1) characterize gene dosage effects and co-dependencies at genomic/transcriptional level in the Ras/MAPK and PI3K/AKT pathways; (2) understand the mutational processes generating such alterations; (3) employ machine learning to identify features in 1) and 2) that are predictive of cellular invasion in this cancer. This integrated framework will highlight pathway vulnerabilities during metastatic onset that may be targetable in the clinic.</p>

Amount: £99,983
Funder: The Wellcome Trust
Recipient: University College London

Developing antisense oligonucleotide therapeutics to target gain-of-function mutations in childhood neurology 02 Nov 2018

<p style="margin-left: 0cm; margin-right: 0cm">The aim of this project is to develop an antisense oligonucleotide (AON) therapeutic approach to target selected gain-of-function mutations that cause childhood neurological disorders. We have selected KCNT1-related infant epilepsy as the primary target disease in this proposal due to the following reasons: 1) this is one of the most frequent genetic causes of infant epilepsies; 2) currently there is no effective treatment; 3) mutations in <em>KCNT1</em> lead to gain-of-function with a marked, measurable increase in neuronal potassium channel current amplitude; 4) cell lines (fibroblast and induced pluripotent stem cells-iPSCs) are being established from patients and readily quantified functional outcome measures are available.</p> <p style="margin-left: 0cm; margin-right: 0cm">In this study, we will design AONs to selectively target a common <em>KCNT1</em> mutation for degradation, optimising the most effective through trials of different AON gene-silencing approaches. The effect of AONs on mutant-allele specific silencing will be evaluated <em>in vitro</em> in human cellular models. The phenotypic rescue of lead AONs on potassium channel function will be evaluated in patient&rsquo;s iPSCs-derived cortical neurons. We expect the success of this project will provide an experimental system and preclinical proof-of-concept of AON therapy applicable for not only KCNT1-related infant epilepsy, but also other childhood neurological disorders caused by gain-of-function mutations.</p>

Amount: £94,290
Funder: The Wellcome Trust
Recipient: University College London

Dissecting endolysosomal trafficking defects in Parkinson's disease 05 Dec 2018

<p style="margin-left: 0in; margin-right: 0in">Endolysosomal trafficking defects are&nbsp;increasingly being implicated in Parkinson's disease (PD). In particular, a number of genes associated with lysosomal storage disorders (LSDs) have been identified as risk factors for developing PD. The precise mechanisms linking endolysosomal genes to PD&nbsp;are not fully understood, but are likely to involve common pathogenic mechanisms. Therefore, through developing a greater understanding of these pathogenic processes, we aim to discover&nbsp;new therapeutic targets in PD.&nbsp;To do this we will study a number of PD-linked genes, including LSD-genes (<em>GBA</em><em>1</em>,&nbsp;<em>SMPD</em><em>1,&nbsp;</em><em>NAGLU</em><em>,&nbsp;</em><em>SLC</em><em>17</em><em>A</em><em>5&nbsp;</em>and&nbsp;<em>ARSB</em>) and&nbsp;<em>Rab39B</em>, encoding&nbsp;an endosomal Rab&nbsp;GTPase. Specifically, we will create novel knockout models&nbsp;of these genes using&nbsp;<em>Drosophila&nbsp;</em>and human PD&nbsp;neuronal cultures,&nbsp;in addition to performing&nbsp;advanced genetic studies. The latter will include a genome-wide association study on the&nbsp;<em>Drosophila&nbsp;</em>Genetic Reference Panel of &gt;200 inbred fly lines harbouring LSD&nbsp;gene loss-of-function. The common biological pathways and genes associated with protection against PD will be identified&nbsp;and compared to those detected by transcriptomic analysis using RNA-sequencing. Targeted genetic and therapeutic drug screening will also be performed on the&nbsp;PD flies. Novel therapies and therapeutic targets will&nbsp;be validated in iPSC-derived dopaminergic neurones and&nbsp;brain tissue from PD patients.&nbsp;</p>

Amount: £1,016,853
Funder: The Wellcome Trust
Recipient: University College London

Assessing Awareness in Severe Dementia 05 Dec 2018

<p style="margin-left: 0cm; margin-right: 0cm">This study is the first to objectively investigate the extent of subjective awareness in severe dementia, its underlying neural correlates and whether awareness changes with environmental stimuli. Transcranial Magnetic Stimulation (TMS), Electroencephalography (EEG), Event Related Potentials (ERPs) and functional Magnetic Resonance Imaging (fMRI) are robust techniques for assessing awareness in clinical groups who are unable to communicate. I will now apply these in dementia to investigate:</p> <p style="margin-left: 0cm; margin-right: 0cm">1) The variation in the level of awareness&nbsp;in people with severe dementia, using TMS-EEG markers.</p> <p style="margin-left: 0cm; margin-right: 0cm">2) In response to visual and auditory stimuli, is there ERP and fMRI evidence of brain activity beyond primary sensory cortices in a fronto-parietal network, reflecting preservation of higher level awareness in people with severe dementia?</p> <p style="margin-left: 0cm; margin-right: 0cm">3) The correlation between different&nbsp;objective biomarkers of subjective awareness, severity of dementia, and clinical and caregiver judgements of&nbsp;subjective awareness.</p> <p style="margin-left: 0cm; margin-right: 0cm">The results will elucidate what people with severe dementia subjectively experience and to what extent they are aware of people and their environment.&nbsp; This novel understanding will support meaningful interactions and communication with family and caregivers,&nbsp;and enable the&nbsp;targeting of interventions and optimisation of environments to&nbsp;improve awareness,&nbsp;quality of life and care for&nbsp;people&nbsp;with severe dementia.</p>

Amount: £633,962
Funder: The Wellcome Trust
Recipient: University College London

An Open-Source Database for Predicting Pharmacokinetics 03 Oct 2018

<p>A free public web resource will be created for academic and industry pharmacometric modellers and data scientists to share standard big datasets and code for the purpose of generating reproducible studies. The ultimate goal is to encourage open research practices through provision of resources needed to facilitate machine learning and mechanism-based approaches for modelling of dose-concentration-response. The repository will allow data users to interact with data generators promoting research collaboration and sharing with a wider audience.</p> <p>The completed project will be a website at the address: <u>www.pkpdai.com</u> and will have 3 overarching aims:</p> <p><strong>Data access: </strong> Links to PKPD datasets amenable to machine learning, the first being clearance (CL) or CL/F for non intravenous administration, where F is the bioavailability.</p> <p><strong>Fostering collaboration: </strong>To download the data and use analytics users will need to register. Upon logging in users will see a simple profile of other users: Name; Institution; Country with an option to send a message to that user (modelled on the PAGE website participant list).</p> <p><strong>Project Showcase: </strong>Summaries, links and other material relating to projects using the database.</p> <p><strong>Milestones:</strong></p> <p>1. Month 6: Website functional with pubmed updating system established, paper submitted to Wellcome Open Research</p> <p>2. Month 7: Workshop at PAGE meeting, email dissemination and set up a Kaggle competition for machine learning prediction of CL.</p> <p>3. Month 8: downloads by &gt;3 academic groups and &gt;3 pharma companies</p> <p>4. Month 12 (end of grant): Workshop at ASCPT, &gt; 50 registered users, 1 manuscript submitted on using database for CL prediction. <strong> </strong></p>

Amount: £49,758
Funder: The Wellcome Trust
Recipient: University College London

Single neuron and network computations in escape decisions 27 Nov 2018

<p style="margin-left: 0in; margin-right: 0in">Computing decisions is a problem that animals must constantly solve, which requires analysing information and selecting appropriate actions. Previous work has demonstrated a role for cortical circuits in learned decision-making paradigms, but we do not know how elementary decision processes, such as integrating evidence, map onto circuit and cellular mechanisms. &nbsp;Our goal is to uncover these mechanisms by investigating instinctive escape decisions in mice. Recent work has identified the superior colliculus and periaqueductal gray as key circuits for escape initiation, providing a unique entry point for investigating decision-making. We aim to explain at the cellular and circuit level the processes of threat stimulus integration and selection of escape behaviour.</p> <p style="margin-left: 0in; margin-right: 0in">Our experimental strategy is to record and stimulate neural activity in the midbrain, while manipulating escape decisions by varying the threat level of sensory stimuli, past experience and the spatial environment. At the circuit level we will make recordings with high-density silicon probes and calcium imaging, while at the single neuron level we will use whole-cell recordings to investigate connectivity and the biophysics of synaptic integration during decision-making. The results from this project will produce mechanistic models of how neurons integrate sensory information and past experience to generate behavioural choices.</p>

Amount: £2,350,667
Funder: The Wellcome Trust
Recipient: University College London

What is special about pandemic HIV-1? How capsid cofactor interactions regulate DNA synthesis, innate immune detection and pandemic potential 27 Nov 2018

<p>The HIV-1 pandemic originates from one of many zoonotic simian lentiviruses. A key unanswered question is: what is special about pandemic HIV-1? Our previous work suggests a pivotal role for lentiviral capsids as molecular machines that determine innate immune evasion capacity and pandemic potential. Lentiviral capsids simultaneously regulate viral DNA synthesis, viral genome uncoating, nuclear entry and integration targeting, through coordinated and dynamic recruitment of host cofactors. The goal of this application is to understand how capsids work by considering the structural changes that result from interactions with known and novel cellular cofactors and drugs, the biological consequences of these changes and how they drive infection, zoonosis and pandemicity.</p> <p>We propose three aims that integrate structural, single-molecule and chemical biology with comparative virology. In aim one we will use state of the art structural approaches to understand cofactor capsid interactions. In aim two we will determine how host cofactors manipulate capsid function to temporally and spatially orchestrate DNA synthesis and genome uncoating to facilitate evasion of innate immunity. In aim three we will use our novel CA inhibitor series as tools to probe capsid function and to develop a new paradigm for treatment of infection.</p>

Amount: £1,027,334
Funder: The Wellcome Trust
Recipient: University College London

The role of cell death in inflammation and inflammation-related disorders 27 Nov 2018

<p style="margin-left: 0cm; margin-right: 0cm">We recently discovered that aberrant cell death induced by death ligands beyond TNF causes lethal inflammation induced by perturbed linear ubiquitination (linUb). Importantly, cell death induction by death ligands other than TNF requires RIPK1 kinase activity in vivo whereas TNF-induced cell death does not. Based thereupon, we will test the following interconnected hypotheses:</p> <p style="margin-left: 0cm; margin-right: 0cm">&nbsp;</p> <ol style="list-style-type: lower-roman"> <li>there is a biochemical basis for the requirement of the kinase activity of RIPK1 for cell death induction by death ligands other than TNF;</li> <li>mice with perturbed linUb can be effectively treated by simultaneously preventing different death ligands, including TNF, but not TNF alone, from inducing cell death;</li> <li>the induction of aberrant cell death by a combination of death ligands, including but not only TNF, is responsible for instigating inflammation-associated diseases in humans, including diseases caused by perturbed linUb and autoimmunity;</li> <li>a cell death aetiology of inflammation-associated disease leaves behind a molecular signature that can be identified by combined cell death and immune profiling which, decisively, in turn reveals a cell death-driven disease aetiology in patients with inflammation-associated disease.</li> </ol> <p style="margin-left: 0cm; margin-right: 0cm">&nbsp;</p> <p style="margin-left: 0cm; margin-right: 0cm">If successful, this research should enable the future identification of patients with a cell death-driven aetiology of inflammation-associated disease and propose effective cell death-inhibitory treatment options for them.</p>

Amount: £2,506,066
Funder: The Wellcome Trust
Recipient: University College London

The typology and function of an integrated spatial and visual cortical system 27 Nov 2018

<p style="margin-left: 0cm; margin-right: 0cm">When we move within an environment, our visual system is bombarded with visual stimulation from the outside world while, at the same time, the head and eyes are also moving. The brain is nonetheless able to integrate these competing inputs into a stable perception of the world. I will investigate two brain regions that are likely to be key players in this process of visuospatial integration: the visual cortex and the retrosplenial cortex (RSP), which processes information essential for navigation such as location, speed, direction and the angular velocity of the head. Recent physiological evidence suggests that the visual cortex integrates signals from the RSP that indicate the motion velocity of the head. This suggests that visual representations in the cortex are context dependent and incorporate egocentric signals to generate a coherent representation of visual motion events in the external world. To develop a biologically realistic model of how the brain performs this computation, we will generate a detailed connectivity map at cellular resolution of the major pathways within these brain areas. By mapping their functional response properties, we will obtain a physiological understanding of how egocentric visual representations are generated and then translated in the RSP for visually-guided behaviour.</p>

Amount: £2,126,007
Funder: The Wellcome Trust
Recipient: University College London

Adaptive myelination in learning and memory 27 Nov 2018

<p>We found that production of new oligodendrocytes (OLs) is stimulated by, and required for, motor skill learning in mice. &nbsp;New OL production was required within 2-3 hours of mice engaging with the motor task, seemingly too soon for full myelin wrapping. We will therefore investigate&nbsp;how, at the cellular level, OLs contribute to early-stage&nbsp;learning, by&nbsp;interfering genetically&nbsp;with&nbsp;pre-myelinating functions of OLs including&nbsp;process outgrowth and&nbsp;ensheathment, or&nbsp;metabolic coupling between OLs and&nbsp;axons. &nbsp;We will also investigate signalling between axons and OLs to&nbsp;ask&nbsp;whether AMPA receptor-mediated&nbsp;synaptic input to OLs&nbsp;selects electrically active axons for myelination over their inactive or less-active neighbours, and whether this contributes to learning. &nbsp;Recently, we found that&nbsp;active OL generation&nbsp;is required for non-motor, &quot;cognitive&quot;&nbsp;learning in a&nbsp;T-maze test, which&nbsp;relies on short-term working memory and longer-term reference memory in a spatial context. &nbsp;We will use additional maze tests&nbsp;to dissociate working and reference memory&nbsp;and&nbsp;test&nbsp;the hypothesis that adult OL genesis is a&nbsp;general requirement for goal-directed learning and&nbsp;memory processes. &nbsp;We will also perform a genetic test of the idea that myelinating OLs, which are&nbsp;extremely long-lived, are required for preserving long-term memories.</p>

Amount: £1,305,661
Funder: The Wellcome Trust
Recipient: University College London

Information-seeking in health and disease 27 Nov 2018

<p style="margin-left: 0in; margin-right: 0in">People spend a substantial amount of time seeking out information (e.g., reading, asking questions, internet browsing). It is theorized that common psychiatric conditions, including depression and anxiety, are characterized by abnormal information-seeking patterns. These patterns could potentially be measured and used to facilitate diagnosis and treatment selection. However, the precise links between information-seeking and psychopathology are unknown. In fact, we know little about how to quantify information-seeking or the mechanisms that control it.&nbsp;&nbsp;</p> <p style="margin-left: 0in; margin-right: 0in">My aim is to understand (i) how people decide to seek or avoid information and (ii) how those decisions relate to mental health. I have developed tasks to quantify key drivers of information-seeking (including valence of information, uncertainty, instrumental utility). I will test participants to assess whether psychopathology symptoms are linked to abnormal influence of these drivers on information-seeking. I will also combine pharmacological manipulation with neuroimaging to examine whether the influence of these drivers is dependent on dopamine &ndash; a neuromodulator that malfunctions in several conditions in which information-seeking is theorized to be altered- and identify the neural computations involved. I will assess whether these drivers are over/under expressed in individuals diagnosed with affective disorders, and conduct experiments to determine how these alterations impact well-being.&nbsp;</p>

Amount: £1,622,804
Funder: The Wellcome Trust
Recipient: University College London

Harnessing tissue-resident CD8 T cells to manipulate hepatic immunity 27 Nov 2018

<p>Hepatitis B virus (HBV) kills two thousand people a day from immune-mediated liver disease. New treatments aim to recapitulate the &ldquo;functional cure&rdquo; seen following natural resolution of infection, with residual virus kept under long-term immune control. Recent work has revealed that tissue-resident T-cells, which cannot be sampled in the blood, play an essential role in frontline immunosurveillance. We therefore hypothesise that profiling T-cells compartmentalised in the liver of subjects with resolved HBV will decipher mechanisms of immune control of this important human pathogen. Capitalising on unique access to intrahepatic T-cells from contrasting infection outcomes, we will define successful local immune responses to HBV. Specific aims include investigating the functional and metabolic adaptations that allow liver-resident T-cells to survive and thrive in this hostile niche, and testing strategies to induce such responses using <em>in vitro</em> and <em>in vivo</em> HBV models. To provide fundamental insights into organ-specific immunity, we will characterise the interplay between gut-translocated bacterial products and a novel population of CD14-expressing CD8+T-cells with both pro- and anti-inflammatory potential in human liver. Results will define &ldquo;gold-standard&rdquo; antiviral T-cells for HBV monitoring and immunotherapy and inform therapeutic manipulation of the balance between hepatic immunopathology and immunoregulation.</p>

Amount: £1,838,275
Funder: The Wellcome Trust
Recipient: University College London

The Long and Winding Road: Connecting Cortex to Cortex Through the Thalamus. 31 Oct 2018

<p>Our current model of the thalamus as a modulator and transmitter of sensory information is difficult to reconcile with the connectivity and physiology of the high-order thalamic nuclei (HOn). The dominance of cortical over peripheral input, variety of cortical areas providing modulation&nbsp;and cell-to-cell diversity in cortical projection targets have made the HOn difficult to understand. I propose that inhibitory circuits are key to understanding the function of diverse HOn pathways since they're in a privileged position to potentially gate behaviourally-relevant pathways and shape the coupling of HOn neurons to cortical areas. I will combine wide-field imaging and extracellular recordings from LP, TRn and vLGn in behaving mice&nbsp;to determine the cortical network affiliation of diverse LP units, whether these networks change&nbsp;with behavioural context, and&nbsp;how inhibitory neurons coordinate activity between LP neurons affiliated with distinct cortical networks during behaviour. Next, I will bi-directionally disrupt inhibition in vLGn and TRn, studying how this affects cortical activity and behaviour and enquiring whether the two types of inhibition have different functions. Lastly, I will search for the circuit substrate of the inhibitory interactions between LP networks revealed in vivo by combining tracer injections and optogenetic circuit mapping in slices.</p>

Amount: £300,000
Funder: The Wellcome Trust
Recipient: University College London

Auditory structured sequence learning on multiple timescales 31 Oct 2018

<p>Regularities play an important role in analysing auditory scenes; for example, by exploiting the predictable sounds of the car engine, a driver can effortlessly ignore this irrelevant noise, freeing cognitive resources to focus on the road. Regularities also play an important role in language, dictating the relationship between syllables in word or the order words in a sentence, and have been studied to better understand language acquisition and evolution. Despite the critical importance of regularities to both language-motivated and auditory scene-motivated research there are few direct interactions between them. Integrating these previously separate fields, this fellowship will test the hypothesis that sequencing abilities studied within the context of scene-motivated and language-motivated sequence learning will depend on common brain mechanisms. Creating novel stimuli consisting of sequences of rapid (scene-motivated) and slower (language-motivated) stimuli, governed by the same complex relationships, sensitivity to regularities will be assessed using behavioural, pupillometry and electroencephalography studies. Sequence processing proficiency will then be compared to other cognitive abilities and used to explore neurodevelopmental language disorders, e.g. dyslexia. This work will develop novel avenues for understanding the role of sequence processing in the brain and provide potential insights into how these neural processes are disrupted in language disorders.<strong><u> </u></strong></p>

Amount: £300,000
Funder: The Wellcome Trust
Recipient: University College London

Neurobiological foundations of flexible social behaviour 31 Oct 2018

<p>A core aspect of healthy social function is the ability to map our private beliefs onto those that we express publicly according to the social context. It may be socially appropriate to express gratitude for a gift we do not want, or remorse for an action we do not regret. My goal is to understand the neurocognitive mechanisms supporting context-appropriate social behaviours and how they are altered in neuropsychiatric conditions.</p> <p>I will use a novel social interaction task which requires subjects to learn a repertoire of context-dependent mappings from private to public beliefs. I will first apply computational modelling to reveal how subjects solve this problem, identifying &lsquo;prediction-error&rsquo; signals that drive changes in &lsquo;private-public&rsquo; mappings. I will then relate these time-varying components to voltammetric recordings of dopamine and serotonin in human striatum during task performance. These neuromodulators are relevant because they are known to support learning and are implicated in neuropsychiatric conditions with prominent social dysfunction. Finally, I will complement the voltammetric recordings with non-invasive whole-brain OPM-MEG recordings, to identify neural areas which provide contextual &lsquo;inputs&rsquo; for updating private-public mappings and are the &lsquo;targets&rsquo; of such updates. This work promises to enhance our understanding of possible routes to social dysfunction.</p>

Amount: £300,000
Funder: The Wellcome Trust
Recipient: University College London

An Integrated Understanding of the NuA4 Coactivator Complex 17 Oct 2018

<p>Coactivators SAGA and NuA4 stimulate transcription by post-translational modifications of chromatin, but also have important roles in DNA repair and mRNA export.&nbsp; Both contain Tra1, a highly conserved 3744-residue protein that belongs to the Phosphoinositide 3-Kinase-related kinase (PIKK) family.&nbsp; Tra1 enables targeting of SAGA/NuA4 to specific genes, by directly interacting with DNA-bound activator proteins, but the molecular details are unknown.&nbsp; Understanding how Tra1 functions within these complexes is critical for elucidating how they cooperate and function in multiple processes.</p> <p>By combining structural, functional and systems biology techniques, we will focus on the Tra1 protein and the NuA4 complex to produce an integrated understanding of their functions.&nbsp; We have two key goals: (1) determining the molecular mechanisms behind activator targeting of Tra1 and their importance for SAGA and NuA4 recruitment during gene activation and (2) solving a complete and high-resolution structure of the NuA4 coactivator complex that will provide an integrated understanding of its functions in transcription and DNA repair.&nbsp; We also have preliminary data in new projects that will expand our research programme beyond the fellowship, by exploring the mechanisms of Tra1 in DNA repair, the relationships between different PIKKs, and the structure and function of histone methyltransferase complexes.</p>

Amount: £630,801
Funder: The Wellcome Trust
Recipient: University College London

From vision to action: Systems analysis of sensorimotor circuitry controlling visually-guided behaviour 15 Nov 2018

<p style="margin-left: 0cm; margin-right: 0cm">Despite the emergence of technologies to record from thousands of neurons during animal behaviour, two major issues are currently limiting the transfer and utilisation of ultra-high-dimensional datasets between neuroscience groups. First, raw data files are often enormous, making data transfer inconvenient and expensive. Second, there is no common format for storing behavioural and neurophysiological data, making it challenging to interpret and work with data from another lab. By the end of this project, we will have provided the neuroscience community with a platform that can solve both challenges. Based on our experience, along with input from other neuroscience labs at UCL, we will develop a universal &ldquo;SysNeuro&rdquo; format for pre-processed, multi-modal, neurophysiology and behavioural data. This will enable labs to exchange compact files that contain all data and metadata relevant to the experiment along with full details of pre-processing algorithms.&nbsp; We will provide open-source software to easily build and manage SysNeuro files and execute advanced data analyses, including deep-learning to discover network dynamics that predict behaviour. Through a symposium at UCL, we will promote the uptake of our platform, provide hands-on training and create a forum to discuss current and future priorities related to data analysis and sharing. Overall, this project will (1) improve utilisation of light-sheet imaging data from our main project, (2) enhance data sharing across the systems neuroscience community and (3) provide easy-to-use tools that lower the barrier to entry for other researchers to flexibly deploy advanced deep-learning analyses.</p>

Amount: £48,349
Funder: The Wellcome Trust
Recipient: University College London

UCL/WT Translational Partnership 2018 - Widening Participation and Enhancing Translational Culture 30 Sep 2018

The biomedical translational strategy of UCL and its partner hospitals is based upon harnessing the wealth of talent and ideas across disciplines to make a difference to patients and their families. The WT Translational Partnership Award supports the pursuit of excellence in the universities tripartite mission "Research, Education and Innovation" and will enhance the knowledge, culture and support available for translation: • Provide funding to develop pilot data enabling progression of projects to our internal Therapeutic Acceleration Fund. Aimed at encouraging Early Career Scientists to take the first step along the translational pathway (RESEARCH) • Enable a greater understanding of translation amongst early career researchers through a mixture of on-line training material and workshops (EDUCATION) • Supporting our Therapeutic Innovation Networks (TINs) in small molecule, biologics, cell, gene & regenerative medicine, devices, diagnostics and repurposing. These "early discovery therapeutic accelerators" will identify and address barriers encountered, share knowledge/best practice and use Industry expertise to progress specific projects (INNOVATION)

Amount: £1,000,000
Funder: The Wellcome Trust
Recipient: University College London

The Future of Maternity Care: challenges and opportunities to achieve person-centred care in the NHS 18 Jun 2018

<p>I propose to review up-to-date research and evidence regarding new developments in technology and health education that aim to&nbsp;improve maternity care in the UK, particularly through improving&nbsp;women&rsquo;s access to information,&nbsp;services, and their own medical records.&nbsp;Parliamentarians will require a balanced and&nbsp;concise summary&nbsp;of the evidence behind these new technologies and a sense of how they will be received by the public and health professionals.</p> <p>Key goals:</p> <ul> <li>Assess the work that has come out of the <em>National Maternity Review</em>, particularly advances in e-health and mobile technology such as the Digital Maternity Toolset being developed by NHS Digital</li> <li>Look more generally at the opportunities for health education in maternal health</li> <li>Explore the possibility of learning from policy innovations in other health systems&nbsp;</li> <li>Engage with a range of stakeholders over the course of the project&nbsp;to assess how policy recommendations&nbsp;will be received and identify&nbsp;potential areas for improvement</li> </ul>

Amount: £6,514
Funder: The Wellcome Trust
Recipient: University College London