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Results

LifeLines 20 Apr 2016

This is the expansion of a project supporting volunteers aged 50 plus to run activities for vulnerable older people to improve health and well-being. These have previously included art classes, creative writing, yoga and computer club. The group will expand across the city, recruiting more volunteers, supporting more than 800 new people and establishing a Men’s Network to encourage older men to socialise regularly. It will also extend its HealthLink scheme to help older people get to medical appointments.

Kilkeel RBL - Saving Our Community Venue 22 Oct 2015

The group is a community and voluntary based organisation providing a range of services and activities to the local community. They received a grant of £10,000 to make improvements to their venue so that it can be used for more classes and activities.

Grant to Royal British Legion Tipton Branch 19 May 2016

Remembering Tipton's World War One Heroes

Grant awarded to The Royal British Legion (Forest Hall) Branch And Club (Tyne & Wear) 20 Nov 1998

Towards improving access and facilities for disabled people at the Forest Hall Ex-Servicemen's Institute.

Grant awarded to Community Service Volunteers (Training and Enterprise NE) (Tyne & Wear) 13 Jul 2004

To provide daycare services to older people living in high rise flats in Newcastle.

ALSPAC The Avon Longitudinal Study of Parents and Children: An international resourcefor population genomics and lifecourse epidemiology. (MH&E AWARD; 75thANNIVERSARY) 01 Sep 2011

This proposal will further develop the Avon Longitudinal Study of Parents and their Children (ALSPAC) resource in ways that render it of maximal value to the scientific community. Extensive data have been collected on over 10,000 mothers initially recruited when pregnant in the early 1990s, their offspring and their partners. This includes a substantial biobank of biological samples, data from repeated clinical assessments and questionnaires on the children, a single clinical assessment and rep eat questionnaires on the mothers, and repeat questionnaires on the partners. The resource will be developed by (1) further questionnaire follow-up as the adolescents transition into adulthood, and their parents as they move towards later middle age; (2) recruitment of the grandchildren of the mothers originally recruited that will total over 1500-2000 over the award period - creating a unique three-generational resource; (3) a clinical examination and further biological sample collection on t he fathers; (4) establishment of the study as a recruit-by-genotype resource; (5) consent from siblings of the original ALSPAC children to enter the study and piloting low-cost data collection from them; (6) developing remote secure access data handling and other approaches to allow maximal utilisation of the data.

Amount: £5,000
Funder: The Wellcome Trust
Recipient: University of Bristol

Investigation of Eph receptor signalling in contact inhibition of locomation and its role in invasion and metastasis in prostate cancer 14 Dec 2010

1) To investigate the mechanism by which Eph receptor signalling controls microtubule dynamics and whether this signaling pathway plays a critical role in regulating cell-contact dependent migration and invasion of prostate cancer cells. 2) To investigate the function of EphB-ephrin-82 interactions in regulating prostate cancer invasion and, metastasis using experimental tumour models.

Amount: £12,143
Funder: The Wellcome Trust
Recipient: University of Bristol

The molecular basis of parasitism in the nematode Strongyloides ratti. 07 Mar 2011

This work aims to discover the molecular basis of nematode parasitism. Nematodes are common and important pathogens of humans. Anti-nematode therapy relies on a few drugs to which there is already resistance. Parasitic nematodes have evolved adaptations (e.g. altered metabolism, immune defence) to be successful parasites. While adaptations to animal parasitism is understood in these rather broad categories, the specific molecular bases of these adaptations is not known. A key question is, wh at molecules do parasitic nematodes use to be successful parasites? The genus Strongyloides spp. include important human parasites. There is also a well studied rodent model, S. ratti. Uniquely among parasitic nematodes, the Strongyloides life-cycle includes both a parasitic female stage and a genetically identical free-living female stage. Differences between these two female forms must be epigenetic, presumably controlled by altered transcription and translation. We will compare the proteom e and transcriptome of the parasitic and free-living females of S. ratti. From this we will define the genes and gene products of the parasitic female stage. This approach exploits the currently advanced S. ratti genome sequencing project. This work will give an understanding of the molecular basis of nematode parasitism, and so define new potential drug targets.

Amount: £272,561
Funder: The Wellcome Trust
Recipient: University of Bristol

Does a mother's dietary intake during pregnancy influence brain development and therefore cognitive ability?. 14 Oct 2008

Foetal and infant nutrition is associated with neurodevelopment and childhood cognition. However, the extent to which poor nutrition is responsible for suboptimal brain development is unclear, because associations between early life nutrition and cognition are heavily confounded by socio-economic status and other lifestyle factors. Many nutrients such as iodine, omega-3 fatty acids and B-vitamins are important in brain development and may have severe consequences if deficient in the diet, althou gh the effect of relatively low levels of these nutrients on cognition is not well understood. We plan to investigate whether exposure to specific nutrients in utero influences cognition. This will be determined by looking at associations between childhood cognition and genetic variants which affect nutrient uptake, metabolism or transport. Cognition in the children will be determined by the Weschler intelligence scale for children (WISC)-III at age 8, and related to both mothers and childs ge notype. The study will be carried-out in a population based cohort of over 14,000 mothers and their children who were recruited during pregnancy and have now been followed up for 16 years. Associations between mothers genotype and childhood cognition will implicate the related nutrient and provide a target for dietary intervention, which could be easily implemented.

Amount: £184,336
Funder: The Wellcome Trust
Recipient: University of Bristol

How is cell migration regulated by the extracellular matrix: role of syndecan-4 and integrin-alpha5beta1 receptors in the regulation of Rho family GTPases?. 23 Jun 2009

I aim to understand how syndecan-4 regulates Rho-family GTPases and integrin-alpha5beta1 to achieve directional cell migration. Specifically I will address: A. Regulation of the principal RhoA suppressor, p190RhoGAP by syndecan-4. I will map the syndecan-4-dependent phosphorylation sites of p190RhoGAP and identify p190RhoGAP-binding partners. Subsequently, I will examine the effects of p190RhoGAP regulation on the activities of RhoA, Rac1 and cell migration. B. Regulation of Rac1 by s yndecan-4. First, I will identify the GTP-exchange factor(s) (GEF(s)) responsible for syndecan-4-dependent Rac1 activation. Second, I will characterise syndecan-4-dependent Rac1 inhibition and turnover through p190RhoGAP. By defining simultaneous activation and turnover pathways, I will resolve mechanisms of precise spatiotemporal regulation and rapid cycling of active Rac1. I will demonstrate how localisation of these events results in directional cell migration in response to syndecan-4 en gagement. C. Regulation of integrin-alpha5beta1 by syndecan-4 that determines adhesive strength. My preliminary experiments have revealed that engagement of syndecan-4 reduces the strength of cell adhesion to integrin ligands. I will identify the mechanism of this novel relationship, focusing on the effect of syndecan-4 engagement on activity and distribution of integrins. Through these aims I will resolve novel mechanisms of GTPase coordination, rapid cycling of active Rac1 and regulat ed cell adhesion.

Amount: £774,917
Funder: The Wellcome Trust
Recipient: University of Bristol

The role of Prdm8 in mammalian eye development. 07 Apr 2008

Although eye development in different organisms produces dramatically different structures, like the compound eye of insects and the camera-like eye of vertebrates, the underlying molecular mechanisms are highly conserved. Animal models have proven to be highly informative of the intrinsic network of transcription factors (TFs) that regulates human eye formation, and mutations in a number of TF genes have subsequently been shown to cause inherited eye and retinal cell type-specific defects in h umans. The aim of the proposed research is to define the role of the putative TF, Prdm8, in eye development and identify its downstream target genes. Adult mice homozygous for a Prdm8 null allele (Prdm8-/-) lack the major class of retinal interneurons, rod bipolar cells. My first goal will be to define the population of genes that are differentially expressed in the developing retinas of wild-type vs. Prdm8-/- mice. My second goal will be to identify the consensus DNA-binding site for Prdm8. Those genes that are: (i) differentially expressed in Prdm8-/- vs wildtype mice, (ii) expressed in the same retinal cell types as Prdm8, and (iii) contain the Prdm8 consensus DNA-binding sequence(s), are likely to be direct downstream target genes for Prdm8, involved in retinal bipolar cell formation.

Amount: £84,439
Funder: The Wellcome Trust
Recipient: University of Bristol

The measurement of whole body and abdominal adiposity in Indian populations: the use of appropriate and available measurements in the assessment of environmental and genetic... 16 Jun 2008

1) To calibrate DXA measures of abdominal adiposity against MRI in a subset of the Hyderabad DXA Study population. 2) To use a combination of basic and DXA derived measures to find the best simple anthropometric measures for assessing whole body and abdominal adiposity in the Hyderabad DXA Study. 3) To use derived measures of adiposity to investigate associations with obesity related genetic variants in a larger Indian cohort. 4) To identify any interactions between genes and environment in the development of DXA measures of adiposity.

Amount: £139,637
Funder: The Wellcome Trust
Recipient: University of Bristol

Vitamin D and cardiovascular risk factors in early life. 16 Jun 2008

1) Examine cross-sectional associations between vitamin D, parathyroid hormone (PTH) and calcium and cardiovascular risk factors (blood pressure, fasting glucose, insulin, HbA1c. lipids and inflammatory markers) in children and adolescents. 2) Examine prospective associations of intrauterine (maternal pregnancy) and childhood (-age 9) vitamin D, PTH and calcium levels with later (-age 15-17) cardiovascular risk factors. 3) Use genetic variants robustly associated with variation in vitamin D status as instrumental variables to determine the causal association of variation in vitamin D with cardiovascular risk factors.

Amount: £139,637
Funder: The Wellcome Trust
Recipient: University of Bristol

10,000 UK genome sequences: accessing the role of rare genetic variants in health and disease. 14 Dec 2009

We propose a series of complementary genetic approaches to find new low frequency/rare variants contributing to disease phenotypes. These will be based on obtaining the genome wide sequence of 4000 samples from the TwinsUK and ALSPAC cohorts (at 6x sequence coverage), and the exome sequence (protein coding regions and related conserved sequence) of 6000 samples selected for extreme phenotypes. Our studies will focus primarily on cardiovascular-related quantitative traits, obesity and related m etabolic traits, neurodevelopmental disorders and a limited number of extreme clinical phenotypes that will provide proof-of-concept for future familial trait sequencing. We will analyse directly quantitative traits in the cohorts and the selected traits in the extreme samples, and also use imputation down to 0.1% allele frequency to extend the analyses to further sample sets with genome wide genotype data. In each case we will investigate indels and larger structural variants as well as SNPs, and use statistical methods that combine rare variants in a locus or pathway as well as single-variant approaches. We will make the sequence data we obtain available for further research purposes, empowering many additional research directions both on these samples and by imputation on further samples from the UK and beyond.

Amount: £104,030
Funder: The Wellcome Trust
Recipient: University of Bristol

Modelling wound re-epithelialisation in the Drosophila embryo 29 May 2009

The main focus of my investigation will be to study the molecular mechanisms behind epithelial sheet contact inhibition of migration and subsequent fusion. The Drosophila embryo wound healing model is an efficient way to study in vivo wound healing, and with many signalling events seemingly conserved across phyla to mammalian wound healing, in the future we hope to translate interesting findings into more complex and clinically relevant models. Our studies will involve live imaging Drosophila embryo wound healing in vivo using confocal microscopy. For this, I will collect stage 15 embryos expressing various key proteins fused to fluorescent reporters in the epidermis; I will wound the embryos on the ventral epithelial surface using laser ablation, as previously described, and image for 3 hours capturing the interaction of epithelial fronts as the wound seals closed. With this method I will: I. Characterise 'the steps of contact inhibition as migrating epithelial cell sheets contact and fuse to one another; in particular, I will live image actin and microtubule dynamics and calcium signals during wound re-epithelialisation and fusion; 2. Investigate epigenetic regulation of wound re-epithelialisation; 3. Reveal mechanical signals during wound closure and determine how they influence wound re-epithelialisation.

Amount: £142,657
Funder: The Wellcome Trust
Recipient: University of Bristol

Genome-wide association study of maternal pregnancy phenotypes and later-life maternal and offspring vascular and metabolic phenotypes. 01 Apr 2009

Our goal is to contribute to understanding mechanisms underlying the association of pregnancy phenotypes with future cardiovascular and metabolic phenotypes in women and their offspring. We will test genetic variation on the Illumina 660W-quad BeadChip for association with pregnancy and later-life phenotypes. Pregnancy phenotypes will include weight gain, blood pressure change, hypertensive disorder of pregnancy (HDP), cholesterol, smoking, diet and alcohol. Later-life phenotypes in mothers and offspring will include fat mass, carotid intima media thickness, blood pressure, glucose, insulin, lipids, smoking, diet, physical activity and alcohol. Our sample size of 7,500-10,100 will enable detection of quantitative trait loci responsible for small proportions of the variance in the continuous phenotypes we will examine: 80% power at = 10-7 to detect 0.35-0.58%. For HDP our study (N=1,950 cases) has 80% power to detect a 1.22 odds ratio at = 10-7. We have agreement to complete from se veral cohorts with relevant phenotypes in mothers and offspring and the ability to complete rapid genotyping to complete replication studies (N=44,900). With these additional 44,900 individuals and our contribution to an existing consortium examining genome-wide data in relation to HDP we will have considerable power to detect robust associations.

Amount: £99,954
Funder: The Wellcome Trust
Recipient: University of Bristol

AMPA receptor endosomal sorting during ischaemia . 04 Feb 2009

Transient global ischaemia induces delayed cell death in hippocampal CA1 neurons, via Ca2+/Zn2+-permeable, GluR2-lacking AMPARs. Following ischaemia, synaptic AMPAR currents in hippocampal neurons show marked inward rectification and increased sensitivity to channel blockers selective for GluR2-lacking AMPARs. This occurs via two mechanisms: a delayed downregulation of GluR2 mRNA expression, and a rapid endocytosis during the OGD insult of GluR2-containing AMPARs, which are replaced by GluR2-lac king receptors. Our preliminary data indicate that ion flux through these early GluR2-lacking receptors contributes to delayed neuronal death, so an investigation into the molecular mechanisms that underlie rapid, OGD-induced AMPAR subunit-switching is crucial to our understanding of the processes involved in ischaemia. Using a combination of confocal imaging, biochemistry and electrophysiology, we will study the endosomal trafficking pathways followed by specific AMPAR subunits in response to O GD and the AMPAR-accessory protein interactions involved. We have preliminary data implicating PICK1 as a regulator of GluR2 internalisation during OGD. In addition, we will use an in vivo transient global ischaemia model and investigate the effects of perturbing the specific trafficking events that we define in vitro, on ischaemia-induced hippocampal neuronal death in vivo.

Amount: £248,202
Funder: The Wellcome Trust
Recipient: University of Bristol

Molecular, genetic and lifecourse epidemiology. 13 Jul 2010

1. I hypothesize that common upstream regulatory pathways of CREB/AhR regulate FSCN1 promoter activity in carcinomas. 2. I hypothesize that CREB/AhR regulates the expression of genes involved in the cancer invasion "program" which are associated with prostate cancer progression. 3. I hypothesize that CREB/AhR and miRNAs act in concert to regulate fascin-1 protein levels in carcinomas. 4. 1 hypothesize that the up-regulation of fascin-1 protein is associated with prostate cancer progression. In addition, I hypothesize that the expression or activation status of regulators of fascin-1 expression such as CREB/AhR and miRNAs are associated with prostate cancer progression. I will test my hypotheses by applying a combination of cell biology and epidemiology approaches, in order to both understand the regulation of FSCN1 in cancer and the translational potential of FSCN1 and its regulators as potential prognostic cancer biomarkers. My unique first year training programme has equipped me with the wide set of skills I require to combine both approaches within a single, unifying PhD project.

Amount: £143,090
Funder: The Wellcome Trust
Recipient: University of Bristol

Biogenesis of the red blood cell cytoskeleton in health and disease 14 Jun 2010

To investigate the expression, associations and localisation of key erythroid cytoskeletal proteins during erythropoiesis. - To determine the role of the erythroid cytoskeleton in protein sorting during enucleation - To understand the mechanism by which cytoskeletal changes result in human red blood cell diseases.

Amount: £143,090
Funder: The Wellcome Trust
Recipient: University of Bristol

Dynamic cell biology programme 14 Jun 2010

My goal is to continue using the zebrafish to learn more about how innate immune cells interact with transformed cells in vivo at the earliest stages of cancer initiation and how these compare with other functions of the immune system. I will have three main objectives: 1. To identify the changes in gene expression of immune cells when faced with transformed cells; 2. To compare these ?cancer cell triggered? changes in gene expression with immune cells exposed to wounds and/or microbial infections; 3. To investigate how the immune response to wounding impacts upon the response to a cancer cell burden, and consequently model minimally invasive cancer surgery.

Amount: £143,090
Funder: The Wellcome Trust
Recipient: University of Bristol