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Results

The collector as consumer in eighteenth century Britain: Dr William Hunter (1718-1783) 16 Jun 2008

This research project aims to enhance the work that I have already completed on Dr William Hunter's lectures on Anatomy to students at the Royal Academy of Arts. The specific purpose of this paper is to identify and convey a particular 18th century aesthetic that valued the role of the craftsman/woman in the fine arts and is discernible in Hunter's teaching at the RA and in his production and display of anatomical specimens. However, this is also part of a wider project that forms a chapter in my PhD thesis: Dr William Hunter and the British School of Artists.

Amount: £479
Funder: The Wellcome Trust
Recipient: University of Glasgow

Vacation Scholarships 2008. 27 May 2008

Not available

Amount: £21,600
Funder: The Wellcome Trust
Recipient: University of Glasgow

Value in People Award. 17 Oct 2007

Not available

Amount: £350,000
Funder: The Wellcome Trust
Recipient: University of Glasgow

The Wellcome Trust Centre for Molecular Parasitology. 29 Aug 2008

We are applying for refunding of core support for our Wellcome Trust Centre, to extend our interactive basic science programmes and our projects to translate appropriate basic findings into products and measures against parasitic disease. Having recruited research leaders heavily in the past 5 years and thus greatly increased our strength in depth and breadth, we aim to address problems in endemic locations and to provide capacity-building both in international research communities and in endem ic locations. Being a Centre also allows us to provide a coherent and broad based approach to public understanding of science, the co-ordination of research networks, participation in scientific community wide initiatives and pump priming of new initiatives. Such strengths need nurture, and so we propose to expand our strengths, and to build our technological base to a level appropriate for our activities. Our key goals are: 1. Develop and nurture our basic research programme 2. Translate ou r basic research towards practical application 3. Strengthen capacity internationally in parasitology 4. Apprise society of the importance of parasitology 5. Consolidate our training programmes 6. Plan succession

Amount: £2,550,183
Funder: The Wellcome Trust
Recipient: University of Glasgow

The Wellcome Trust Centre for Molecular Parasitology 16 Sep 2008

We are applying for refunding of core support for our Wellcome Trust Centre, to extend our interactive basic science programmes and our projects to translate appropriate basic findings into products and measures against parasitic disease. Having recruited research leaders heavily in the past 5 years and thus greatly increased our strength in depth and breadth, we aim to address problems in endemic locations and to provide capacity-building both in international research communities and in endem ic locations. Being a Centre also allows us to provide a coherent and broad based approach to public understanding of science, the co-ordination of research networks, participation in scientific community wide initiatives and pump priming of new initiatives. Such strengths need nurture, and so we propose to expand our strengths, and to build our technological base to a level appropriate for our activities. Our key goals are: 1. Develop and nurture our basic research programme 2. Translate ou r basic research towards practical application 3. Strengthen capacity internationally in parasitology 4. Apprise society of the importance of parasitology 5. Consolidate our training programmes 6. Plan succession

Amount: £210,000
Funder: The Wellcome Trust
Recipient: University of Glasgow

Student Elective Prize for Mr Matthew A Rutherford 29 Aug 2008

''Regulation of aldosterone production by angiotensin related peptides''.

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

Student Elective Prize for Mr James Kinsella 29 Aug 2008

An investigation into early predictors of recovery of ventricular function in patients with low function during the acute phase of MI

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

Open Access Award. 31 Oct 2006

Not available

Amount: £30,000
Funder: The Wellcome Trust
Recipient: University of Glasgow

Exploiting ES-62 to dissect dendritic cell signals regulating initiation and the phenotype of the inflammatory response. 28 May 2007

The core aim of the project is to dissect the signalling mechanisms underlying ES-62-mediated subversion of dendritic cell (DC) maturation to a phenotype that drives hyporesponsive/antiinflammatory T cell-mediated immune responses. Specifically, the major objectives of the project are 1. Define whether ES-62 subverts DC maturation by signalling via a TLR4/PAF-co-receptor complex 2. Identify key signals regulating the switch converting DCs from a pro- to anti-inflammatory phenotype 3. Define whether modulation of the DC signals targeted by ES-62 mimics the phenotype of immune responses associated with ES-62 in vivo By dissecting the molecular mechanisms underlying how ES-62 subverts DC maturation, we aim to identify candidate immunomodulatory targets to facilitate novel drug development for inflammatory disease. This project will be complemented by, and will achieve added value, in terms of reagents and training, by on-going projects identifying the molecular targets of the immunomodulatory actions of ES-62 in B cells and mast cells within our longstanding collaborative grouping (MM Harnett, AJ Melendez and W Harnett).

Amount: £135,945
Funder: The Wellcome Trust
Recipient: University of Glasgow

Unravelling the in vivo immune response against Schistosoma mansoni eggs 10 Feb 2014

Schistosomiasis is the second-most socioeconomically devastating parasitic disease. After infection, Schistosoma mansoni eggs become trapped in the smallintestine and the liver. These eggs drive a chronic immune response that generates fibrosis, causing a debilitating and eventually fatal loss of organ function. Drugs to reduce this inflammation are not available, and much remains to be learned about this pathogenic immune response against S. mansonieggs in vivo. Here we propose a detailed analysis of the soluble and cellular mediators thatinduce responses to S. mansoni eggs in the small intestine and the liver of mice in vivo. We will use novel tools to generate heretofore-unavailable insights into these mechanisms. These include recently developed flow cytometric analyses of immune cell populations, cell sorting, genetically modified mouse strains, and cutting-edge in vivo techniques. We aim to identify the specific cells that drive pathogenic responses to S. mansoni, andthe precise cellular sources of the soluble mediators that control this response. Our results will not only produce a detailed understanding of the cellular interactions between immune cells that respond to S. mansoni eggs, transferable to other parasitic infections or even allergic responses, but mayalso present targets for the specific immunosuppression of Schistosomiasis.

Amount: £52,266
Funder: The Wellcome Trust
Recipient: University of Glasgow

Natural peptidase inhibitors of trypanosomatids. 08 Feb 2007

We shall characterise the roles of two unusual classes of natural peptidase inhibitors in the trypanosomatid parasitic protozoa Leishmania major and Trypanosoma brucei. Neither inhibitor has a mammalian orthologue. The first, inhibitor of serine peptidase (ISP), is similar to bacterial ecotin. We hypothesise that the parasite ISPs inhibit host serine peptidases, thereby facilitating infection and pathogenicity. We shall generate and use ISP-deficient mutants of L. major and T. brucei to inv estigate how ISP influences host-parasite interactions (eg Leishmania with neutrophils and macrophages in vitro and in vivo: T. brucei proliferation and CNS invasion). We shall characterise the inhibitory properties of ISPs, and their expression and trafficking within the parasites, in order to identify the potential key mammalian targets enzymes and so informed insights into the roles of parasite ISPs. The second natural peptidase inhibitor is ICP (inhibitor of cysteine peptidase). Analy sis of a T. brucei ICP-deficient mutant suggests that the inhibitor modulates endogenous CP activity. By generating a CP-deficient mutant and comparing its phenotype with the ICP-deficient mutant, we shall study the contribution of cysteine peptidase (CP) activity to T. brucei infection and pathogenicity, particularly using a blood brain barrier model, and elucidate the functional role of the parasite s ICP.

Amount: £318,841
Funder: The Wellcome Trust
Recipient: University of Glasgow

Structure/Function analyses of the neural circuitry controlling male courtship behaviour in Drosophila. 28 Jun 2007

Reproduction and courtship are essential components of the behavioural repertoire of Drosophila melanogaster. A number of genes are involved in building the potential for these behaviours into the central nervous system (CNS), most notably the sex determination genes fruitless (fru) and doublesex (dsx). Yet how do fru and dsx generate a sexually dimorphic nervous system, and what can we learn from these genes to understand how complex behaviour may be encoded? We have developed a unique set of m olecular genetic tools to dissect the function of Fruitless-expressing neurons in the CNS. Using these same strategies we are generating complimentary reagents to extend our structure/function analyses to the dsx gene. We are exploiting these reagents to study how the neural circuitry underlying sexual behaviour is built into the nervous system during development, and how this circuitry functions in the adult. We have two specific aims; firstly, we will continue to dissect the relative roles of Fru isoforms in male neuronal differentiation and sexual behaviour by the generation and characterization of fru isoform-specific mutants; secondly, we are investigating Fru- and Dsx expressing neurons associated with motor output, notably those controlling male copulatory behaviour and courtship song production.

Amount: £297,695
Funder: The Wellcome Trust
Recipient: University of Glasgow

Do food representations mediate the relationship between self-control and body weight? 01 Apr 2016

In line with the grounded theory of desire and motivated behaviour (Papies and Barsalou, 2015), Papies (2013) demonstrates that hedonic and situational mental representations underlie desire to eat attractive unhealthy food. The ability to resist this desire is called self-control (SC). Although there have been a number of attempts of explaining trait SC (see De Ridder et al., 2012), it has remained unclear how it precisely operates. This study aims at expanding on Papies (2013) by investigating the relationship between representations of unhealthy foods, SC and body weight outcomes (indicated by body mass index, BMI). Thus four predictions are made: (1) trait SC will be negatively associated with BMI; (2) hedonic and situational representations of tempting food will be associated with higher BMI and with lower SC scores; (3) health representations of tempting food will be associated with lower BMI and with higher SC scores; and (4) the association of SC and BMI will be mediated by hedonic, situational, and health representations of tempting foods. Feature listing task (Papies, 2013), Self-Control Scale (Tangley et al., 2004) and information about weight and height will be used to test the hypotheses.

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

Open access block grant 2016/17 30 Sep 2016

Not available

Amount: £77,697
Funder: The Wellcome Trust
Recipient: University of Glasgow

Recognition of BRCA1 deficient mammary tumour cells by γδ T cells 27 Apr 2017

gammadelta T cells are immune cells, which express a T cell receptor whilst behaving like innate immune cells. There are two main subsets of gammadelta T cells in mice. CD27+ (IFNg-producing) gammadelta T cells are anti-tumourigenic, whilst CD27— (IL-17-producing) gammadelta T cells are pro-tumourigenic. However, the function of the anti-tumourigenic properties of CD27+ gammadelta T cells are not entirely known. Previous studies have shown that CD27+ gammadelta T cells kill cancer cells using the NKG2D receptor that binds stress signals that are not normally present in healthy tissue. The key goal of this project is to determine whether CD27+ gammadelta T cells kill BRCA1-deficient cancer cells through the NKG2D receptor due to the expression of stress ligands on the cancer cells. BRCA1 is a protein involved in DNA damage repair. My host lab has found that BRCA1-deficient breast cancer cells upregulate NKG2D ligands, suggesting that increased DNA damage leads to expression of stress signals. To address this goal, we will use techniques including western blot and flow cytometry following co-culture of CD27+ gammadelta T cells with cancer cells. It is hoped that robust T cell therapy will become a reality once we better understand the mechanisms of gammadelta T cells.

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

Access to the skin by African trypanosomes 27 Apr 2017

African trypanosomes are protozoan parasites that cause both African trypanosomiasis in humans and Nagana in animals. They are transmitted by the bit of a tsetse fly. Until recently the disease was considered a blood disease, however evidence suggests that parasites sequester to the skin and these extravascular parasites can be transmitted to the tsetse vector as it takes a bloodmeal. therefore, sequestration to the skin is an important feature of the disease. This project will try to understand the mechanism of parasites sequestration. the project will try to address these questions: are trypanosomes found in the skin different to those found in the blood? Are they expressing different genes that allow them to escape the vasculature and invade the skin? In order to answer these questions, the transcriptome of skin-dwelling and blood-dwelling parasites will be compared. This will identify any gene expression differences that are associated with extravascular sequestration, leading possible mechanisms of tissue invasion. This project will generate important information that will lead to the development of new hypotheses regarding the mechanism of parasite sequestration that will form the basis of future research for my host laboratory.

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

Causal feature transfer in different face categorisation tasks 01 Apr 2016

The research seeks to study how the causal feature transfer of face representations in the brain may depend on the categorisation task itself. Subjects would perform two face discrimination tasks – one for gender and one for the six basic emotional expressions (anger, disgust, fear, happiness, sadness, surprise) – with stimulus pixels sampled using the Bubbles method. MEG measures would be used to examine in a first stage which nodes are maximally task-modulated by computing the time-varying Mutual Information between MEG source activity and tasks. For each of these task-sensitive nodes, we would then compute the Mutual Information between the sampled pixels and the MEG node activity. Between these two analyses we could separate, in the set of task-varying nodes, the subset of nodes coding categorization-specific features, from those coding only the semantics of the categorization task. In a final stage, we would reconstruct the network of nodes that code and transfer task-related features. From a theoretical perspective, this latter step is important to dissociate a code that the experimenter can decode, from a code that the brain uses for data transmission.

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

Provision for public engagement. 15 Jul 2014

Modern approaches to parasitological research are multidisciplinary requiring many and varied expertise that a Centre best employs and exploits. Based upon polyomics and extensive bioinformatic/modelling platforms coupled with cutting edge imaging and novel, in house molecular parasitological methodologies the WTCMP will continue to play a leading role in tropical disease research. Primarily focussing on the molecular and cell biology of apicomplexan and trypanosomatid parasites, we address the major problems caused by parasitic infection in the tropics in a setting continuously strengthened by responsive investment in infrastructure and recruitment of promising group leaders. Translation is principally envisaged to be discovery and development of drug targets and vaccine candidates. WTCMP will continue to provide excellent training at pre-and post-graduate levels, mentoring across the career spectrum. WTCMP will accelerate the development of activities and partnerships in disease ende mic regions (DER) notably via the Wellcome Trust Liverpool Glasgow Centre for Global Health (WTLGCGH) initiative providing access to any relevant Glasgow expertise whilst allowing WTCMP-centred clinical engagement. Polyomics (particularly metabolomics) and modelling will be central to DER engagement allowing integration of our interactions with DER into a unified approach. WTCMP outreach will continue to inform the public of our activities and the problems we address.

Amount: £435,499
Funder: The Wellcome Trust
Recipient: University of Glasgow