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VALUE IN PEOPLE AWARD. 30 Aug 2006

Not available

Amount: £300,000
Funder: The Wellcome Trust
Recipient: University of Edinburgh

The Social, Medical and Political Response to Infertility in Later Twentieth-Century Scotland (1950-1990). 14 Jun 2006

This study will explore the interface between infertility, sexual dysfunction, health and sexuality in Scotland between circa 1950 and 1990. It will examine reproductive pathologies, technologies and ethics in terms of both the formulation and medical implementation of infertility-related policy, and gauge how medical ideologies and agencies interacted with broader socio-legal concerns and processes. The project will address the two major areas of contention within the history of infertility: aetiological debates and the implications of treatment. It will deconstruct the major causal theories debated in later twentieth-century Britain, relating them to broader social concerns and medical ideologies. It will also examine the social, legal, moral and ethical implications of treatment, and the social politics surrounding the desirability of new technologies. Techniques devised to treat the condition have raised highly complex and contentious issues which go far beyond the technical and medical considerations that have received most publicity to date. Therefore, an examination of the social context and contestation surrounding these issues will be central to the research. The study will compare the Scottish experience with the remainder of the United Kingdom, in order to explore whether there was a distinctively Scottish dimension to the social politics of reproduction in this period, given Scotland's separate traditions of law, local government and medical practice, and the distinctive influence of the Scottish Churches on governance north of the Border.

Amount: £189,579
Funder: The Wellcome Trust
Recipient: University of Edinburgh

Identification and characterisation of Wnt target genes in the developing cerebral cortex. 20 Oct 2005

All higher mental and cognitive functions unique to humans depend on the neocortex. In order to fulfill these functions the cortex requires an enormousvariety of neurons. The general aim of my research is to contribute to our understanding of the patterning mechanisms which lead to the generation of these different cortical neurons during embryonic development.I started to address this problem by analyzing cortical development in the extra-toes mousemutant which lacks the Gli3 zinc finger transcription factor. In the Gli3 mutant cortex, the expression of several Wnt genes is severely altered and apical/basal cell polarity, an important determinant of stem cell characteristics, is lost in cortical progenitor cells. By combining transgenicand knock-out approaches with tissue and cell culture experiments, I want to identify and characterize genes which are regulated by Wnt molecules and whichmediate their functions. From these analyses, I expect to gain important insights into an important but poorly understood aspect of Wnt gene function in the developing cortex.

Amount: £570,959
Funder: The Wellcome Trust
Recipient: University of Edinburgh

From mitosis to invasion: studies on invadolysin - a novel, essential metalloprotease. 21 Feb 2006

Through analysis of Drosophila mutations and examination of human cultured cells, we identified invadolysin, a novel essential metalloprotease that provocatively links mitosis with cell migration. Elucidating how invadolysin functions will lay the groundwork for future studies of both normal development and human diseases (e.g. inflammatory, angiogenic, reproductive, and cancer).The investigation of invadolysin is now a major focus of my research programme, with the specific aims of this proposal being:· to determine whether invadolysin is expressed as structurally and functionally distinct forms in fly and vertebrate cells.· to identify substrates and regulators of invadolysin.· to examine invadolysin in cell migration in vertebrate and fly cells.I propose to combine the power of Drosophila as a model organism amenable to genetic and cytological analyses with the biochemical accessibility and medical relevance of human cells to address the cell biology of invadolysin and its role in cell migration during the 3 years of this research proposal. The present application would support the move of my research group to an environment ideally suited to comparative analysis of cell migration and medical applications in the new Queen's Medical Research Institute, part of the College of Medicine and Veterinary Medicine at the University of Edinburgh.

Amount: £843,354
Funder: The Wellcome Trust
Recipient: University of Edinburgh
Amount: £4,576
Funder: The Wellcome Trust
Recipient: University of Edinburgh
Amount: £9,152
Funder: The Wellcome Trust
Recipient: University of Edinburgh

'Psychiatry and Criminal Responsibility: Legal, Medical and Historical Perspectives on Psychiatry in the Courtroom' workshop to be held at the University of Edinburgh on 8-9 March 2006. 08 Feb 2006

Psychiatry and Criminal Responsibility: Legal, Medical and Historical Perspectives on Psychiatry in the Courtroom Drs Crozier and Tadros are in the initial phases of a projected long term research project in the interdisciplinary area of the history of forensic psychiatry and law. This area crosses over both Dr Crozier's historical interests in the development of psychiatric knowledge in the nineteenth and twentieth centuries, and Dr Tadros' legal expertise in criminal responsibility. The focus of this project is to build on the growing interest in Science Studies with science and the law. Dr Crozier and Dr Tadros co-supervise a PhD student working in this area and are hoping to encourage more students to study with them at the University of Edinburgh. Holding a workshop that explores historical and legal aspects of criminal responsibility in relation to psychiatric practice will allow them to bring together scholars from history of medicine, law and psychiatry in order to develop an interdisciplinary dialogue that will help develop a multi-faceted approach to the problem. Such dialogue will encourage reflection on the problem from a variety of angles, and will allow participants to meet colleagues from other scholarly fields whom they would otherwise not had the opportunity to meet. Many of the papers being presented - by historians, lawyers and psychiatrists - will have an historical focus, and so will address important problems in the history of forensic psychiatry.

Amount: £3,000
Funder: The Wellcome Trust
Recipient: University of Edinburgh

Control of chromosome segregation during meiosis. 28 Mar 2006

During meiosis, a single round of DNA replication is followed by two rounds of chromosome segregation. Homologous chromosomes are segregated during meiosis I, whereas sister chromatids are segregated during meiosis II, which resembles mitosis in many aspects. This requires several modifications to the segregation machinery, including the way cohesion between sister chromatids is regulated. During mitosis, sister chromatid cohesion is lost simultaneously along the entire length of chromosomes, which triggers the onset of sister chromatid separation. However, in meiosis, sister chromatid cohesion is lost in a step-wise manner. Loss of cohesion on chromosome arms in meiosis I abolishes the linkage between homologues and allows them to segregate. Cohesion between sister chromatids is, however, maintained around the centromeric regions to keep them together until meiosis II. I propose to elucidate the mechanism that protects cohesion around the centromere during meiosis I, using budding yeast as a model system. I intend to identify and characterize the proteins that prevent loss of centromeric cohesion during meiosis I (protector proteins). I will then investigate the mode of action of protector proteins by analyzing their interactions with each other and with the factors that generate cohesion (cohesins). Finally, I will determine how protector proteins are themselves regulated.

Amount: £30,028
Funder: The Wellcome Trust
Recipient: University of Edinburgh

Understanding how mammalian genomes are packaged in complex chromatin structures. 13 Dec 2005

Studying chromatin is essential to understanding fundamental cellular processes that act on DNA, such as transcription, replication and repair and how it affects many human diseases. Although we have a clear understanding of the structure of the nucleosome we know very little about higher levels of chromatin folding or how it is regulated. The chromatin architecture of mammalian genomes is heterogeneous and I have previously shown that the gene-rich regions of the human genome have a more open higher-order chromatin conformation than gene-poor regions. Constitutive heterochromatin is molecularly distinct from euchromatin. I have shown that both human and mouse satellite-containing centromeric heterochromatin has a compact higher-order chromatin structure. In this proposal I aim to identify factors responsible for regulating the conformation of the chromatin fibre in heterochromatin and examine their mechanism of action. Using a biophysical assay I will determine whether histone and DNA modifications have the capacity to alter the conformation of the chromatin fibre. Using a further development of this technique to purify centromeric heterochromatin, I will examine whether the higher-order 30nm chromatin fibre has a structural RNA component that can modulate its conformation, and will identify new protein components of the chromatin fibre.

Amount: £512,274
Funder: The Wellcome Trust
Recipient: University of Edinburgh

The role of the human cathelicidin LL-37 as an immunomodulator in infectious lung disease. 13 Dec 2005

Cationic host defence peptides (CHDP) are key components of innate defences, recently proposed as potent immunomodulators. LL-37 is a CHDP produced by neutrophils and epithelial cells, and upregulated during infection and inflammation. I have discovered that LL-37 promotes epithelial cell apoptosis,but inhibits neutrophil apoptosis. The differential effects of LL-37 and the underlying mechanisms will be characterised and contrasted in vitro, examining: a) priming of beneficial airway epithelial cell apoptosis through altered Bcl2 family gene expression, as a defence against infection, and b) inhibition of neutrophil apoptosis through activation of MAPK and NFkB pathways, promoting bacterial killing. I propose that these effects of LL-37 enhance innate host defence in acute infectious lung disease, but contribute to disease pathogenesis in chronic exposure, such as occurs in cystic fibrosislung disease. The in vivo contribution of these LL-37-mediated effects to the clearance of pulmonary Pseudomonas aeruginosa infection in murine models will be defined, and the significance of chronic LL-37 exposure to cystic fibrosis lung disease pathogenesis will be determined. A clear understanding of these immunomodulatory effects of LL-37 in vitro and in vivo is required to establish physiological significance and enable appropriately targeted development of synthetic derivatives as therapeutics for antibiotic-resistant infections.

Amount: £581,392
Funder: The Wellcome Trust
Recipient: University of Edinburgh

Paracrine control of renal function: extracellular nucleotides and sodium reabsorption. 30 Aug 2006

Paracrine control of renal function: extracellular nucleotides and sodium reabsorption Extracellular nucleotides modulate cellular function through interaction with the P2 receptor family. Studies in cell lines have shown that these receptors are powerful regulators of renal sodium transporters and thus can exert a major impact on volume status. Nevertheless, using cell systems to model a complex, highly polarised epithelium compromises meaningful integration into systems physiology; phenotypic delineation of "proximal" and "distal" cell models is not absolute and transporter polarity is often lost in culture. I have demonstrated P2 receptor expression in the rat kidney and performed studies providing evidence for in vivo control of renal sodium transport by ATP. This proposal will extend my initial findings, demonstrating paracrine control of both proximal tubule and collecting duct sodium transport via P2 receptor activation. The application is timely, given that the therapeutic potential of this system has been realised in other epithelia. Moreover, this field represents a clear opportunity for expansion in the future. In order to place myself in a competitive position, this project will also make a novel transgenic mouse carrying a "floxed" allele, allowing targeted deletion of the P2Y1 receptor. This powerful tool will allow dissection of the function of tubule P2Y1 receptors in control of systemic sodium homeostasis.

Amount: £7,087
Funder: The Wellcome Trust
Recipient: University of Edinburgh

Paracrine control of renal function: extracellular nucleotides and sodium reabsorption. 22 Nov 2005

Paracrine control of renal function: extracellular nucleotides and sodium reabsorption Extracellular nucleotides modulate cellular function through interaction with the P2 receptor family. Studies in cell lines have shown that these receptors are powerful regulators of renal sodium transporters and thus can exert a major impact on volume status. Nevertheless, using cell systems to model a complex, highly polarised epithelium compromises meaningful integration into systems physiology; phenotypic delineation of "proximal" and "distal" cell models is not absolute and transporter polarity is often lost in culture. I have demonstrated P2 receptor expression in the rat kidney and performed studies providing evidence for in vivo control of renal sodium transport by ATP. This proposal will extend my initial findings, demonstrating paracrine control of both proximal tubule and collecting duct sodium transport via P2 receptor activation. The application is timely, given that the therapeutic potential of this system has been realised in other epithelia. Moreover, this field represents a clear opportunity for expansion in the future. In order to place myself in a competitive position, this project will also make a novel transgenic mouse carrying a "floxed" allele, allowing targeted deletion of the P2Y1 receptor. This powerful tool will allow dissection of the function of tubule P2Y1 receptors in control of systemic sodium homeostasis.

Amount: £171,774
Funder: The Wellcome Trust
Recipient: University of Edinburgh

Investigating genetic leanness: what goes "right" in obesity-resistance. 29 Jun 2006

Metabolic Syndrome (visceral obesity, insulin resistance, type2 diabetes, hypertension) is now highly prevalent, in part due to increased consumption ofhigh fat diets. However, even with dietary excess some humans and rodent strains resist Metabolic Syndrome. We have recently described a novel and unexpected phenotype of high fat diet-induced fat loss and insulin sensitisation in a unique polygenic model of leanness (L mice). This 'superlean' phenotype is associated with a pronounced down-regulation of adipose tissue glucocorticoid action (via the enzyme 11b-HSD-1), a phenomenon that occurs in other obesity-resistant strains (e.g. A/J mice). Our project will:1. Map the gene expression patterns that underlie the novel 'superlean' adipose tissue phenotype of high fat fed L mice using microarrays.2. Investigate whether high fat diet-induced down-regulation of adipose glucocorticoid action (e.g. 11b-HSD-1) is a key adaptation in a panel of obesity-resistant mice (A/J, SWR/J, MF1, 129 and L). We predict that glucocorticoid-regulated pathways will be intimately involved in the protective adaptation of adipose tissue to fatty diets. Novel genes from the microarrays will be screened across the above strains to identify common molecular pathways. Understanding the molecular basis of conserved obesity-resistance mechanisms offers a powerful alternate strategy for identifying future Metabolic Syndrome therapeutics.

Amount: £473,300
Funder: The Wellcome Trust
Recipient: University of Edinburgh

Analysing the interactions of arthropod-borne viruses with their arthropod host. 01 Jun 2006

Emerging and re-emerging diseases, many of which are arthropod-borne viruses (or arboviruses), remain a major threat to public health. These viruses can cause serious, sometimes deadly, illness, with symptoms ranging from fever, arthritis to encephalitis and hemorrhagic fever. While our understanding of the mammalian immune response is very detailed, we still only have limited knowledge as to how the arthropod vector deals with virus infection. The arthropod immune system has ways of dealing with bacteria and parasites, and the signalling pathways are well characterised for the model organism Drosophila melanogaster. From what we know so far from disease carrying mosquitoes, it is safe to assume that their signalling mechanisms are very similar. The goals of this project are to understand how arthropod-borne viruses spread through the arthropod host, where, how and what signalling pathways are activated in response to viral infection, and what the consequences at the cellular and molecular level are for the arthropod. We will also try to find whether any viral proteins are necessary to counteract any antiviral defences. In the first instance we will use Semliki Forest virus, an arthropod-borne member of the Togaviridae family, but in principle the studies are applicable to and could be extended to other arboviruses.

Amount: £546,214
Funder: The Wellcome Trust
Recipient: University of Edinburgh

Funds for administrative support. 26 Apr 2006

Wellcome Trust Cardiovascular Research Initiative. The University of Edinburgh has had considerable recent success in setting up new interdisciplinary centres for biomedical research and the intention of the University to institute a Centre for Research in Cardiovascular Biology (CRCB) was highlighted in the submission for the 1996 RAE well in advance of publicity for the CVRI. The CRCB will be a network of interacting groups within an interdisciplinary 'centre without walls'. A Scientific Advisory Board (SAB) will provide the necessary management structure and administrative support for the Initiative to ensure quality in both research and training. As indicated in our original submission, the SAB will comprise Profs Fox, Haslett, Seckl, Webb and Wyllie, as well as all senior and principal fellows related to the Initiative. Therefore, it is envisaged that Dr Mullins would be a member of the SAB from the outset and that Dr Brown would join in due course. The leader of the Initiative will be Prof Webb, a clinical pharmacologist and clinician in cardiovascular medicine who has a background in cardiovascular science, a major research interest in endothelial function, and whose work bridges clinical and laboratory based-research. This group has the following major responsibilities: In research: To review overall strategy and focus, and set the priorities for research; to review ongoing research programmes and assess new proposals for funding; to assess proposals for senior or principal fellows; and to consider applications from potential visiting research staff. In training: To review ongoing training fellowships; to approve and prioritise new training opportunities and requirements; to consider applications for research leave in the UK or abroad to learn new techniques; to implement a programme of research seminars; and to liaise with the University Faculty of Medicine and, where relevant, with the Postgraduate Dean to address and facilitate clinical training needs, a role which the four clinical professors of medicine who are members of the SAB are particularly well placed to accomplish.

Amount: £45,000
Funder: The Wellcome Trust
Recipient: University of Edinburgh

Balance of funds awarded to Edinburgh CVRI. 26 Apr 2006

Wellcome Trust Cardiovascular Research Initiative. The University of Edinburgh has had considerable recent success in setting up new interdisciplinary centres for biomedical research and the intention of the University to institute a Centre for Research in Cardiovascular Biology (CRCB) was highlighted in the submission for the 1996 RAE well in advance of publicity for the CVRI. The CRCB will be a network of interacting groups within an interdisciplinary 'centre without walls'. A Scientific Advisory Board (SAB) will provide the necessary management structure and administrative support for the Initiative to ensure quality in both research and training. As indicated in our original submission, the SAB will comprise Profs Fox, Haslett, Seckl, Webb and Wyllie, as well as all senior and principal fellows related to the Initiative. Therefore, it is envisaged that Dr Mullins would be a member of the SAB from the outset and that Dr Brown would join in due course. The leader of the Initiative will be Prof Webb, a clinical pharmacologist and clinician in cardiovascular medicine who has a background in cardiovascular science, a major research interest in endothelial function, and whose work bridges clinical and laboratory based-research. This group has the following major responsibilities: In research: To review overall strategy and focus, and set the priorities for research; to review ongoing research programmes and assess new proposals for funding; to assess proposals for senior or principal fellows; and to consider applications from potential visiting research staff. In training: To review ongoing training fellowships; to approve and prioritise new training opportunities and requirements; to consider applications for research leave in the UK or abroad to learn new techniques; to implement a programme of research seminars; and to liaise with the University Faculty of Medicine and, where relevant, with the Postgraduate Dean to address and facilitate clinical training needs, a role which the four clinical professors of medicine who are members of the SAB are particularly well placed to accomplish.

Amount: £14,243
Funder: The Wellcome Trust
Recipient: University of Edinburgh

Identification of the kinases and phosphatases that regulate phosphorylation and activity of the Na-K-2Cl cotransporter in response to environmental change 31 Oct 2005

The Na-K-2Cl cotransporter plays important roles in regulating the compositionand volume of cells and body fluids. Its activity changes in response to diverse stimuli due to its phosphorylation at several sites. We will test the hypothesis that regulation of cotransporter activity involves phosphorylation of the cotransporter at multiple sites by several different kinases and phosphatases and aim to identify the enzymes and sites involved. We will use ferret red cells as a powerful functional model of mammalian cotransport, and cloned cotransporter expressed in HEK-293 cells so we can exploit molecular biological techniques. We will:· Identify proteins that co-precipitate with the cotransporter by mass spectroscopy following their isolation from red cells by blue native gel electrophoresis, co-immunoprecipitation, and pull-down assays using cotransporter with genetically-modified kinase and phosphatase binding sites.· Identify sites on the cotransporter that are phosphorylated by mass spectroscopy, 2D electrophoresis, and using sequence information from cloning studies.· Analyse how cotransporter activity

Amount: £286,216
Funder: The Wellcome Trust
Recipient: University of Edinburgh

Core support for Wellcome Trust Centre for Cell Biology. 20 Sep 2006

The broad aim of the Wellcome Trust Centre is to create a world-class research grouping that is at the forefront of research on fundamental aspects of cell biology. Since the creation of the Centre four years ago, we have made significant progress towards this aspiration. We appointed a core of professorial level scientists who are leaders in their fields plus more junior group leaders who have acquired fellowships in open competition. Our most important assets are the individual scientists who direct and manage their independently funded research groups and whose ability largely determines our research output. The Centre's specific goal is to make discoveries that take the understanding of cells to new levels. We believe that creative research of this kind flourishes where interaction, scientific rigour and constructive criticism are pervasive. The core funding associated with being a Centre allows us to realise these ideals. We have promoted a culture of scientific excellence through communal scientific activites that reinforce our ethos (seminars, retreats, Fellows Meetings, etc) and through sharing of state-of-theart core resources, equipment and facilities. In future, we intend to strengthen our scientific profile in several ways. 1. We will continue to seek cell biologists of excellence for our faculty. 2. We will improve the Centre's instumentation stock in order to maintain our status at the cutting edge in a time of feverish technological development. 3. We will develop our "outreach" activities in order to more effectively communicate the excitement of our research to the public. 4. We will enhance our mentoring of scientists at all levels. 5. We will seek to institute a PhD programme that will allow us to stimulate and educate a new generation of scientists.

Amount: £1,539,302
Funder: The Wellcome Trust
Recipient: University of Edinburgh

Core support for Wellcome Trust Centre for Cell Biology. 22 May 2006

The broad aim of the Wellcome Trust Centre is to create a world-class research grouping that is at the forefront of research on fundamental aspects of cell biology. Since the creation of the Centre four years ago, we have made significant progress towards this aspiration. We appointed a core of professorial level scientists who are leaders in their fields plus more junior group leaders who have acquired fellowships in open competition. Our most important assets are the individual scientists who direct and manage their independently funded research groups and whose ability largely determines our research output. The Centre's specific goal is to make discoveries that take the understanding of cells to new levels. We believe that creative research of this kind flourishes where interaction, scientific rigour and constructive criticism are pervasive. The core funding associated with being a Centre allows us to realise these ideals. We have promoted a culture of scientific excellence through communal scientific activites that reinforce our ethos (seminars, retreats, Fellows Meetings, etc) and through sharing of state-of-theart core resources, equipment and facilities. In future, we intend to strengthen our scientific profile in several ways. 1. We will continue to seek cell biologists of excellence for our faculty. 2. We will improve the Centre's instumentation stock in order to maintain our status at the cutting edge in a time of feverish technological development. 3. We will develop our "outreach" activities in order to more effectively communicate the excitement of our research to the public. 4. We will enhance our mentoring of scientists at all levels. 5. We will seek to institute a PhD programme that will allow us to stimulate and educate a new generation of scientists.

Amount: £1,726,327
Funder: The Wellcome Trust
Recipient: University of Edinburgh