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Results

Mitochondrial probes for oxidative stress. 08 Feb 2006

Mitochondrial probes for oxidative stress Interest has recently been focused on the damage caused to mitochondria by reactive oxygen species (ROS) such as hydroxyl (HO·), peroxyl (HO2·) and superoxide (O2·) radicals. Such damage appears to be causal in the universally experienced, but poorly understood, process of ageing. Thus, the extension of lifespan when there is calorie restriction in the diet of rats appears to arise at least in part from reduced oxidative damage to mitochondria. Furthermore, murine life span can be extended by overexpression of catalase targeted to mitochondria, where the increased removal of hydrogen peroxide will reduce ROS production and consequent damage. Oxidative stress is also important in a range of pathologies including the accelerated atherosclerosis associated with diabetes. Mitochondria are particularly susceptible to oxidative stress because much of the intracellular production of ROS arises in these organelles, particularly when a large proton motive force is generated by mitochondria respiring, but not producing ATP. Understanding the role and significance of ROS generated in mitochondria in ageing and pathologies where oxidative stress appears important has been hampered by a lack of mitochondria-targeted probes that specifically detect radicals. The aim of this research is to develop such generally useful probes and to use them to test the hypothesis that increased production of ROS in mitochondria is a major contributor to oxidative damage during hyperglycaemia (important in diabetes). The only technique that observes radicals directly and to the exclusion of all non-radical species is electron paramagnetic spectroscopy (EPR). The technique is very versatile and is useful in studies extending from simple chemical reactions in the test tube to the observation of radicals in vivo. Thus, the probes to be developed are for use with EPR spectroscopy. The specific objectives are to: (i) Design and synthesise new hydroxylamine H-atom transfer probes for EPR spectroscopy. (ii) Characterisation of their chemical reactivity with radicals and the longevity of the EPR signal produced in the presence of ascorbic acid. (iii) Determination of uptake into isolated mitochondria and whole cells. (iv) Application of probes to investigate the role of mitochondrial dysfunction in oxidative damage in hyperglycaemia (and to protect cells against cellular ageing).

Amount: £2,060
Funder: The Wellcome Trust
Recipient: University of Glasgow

Disease and Culture in Early Modern Italy. 10 Nov 2005

The pilot study will investigate the wide variety of cultural responses to large-scale epidemic disease, principally in Italy and against the backdrop of plague during the sixteenth century. The study will question generally accepted ideas (William McNeill, Alfred Crosby, and others) that epidemic catastrophe brought on widespread pessimism, otherworldly philosophies, and the decline of vigorous state formations). For the most catastrophic plague wave of the sixteenth century, 1575-7, the relationship was more nearly the reverse. The principal source for viewing this relationship will be the plague tract as it developed and multiplied through the sixteenth century. Written by university doctors, practicing medics, members of newly established health boards, and parish priests, these sources provide not only changing attitudes toward medical practice; they express fears and hopes and devise means for combating their hidden enemy from ritual purges to social policy. Around three hundred of them survive for sixteenth-century Italy, scattered through rare book rooms and archives; less than handful are available in modern editions. Along with demographic sources, chronicles, and literary works (novelle), this pilot study will explore these largely untapped sources to chart psychological and cultural reactions to epidemic disease from periods of low plague mortalities to the catastrophic years, 1575-7.

Amount: £20,269
Funder: The Wellcome Trust
Recipient: University of Glasgow

VALUE IN PEOPLE AWARD. 30 Aug 2006

Not available

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

The Wellcome Centre for Molecular Parasitology 20 Sep 2006

The Wellcome Centre for Molecular Parasitology The Centre originated in 1987, when Anty Tait and Dave Barry were funded by the Wellcome Trust to set up the Wellcome Unit of Molecular Parasitology, to apply molecular, genetic and biochemical technologies to the investigation of basic questions in the biology of parasites. The Unit had some core funding and was based in the Dept Veterinary Parasitology (Tait) and the Institute of Genetics (Barry), on separate campuses of the University of Glasgow. In 1994, via a grant for the Wellcome Trust, the Unit was amalgamated in new laboratories in the Anderson College. At the quinquennial review in 1998, the Unit applied successfully for Wellcome Trust Centre status. In June 2005, the Centre will move to the new Glasgow Biomedical Research Centre (JIIF/SRIF funded), along with immunobiologists and structural biologists. The Centre is a hub of parasitologists using a wide range of modern approaches to understanding aspects of the organismal biology of parasites. Its missions are: Form a centre of excellence for the molecular and genetic study of parasites Provide and sustain a modern laboratory environment Provide quality research training for science and veterinary graduates. The Centre has 8 research groups (and Acosta-Serrano from Sept 2003), studying mainly 5 parasite genera and the free-living nematode C. elegans, an excellent model for parasitic nematodes, which are diffi8uclt to study. Its research programmes are integrated into three of these themes. The first is the generation of diversity, which is core to the success of parasites. The second, which overlaps with the first, is the control and synthesis of surface molecules, many of which are key to host-parasite interaction. The third is differentiation through the life and cell cycle, steps essential for colonisation of, and transmission between, hosts. Due to the several levels of discussion within the Centre, there is much exchange of ideas within each theme and several of the groups have major collaborations, through to publication level.

Amount: £319,481
Funder: The Wellcome Trust
Recipient: University of Glasgow

Interactions and structures in antigenic variation. 28 May 2007

Recent discoveries have changed traditional views of antigenic variation in trypanosomes1. It is important now to define fundamental facts at the host-parasite interface in the chronic phase of infection. My aims are to answer the following questions: 1. How sequence-related are VSGs that are expressed sequentially in the chronic phase of infection, and do they cross-react serologically? 2. If they are cross-reactive, how do trypanosomes expressing them survive? 3. What are the epitope specificities of responding antibodies? 4. What is the structure of exposed epitopes of the variant surface glycoprotein, and to what extent do naturally present mutations alter them? Answers to those questions will help answer a core question about antigenic variation: 5. What are the contributions to antigenic variation of total gene switching, segmental gene conversion, and point mutation?

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

The roles for Slit/Robo proteins in the regulation of chemokine function and cell movement. 28 May 2007

Since the discovery of its importance in the development of the nervous system, the Slit/Robo signalling pathway has become more and more remarkable among pathways of intercellular communication. Initially identified for roles in axon guidance, it is now clear that the Slit/Robo system regulates a complex range of other biological processes involved in the development and growth of various organs and tissues. Moreover, the Slit/Robo signalling axis has also been implicated in cancer. Most recently a role for Slit/Robo in regulating chemokine-dependent leukocyte migration during immune and inflammatory responses, has been demonstrated. In spite of the clear biological importance for Slit/Robo in these diverse biological systems, there remain many unanswered questions of relevance to Slit/Robo function. It is the aim of this project to take 2 approaches to studying the biology of this system. Specifically we propose to examine, in detail, roles for Slit/Robo signalling in the control of leukocyte migration and in addition, we propose to use biochemical and cellular approaches to detail the mechanism of Slit/Robo transmembrane signalling. The aims of our project are: 1) To examine the roles for Slit/Robo in the regulation of chemokine-dependent leukocyte migration 2) To examine the cellular mode of action of Robo by directly imaging its cell membrane positioning and oligomerisation status and its association with chemokine receptors or their downstream signalling components.

Amount: £135,945
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

Regulation of RNA polymerase III transcription by Maf1 in mammals . 27 Feb 2007

The rate of transcription by RNA polymerase (pol) III is a major determinant of a cell s capacity to grow. As such, it is subject to stringent controls that ensure output is appropriate for prevailing conditions. Abnormally elevated pol III transcription is a feature of hyperproliferative and cardiovascular diseases. Genetic and biochemical studies have shown that in Saccharomyces cerevisiae a repressor called Maf1 binds and inhibits pol III in response to a wide range of stresses, such as DN A damage or nutrient deprivation. Indeed, evidence has been presented that Maf1 mediates pol III regulation under all circumstances examined in this yeast. We have found a homologue of Maf1 that potently represses pol III transcription in mouse and human cells. However, the situation is much more complex in mammals, which express a variety of factors that control pol III transcription directly and are not found in yeast, including RB, p53 and c-Myc. This project aims to characterise the phys iological role of Maf1 in mammals, by identifying conditions where it mediates a pol III regulatory response. It also aims to determine the mechanism(s) used by Maf1 to inhibit transcription.

Amount: £115,258
Funder: The Wellcome Trust
Recipient: University of Glasgow

An investigation of the roles for leukocyte and lymphatic endothelial cell D6 in the orchestration of the in vivo inflammatory response. 08 Feb 2007

Much is known about initiation and maintenance of inflammation but less about the resolution of this response. Prominent amongst inflammatory regulators are chemokines. We have identified an atypical chemokine receptor which we have called D6. D6 binds all CC-chemokines involved in regulating inflammatory responses. In vitro studies have shown that D6 is a scavenging receptor for CC-chemokines and in vivo studies have revealed a role for D6 in the removal of inflammatory CC-chemokines from infla med sites. TPA application to skin leads to the development of a psoriasis-like pathology in D6-null mice. D6 therefore is involved in the resolution of inflammation. Despite evidence for the important in vivo roles for D6 we have a limited understanding of the cellular basis for D6 function. We have reported D6 expression on lymphatic endothelial cells (LECs) in tissues. However we have recently detailed expression of D6 on leukocytes in inflamed sites. This indicates that leukocyte and LEC-exp ressed D6 may contribute in distinct ways to the resolution of inflammatory responses and indeed to the regulation of immune responses. We propose to investigate the relative roles played by leukocyte and LEC-D6 in the regulation of inflammatory responses and the movement of leukocytes to lymph nodes.

Amount: £199,345
Funder: The Wellcome Trust
Recipient: University of Glasgow

Regulating the redox conditions withn the mammalian endoplasmic reticulum 26 Jun 2009

The proposed research will address three specific areas. Firstly we will determine how oxidative stress within the endoplasmic reticulum (ER) is regulated. Here we will focus on how the activity of the ER oxidases that are potentially responsible for the production of reactive oxygen species in the ER are regulated. Our goal will be to fully understand their mechanism of action so that we can predict how they contribute to oxidative stress. Secondly we will characterise the role of ER enzyme s in protecting the cell from alterations in redox status and ER-generated ROS. Our goal will be to identify and characterise key components that prevent excessive oxidative stress. Finally we aim to identify novel components that are involved in regulating the levels of the redox buffer within the ER and in sensing ER generated oxidative stress. Here our goal will be to develop methodologies to monitor cellular redox status and to use these tools to identify cellular proteins whose function is to maintain redox homeostasis.

Amount: £1,291,775
Funder: The Wellcome Trust
Recipient: University of Glasgow
Amount: £1,480
Funder: The Wellcome Trust
Recipient: University of Glasgow

Quasispecies evolution in the progression of FIV infection. 07 Jul 2009

Feline immunodeficiency virus (FIV), a lentivirus that occurs in cats worldwide, is a ubiquitous feline pathogen. Infected cats may progress from the primary acute phase, through a variable latent phase until finally developing AIDS in the terminal phase, mirroring the progression of human immunodeficiency virus (HIV) infection in people. Therefore, as well as being an important area for veterinary research, FIV research has comparative value for understanding the progression of HIV infection in human patients. Although we have been diagnosing FIV infection for over 20 years, the outcome of infection is variable depending on the infecting strain; consequently the proportion of naturally infected cats that develop second stage disease is unknown. The key goals of this project are to address host and viral factors that may determine the different outcomes with the aim of developing a test that will provide useful prognostic information.

Amount: £356,105
Funder: The Wellcome Trust
Recipient: University of Glasgow

Value in people award. 21 Oct 2008

Not available

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

Grant to Alzheimer's Society 25 Sep 2017

As requested by the donor towards support for people with dementia.

Amount: £250
Funder: Quartet Community Foundation
Recipient: Alzheimer's Society

Health ethics in the age of autonomy: public engagement with the social challenges of health policy. 18 Apr 2007

The proposed research will argue that public policy in the field of health (broadly understood) must develop greater capacities to respond to social dilemmas that cannot be successfully addressed by deferring to autonomy (choice). Although other work is underway to address similar issues in public health - particularly the tensions between individual and public interests - the proposed research will aim to supplement this by performing a number of key tasks. The research will conduct detailed analysis of ethical principles and cultures that are related to the autonomy paradigm that can obstruct efforts to address social issues. In this respect it will investigate how recasting the nature and importance given to the principles of autonomy and choice in health care could be beneficial. The project will examine current efforts to engage the public and professionals in dialogue on health policy and utilise insights from political philosophy to help implement this work more rigorously within the public sector by developing an account of public reason. The research will go beyond current work in the field by formulating a framework that is able to help ethically regulate this dialogue between the public, professionals and policy makers.

Amount: £139,050
Funder: The Wellcome Trust
Recipient: University of Glasgow

The Wellcome Centre for Molecular Parasitology 20 Dec 2006

The Wellcome Centre for Molecular Parasitology The Centre originated in 1987, when Anty Tait and Dave Barry were funded by the Wellcome Trust to set up the Wellcome Unit of Molecular Parasitology, to apply molecular, genetic and biochemical technologies to the investigation of basic questions in the biology of parasites. The Unit had some core funding and was based in the Dept Veterinary Parasitology (Tait) and the Institute of Genetics (Barry), on separate campuses of the University of Glasgow. In 1994, via a grant for the Wellcome Trust, the Unit was amalgamated in new laboratories in the Anderson College. At the quinquennial review in 1998, the Unit applied successfully for Wellcome Trust Centre status. In June 2005, the Centre will move to the new Glasgow Biomedical Research Centre (JIIF/SRIF funded), along with immunobiologists and structural biologists. The Centre is a hub of parasitologists using a wide range of modern approaches to understanding aspects of the organismal biology of parasites. Its missions are: Form a centre of excellence for the molecular and genetic study of parasites Provide and sustain a modern laboratory environment Provide quality research training for science and veterinary graduates. The Centre has 8 research groups (and Acosta-Serrano from Sept 2003), studying mainly 5 parasite genera and the free-living nematode C. elegans, an excellent model for parasitic nematodes, which are diffi8uclt to study. Its research programmes are integrated into three of these themes. The first is the generation of diversity, which is core to the success of parasites. The second, which overlaps with the first, is the control and synthesis of surface molecules, many of which are key to host-parasite interaction. The third is differentiation through the life and cell cycle, steps essential for colonisation of, and transmission between, hosts. Due to the several levels of discussion within the Centre, there is much exchange of ideas within each theme and several of the groups have major collaborations, through to publication level.

Amount: £12,125
Funder: The Wellcome Trust
Recipient: University of Glasgow

Molecular Functions in Disease 16 Jun 2008

1. To assess the global changes in a Plasmodium genome that are associated with the loss of the ability to commit to sexual development (produce gametocytes). 2. To provide a causal link between the observed changes and gametocytogenesis.

Amount: £141,567
Funder: The Wellcome Trust
Recipient: University of Glasgow

Functional, biochemical and structural analyses of Plasmodium falciparum pyruvate dehydrogenase complex and glycine cleavage systems. 16 Jun 2008

To investigate the precise role of the giant multi-enzyme complex pyruvate dehydrogenase (PDH) in P. falciparum via genetic, molecular biology, biochemical and biophysical techniques. Specifically to answer the following questions: a. Is PDH required for Plasmodium growth during intra-erythrocytic development? b. What is the precise function of apicoplast-located PDH? c. How is the activity of PDH regulated in the absence of genes encoding PDH kinases and phosphatases? d. Are there biochemical and structural peculiarities in PDH that are exploitable for future drug development?

Amount: £141,567
Funder: The Wellcome Trust
Recipient: University of Glasgow