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Lund University

Lund University

46 Projects, page 1 of 10
  • Funder: UK Research and Innovation Project Code: ES/L012014/1
    Funder Contribution: 332,457 GBP

    The project addresses Theme I: Agriculture and growth. The project aims to analyse broad based agricultural growth from a gender perspective and to situate these processes locally, against the backdrop of specific national policies and broader demographic, socio-economic and climate related changes. The objective of the study is to assess under what social and institutional conditions pro-poor agricultural growth entrenches or redresses gender based differences in access to agrarian resources and what consequences this has for linkages to the nonfarm sector. Three key research questions guide inquiry: 1. How can the consequences of gender differentiated access to productive and institutional resources during processes of broad based agricultural growth be understood? 2. How can linkages between agriculture and the nonfarm sector be analysed from a gender perspective, given that nonfarm income may be important in alleviating inferior access to agrarian resources among women in particular? 3. What village level characteristics are relevant to understanding the dynamics of broad based agricultural growth and nonfarm/farm interaction from a gender perspective? The project will use a mixed-methods, longitudinal, multi-scalar approach which enables comparison of growth dynamics across countries, regions, villages and households, while situating individuals within households. The method addresses the lack of comparative data on gender and growth, village level institutions and intra-household relationships through combining quantitative and qualitative data collection. The quantitative data builds on existing data from Ethiopia, Ghana, Kenya, Malawi, Mozambique, Nigeria, Tanzania and Zambia collected in 2002 and 2008, covering close to 4000 households in 84 villages. A third round of quantitative data is currently being collected in Ghana, Kenya, Malawi and Zambia and funding is applied for to cover data collection also in Tanzania and Mozambique. The 2013/2014 cross-section would cover 2466 households in 56 villages and two rounds of panel data for six countries. This will address a research gap in relation to the lack of longitudinal data. The sustainability of growth processes will therefore be possible to document. The quantitative data will enable assessing the existence and drivers of pro-poor agricultural growth, the location of such dynamics to particular regions and villages and whether female headed households are discriminated against in these processes. Qualitative data on social and institutional village characteristics as well as intra-household gender dynamics will be collected in villages involved in pro-poor agricultural growth as well as villages having experienced withdrawal from agricultural markets. The purpose is to document village level institutional frameworks with respect to gendered access to productive resources within and outside agriculture. Academic results will be disseminated through articles in world leading, peer reviewed journals, research reports published on the project website and research briefs circulated through ELDIS and the project advisors. Non-academic stakeholder involvement is ensured through an inaugural as well as concluding stakeholder workshop. Results will be popularized through written reports directed towards non-academic stakeholders and oral presentations in events organized by such stakeholders.

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  • Funder: UK Research and Innovation Project Code: NE/I00162X/1
    Funder Contribution: 78,431 GBP

    Almost all species have parasites that infect them, take resources from them and potentially cause disease. The parasite has a set of genes that makes it able to exploit the host. In return, the host has evolved genes which code for resistance mechanisms to reduce, or even eliminate, the negative effects of a parasite. Some of these genes are known, but it is clear that many more are yet to be identified. There is now good evidence that the effectiveness of these genes in fighting off a parasite can depend on the environmental conditions that the host lives under. If you keep a particular organism under controlled conditions in the laboratory it may, for example, be resistant to a parasite at one temperature but susceptible at another. In other words some resistance genes are only functional in particular environments. But what does this laboratory-observed phenomenon mean for natural populations? The question is particularly relevant in the face of current environmental change where organisms in some areas are facing considerable change in environmental conditions, such as temperature and CO2 levels. Natural populations of organisms usually consist of a large number of individuals that are slightly different from each other. Plants in a population will, for example, differ in size and start flowering at slightly different times. These differences are due to individual variation in the genes controlling traits such as growth and flowering time. Such genetic variation is crucial to a populations' ability to adapt to new conditions. If a new type of parasite infects a host population it will be those individuals with the genes and gene variants best able to eliminate or reduce this particular infection that will be most likely to survive and reproduce. As many parasites may, potentially, invade a population it is clear that populations with a larger combination of different genes and gene variants will have the higher chance of withstanding a new infection. But what if the effect of different genes changes as a result of environmental factors such as temperature? We know that some genes may only be functional in certain environments. If specific genes involved in resistance are, for example, consistently less able to function at high temperatures, then it will mean a functional decrease in genetic variation for resistance at these higher temperatures, and hence a higher risk of infection in the population. The current proposal sets out to map out the impact of such genome-environment interactions. It will do this by measuring genetic variation in parasite resistance in different populations of the plant Arabidopsis thaliana (Thale Cress) under different temperature regimes and with different levels (and types) of parasite infection. It aims to understand how a temperature increase will change the ability of host populations to adapt to new parasites - and whether this will vary with the type of infection. The results will be important for our ability to predict the spread and negative impact of parasites under changing environmental conditions. The research will therefore have immediate application in wildlife management and conservation. It will also provide essential knowledge to crop managers and breeders in their attempts to develop strategies for secure food production in future climates.

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  • Funder: UK Research and Innovation Project Code: BB/E017096/1
    Funder Contribution: 383,430 GBP

    As a consequence of its physiological functions the liver is exposed to a wide variety of pathogens and toxic insults. Consequently it is capable of protecting itself against infections entering from the blood by mounting a vigorous immune response. The earliest response triggered is called the 'innate immune response' and this is very old in evolutionary terms. We believe that this response will be critical in determining the outcome of liver damage. Such responses may be effective at removing the infectious organism but in the process may cause 'collateral' damage to the liver and to counteract this the liver can regenerate and thereby restore normal tissue architecture and function. If the balance between the immune response and the repair response is not carefully controlled the result is persistent, irreversible tissue damage, scarring and eventually cancerous change. The liver cell types most commonly targetted in these process, hepatocytes and cholangiocytes contribute to persistent damage by secreting factors that promote continuing activation of the immune system which leads to more damage and eventually to the development of a cancerous transformation of the liver cells. We propose that a family of proteins called tumour necrosis factor receptors found on the surface of liver cells are critical in determining whether injury results in removal of the injurious factor, regeneration, repair and full recovery or continuing damage, scarring and cancerous change. These receptors are activated by specific factors (ligands) in the local environment and the outcone of such activation is important for a wide range of cell functions including determining whether a cell dies or proliferates. If a cell continues in the proliferative state control is lost and it can become a cancerous cell. Thus how, when and where these receptors are activated will determine the balance between resolution/regeneration on one hand and persistent damage and cancerous change on the other. We have developed techniques to grow human cells out of liver tissue that is removed during liver transplantation allowing us to set up systems to study these processes using human liver cells rather than relying on animal models which do not always accurately represent what takes place in humans. We shall now use the human cells in tissue culture to investigate how the tumour necrosis factor receptors (TNFr) determine the balance between liver damage and repair and their involvement in cancerous change in the liver. We plan to carry out specific experiments to determine a) the factors that control whether TNF receptors are present in the liver b) how these receptors control the fate of liver cells c) how the 'innate' immune system can activate these processes. d) whether this response can lead to cancerous change in liver cells These studies will tell us a great deal about how the liver responds to injury and the role of the innate immune system in this process. The results will not only provide new information on how the normal liver functions and responds to damage but may also suggest new approaches to developing therapies in which the liver response to injury can be manipulated in favour of regeneration and repair without risking cancerous change.

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  • Funder: UK Research and Innovation Project Code: MR/Y034252/1
    Funder Contribution: 595,590 GBP

    Food security is one of the most pressing challenges that humans will face this century. A growing population, shifting dietary habits and a changing climate are placing unprecedented pressure on crop production. Future crops must therefore be resilient to climate change and (a)biotic stresses. Whilst modern crop varieties have been bred for high yields, this has led to a reliance on a diminished number of crop species and varieties, resulting in a vulnerability to pests and disease and a changing climate. Leveraging the genetic diversity that exists across different crop cultivars and landraces offers an opportunity to sustainably increase food production and close yield gaps by ensuring that crops are optimised to current and future environments. However, identifying the molecular mechanisms that underpin crop physiological responses to environmental stress is complex. Crops express phenotypic traits according to interactions between their genomes, the environment and how they are managed. Identifying how a given crop cultivar will respond to different environmental conditions is key to guiding breeding programmes. Phenotyping studies are underpinned by testing how crop genomes respond to environmental conditions, and how these conditions affects overall yields and the resilience of the crops to stress. However, this is resource intensive and limited in scope by the time and environment that the crops are grown under. There is a critical need to harness novel remote sensing techniques and state-of-the-art modelling approaches to model how genetically-regulated crop biochemical, structural and physiological traits affect yields, under different environmental scenarios. Closing this genotype to field-scale gap requires robust scaling methodologies that can be deployed at high throughputs. Leveraging our understanding of genetic controls on physiological traits and fluxes will enhance our ability to predict how crop genomes will respond under different environmental conditions.

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  • Funder: UK Research and Innovation Project Code: BB/D015308/1
    Funder Contribution: 337,183 GBP

    Enzymes are the molecules that catalyse biological reactions. Almost all enzymes are proteins, and they are large and complicated molecules. This is inevitable, because of the job they have to do. All enzymes work by being able to stabilise the 'transition state', which is the highest energy part of the reaction pathway. They therefore have to be able to recognise, and bind to, the starting materials of the reaction ('substrates'), the transition state, and the products of the reaction. This means that an enzyme has to be flexible, to accommodate these three stages of the reaction, which always have different shapes and (usually) a different distribution of electric charges. This much is known, but much else is surprisingly poorly understood. It was for example suggested a long time ago that enzymes undergo 'induced fit', in which binding of the substrate causes the structure of the enzyme to change, in order to better match the transition state. However, more recently it has become clear that enzymes may undergo induced fit motions even in the absence of substrates. In which case the question arises; what exactly does the substrate do? For example, does it change the motions of the enzyme, or does it stop them, by freezing the enzyme in an active state? Or does it redirect the motion so that the enzyme 'pushes' the substrate in the appropriate way to help the reaction to happen? These are fundamental questions, which are important to answer because they will enable us to engineer better enzymes in future. The enzyme being studied here functions to digest RNA, and is called barnase. Rather than study binding of substrate, we will study inhibitors, which are more stable. We will study two different types of inhibitor: a mimic of the substrate, plus a naturally occurring protein inhibitor. The technique we will use is nuclear magnetic resonance (NMR), which provides detailed information about motional states of individual atoms in the enzyme. We have been developing a novel technique to characterise alternative states of proteins, that are only populated a few percent: these are the types of states involved in these induced fit motions. The purpose of this research is to make detailed comparisons of our technique to other NMR techniques for probing alternative states, in particular a technique called relaxation dispersion. Relaxation dispersion is an exciting measurement, because it provides timescales and populations of alternative states. However, it is only sensitive to a relatively limited range of timescales, between about 10-3 s and 10-6 s. There are other NMR techniques that can look at the range from 10-9 s and faster, but so far nothing that can look in the intermediate range, between 10-6 and 10-9 s. This is a big gap, and one that includes many of the motions that are suspected to be important for enzyme function. Our research will provide a complete picture of what motion is happening, where in the protein, and how fast. We will also measure whether motions of different atoms are correlated, that is, whether they are part of the same movements or are independent. These are detailed measurements, but they will for the first time enable us to say with confidence how the protein moves, and therefore how the motions relate to its function.

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