We are seeking funding to acquire a microarray robot for bioscience research. These machines are in effect printers that instead of ink, print biological samples in the form of spots on a surface such as a slide or membrane. The power of microarrays and their value to life science research is immense because entire libraries of molecules from complex biological systems can be represented in the form of tens of thousands of spots in an area no bigger than a postage stamp. With these arrayed libraries, we can explore interactions between molecules, test for biological activities, screen for new drugs and discover new enzymes. This technology was first applied to nucleic acids (DNA and RNA), but microarrays are now used for research into proteins, carbohydrates, lipids and small molecules. The technology is especially powerful for deciphering interaction networks between genes and proteins and for large scale screening of antibodies, enzymes and other bio-molecules. Furthermore, the latest generation of microarray robots are also advanced manufacturing devices capable of fabricating sensors and assays and can be used for performing multiplexed (many simultaneously) microscale experiments in-situ within the controlled environment of the machine. The equipment that we are requesting will be custom manufactured with bespoke features that greatly enhance its capacity and versatility, by a globally-leading UK company. By embedding this equipment within a new Biosystems Engineering unit at Newcastle University, we will create a truly world-class microarray technology hub that will accelerate research in food security, bioenergy and industrial biotechnology and health bioscience. By working with locally based but globally active industry partners we will use this equipment to drive translational research towards commercialisation. The equipment will also ensure that a new generation of UK students will have access to state-of-the-art technology, bringing a lasting legacy of research benefits.

There is an unmet need to improve the number and quality of organs transplanted. The stress following lack of oxygen and when blood supply is reinstated results in production of molecules which modify the proteins involved in inflammation, called chemokines. These modified chemokines could be novel biomarkers in assessing organ quality before transplantation. We have developed a novel antibody for modified-chemokine; we will quantify the ratio of native to modified-chemokine in transplant patient samples. We will also use a second detection method using mass spectrometry in order to corroborate the results. This will allow transplant patient stratification.

Fewer and fewer children now play outside. This reduction in outdoor active play - or 'playing-out' - has led to a whole range of concerns around health, wellbeing and development as well as continued international calls-to-action to address the issue. Factors behind reductions in playing-out include an increased reluctance of parents to allow children to be unsupervised outside due to concerns about the safety of their neighbourhoods, and in particular, increasing traffic and 'strangers'. As fewer children play outside, neighbourhoods, towns and cities are becoming 'play deserts', places where there are neither formal nor informal opportunities for outdoor play, and where play is simply not welcome anymore. While children play outside less and less, children play online more and more. The under 9s use the internet to search for information, to socialize and to play games. But, while the under 9s are readily understood to consume increasing amounts of content online, they continue to have little opportunity to create and share their own digital content about their lives. This is made worse by an extensive focus on video media for sharing experiences using social media platforms such as YouTube and Vine, where parents and society share many concerns around children's internet safety, and where formal services such as YouTube Kids emphasizes the child as a content consumer, rather than producer. We respond to these real-world interrelated problems by investigating the opportunity for Internet of Things (IoT) technologies to enable children to transform their neighbourhoods into digitally enhanced playgrounds and adventures. IoT refers to the idea that objects within our environments can be continually connected with the environment and the internet to offer new kinds of services. We think about IoTs as an entirely new mode of digital content that children (or anyone) can create and share. We imagine, for example, how IoT technologies can scaffold a child's play - e.g. a child can create an IoT to augment bricks in a wall to provide temporal targets for her football practice - as well as provide alternative modes to document and share play - e.g. a child can share media of her football practice, and her play's meta-data can be used to program another child's IoT to test and compare their own skills. We propose that by creating new opportunities for play which draw on children's interests and use in digital and social technologies that we can motivate children to play out more. In order to facilitate these kinds of interactions we need to understand and test the kind of support children would need to set-up their own IoTs for playing out, as well as how children would negotiate and create stories around this content which they could safely share. We think making use of the data sensed and collected about a child's play with IoTs could be an interesting way to both record the experience of a child's play while preserving a child's anonymity, and help them share that play with others to try out. This project will pursue an action orientated 'in the wild' program of research, working directly with the Cedarwood Trust in Meadow Well, BeChange in Aylesham, Playing Out CIC in Bristol and SAMLabs. Together we will co-design and develop technologies which support the under 9s in creating digitally-augmented outside play. We will use participatory design methods to achieve this, working closely with under 9s in both communities to design the tools and the kinds of play they facilitate. We are keen to know whether our 'Playing Out' IoT changes children's play behaviours, changes a child's relationship with their neighbourhood, impacts on the play opportunities in a community, or improves parent-child interactions. To help us understand the impact of our technology we will undertake observations, interviews and questionnaire surveys in both locations. We will also undertake a content analysis of the kinds of play created.

Despite the widespread availability of antibiotics, infection deep in the lung (pneumonia) remains an important cause of death in older people, as well as in critically ill patients in intensive care units. Our lungs contain a population of cells that sit in the air pockets of the lung and sense the presence of bugs. These cells are called alveolar macrophages (AMs). When AMs sense bugs in the lung, they kill them and if necessary send signals to the wider immune system for more help. Our study wishes to find out if AMs work less well as we get older, or when we are critically ill, as this may explain why we become susceptible to pneumonia. We know that a natural chemical in the body, called granulocyte-macrophage colony-stimulating factor (GM-CSF), maintains the health of our AMs. A further aim of our study is to determine whether giving GM-CSF as an inhaled drug, directly into the lung, might boost the function of AMs. If it does, this would provide the impetus for further research to see if GM-CSF could be given to people at very high risk of pneumonia (for example those in intensive care units), to prevent infection. This may have great advantages, because GM-CSF is not an antibiotic. The very heavy use of antibiotics in intensive care units has led to the emergence of "superbugs" that are not killed by antibiotics, and there is an urgent need to develop safe treatments that might boost immune cells such as AMs, instead of relying entirely on antibiotics. Nearly all of our information on how GM-CSF improves the function of AMs comes from studies in mice. We need to understand better how human AMs kill bugs, we need to know if this goes wrong as we get older or become critically unwell, and we need to know if GM-CSF can improve things. These issues have driven the design of our study. We shall ask 20 young volunteers (aged 18-30) and 20 older volunteers (60 or over) to come to the hospital on three days. On day one and day two they will inhale GM-CSF or a placebo, but neither they nor the research team will know which they inhaled. Each session will last about an hour. On day three they will come back for a telescope test of the lungs (bronchoscopy), where they are closely monitored and fluid is instilled into the a small area of the lung and gently sucked back. The fluid sucked back contains millions of AMs. The test lasts about 20 minutes and the person rests in hospital afterwards for a few hours before going home. Separately, a group of critically ill patients in the ICU will have the same protocol, i.e. GM-CSF or placebo on days 1 and 2, and bronchoscopy on day 3. In a final variation, the young volunteers will come back at least one month later, and have the same procedures done again, except that if they received GM-CSF first time round they will receive placebo the second time, and vice versa. We can take the AMs to the lab and study how well they eat bugs. We can block the function of specific molecules in the AMs and if this prevents the anti-bug effects we can infer that these molecules must be important for AM function. This way we shall build up a profile of the key molecules at the surface of the AM ("receptors") or inside the AM. Once we have the results we can "unblind" ourselves to find out who had GM-CSF and who had placebo. In this way we can piece together the answers to our questions - how do human AMs get rid of bugs? Do ageing and critical illness reduce the function of AMs and, if so, how? Does GM-CSF restore good function to AMs? The study will generate entirely new information on the function of human AMs. If GM-CSF is safe and boosts AM function we shall take this information forward to work out if inhaled GM-CSF can effectively and safely prevent pneumonia in patients who are at highest risk.

To sustain life, cells must be able to divide into two genetically identical daughters. During cell division, chromosomes must be precisely apportioned into the two daughter cells so that all the genetic information remains intact. Although surveillance mechanisms exist to ensure the accuracy of this process, errors can occur. These errors can lead to cells with the wrong numbers of chromosomes and to birth defects, miscarriage, cancer and ageing. One of the key proteins involved in error correction is an enzyme known as Aurora B, and work from many laboratories has shown that Aurora B acts early during cell division to minimise mistakes. However, it is clear that the error correction machinery is not foolproof, and certain types of error are not detected during the early stages of cell division. The aim of this project is to understand how cells deal with persistent errors and, in particular, to determine how Aurora B regulates chromosome sorting during the late stages of cell division to make sure that accurate inheritance of genetic material is maintained.