A LINGUISTIC ATLAS OF LATE MEDIAEVAL ENGLISH (McIntosh, Samuels and Benskin: 1986) comprises four volumes and offers a conspectus of the dialectal variation to be found in written Middle English between ca 1350 and ca 1450. It lists and maps an inventory of linguistic forms (derived from a questionnaire of 300 items) from the written outputs of over 1,000 scribes. It has become an indispensible reference tool to scholars working on the language and literature of the Middle English period. \n\nThe aim of the present project is to make this invaluable resource more accessible and flexible as an interactive website (e-LALME). e-LALME will be available to every user from their own desktop and will be linked to a Linguistic Atlas of Early Middle English (LAEME) and a Linguistic Atlas of Older Scots (LAOS) (to be on-line in 2007). In addition links may be made to the on-line open-access dictionaries: the Dictionary of the Scots Language, the Middle English Compendium and the Anglo-Norman Dictionary.There is also the possibility of links to and from other related electronic resources, such as the Oxford English Dictionary. A link to the on-going Middle English Grammar Project's database (Glasgow / Stavanger) is envisaged.\n\ne-LALME will be a digitized, on-line version of the present volumes, corrected and variously augmented. It will include more canonical maps than the present volumes, and the potential for users to make maps to their own specifications from the e-LALME data-base. The corrections will include review, and possible revision, of problematic localizations of some scribal dialects. It is intended that in e-LALME the summary descriptions of sources will be searchable not only by manuscript, repository and place of dialectal origin, but additionally will permit searches organised by manuscript date, by text, by edition and other bibliographical information, and by persons and places.\n\nSoftware already under development will be provided to allow users to apply the 'fit' technique computationally, for localizing and evaluating dialectal material not so far incorporated in the atlas.\n\nLike LAEME and LAOS, e-LALME will also have direct links to a Corpus of Etymologies being compiled by Roger Lass. For each spelling-type of each word listed in e-LALME there will be an etymology tracing its history back to the period of the earliest English, including an etymological pathway related to a linked Corpus of Sound Changes.\n\ne-LALME will provide a powerful resource not only for dialectology, but also for historical linguistics and socio-linguistics, medieval literature and historical studies. Further, its general accessibility and flexibility will make it a valuable interactive tool for teaching the History of English.

Why do humans but not apes acquire language? According to a standard view (Tomasello 2008; Scott-Phillips 2014) humans alone acquire language because we possess biological adaptations for Theory of Mind ('ToM') - the ability to think about others' mental states - that great apes lack. These enable us to act with and attribute the 'Gricean' (Grice 1957) communicative intentions that are necessary for natural language development. Since great apes lack ToM, they can neither attribute communicative intentions nor acquire language. Problematically for the standard view, the ToM needed for Gricean communication seem to develop only with the mastery of certain natural language forms - 'realis complement clause' syntax - around children's fourth birthday. If the mindreading needed for Gricean communication is itself language dependent, then it cannot contribute to an explanation of children's language acquisition. Since new empirical data (Krupenye & Kano, 2017) also shows that the ToM of great apes is similar to that of pre-verbal infants, the standard view leaves the absence of language in great apes unexplained. To dissolve these explanatory puzzles, the Communicative Mind project will develop a new account of the relationship between ToM, language, and communication. Building on the PI's previous work, which shows that infants and apes alike can engage in socio-cognitively undemanding forms of 'minimally Gricean' communication, the project will establish that key socio-cognitive differences between humans and apes are culturally learned, not biologically inherited. They emerge because humans but not apes can use syntactically structured utterances to communicate, and because on the back of this ability generations of language-users have developed linguistic tools for theorising about mental states. Thus, it is not ToM that explains the development of language, but syntax and the cultural evolution of language that explains the development of ToM. Children learn to use these tools in ontogeny, through cultural practices of conversation and storytelling, and thereby acquire new tools for thinking about minds. The Communicative Mind will develop new accounts of the evolution of language in phylogeny, and of the development of ToM in ontogeny. In years 1 and 2 of the project, the PI (a philosopher) will work with a developmental psychologist to conduct a series of pioneering studies to illuminate the developmental relationship between complement clause syntax mastery and the ability to represent what others know. By using, for the first time, both verbal and non-verbal paradigms to study the development of children's mastery of embedded, hierarchically structured complement clause forms, we will generate new knowledge of the cognitive mechanisms that support the development of children's mindreading and language. In years 3 and 4 of the project, the PI will work with a linguist to shed new light on the emergence of complement clause syntax in human history. We will develop a new account of the phylogenetic emergence in humans of a cognitive architecture that allows us, but not our great ape cousins, to use syntactically structured language. Subsequently we will use comparisons of existing languages to develop an account of the cultural evolution of complement-clause like syntax in natural languages. These subprojects will combine to give an account of the cultural origins of the ability to use language to represent others' perspectives on the world. We will show how linguistic tools for ToM can be created and learned through processes of communicative interaction, and describe the new representational tools with which they imbue speakers. By showing that uniquely human cognitive traits emerge through communication, we will demonstrate the fundamentally social foundations of human thought. Subsequently we will use our findings to develop educational tools to support children's learning.

Flow and mixing of fluids and granular materials occur in a wide range of processes. In nature, methane venting from ocean sediments represents a significant source of greenhouse gas, and the emission rate is intimately linked with complex interactions between the sediment and the rising methane gas in the form of bubbles or channels. Another example is the migration of gas through volcanic magma - a mixture of solid crystals and liquid melt - where the specifics of the complex flow patterning of the gas transport is thought to influence volcanic eruption behaviour. In the engineering sector, handling of granular suspensions and deformable porous materials are key in a wide range of industries from oil and gas, to food processing and pharmaceuticals. Despite the abundance and importance of such processes, fundamental knowledge of the physics that control them is lacking in many areas. These systems are inherently difficult to predict and control because of the very complex interactions taking place between the granular materials, liquids and gases during flow. The main aim of the project is to uncover the physics of two unknown mechanisms, namely the role of fluid viscosity and grain-fluid interactions in controlling the flow behaviour of frictional fluids and deformable materials. Using both experiments and computer simulations, we will explore the full range of viscosity ratio; high viscosity fluids injected into low viscosity host fluids and vice versa, where the host fluid contains granular materials of a range of concentrations, shapes and sizes. Where the two fluids meet, the meniscus will push or pull on the grains depending on the wetting properties, e.g. whether the grains are hydrophilic ("water-loving") or hydrophobic ("water-hating"). Through finely controlled experiments matched with theory and simulations we will reveal the effect of wetting on the flow behaviour. The new insight will be incorporated into models that will allow a much more accurate prediction of frictional flow behaviour, and ultimately to improving forecasting of natural events such as volcanic eruptions, and to optimize industrial processing of granular suspensions and deformable materials.

Post combustion CO2 capture from flue gas streams by amine based species will form a major component of the strategy for CO2 mitigation in the short and medium term. The wide spread uptake of this technology necessary to make a significant impact will require the production of many thousands of tonnes of amines with consequent atmospheric release either in small but still significant amounts during production, transport, use, recycling and disposal or in larger amounts following accidental release or plant failure. Very little is known about the atmospheric lifetimes or degradation products of even simple amines or the more complex amines that have been proposed for carbon capture (e.g. monoethanolamine - MEA). The overall objective of this project is to fill this gap in our knowledge on the gas phase oxidation of amines. The very limited studies that have taken place to date show that both gas phase and heterogeneous oxidation is important. The focus of this project is gas phase chemistry, but we have colleagues in Leeds and collaborators in the University of Oslo who are experts on the heterogeneous process, so that there will be a good flow of information between the two communities. The first component of the project is the measure the rate coefficients for the reaction of a variety of amines with important atmospheric oxidants such as the OH, NO3 and Cl radicals and ozone (O3). These rate coefficients will be measured under isolated conditions, focusing on just this first step in the amine oxidation process. The measurements will be performed using techniques such as laser flash photolysis and laser induced fluorescence. The resulting rate coefficients will allow us to calculate the atmospheric lifetimes of the amines and hence the spatial spread of any pollution. The second component of the project will be to determine the chemical mechanism for the production of first and subsequent generation products for selected important amines such as MEA. This will be achieved both by determining the position of the initial radical attack on the amine (i.e. for a simple amine such as CH3NH2, what fraction of the H atoms abstracted comes from the CH3 or NH2 groups?) and by observing the concentrations of the stable products, primarily by IR spectroscopy. Amine oxidation following attack at the RNHR group to form NR2 radicals has the potential to form highly toxic nitrosamines following reaction of NR2 with NO. By determining the rate coefficients for NR2 formed from selected important amines, with NO and O2, the third component of the project will asses the potential for nitrosamine formation. The final component of the project is to combine the above information and incorporate into a comprehensive chemical model of the atmosphere - the Master Chemical Mechanism, MCM - to assess the potential for amines to contribute to ozone production (air quality and climate change implications) and other atmospheric issues. The project will involve interactions with industrial groups and legislative organisations. Whilst the primary focus is on amines from carbon capture, amines are produced from a variety of sources - e.g. marine environment, so the project has wider applications and potential.

Iron is essential for life. It is required not only for the synthesis of haemoglobin, which carries oxygen around our bodies, but also for the function of the enzymes that generate energy inside our cells. Indeed, iron deficiency reduces exercise capacity, even when haemoglobin levels are normal. At the same time, too much iron within the cells is toxic because it promotes the production of damaging oxidants. Therefore, the control of iron levels is essential for the healthy functioning of our tissues. Tissues get their iron from the blood. Iron in the blood comes from three different sources; the spleen where iron is recycled from old blood cells, the liver where iron is stored, and the gut where iron is absorbed from the diet. Iron is exported from these organs into the blood by an iron-exporting protein called ferroportin. When iron levels in the blood get too high, the liver produces a hormone called hepcidin that blocks ferroportin so that blood iron levels return to normal. Inflammation also stimulates the production of hepcidin. Because of this, many patients with inflammatory conditions like heart disease and kidney disease have too much hepcidin in their blood. This inhibits the absorption of iron from the gut and causes iron to be locked inside the liver and the spleen. This is why many patients with chronic conditions have low iron levels in the blood and are described as "iron-deficient". In recent years, studies in these patients have shown that this iron deficiency worsens heart failure and increases mortality. There are now many efforts directed at finding the best way to treat this iron deficiency. Giving these patients oral iron does not work because iron absorption in the gut is blocked by hepcidin. A new treatment involving direct infusion of iron into the blood (by intravenous means) has been developed and rolled out to treat iron deficiency in patients with heart disease. In the past 5 years, work in my lab has discovered that heart cells use ferroprotin to control the amount of iron inside them. When we made mice that lacked ferroportin just in the heart, but had intact ferroportin in the gut, spleen and liver, these mice developed fatal heart failure because of too much iron being retained in heart cells. Like ferroportin at other sites, ferroportin in the heart can also be blocked by hepcidin. Based on this discovery, we hypothesise that high levels of hepcidin in patients also block ferroportin in heart cells, causing iron to be retained in the heart. When iron availability in the blood is low, this iron retention could protect the heart from becoming iron-depleted. However, when iron availability in the blood is high, especially after intravenous iron infusion, this retention could cause toxic iron accumulation in the heart. The aim of the research is to test this hypothesis. We will do this using both a mouse model of heart failure and human samples. The research will be conducted at the University of Oxford by my team in collaboration with clinicians who study and treat iron deficiency in heart failure patients. If our studies show that our hypothesis is true, then they will change how clinicians treat iron deficiency in heart failure patients who have raised hepcidin. One possible change is to give these patients compounds that lower hepcidin first (these are already being tested in clinical trials for other conditions). The advantage of lowering hepcidin is that it corrects iron deficiency in the blood (by unblocking ferroportin in the gut, liver and spleen) and also restores the ability of heart cells to control their iron levels and avoid iron toxicity (by unblocking ferroportin in the heart).