Traditionally the exploitation of ocean mineral resources has been mainly limited to oil, gas and coal extraction. It is only recently that the economics of mining other minerals has weighed in favour of substantial deep ocean exploration. Due to the challenging environments, extensive surveying of the seabed to inform mining choices is difficult. This increases financial risk as well as the potential for needless damage to surrounding ecosystems. We propose to develop X-ray fluorescence spectrometer technology based on wide bandgap semiconductors that would enable surveying and characterisation of deep ocean geology in situ. This would eliminate the current problems associated with deep ocean geological surveying and revolutionise deep sea mineral prospecting.

The project will also benefit from collaboration with Sussex Partnership NHS Foundation Trust. This project will draw on personality and attachment theory, a systematic review in the first year, qualitative and quantitative experimental/empirical methods to: (i)investigate the personal characteristics/qualities that clinicians look for in a briefly-trained therapist; (ii) investigate the extent to which these qualities engender trust: and (iii) develop and evaluate a screening process for the use of this information in the selection of briefly-trained therapists within NHS mental health services for patients with psychosis.

Abstracts are not currently available in GtR for all funded research. This is normally because the abstract was not required at the time of proposal submission, but may be because it included sensitive information such as personal details.

DNA is the genetic material which encodes the information that determines the ability of our cells to function. DNA is assembled from building blocks called base pairs, and the sequence of the base pairs is used to create the enzymes and proteins that carry out the work within a cell. Since each individual originates from a single cell, the genetic material of each cell in a body should be identical. However, cells have to go through multiple divisions to generate an organism, which necessitates that our DNA is replicated accurately. Additionally, our DNA is constantly subjected to damage, from both external and internally generated damaging agents. To maintain genetic stability, that is, the correct sequence of base pairs in our DNA, which is critical for the health of the individual and for cancer avoidance, cells have a repertoire of mechanisms that serve to repair any damage to the DNA during replication or from DNA damaging agents. A particularly dangerous lesion is when a break occurs in both DNA strands in close proximity. Such a lesion is called a DNA double strand break (DSB). If a DSB remains unrepaired, the cell will be unable to replicate and can die. Perhaps even worse, if the DSB is misrepaired, the sequence of base pairs can become changed, which is a step in the development of cancer. DNA is embedded in a coat of proteins called histones, which collectively generate a protective shield to the DNA called chromatin. However, chromatin can be refractory to the repair processes. Additionally, a range of metabolic processes take place on the DNA, which can also inhibit the repair process. The genetic information encoded in the DNA is employed to generate proteins, the worker molecule of a cell. Transcription is the first step by which proteins are assembled from the genetic sequence, and transcription can be inhibitory to the DSB repair process. Thus, the cell has evolved processes that allow the chromatin to be remodelled to facilitate DSB repair and that allow transcription in the vicinity of a DSB to be inhibited. Although, we have a good understanding of the core DSB repair processes, we have relatively little understanding of how chromatin becomes remodelled to facilitate repair to occur nor how the repair process interface with processes such as transcription. We have identified a number of new proteins that are required for the inhibition of transcription in the vicinity of a DSB. The aim of this proposal is to learn more about how these proteins function at DSBs taking place near transcribed genes. We also plan to test whether this process prevents a particularly dangerous form of inaccurate repair, termed a chromosomal translocation. This is important because chromosomal translocations are frequently observed in cancer cells and can contribute to disease progression. Thus, understanding how these processes work in greater detail could help us understand how we are protected against cancer.

The project will consider a mathematical model for studying plant cell evasion by the pathogen magnaporthe oryzae, commonly known as the rice blast fungus. This fungus results in annual losses of 11 - 18% of the global rice yield whereby a 10% yield loss accounts for crops that would feed 60 million. We intend to derive, analyse and numerically solve a diffuse interface formulation of the problem. This will involve the coupling of two diffuse interface equations; a scalar phase field one for the evolution of the fungus and a vector valued one for the system of re-action diffusion equations (RDEs) that model the densities of proteins on the tumour's surface. We will discretise these equations using adaptive finite element approximations. The resulting approximations will be solved using the adaptive nite element tool box ALBERTA.