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«16th September 2013 Lay Abstract Booklet Poster number First name Surname Department Title of poster 1 Fatimah Alsaffar Oncology Molecular ...»

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Faculty of Medicine, Dentistry and Health

16th September 2013





number First name Surname Department Title of poster

1 Fatimah Alsaffar Oncology Molecular characterisation of Ti M P3

mutations responsible for sorby's fundus


2 Israa Al- ScHARR Gender related differences among type 2

Rawashdeh Diabetes patients in Jordan 3 Marwa Mahmoud Cardiovascular The potential role of developmental genes in Science the spatial distribution of atherosclerosis 4 Hannah Thornton Medical School Structure-function studies on gly1 homologues 5 Sharonjit Gill Infection & Characterization of Human Lung Immunity Macrophages 6 Marta Krasuska School of Clinical Can quality of life stay the same when health Dentistry changes?

7 Chris Webster Neuroscience The cellular role of the C9ORF72 protein 8 Sarah Waite Human The Role of Calcium and Potassium Metabolism Channels in the Initiation of Labour Contractions 9 Sarah Dawson Cardiovascular Identifying OPG binding partners on Science pulmonary arterial smooth muscle cells 10 Daniel Cozens Infection & The potential use of tetraspanins as the next Immunity generation of antimicrobials 11 Tracey Moore Nursing & Why nurses feel they fail to recognise and Midwifery respond effectively to patient deterioration a qualitative study 12 Cassy Ashman Neuroscience PTEN signalling pathways as a therapeutic target in cell models of motor neuron disease 13 Ismael Gauci Cardiovascular The Roles of Homeobox genes in endothelial Science

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Sorsby’s fundus dystrophy (SFD) is an inherited eye disease that leads to blindness in middle age. It is caused by mutations in the protein tissue inhibitor of metalloproteinases-3 (TIMP3). Twelve different mutations in TIMP3 have been discovered in independent families but all of those examined to date cause the molecule to cross-link to itself, forming protein dimers. These dimers appear to resist the normal turnover processes in the eye and gradually accumulate in the retina, causing the light sensing cells there to die. This is exacerbated by the formation of new blood vessels, which can directly impair vision or cause the retina to become detached, leading to sudden blindness. Ten of the known mutations lie in the same part of the molecule (the carboxyl-terminal domain), and would be expected to have similar effects. However there are also two novel mutations that have not been studied. One of these affects the opposite end of the TIMP3 molecule (the amino terminal domain) and one, known as a splice site mutation, affects a part of the DNA that doesn’t actually code for the protein itself, but affects how it makes the messenger RNA (mRNA) molecule that acts as an intermediary in protein synthesis.

While the consequence of these novel mutations on the TIMP3 protein is unknown, they still cause the same disease, and so we hypothesize that they will also result in accumulation of TIMP3 dimers. To test our hypothesis, we created TIMP3 gene constructs corresponding to both the splice site and amino-terminal domain mutations and introduced these into mammalian cells. We then examined the TIMP3 mRNA and/or protein produced by these cells to see if it resulted in TIMP3 dimers, consistent with our hypothesis. Confirmation of this should provide convincing evidence that TIMP-3 dimerisation is critical to the pathogenesis of SFD.

Name of Student: Israa Al-Rawashdeh Department: ScHARR Authors: Israa Al-Rawashdeh Title: Gender related differences among type 2 Diabetes patients in Jordan Background: Diabetes is a common chronic medical condition in Jordan where almost one in five adults has diabetes. Most cases are type2 diabetes which usually develops gradually in later life. Worldwide, many previous studies have shown differences between men and women with diabetes that may have an influence on their attitudes and behaviour in taking care for diabetes and therefore their health, wellbeing and quality of life.

These differences can be clinical, psychosocial, or behavioural. For example; women are found to be more compliant regarding diet and prescribed medications and more successful in losing weight than men. Moreover, women with diabetes tend to use more healthcare services and have a higher illness rate compared with men. In addition, women report higher levels of social support from their diabetes health care team than men do.

Nonetheless, men show better health outcomes, better sugar control measures and less depression rates.

Still, there is a lack of research about gender based differences among diabetes type 2 patients in Jordan.

Aim and Objectives: The study aims to investigate whether there is an association between gender and clinical, psychosocial, and behavioural outcomes among type 2 diabetes patients in Jordan.

Research question: In T2DM patients in Jordan, does gender predict:

- Clinical outcomes e.g. glycemic control?

- Psychosocial outcomes e.g. self reported wellbeing?

- Health related behaviours e.g. self management, diet, physical activity, use of medications?

Methodology: The study will use a cross-sectional quantitative research design, where a questionnaire will be used to gather data from T2DM patients in the form of an interview.

Name of Student: David Baker Department: Neuroscience Authors: David Baker, Daniel Blackburn, Laura Ferraiuolo, Paul Heath, Janine Kirby and Pam Shaw.

Title: Do astrocytes change their behaviour in motor neuron disease?

Motor neuron disease (MND) is a devastating disorder of the cells that transmit information about movement from the brain to the muscles. This disorder usually leads to death within around 3 years of symptom onset. There is currently no cure and only one treatment, which extends life by about 3-5 months. Around 10% of MND cases are linked to inherited genetic defects (known as familial MND) whereas the remaining 90% of cases (known as sporadic MND) have no known familial link. Motor neurons are not the only cells affected by MND, other types of cells within the central nervous system, called astrocytes, oligodendrocytes and microglia, are also affected in the disease and impact upon survival of neurons. My project focuses on analysing the behaviour of astrocytes throughout the disease course of an animal model of motor neuron disease. This animal model is based upon one of the genetic mutations that has been identified as causing familial forms of the disease. By looking at how genes are expressed in the astrocytes of the animal model at different disease stages I hope to identify behaviour that can be corrected or modified, with the ultimate aim of expanding our knowledge of these cells in MND and benefitting patients.

Name of Student: Cassy Ashamn Department: Neuroscience Year of Study: First Authors: Cassy Ashman, Dr Ke Ning, Professor Pamela Shaw Title: PTEN Signalling Pathways as a Therapeutic Target in Cell Models of Motor Neuron Disease Motor Neuron Disease (MND) is a fatal neurodegenerative disorder with a typical duration of 3 to 5 years. In MND, the motor neurons which are the nerve cells that connect the brain to the muscles of the body characteristically die, subsequently presenting patients with muscle wasting and paralysis. While the majority of MND cases are sporadic in origin, 5-10% are familial cases with genetic mutations. Recently a new mutation in a gene called C9ORF72 of unknown function was found to be the most common genetic cause of MND to date.

Healthy cells have intrinsic biochemical pathways which are in a balance between promoting cell survival and cell death. For example, excess cell survival may lead to cancer but in turn excess cell death such as that seen in MND can lead to neurodegeneration. In our study, we aim to help tip the balance towards cell survival. To do this, we are going to manipulate a well understood cell survival pathway where the activation of a component called AKT promotes cell survival. In cells, AKT activation is normally stopped by another molecule called PTEN, thus, by preventing the action of PTEN, we hope to increase cell survival. We are going to test drugs that modulate PTEN’s activity hoping that they may translate to the clinic.

We are first going to test these drugs on different cell models of MND, including mouse motor neuron-like cells called Neuroblastoma Spinal Cord cells (NSC34 cells). In addition we are going to use a novel technique of turning patient skin cells (Fibroblasts) from patients with C9ORF72-positive MND into motor neurons. By comparing different cell models of MND we can validate if these modulators can increase cell survival in many models of disease.

Name of Student: Helen Cameron Department: Human Communication Sciences Year of Study: First Authors: Helen Cameron, Dr Tom Muskett, Dr Richard Body Title: Clinical and everyday interactions of young children with autism Background: This study aims to examine the interactions of young children and their communication partners across two contexts: speech and language therapy sessions and everyday activities at home, such as dinner time and play time. Parents are frequently trained and encouraged to complete therapy activities with their children at home in between sessions but little is known about how such therapeutic interactions occur at home between parents and their young children with autism.

Method: Five families of children with autism aged 2-6 years will take part in the study. Video recordings will be made of four routine speech and language therapy sessions and families will also make recordings of everyday interactions occurring at home between sessions. The recordings will be transcribed in fine detail and analysed to examine interesting features of interaction which may help us better understand how adults promote language and social communication during interaction episodes with young children with autism.

Results: Findings are not yet available as data collection for this project has not commenced. It is expected that video recordings will commence in late 2013.

Discussion: Findings will be discussed in the context of existing research on interactions involving young children with autism.

Conclusion: It is hoped that the findings of this project will contribute to our understanding of interactions involving young children with autism.

Name of Student: Daniel Cozens Department: Infection and Immunity Year of Study: Second Authors: D. Cozens, R.C. Read, S. MacNeil, L.J. Partridge, P.N. Monk Title: The Potential Use of Tetraspanins as the Next Generation of Antimicrobials Hospital acquired infections are a current major problem in healthcare, resulting in increased mortality of patients (15,000 in the UK a year) and a massive cost burden ((£1Bn annually in the NHS). The problem has been exacerbated through the rise of antibiotic resistance, with dramatic reductions in success rate from some antibiotics in treating a number of clinically important diseases, from TB to Salmonella. This raises a possible scenario where patients may regularly experience life threatening complications from infections of wounds caused by routine operations.

With a lack of new antibiotics currently in the pipeline, scientists are increasingly looking to more novel sustainable methods to prevent infections. One method under investigation involves the development of antiadhesive therapeutics. These work by stopping the bacteria from binding onto the host, the first step in the progression to disease.

This technique exploits a family of proteins found within the human body, known as tetraspanins, which have a role in the organisation of the surface of the cell, making patterns of receptors readily identifiable to potential pathogens, aiding their attachment. By interfering with these tetraspanins, bacterial attachment can be discouraged and in theory infection prevented.

Humans cells, when pretreated with synthetic peptides based on sections of tetraspanins are protected against a number of common pathogens. The peptides can also reduce the migration of bacteria between cells, halting the spread of an infection. Bacterial number was reduced by up to 50%, which, if replicated in real life, can help the body control an infection and improve survival rates.

The mechanism by which this therapy works is currently being researched, in a hope of increasing its efficiency and giving insight into the role of tetraspanins in the cell. If successful it is hoped that these can then be used in a cream, similar to Savlon©, which can be used on cuts and burns, to act as a barrier to common infections, such as MRSA, reducing the burden of resistant bacteria on healthcare.

Name of Student: Sarah Dawson Department: Cardiovascular Science Year of Study: Second Authors: Sarah Dawson, Josephine Pickworth, Christopher Newman, Sheila Francis, Allan Lawrie Title: Identifying OPG binding partners on pulmonary arterial smooth muscle cells Pulmonary arterial hypertension (PAH) is a rare but serious lung disease that significantly affects quality of life and greatly reduces the lifespan of those affected. Pulmonary arteries are the blood vessels that carry the blood from the heart to the lungs to pick up oxygen. As PAH develops, the smaller branches of the pulmonary arteries become thickened, making it harder for the heart to pump blood through the vessels. This results in an increase in blood pressure within the pulmonary arteries and lowers oxygen carrying capacity. Over time, pulmonary arterial smooth muscle cells (PA-SMCs) within the pulmonary arteries migrate and divide uncontrollably, causing the vessels to thicken. Although current treatments are affective in alleviating symptoms by relaxing the vessels, they have only modest impact on patient survival rates. We have identified the protein, osteoprotegerin (OPG), as an important mediator in the development of PAH. Although we know OPG plays an important role in disease development, we do not know how OPG alters signalling inside smooth muscle cells to induce cell migration and division.

Aims: To identify the OPG signalling pathway in PA-SMCs and the protein to which OPG binds to induce cell division.

Methodology: OPG binding partners were identified following expression of human membrane proteins on HEK293 cells (Retrogenix, Sheffield, UK). Interactions were subsequently confirmed in PA-SMCs by coimmunoprecipitation.

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