There is a wide variety of researh undertaken in the School of Life Sciences. Here are just some examples of the work our postgraduate researchers have undertaken.
Examining the effects of integrative neuromuscular training on fundamental movement skills, physical activity and body fatness in primary school children
PI: Prof Mike Duncan
Highlights: In childhood acquisition of fundamental movement skills (e.g. Catching, throwing, jumping) has important implications for participation in lifelong physical activity. Essentially, if a child does not master the skill of catching they may then avoid all activities that involve that skill. UK data are suggestive that many children are not mastering these skills in primary school. We are working with Prof David Stodden from the University of South Carolina, USA in examining the practicality and effectiveness of a school based training programme involving resistance exercises and skill acquisition sessions on children’s physical activity levels, their mastery of fundamental movement skills, physical fitness and levels of body fatness.
Virulence mechanisms of Propionibacterium acnes in association with lumbar disc herniations
Highlights: The pathogenic role of Propionibacterium acnes (P. acnes) in acne is well documented Evidence now highlights the potential importance of P. acnes in a number of clinical infections including sarcoidosis, sciatica and discitis. Recent work (Coventry University in collaboration with Aston University and the Spine Centre of Southern Denmark) has demonstrated the presence of P. acnes in disc tissue isolated from patients undergoing lumbar discectomy. The research team are currently investigating the pathogenicity traits of P. acnes isolated from lumbar disc herniations compared to P. acnes isolated from the skin. This projects aims to establish if P. acnes infection within ruptured disc tissue can be attributed to vertebrae bone oedema and associated physiological pain. Such findings may inform future NHS treatment options for the treatment of back pain associated with ruptured discs.
Tumorigenesis, why transcription in cancer cells does not respond to extreme stabilisation of mRNAs in the cytoplasm?
PI: Dr. Igor Morozov
Highlights: Cancer is a genetic disease which is caused by deregulation of expression of a plethora of genes at the level of transcription (mRNA production), translation (protein production) and mRNA degradation. Studies in the last five years have revealed three important observations. Firstly, it has also been established for wild type cells that events in the nucleus (e.g. transcription) define the fate of mRNA in the cytoplasm (e.g. mRNA stabilisation, degradation or translation). Secondary, transcription, translation and RNA degradation are all intricately related to each other and deregulation of these processes can lead to cancer. Finally, the level of translation and the rate of mRNA degradation are abnormally altered in cancer cells. Surprisingly, it has also been found that the rate of mRNA degradation in the cytoplasm signals back to the nucleus and regulates the rate of transcription. These data clearly suggest the presence of a novel buffering mechanism in normal cells which maintains the proper level of mRNA for a balanced protein production. We propose that such buffering mechanism which exists in normal cells and allows the nucleus to sense events in the cytoplasm and therefore maintain the correct level of mRNA is broken in the cancer cells. The aim of this project is to identify mRNA decay factor(s) which no longer influence(s) the rate of transcription in cancer cells.
Research on drug-induced cardiac injury
Name of PI: Professor Helen Maddock
Highlights: Professor Maddock and her research team are working on projects which include the development of physiologically relevant non-clinical heart assays and investigation and/or detection of drug-induced cardiac injury including current and novel oncology therapies. Many of these research projects are in collaboration with Cardiology and Oncology clinicians, Clinical Biomedical Scientists and experts within the Pharmaceutical Industry.
Professor Maddock is also founder and Chief Scientific Officer, of InoCardia Ltd, a Coventry University spin-out company. InoCardia supports providing undergraduate and postgraduate commercially aligned learning opportunities to students within the School of Life Sciences and offers placements, internships and job opportunities within the company. Recently Professor Helen Maddock and her team have discovered a method to efficiently test drugs to analyse the risk of side effects to the heart. This breakthrough in how drugs are reliably tested for effects on the heart could save thousands of lives as well as billions of pounds.
Professor Maddock has attracted research funding from the British Heart Foundation, Heart Research UK, British Pharmacological Society, European Regional Development Fund, InnovateUK and the NC3Rs.
Cardioprotection via Late reperfusion activation of adenosine receptors
Highlights: There is evidence to show that the activation of Adenosine receptors can protect the heart from ischaemia / reperfusion injury when administered either before ischaemia or at reperfusion. Preliminary data from our lab suggests that pharmacological activation of A3 adenosine receptors 15 or 30 minutes late in reperfusion can still mediate cardioprotection and has been linked to upregulation of Akt and Erk1/2.
It is possible that adenosine receptor activation could offer a novel modality of cardioprotection that would be of significant benefit in the various treatments of myocardial ischaemia. The study will examine lethal ischaemia/reperfusion injury and determine whether pharmacological agents are able to protect the myocardium when given post-reperfusion and determine the associated roles of cell survival signalling pathways. Data obtained from this project will be used to support a full Grant Application to the British Heart Foundation and the Medical Research Council.
Control of cellular polarity; roles in cellular migration and tissue regeneration
Highlights: Cell polarity has been long established as a key controller of spatial asymmetrical organization of cellular components and having a role at not just the cell but also tissue level, processes such as cell migration and motility are all dependent on cell polarity. Many processes are known to be effected by both diseases such as cancer as well as during ageing and cellular senescence. Crucial to the functionality of cell polarity in both cancer and ageing environments are the apico-basal cell polarity complexes such as human polarity liver kinase (LKB1) and the protein kinases AMPK and Par1 along with intra-cellular G-proteins such as RhoA. Equally, the tight-junction proteins such as the Claudin’s, occludin, and tricellulin and their intra-cellular scaffold proteins ZO-1, 2 and 3 have all be shown to be crucial in maintained function of cell polarity and their differential expression and distribution within disease and aged tissues. Most recently, adhesion molecules such as Jam1 and 2 have been implicated in regulation of stem cell fate. This project stream looks to address some of these issues and interactions in the human liver, both with cell based and clinical samples.