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The STMTI Scheme

STMTI has been designed to provide a first-class training programme that will create a cadre of clinical academics with strong training in translational medicine and therapeutics, building on established collaborations among internationally competitive scientists within four Scottish clinical academic institutions and a leading global pharmaceutical company, Pfizer. STMTI will focus on translational approaches to disorders of high clinical priority in which considerable unmet clinical need remains, and where there is compelling opportunity for ‘bench to bedside’ transition. Thus, the focus is on cardiovascular/metabolic, inflammation, musculoskeletal, neuroscience and reproductive health themes.

STMTI builds on a well-established collaboration among academia, industry, NHS and government, combining complementary strengths in drug discovery and the various stages of drug development. Critically, all relevant enabling tools – bioinformatics, genetics, proteomics, imaging, biomarker development and high-quality phenotyping – are available in Scotland. STMTI employs established, well-developed and nationally networked clinical research facilities, and an associated Scottish-wide research education programme. STMTI thereby creates an innovative interdisciplinary TMT training programme that will allow seamless academic career progression for outstanding clinicians: from clinical PhD training, to academically-protected clinical lectureships. STMTI will place its fellows in an enviable and highly competitive position for a career in TMT and ultimate appointment to senior academic positions.

The centrepiece of our programme will be a PhD that includes formal teaching in a wide range of translational and pharmacological skills, and a project which takes experimentation in the laboratory through to proof-of-concept studies in humans. We have assembled an outstanding faculty of PhD supervisors spanning a wide choice of skills and experience in basic and clinical science. There will be opportunities for regular research meetings between fellows, under the umbrella of the Scottish Society for Experimental Medicine, and through an annual Translational Medicine and Therapeutics Symposium where trainees will present their work and future plans.

STMTI Fellows

Below are short biographies for those Fellows already appointed to STMTI, along with a brief summary of their projects:

Dr Hannah Bayes



Dr Hannah Bayes is a Respiratory Specialty Registrar within the West of Scotland and is currently undertaking a PhD through the STMTI scheme at the Institute of Infection, Immunity and Inflammation at the University of Glasgow.  Dr Bayes has a clinical and research interest in cystic fibrosis, chronic pulmonary sepsis and the role of the aberrant immune response in the pathogenesis of pulmonary disease.  Dr Bayes’ research is examining the role of novel T helper cell subsets in the pathogenesis of cystic fibrosis, specifically in response to chronic Pseudomonas aeruginosa infection.

Cystic fibrosis (CF) is the commonest life-threatening inherited condition in the UK.  The main cause of death is chronic pulmonary sepsis, in most cases with the bacterium Pseudomonas aeruginosa.  A chronic inflammatory response is established in the airways in response to the organism and eventually leads to irreversible bronchiectasis.  Neutrophils are a major component of the cellular influx that accumulates and, whilst contributing to host defense, also produce tissue injury.  Two novel subsets of T helper lymphocytes have recently been described, namely Th17 and Th22 cells. Th17 cells predominantly produce IL-17, a cytokine that orchestrates neutrophilic responses.  The role of Th22 cells remains to be clearly defined, but may include an important pulmonary defense mechanism.  The aim of Dr Bayes’ PhD project is to characterize the human T helper cell response to Pseudomonal infection and to determine the role of Th17 and Th22 cells in the pathogenesis of chronic pulmonary pseudomonal infections.  The results of this investigation will define the role that these novel T helper cells and their related cytokines play in the lung disease of CF and might allow targeting of these immune responses as a potential therapy in this condition.



Dr Shyamanga Borooah

Dr Shyamanga Borooah

Dr Borooah is working towards a career as a clinician scientist specialising in regenerative approaches for ophthalmic disease.  He graduated in medicine from Imperial College in 2001gaining an intercalated BSc with honours in Neuroscience in 1998. He completed his early postgraduate training in London and moved to Scotland to join the South East Scotland training scheme in Ophthalmology.  Currently, he is undertaking a PhD under the Wellcome Trust STMTI scheme at the MRC Scottish Centre for Regenerative Medicine. His project is entitled “Using Induced Pluripotent Stem Cells to Investigate Macular Degeneration”.

Macular degenerations are the most common causes of blindness in the developed world.  Complex interactions between retinal cells are thought to be key to disease pathogenesis. Currently, there are few treatments available to treat these diseases. Consequently, macular degenerations place a considerable burden on patients and financially on health service providers worldwide.   There is a need for suitable disease relevant models to help investigate disease pathogenesis and develop treatments.  Recent advances in cell biology now enable the production of retinal cells from skin using induced pluripotent stem cells.  This offers the advantage of producing an almost unlimited supply of specialised human cells which would otherwise be difficult to obtain. Using retinal cells derived from well phenotyped families carrying a gene for an inherited macular degeneration, my project aims to develop an in vitro humanised model. The model will be used to probe disease mechanisms in macular degeneration, with the ultimate of aim of using the model as a test bed for drug discovery and crucially patient clinical treatments.


Dr Victoria Campbell

Dr Victoria Campbell

Dr Victoria Campbell graduated from Imperial College School of Medicine, London, in 2004. During this time she undertook an intercalated honours degree in Medical Sciences with Immunity and Pathology.  She completed her general medical training in London before relocating to Edinburgh to as a Haematology Specialist Registrar. She is currently undertaking a PhD through the STMTI scheme at the Paul O’Gorman Leukaemia Research Centre at the University of Glasgow.

Dr Campbell’s project is designed to determine the role of Hedgehog signalling in conferring chemoresistance in myeloid malignancies and evaluate the efficacy of targeting the Hh pathway alone or in combination with current treatment in CML and AML.

Acute myeloid leukaemia (AML) and chronic myeloid leukaemia (CML) are blood disorders which originate from a defect in the stem cells found in the bone marrow.  Current therapies are effective at eliminating the bulk of the leukaemia but are often unable to eradicate all the stem cells which sustain the disease.  These stem cells have the capacity to reproduce themselves, a process called ‘self-renewal’, producing more malignant cells.  Self-renewal is controlled by many different factors within the stem cell.  One of these factors which may be abnormal in cancer and leukaemia is the “Hedgehog pathway” which helps to control how cells grow and divide.  A number of drugs which target the Hedgehog pathway have recently entered clinical trials.  In order to effectively use these drugs, it is important to understand in what ways the Hedgehog pathway is modified in those with the disorders.  



Dr David Dorward



Dr David Dorward studied medicine at the University of Edinburgh (graduated 2006), during which time he completed an intercalated honours degree in Experimental Pathology.  He went on to complete both Foundation and Core Medical Training in South East Scotland.  His PhD entitled “Evaluating the effects of neutrophil induced 'damage'-associated molecular patterns (DAMPs) in infective lung injury” aims to explore the role of mitochondrial DAMPs in the propagation of pneumonia and to assess potential therapeutic interventions.

Despite the widespread use of antibiotics, pneumonia still causes millions of deaths worldwide each year. In response to infection neutrophils, cells vital to the body’s defence mechanism, enter the lung releasing large numbers of bug-killing proteins.  In doing so lung cells are also killed, spilling their contents into the surrounding tissue.  A variety of these products (DAMPs) appear to be crucial in propagating a vicious cycle of neutrophil recruitment and lung damage.  Exactly which DAMPs cause this to occur, and whether different DAMPs are released in different types of pneumonia, is not known.  Dr Dorward's study aims to identify those DAMPs important in severe pneumonia, examine their effects on neutrophil function and assess the effect of blocking the action of specific DAMPs.  Using newly designed imaging techniques it is possible to study individual cells in the laboratory and molecular events within mice with pneumonia in real time.  This helps understand the damaging effects of DAMPs more effectively and identify key areas to target in the development of new drugs to treat pneumonia.


Dr Scott Mackenzie



Dr Mackenzie graduated in medicine from the University of Glasgow in 2004, having completed an intercalated BSc in medical science in 2002.  Following early clinical training in Glasgow, he commenced specialty training in diabetes and endocrinology in North-West England in 2008.  He is now pursuing a research interest in the field of endocrinology with a PhD at the Queen’s Medical Research Institute, Edinburgh, under the supervision of Professor Brian Walker.

Dr Mackenzie’s project aims to assess the role of the glucocorticoid hormone corticosterone in cardiovascular disease and adrenal insufficiency.  Professor Walker’s group have made a number of key discoveries highlighting the role of cortisol in metabolic syndrome, which have translated into novel therapies for type 2 diabetes, the 11βHSD1 inhibitors.  As a less abundant glucocorticoid in plasma, corticosterone has been very little studied in humans.  However, recent evidence points to mechanisms whereby intracellular concentrations of corticosterone are regulated by trans-membrane proteins, the ABC transporters. Tissue specific expression of these transporters may allow corticosterone preferential access to CNS centres which regulate adrenal function, suggesting the hormone may be important in determining overall glucocorticoid exposure.  In a series of in vivo and in vitro human studies, the project aims to establish whether trans-membrane trafficking of corticosterone accounts for a distinct role for the hormone in human health.  Confirming a distinct physiological role for corticosterone may be of direct clinical relevance in adrenal insufficiency, and also provide a novel therapeutic target for therapies aimed against metabolic syndrome.


Dr Kenneth Muir



Dr Muir graduated in Medicine at the University of Dundee in 2002 having also completed an intercalated degree in Physiological Sciences. He began training in Diabetes and Endocrinology following 16 months working as a diabetes research fellow in New Zealand. His research, which will be based at the Institute of Medical Science at the University of Aberdeen, will be to investigate the potential of reprogramming non-endocrine pancreatic cells to an endocrine lineage using adenoviral mediated delivery of transcription factors. Human tissue left over from islet cell transplants carried out at the Scottish Islet Isolation and Transplantation Unit in Edinburgh will be used for the reprogramming.

The discovery of insulin by Banting and Best in 1922 revolutionised the treatment of type 1 diabetes mellitus. Despite significant progress using analogue insulin and pump devices to more closely mimic normal physiology, we still cannot completely negate the risk of microvascular complications even with optimal control. Moreover, with stringent control, hypoglycaemia becomes increasingly common. Islet cell transplantation may offer the best hope of a cure, however the lack of suitable donors creates a significant mismatch between supply and demand. Approximately 98% of pancreas tissue is unused from each islet cell transplant. The aim of this project is investigate the feasibility of reprogramming these cells to an endocrine lineage and thus potentially increasing the availability of donor material.


Dr Marta Seretny

Dr Marta Seretny

Dr Marta Seretny is a specialty registrar in Anaesthetics in South East Scotland. Early in her postgraduate career she pursued formalised research training and completed an MSc in Public Health Research at Edinburgh University. The Msc allowed her to gain training in Epidemiology, Advanced Statistics, Research Ethics, Qualitative Research, Protocol Development, Clinical Trials, Systematic Reviews and Medical Sociology. During her MSc she became involved with the Edinburgh Critical Care research group.

Dr Seretny is currently undertaking a PhD through the STMTI scheme at the University of Edinburgh. Her project utilises functional magnetic resonance imaging (fMRI) to assess the importance of central sensitisation in the development and treatment of chemotherapy induced peripheral neuropathy.

Annually, in the UK around 60,000 patients receive potentially neurotoxic chemotherapy for cancer treatment. Up to 96% of these patients will develop neuropathy. For many this will limit further treatment, having a major impact on their quality of life, function and potentially survival.

Cancer induced peripheral neuropathy (CIPN) is a complex clinical problem. The underlying pathophysiological mechanisms are not fully understood, and consequently the treatment options are limited and often ineffective.

New treatment options for CIPN are urgently needed. However, assessing new treatments in this patient group is challenging due to limited understanding of the mechanism underlying CIPN development, the neurobiological variability between individuals, and the important influence of placebo effect and patient expectation. Many of these challenges can be overcome by using neuroimaging techniques, which enable a robust, sensitive and non-invasive method of addressing these issues.



Dr Kave Shams

Dr Kave Shams

Dr Kave Shams studied Medicine and Pharmacology at Edinburgh University and is now a Dermatology Registrar in the West of Scotland. His main clinical and research interest is inflammatory skin conditions, in particular psoriasis, which is a condition that profoundly impacts those affected. Although there have been significant advances in psoriasis research, there exists a continued need to better understand and treat psoriasis.

Dr Shams obtained a postgraduate certificate in Translational Medicine from Edinburgh University in 2011. He commenced his PhD entitled “The regulation of the chemokine receptor D6 in cutaneous inflammatory disease” at Glasgow University in 2012, under the supervision of Professor Gerry Graham and Professor David Burden. Chemokines have emerged as the principal regulators of leukocyte migration and are important therapeutic targets. The atypical chemokine receptor D6, which is the focus of Dr Shams’ PhD, lacks the ability to signal, but instead internalises and degrades pro-inflammatory chemokines. We know that D6 plays a key role in psoriasis pathogenesis, where high D6 levels appear to be protective. Dr Shams’ PhD aims to better understand the role D6 plays in psoriasis and other inflammatory skin diseases and to elucidate how D6 levels are differentially regulated. The results of the project will lead to a greater understanding of 1) how D6 is regulated in the skin and 2) the value of D6 as both a marker and a novel therapeutic target in psoriasis and other inflammatory skin conditions.


Dr Karolina Skorupskaite

Dr Karolina Skorupskaite

Dr Skorupskaite graduated from the University of Edinburgh in 2009 with class Bsc Honours in Reproductive Biology. She started specialist training in Obstetrics and Gynaecology in South East Scotland. Reproductive Endocrinology and Infertility is her area of interest and she is currently researching the role of kisspeptin and neurokinin B in human reproduction. Her PhD is at the MRC Centre for Reproductive Health at the Queen’s Medical Research Institute, Edinburgh, under the supervision of Professor Richard Anderson and Dr Jyothis George.
 
Pulsatile secretion of Gonadotropin Releasing Hormone (GnRH) is central to the regulation of reproduction. Two newly discovered hypothalamic peptides, kisspeptin and neurokinin B regulate GnRH through their stimulatory effects, although their relative contributions are unknown. This neurokinin b-kisspeptin pathway might be contributing to the increased frequency of GnRH pulse secretion and therefore LH pulsatility that characterise Polycystic Ovary Syndrome (PCOS), the commonest endocrine disorder of reproductive age and the leading cause of anovulatory infertility. PCOS therefore serves as a model to further study the interaction of these hypothalamic neuropeptides in scenario of LH hypersecretion. This has a potential for developing novel therapies in patients with PCOS, where the selective suppression of increased LH is desirable.

Negative feedback exerted by estradiol is core to the control of GnRH secretion in early follicular phase. However, for an ovulatory LH surge to happen this negative feedback changes to positive estradiol feedback, the mechanism of which is unknown. Animal data suggest that kisspeptin might be partially responsible for this stimulatory effect on LH midcycle surge, necessary for ovulation. By administering kisspeptin and neurokinin B antagonist we might be able to trigger and suppress the LH surge, respectively.

I am to manipulate neurokinin B-kisspeptin pathway by specific agonists and antagonists to delineate the hierarchical contribution of these hypothalamic peptides in the regulation of reproductive axis. These studies have the potential of developing novel therapies for conditions characterised by abnormal LH secretion as well as ovulation suppression (i.e. contraception) and ovulation induction (i.e. in assisted reproduction).


Dr Victoria Snowdon



Dr Snowdon graduated from Nottingham University in 2003.  As part of her degree she undertook a BMedSci in Molecular biology looking into how CD14 binds apoptotic cells, this experience inspired her to want to do more research. After house jobs in Cheltenham and Derriford Hospital, Plymouth, and 6 months of A&E at Leeds General Infirmary, she did her general medical rotation at Derriford Hospital, completing her membership of the Royal College of Physicians in 2007.  She got her NTN in Gastroenterology in 2008.  Shortly into her registrar training, she decided that she wanted to sub-specialise in Hepatology.  Hepatology is a speciality that currently remains relatively lacking in successful therapies despite great advances in basic scientific understanding of the liver.  With this in mind, Victoria approached Professor John Iredale, a lead in academic hepatology, about undertaking a PhD in his laboratory in the Centre for Inflammation Research, Queens Medical Research Institute, University of Edinburgh.   After discussion she designed a translational research project building on work already being done by Jonathan Fallowfield into the peptide hormone, Relaxin.  With this project she succeeded in gaining a Scottish Translational Medicine Therapeutics Initiative (STMTI) Fellowship.

The project is entitled ‘Relaxin as a haemodynamic modulator of liver disease’.  It concentrates on Hepato-renal syndrome (HRS), one of the high mortality consequences of liver disease and portal hypertension.  The hypothesis is that Relaxin can beneficially modulate the haemodynamic changes responsible for HRS and can therefore be a novel therapeutic agent.  The project involves in -vitro, in-vivo work and a clinical study.  Understanding into how Relaxin works at a molecular level in liver disease and mechanisms for HRS development are still being unravelled.  Using models of HRS Victoria will explore this in more detail in the hope of improving therapies for this fatal condition.  Victoria's aim, after completing her PhD, is to return to clinical training as a clinical lecturer in order to pursue a career as an academic hepatologist focussing on translational research.


Mr Ben Stutchfield



Mr Stutchfield began his specialty surgical training in 2008, working towards a career in transplantation/hepatobiliary surgery.  He is interested in the application of cell therapies to support the failing liver and has been working towards a period of translational research in this area.

In the UK, the incidence of chronic liver disease is increasing exponentially, along with this has come an increase in the incidence of hepatocellular carcinoma.  The treatment for this is resection of the portion of the liver containing the tumour.  While the normal liver can regenerate following resection of up to 75% of its volume, regeneration of the fibrotic or cirrhotic liver is impaired.  Cell therapies offer much promise in coordinating and facilitating liver regeneration.  The macrophage has a central role in liver regeneration, promoting hepatocyte proliferation, activating hepatocyte progenitor cells, and remodelling liver parenchyma.  Recent preclinical studies by the Forbes group have demonstrated that macrophage therapy can also reduce fibrosis and stimulate regeneration of the chronically injured liver.  Mr Stutchfield aims to continue this work in a surgical context by studying the effects of macrophage therapy in a mouse model of partial hepatectomy and fibrosis.  In working towards clinical application, the therapy will be further evaluated in a pig model of surgical liver regeneration which closely mimics the human situation.


Dr Jonathan Weir-McCall

Dr Jonathan Weir-McCall

Dr. Jonathan Weir-McCall graduated in 2007 from the University of Aberdeen.  His junior doctor years were spent in St Mary’s in London, before he started his Radiology training in Guy’s and St Thomas’, London.  In 2009 he took up a clinical lecturer post in Ninewells Hospital with a major research interest in cardiovascular magnetic resonance imaging.  He is currently undertaking a period of research funded by the Wellcome Trust under the Scottish Translational Medicine Therapeutics Initiative looking at the effects of lung disease on the heart and pulmonary vasculature using cardiac magnetic resonance imaging. 

Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of mortality in the UK, and is the only leading cause of mortality that is increasing in prevalence, with approximately 30,000 people in the UK dying each year.  Despite being a condition affecting the lungs, up to 30% of people with COPD will die of heart disease, and the link is not fully understood.  Raised pulmonary pressures cause right heart remodeling and failure, however these changes occur even before the pressures are markedly raised.   Recently, a relationship has also been suggested between COPD and increased pulmonary arterial stiffness, which is important as arterial stiffening puts an increased workload on the heart.  MRI can assess both the distensibility of vessels and the pulse wave velocity (speed of the pressure wave with the blood vessels), both of which are established markers of arterial stiffness.  The PWV of the pulmonary arteries may be an essential determinant of right heart load in COPD, and a clinically useful indicator of cardiovascular risk.  Better understanding of the role of the pulmonary arteries in right heart failure in COPD has the potential for early disease detection, and to lead to new avenues for the treatment of this common condition.



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Last modified: 28 January 2014   2007 The University of Edinburgh