Postgraduate research opportunities 

Cardiovascular and Medical Sciences

blood cells

Our strength is in identifying and designing novel therapeutic strategies that will lead to clinical trials.

PhD Research Projects

Project Title: Non-coding RNA in vascular pathophysiology

Supervisor : Professor Andrew H Baker

Research area: Vascular disease and therapy

Project outline: The central hypothesis is that long non-coding RNA (lncRNA) fundamentally control pathological remodelling of the vasculature and that manipulation of lncRNAs can prevent the pathogenesis of vascular pathologies. This project will envelop these concepts in a portfolio of studies that encompass vascular biology and therapy, focusing on in vitro and in vivo models, and analysis of human biological samples. A great deal of recent interest has focused on the role of RNA as regulators of gene and protein expression in the vessel wall in homeostasis and pathology. LncRNA are tissue-specific and developmentally regulated and abnormal lncRNA expression is known to cause developmental abnormalities and human diseases, such as cancer and cardiovascular disorders. Here, we will deepen our fundamental understanding of the role of lncRNA in individual cellular compartments of the vessel wall, performing these studies across related vascular remodelling pathologies to maximise knowledge gain and potential for translation to man.

Project aims: To answer the following:

  • What controls the expression of vascular lncRNA in response to vascular injury?
  • How do growth factors and cytokines affect this?
  • What is the mechanism of action of defined vascular lncRNA?
  • How does modulation of the lncRNA affect vascular cells and phenotype?
  • Can we engineer lncRNA using CRISPR/Cas systems?

Techniques used: The project will use a number of important in vitro and in vivo models to assess the dynamics of lncRNA function. The project will use standard, as well as novel systems to assess lncRNA function in cultured primary vascular cells. The expression of candidate lncRNAs will be assessed in cycling and non-cycling cells in response to key stimuli, for example growth factor/cytokine combinations that my work has previously showed to provide synergistic effects on vascular phenotypes (migration, protease expression etc). The cell signalling events that mediate such effects will be analysed using small molecule inhibitors. To monitor the effects of lncRNA manipulation in individual vascular cell types and between vascular endothelial and smooth muscle cells, lentivirus (LV) signalling pathway reporters will be used. We will also use available fluorescent reporters for cell phenotypes such as proliferation and apoptosis, as well as fluorescent cell cycle reporter vectors. Strategies to induce overexpression/ knockdown of lncRNA in cell culture will include siRNA, shRNA, LV and adenovirus systems as well as CRISPR/Cas.

References: 

  • Denby L, Ramdas V, Lu R, Conway B, Grant JS, Dickinson B, Aurora AB, McClure J, Kipgen D, Delles C, van Rooij E and Baker AH. MiRNA-214 antagonism leads to protection from renal fibrosis. J Am Soc Nephrol, 2013, In Press.
  • McDonald RA, White KM, Wu J, Cooley BC, Robertson KE, Halliday CA, McClure JD, Francis S, Lu R, Kennedy S, George SJ, Wan S, van Rooij E, H Baker AH. MiRNA-21 is dysregulated in response to vein grafting in multiple models and genetic ablation in mice attenuates neointima formation.European Heart Journal, 2013, 34(22):1636-43.
  • Caruso P, Dempsie Y, Stevens H, McDonald RA, Long L, Lu R, White K, Mair K, McClure JD, Southwood M, Upton P, Xin M, van Rooij E, Olson E, Morrell NW, Maclean MR and Baker AH. A role for miR-145 in pulmonary arterial hypertension: Evidence from mouse models and patients samples. Circulation Research, 2012, 111: 290-300. PMID: 22715469

Contact address and email:

Professor Andrew H Baker PhD FRSE
British Heart Foundation Professor of Translational Cardiovascular Sciences
Institute of Cardiovascular and Medical Sciences BHF Glasgow Cardiovascular Research Centre University of Glasgow
126 University Place
Glasgow, G12 8TA
Tel No: 0141 330 1977
Fax No: 0141 330 5339
Email: Andrew.H.Baker@Glasgow.ac.uk

 

 

Project Title: Regulation of Aldosterone Production by novel RNA Molecules.

Supervisor: Prof Eleanor Davies, Dr Scott MacKenzie

Research area: Cardiovascular Endocrinology

Project outline:The steroid hormone aldosterone is produced by the adrenal gland and plays an important role in blood pressure control. Increased levels of the hormone are associated with hypertension, cardiovascular disease, stroke, obesity and diabetes and play a role in the pathogenesis of these common diseases. Therefore, understanding the molecular mechanisms involved in the regulation of this important hormone is essential.
Recent studies have shown that non-coding RNAs (microRNAs and long non-coding RNAs) can have a significant impact on mammalian regulatory mechanisms and our current studies show that this is also true of aldosterone production. This project will combine our extensive experience of aldosterone research with cutting edge molecular biology and bioinformatic methods to examine non-coding miRNA profiles in the adrenal gland and in the circulation of patients with excess aldosterone production. The effect of non-coding RNAs whose profile is altered, on aldosterone production and other cellular processes e.g cell divison, apoptosis, angiogenesis will be examined using standard laboratory techniques.

Summary aim: This project has the potential to identify novel molecular mechanisms that regulate the production of the steroid hormone aldosterone. Understanding the regulation of aldosterone production is central to unravelling its role in common conditions such as hypertension, stroke, obesity and diabetes. A detailed knowledge of its regulation and production will aid the development of new therapeutic interventions for these common conditions.

Techniques used: Cell culture, qRT-PCR, transfection, ELISA, Western blotting, DNA sequencing, RNA-Seq screening, Bioinformatics

References:

  • Robertson S, MacKenzie SM, Alvarez-Madrazo S, Diver LA, Lin J, Stewart PM,Fraser R, Connell JM, Davies E. MicroRNA-24 is a novel regulator of aldosterone and cortisol production in the human adrenal cortex. Hypertension. 2013 Sep;62(3):572-8.
  • Connell JM, MacKenzie SM, Freel EM, Fraser R, Davies E. A lifetime of aldosterone excess: long-term consequences of altered regulation of aldosterone production for cardiovascular function. Endocr Rev. 2008 Apr;29(2):133-54.
  • Alvarez-Madrazo S, Mackenzie SM, Davies E, Fraser R, Lee WK, Brown M, Caulfield MJ, Dominiczak AF, Farrall M, Lathrop M, Hedner T, Melander O, Munroe PB, Samani N, Stewart PM, Wahlstrand B, Webster J, Palmer CN, Padmanabhan S, Connell JM. Common polymorphisms in the CYP11B1 and CYP11B2 genes: evidence for a digenic influence on hypertension. Hypertension. 2013 Jan;61(1):232-9.

Contact address and email:

Professor Eleanor Davies
Professor of Molecular Endocrinology
Institute of Cardiovascular and Medical Sciences
BHF Glasgow Cardiovascular Research Centre
126 University Place
Glasgow G12 8TA
Eleanor.davies@glasgow.ac.uk

Project Title: Adipose tissue function in preeclampsia

Supervisor: Dilys Freeman

Research area: Diabetes, Renal, Endocrinology and Metabolism

Project outline: Preeclampsia is a leading cause of pregnancy-related maternal and offspring mortality and morbidity, occurs in 2-10% of pregnancies and is unique to humans. It is a multi-factorial disease with a number of presenting phenotypes caused by a primary defect in trophoblast invasion followed by an atypical maternal vascular response resulting in hypertension and proteinuria. Maternal obesity is a risk factor for preeclampsia and an abnormal maternal metabolic adaptation to pregnancy, reflective of metabolic syndrome, is a key feature of the disease. Maternal gestational hyperlipidaemia is a physiological response and provides for the energy demands of the fetus as well as supplying lipid precursors necessary for fetal development. In healthy pregnancy, mothers store fatty acids in adipose tissue and, as a consequence of the action of pregnancy hormones, maternal insulin resistance develops in mid to late gestation. This leads to increased adipocyte lipolysis, up-regulation of VLDL synthesis by the liver and gestational hypertriglyceridaemia. We have previously shown that in preeclampsia, there is evidence that mothers are less able to expand their adipose tissue and their adipocytes are more insulin resistant resulting in increased lipolysis. Excessive lipolysis and reduced capacity to store fatty acids in adipose tissue, such as is seen in type 2 diabetes, can lead to ectopic fat accumulation in the liver and other tissues with downstream pathological consequences resulting from lipotoxicity. The consequences of inappropriate fatty acid handling in pregnancy can include vascular dysfunction, increased insulin resistance and defects of long chain polyunsaturated fatty acid metabolism.

Project aims: The aim of this project is to explore in more detail the adipose tissue defects in preeclampsia. In particular the regulation of adipocyte lipolysis and lipogenesis will be studied and the mechanisms for the limited expansion or pre-adipocytes to form mature adipocytes examined.

Techniques used: Metabolic assays in adipocytes using ex-vivo tissue biopsies. Gene and protein expression of regulators of adipocyte differentiation. Cell culture of preadipocytes.

References:

  • Jarvie E, Hauguel-de-Mouzon S, Nelson SM, Sattar N, Catalano PM, Freeman DJ Lipotoxicity in obese pregnancy and its potential role in adverse pregnancy outcome. Clinical Science 2010;119:123-9
  • Huda SS, Forrest R, Paterson N, Jordan F, Sattar N, Freeman DJ. In preeclampsia, maternal third trimester subcutaneous adipocyte lipolysis is more resistant to suppression by insulin than in healthy pregnancy Hypertension 2014;63(5):1094-101
  • Mackay VA, Huda SS, Stewart FM, Tham K, McKenna L, Martin I, Jordan F, Brown E.A, Hodson L, Greer IA, Meyer BJ, Freeman DJ. Preeclampsia is associated with compromised maternal synthesis of long chain polyunsaturated fatty acids leading to offspring deficiency Hypertension 2012;60(4):1078-85

Contact address and email:

Dilys.Freeman@glasgow.ac.uk
Institute of Cardiovascular and Medical Sciences
West Medical Building, University of Glasgow.

Project Title: Runx1 and Heart Disease Post-Myocardial Infarction

Supervisor: Dr C Loughrey, Dr S Nicklin, Ewan Cameron

Research area: Heart Research

Project outline: Coronary heart disease (CHD) leading to myocardial ischaemia is the predominant cause of heart failure (HF) and premature mortality in the UK. CHD occurs when the blood vessels of the heart (coronary arteries) become narrowed by fatty material (atheroma) and reduce blood flow to heart muscle (myocardial ischaemia). If the coronary artery is occluded then an area of lethal tissue injury in heart muscle called a myocardial infarction (MI) can be produced. The subsequent structural and functional changes in the surviving heart muscle can lead to poor cardiac pump function and HF. Novel therapeutic strategies to preserve cardiac pump function are urgently needed to treat patients with myocardial infarction and thereby improve patient survival rates and quality of life.
The Runx family of genes (Runx1,2&3) encode for DNA binding transcription factors (Runx1,2&3) which regulate gene expression. Recently, increased Runx1 expression has been demonstrated in the hearts of patients with MI. In line with these data, our recent work demonstrates increased Runx1 expression in a mouse model of MI. However, despite these observations, the role Runx1 plays in heart function remains unknown. We have made a novel and exciting discovery that higher Runx1 expression levels correlate with poor cardiac pump function. In order to corroborate this finding, we have produced a heart-specific knockout of Runx1. When MI is induced in this transgenic model, cardiac pump function is markedly improved suggesting that reducing Runx1 expression in the heart is a potentially novel therapeutic approach to limit the progression of cardiac dysfunction in patients with MI.

Project aims: This studentship will investigate whether reduction of Runx1 levels in the heart via somatic gene transfer using viral gene transfer vectors can improve cardiac pump function in a mouse model of MI.

Techniques used: The project will enable the student to be trained in in vivo rodent models of MI, integrative physiology, molecular biology and gene transfer approaches.

References:

  • McMurray et al. European journal of heart failure. 2012;14:803-869.
  • Kubin et al. Cell stem cell. 2011;9:420-432.
  • Loughrey et al. The Journal of physiology. 2004;556:919-934.

 

Contact address and email:

christohper.loughrey@glasgow.ac.uk

Project Title: H. pylori infection and gastric acid secretory function throughout the stomach and in particular at the gastroesophageal junction

Supervisor : Professor Kenneth E.L. McColl

Research area: Upper gastrointestinal pathophysiology

Project outline: The incidence of oesophageal adenocarcinoma has risen by 3-4 fold over the past thirty years in the Western world. The recognised environmental risk factors (obesity and smoking) explain less than 10% of this increase. Epidemiological data indicate a strong negative association between H. pylori infection and oesophageal adenocarcinoma and if directly linked, the rise in cancer could be attributed to the fall in H. pylori infection. The infection can reduce gastric mucosal acid secretion, though there is very little information on this effect in the general population and no information on this effect on the mucosa closest to the gastroesophageal (GO) junction which is recognised to be most important in inducing oesophageal adenocarcinoma. H. pylori suppression of acid secretion by the gastric mucosa close to the GO junction would provide a plausible mechanism for the rising incidence of oesophageal adenocarcinoma. We propose to investigate acid secretion by the total gastric mucosa and, in particular, of the mucosa close to the gastroesophageal junction in H. pylori-infected and uninfected healthy volunteers. 

Project aims: 50 H. pylori positive and 50 H. pylori negative healthy volunteers with be compared with respect to the following: (i) intragastric acidity following a meal in the main body region of the stomach; (ii) intragastric acidity following a meal close to the gastroesophageal junction; (iii) parietal cell density in different regions of the stomach including the main body of the stomach and close to the gastroesophageal junction; (iv) the position of the squamo-columnar junction relative to the high pressure point of the lower oesophageal sphincter.

Techniques used: The study will employ the following techniques which we established in our department: (i) 14C urea breath test; (ii) quantitative assessment of parietal cell density in biopsies obtained from ten different regions of the stomach; (iii) high resolution pH-metry in which we monitor the acidity in twelve different regions of the stomach under fasting conditions and following a standard meal; (iv) high resolution manometry of the lower oesophageal sphincter; (v) determination of the position of the squamo-columnar junction relative to the pH step-up point and lower oesophageal sphincter high pressure region by means of endoscopic clipping of radiopaque clip and then fluoroscopy simultaneous with pH- metry and manometry.

References:

  • Robertson E V, Derakhshan M H, Wirz A A, Lee Y Y, Seenan J P, Ballantyne S A, Hanvey S S, Kelman A W, Going J J, McColl K E L. Central obesity in asymptomatic volunteers is associated with increased intra-sphincteric acid reflux and lengthening of cardiac mucosa. Gastroenterology, 2013; 145: 730-739.

 

Contact address and email:

Professor Kenneth E.L. McColl, MD, FRCP, FMedSci, FRSE,
Institute of Cardiovascular & Medical Sciences,
University of Glasgow,
44 Church Street,
Glasgow, G11 6NT.
Tel: 0141 211 2513
Email: Kenneth.McColl@glasgow.ac.uk

Project Title: Role of IL-33 in cardiovascular inflammation

Supervisor: Dr Ashley Miller

Research area: Cardiovascular inflammation

Project outline: The main focus of my research is to investigate the role of the immune system in cardiovascular diseases. Evidence is now accumulating that during obesity tissues such as arteries and adipose develop chronic low-grade inflammation that likely contributes to metabolic consequences such as type 2 diabetes. Immune cells, such as macrophages and T cells, and the resident vascular cells and adipocytes secrete a variety of pro-inflammatory cytokines and chemokines. Recent studies demonstrate that the infiltrating T cells display a Th1 pattern of activation with enhanced IFN? production, and that an imbalance may exist in obese adipose between dominant Th1 responses and reduced Treg or Th2 responses. This in turn leads to macrophage recruitment and a switch from a protective alternatively activated (M2) macrophage to a classically activated (M1) pro-inflammatory phenotype. We have shown that the IL-1 family cytokine, IL-33, and its receptor ST2 can play a key protective role in systemic and vascular inflammation in atherosclerosis and obesity, and current work is focused on identifying the mechanisms of IL-33-induced protection. In particular we plan to study the phenotype of cellular immune infiltrates induced into adipose tissue and arteries, and elucidate the metabolic consequences of IL-33 signalling.

Project aims:

  • To study the metabolic consequences of IL-33 signalling in adipose tissue and arteries
  • To identify the immune cells recruited to adipose tissue and arteries in response to IL-33
  • To elucidate the chemokines responsible for recruitment of immune cells to adipose tissue in response to IL-33.

Techniques used:

  • FACS
  • PCR
  • Immunohistochemistry
  • Luminex
  • Cell culture – macrophages, adipocytes, endothelial cells
  • Animal models of obesity/diabetes and atherosclerosis

References:

  • Miller AM, Asquith DL, Hueber AJ, Holmes W, McKenzie A, Xu D, Sattar N, McInnes IB, Liew FY (2010) IL-33 induces protective effects in adipose tissue inflammation during obesity in mice. Circ. Res. 107: 650-658.
  • Weir RAP, Miller AM, Murphy GEJ, Clements S, Steedman T, Connell JMC, McInnes IB, Dargie HJ, McMurray JJC (2010) Serum soluble ST2: a potential novel mediator in left ventricular and infarct remodeling following acute myocardial infarction. JACC. 55: 243-250.
  • Miller AM, Xu D, Asquith DL, Denby L, Li Y, Sattar N, Baker AH, McInnes IB and Liew FY (2008) IL-33 Reduces the Development of Atherosclerosis. J. Exp. Med. 205: 339-346.

Contact address and email:

Institute of Cardiovascular & Medical Sciences
C437, BHF Glasgow Cardiovascular Research Centre
126 University Place
University of Glasgow,
Glasgow, G12 8TA
Ashley.Miller@glasgow.ac.uk

Project Title: Assessing the counter-regulatory renin angiotensin system in cardiovascular disease

Supervisors : Dr Stuart Nicklin (with Dr Christopher Loughrey, Professor Graeme Milligan, Prof Andrew Baker)

Research area: Institute of Cardiovascular & Medical Sciences

Project outline: The renin angiotensin system (RAS) is a hormonal cascade mediating cardiovascular function. The RAS is key to the development of cardiovascular diseases, including hypertension, cardiac remodelling and atherosclerosis. A counter-regulatory RAS exists, centered on the angiotensin converting enzyme (ACE) homologue ACE2 and angiotensin 1-7 [Ang-(1-7)], highlighting additional key mediators of the RAS which may be therapeutic targets in cardiovascular disease. We have also discovered that Ang-(1-9), a metabolite of the Angiotensin II precursor angiotensin I, is a RAS hormone. We have demonstrated that Ang-(1-9) is able to antagonise the pathophysiological effects of AngII in cardiomyocytes, fibroblasts and vascular smooth muscle cells via the angiotensin type 2 receptor. We are now investigating the effects of Ang-(1-9) in cardiovascular disease models including hypertensive cardiomyopathy, myocardial infarction and acute vascular injury in order to understand its molecular mode of action and its therapeutic potential.

Project aims: To dissect mechanisms of action of angiotensin-(1-9) in cardiovascular disease and explore therapeutic options.

Techniques used: Cell culture in both primary cells and cell lines and in vivo models of cardiovascular disease, molecular biology techniques, construction and testing of replication deficient viral gene transfer vectors.

References:

  • C McKinney, C Fattah, C Loughrey, SA Nicklin. (2014). Cardiac and vascular remodelling: effects of the counter-regulatory renin angiotensin system peptides, Ang-(1-7) and Ang-(1-9). CLINICAL SCIENCE, 126: 815-827.
  • Flores-Munoz, M., Smith, N. J., Haggerty, C., Milligan, G, and Nicklin, S. A. (2011) Angiotensin1-9 antagonises pro-hypertrophic signalling in cardiomyocytes via the angiotensin type 2 receptor. The Journal of Physiology, 589 (4). pp. 939-951. ISSN 0022-3751
  • M Flores-Muñoz, LM Work, K Douglas, L Denby, AF Dominiczak, D Graham, SA Nicklin. (2012). Angiotensin-(1-9) attenuates cardiac fibrosis in the SHRSP via the angiotensin type 2 receptor. HYPERTENSION, 59(2):300-307.

 

Contact address and email:

Stuart A Nicklin BSc (Hons) PhD
Reader
Institute of Cardiovascular and Medical Sciences
BHF Glasgow Cardiovascular Research Centre
College of Medical, Veterinary and Life Sciences
University of Glasgow
126 University Place
Glasgow G12 8TA
Email: stuart.nicklin@glasgow.ac.uk
Tel: +44 (0)141-330-2521
Fax: +44 (0)-141-330-6997

Project Title: Developing Therapeutic approaches for haemorrhagic stroke

Supervisor : Dr. Tom Van Agtmael

Research area: Mouse genetics, haemorrhagic stroke, molecular cell biology, extracellular matrix, vascular disease, collagen, endoplasmic reticulum stress

Project outline: Stroke costs UK Society ~£8 billion annually with haemorrhagic stroke accounting for 15% of adult and 50% of paediatric stroke. There are no treatment available for haemorrhagic stroke, in part due to a poor understanding of the underlying molecular cause.
Collagen IV is the major component of a type of extracellular matrix called the basement membrane that provides essential structural support to blood vessels. We and others have shown that mutations in COL4A1 or COL4A2 (encoding collagen IV proteins) cause familial and sporadic haemorrhagic, indicating these mutations may be more common than previously expected and a potential contribution to stroke in the general population (1). Our results also reveal that endoplasmic reticulum (ER)-stress due to intracellular accumulation of mutant collagen IV is associated with disease development, and that treatment of collagen IV mutant cells can reduce ER-stress (2). This provides a golden opportunity to identify the disease causing mechanisms and explore therapeutic approaches for collagen IV diseases including haemorrhagic stroke.
We have brought together a unique cohort of cell lines from patients and animal models with Col4a1 mutations to investigate the disease mechanisms of these mutations and determine how cells respond to these mutations. The identified pathways will then be modified in cell line and animal models to investigate their role in disease development and identify their potential as a therapeutic target. As FDA approved compounds are available, this will directly inform on and may identify therapeutic approaches for haemorrhagic stroke.

Project aims:

  • Exploring genetic and high throughput approaches to identify pathways that influence disease development
  • Identify the ability of small compounds to prevent the pathological effects of collagen IV mutation in cells.
  • Modification of disease development in animal models

Techniques used: State of the art imaging techniques including 3-dimensional electron microscopy, confocal microscopy and atomic force microscopy. Molecular cell biology, animal models, MRI imaging, transcriptomics.

References:

  • Plaisier E, et al. Role of COL4A1 Mutations in the Hereditary Angiopathy with Nephropathy, Aneurysm and Cramps (HANAC) Syndrome. New Eng J Med 2007, 357, 2687-2695
  • Murray LS et al. Chemical chaperone treatment reduces intracellular accumulation of mutant collagen IV and ameliorates the cellular phenotype of a COL4A2 mutation that causes haemorrhagic stroke. Hum Mol Genet 2014, 23:283-92

Contact address and email:

tom.vanagtmael@glasgow.ac.uk
Dr. Tom Van Agtmael
Institute of Cardiovascular & Medical Sciences
College of Medical, Veterinary and Life Sciences
Davidson Building
University of Glasgow
University Avenue
Glasgow, G12 8QQ
United Kingdom
Phone: +44 (0)141 330 6200

Overview

Cardiovascular disease is projected to remain the single leading cause of death over the next two decades, accountable for considerable disability and reduction in the quality of life, therefore research is vital to advance its diagnosis, treatment and prevention.  

The Institute of Cardiovascular and Medical Sciences (ICAMS) is a successful and vibrant Research Institute with outstanding training and learning opportunities. Our purpose-built British Heart Foundation (BHF) Cardiovascular Research Centrehouses state-of-the-art laboratories and facilities and we are one of only six BHF Centres of Excellence in the UK.  Our research strengths have been integrated into substantial, well-resourced thematic programmes that build on the strengths of individual, clinical and non-clinical principal investigators.   Working in basic, translational and clinical research, our strength is in elucidating mechanisms of cardiovascular disease, identifying biomarkers of disease, identifying therapeutic targets and developing and designing novel therapeutic strategies that will lead to clinical trials.

Study options

PhD programmes in the Institute of Cardiovascular and Medical Sciences (ICAMS) last 3-4 years, with individual research projects tailored around the expertise of principal investigators within the Institutes. Basic and clinical projects are available for study. A variety of approaches are used, including molecular biology, biochemistry, epidemiology, mathematical modelling, bioinformatics, genetics, cell biology (including advanced in vitro and in vivo imaging), immunology and polyomics (genomics, transcriptomics, proteomics, metabolomics etc).

Specific areas of interest include:

  • Vascular science and medicine
  • Cardiovascular biology and cell signalling
  • Cardiovascular gene therapy for the treatment of vascular disease
  • Basic and clinical cerebrovascular disease e.g stroke 
  • Stem cell therapies for Cerebrovascular disease
  • Genetics, genomics and systems medicine 
  • Adrenal Corticosteroids in cardiovascular disease
  • Diabetes , obesity, metabolic and renal disease
  • Cardiovascular imaging
  • Cardiovascular clinical trials
  • Sport & Exercise Science& Medicine

Supervisors

All our postgraduate research students are allocated a supervisor who acts as the main source of academic support and research mentoring.

You may want to identify a potential supervisor and contact them to discuss your research proposal before you apply.

Entry requirements

Awarded or expected 1st class or high upper 2nd class BSc degree.

English Language requirements for applicants whose first language is not English.

English Language requirements for applicants whose first language is not English.

Fees and funding

Fees

2016/17

  • £4,121 UK/EU
  • £18,900 outside EU

Prices are based on the annual fee for full-time study. Fees for part-time study are half the full-time fee.

Additional fees for all students:

  • Submission by a research student £440
  • Submission for a higher degree by published work £890
  • Submission of thesis after deadline lapsed £140
  • Submission by staff in receipt of staff scholarship £680
  • Research students registered as non-supervised Thesis Pending students (50% refund will be granted if the student completes thesis within the first six months of the period) £250
  • General Council fee £50
  • Depending on the nature of the research project, some students will be expected to pay a bench fee to cover additional costs. The exact amount will be provided in the offer letter.

2017/18

  • £4,195 UK/EU*
  • £19,500 outside EU

Prices are based on the annual fee for full-time study. Fees for part-time study are half the full-time fee.

* We expect that tuition fees for EU students entering in 2017 will continue to be set at the same level as that for UK students.  However, future funding arrangements for EU students will be determined as part of the UK’s discussions on its future relationship.  If you are thinking of applying for 2017 entry, we would encourage you to do so in the usual way. For further information, please see the Research Councils UK statement on international collaboration and Universities UK Brexit FAQs for universities and students.

Additional fees for all students:

  • Fee for re-submission by a research student: £460
  • Submission for a higher degree by published work: £1,050
  • Submission of thesis after deadline lapsed: £250
  • Submission by staff in receipt of staff scholarship: £730
  • Research students registered as non-supervised Thesis Pending students (50% refund will be granted if the student completes thesis within the first six months of the period): £300
  • Registration/exam only fee: £150
  • General Council fee: £50

Alumni discount

A 10% discount is available to University of Glasgow alumni. This includes graduates and those who have completed a Junior Year Abroad, Exchange programme or International Summer School at the University of Glasgow. The discount is applied at registration for students who are not in receipt of another discount or scholarship funded by the University. No additional application is required.

 

Funding

Support

Resources

Our laboratories are well resourced and we offer a wide range of cutting-edge research facilities, including core facilities in:

  • Optical Imaging
  • Electrophysiology
  • Magnetic Resonance Imaging
  • Spectroscopy
  • Cell Biology
  • High throughput genotyping
  • Phenotyping
  • Clinical trials
  • a wide range of cellular, molecular and biochemical analysis tools. 

Our excellent facilities underpin a bench to bedside approach that will equip you with research specific and generic training and skills complementary to a wide range of career options.  We can tailor your study pathway to the precise aspects of cardiovascular research that suit your objectives.

You will emerge equipped with the skills necessary for a career in the highly competitive field of cardiovascular science and medicine. Future career opportunities include basic and clinical cardiovascular research in academia or industry, education, NHS, Clinical Biochemistry, public health bodies, media and publishing, funding agencies and scientific charities.

Graduate School

The College of Medical, Veterinary and Life Sciences Graduate School provides a vibrant, supportive and stimulating environment for all our postgraduate students. We aim to provide excellent support for our postgraduates through dedicated postgraduate convenors, highly trained supervisors and pastoral support for each student.
 
Our over-arching aim is to provide a research training environment that includes:

  • provision of excellent facilities and cutting edge techniques
  • training in essential research and generic skills
  • excellence in supervision and mentoring
  • interactive discussion groups and seminars
  • an atmosphere that fosters critical cultural policy and research analysis
  • synergy between research groups and areas
  • extensive multidisciplinary and collaborative research
  • extensive external collaborations both within and beyond the UK 
  • a robust generic skills programme including opportunities in social and commercial training