Postgraduate research 

Cardiovascular & Medical Sciences PhD/iPhD/MD/MSc (Research)

Travel advice for postgraduate research students

The latest Scottish Government guidance confirms that most students should not plan to travel to term-time accommodation at this point. Where there is a time-sensitive element to your course, a small number of students will be able to travel.

There are some exceptions to this advice, with the following groups of students allowed to be on campus:

  • those who have remained over the winter break;
  • those whose attendance is critical and whose education cannot be delivered remotely or postponed, essential placements, or for reasons of student wellbeing

Please continue to observe the latest Scottish Government guidance and local restrictions.

If you are travelling to a term-time address from within the UK, you should book a test for the date of your arrival.

 

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Travel advice for international students

Semester began on 11 January and the majority of learning and teaching is being delivered online. The latest Scottish Government guidance confirms that most students should not plan to travel to term-time accommodation at this point. 

Unless you need to be at the University for in-person teaching, please delay your travel for now. We will update all students when the Scottish Government advise it is safe for students to travel.

From Monday 18 January, the small number of students who do travel to Scotland from abroad must:

  • have proof of a negative PCR test (or similar test with at least 99% specificity and 97% sensitivity for detecting COVID-19) taken a maximum of 72 hours before travel. See the Scottish Government’s guide: Pre-departure coronavirus testing
  • self-isolate for 10 days on arrival. Our International Student Support Team will provide assistance following arrival in Glasgow.
  • not book a Lateral Flow test at the University's testing centre.

Students who do fly into Glasgow are invited to complete the University’s Travel Plans form, which gives the option of an airport transfer.

Whether you join us in Glasgow or study from home, please know that we are with you every step of the way, and will do all that we can to ensure that your student journey at the University of Glasgow is both a successful and enjoyable one.

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blood cells

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

  • PhD: 3-4 years full-time; 5 years part-time;
  • Integrated PhD: 5 years full-time;
  • MD (Doctor of Medicine): 2 years full-time; 4 years part-time (for medically-qualified graduates only) part-time;
  • MSc (Research): 1 year full-time; 2 years part-time;

Research projects

Self-funded PhD opportunities

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Investigating disease mechanisms of collagen IV disease including intracerebral haemorrhage

Supervisors: Tom Van Agtmael and Alyson Miller

15% of strokes are due to intracerebral haemorrhage (ICH), for which there is no treatment. and absence of specific effective treatments indicates increased knowledge of its pathomolecular basis is required. Recent genetic data has identified an important role for the protein collagen IV in stroke due to haemorrhage. Mutations in collagen IV also cause eye, kidney and muscle disease for there are also no treatments. We and others have showed the mutations and variants in collagen can cause defects to the extracellular matrix as well as a cell stress response called ER stress.

This project will use a powerful set of bespoke mouse models to determine in vivo the relative contribution of BM defects and ER stress to ICH as well as eye and kidney defects due to collagen IV. This will be combined with vascular physiology and molecular approaches, including transcriptomics and/or proteomics, to identify novel mechanisms.

Importantly, you will validate these mechanisms in patients. This project can be tailored to the interests of the candidate but will transform our knowledge of molecular mechanisms of stroke and disease due to collagen. This will aid development of precision medicine treatments.

Techniques used: you will be trained in a large variety of techniques crossing animal models of stroke, analysis of vascular function, molecular and biochemical approaches, imaging etc.

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Developing gene therapy approaches for stroke, eye and kidney disease due to mutations in collagen

SupervisorsTom Van Agtmael and Mark Bailey (SoLS)

Mutations in collagen IV cause a severe genetic disorder that includes brain bleeding, eye and kidney disease. In addition rare mutations also contribute to stroke in the general population. There are no treatments available for these disease, and the complex nature of the disease further hinders treatment development.

A gene therapy based approach is therefore an attractive solution to develop a potential cure for this disease.

Using a panel of cell lines from patients and endothelial cells with mutations, you will investigate different gene therapy approaches to silence the expression of collagen IV mutations. This would involve developing different strategies and introduce them into cell culture to determine if they can overcome the cell defects of these mutations. If successful this could be translated into treatments for our animal models of diseases due to collagen mutations.

Techniques used: You will use a large variety of molecular biology approaches for the design and cloning of gene therapy approaches, cell culture, analysis of endothelial cell function (eg. angiogenesis assays), biochemical and molecular analysis, imaging etc.

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Investigating the role of endoplasmic reticulum stress as mechanisms of cardiovascular disease

Supervisors: Tom Van Agtmael and Christian Delles

Vascular diseases including haemorrhagic stroke are a major health problem for which there is an urgent need for treatments. Increasing our understanding of the underlying molecular disease mechanisms will aid in the development treatment strategies.

We have previously identified that mutations in the genes Col4a1 and Col4a2 cause stroke and vascular disease. These mutations cause defects to the extracellular matrix and a cell stress response called endoplasmic reticulum (ER) stress, caused by misfolding of the mutant collagen protein. Interestingly ER stress has also been observed in other vascular diseases in the general population including high blood pressure and heart failure. However, the actual role of ER stress to these diseases including Col4a1 disease remains unclear.

To address this gap in our knowledge, in this project you will employ novel mouse models that we generated to determine in vivo the role of ER stress in disease. Combined with cell culture models, imaging and proteomics/next generation sequencing you will investigate the molecular mechanisms by which ER stress affects the vasculature. In so doing, this project will increase our fundamental understanding of ER stress and may help the development of novel disease-mechanism based treatments for vascular disease such as stroke, and/or hypertension.

Techniques used: you will be trained in a large variety of techniques using animal models, cell culture, molecular and biochemical approaches, imaging, as well as RNASeq and proteomics etc.

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MIRomics in Hypertension and Cardiovascular Disease.  

Supervisor: Prof Eleanor Davies, Dr Scott MacKenzie

Research area: Hormones and the Cardiovascular System

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, atrial fibrillation, ventricular hypertrophy and stroke,. Therefore, understanding the mechanisms involved in the regulation of this important hormone is essential.

We have shown that non-coding RNAs (microRNAs and long non-coding RNAs) can have a significant impact on aldosterone production and a number of miRNAs are dysregulated in patients with aldosterone excess.

In this project, we wish to examine the role of non-coding miRNAs in aldosterone production and investigate their utility as therapeutic agents to lower levels of aldosterone. This project will combine our extensive experience of cardiovascular and hormone research with cutting edge molecular/cellular biology and bioinformatic methods.

Summary aim:

Understanding the regulation of aldosterone production is central to unravelling its role in common conditions such as hypertension, stroke and obesity. This project has the potential to identify novel mechanisms that regulate the production of aldosterone and identify therapeutics targets to modify its production.

Techniques used: 

Cell culture, qRT-PCR, cell transfection, ELISA, Western blotting, DNA sequencing, RNA-Seq screening, Bioinformatics.

References: 

  1. Robertson S, Diver LA, Alvarez-Madrazo S, Livie C, Ejaz A, Fraser R, Connell JM, MacKenzie SM, Davies E. Regulation of Corticosteroidogenic Genes by MicroRNAs. Int J Endocrinol. 2017
  2. MacKenzie SM, van Kralingen JC, Davies E.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.
  3. 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.

Contact:

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

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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

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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 email: christohper.loughrey@glasgow.ac.uk

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Assessing therapeutic strategies to target the counter-regulatory renin-angiotensin system in cardiovascular disease

Supervisors: Dr Stuart Nicklin (with Dr Christopher Loughrey, Dr Lorraine Work)

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 cardiac remodelling in hypertension and heart failure and atherosclerosis. A counter-regulatory RAS exists, centred 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 therapeutic approaches for peptides and enzymes of the counter-regulatory axis of the renin angiotensin system using adenoviral and adeno-associated viral gene transfer vectors and extracellular vesicles as delivery vehicles in cardiovascular disease models including hypertensive cardiomyopathy, myocardial infarction and acute vascular injury.

Project aims: To develop and assess molecular therapeutic approaches to deliver counter-regulatory renin angiotensin system components in cardiovascular disease.
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, isolation and characterisation of extracellular vesicles.

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, isolation and characterisation of extracellular vesicles.

References:

  • C Fattah, K Nather, CS McCarroll, M Hortigon, V Zamora Rodriguez, M Flores-Munoz, L McArthur, L Zentilin, M Giacca, RM Touyz, GL Smith, C Loughrey, SA Nicklin. Gene therapy with angiotensin-(1-9) preserves left ventricular systolic function post-myocardial infarction via a direct inotropic effect. (2016). THE JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 68: 2652-2666.
  • 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.
  • 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.
  • A Pashova, LM Work and SA Nicklin. (2020). The role of extracellular vesicles in neointima formation post vascular injury. CELLULAR SIGNALLING, 18;76:109783. doi: 10.1016/j.cellsig.2020.109783.
  • McFall A, Nicklin SA, Work LM. The counter regulatory axis of the renin angiotensin system in ischaemic stroke: insight from preclinical studies and potential as a therapeutic target. CELLULAR SIGNALLING, 2020 Dec;76:109809. doi: 10.1016/j.cellsig.2020.109809. Epub 2020 Oct 13.

Contact address and email:

Professor Stuart A Nicklin BSc (Hons) PhD
Professor of Cardiovascular Molecular Therapy
Institute of Cardiovascular and Medical Sciences
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

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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

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Overview

The Institute of Cardiovascular & 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 Centre houses 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.

Individual research projects are tailored around the expertise of principal investigators within the institute. 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

Study options

PhD

  • Duration: 3/4 years full-time; 5 years part-time

Individual research projects are tailored around the expertise of principal investigators.

MSc (Research)

  • Duration: 1 year full-time; 2 years part-time

MD (Doctor of Medicine)

  • Duration: 2 years full-time; 4 years part-time (for medically-qualified graduates only)

Integrated PhD programmes (5 years)

Our integrated PhD allows you to combine Masters level teaching with your chosen research direction in a 1+3+1 format. 

International students with MSc and PhD scholarships/funding do not have to apply for 2 Visas or exit and re-enter the country between programmes. International and UK/EU students may apply.

Year 1

Taught masters level modules are taken alongside students on our masters programmes. Our research-led teaching supports you to fine tune your research ideas and discuss these with potential PhD supervisors. You will gain a valuable introduction to academic topics, research methods, laboratory skills and the critical evaluation of research data. Your grades must meet our requirements in order to gain entry on to a PhD research programme. If not, you will receive the Masters degree only.

Years 2, 3 and 4

PhD programme with research/lab work, completing an examinable piece of independent research in year 4.

Year 5

Thesis write up.

All applicants must have full funding before starting their iPhD programme.

Entry requirements

A 2.1 Honours degree or equivalent.

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English language requirements

For applicants whose first language is not English, the University sets a minimum English Language proficiency level.

International English Language Testing System (IELTS) Academic module (not General Training)

  • overall score 6.5
  • no sub-test less than 6.0
  • or equivalent scores in another recognised qualification

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Fees and funding

Fees

2021/22

  • UK fee to be confirmed by ukri.org (2020/21 fee was £4,407)
  • International & EU: £23,000

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:

  • Re-submission by a research student £540
  • Submission for a higher degree by published work £1,355
  • Submission of thesis after deadline lapsed £350
  • Submission by staff in receipt of staff scholarship £790

Depending on the nature of the research project, some students will be expected to pay a bench fee (also known as research support costs) to cover additional costs. The exact amount will be provided in the offer letter.

Alumni discount

We offer a 10% discount to our alumni on all Postgraduate Research and full Postgraduate Taught Masters programmes. This includes University of Glasgow graduates and those who have completed Junior Year Abroad, Exchange programme or International Summer School with us. 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.

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2020/21 fees

  • £4,407 UK/EU
  • £21,920 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:

  • Re-submission by a research student £525
  • Submission for a higher degree by published work £1,315
  • Submission of thesis after deadline lapsed £340
  • Submission by staff in receipt of staff scholarship £765

Depending on the nature of the research project, some students will be expected to pay a bench fee (also known as research support costs) to cover additional costs. The exact amount will be provided in the offer letter.

Alumni discount

We offer a 20% discount to our alumni commencing study in Academic session 2020/21, on all Postgraduate Research and full Postgraduate Taught Masters programmes. This includes University of Glasgow graduates and those who have completed a Study Abroad programme or the Erasmus Programme at the University of Glasgow. This discount can be awarded alongside other University scholarships. 

Funding for EU students

The Scottish Government has confirmed that fees for EU students commencing their studies 2020/21 will be at the same level as those for UK student.

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Funding

The iPhD  is not supported by University of Glasgow Scholarship/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 & 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 overarching 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

How to apply

Identify potential supervisors

All Postgraduate Research Students are allocated a supervisor* who will act 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. Please note, even if you have spoken to an academic staff member about your proposal you still need to submit an online application form.

You can find relevant academic staff members with our staff research interests search.

*iPhD applicants do not need to contact a supervisor, as you will start your programme by choosing a masters from our Taught degree programmes A-Z [do not apply directly to a masters].


Gather your documents

Before applying please make sure you gather the following supporting documentation:

  1. Final or current degree transcripts including grades (and an official translation, if needed) – scanned copy in colour of the original document.
  2. Degree certificates (and an official translation, if needed): scanned copy in colour of the original document
  3. Two references on headed paper and signed by the referee. One must be academic, the other can be academic or professional [except iPhD applicants, where only one academic or professional reference is required]. References may be uploaded as part of the application form or you may enter your referees contact details on the application form. We will then email your referee and notify you when we receive the reference.  We can also accept confidential references direct to rio-researchadmissions@glasgow.ac.uk, from the referee’s university or business email account.
  4. Research proposal, CV, samples of written work as per requirements for each subject area. iPhD applicants do not need to submit any of these as you will start your programme by choosing a masters.

Notes for iPhD applicants

  • add 'I wish to study the MSc in (chosen subject) as the masters taught component of the iPhD' in the research proposal box
  • write 'n/a' for the supervisor name

Apply now

I've applied. What next?

If you have any other trouble accessing Applicant Self-Service, please see Application Troubleshooting/FAQs. 


Contact us

Before you apply

PhD/MSc/MD: email mvls-gradschool@glasgow.ac.uk

iPhD: email mvls-iphd@glasgow.ac.uk

After you have submitted your application

PhD/MSc/MD/iPhD: contact our Admissions team

Any references may be submitted by email to: rio-researchadmissions@glasgow.ac.uk