Postgraduate research 

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

Start dates for incoming postgraduate research students

1 October 2020 is the preferred date to start your PhD [or the date on your offer letter].

We will run a full on-line induction and training programme that may be taken remotely for the first month. Most of our doctoral researcher training programme will also be available online and we will offer many remote opportunities to help you become part of the Graduate School and wider University community.  

Research that involves laboratory work may start following the completion of induction (all labs are currently up and running).

Some types of research (such as non-laboratory work) and supervision can be carried out entirely remotely and this may be the most appropriate way for you to work at the moment.  Contact your supervisor, if you believe this applies to your research to discuss requirements for home/remote working. You may also require the agreement of the subject, school or institute convener if you wish to carry out your PhD remotely for a fixed period. You may not continue remotely unless an adequate plan is agreed to ensure sufficient work can be undertaken prior to starting the experimental work. It is important that starting remotely does not affect the overall PhD timescale.

Delayed start dates

We understand there may be good reasons to delay:

  • If it is necessary to travel to Glasgow to begin your research, but there are restrictions preventing travel at this time, then a delay to 5 January 2021 is encouraged [when we will run full on-line induction and training programme]. You may also delay to another start time with the agreement of your supervisor and Graduate School.
  • For subjects where laboratory work is required to commence immediately following on-line induction and training and you are unable to come to Glasgow, you should consider delaying your start-date. Contact your supervisor or the Graduate School in this instance.
  • If your research involves objects, artefacts, archives or fieldwork, you should discuss this with your supervisor. Some kinds of work may be able to be started remotely; in other cases, it may be advisable to delay the start-date.
  • External government sponsors may prefer a delay and the University is happy to support this.

From our point of view, there is no disadvantage in deferring your PhD to a later agreed start date. Scholarship holders should check that this can still be provided with a delayed start.

Office and study space

At present, current staff and research students are not using office spaces on campus. We do not have a confirmed date for the return to office use, but all work that can be undertaken off-campus (ie is not lab-based) should be done at home or remotely at present.

Some study spaces are becoming available on campus with a booking system in place, such as the postgraduate study space in the University Library.

International/EU students remotely starting a funded PhD

You should check with your funder that you can be paid a stipend if you are not in the UK. If you are in receipt of a scholarship, you should contact the Graduate School for advice on opening a bank account to allow stipend payments.


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.

Research projects

Self-funded PhD opportunities

MicroRNAs 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, stroke, obesity and diabetes.

Therefore, understanding the 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.

In this project, we wish to examine the role of non-coding miRNAs in aldosterone production and related cardiovascular disease, study their effect on cellular processes and investigate their utility as circulating biomarkers of disease. This project will combine our extensive experience of cardiovascular and hormone research with cutting edge molecular/cellular biology and bioinformatic methods.

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: 

  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 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

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

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.

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

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

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

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