Current postgraduate opportunities

Funded PhD Scholarships starting autumn 2016 are available in research teams on Hull York Medical School's Hull campus, funded by the University of Hull. Multiple positions are available for two clusters of projects in successful and growing research areas, as detailed below.

These positions are available as either full-time UK/EU PhD Scholarships including fees at home/EU rate and maintenance stipend (£14057 for 2015-16), or full-time International PhD Fee Bursaries covering full fees at the international rate. The funding covers three years' study, dependent on satisfactory progress. In order to qualify applicants require a strong academic record (minimum of undergraduate degree with class 2.1 or equivalent) and good English language ability (native speaker or IELTS 7.0). PhD students at Hull York Medical School follow modules for research and transferable skills development and gain a Masters level Certificate in Research Training, in addition to their research degree.

Project supervisors will welcome informal enquiries from potential applicants. The closing date for formal applications is 29th February 2016. Shortlisting and interview will take place as soon as possible after the closing date, with successful applicants being informed by 30th April 2016 at the latest.

Projects in new and emerging areas of platelet biology

Projects in clinical research into cardiovascular, respiratory and metabolic medicine

Additional project in applied health research


Projects in new and emerging areas of platelet biology

This cluster of projects is focussed on understanding the role of blood platelets in thrombo-inflammation. They are based in a strong team of six collaborating laboratory scientists, with strong links to clinical researchers. Thrombosis and haemostasis research is a major theme in the HYMS strategic plan and has attracted £1.5 million in external research funding as well as been an area of significant internal investment. The students will join an active research centre which currently includes 4 post-doctoral scientists and 12 PhD students, supported by regular laboratory meetings, seminars and journal clubs.

  • Platelet Project 1: Resolution of thrombo-inflammation through targeting of platelet inflammatory signalling.

    Inflammation is a complex process that is initiated to combat infection.  Innate immune cells such as macrophages, leukocytes and dendritic cells use pattern recognition receptors (PRRs) on their surface to recognize damaged cells through their expression of danger-associated molecular patterns (DAMPs).  Activation of PRRs on immune cells activates signalling cascades resulting in the release of chemical messengers such as cytokines and chemokines.  In addition to established immune cells, blood platelets possess a number of proinflammatory actions including release of chemokines, cytokines and other chemicals promoting the recruitment of inflammatory cells.

    Blood platelets are a group of cells that circulate and function to repair damage to the blood vessel wall through the formation of blood clots. However in heart disease platelets become hyperactive and drive pathological thrombosis that leads to myocardial infarctions (heart attacks). Emerging evidence suggests that platelet inflammatory functions require receptors that are important for innate immunity. These receptors, including scavenger and toll-like receptors (TLR), allow platelets to scan the blood for foreign microbes or damaged cells. The inflammatory functions of platelets activated upon encountering DAMPs likely evolved as part of general protection against infection. Interestingly, endogenous DAMPs including are associated with platelet hyperactivity, accelerated thrombosis and heart disease, suggesting a link between the immune function of platelets and atherothrombosis though the mechanism is not clear.

    In this project you will study new mechanisms of pathobiology that focus on how blood platelets respond to DAMPs to promote inflammation and thrombosis. You will use molecular and cell biology techniques including phosphoflow cytometry, immunoprecipitation/immunblotting, ELISA, physiological thrombosis assays and high-resolution microscopy to determine how platelets response to distinct DAMPs and identify the receptor-signaling pathways involved. This is an excellent opportunity for training in basic cell and molecular biology techniques, and in the study of cellular signal transduction and systems biology.  The student will join a team of three Post-doctoral Research assistants and three PhD students that utilizes multidisciplinary approaches to characterizing the molecular mechanisms regulating platelet function.

    Supervisor: Professor Khalid Naseem with Dr Monica Arman. For informal enquires contact

    All applications MUST BE submitted online at  For more information please see

     The deadline for applications is 29 February 2016.

  • Platelet Project 2: Do Danger Associated Molecular Patterns (DAMPS) cause dysfunction of pluripotent stem cells differentiation, megakaryocyte maturation or proplatelet formation?

    Cardiovascular diseases are characterised by increased oxidative stress. In these diseases patients have increased circulating levels of oxidised lipids, called lipid peroxides, which are associated with plasma lipoproteins such as low density lipoprotein (LDL). Oxidation of LDL (oxLDL) converts it to a danger associated molecular pattern (DAMP) containing particle, which is highly proinflammatory and induces phenotypic changes in the cells it interacts with. In the blood it causes platelets to become hyperactive which can lead to increased thrombosis.

     In addition to its effects within the blood, LDL can penetrate the blood vessel wall and influence cells outside the vascular system.  One such cell is the megakaryocyte, which is descended from pluripotent stem cells, and is the precursor of blood platelets. The location of megakaryocyte maturation, development, and eventual initiation of platelet production is the subendothelial matrix, the area in which oxLDL and other DAMPs will be present. The oxidized phospholipids found in oxLDL have genomic effects that induce cell proliferation and increased invasiveness suggesting that accumulation of oxidised lipids in the blood vessel wall could change the phenotypic properties of the megakaryocyte.  However the influence of oxidised lipids on megakaryocyte function and platelet function is completely uncharacterised. We hypothesise that elevated levels of oxidised phospholipids will induce alterations in megakaryocyte function, leading to platelet functional changes, which could underlie the hyperactivation of the platelet within patients with cardiovascular disease. 

    The student will use a wide range of biological assays, including transfection of primary megakaryocytes, spreading and migration assays, western blotting, pro-platelet formation, ploidy analysis via FACS, fluorescence and confocal microscopy in both 2D and 3D environments, to understand the effect of oxLDL on megakaryocyte function. It would suit a student with a background in biology, biochemistry, medicine or pharmacology. The student will join a team of post-doctoral scientists and PhD students who use multidisciplinary approaches to characterising molecular mechanisms regulating platelet and megakaryocyte function.

    Supervisor: Dr Simon Calaminus with Professor Khalid Naseem. For informal enquiries contact

    All applications MUST BE submitted online at  For more information please see 

    The deadline is 29 February 2016.
  • Platelet Project 3: Deciphering the molecular mechanisms that mediate bacterial killing by human platelets

    Platelets are blood cells that play a critical role in cessation of bleeding. However they also have important immunological functions. Platelet activation is involved in antibacterial host defence by secreting antimicrobial peptides like Platelet Factor 4 (PF4) or modulating leukocyte responses and inflammation. In some infections the formation of platelet aggregates upon platelet activation might be a beneficial way to trap and contain bacteria within clumps. For some bacterial species, bacteria internalisation within individual platelets has been reported.

    Although platelet activation to undergo secretion and/or aggregation takes place in response to a wide range of bacteria, the effect on bacterial survival has been poorly investigated. In this study we propose to perform a detailed characterisation of the molecular mechanisms by which human platelets mediate bacterial death. A range of Gram-positive and Gram-negative bacteria will be systematically tested for susceptibility to PF4-mediated killing, and the mechanisms regulating PF4 release and its interaction with these pathogens will be characterised. Furthermore internalisation of bacteria within platelets and the molecular pathways underlying this process will be explored. The study will focus on the role of specific platelet surface receptors involved in immunity (e.g. FcgammaRIIA receptor recognising IgG-coated bacteria, Toll-like receptors, CD36 scavenger receptor) and platelet signalling pathways controlling cytoskeleton rearrangements involved in exocytic (e.g. PF4 release) and endocytic (e.g. bacteria internalisation) responses to bacteria.

    The student will join a research team that utilises multidisciplinary approaches to study platelet-pathogen interactions. He/she will use a number of molecular and cell biology techniques including confocal and fluorescence microscopy, flow cytometry, western blotting, and immunoprecipitation to examine how platelets respond to bacteria. This is an excellent opportunity for training in basic cell and molecular biology techniques, and in the study of cellular signal transduction and bacteria-host cell interactions.

    Supervisor: Dr Monica Arman with Dr Simon Calaminus. For informal enquiries contact

    All applications MUST BE submitted online at  For more information please see

    The deadline is 29 February 2016.

  • Platelet Project 4: Understanding the mechanisms connecting platelets to muscle stem cell function and skeletal muscle regeneration

    Platelets affect regeneration in several tissues including liver, bone and connective tissue. Recent evidence suggests that platelet-derived molecules (PDM) promote skeletal muscle regeneration after injury. However these platelet-driven effects, although exciting at the preclinical level, have faced challenges in clinical applications and their effectiveness remains controversial. Therefore there is a need to better understand the molecular interactions between platelet signalling and myofibre repair capacity.

    Skeletal muscle stem cells, called satellite cells, play a major role in muscle repair in response to injury. They become activated by growth factors and are considered the key rate-limiting step for successful repair. This project will test the hypothesis that platelets promote skeletal muscle regeneration by means of their secreted molecules. Key growth factors secreted by platelets include vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF) and fibroblast growth factor (Fgf), and all are known to regulate myogenesis in several experimental settings. In order to pinpoint key molecular events, we will examine the cross-talk between platelet signalling and skeletal muscle stem cells in the context of muscle fibre regeneration. We will establish the effect of different platelet-derived molecules in myofibre regeneration at the cellular level and we will also determine whether platelet enrichment is beneficial for muscle regeneration after injury in vivo.

    The project will involve use of a wide spectrum of experimental tools including basic cell and bio-molecular techniques such as cell culture systems, fluorescence microscopy, protein biochemistry, histology and gene expression. The project has implications for regenerative medicine and there will be scope to translate biochemical findings to in vivo patho-physiological conditions of muscle damage using genetically modified mice, pharmacological approaches to modulate platelets, and delivery of PDM to injured muscle. The student will join an interactive research environment with expertise in platelet biology and skeletal muscle molecular physiology and will use modern approaches for dissecting the molecular mechanisms that modulate muscle stem cell function by platelets.

    Supervisor: Dr Antonios Matsakas with Professor Khalid Naseem and Dr Roger Sturmey. For informal enquiries contact

    All applications MUST BE submitted online at  For more information please see

    The deadline is 29 February 2016.

  • Platelet Project 5: Examining the role of adipokines in the prothrombotic state of metabolic syndrome

    Mounting evidence suggests that inflammation participates in the pathogenesis of type 2 diabetes (T2D), with immunomodulatory strategies for treating this condition being currently explored. Cells and mediators of the immune system have been found altered in metabolic syndrome (diabetes and obesity) in various tissues. In T2D patients platelets circulate in a hyperactivated state and platelets themselves contribute to sustaining the inflammatory processes that are at the root of T2D. Metabolic syndrome is accompanied by abnormal release of adipokines (resistin, leptin, visfatin, adiponectin and others) by the adipose tissue. Resistin has received particular attention as a potential link between inflammation and metabolic disease.

    Despite the great interest in resistin as a participant in the pathogenesis of metabolic syndrome, virtually no studies have addressed its role in modulating platelet function and potentially contributing to the prothrombotic state. Two of the proposed resistin receptors, TLR-4 and CAP1, are expressed in platelets and are intimately linked with inflammatory responses. We hypothesise that resistin shifts platelets into a prothrombotic state by interfering with the signalling and metabolic routes that control platelet activation. The student will investigate this by studying the effects of resistin on an array of platelet functions, including glucose and oxidative metabolism, and will dissect the signalling pathways that mediate those effects.

    The project will offer an excellent opportunity for training in the use of a wide spectrum of cutting edge cell, molecular biology and biochemistry techniques, including flow cytometry, immunoblotting, fluorescence microscopy and metabolic profiling. In addition, there will be scope within the project to translate our findings to in vivo patho-physiological conditions of insulin resistance and other metabolic conditions. The student will join a team of a post-doctoral scientist and other PhD students who use multidisciplinary approaches to characterise the molecular mechanisms regulating platelet function. The team is embedded in a research environment with wide expertise in platelet biology, cell biology and metabolism.

    Supervisor: Dr Francisco Rivero with Dr Roger Sturmey and Professor Khalid Naseem. For informal enquiries contact

    All applications MUST BE submitted online at  For more information please see

    The deadline is 29 February 2016.

Projects in clinical research into cardiovascular, respiratory and metabolic medicine

This cluster of projects is focussed on improving our understanding and treatment of respiratory conditions (lung fibrosis, sarcoidosis and the effects of human Rhinovirus), superficial venous insufficiency, and diabetes. They are led by dynamic early/mid-career researchers within clinical research groups with a strong track record of publication and external grant funding (£3.7 million in the last few years). The University is currently building a new Health Hub building which is due for completion in 2017 and will act as a major nucleus for clinically-related researchers on campus, and there is also dedicated well equipped laboratory space in hospital locations.

  • Clinical Project 1: The endovenous revolution in varicose vein surgery – assessing the impact and prioritising future areas of research

    Superficial venous insufficiency (varicose veins) is a common problem affecting 20-30% of the UK adult population. It can cause significant symptoms, quality of life limitations and complications. Traditional treatment involved a surgical operation under general anaesthetic from which patients took several weeks to recover. The Academic Vascular Surgical Unit in Hull pioneered the development of new minimally invasive “walk in, walk out” treatment performed under local anaesthetic. This new treatment utilises laser energy, delivered from a catheter within the vein, to seal it. A recent NIHR HTA funded multicentre RCT demonstrated the superiority of endovenous laser ablation over traditional surgery in terms of clinical and cost effectiveness (Brittenden et al, N Eng J Med 2014; 371: 1218-1227). As a result the National Institute for Health and Care Excellence recommended that endovenous laser ablation should be the primary treatment option in patients with varicose veins (

    This project has as its first aim to assess the impact of this endovenous revolution. Routinely collected national Hospital Episodes Statistics (HES) and Patient Reported Outcome Measures (PROMs) data will be interrogated from 2010 – 2015 to investigate any change in clinical practice throughout the UK over this time, to assess the effect on patients quality of life,  and to model cost implications for the NHS. Secondly the student will work with the surgical team to prioritise areas of future venous research, using a Delphi approach to survey members of the Venous Forum of the Royal Society of Medicine. The project gives an opportunity for a graduate in health sciences and related subjects to gain expertise in data analysis and clinical research approaches in an area of medicine which has a wide impact on patients' quality of life.

    Supervisors: Professor Ian Chetter and Mr Tom Wallace with Mr Daniel Carradice. For informal enquiries contact

    All applications MUST BE submitted online at  For more information please see

    The deadline is 29 February 2016.

  • Clinical Project 2: The use of Precision Cut Lung Slices to investigate the effect of the Human Rhinovirus on cough and airway inflammation

    The human Rhinovirus (RV) is the major cause of the common cold.  There are no current treatments or vaccines for the virus other than over the counter preparations to alleviate symptoms.  For most people, RV infection will resolve without the need for medical intervention, however for some individuals complications can occur.  These can include the post viral cough leading to a chronic cough and for those who already have chronic lung diseases such as asthma and Chronic Obstructive Pulmonary Disease (COPD), a RV infection is one of the leading causes of exacerbations.  Additionally, RV may lead to other respiratory infections including pneumonia in susceptible individuals.

    There are thought to be over 100 different RV serotypes making it difficult to produce a vaccine.  In addition, like most respiratory diseases or infections, there is a lack of effective preclinical models, making drug development difficult.  There is no known mouse or guinea pig RV so studies have been limited to infecting human volunteers. 

    The aim of the current research project is to develop the Precision Cut Lung Slice (PCLS) lab-on-a-chip model (in collaboration with Chemistry) using human tissue to investigate the RV and its role in post viral cough and airways inflammation.  Over the first year the PCLS model will be developed and infection of tissue will be perfected and characterised.  Over the second and third year the student will investigate the effect of RV on the tissue and its secretions.  We hypothesise that RV infection will alter expression of channels and receptors which we have shown to be involved in cough and airway inflammation, causing the lung tissue to become hyper responsive to bronchoconstrictive agents.  This work will develop a more realistic model to study how RV causes cough and exacerbations in those already suffering from inflammatory airways diseases and it is hoped that this information can be used to develop novel therapies.

    Supervisor: Dr Laura Sadofsky with Dr Chris Cawthorne  . For informal enquiries contact

    All applications MUST BE submitted online at  For more information please see

    The deadline is 29 February 2016.
  • Clinical Project 3: Mechanisms of lung fibrosis in autoimmunity

    Pulmonary fibrosis is a progressive incurable disease of older people with a prognosis worse than many cancers. Median survival is only about 3 years from diagnosis. There is a strong association between pulmonary fibrosis and autoimmune diseases including rheumatoid arthritis and scleroderma. However, the mechanisms responsible for driving lung scarring in autoimmune conditions are unknown, and immunosuppressive drug therapy, whilst effective for controlling joint and skin inflammation, has little or no effect on pulmonary fibrosis.

    Our group has been investigating the role of interactions between the lung vasculature and endothelium, and circulating blood platelets, in pulmonary fibrosis. We have demonstrated that blood platelets from patients with pulmonary fibrosis are more responsive to stimulation (Crooks et al, PLoS One 2014;9:e111347), and that vascular endothelial cells can be activated in response to bleomycin (Williamson et al in preparation), a cytotoxic drug known to cause pulmonary fibrosis. We hypothesise that autoimmune diseases are associated with abnormalities of the lung endothelium and blood platelets that promote platelet-endothelial interaction and retention and activation of pro-fibrotic platelets within the lungs.

    In this project the student will test our hypothesis by exposing pulmonary microvascular endothelial cells and platelets to autoantibodies that are found in the serum of patients with autoimmune diseases. Endothelial cell and platelet activation will be measured, and adhesion interactions will be examined in a flow chamber system. Promising mechanisms will be tested in a rodent model of pulmonary fibrosis, and confirmed by staining human lung pathology biopsy specimens.

    This PhD studentship will contribute to research supported by a £50k bequest from the family of the late Kathleen Garthwaite, a former patient who suffered from pulmonary fibrosis associated with autoimmunity.

    Supervisor: Dr Simon Hart. For informal enquiries contact

    All applications MUST BE submitted online at  For more information please see

    The deadline is 29 February 2016.
  • Clinical Project 4: Determination of macrophage phenotype in sarcoidosis

    Sarcoidosis is a chronic inflammatory disease of unknown cause which commonly affects the lungs, lymph nodes, skin, and eyes. It causes significant morbidity and may shorten lifespan. Histologically the disease is characterized by granulomatous inflammation composed of monocytes/macrophages and lymphocytes, similar to that found in certain infectious diseases although no inciting microbe has been proven as a causative agent. This project will investigate the factors that promote the unique macrophage phenotype found in sarcoidosis, characterized by expression of the enzymes angiotensin converting enzyme (ACE) and vitamin D 1-alpha hydroxylase (CYP27B1).

    The student will characterize the phenotype of monocyte/macrophage cells in culture in the laboratory. Primary monocyte-derived macrophages and cell lines cultured in vitro will be stimulated with cytokines and microbial molecule agonists of Toll-like receptors and NOD receptors. Dose dependent effects on expression of ACE and CYP27B1 will be determined by a variety of techniques including intracellular flow cytometry, Western blotting, and quantitative PCR. Once pathways responsible for the sarcoidosis macrophage phenotype in cultured cells are identified, evidence for pathway activation will be sought in primary blood monocytes and in pathology tissue sections from patients with sarcoidosis.

    This PhD studentship will join a project supported by a recently awarded grant from the British Lung Foundation to study how monocytes regulate immune responses in the blood of patients with sarcoidosis.

    Supervisor: Dr Simon Hart. For informal enquiries contact

    All applications MUST BE submitted online at  For more information please see

    The deadline is 29 February 2016.
  • Clinical Project 5: Effect of exercise on acute fluctuations of hyperlipidaemia and metabolic flexibility in patients with type 2 diabetes: identification of novel biomarkers for cardiovascular risk

    Hyperglycaemia and hyperlipidaemia are well-recognised risk for atherosclerosis.  Although fasting samples are commonly used for the assessment of lipid and glucose status, people spend most of their time in the postprandial state. There are fluctuations in glucose and lipid levels between pre and post-meal periods. Postprandial hypertriglyceridemia and hyperglycaemia seem to be associated with cardiovascular risk. It is uncertain whether this was simply due to high average levels or due to fluctuations of lipids or glucose between pre and postprandial states. Our recent work showed that acute hyperlipidaemia either in patients with insulin resistance or in healthy subjects caused insulin resistance and increased platelet hyperactivity, a marker of atherosclerotic risk. 

    This study aims to examine whether fluctuant hyperlipidaemia has a greater effect than constant hyperlipidaemia on endothelial and inflammatory markers, and their relationship to novel miRNA expression that may identify new biomarkers.

    The effect of fluctuation of lipid levels will be compared to constant hyperlipidaemia during a constant hyperglycaemic state employing a hyperglycemic insulin clamp technique in patients with type 2 diabetes. In accord with the ectopic fat hypothesis of insulin resistance, these studies will be repeated following 3 months of supervised exercise to determine changes in the metabolic parameters and markers. Lipid infusions will be used instead of a lipid rich meal to avoid variability in gut absorption and to exclude the possible response of intestinal derived incretin hormones and their effect on insulin secretion.

    This project will involve cross-faculty collaboration between Hull York Medical School and Sports, Health and Exercise Sciences. This studentship would be suitable from applicants with a background in dietetics, sports science or clinical medicine. The student will be trained in clinical trials methodology, insulin clamp techniques, indirect calorimetry (to assess metabolic flexibility), Endopat for measuring endothelial function, measurement of oxidative stress and endothelial markers and measurement of microRNA. 

    Supervisor: Dr T Sathyapalan with Dr David Hepburn and Professor Sean Carroll. For informal enquiries contact

    All applications MUST BE submitted online at  For more information please see

    The deadline is 29 February 2016.

Additional project in applied health research

In addition to the University of Hull PhD Scholarships above, there is currently a studentship available in applied health research. It carries the same requirements and benefits (fees, and for home/EU students a stipend) as the others, and the same deadline for applications applies. It will be based in the Supportive care, Early Diagnosis and Advanced disease (SEDA) research group on HYMS's Hull campus. This is a very active and expanding group consisting currently of 7 academics, 8 research fellows and 12 research students. It has attracted over £3 million in external grant funding over the last three years and is part of a major new initiative to establish an Institute of Clinical and Applied Health Research in Hull.

  • Applied health research project: How healthy are older migrants?

    Health between migrants and the local population often differs in that migrants frequently have a health advantage over the resident population when they first enter a country. This so called healthy migrant effect might diminish over time. 

    Australia, which has rigorous health requirements on migrants, has an increasing proportion of foreign born population (27.7% in 2013) who come from the UK (5.3% of total population), followed by New Zealand, China, India and Vietnam. Even though a favourite migration country, the population is ageing and research on migrant health is sparse as in many other countries. 

    We work closely with colleagues in Australia and this studentship provides an opportunity to interrogate a large dataset to explore the impact of ageing on a large migrant community. This project will examine the health of older migrants using the Dynamic Analyses to Optimise Ageing (DYNOPTA) dataset which combines 9 Australian longitudinal studies for ageing (over 50000 participants). This longitudinal dataset contains the relevant information for this study, for example: country of birth, health behaviours and conditions, activity limitations, mental and cognitive health, and use of services. 

    The aim of the project will be to compare the mortality and morbidity (both physical and mental health) of older migrants with the local-born population. Differences will be related to factors such as: (1) duration of residence, education, language spoken, access to services and caring responsibilities; and (2) variations in health behaviour such as smoking, drinking and physical activities. Although conducted in a non-UK dataset, the study will use generalizable skills and generate generalizable findings. 

    This project is suitable for a student with good quantitative skills (e.g. degree in statistics, computer science, geography etc.). The PhD will offer the opportunity to expand quantitative skills with demographic methods and standard measures of health inequalities.  Interrogating large datasets is a key strategic area of the new Institute of Clinical and Applied Health Research in Hull and the student's research will be a part of that initiative. 

    Supervisors: Dr Pia Wohland and Professor Miriam Johnson. For informal enquiries contact

     All applications MUST BE submitted online at: The deadline is 29 February 2016.

    For more information please follow this link   


Separate BHF-funded project in platelet biology

There is also a prestigious British Heart Foundation PhD studentship available, which attracts a higher stipend than standard studentships in order to attract outstanding candidates. It is based in the same team as the other platelet projects, and could be available earlier than the other positions (start date to be agreed with the successful candidate).

  • BHF studentship: The role of coronin in platelet cytoskeletal changes and cardiovascular function

    A British Heart Foundation funded PhD position is available for an outstanding student to study the signal transduction pathways that regulate the function of blood platelets. It is based at the Hull campus of Hull York Medical School supervised by Dr Francisco Rivero and Professor Khalid Naseem. 

    In this project we will investigate the role of the cytoskeleton protein coronin in the regulation of platelet adhesion, activation and aggregation and its potential influence on development of cardiovascular disease. The studentship provides an excellent opportunity to receive training in basic cell and molecular biology techniques (immunoblotting/immunoprecipitation, flow cytometry, fluorescence/confocal microscopy, proteomics) in the study of cellular signal transduction. The student will join a research team that utilises multidisciplinary approaches to identify new mechanisms regulating platelet function and determine if these newly identified mechanisms can be targets for prevention and treatment of arterial thrombosis.     

    Informal enquiries should be addressed to Dr. Francisco Rivero (, Prof. Khalid Naseem ( or Mrs. Helen Procter (

    The post is a full-time studentship for 3 years, depending on satisfactory progress, funded by the British Heart Foundation. It includes stipend at an enhanced rate, tuition fees and bench fees for a UK/EU student. The start date is open to negotiation (earliest 1 April 2016). The deadline for applications is 29 February 2016. 

    Applicants should hold First or Upper Second Class Honours degree or equivalent, and an MSc (with distinction) in biochemistry, biomedical sciences, pharmacology or a related area of biological sciences. The position is open only to EU/UK applicants. Applicants for whom English is not their native language will need to demonstrate adequate proficiency (IELTS 7.0).