Find out more about self-funded PhD projects in areas of biomedical science.
We already have supervisors active and engaged in the research topic in our School of Life Sciences.
Fixed term contract for 3 years, commencing September 2023.
Bursary of £17,668 per annum and a full fee-waiver for UK and International tuition fees.
Closing date: Friday 26 May 2023
Interview date: June 2023
Project supported by Anglia Ruskin University and the Cambridge Philosophical Society.
About Anglia Ruskin University:
Anglia Ruskin is a vibrant workplace and our university is recognised both nationally and internationally. We have ambitious plans for the future, and we are determined that our students and staff will realise their full potential. Our main campuses in the cities of Cambridge, Chelmsford, London and Peterborough have been transformed with major capital investment. With an annual turnover of over £200m, we are a major force for higher education and one of the largest universities in the East of England.
About the project:
Acute respiratory distress syndrome (ARDS) is a pressing and current health concern resulting in ~20% intensive care unit admissions and nearly 50% mortality in critical care patients1. More recently, COVID-19 has been identified as a major cause of ARDS associated with high mortality and prolonged stay in intensive care unit2. A common pathophysiology in ARDS is breakdown of the pulmonary microvasculature leading to pulmonary edema formation (water on the lungs) and low blood oxygen in patients2. Current treatment options, such as mechanical ventilator treatment, can actually exacerbate the degree of lung injury3. This research project focuses on identifying new and targeted therapeutic tools to improve pulmonary microvascular function in settings of ARDS.
Our research is focused on understanding the signalling molecules which regulate the pulmonary microvasculature and how this knowledge can be used to develop new treatments for patients with ARDS. More recent studies have focused on the expression and function of novel GPCRs in the lung endothelium in settings of ARDS4,5. While the evolutionary function of these taste receptors in extraoral locations appears unconventional, we previously identified that these novel GPCRs play a key role in regulating the microvasculature using both in vitro and in vivo studies.
The objective of this project is to further our understanding of these novel GPCRs with the aim of developing novel therapeutic tools which will reduce the hyperpermeable state of the pulmonary vasculature. Studies will focus on investigating the molecular mechanisms underlying these therapeutic tools (in vitro studies) as well as understanding their physiological (in vivo studies) and clinical implications in settings of ARDS.
The 3-year PhD project will be based in the research laboratories in Anglia Ruskin University along with support from collaborators at the University of Cambridge (UK) and Brown University (USA).
References:
About the Studentship:
A 3-year studentship is offered, intended to start in September 2023, providing a tax-free stipend of £17,668 per annum plus tuition fees at the UK and International rate. Due to funding restrictions, this studentship is only available as a full-time position.
Project location: Cambridge campus. Prospective candidates who would not be Cambridge-based are encouraged to contact the principal supervisor prior to application (contact details below).
Candidates for this PhD Studentship must demonstrate outstanding qualities and be motivated to complete a PhD within 3 years.
Qualifications:
Applicants should have a minimum of a 2.1 Honours degree in a relevant discipline and a relevant level 7 (or equivalent) qualification (e.g., Masters degree). An IELTS (Academic) score of 6.5 minimum (or equivalent) is essential for candidates for whom English is not their first language.
In addition to satisfying basic entry criteria, the University will look closely at the qualities, skills, and background of each candidate and what they can bring to their chosen research project in order to ensure successful and timely completion.
Previous experience with molecular or cell biology techniques is essential with experience in mammalian cell culture, protein and mRNA analysis (e.g. Western blot, ELISA, qPCR) desirable.
How to apply:
To apply, please visit Biomedical Science PhD, click 'Apply online' and complete the application form for full-time study with a start date of September 2023. Please ensure the reference ‘PhD Studentship Sedgwick: Investigating how novel orphan receptors regulate the pulmonary endothelium to identify new therapeutic targets for patients with acute respiratory distress syndrome' is clearly stated on the application form, under the title ‘Outline of your proposed research’. Within this section of the application form, applicants should include a 500-word outline of the skills that they would bring to this research project and detail any previous relevant experience.
Interested applicants should direct initial queries about the project to Dr Havovi Chichger via email: [email protected]. For enquiries regarding the process and eligibility please contact [email protected].
Interviews will be scheduled for June 2023.
We value diversity at Anglia Ruskin University and welcome applications from all sections of the community.
Closing Date – 26 May 2023.
Fixed term contract for 3 years, commencing September 2023.
Bursary of £17,668 per annum and a full fee-waiver for UK and International tuition fees.
Closing date: Friday 26 May 2023
Interview date: June 2023
Project supported by Anglia Ruskin University and the Cambridge Philosophical Society.
About Anglia Ruskin University:
Anglia Ruskin is a vibrant workplace and our university is recognised both nationally and internationally. We have ambitious plans for the future, and we are determined that our students and staff will realise their full potential. Our main campuses in the cities of Cambridge, Chelmsford, London and Peterborough have been transformed with major capital investment. With an annual turnover of over £200m, we are a major force for higher education and one of the largest universities in the East of England.
About the project:
During the past 100 thousand years, humans spread around the world, encountering and adapting to new environments. These local adaptations are responsible for much of the regional variation in phenotypes seen across the human species range. However, more recently migrations have brought distantly related populations back into contact with each other. Admixture occurs when these distantly related populations exchange genes, and this process has the potential to be a strong force in very recent human evolution. What happens to the genes and phenotypes that previously diverged when populations come back together?
The people of Madagascar offer an ideal opportunity to study the role of post-admixture selection in human evolution. The Malagasy people descend from two of prehistory’s great migrations: The Bantu expansion of farming peoples across sub-Saharan Africa, and the Austronesian Expansion of seafaring peoples that began in Island Southeast Asia and spread across the Pacific and Indian Oceans. These African and Southeast Asian populations arrived on the previously unpopulated island of Madagascar and began mixing around 2000 years ago. As such, the Malagasy have a unique mixture of genes and culture not seen anywhere else in the world, and the people have remarkable levels of phenotypic diversity. Has natural selection favoured either the African or Asian derived ancestries or phenotypes during the 2000 years that people have been evolving in Madagascar? Do Malagasy people tend to marry people with similar genes and phenotypes to themselves, and if so, how his this affected their evolution?
This project will use genomic SNP data sampled coupled with extensive phenotypic data from 300 married couples in Madagascar. The project will require the student to develop population genomic and bioinformatics skills. The student will also have the opportunity to visit Madagascar and contribute to ongoing data collection efforts there. The student will receive training in genomics and bioinformatics from Dr Hodgson and Prof Manica, and training in anthropological field methods from Dr Hodgson and Dr Rakotoarivony. The student will also be a member of the Evolutionary Ecology Research Group at Cambridge University led by Prof Manica.
Aim 1: Develop a methodology for identifying and testing for post-admixture natural selection.
Aim 2: Identify genes involved in skin colour and 3D face shape variation, and test for evidence of selection in these genes.
Aim 3: Test for evidence of natural selection in genes involved in resistance to malaria.
Aim 4: Test for evidence of assortative mating with respect to genes and phenotypes related to African and Southeast Asian ancestry.
Supervisory Team:
Dr Jason Hodgson, Senior Lecturer in Bioinformatics and Big Data, School of Life Sciences, Anglia Ruskin University
Prof Andrea Manica, Professor of Evolutionary Ecology, Dept. of Zoology, Cambridge University.
Dr Rindra Rakotoarivony, Lecturer, University of Antananarivo, Madagascar
References:
About the Studentship:
A 3-year studentship is offered, intended to start in September 2023, providing a tax-free stipend of £17,668 per annum plus tuition fees at the UK and International rate. Due to funding restrictions, this studentship is only available as a full-time position.
Project location: Cambridge campus. Prospective candidates who would not be Cambridge-based are encouraged to contact the principal supervisor prior to application (contact details below).
Candidates for this PhD Studentship must demonstrate outstanding qualities and be motivated to complete a PhD within 3 years.
Qualifications:
Applicants should have a minimum of a 2.1 Honours degree in a relevant discipline and a relevant level 7 (or equivalent) qualification (e.g., Masters degree). An IELTS (Academic) score of 6.5 minimum (or equivalent) is essential for candidates for whom English is not their first language.
In addition to satisfying basic entry criteria, the University will look closely at the qualities, skills, and background of each candidate and what they can bring to their chosen research project in order to ensure successful and timely completion.
Previous experience with genomics and bioinformatics is highly desired.
How to apply:
To apply, please visit Biomedical Science PhD, click 'Apply online' and complete the application form for full-time study with a start date of Sept 2023. Please ensure the reference ‘PhD Studentship Sedgwick: Understanding the roles of admixture and natural selection in phenotypic diversity of the people of Madagascar' is clearly stated on the application form, under the title ‘Outline of your proposed research’. Within this section of the application form, applicants should include a 500-word outline of the skills that they would bring to this research project and detail any previous relevant experience.
Interested applicants should direct initial queries about the project to Dr Jason Hodgson via email: [email protected]. For enquiries regarding the process and eligibility please contact [email protected].
Interviews will be scheduled for June 2023.
We value diversity at Anglia Ruskin University and welcome applications from all sections of the community.
Closing Date – 26 May 2023.
Cardiovascular, Translational Biomedicine
Background: Macrophages play a critical role in homeostasis and diseases. They can change their phenotype to perform differential activities in different phases of inflammatory response.
Polarized macrophages are broadly classified into two groups:
It has been demonstrated that M1/M2 switch plays critical role in inflammation which is dependent on various factors such as bioavailability of different subsets of monocytes and macrophages, sequential monocytes recruitment into the tissue in the process of inflammation or response to different conditions. Furthermore, the misbalance of M1/M2 switch can lead to chronic inflammatory diseases. Undoubtedly the generation of novel anti-inflammatory drugs regulating M1/M2 switch is an important step for pharmacological intervention of chronic inflammatory-based diseases. Unfortunately, the current drug screening strategies are not based on macrophage polarization. The development of a phenotypic macrophage high-throughput assay will provide a platform for screening of pro or anti-inflammatory properties of the candidate molecule (preclinical drug validation) or FDA approved drugs library and selected compound libraries with known anti-inflammatory activity (clinical drug validation).
Main goal and objectives: The main goal of the study is to develop and validate a novel phenotypic macrophage high-throughput cell-based assay for anti-inflammatory drug screening activity. The two main objectives are:
Methodology: Cell culture and cell-based essays, western blotting, ELISA approaches.
Collaborations: This project is based on academic and industrial collaborations with Reading University and Innaxon, UK respectively.
Outcomes: Results from this project will evaluate the potential of the phenotypic macrophage high-throughput assay for drug screening as well as provide important information about the effect of the candidate molecules on macrophage polarisation and will contribute to their preclinical/clinical validation. This will represent a finding of great public and commercial impact as currently there are no macrophage cell-based phenotypic assays for drug screening. The proposed project will have a commercial value and we plan to secure protection of the arising intellectual property.
This project is self-funded.
Details of studentships for which funding is available are selected by a competitive process and are advertised on our jobs website as they become available.
If you wish to be considered for this project, you will need to apply for our Biomedical Science PhD. In the section of the application form entitled 'Outline research proposal', please quote the above title and include a research proposal.
Cardiovascular, Translational Biomedicine
Background: Toll-like receptors (TLRs) serve as pattern recognition receptors within the immune system. Among these receptors TLR4 is activated in response to bacteria and other non-bacterial ligands such as heat shock proteins, small fragments of hyaluronan, and even oxidised low density lipoproteins (oxLDL) in immunocompetent cells. TLR4 expression has been described in monocytes and microphages. TLR4 and different macrophage subsets have been shown to be implicated in inflammatory related diseases suggesting that understanding mechanisms of modulation of TLR4 signalling may be of great importance for pharmacological treatment of atherosclerosis.
Although existing TLR4 antagonists have been discontinued from clinical trials due to lack of efficacy, recently, a novel compound family designed as small molecule TLR4 antagonists have been developed to specifically modulate TLR4 signalling. We have recently shown that one of these molecules (AXO-102) negatively regulated in vivo and in vitro TLR4 signalling in vasculature and inhibited early rupture and incidence of aneurysms formation.
Main goal: This project will investigate the potential of IAXO-102 and other mimetic molecules to modulate the macrophage polarisation (formation of specific subsets) in response to sterile inflammation.
There are three main objectives:
Methodology: Cell culture and cell-based essays, western blotting, ELISA and antibody array approaches.
Collaborations: This project is based on academic and industrial collaborations with Reading University and Innaxon, UK respectively.
Outcomes: The results from this study will validate the potential of novel TLR4 antagonists as candidates for pre-clinical studies for pharmacological intervention of atherosclerosis.
This project is self-funded.
Details of studentships for which funding is available are selected by a competitive process and are advertised on our jobs website as they become available.
If you wish to be considered for this project, you will need to apply for our Biomedical Science PhD. In the section of the application form entitled 'Outline research proposal', please quote the above title and include a research proposal.
Cardiovascular, Translational Biomedicine
Various disease states damage the function of blood vessels, including diabetes, atherosclerosis and bacterial infections. The level of injury is dependent on the physiological insult and vascular bed. Maintenance of an intact endothelium is vital to prevent infiltration of immune cells or fluids. Platelets interact with the endothelium under conditions where the vessel wall is damaged, resulting in adhesion and aggregation of platelets to form a clot and arrest bleeding. The cell signalling mechanisms which regulate endothelial integrity and platelet aggregation are currently studied however the precise molecular mechanisms resulting in breakdown of barrier integrity and subsequent platelet interactions is not wholly understood.
The project will investigate novel mechanisms which regulate the cross-talk between the platelets and endothelium in settings of vascular disease. In particular, the research will focus on systemic factors associated with diet and the microenvironment at sites of vascular injury.
Research methods will include cell culture and platelet aggregation studies, as well as biochemical assays such as Western blotting and PCR analysis.
This project is self-funded.
Details of studentships for which funding is available are selected by a competitive process and are advertised on our jobs website as they become available.
If you wish to be considered for this project, you will need to apply for our Biomedical Science PhD. In the section of the application form entitled 'Outline research proposal', please quote the above title and include a research proposal.
Atherosclerosis is a disease of the arteries which develops from localised inflammation in the artery wall. This occurs concomitant with a build-up of fatty deposits, dead cells and mineral deposits at these sites. Everyone develops some degree of atherosclerosis and overtime, depending on genetic and lifestyle factors such as a fatty diet and exercise, these lesions can become weak and rupture. A ruptured lesion will cause localised blood clotting. These clots can break away from the vessel wall and migrate with the blood flow to smaller arteries where blockage can occur, causing vascular diseases such as heart attacks, stroke and peripheral limb ischaemia. Currently, 420 people a day in the UK will die from cardiovascular diseases, with 7 million people living with the consequences of the disease.
Atherosclerotic inflammation and mineralisation are considered to be the end points of the development of atherosclerotic lesions. Thus, these two processes have the potential to be used as markers of atherosclerotic lesions likely to rupture, and may help in indicating patients at risk of developing the clinical consequences (heart attack and stroke). The mineral deposits in atherosclerotic lesions are formed from calcium hydroxyapatite deposition in a manner similar to bone formation. Bone material is produced by osteoblasts and osteoblast-like cells have been found in atherosclerotic lesions. These cells are thought to arise by the transformation of the resident vascular smooth muscle cells to an osteoblast-like phenotype. However, the biological processes regulating the cell transformation and subsequent mineralisation remain unclear.
This project will investigate novel mechanisms by which mineralisation occurs during the development of atherosclerosis and in particular, the role that localised inflammation plays in this process. The main objectives are to:
Research methods will include cell culture studies and biochemical assays including Western blotting, ELISA and qPCR analysis.
The expected outcome is an improved understanding of the processes by which vascular smooth muscle cells are induced to adopt an osteoblast-like phenotype and in particular, the signalling mechanisms involved.
This project is self-funded.
Details of studentships for which funding is available are selected by a competitive process and are advertised on our jobs website as they become available.
If you wish to be considered for this project, you will need to apply for our Biomedical Science PhD. In the section of the application form entitled 'Outline research proposal', please quote the above title and include a research proposal.
Cardiovascular, Connective tissue, Translational Biomedicine
Osteoarthritis (OA) is the most frequent of the arthritides with an incidence of 1 in 10 in those over 60 years of age. The disease is typified by the degradation and chronic loss of the cartilage that covers the ends of the bones. Currently, there is no cure for osteoarthritis beyond pain relief and joint replacement. Hyaline cartilage functions by providing both low friction surfaces in the joint and impact absorbance during locomotion. Chondrocytes are the principal cell type of hyaline cartilage and produce the extracellular matrix (ECM) which, provides the tissue with the capacity to resist mechanical load. The progression of the disease is characterised by an irreversible loss of the tissue and by chondrocyte cell death.
Osteoarthritis is linked most frequently to the “wear and tear” processes accompanying a lifetime of joint use and episodic joint inflammation. This project will investigate novel mechanisms involved in cartilage degradation and in particular, the intracellular signalling pathways, which regulate the degradative processes.
This project will investigate the mechanisms by which cartilage is induced to degrade, using cell culture models. The main objectives are to:
Research methods will include tissue and cell culture studies, and biochemical assays including Western blotting, ELISA, zymography and qPCR analysis.
The expected outcome is an improved understanding of the signalling mechanisms involved in cartilage degradation, which may identify future therapeutic targets for reducing the degradation of cartilage in the arthritides.
This project is self-funded.
Details of studentships for which funding is available are selected by a competitive process and are advertised on our jobs website as they become available.
If you wish to be considered for this project, you will need to apply for our Biomedical Science PhD. In the section of the application form entitled 'Outline research proposal', please quote the above title and include a research proposal.
Around 12 million people in the UK are diagnosed with respiratory diseases such as obstructive pulmonary disease, respiratory distress syndrome and pulmonary hypertension. Patients with respiratory disease suffer from a range of pathologies, such as hypoxia and pulmonary edema, associated with cardiovascular complications and increased mortality. One of the hallmarks of this group of diseases is disruption of the pulmonary microvasculature however despite significant efforts in the field, there is still no effective treatment to reduce this injury in patients with respiratory disease.
In respiratory diseases, there is an increase in oxidative stress and actin remodelling in the pulmonary endothelium, resulting in breakdown of the vasculature. We have identified a novel protein in the pulmonary endothelium, p18/LAMTOR1, which is downregulated in respiratory disease models. Proposed studies are needed to understand the mechanism through which this novel protein maintains a healthy endothelium. The research question for this PhD project is therefore: does p18/LAMTOR1 regulate oxidative stress and actin remodelling in the pulmonary endothelium? Proposed studies will address a new area of research which will develop our understanding of p18/LAMTOR1 in the endothelium and provide data to support a potential therapeutic target to improve microvascular function in patients with respiratory diseases.
Research will be performed using a range of in vitro techniques with healthy pulmonary arterial endothelial cells (HPAEC) to measure the role of p18/LAMTOR1 in regulating oxidative stress, actin remodeling and barrier function in the pulmonary endothelium.
Findings are anticipated to establish p18/LAMTOR1 as a key protein which regulates the pulmonary endothelium. The PhD will give insight into the mechanism through which p18/LAMTOR1 maintains the endothelium and expand our understanding of the novel role of the protein in the lung. Studies are anticipated to implicate p18/LAMTOR1 as a therapeutic target in maintaining a healthy endothelium.
This project is self-funded.
Details of studentships for which funding is available are selected by a competitive process and are advertised on our jobs website as they become available.
If you wish to be considered for this project, you will need to apply for our Biomedical Science PhD. In the section of the application form entitled 'Outline research proposal', please quote the above title and include a research proposal.
Increased gastric permeability is associated with metabolic diseases such as diabetes and obesity. Maintenance of a healthy, intact intestinal epithelial barrier is vital to prevent inflammation and septicemia seen in these diseases. The intact barrier is preserved through the formation of junctional complexes between intestinal epithelial cells. We have recently shown that the activation of sweet taste receptors, by sweeteners, increases leak across the intestinal epithelium by breakdown of these junctional complexes. We have further demonstrated that sweeteners increase the ability of model bacteria, in the gut microbiota, to damage intestinal epithelial cells. In contrast, far less is understood about bitter taste sensing in the intestinal epithelium, despite the high number of bitter taste receptors in the G-protein coupled receptor family. Interestingly, increased expression of bitter taste receptor T2R38 observed in the specialized gastrointestinal tract cells of obese patients. Preliminary studies from the laboratory, using intestinal epithelial cells, show that stimulation of T2R38, by phenylthiourea, increases breakdown of tight junctions maintaining the epithelial barrier and increased leak. The research project will therefore address the hypothesis that bitter taste sensing regulates the intestinal epithelium through acting on microbiota and intestinal epithelial cells. By understanding the mechanisms regulating these processes, we aim to develop novel therapeutic targets to improve intestinal epithelial barrier function and therefore reduce inflammation and septicaemia in patients with metabolic disease.
To test this hypothesis, studies will be performed using a combination of microbiology and cell culture studies using two model gut bacteria (E.coli NCT, E. faecalis) and a transformed cell model of the intestinal epithelium (Caco-2 cells). These two models, currently used in the laboratory, will be studied as a co-culture using bitter taste agonists to study the functional response. Key outcomes are changes in metabolism or pathogenic effect of bacteria on the epithelium and breakdown of the intestinal epithelial barrier.
Findings from the project will demonstrate the molecular mechanisms through which activation of bitter taste receptors can regulate function of the intestinal epithelium. This investigation is anticipated to demonstrate that taste receptors represent novel therapeutic targets in the treatment of inflammation and septicaemia in patients with metabolic diseases.
This project is self-funded.
Details of studentships for which funding is available are selected by a competitive process and are advertised on our jobs website as they become available.
If you wish to be considered for this project, you will need to apply for our Biomedical Science PhD. In the section of the application form entitled 'Outline research proposal', please quote the above title and include a research proposal.
Dr Arjune Sen (University of Oxford)
Genetics, Bioinformatics
This project aims to explore one of the promising areas of epilepsy genetics: the role of clock genes in development of seizures and its contribution to pharmaco-resistance in epilepsy. Epilepsy is a distressingly common neurological disorder characterised by aberrant bursts of electrical activity in the brain, or seizures, leading to various symptoms, including altered consciousness, unusual behaviours, and uncontrolled movements. Literature shows an apparent link between both seizure frequency and type of epilepsy to the circadian cycle - the internal process that regulates our daily physical, mental and behavioural changes. Circadian rhythm is the result of the expression of a set of clock genes. The interaction, regulation and expression of clock genes is vital for the homeostasis and tuning of many important functions, including the sleep/wake cycle and day/night activity patterns. Recent studies demonstrate that clock genes are altered in neurodevelopmental disorders and identified common associations between seizures and sleep-wake states. The frequency of seizures can be associated to a specific time of the day, for example being highest in the middle of the wake period, thus suggesting an important role of ‘time-of-day’ factors in the expression of the seizures. It can, therefore, be hypothesised that alterations of specific clock genes link to the onset of seizures and to the type of epilepsy. Exploration of whether circadian rhythms control distinct mechanisms of neuronal hyperexcitability might offer new insights into seizure genesis and lead to new therapeutic strategies. One further application will also be to identify specific associations between disrupted clock genes/mechanisms and pharmaco-resistance in epilepsy, which is failure to achieve seizure control with anticonvulsant medications. Specific associations between altered clock genes/mechanisms and epilepsy will serve as biomarkers of vulnerability to epilepsy and pharmaco-resistance and will facilitate the development of personalized treatments in the longer run.
To address the aims and objectives of the proposed study, data from the 100,000 genomes project, led by Genomics England, will be used. The neurology domain of the Genomics England project (GEL) comprises the whole-genome sequencing (WGS) data of thousands of people with epilepsy, including their detailed clinical information and family history. We already have access to the GEL research environment and any new projects are readily approved by the GEL research team. The whole-genome sequences of epilepsy cases will be screened for rare variants in a curated list of clock genes by utilizing different bio-informatic tools involved in next generation sequencing data analysis. The variants will further be analysed for different parameters, including their frequency in different public databases and their pathogenicity, which will be evaluated using in-silico tools. The final set of credible clock gene variants will be clinically evaluated using the available clinical information of these cases.
Better understanding how circadian mechanisms contribute to regulation of seizures would have important clinical applications including: i) diagnosing the type of epilepsy, ii) determining specific associations between the onset of seizures and alterations of genes that regulate sleep patterns iii) identifying possible causes for pharmaco-resistance.
This project is self-funded.
Details of studentships for which funding is available are selected by a competitive process and are advertised on our jobs website as they become available.
If you wish to be considered for this project, you will need to apply for our Biomedical Science PhD. In the section of the application form entitled 'Outline research proposal', please quote the above title and include a research proposal.