southampton

About

With expertise in regenerative medicine, physiology, engineering, orthopaedics, prosthetics and orthotics, rehabilitation and assistive technologies, epidemiology and clinical trial design, we aim to improve lives by delivering improved treatments, increasing the speed to market of musculoskeletal-focused technology and training the next generation of scientists and engineers.

The population across the globe is living longer, which brings a number of healthcare challenges, especially in musculoskeletal health. The burden of age-related disease and injury is rising rapidly, having a detrimental impact on people’s quality of life and increasing the costs of healthcare provision. Loss of muscle mass and function is the leading reason for loss of independence in later life, and causes impaired mobility, falls, fractures, physical disability, increased insulin resistance and associated co-morbidities, and mortality. The number of hip fractures is expected to rise to 6.3 million by 2050 and the number of diabetic lower limb amputations has now risen to 7,000 per year in the UK and over 70,000 in the USA.

The University is working to meet these challenges by creating networks of experts working in interdisciplinary musculoskeletal health research to develop new technologies, interventions and practices that will have a positive effect on people’s lives:

FortisNet is an interdisciplinary research network of clinical, academic and industrial partners that aims to develop products and services to transform musculoskeletal health. Launched in 2016, we have fostered over 50 new collaborations with other universities from across the UK, the NHS and industry. We have developed courses with national partners to help innovators understand how to bring medical technologies to market, and through investment in interdisciplinary studentships we are working to dissolve discipline boundaries, to train a new generation of life scientists and engineers for the benefit of society.
MyAge (Muscle resilience across the life course: from cells to society) is one of eleven UK Ageing Networks, funded by the Biotechnology and Biological Sciences Research Council and Medical Research Council. Led by the Institute for Life Sciences, together with partners from Birmingham, Nottingham and Imperial, the network will guide the future of muscle resilience research through roadmap development and interdisciplinary collaboration.

Research highlights

Muscle analytics for elite sports

Digital

Future societies and communities

Health and wellbeing

PhD Researcher Dr Devon Lewis is developing a new type of wearable muscle sensor to accelerate injury recovery and performance training in elite sports.

Black and white image of a mother holding her young baby close.

Preventing the transmission of non-communicable disease risk between generations

Health and wellbeing

Research from the Developmental Origins of Health and Disease Centre demonstrates how the diet and lifestyle choices of prospective parents and pregnant mothers can affect the long-term health of their children.

An extreme close-up of the tip of an injection needle, with a drop of nanoclay sitting at the tip.

Using nanoclay gel to regrow, repair and replace damaged cells

Health and wellbeing

Southampton researchers have developed an innovative medical clay that can be used to apply regenerative medicine to patients with musculoskeletal conditions.

People

Dr Janos Kanczler

Lecturer

Connect with Janos

Email: [email protected]

Tel: +44 7584496150

ORCID

Professor Jasmin Godbold

Professor

Research interests

Changes in seafloor biodiversity and ecosystem functioning
Effect of human activities and environmental change on species-environment interactions
Trait-expression in benthic invertebrates

Accepting applications from PhD students

Connect with Jasmin

Email: [email protected]

Tel: +44 23 8059 3639

ORCID

Professor Jaswinder Sethi BSc DPhil FRSB

Professor of Immunometabolism

Research interests

Immunometabolism
Obesity
Metabolic diseases

Accepting applications from PhD students

Connect with Jaswinder

Email: [email protected]

Tel: +44 2381208502

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ORCID

Twitter

Dr Jay Amin BM, MRCPsych, PhD

Assoc Prof in Psychiatry of Older Age

Research interests

Developing our understanding of the role of inflammation in Lewy body dementia and Alzheimer's disease, including how it affects disease progression.
Undertaking cohort studies exploring clinical outcomes in dementia.
Undertaking clinical trials testing novel treatments in dementia.

Accepting applications from PhD students

Connect with Jay

Email: [email protected]

Tel: +44 2380475206

ORCID

Dr Jeff Thompson

Lecturer

Research interests

Evolution of animal body plans
Macroevolution
Molecular Palaeobiology

Accepting applications from PhD students

Connect with Jeff

Email: [email protected]

ORCID

Dr Jennifer Williams

Lecturer

Research interests

Responsible and trustworthy audio processing applied to a variety of domains and use-cases;
Audio AI safety in terms of usability, privacy, and security;
Ethical issues of trust for audio AI (deepfake detection, voice-related rights, and speaker and content privacy).

Accepting applications from PhD students

Connect with Jennifer

Email: [email protected]

Tel: +44 7395826770

ORCID

Dr Jeremy Blaydes

Associate Professor

Research interests

Transcriptional responses to pathways: roles in the causes and treatment of cancer Intra-cellular stress-response pathways are activated in response to potentially deleterious conditions in the cell’s environment. In single celled organisms these pathways are generally involved in ensuring the survival and replication of the individual cell. In complex multi-cellular organisms such as man, they are critical in maintaining the normal function of each organ in the body, and the survival of the organism as a whole. Stress-response pathways play a key role in the patho-physiology and treatment of many diseases, including cancer.At almost every stage of the development of a tumour, cells are exposed to some form of stress. Examples include exposure to toxic compounds or radiation, loss of contact with other cells or the extra-cellular matrix, lack of oxygen (hypoxia), acidic pH, the activation of oncogenes, induction of cellular senescence, oxidative damage or depletion of essential metabolites. In some circumstances, the activation of a stress-response pathway will actually help the tumour cell to survive and proliferate. In other situations the response is cell cycle arrest or programmed cell death (apoptosis), providing a barrier to further tumour development that the tumour may ultimately circumvent through the acquisition of a mutation in one of the genes within the stress-response pathway. The p53 tumour suppressor protein is a key component of one such stress-response pathway, and virtually all cancers loose functionality of the p53-stress response pathway. Many current and prospective treatments for cancer work by either inhibiting, or re-activating stress response pathways.Our work focuses on the role of regulators of gene transcription in the response of cancer cells to stress. We have a long-standing interest in the p53 protein, a stress-activated transcriptional activator. We have also developed interests in other pathways which regulate gene transcription and cancer cell proliferation in response to stress and changes in cell metabolism. We aim to determine the role of these pathways in the development of cancer, and establish the potential for targeting components of the pathways for cancer therapy.Our group is based in the purpose-built Somers Cancer Research Building. Modern, well equipped laboratories provide us with an excellent research environment, and the opportunity to interact with researchers working on related areas of cancer biology.
Some Example Projects: Regulation of HDM2 and HDMX proteins The HDM2 oncoprotein is the major negative regulator of p53 function in the cell. In the late 1990s work from a number of groups, including Blaydes et al , demonstrated that HDM2 could be targeted in cancer cells to re-activate the p53 stress-response pathway. Subsequently, small molecule inhibitors of HDM2 have been developed that show great promise in pre-clinical trials. We have undertaken a series of projects examining how HDM2, and its paralogue HDMX is regulated in cancer cells (see Phillips et al, 2010, 2008, 2007, 2006a, 2006b and Phelps et al 2005, 2003). A particular interest of our work has been how HDM2 and HDMX protein synthesis is controlled in response to cell-signalling pathways in different cell types, and how this affects p53 function in these cells.
Role of CtBP transcriptional repressors in cancer cell proliferation and survival In common with p53, CtBP1 and CtBP2 proteins were discovered through their physical association with a viral oncoprotein. We have shown that CtBPs also interact with HDM2 protein, and can consequently regulate p53 function (Mirnezami et al, 2003). The main function of CtBPs is as transcriptional co-repressors. They are involved in a range of cellular processes, depending upon the transcriptional repressor that recruits them to DNA, and they suppress the transcription of genes that cause apoptosis (reviewed in Bergman et al, 2006a). CtBP activity is modified by UV radiation and glycolytic metabolism, suggesting that CtBPs regulate cell survival in response to cellular stress. From 2004 The Breast Cancer Campaign has funded work in our laboratory to study the role of CtBPs in breast cancer. Our studies have progressed from studies of the basic mechanisms whereby CtBPs control breast cancer proliferation and survival (Birts et al 2011 and Bergman et al 2009, 2006a) to their impact on the response to current chemotherapies (Birts et al 2010) to the demonstration that CtBPs are themselves a therapeutically tractable potential molecular target for cancer therapy (Birts et al 2013). Our group was named Breast Cancer Campaign “Team of the Year 2011” on the basis of this work.

Connect with Jeremy

Email: [email protected]

Tel: +44 2381205170

ORCID