|Funding for:||UK Students, EU Students, International Students|
|Funding amount:||See advert for details|
|Placed On:||5th September 2023|
|Closes:||1st November 2023|
The GW4 BioMed2 MRC DTP is offering up to 22 funded studentships across a range of biomedical disciplines, with a start date of October 2024.
These four-year studentships provide funding for fees and stipend at the rate set by the UK Research Councils, as well as other research training and support costs, and are available to UK and International students.
About the GW4 BioMed2 Doctoral Training Partnership
The partnership brings together the Universities of Bath, Bristol, Cardiff (lead) and Exeter to develop the next generation of biomedical researchers. Students will have access to the combined research strengths, training expertise and resources of the four research-intensive universities, with opportunities to participate in interdisciplinary and 'team science'. The DTP already has over 90 studentships over 6 cohorts in its first phase, along with 38 students over 2 cohorts in its second phase.
The 80 projects available for application, are aligned to the following themes;
Applications open on 4nd September 2023 and close at 5.00pm on 1st November 2023.
Studentships will be 4 years full time. Part time study is also available.
Infection, Immunity, Antimicrobial Resistance & Repair
Phages are viruses that infect bacteria and the most abundant biological entity on Earth. Given the escalating threat of antimicrobial resistance, phages have gained renewed interest for the treatment of bacterial infections, offering a personalised approach to treatment. Using cryoelectron microscopy, our objective is to characterise and subsequently enhance the efficiency of selected phages, expanding their versatility and applicability in the field of medicine.
With the rise of antibiotic-resistant bacteria posing a significant threat to public health, there has been a growing recognition of the potential of bacteriophages (phages) as an alternative or complementary approach to traditional antibiotics. When a phage infects a bacterium, it binds to specific receptors on the surface of the cell and injects its genetic material into the host. It then hijacks the host's machinery, using it to replicate its own genetic material and produce new phage particles. Phages exhibit self-catalytic amplification at the site of infection, ultimately being eliminated from the body when they exhaust their host population. Unlike antibiotics, phages have evolved to infect and kill specific bacteria over millions of years, avoiding the collateral damage to the commensal microbiome. Their abundance, diversity and specificity make them a potent, low-cost, near-limitless resource for personalised antimicrobials.
However, phage therapeutics face two significant challenges. First, the specificity of phages is also their greatest limitation for therapy. Phages must be selected that infect a pathogen specific to a patient. This requires additional time and resources to screen large phage biobanks for appropriate phages, and poses significant regulatory challenges as each phage could potentially require its own authorisation as a medicine, rendering phage therapy time consuming and cost-prohibitive. Second, the innate immune system eliminates phages from the body by recognising specific peptides on the phage surface, thereby diminishing their ability to locate and eradicate target bacteria.
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