On the Biomedical Science MRes - Infection and Immunity pathway you will be taught the essentials of conducting high quality research through a range of core modules as well as gaining a detailed knoweldge in the area of Infection and Immunity before undertaking your research project.
St George's is home to world leading researchers who are tackling some of the greatest health challenges of the 21st century. The MRes is made up of 180 credits, all modules below must be studied and will equip you with the skills and knowledge to conduct high quality research.
|Research methods||15 credits|
|Research project planning and management||15 credits|
|Research project||105 credits|
Specialist module - Infection and Immunity
The specialist Infection and Immunity module is 30 credits and will cover the broad area of infectious disease, taking advantage of active research taking place at St George’s by exploring some of the specific causes of infection such as tuberculosis, malaria, MRSA and viral infections such as HIV. You will learn about the cellular and molecular responses to infection, including innate and adoptive immune responses and those responses that are deleterious.
The module will provide insight into the pathogenesis of infection and the virulence mechanisms involved. It will also demonstrate how an understanding of these processes drives vaccine development, antibiotic treatment and immunotherapy. The module will also provide you with insight into how new sequencing technologies and ‘omics’ methodologies are providing novel insights into the human microbiota, susceptibility to infection, tracking of infectious disease and mechanisms underlying resistance to antibiotics.
Past research projects
The substantive research project is worth 105 credits and you can view past student projects below.
Bioinfomatic approaches to meta-data analysis of drugs and drug targets
Aims: Understand how NF-kB signalling is inhibited during human cytomegalovirus replication.
Brief Overview: Human cytomegalovirus is major human pathogen affecting both immunocompetent and immunodeficient patient populations. We and others have discovered that the NF-kB inflammatory signalling pathway is important for HCMV replication. Moreover, we have discovered a novel mechanism by which we believe HCMV antagonizes NF-kB signalling. Therefore, we will investigate antagonism of NF-kB signalling in HCMV infected cells. The Strang laboratory is an open, welcoming, multi-disciplinary environment. As in previous years, motivated students who work to high standards may see their work published in high quality professional journals.
Methods used for data collection: Standard molecular and cellular techniques for protein and gene expression analysis. Chemical biology and chemical genetics.
Mechanistic characterisation of ADAM 10 activation of reactive oxidant production in the airway epithelium
Aims: The aim of the project is to define and characterise the unprecdented mechanism which couples ADAM 10 activation to thrombin formation and protease activated receptor 1 stimulation.
Brief Overview: Our laboratory is investigated in the molecular basis of allergenicity and understanding how interactions between allergens and infections cause exacerbations of asthma which challenge its clinical management. Recent studies in our laboratory have unexpectedly identified A Distintegrin and Metalloprotease (ADAM) 10 as a key component of a chain reaction in which certain allergens and viruses converge to trigger the production of reactive oxidant species (ROS). This is significant because ROS activate the expression of genes important in allergy and because people with allergic asthma have impaired defences against oxidative stress. An intriguing feature of this chain reaction is that it is a cycle with the potential for self-sustaining activity before it is terminated. The cycle involves the activation of thrombin by what we believe is an unprecedented mechanism. The aim of the project is to define and characterise that mechanism.
Methods used for data collection techniques: A combination of biochemical, cellular and molecular approaches will be used, including fluorescent antibody labelling, SDS-PAGE, Western blotting, siRNA knockdown, enzyme-substrate reactions, and protein purification.
Inflammatory mediator production resulting from interactions between house dust mite allergens and stimulation of virus pattern recognition receptors
Aims: To investigate the relationship between ROS production and inflammatory mediator upregulation in airway epithelial cells following exposure to allergens and virus surrogates.
Brief Overview: We have discovered that the major house dust mite allergen called Der p 1, which is a cysteine peptidase, unexpectedly activates a signalling pathway which converges with the production of reactive oxidants (ROS) triggered when virus pattern recognition receptors (TLR3, MDA5, RIG-I) are stimulated. There is considerable interest in this mechanism because of its potential relevance to the triggering of asthma exacerbations. Transcription factors which promote the expression of cytokines responsible for the development and maintenance of allergy are redox sensitive, and many people with asthma have impaired antioxidant defences leading to oxidative stress and increased gene expression. As a key step in exploring this interaction between allergen- and virus-dependent signalling we now wish to establish which mediators are upregulated.
Methods used for data collection techniques: General cell and molecular biological approaches, Click chemistry, quantitative protein determination, ELISA/chemiluminescent assay, fluorescent antibody labelling, fluorescent intracellular probe labelling and reaction kinetics.
Identification of glucose transporters in the airway epithelium and their role in glucose homeostasis
Aims: To further identify glucose transporter isoforms in the airway and distal lung epithelium and characterise their transport function.
Brief Overview: We have identified some glucose transporters that are important for glucose homeostasis across the airway epithelium (GLUT1, 2 and 10). However, there remain a number of other isoforms that have been identified by transcriptomic screening that may also have important function. This project will investigate the expression of GLUT and SGLT mRNA in primary airway cells and tissue from mouse and human. The abundance and localisation of key isoforms will be investigated using protein biochemistry and histological techniques. The function of these transporters and their role in glucose homeostasis across the lung epithelium will also be investigated using glucose transport assays. The identification of functionally important glucose transporters will be aided by the use of mice in which GLUT isoforms (1,2,5 and 10) and SGLT1 have been genetically knocked out.
Methods used for data collection: Mouse and human airway cell culture, PCR, western blot, immunohistochemistry, glucose flux measurement.
Last Updated: Tuesday, 21 March 2017 09:12