Module overview
The module comprises an introduction/revision to inflammatory mediators and a detailed survey of the way that they interact in different diseases. This information is integrated in the context of a number of human diseases affecting a range of different tissues within the body. Strategies that are used to devise new therapeutic approaches to inflammatory disease are discussed within each topic.
Aims and Objectives
Learning Outcomes
Learning Outcomes
Having successfully completed this module you will be able to:
- Distinguish the mechanisms of oncogenic activation of Myc and explain how Myc can function as a transcriptional activator or a transcriptional repressor
- Describe how intervention in key signalling pathways may be used to treat inflammatory disease of the CNS.
- Outline the role of mTOR, PI 3-kinase and Ras/ERK signalling in diseases such as cancer and cardiac hypertrophy and describe strategies for tackling the defects in cell signalling that give rise to specific diseases
- Discuss the implications of a sample of current research in this field for our understanding of cellular signalling.
- Explain the physiological roles of the mTOR (mammalian target of rapamycin) pathway in cellular regulation and the immune system, and the mechanisms by which mTOR signalling is activated by hormones and growth factors
- Explain the biological role of cytokines in health and disease and describe the basic function of the different Toll like receptors and cytokine receptors
- Explain the fundamental principles that underlie intracellular signalling pathways, and describe how cell surface receptors activate major signalling pathways such as PI 3-kinase/Akt and Ras/ERK
- Identify members and roles of the Myc/Max family of transcriptional regulators
- Describe how the signalling pathways of cytokine receptors are activated and explain the importance of regulation
- Describe how signals are transduced from cell surface receptors to regulate the transcription of nuclear genes
- Outline the importance of apoptosis during embryonic development and in the maintenance of appropriate cell number.
- Review the possible mechanisms that control the innate and acquired immune responses in the central nervous system
- Explain the similarities and differences between the induction of apoptosis by extrinsic and intrinsic pathways and describe some of the characteristic changes to cellular components during the execution stage of apoptosis
Syllabus
The module comprises an introduction/revision to inflammatory mediators and a detailed survey of the way that they interact in different diseases. This information is integrated in the context of a number of human diseases affecting a range of different tissues within the body. Strategies that are used to devise new therapeutic approaches to inflammatory disease are discussed within each topic.
Learning and Teaching
Teaching and learning methods
The module will comprise of lectures and a final revision lecture (if required), research paper seminars and independent study.
Students will have access to a list of selected literature for further reading around each topic.
The module will comprise of lectures and a final revision lecture (if required), research paper seminars and independent study.
Students will have access to a list of selected literature for further reading around each topic.
Type | Hours |
---|---|
Independent Study | 126 |
Lecture | 24 |
Total study time | 150 |
Resources & Reading list
Internet Resources
Older editions of the last three textbooks are available for free at the NCBI Bookshelf.
Textbooks
H. Lodish et al (2008). Molecular Cell Biology.
Kindt et al (2006). Kuby Immunology.
B. Alberts et al (2009). Essential Cell Biology.
Murphy et al (2008). Janeway’s Immunobiology.
B. Alberts et al (2008). Molecular Biology of the Cell.
Marks et al (2009). Cellular Signal Processing.
Assessment
Summative
This is how we’ll formally assess what you have learned in this module.
Method | Percentage contribution |
---|---|
Literature review with presentation | 35% |
Written assessment | 65% |
Referral
This is how we’ll assess you if you don’t meet the criteria to pass this module.
Method | Percentage contribution |
---|---|
Literature review with presentation | 35% |
Written assessment | 65% |