Current Portfolio
- Epilepsy
- Bone disease
- Nanotoxicity testing
- Abdominal pain studies
- Brain cell imaging
- Huntington's disease
- Breast Cancer
- Viral encephalitis
- Chronic pain in arthritis and fibromyalgia
- Bacterial infection in cystic fibrosis
- Advances in human neuroscience
- Neurofibromatosis
- Hypersecretion of mucus in asthma
- Premature birth
- A clearer picture of pain relief
- Tissue engineering of human liver
- Creating knockout tissues
- Skin cancer
- Magnetoencephalography (MEG)
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Premature birth
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2007 – 2010 Research Assistant Development of a human tissue model for investigating uterine functionDr Rachel Tribe & Professor Michael Taggart |
Dr Rachel Tribe is a Senior Lecturer in Cell Signalling at the Maternal and Fetal Research Unit of St Thomas’ Hospital, King’s College London.
Professor Michael Taggart holds the Chair of Reproductive Sciences at the Institute of Cellular Medicine, Newcastle University.
Problematic labour, which includes dysfunctional labour and preterm labour, affects approximately 30% of all pregnancies in the UK and is associated with high rates of maternal and fetal mortality. Both conditions are linked with inappropriate activation of uterine muscle. To develop better therapeutic strategies for treating problematic labour, more needs to be known about how human uterine muscle is regulated during pregnancy and labour.
Much research into uterine function has been conducted on pregnant animals, as an appropriate ex vivo human model is lacking. There is an over-reliance on the use of transgenic mice for determining the functional impact of individual genes in human biology. There are inherent problems with this approach as mice do not represent a good model for human pregnancy.
The main aim of this Dr Hadwen Trust-funded project, therefore, is to address this issue by developing a validated method for transfecting human uterine smooth muscle tissue, to alter gene expression and contractile function. This new model will subsequently be employed to determine the contribution of signalling events to uterine contraction; and to assess the role of inflammatory cytokines implicated in preterm and term labour.
The development of this human tissue model will provide an alternative to genetically modified animals and other in vivo animal ‘models’ of preterm labour. The research will be useful to the wider scientific community and will, potentially, be employed to determine the efficacy of therapies designed to stop preterm labour.