Epithelium reconstruction of a tissue engineered oesophagus for therapy of oesophageal atresia

Dr Paola Bonfanti, University College London

Oesophageal atresia (OA) is a severe congenital condition, where instead of connecting the throat to the stomach; the oesophagus ends in a blind-ended pouch, and requires surgical intervention to try to connect the upper and lower parts. One novel treatment option may be a tissue engineering approach, using stem cells grown on an a 3-D scaffold, to create a new biological structure that could be implanted in to patients. This would represent one lifetime therapy, and could have a significant impact on quality of life and cost to the NHS. With an overall objective of developing an implantable oesophageal scaffold, Dr Bonfanti’s aim is to generate the layer of tissue that will line the oesophagus.


Understanding the link between the obesity gene FTO and gut hormones in order to develop targeted preventative and therapeutic strategies for obesity

Professor Rachel Batterham, University College London

In the UK, around 16 million people are obese, a figure which is expected to continue to rise. Obesity is responsible for more than half the Type 2 Diabetes incidence, and a quarter of heart disease cases which results in 3.5 million preventable deaths each year. For a long time, obesity has been considered a result of a lack of will power, however it is recognized by the World Health Organisation as a disease, and much research has shown that a number of factors, such as genetics can make an individual more likely to become obese. Understanding the biology and identifying ways to prevent or treat obesity are key to combating the growing worldwide obesity epidemic.

The aim of Professor Rachel Batterham’s work is identify targets to treat and prevent obesity. As head of the UCL Centre for Obesity Research and UCL Hospitals’ Obesity and Bariatric Surgery Services, she is in a unique position to combine laboratory research and clinical studies on patients.

This study has two components; an exercise study of normal weight volunteers to see if exercise can correct the increased appetite and ghrelin levels seen in people with the obesity risk form of FTO, and an investigation of the influence of genetics on the outcomes of bariatric surgery.


Modulation of MER tyrosine kinase (MERTK) signalling in liver failure: a therapeutic strategy to reverse monocyte dysfunction and susceptibility to infection

Dr Harry Antoniades, Imperial College London

Acute liver failure (ALF) is a life-threatening illness that commonly occurs in previously healthy individuals in their 30’s. Infection is very common complication in ALF and is associated with premature death in over 50% of these patients. Dr Antoniades is studying the role of a critical regulator (MER tyrosine kinase) of infection fighting immune cells called monocytes. In ALF, these cells mount inadequate responses to bacteria and are strongly associated with increased susceptibility to infection and increased mortality rates encountered in patients. Currently, the research team is trying to manipulate the function of these immune cells by altering the activity of this regulatory switch in order to boost the function of these cells in human and experimental models of liver failure.


 Preventing Type 1 Diabetes

Professor Molly Stevens, Imperial College London

Type 1 diabetes (T1D) is an autoimmune condition, where beta cells (the insulin producing cells of the pancreas) are destroyed by T-cells, a type of immune cell. This causes problems with controlling the amount of sugar in the blood and results in long term consequences such as nerve damage and kidney failure.  T1D is managed by insulin injections, with no treatments currently available to cure the condition.

In this project lead by Professor Stevens, the researchers are using state of the art approaches to stop the destruction of beta cells. To do this, they are developing tiny particles which can attract the damaging T-cells, and destroy them.  If successful, this will allow beta cells to be protected, and prevent T1D.


Generation of human insulin-producing cells for cell replacement therapy of diabetes

Prof Shimon Efrat, Tel Aviv University       

In both Type 1 and Type 2 diabetes, the insulin producing cells of the pancreas, beta cells, are destroyed or malfunction.  Restoring the function of these cells is central to diabetes treatment, as current therapies cannot prevent the complications of diabetes due to difficulty in regulating blood glucose levels.  Several recent studies have provided evidence of a reservoir of dedifferentiated beta cells, which have lost their function.  These cells could be exploited to try to restore the beta cell population. Previous work by Professor Efrat’s team developed a method to track the dedifferentiation of beta cells and showed that it is possible to redifferentiate them, to cells that are capable of producing, storing and releasing insulin in response to glucose stimulation.  They also identified several pathways involved in the dedifferentiation, and hypothesise that blocking these would help to maintain a population of functional B cells. In this project, the researchers will use small molecules to block these pathways to investigate if the cells redifferentiate and become functional pancreatic beta cells.

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