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"Adopt a Project"
The group have donated thousands of pounds to various research projects over the years, they are listed below |
VEGF165b in Diabetic Retinopathy
| Our September 2002 speaker – Dr Moira Murphy, Director of Research, Diabetes UK, sparked an interest in the "Adopt a Project" scheme. Members felt they would like our fund-raising efforts to be channelled into a specific scheme, rather that for it to disappear into the larger "pot". With this remit, the Secretary contacted the Research Department and obtained details of the scheme, and specifically into three local projects requiring funding. These details were passed to the members at our November 2002 meeting and a vote was taken. We wish we could have funded all of the projects, but could only afford one. The decision was made to donate £1,000 to Dr. Churchill’s project at the Bristol Eye Hospital – The role of VEGF165b in diabetic retinopathy. The project begins on 1 March 2003 and runs until 28 February 2006. Dr Amanda Churchill Phd. FRCOphth. is Consultant Senior Lecturer at Bristol University Department of Ophthamology and runs the Genetics and Childhood Eye diseases clinics at the Bristol Eye Hospital. (See Links page) |  |
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Project summary
New blood vessel growth is critical for the development of severe diabetic retinopathy. This blood vessel growth is stimulated by a vascular growth factor call VEGF. Research has recently discovered a new form of VEGF that appears to block the effects of normal VEGF. This new form (VEGF165b) has a different structure at the end of the molecule and appears to be able to stop vascular cell growth in culture.
This study will measure the expression of VEGF165b in normal and diseased eyes, test whether it is able to prevent retinal blood vessel growth in the laboratory, and whether injection of VEGF165b into the eyes of diabetic animals can prevent or treat retinopathy. |
Dr Harper
| Our March 2004 speaker was Dr Steve Harper, who attended on behalf of our "Adopted Project" VEGF165b in Diabetic Retinopathy. We learned that this research project is a multi-discipline one. Dr Harper is a Kidney specialist. The unwanted microvascular growth caused by VEGF165 is found in Cancer, Kidney and Heart disease as well as in diabetic retinopathy. This growth of small vessels is what gives a tumour a blood supply to enable it to spread and grow. The 165b variant appears to switch off the additional growth. Dr Harper volunteered to speak to us again next year to tell us of any further advances the team make |  |
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Further support
| At the May 2004 meeting it was decided to give further support to the VEGF165b in diabetic retinopathy project at Bristol Eye Hospital. The sum of £2,000 being donated. |  |
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Research Update
A protein present in normal body tissue can prevent further growth in tumours, researchers have found.
A tumour can grow only if its blood supply also expands to provide it with essential nutrients.
The protein, discovered by Bristol University researchers, appears to block the growth of blood vessels past a certain size.
The researchers hope their work, published in Cancer Research, will lead to new cancer treatments.
The key protein is one of a group known as vascular endothelial growth factors (VEGF).
Most forms of VEGF stimulate blood vessel growth, including the new vessels formed as a tumour begins to develop.
However, the Bristol team have identified a form called VEGF 165b, which appears to have the opposite effect by inhibiting the growth of new blood vessels required for tumours to grow above one millimetre in size.
The researchers have also found that this form of VEGF is generally found in many normal parts of the body, including the prostate, but not in prostate cancer.
Starvation
They hope it may eventually be possible to use VEGF 165b to prevent tumour growth by effectively starving it of nutrients.
The Bristol team believe that the fact that the protein is produced naturally by the body could make it more effective than other anti-cancer agents.
Many new cancer therapies are based on starving the tumour of nutrients by attacking the tumour blood supply rather than the cancer cells.
Blocking VEGF using antibodies has recently been shown to be effective in large-scale trials in colorectal cancer in the US.
New blood vessel growth is also necessary for many normal body functions.
These include the development of the embryo and, in adults, wound healing, the development of the placenta in pregnancy and of muscles during physical training programmes.
However, it is thought that adults can live healthily without blood vessel growth for extended periods of time.
This blood vessel growth is controlled by many factors, but VEGF is the most powerful factor.
Researcher Dr Dave Bates said: "Now that we have found out that this protein works in living tissues, we need to find the best way of using it in cancer, with tumour models.
"We also need to try it in models of other diseases where blood vessel growth is necessary, such as diabetes, age-related macular degeneration and arthritis."
Story from BBC NEWS: |
Dr Olga Konopatskaya
 Dr Olga Konopatskaya from the Microvascular Research Laboratory at Bristol University gave the group an update on our “Adopted Project” VEGF165b in diabetic retinopathy.
It was reported that very good progress had been made. The team are now ready for the next stage which includes testing on laboratory mice by a specialist laboratory. |
Two more projects
The group decided to adopt two projects this year, donating £1,000 to each.
Descriptions of the projects are shown below.
CD8 T cells in human type 1 diabetes
CD8 T cells in human type 1 diabetes
Dr Florence Susan Wong, University of Bristol
Studies to increase the understanding of autoimmune disease, to find out why T cells attack and destroy the B -cells in the pancreas, thus causing diabetes.
ChREBP
Carbohydrate-Responsive Element-Binding Protein (ChREBP) as a negative regulator of Pdx-1 Gene expression in Pancreatic Islet B -cell Differentiation and Function
Dr Isabelle Leclerc and Professor Guy Rutter. University of Bristol
Failure of Pancreatic Islet B-cells to produce insulin and to release the hormone in response to elevated glucose concentrations causes diabetes. Mutations in various gene transcription factors are responsible for most forms of a subtype of Type 2 diabetes where islets become "blind" to glucose.
Investigate the role of the newly described (ChREBP) transcription factor with regards to glucose sensing and insulin secretion in Pancreatic Islet B -cells.
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Prevention of diabetic cardiomyopathy
 | | In March 2008 the group presented a cheque for £1,000.00 towards the Diabetes UK Adopt a Project Scheme. We are supporting a project at Bristol Heart Institute researching the prevention of diabetic cardiomyopathy by the vitamin B1 analogue Benfotiamine, a global approach to improve angiogenessis and cardiomyocyte survival. The research is being run by Professor Paolo Maddedu and Dr Constanza Emanueli. |
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