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Manchester University picketed over 'pitiless and medically irrelevant' GM mouse experiments
Posted 11 March 2013
- Animal Aid brands Manchester University GM mice research programme as ‘pitiless, shameful and medically irrelevant’
- Genetically modified mice with extreme heart damage forced to endure punishing ‘swimming’ regime
- Others, with severe neurological damage, are forced to hold on to hanging wire
- More than 46,000 mice used by the University in just one year
- Evidence shows that ‘reprogrammed’ rodents fail as models for human heart disease
- For every GM mouse used in an experiment, hundreds more die or are killed
A Reality TV roadshow is coming to Manchester on Tuesday 12 and Wednesday 13 March to expose a long-running series of experiments on genetically modified mice conducted at Manchester University.
The centrepiece of the two-day Animal Aid visit is a converted ambulance emblazoned with stark protest imagery and messages. A three-minute film, which includes footage of a variety of GM mouse experiments, will be screened continuously from the side of the vehicle. The ambulance will be stopping at numerous locations around the city and the university, reaching as many residents and students as possible. The protest marks the start of a determined campaign with a simple objective – to bring an end to the experiments.
The Manchester experiments that focused on heart disease have been funded in large part by the British Heart Foundation. They have involved genetically altering mice so that they are prone to develop heart failure. Some were then subjected to a crude surgical procedure, which led to the heart growing unnaturally and failing to pump effectively. A similar effect was achieved in other mice through a constant administration of drugs. For a number of these reprogrammed and damaged mice, the torment continued when they were forced to swim for up to 90 minutes twice a day for 28 days. Mice dislike swimming, and are reported to have a fear of drowning.
Despite years of such research, benefits for human patients are still nowhere in sight. An accurate representation of human heart failure and other cardiovascular diseases cannot be reproduced in mice for many reasons. Apart from the obvious genetic1 and physiological differences, a mouse heart beats at 600 times per minute compared with the human average of 72. In addition, notes Animal Aid’s scientific Briefing on the Manchester experiments, ‘the damage induced in the animals is fundamentally different from the human disease it supposedly “models” ’. The Briefing goes on to set out examples from the scientific literature where apparently promising results from heart disease experiments on GM mice failed to translate into clinical progress.
There are numerous productive non-animal methods of conducting heart disease research. They include the use of stem cells, microarrays (small membranes of slides containing samples of genes), computer modeling, as well as more traditional clinical, autopsy and epidemiological studies2.
In a separate series of experiments – whose declared purpose was to ‘advance our knowledge’ – a strain of mice was created by disabling (‘knocking out’) a gene known to be essential for life. The resulting progeny had reduced brain size and suffered severe loss of coordination, whole-body tremor and other symptoms. To test the extent of the damage, the mice were turned on their backs to see how long it took them to right themselves, and also forced to hold on to a hanging wire. These mice were so severely brain-damaged that they generally died within three weeks of birth.
In 2011, the university acknowledged that it had used and killed more than 46,000 mice, a high proportion of whom were genetically modified. Unrecorded were the many mice killed because they were ‘surplus’ or ‘failures’.
The Manchester protest comes in the wake of the publication last month of a landmark new Animal Aid report called Science Corrupted: the nightmare world of GM mice. Drawn from mouse researchers’ own papers published in scientific journals, the report concludes that the UK-wide research programme to tackle major human diseases by breeding and experimenting on genetically modified mice has become ‘frenzied, scientifically irrational and terrifyingly cruel’.
Says Animal Aid’s Scientific Consultant, Dr Adrian Stallwood:
‘The Manchester experiments are “basic” research, involving the laboratory destruction of animal physiology and anatomy in the hope of finding out something clinically relevant. It represents the primacy of curiosity over compassion, with both human patients and animals suffering. The research can fairly be described as pitiless, shameful and medically irrelevant. Much of the funding for the heart research comes from the British Heart Foundation – a charity that depends on the goodwill of the general public. That public has been poorly served. We urge Manchester University to take the humane and rational step of ending these experiments immediately.’
- Read Animal Aid’s scientific Briefing on the Manchester experiments.
- Read Science Corrupted and watch a short film about GM mouse research, including footage of a variety of GM mouse experiments.
- For more information or to arrange an interview, call Andrew Tyler: 01732 364 546.
- Dr Adrian Stallwood MBBS is a specialty doctor in emergency medicine in West Wales, and a clinical teacher of medical undergraduates at Cardiff University.
Notes to Editors
- Mice share around 80 per cent of genes with human beings but the way those genes function and are regulated varies greatly in the two species. Adding or subtracting a gene or two (the main alterations done to GM mice) does not overcome the fundamental biological differences between humans and rodents. And, as important as genes might be, they represent a tiny fraction (about 2 per cent) of a person’s DNA that – in sum total – governs his or her development and functioning.
- For more details of non-animal research methods, see: Our Non-animal Research Methods for Cancer, Cardiovascular Disease, Parkinson's Disease and Alzheimer's Disease factsheet.