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The Pusztai affair is a controversy that began in 1998. Scientist went public with the initial results of unpublished research he was conducting at the in Aberdeen, Scotland, investigating the possible effects of upon rats. Pusztai claimed that the genetically modified potatoes had stunted growth and repressed the rats' immune systems while thickening their gut mucosa.
Initially supported by the Rowett Institute, his comments on a British television programme caused a storm of controversy and the Rowett Institute withdrew its support. Pusztai was suspended and misconduct procedures were used to seize his data and ban him from speaking publicly. The Institute did not renew his annual contract and Pusztai was criticized by the British Royal Society and some other scientists for making an announcement before his experiment was complete or peer-reviewed, and for the experiment's design, methodology and analysis.
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Some of the data from the study was eventually published in The Lancet in 1999 after five out of six peer reviewers approved of the study – triggering further controversy. Contents.Background Before 1995, no peer-reviewed studies had been published investigating the safety of using human or animal feeding trials. In 1995 the Scottish commissioned a £1.6 million three-year research study to assess the safety of. The potatoes had been developed by biochemist John Gatehouse at Cambridge Agricultural Genetics (later renamed Axis Genetics) and had recently completed two years of field trials at. The GNA gene from the (snowdrop) plant was inserted into the potato, allowing the GNA to be. This lectin has been shown to be toxic to some insects.Twenty-eight studies were proposed, of which eight were selected for peer review by the.
From these eight the 's proposal was chosen and a combined team of academics from the, the and the Rowett Institute was assembled, and coordinated by Pusztai.Although the tested potatoes were not a commercial variety and not intended for human consumption a contract was signed with Cambridge Agricultural Genetics, which included a profit-sharing agreement, if potatoes developed using this technology were approved and released commercially. In earlier ten-day feeding trials on GNA-fed rats, Pusztai concluded that they did not significantly affect growth, despite some of the small intestine and a slight decrease of gut activity. Experiment The experimental potatoes had been with the (GNA) from the (snowdrop) plant, allowing the GNA to be.
This lectin is toxic to some insects. Rats were fed raw and cooked genetically modified potatoes, using unmodified as. One control group ate an unmodified Desiree Red potato spiked with the GNA snowdrop lectin. Twelve feeding experiments were conducted, ten short-term (10 days) and two long-term (110 days). Before the experiment Pusztai and his team said they expected no differences between the rats fed modified potatoes and rats fed the non-modified ones.The potatoes were chosen because they were deemed to non-genetically modified Desiree Red potatoes. The study used two lines of potato, both with the GNA gene inserted.
They were grown in the same conditions as the non-genetically modified parent plant. According to Pusztai, the potatoes were not substantially equivalent, as one of the transgenic lines contained 20 percent less than the other, and the and sugar contents varied by up to 20 percent among the three lines. Pusztai claimed that these differences were reason enough to discontinue further experimentation.Their experiment showed a difference in the thickness of the stomach. The mucosa of rats fed raw or cooked potato modified with the GNA gene was thicker than that of rats fed the unmodified potato. The length in the was greater on rats fed the raw modified potato, although there was no statistical difference observed in the rats fed the cooked potato. As these effects were not observed in rats fed the control potatoes spiked with GNA, Pusztai concluded that the differences were a result of the transformation procedure, rather than the presence of GNA.
Pusztai's collaborator Stanley Ewen said that the used as a could likely be the cause of the observed changes. Announcement On June 22, 1998 Pusztai revealed his research findings during an interview on 's current affairs programme titled 'Eat up your genes'. He was given permission to do the interview by Rowett Institute Director Philip James. Rowett's press officer was present at the start of filming. During the interview Pusztai said he had 'concerns that some of the testing techniques are not up to what we thought it was necessary to do, and therefore we should have more testing.' When asked why he felt concerned, he said 'it was because we had done some experiments which made us feel concerned' and discussed his results in general terms.Pusztai later said that at the time of the interview he was not sure if he should reveal results from experiments that had not been completed and did not think the programme would be hostile toward genetically modified food. He estimated that the experiments were 99 percent complete when the interview was conducted.
He said that the rats in his experiments suffered stunted growth and had suppressed immune systems and that more safety research was required. He also said, 'If you gave me the choice now, I wouldn't eat it' and it was 'very, very unfair to use our fellow citizens as guinea pigs'. Reaction World in Action issued a press release the day before the broadcast, stimulating numerous phone calls to Pusztai and the Institute from government, industrial, non-governmental and media organisations. James says he was dismayed that unpublished data had been released and withdrew Pusztai from any further media commitments that morning. He eventually suspended Pusztai, used misconduct procedures to seize his data, banned him from speaking publicly and did not renew his annual contract.Confusion reigned over just what experiments had been conducted. Pusztai had mentioned two lines of genetically modified potatoes, meaning the two GNA lines, and this was reported by the media.
The Rowett institute mistakenly assumed the media was talking about a second line transformed with (ConA), a lectin that is toxic to mammals. Transgenic ConA Potatoes had been developed, but had never been tested. Two press releases issued by the Rowett Institute on the 10th and 11th praised Pusztai's research and supported increased safety tests on. The press releases also said that the potatoes were modified with ConA, adding to the confusion. Pusztai claimed that he had not seen the press releases before they went out and had no opportunity to correct the mistake. James says that he drafted it and Pusztai rewrote one section, but did not see the final copy.
The mistaken belief that the ConA gene was inserted into the potato led scientist and Agricultural Minister to release statements to the media saying that the findings were not surprising, as a known poison had been added to the potato. Some scientists still dismiss Pusztai's work over this error.
Audit The Rowett Institute audited Pusztai's work on 22 October 1998. It concluded that his data did not support his conclusions. In February 1999, 22 scientists from 13 countries, organised by, published a memo responding to the audit. It stated that their independent examination supported Pusztai's conclusions and that he should have been concerned by his findings.Royal Society peer review On 19 February the publicly announced that a committee would review his work. Reporters Laurie Flynn and Michael Sean Gillard claimed that this was an unusual step, as the Royal Society did not normally conduct peer reviews. The data were sent to six anonymous reviewers and the resulting review was published in June 1999. It stated that Pusztai's experiments were poorly designed, contained uncertainties in the composition of diets, tested too few rats, used incorrect statistical methods and lacked consistency within experiments.
Pusztai responded by saying the reviewers had reviewed only internal Rowett reports, which did not include the design or methodology of the experiments. Lancet response The editors of published an editorial in May 1999 in which they denounced all parties involved, criticizing Pusztai for 'unwisely' announcing his results on television and stating that scientists should publish 'results in the scientific press, not through the popular media'; the editorial also denounced the Royal Society's review as 'breathtaking impertinence'. Publication The data were published as a letter in The Lancet in October 1999, co-authored by Ewen. It reported significant differences in the thickness of the gut of rats fed genetically modified potatoes (compared to those fed the control diet), but no differences in growth or immune system function were suggested.The letter was reviewed by six reviewers – three times the Lancet's usual number. Four reviewers found it acceptable after revisions. A fifth thought it was flawed, but wanted it published 'to avoid suspicions of a conspiracy against Pusztai and to give colleagues a chance to see the data for themselves'.
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The sixth, John Pickett of the, also said it was flawed. After consulting with the Royal Society, Pickett publicly criticised The Lancet for agreeing to publish the study. The study, which used data held by Ewen, who was not subject to the veto of Pusztai's work, reported differences in thickness of the gut between control and test subjects, but did not mention growth or immunity problems.The published work was criticised on the grounds that the unmodified potatoes were not a fair control diet and that any rats fed only potatoes would suffer from protein deficiency. Pusztai responded to these criticisms by saying that all the experimental diets had the same protein and energy content, and that the food intake of all rats was the same.
In an interview, Pickett later said that Lancet editor must have had a political motive for publishing the paper because the referees had rejected it. Randerson, James (15 January 2008). The Guardian. The Guardian. Retrieved 5 December 2017. Domingo JL (2007). 'Toxicity Studies of Genetically Modified Plants: A Review of the Published Literature'.
Critical Reviews in Food Science and Nutrition. 47 (8): 721–733. ^ Arpad Pusztai GM Food Safety: Scientific and Institutional Issues Science as Culture, Volume 11 Number 1 March 2002. 2016-02-01 at the. ^ Ewen SW, Pusztai A (October 1999). 'Effect of diets containing genetically modified potatoes expressing Galanthus nivalis lectin on rat small intestine'. 354 (9187): 1353–4.
Murdock, L. L.; Shade, R. 'Lectins and Protease Inhibitors as Plant Defenses against Insects'. Journal of Agricultural and Food Chemistry.
50 (22): 6605–6611. ^ James Randerson January 15, 2008. Pusztai, A.; Koninkx, J.; Hendriks, H.; Kok, W.; Hulscher, S.; Van Damme, E.
M.; Peumans, W. J.; Grant, G.; Bardocz, S. 'Effect of the insecticidal Galanthus nivalis agglutinin on metabolism and the activities of brush border enzymes in the rat small intestine'. The Journal of Nutritional Biochemistry. 7 (12): 677–682. ^ (PDF). 21 August 1998.
Archived from (PDF) on 27 September 2011. James Meikle (5 October 1999). The Guardian. Canadian Health Coalition. 10 November 2000.
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^ Brian Tokar Redesigning life?: the worldwide challenge to genetic engineering Pg 58. The Guardian February 13, 1999 archived Berkeley University. The Economist. Aug 13, 1998.
^ (PDF). 8 March 1999. ^ Enserink, M. 'Science in Society: Institute Copes with Genetic Hot Potato'. 281 (5380): 1124–5. February 12, 1999. ^ Rowell, Andrew (2003).
Don't worry, it's safe to eat: the true story of GM food, BSE, & Foot and Mouth. The Guardian. 12 February 1999. Archived from on September 7, 2011. Cite uses deprecated parameter deadurl=. Nina Vsevolod Fedoroff & Nancy Marie Brown.
Mendel in the kitchen: a scientist's view of genetically modified foods. P. 178. Gaskell, George and Bauer, Martin W., editors, 'Biotechnology, 1996–2000, the years of controversy', p. The GM food debate, National Museum of Science and Industry,. The Guardian, 12 February 1999, Retrieved 12 November 2010. ^ Laurie Flynn and Michael Sean Gillard for The Guardian, October 31, 1999.
Murray, Noreen et al., (1999) The Royal Society, 1 June 1999, Retrieved 28 November 2010. Editors of the Lancet. The Lancet 353(9167):1811, May 29, 1999. Enserink, Martin (1999).
'The Lancet Scolded Over Pusztai Paper'. 286 (5440): 656a–656.
Enserink, M. 'Bioengineering: Preliminary Data Touch Off Genetic Food Fight'. 283 (5405): 1094–5. Kuiper, H.
A.; Noteborn, H. M.; Peijnenburg, A. (October 1999). 'Adequacy of methods for testing the safety of genetically modified foods'. 354 (9187): 1315–1316.
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46: S2–x2.External links. The Guardian. Full account of the affair by Arpad Pusztai.
Potocki–Lupski syndromeOther names17p11.2 microduplication syndromePotocki–Lupski syndrome ( PTLS), also known as dup(17)p11.2p11.2 syndrome, trisomy 17p11.2 or duplication 17p11.2 syndrome, is a involving the of 11.2 on the of human (17p11.2). The duplication was first described as a in 1996. In 2000, the first study of the disease was released, and in 2007, enough patients had been gathered to complete a comprehensive study and give it a detailed clinical description.
PTLS is named for two researchers involved in the latter phases, Drs. And of.PTLS was the first predicted of a ( or ) where both reciprocal recombinations result in a contiguous gene syndrome. Its reciprocal disease is (SMS), in which the chromosome portion duplicated in PTLS is deleted altogether.Potocki–Lupski syndrome is considered a, predicted to appear in at least 1 in 20,000 humans.Symptoms of the syndrome include, and other disorders unrelated to the listed symptoms.
Contents.Characteristics Clinically, PTLS presents as a milder syndrome than SMS, with distinct characteristics, though PTLS can be mistaken for SMS. Both syndromes are characterized by multiple. A key feature which appears in 80% of cases is. Other unique features of Potocki–Lupski syndrome include, abnormal, and.After noting that autism is commonly associated with PTLS, researchers at the and the a PTLS ' where the chromosome segment was duplicated, and examined the of these mice versus those without the anomaly (the ').
One human autism-related symptom is abnormal. The researchers observed that the mice of both sexes had a slight impairment of their preference of a (i.e., a living, breathing mouse) over an one — the average human will prefer the social target — and preferred to explore newly introduced mice instead of familiar ones, unlike the typical human and mouse preference of a friend over a stranger, demonstrating a change in their liking of. They also found that male mice, in some scenarios, showed increased and than the. Anatomically, the engineered mice had a decreased and an alteration in the of several genes in the. Molecular genetics Both Potocki–Lupski and Smith–Magenis syndromes arise through a faulty mechanism. Both appear to involve a 1.3-3.7 chromosome section in that includes the inducible 1 ( ) gene.
Other have been identified within the duplicated section, including, and.In mice of the subfamily, a 32-34 region of chromosome 11 is to 17p11.2, meaning that they contain the same genes in the same order and orientation. This conserved sequence has been exploited to learn more about SMS and PTLS. Through genetic studies on both and humans, it has been discovered that RAI1 is likely the gene responsible for these syndromes.
For example, in one study, it was shown that mice with one copy of the RAI1 gene and 3 copies of each of the other 18 genes in the described region of chromosome 11 appeared and behaved like the control mice with the described region intact. In other words, RAI1 is -sensitive. This provides evidence that it is the number of RAI1 present that affects the symptoms of PTLS and SMS. It is therefore believed that RAI1 is the critical gene involved in these disorders; however, since no cases of RAI1 duplication alone have been identified, this has not been concluded.One group has noted that, in a mouse model, the in the duplicated segment were also, suggesting some new for analysis, including,.
Diagnosis The duplication involved in PTLS is usually large enough to be detected through alone, though there is a high rate. To ascertain the diagnosis when results are unclear or negative, more sophisticated techniques such as analysis and (aCGH) may be used. Management.