April: I’ve compiled a few articles on GMO monkeys. Once again, knowledge is way ahead of wisdom, and the long term consequences could be…?
I understand how animals can further science, but at this point in our evolution, I also know that these companies have no intention of finding cures. These companies are in the business of research: not the business of cures.
SC issues show cause over release of monkeys
June 20, 2010
KATHMANDU, June 20: The Supreme Court on Sunday issued a show cause notice to the government over the release of rhesus monkeys from Lele Research Center to Shivapuri National Park.
As per the order, the Office of the Prime Minister and Council of Ministers, Ministry of Forest and Soil Conservation and Department of National Parks and Wildlife Conservation will have to furnish clarification over the government´s decision.
A Public Interest Litigation was filed by the Law Students Society of Nepal against the release of genetically modified primates into the park on Friday.
The applicants have argued that the release of 263 monkeys is in violation of national and international environmental laws and principles regarding biological diversity conservation. They have also said that the release violates people´s constitutional right to safe environment and health.
The applicants have requested the court to issue mandamus in the name of respondents to capture all released monkeys and rehabilitate them by adhering to the internationally recognized guidelines and by applying precautionary measures.
They have also requested the court to issue a directive in the name of respondents to draft and issue necessary rules, guidelines and policies to regulate future cases of wildlife rehabilitation.
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Introducing ANDi: The first genetically modified monkey
January 16, 2001 (note date)
Oregon researchers have created the first genetically modified monkey. ANDi, a playful, coffee-colored rhesus monkey born on October 2nd 2000, has been engineered to carry a gene from another species. The work demonstrates that a foreign gene can be delivered and inserted into a primate chromosome. The researchers anticipate that gene insertions in the monkey will lead to primate models of human diseases—like Alzheimer’s, diabetes, heart disease and obesity—that will offer a more robust testing ground for new drugs, gene therapy and modified stem cells.
“Our ultimate goal is to produce human disease models. Primates show human pathology better than mice, which, in many cases, are the only systems we have for modeling human diseases,” says Anthony Chan, of the Oregon Regional Primate Research Center, in Beaverton. The report is published in this week’s issue of Science.
Chan’s goal was to show that a foreign gene can be inserted into a monkey’s chromosome and produce a functional protein. The GFP gene was chosen because the protein it produces emits a fluorescent green glow that can easily be seen through a microscope. Eventually scientists want to insert human disease genes and study disease progression in monkeys, says Chan.
Tissue samples taken from ANDi’s cheek, hair, umbilical cord and placenta confirm that the cells contain the GFP gene and corresponding mRNA; the molecule that bridges the gap between DNA and protein. However, when the tissue was examined under the microscope, no green protein could be seen.
“Maybe the quantity of protein is too small to be seen or maybe the mRNA is not being translated,” says Chan. The team will continue to monitor ANDi for GFP; some transgenic animals do not produce any foreign protein until after the first year.
(LEFT)Virus particles carrying the GFP gene are injected into the unfertilized egg. The gene (white) is released from the virus and incorporated into the chromosome. (RIGHT)About 6 hours after introducing the virus scientists artificially fertilize the egg by injecting a sperm from a male rhesus. The fertilized egg then begins to grow and divide. Two to three days later when the egg has divided twice and become a four-celled embryo it is implanted into a surrogate mother.
Courtesy Oregon Regional Primate Research Center
To create ANDi, Chan and his colleagues injected 224 unfertilized rhesus eggs with a virus carrying the GFP gene. The virus’s job is to integrate the gene into a random site on one of the chromosomes. Six hours later, each egg was artificially fertilized by sperm injection. Roughly half of the fertilized eggs grew and divided, reaching the four-cell stage. Forty were chosen and implanted into twenty surrogate mothers—two per mother. Of these, three healthy males were born and two twin males were stillborn. ANDi was the only live monkey carrying the GFP gene.
Curiously, green fluorescent protein was produced in both stillborn males. Their hair and toenails had a green glow when examined under fluorescent light. It is not clear whether their deaths were due to the protein or to the twin pregnancy, which is rare and risky in rhesus.
It will take considerably more research before monkeys like ANDi are common research animals in the lab. “We need to become more efficient at producing transgenic animals,” says Chan. “We need to learn when is the best time to inject the virus, how long to wait before fertilizing the eggs, and when to implant the embryos. We need to adjust the timing of a lot of steps and make a lot of improvements,” he added.
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“Meddling with the building blocks of life is extremely dangerous,” said Peter Wood, a spokesman for People for the Ethical Treatment of Animals. “It goes right to the core of the research philosophy, which is ‘I can do with animals as I please. I can even change their physiology.'”
Wood also said he doubted the work would yield new discoveries to treat human diseases.
Animal rights activists were critical of the new research.
But Dr. John Strandberg, director of comparative medicine at the National Institutes of Health, disagreed. He said monkeys could prove to be very useful in studying human diseases.
“The genetically modified animals in the lab have been principally mice, which are good but far removed from humans. How relevant their results are to humans is questionable,” he said. “The closer you can get to the human situation, the more accurate are the results you get.”
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Next step — humans?
So now that scientists have put a jellyfish gene into a monkey, do they now want to insert a gene from a non-human animal into a human being?
No, said Schatten. “We don’t support any extension or extrapolation of this work from laboratory animals to humans.”
Several scientists and ethicists interviewed by CNN said they don’t know of anyone who’s interested in inserting animal genes into humans because it could be risky and has no known medical use.
But bioethicist Art Caplan at the University of Pennsylvania said even though no one’s interested now, the work with ANDi is a “baby step to genetically engineering ourselves, but we still have a long way to go.
“The time for the public to discuss the ethics of genetic engineering is now, even though we’re just at the start of the genetic trail,” he added.
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GM monkeys given incurable brain disease
Roger Highfield, Science Editor
Published: 12:56PM BST 19 May 2008
American scientists carried out the experiment – which has been criticised by the RSPCA – as part of research into possible future treatments for Huntington’s disease.
It is believed to be the first time that primates have been genetically modified to have a human ailment.
The achievement by scientists at the National Primate Research Centre could pave the way for creating genetically modified primates with other severe degenerative brain conditions such as Parkinson’s disease, Fragile X and Alzheimer’s disease.
But even researchers accustomed to animal research say working with GM monkeys should only be a last resort
And the RSPCA condemns the creation of primates that were designed to suffer.
“We understand that medical research is vital, but there are many different ways of carrying out research on these diseases without using primates,” a spokesman said. “The animal suffering involved, in our view, would be considerable.”
People are born with the faulty gene responsible for Huntigton’s disease but symptoms typically do not appear until middle age.
They may include uncontrolled movements, mood swings, cognitive decline, balance problems, and eventually losing the ability to walk, talk or swallow. It affects five to 10 people in every 100,000.
There is no known treatment to halt progression of the disease, only medications to relieve symptoms. Death typically occurs 15 to 20 years after onset.
In the journal Nature Dr Anthony Chan and colleagues at Yerkes, part of Emory University, Atlanta, said one of two surviving rhesus macaque monkeys engineered to have the defective gene that causes Huntington’s in humans is alread showing tell-tale symptoms aged just 10 months.
The team chose Huntington’s because the hereditary disease is untreatable.
Researchers often study laboratory animals such as mice to get insights into the underlying biology of diseases and to test treatments. But when it comes to brain disease, rodents come a poor second to monkeys and other primates that are much more similar to people .
“Rodent species can capture some of the characteristics of the disease, but they have not been satisfactory in being able to really capture the essence of the disease,” said Stuart Zola, head of the Yerkes centre. “Now we have a genetically modified nonhuman primate that really has captured the clinical signs that we see in patients with Huntington’s disease.”
The researchers also chose Huntington’s as the disease for creating the genetically modified monkeys with an eye toward simplicity – because it is linked to mutations in a single gene.
Huntington’s disease is one of a number of degenerative diseases marked by build up of a malformed proteins in brain cells.
In all, the Yerkes team engineered five rhesus macaque monkeys to develop the disease. The brains of one set of twins, who died a day after birth, contained clumps of the mutant protein while the lone animal, who died a month after birth, jerked involuntarily.
Recently Prof David Rubinsztein and colleagues at the University of Cambridge announced that they have identified a number of candidate drugs to investigate further which encourage cells to “eat” the malformed proteins that lead to the disease.