"UNWITTING CREATOR"
Disgraced Korean scientist Hwang Woo-Suk may have unwittingly created the first human stem cell by parthenogenesis
Japan makes fourth-generation cloned pig
TOKYO
Japanese researchers have created a fourth-generation cloned pig in a world-first achievement that could lead to new transplant treatments for humans. It is the first time that scientists have cloned such a large animal over successive generations, said Hiroshi Nagashima, a bioscientist leading the project at Meiji University.
He said the male pig-whose forebearers starting from his great-grandfather were also cloned in laboratories-was born on July 23 at the university. "This shows that a large mammal can be cloned over multiple generations," Nagashima said. "It had been said that cloning animals over several generations causes problems because the genetic material in the nucleus of the donor cell degrades with each successive generation."
US researchers had earlier cloned sixth-generation mice. But Nagashima said that his project was more useful as a pig is closer to a human being than a mouse. If research in the area progresses, organs and cells of cloned pigs could be transplanted to humans to treat various diseases, he said. One example would be to transplant a cloned pig's pancreas, which produces insulin, to a human diabetic.
Fake real
WASHINGTON
While faking the first human embryo-cloned stem cells, disgraced South Korean scientist Hwang Woo-Suk in 2004 unwittingly created the first human stem cell derived by parthenogenesis. An analysis of Hwang's work published in Stem Cell by Kitai Kim and George Daley of the Children's Hospital Boston Stem Cell Program, shows that the stem cells Hwang obtained contained genetic material only from the donor egg and had not been cloned from a human embryo.
Hwang and his team "unwittingly created something entirely different-the world's first human embryonic stem cell to be derived by parthenogenesis," the two US researchers said. "We now know that the Korean's first supposed nuclear-transfer-derived stem-cell line was actually derived from the woman's egg alone," said Daley.
Parthenogenesis is a method of reproduction, common in plants and in some reptiles, in which the female can generate offspring without the contribution of the male, through artificial activation of unfertilized eggs. Parthenogenesis in mammals is seemingly very difficult.
In cloning, the nucleus of an egg is replaced with the nucleus from a cell in a different body to produce, theoretically, genetically identical embryonic stem cells. That is what Hwang claimed he did in 2004. A year later, however, he confessed that his entire body of research on stem cells published in Science had been faked.
Schizophrenic mouse may aid drug testing
WASHINGTON
Researchers have created a schizophrenic mouse that will allow testing of new drugs and treatments before they are used on humans. The scientists used genetic engineering to create mice whose brain structures and behavior are similar to the two million persons suffering from schizophrenia in the United States.
The new mouse will allow researchers to track the progression of the disease in mice, which parallels the human counterpart. Previously, researchers could only induce the symptoms of schizophrenia, such as delusions, mood changes, and paranoia, by administering drugs.
The mouse model was made possible by the recent discovery of a gene, DICS1, which produces a protein that helps nerve cells take their proper place in the brain. A person or a mouse without it is more prone to suffer schizophrenia, the study said. The new mouse produces an incomplete, shortened version of the DICS1 protein, which interferes with the workings of the brain.
These mice matured with symptoms of schizophrenia. With magnetic resonance imaging, researchers confirmed that their brains shared the structures of schizophrenic mice.
Researcher Akira Sawa of Johns Hopkins University said the engineered mice were not as mentally ill as humans with the disease, because sufferers have more than one genetic defect. "However, this mouse model will help us fill many gaps in schizophrenia research," Sawa said. "We can use them to explore how external factors like stress or viruses may worsen symptoms. The animals can also be bred with other strains of genetically engineered mice to try to pinpoint additional schizophrenia genes."
Breakthrough in multiple sclerosis
PARIS
Investigators reported the biggest breakthrough in decades into the genetic drivers for multiple sclerosis (MS), identifying two genes that each boost the risk of developing this tragic disease by up to 30 percent.
In MS, the immune system attacks myelin, the fatty sheath that protects the cells of the central nervous system, rather like plastic insulation that protects electrical cables. As a result, "short circuits" occur in the body's messaging system, because nerve signals get slowed or blocked. This leads to difficulties in movement and coordination, muscle weakness, cognitive impairment, slurred speech, and vision problems.
Until now, investigations of the human genome have turned up only a cluster of variants of genes on chromosome 6, in the so-called major histocompatibility complex, which regulates the immune system. But these genes were identified in the mid-1970s, leaving frustrated doctors to hunt for other culprits in the complex cascade of processes involved in MS.
The new suspects play a role in guiding key immune cells, called T cells, which patrol the body for intruders. They carry the name of interleukin-7 receptor alpha, or IL7R-alpha, located on chromosome 5, and interleukin-2 receptor alpha (IL2R-alpha) on chromosome 10, which has previously been associated with type 1 diabetes. A single change in the genetic code in IL7R, and two changes in IL2R create the dangerous variants. Each variant appears to boost the risk of MS by between 20 and 30 percent.
"Our finding is very important, because the genetic factors that are already known to be associated with multiple sclerosis only explain less than half of the total genetic basis for the disease," said Simon Gregory, a geneticist at Duke University in Durham, North Carolina, who took part in the IL7R work.
The two studies published simultaneously by Nature Genetics and the New England Journal of Medicine were carried out by two groups of scientists from the United States and Cambridge University, England.
The genetic variants were unearthed thanks to a comparison of more than 20,000 samples of DNA provided by patients diagnosed with MS and those without the disease living in the US and Europe.
"People have been looking for genes involved in MS for 30 years," said David Hafler, a professor of neurology at Harvard Medical School, a lead author on the IL2R study. "Why weren't they found? The answer is, you couldn't do it without the sequence of the human genome."
Gene therapy in pioneering eye operation
LONDON
Doctors at Britain's Moorfields Eye Hospital have carried out the first attempt to cure a sight disorder using gene therapy on 23-year-old Robert Johnson, who was born with an inherited disorder that stops his retina detecting light properly. His condition, which meant he could see only outlines of objects, was getting worse with age, but now it is hoped his sight will improve.
The operation saw surgeons injecting copies of the faulty RPE65 gene into the back of Johnson's eye, a procedure that required pinpoint precision. It was carried out following years of research involving the hospital and the Institute of Opthalmology at University College London.
"We have been developing gene therapy for eye disease for almost 15 years, but until now we have been evaluating the technology only in the laboratory," said lead researcher Prof. Robin Ali. "Testing it for the first time in patients is very important and exciting and represents a huge step towards establishing gene therapy for the treatment of many different eye conditions."
It is likely to be several months before full results of the trial are available.
Mice experiment shows sight adaptation
CHICAGO
An experiment involving genetically engineered mice illustrates how the earliest primates acquired full-color vision tens of millions of years ago, and demonstrates just how adaptable mammalian brains are. By genetically engineering mice with a human gene that codes for a light sensor that the rodents do not usually possess, researchers were able to create transgenic mice that could see in full color.
Mice, like most mammals, have dichromatic vision. They typically view the world with a limited color palette, which in human terms registers yellows, blues, and grays. Their brains did not evolve to handle the more complex color spectrum that among mammals is the unique preserve of primates and which allows humans to see five colors in a rainbow, according to the study published in Science.
To be sure that these transgenic mice could "rewire" their brains to use the new visual information, the researchers used a classic preference test. Mice set before three light panels were trained to touch the one panel that appeared to differ from the other two. A correct answer was rewarded with a drop of soymilk.
The genetically engineered mice chose the correct panel in 80 percent of the trials, while a "control" group of normal mice chose correctly one third of the time-a score that could be arrived at by guessing randomly among the three panels.
The new abilities of the genetically engineered mice indicate that the mammalian brain possesses a flexibility that permits a nearly instantaneous upgrade in the complexity of color vision, the authors of the study wrote.
"If you gave mice a new sensory input at the front end, could their brains learn to make use of the extra data at the back end?" said Jeremy Nathans, a professor of molecular biology and genetics, neuroscience and ophthalmology at Johns Hopkins School of Medicine. "The answer is, remarkably, yes. They did not acquire additional generations to evolve new sight."
The experiment mimics how our earliest primate ancestors acquired trichromatic vision, by "engineering" genetic changes that made the mice produce a third photoreceptor that registered longer wavelengths of light, Nathans said. "What we are looking at in these mice is the same evolutionary event that happened in one of the distant ancestors of all primates and that led ultimately to the trichromatic color vision that we now enjoy."
Mammals that have trichromatic vision have three types of light- sensitive cells in the retina fine-tuned to wavelengths that appear blue, green, and red. Researchers think this kind of vision evolved about 40 million years ago, or more, when an early ancestral primate inherited an additional, or third, photoreceptor thanks to random mutations that created a variant of one receptor gene located on the X chromosome.
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