Why We Go Deaf, and Get Addicted
Japanese rice could take place of insulin shot
A BOWL OF RICE FOR DIABETICS...
TOKYO
Japanese laboratories have developed rice plants that could free serious diabetes patients from regular insulin injections by promoting their own bodies' production of the key hormone. The genetically modified rice was developed jointly by the National Institute of Agrobiological Sciences (NIAS), private-sector Japan Paper Industries, and Sanwa Kagaku Research Institute.
Fumio Takaiwa, head of the NIAS research team, said it was the first time that a foodstuff had been developed as an effective treatment for diabetes, which afflicts more than 150 million people worldwide, 6.9 million in Japan.
The newly-developed rice strain contains a high level of another hormone, the GLP-1, which promotes the pancreas' release of insulin. The development is "epoch-making...as it enables us to eat the staple food of Japanese, increase insulin secretion, and lower glucose levels in blood," in type 2 diabetics, the three research partners said. A standard Japanese helping of rice at every meal is believed to be enough to control glucose levels.
The project aims at commercializing the rice in two to three years but research director Takahito Jomori at Sanwa Kagaku admitted it could take longer for it to be available to consumers.
...AND A GENE TO PRODUCE INSULIN
JERUSALEM
Israeli scientists say they had successfully used genetically modified embryonic stem cells to produce insulin in mice, which could eventually be used to help treat diabetes.
"This method could in the future be used mainly as a treatment against juvenile diabetes," said Shimon Efrat, Tel Aviv University professor who conducted the research, published in the Proceedings of the National Academy of Sciences.
He said his team had used stem cells from embryonic livers and modified them by introducing a gene that produces insulin. Transplanted into diabetic mice, the cells maintained normal blood sugar levels for several months, he said. The cells could be used within several years to help treat diabetics if a way is found for them to avoid being rejected by the immune system, Efrat said.
SPEAKING FOR THE DEAF
PARIS
Experiments with a batch of engineered mice have shown exciting genetic clues about why humans often suffer from worsening deafness as they get older.
The evidence points to a rodent gene called Ink4d, which plays a role in sensory hair cells in the inner ear. These cells are the magic behind the so-called Organ of Corti, a structure about two inches long that spirals along the cochlea and is the vital link in the ability of mammals to hear. The organ is filled with fluid that moves in response to sound waves.
Thousands of cells with tiny hairs line the organ, and when they move in response to the fluid, they generate electrical signals that stimulate fibers in the auditory nerve connected to the brain. This is how we perceive sound.
The problem is that sensory hair cells do not regenerate once they have been lost: the cells carry on dividing until just after a child is born, and then the process abruptly stops.
So if the cells are damaged by loud noise or-in some individuals-when the cells die off in significant numbers in later life, the result is progressive hearing loss.
Why these cells do not regenerate may now be explained in part thanks to Ink4d, say researchers at the House Ear Institute in Los Angeles. Following up evidence that Ink4d plays a role in preventing cells from dividing, the team created mice whose genetic code had been modified to lack this gene.
Sensory hair cells started dividing among adult mice with the deleted gene. It was not all good news, however: without the restraining influence of Ink4d, the divided cells eventually committed suicide under a process called apoptosis, and the mice became progressively deaf.
The findings are good because they lead to a new understanding about progressive hearing loss and tease out fresh ideas about how it may eventually be cured. It could be, for instance, that an inherited, malfunctioning form of Ink4d could make people more vulnerable to progressive deafness than others. This mutant form of the gene could unleash cell death among sensory hair cells.
The research also throws open the intriguing path of trying to reverse deafness by removing cell-division inhibitors through gene therapy. That would encourage the cells to grow again, but the apoptosis problem, shown in the mice, shows one of the big hurdles that would lie ahead. The study is published in Nature Cell Biology.
UPBEAT NEWS FOR ALZHEIMER'S VICTIMS
PARIS
Victims of Alzheimer's disease may benefit from lithium, a drug that has been used for decades to treat manic depression, research carried out on lab mice suggests.
Lithium prevented the buildup of protein deposits in the brains of rodents that had been genetically engineered to replicate Alzheimer's symptoms, the study published in Nature says.
Researchers led by Peter Klein of the University of Pennsylvania School of Medicine experimented with lithium and kenpaullone-molecules that are known to block the molecular mechanism that forms amyloid plaques and tangled fibrils called tau, which characterize Alzheimer's. These compounds specifically target an enzyme called glycogen synthase kinase-3 (GSK-3).
In a commentary, Bart De Strooper of the Katholieke Universiteit in Leuven, Belgium and James Woodgett of the Ontario Cancer Institute in Toronto said the tests, by using live animals, provided exciting support for previous lab-dish experiments that used lithium against Alzheimer's cells. But a long path lay ahead before lithium or something like it could be used on humans, they said. "A more focused clinical trial will be needed to decide whether lithium-and later more selective GSK-3 inhibitors-becomes a new weapon in the arsenal of drugs to treat Alzheimer's disease."
FROM ENDING TO SAVING LIVES?
PARIS
American and French researchers say the French-made anti-abortion pill is also a potential therapy for treating psychotic depression. Use of the RU486 pill dampens surges of cortisol, a stress hormone that has been linked to this form of depression, they report in the Biological Psychiatry.
The work was carried out by Etienne-Emile Baulieu, the inventor of RU486, and a team from Stanford University in California. A preliminary trial was carried out on a group of 30 volunteers, men and women aged 25 to 74, who were given doses equal or superior to that used to terminate a pregnancy.
Episodes of psychotic depression cannot be controlled by normal antidepressants, and victims of the condition feel so low that many commit suicide.
Baulieu said RU486 "can save lives" in tackling such episodes. "A week's treatment with RU486 helps the patient to overcome the danger, and return to normal medication," he said. But he stressed it was not a therapy for people who suffered chronic manic depression or "reactional" depression to things that went wrong in life. "The role of cortisol secretion in depressions has been studied for more than 20 years... [but] the precise way in which corticoids [adrenal cortex hormones] act on the brain needs further research," he said.
DENGUE AND THE ORIGINAL SIN
PARIS
Scientists believe they can explain why dengue fever, which affects up to 50 million people a year, mainly in tropical developing countries, is such a peculiarly vicious disease.
Someone who is infected twice by the dengue virus often suffers worse symptoms the second time they catch the disease. This is unusual, for it is the reverse of what normally happens when someone is infected again by the same disease-the body is resistant, because the immune system is already primed to attack the invading microbe.
A British-Thai team of immunologists found that the answer lies in the four subtypes of the virus. In Thai volunteers with dengue, those who were infected a second time with a different strain from the first were found to have very few T-cells that had been programmed to fight the new strain. In addition, immune cells were prone to molecular prompts to commit suicide or apoptosis. With many defenses inoperative or weakened, the virus spread more easily and the patient became sicker.
The team, led by Gavin Screaton of John Radcliffe Hospital in Oxford, England, have coined the term "original antigenic sin" to describe how the T-cells are oriented only towards fighting the initial dengue subtype and cannot identify and combat a different strain. "Original antigenic sin" is worrying news for the elusive hunt for a dengue vaccine because someone who is immunized with only one strain of the virus could, thanks to apoptosis, end up in a worse state if they are infected by a different strain.
The task will be to look for specific characteristics called epitopes, on each of the four virus strains that can safely activate antibodies, the immune footsoldiers, which alert T-cells to an intruder, the authors say. "If we can identify enough of these, it may be possible to incorporate them into a dengue vaccine that would improve safety by avoiding potential antibody enhancement or cross-reactivity in T-cell responses," they say.
Around 2.5 billion people live in countries that are vulnerable to dengue.
THE EARLIER, THE MORE DEPENDENT
PARIS
The earlier the age at which smoking starts the greater the degree of nicotine dependency in later life, according to a French study carried out on rats but which results, the researchers led by Pier Vincenzo Piazza said, were "relevant for extrapolation to humans."
The researchers introduced groups of rats to nicotine at two different ages: around adolescence (from about a week before puberty to a few days after it) and in postadolescence. When the rats reached adult age they were enabled to choose for themselves the amount of nicotine they wanted by sticking their snouts into a special hole in their cage. The rodents that had been initiated at the earliest age showed more interest in the nicotine, made more effort to get it, and helped themselves to substantially stronger doses than those that had been introduced to the drug when they were more mature.
The team found changes in some genes of the rats exposed to nicotine before puberty, and suggested these changes accounted for the extra sensitivity to the drug.
The team also said they had discovered the role played by a brain stress receptor in craving for cocaine. They deactivated this receptor (called GR) in a group of rats and mice and then repeated the earlier experiment, replacing the nicotine with cocaine. Rats belonging to a control group with "GR" were addicted: they took regular doses of the drug and their behavior showed clear signs of its effect. The animals without "GR" were much less interested in the drug. "These results are a first therapeutic lead for [treating] cocaine dependency," the researchers say in the Journal of Neuroscience.
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