Once again the cure is as bad as the illness. It seems as if going green can really cause someone to turn green. Those reusable grocery bags can make you sick.
Remember the good old days, when you went to the grocery store and brought food home in brown paper bags. Those bags were great, they had so many uses once you brought them home, everything from "trick or treating," to trash bags. Heck, they even inspired a popular comedian "The Unknown Comic"
Throughout my school years every text book I had was named Walbaums, because they were protected by brown paper bags from my mom's favorite Supermarket.
But those bags used paper and the environmentalists wanted to save the rain forests so they switched to those thin plastic bags. The plastic could still be used for Halloween, and are perfect for your wet bathing suits when coming home from the beach. But plastic uses petroleum and take centuries to decompose so the environmentalists didn't like them either. To be honest neither do I, they aren't really strong enough to hold the groceries without tearing.
Enter the reusable grocery bags, they are good for groceries and Halloween, but you can't use them for book covers. It doesn't kill trees and will slow the build-up of plastic in the land fills. The only real problem with them is they are great incubators of E.coli, and salmonella
Tests on shoppers' bags revealed half contained traces of E.coli, a lethal toxin which killed 26 people in Scotland in 1996 in one of the worlds worst food poisoning outbreaks.
Scientists also found many were contaminated with salmonella.
Researchers blame the fact that consumers do not realise reusable bags need to be washed regularly at high temperatures to kill off bugs deposited by raw meat packaging.
They warned the levels of bacteria they found were high enough to cause a wide range of serious health problems and even death.
Think of it this way, the environmentalists may save the rain forests, and clean up land fills, with the unintended consequence of killing children, as kids are particularly vulnerable to the effects of organisms such as E.coli.
The tests were carried out by experts at the University of Arizona, who stopped a total of 84 shoppers in Tucson, Los Angeles and San Francisco to check the state of their bags.
The popularity of reusable eco-friendly shopping bags has soared in Britain, as in the US, as the growth in the recycling culture means fewer consumers rely on disposable plastic bags.
Many of the new bags are made from jute or woven polypropylene.
But while they are better for the environment, the new research suggests they could be harmful to health if not cleaned regularly.
Oh and the hotter the climate, the worse the contamination so imagine what will happen if Al Gore is telling the truth (about climate change, not that massage in the hotel)
Professor Charles Gerba, who led the study said: "Our findings suggest a serious threat to public health, especially from bacteria such as E.coli, which were detected in half of the bags sampled.
"Consumers are alarmingly unaware of these risks and the critical need to sanitise their bags on a weekly basis."
A poll revealed 97 per cent of shoppers who used eco-friendly bags never washed or bleached them.
Here's an idea, throw out the reusable bags and the plastic and lets go back to the best option of all, paper bags. Think of all the trees and plastic we won't be using for book covers.
Thursday, July 1, 2010
Saturday, June 5, 2010
Two Drugs Appear to Surpass Landmark Novartis Leukemia Treatment
By PETER LOFTUS
CHICAGO—Novartis AG's Gleevec is one of the closest things to a miracle drug to come out of the battle against cancer in recent years. But new research suggests two newer drugs are even more effective for the form of leukemia whose treatment Gleevec has transformed.
In separate studies published Saturday, Bristol-Myers Squibb Co.'s Sprycel and Novartis's Tasigna each were superior to Gleevec in treating people with newly diagnosed chronic myeloid leukemia. The two newer drugs are currently approved to treat patients whose disease persisted after trying Gleevec.
The new studies could help widen the patient populations for both Sprycel and Tasigna if doctors begin choosing them over Gleevec for newly diagnosed patients.
Switzerland-based Novartis has already applied for regulatory approval to market Tasigna as a first-line treatment, and New York-based Bristol said it is in the process of doing so for Sprycel. Some doctors may not wait for formal regulatory approval to try the newer drugs as first-line treatments.
But some doctors might still stick with Gleevec until Tasigna and Sprycel can demonstrate a long-term survival advantage over Gleevec. Also, Gleevec could be viewed as a more cost-effective option when the drug loses patent protection and cheaper generic versions become available in coming years.
"We don't know yet about long-term survival," said Sonali Smith, oncologist at the University of Chicago Medical Center. "We probably won't have that data for quite some time."
Gleevec was introduced in 2001 and quickly became the standard of care for people newly diagnosed with CML, a cancer of the blood, based on its ability to induce remission and significantly improve survival versus older drugs, with relatively low toxic effects.
Studies have shown at least 80% of Gleevec users were still alive eight to 10 years after beginning therapy, much higher than the historical survival rate of less than 20% for CML patients before Gleevec. Gleevec had world-wide sales of $3.9 billion last year.
But not all patients improve on Gleevec, and newer drugs were initially aimed at helping these patients. Sprycel was introduced in 2006 and had 2009 sales of $421 million. Tasigna, which came out in 2007, had 2009 sales of $212 million.
Both Sprycel and Tasigna are more potent in going after a certain molecular target than Gleevec, so researchers studied whether they would work better than Gleevec in the first-line setting. Results were released at the annual scientific meeting of the American Society of Clinical Oncology and published simultaneously by the New England Journal of Medicine on Saturday.
In the Bristol-funded Sprycel study of 519 newly diagnosed CML patients, some 77% of Sprycel users had "complete cytogenetic" responses after 12 months of follow-up, versus 66% in the Gleevec users. This is one measure of remission, when the disease is virtually undetectable in bone marrow.
In a separate, 846-patient study supported by Novartis, some 80% of Tasigna users had complete cytogenetic responses, versus 65% of Gleevec users.
Both studies, while not designed identically, also looked at another measure of remission, known as major molecular response. This was achieved in about 44% of Tasigna users after 12 months, versus 22% for Gleevec. In comparison, the corresponding rates in the Bristol study were 46% for Sprycel and 28% for Gleevec.
Novartis also released data showing Tasigna continued to be superior to Gleevec after 18 months of follow-up.
Hagop Kantarjian, an oncologist at University of Texas M.D. Anderson Cancer Center in Houston who served as an investigator in both trials, said Sprycel and Tasigna were superior to Gleevec at inducing remissions, but some doctors may want to wait for three- to five-year follow-up data before substituting these drugs for Gleevec.
There were various side-effects associated with each drug in the studies, such as skin problems and headaches for Tasigna and accumulation of fluid in the chest for Sprycel. But Charles Sawyers, a cancer specialist at the Memorial Sloan-Kettering Cancer Center in New York, wrote in an editorial in the NEJM that all three drugs have "outstanding safety profiles."
Dr. Sawyers raised the question of whether the new data would render Gleevec "forever enshrined in the history of oncology but no longer useful." But he said Gleevec may get new life when it goes generic: "With rising pressure to balance cost and efficacy, patients and payers may be forced to select the cheapest among three excellent treatment options."
Novartis has patent protection for Gleevec in the U.S. until 2015.
Dr. Kantarjian said Sprycel and Tasigna would have to show significant improvement in survival to justify their prices versus generic Gleevec in first-line CML.
Pfizer Inc. is developing a similar CML drug, bosutinib, that would compete against the others if it reaches the market.
CHICAGO—Novartis AG's Gleevec is one of the closest things to a miracle drug to come out of the battle against cancer in recent years. But new research suggests two newer drugs are even more effective for the form of leukemia whose treatment Gleevec has transformed.
In separate studies published Saturday, Bristol-Myers Squibb Co.'s Sprycel and Novartis's Tasigna each were superior to Gleevec in treating people with newly diagnosed chronic myeloid leukemia. The two newer drugs are currently approved to treat patients whose disease persisted after trying Gleevec.
The new studies could help widen the patient populations for both Sprycel and Tasigna if doctors begin choosing them over Gleevec for newly diagnosed patients.
Switzerland-based Novartis has already applied for regulatory approval to market Tasigna as a first-line treatment, and New York-based Bristol said it is in the process of doing so for Sprycel. Some doctors may not wait for formal regulatory approval to try the newer drugs as first-line treatments.
But some doctors might still stick with Gleevec until Tasigna and Sprycel can demonstrate a long-term survival advantage over Gleevec. Also, Gleevec could be viewed as a more cost-effective option when the drug loses patent protection and cheaper generic versions become available in coming years.
"We don't know yet about long-term survival," said Sonali Smith, oncologist at the University of Chicago Medical Center. "We probably won't have that data for quite some time."
Gleevec was introduced in 2001 and quickly became the standard of care for people newly diagnosed with CML, a cancer of the blood, based on its ability to induce remission and significantly improve survival versus older drugs, with relatively low toxic effects.
Studies have shown at least 80% of Gleevec users were still alive eight to 10 years after beginning therapy, much higher than the historical survival rate of less than 20% for CML patients before Gleevec. Gleevec had world-wide sales of $3.9 billion last year.
But not all patients improve on Gleevec, and newer drugs were initially aimed at helping these patients. Sprycel was introduced in 2006 and had 2009 sales of $421 million. Tasigna, which came out in 2007, had 2009 sales of $212 million.
Both Sprycel and Tasigna are more potent in going after a certain molecular target than Gleevec, so researchers studied whether they would work better than Gleevec in the first-line setting. Results were released at the annual scientific meeting of the American Society of Clinical Oncology and published simultaneously by the New England Journal of Medicine on Saturday.
In the Bristol-funded Sprycel study of 519 newly diagnosed CML patients, some 77% of Sprycel users had "complete cytogenetic" responses after 12 months of follow-up, versus 66% in the Gleevec users. This is one measure of remission, when the disease is virtually undetectable in bone marrow.
In a separate, 846-patient study supported by Novartis, some 80% of Tasigna users had complete cytogenetic responses, versus 65% of Gleevec users.
Both studies, while not designed identically, also looked at another measure of remission, known as major molecular response. This was achieved in about 44% of Tasigna users after 12 months, versus 22% for Gleevec. In comparison, the corresponding rates in the Bristol study were 46% for Sprycel and 28% for Gleevec.
Novartis also released data showing Tasigna continued to be superior to Gleevec after 18 months of follow-up.
Hagop Kantarjian, an oncologist at University of Texas M.D. Anderson Cancer Center in Houston who served as an investigator in both trials, said Sprycel and Tasigna were superior to Gleevec at inducing remissions, but some doctors may want to wait for three- to five-year follow-up data before substituting these drugs for Gleevec.
There were various side-effects associated with each drug in the studies, such as skin problems and headaches for Tasigna and accumulation of fluid in the chest for Sprycel. But Charles Sawyers, a cancer specialist at the Memorial Sloan-Kettering Cancer Center in New York, wrote in an editorial in the NEJM that all three drugs have "outstanding safety profiles."
Dr. Sawyers raised the question of whether the new data would render Gleevec "forever enshrined in the history of oncology but no longer useful." But he said Gleevec may get new life when it goes generic: "With rising pressure to balance cost and efficacy, patients and payers may be forced to select the cheapest among three excellent treatment options."
Novartis has patent protection for Gleevec in the U.S. until 2015.
Dr. Kantarjian said Sprycel and Tasigna would have to show significant improvement in survival to justify their prices versus generic Gleevec in first-line CML.
Pfizer Inc. is developing a similar CML drug, bosutinib, that would compete against the others if it reaches the market.
Friday, May 28, 2010
This is wonderful!
8-month-old deaf toddler Jonathan reacts to the activation of his cochlear implant.
Tuesday, May 11, 2010
Snakebites About to Get a Lot More Deadly
The cure for North American coral snake bite is about to disappear. Why an unprofitable anti-venom may end up costing lives.
By Glenn Derene
As venomous snakes go, the coral snake is a clumsy biter. Unlike pit vipers such as rattlesnakes and cottonmouths, which have gruesomely efficient fangs that articulate forward during a strike and inject venom like hypodermic needles, the brightly colored coral snake has small, rear-facing fangs that guide venom into a wound. This process doesn't always work well--experts estimate that 25 percent of coral snake envenomations are dry bites--which is perhaps why the coral is so unaggressive. The snake is found throughout Florida, as well as in parts of Alabama, South Carolina, Louisiana, Texas and Arizona, but there are generally only about 100 or so bites each year.
What the coral lacks in belligerence, it makes up for in neurotoxicity. Unlike bites from pit vipers, which cause immense pain and swelling at the wound site, coral snake victims usually report little pain after being bitten. But the effects begin to show within hours, with symptoms such as tingling sensations in the extremities, dysarthria (slurred speech) and ptosis (droopy eyelids). Then a victim's lungs shut down. "The venom acts as a neuromuscular blockade to the lungs," University of Florida professor of medicine Craig Kitchens says. "Without antivenom, you need artificial respiration or you die."
Unfortunately, after Oct. 31 of this year, there may be no commercially available antivenom (antivenin) left. That's the expiration date on existing vials of Micrurus fulvius, the only antivenom approved by the Food and Drug Administration for coral snake bites. Produced by Wyeth, now owned by Pfizer, the antivenom was approved for sale in 1967, in a time of less stringent regulation.
Wyeth kept up production of coral snake antivenom for almost 40 years. But given the rarity of coral snake bites, it was hardly a profit center, and the company shut down the factory that made the antivenom in 2003. Wyeth worked with the FDA to produce a five-year supply of the medicine to provide a stopgap while other options were pursued. After that period, the FDA extended the expiration date on existing stock from 2008 to 2009, and then again from 2009 to 2010. But as of press time, no new manufacturer has stepped forward.
Antivenom shortages are a surprisingly common occurrence. The entire state of Arizona ran out of antivenom for scorpion stings after Marilyn Bloom, an envenomation specialist at Arizona State University, retired in 1999. Bloom had been single-handedly making all the scorpion antivenom for state hospitals. Recently, Merck & Co, the only FDA-licensed producer of black widow antivenom, has cut back distribution because of a production shortage of the drug. In a 2007 report, the World Health Organization listed worldwide envenomations as a "neglected public health issue."
New scorpion and black widow antivenoms are currently in the pipeline, thanks to efforts by several poison-control associations to speed foreign drugs into the market through FDA research programs. There is also a coral snake antivenom produced by Mexican drug manufacturer Instituto Bioclon that researchers believe could be even more effective and safe than the outgoing Wyeth product. But that drug, Coralmyn, is not currently licensed for sale by the FDA. The tests required for licensing would cost millions of dollars, and for such a rare treatment (there are 15 times as many scorpion stings per year as coral snake bites), it could take decades for Bioclon to make its money back.
Envenomation experts express exasperation and disbelief at the situation. "It's ridiculous that we're losing a technology that we already have," says Joe Pittman, a snakebite treatment specialist at the Florida Poison Information Center in Tampa. "It's even more ludicrous that we have a product that's available, and we have to jump through so many hoops to get it approved." In July 2009, an FDA advisory board determined that Coralmyn qualified for an accelerated approval process, but there is still no one with the estimated $3 million to $5 million to pay for the required studies.
"Nobody in this situation is being a bad actor," says Eric Lavonas of the Rocky Mountain Poison and Drug Center. "We just don't have a system set up to deal with it." With no adequate replacement for coral snake antivenom, hospitals are likely to appeal to local zoos, many of which maintain small stocks for their staff. But zoos are under no obligation to provide the medicine.
If and when shortages do occur, many hospitals will have no other option but to intubate coral snake bite victims on ventilators for weeks until the effects of the toxin wear off--potentially costing hundreds of thousands of dollars per bite. "It's probably going to end up costing us far more not to deal with this than to deal with it," Lavonas says, "both in human suffering, and in dollars and cents."
By Glenn Derene
As venomous snakes go, the coral snake is a clumsy biter. Unlike pit vipers such as rattlesnakes and cottonmouths, which have gruesomely efficient fangs that articulate forward during a strike and inject venom like hypodermic needles, the brightly colored coral snake has small, rear-facing fangs that guide venom into a wound. This process doesn't always work well--experts estimate that 25 percent of coral snake envenomations are dry bites--which is perhaps why the coral is so unaggressive. The snake is found throughout Florida, as well as in parts of Alabama, South Carolina, Louisiana, Texas and Arizona, but there are generally only about 100 or so bites each year.
What the coral lacks in belligerence, it makes up for in neurotoxicity. Unlike bites from pit vipers, which cause immense pain and swelling at the wound site, coral snake victims usually report little pain after being bitten. But the effects begin to show within hours, with symptoms such as tingling sensations in the extremities, dysarthria (slurred speech) and ptosis (droopy eyelids). Then a victim's lungs shut down. "The venom acts as a neuromuscular blockade to the lungs," University of Florida professor of medicine Craig Kitchens says. "Without antivenom, you need artificial respiration or you die."
Unfortunately, after Oct. 31 of this year, there may be no commercially available antivenom (antivenin) left. That's the expiration date on existing vials of Micrurus fulvius, the only antivenom approved by the Food and Drug Administration for coral snake bites. Produced by Wyeth, now owned by Pfizer, the antivenom was approved for sale in 1967, in a time of less stringent regulation.
Wyeth kept up production of coral snake antivenom for almost 40 years. But given the rarity of coral snake bites, it was hardly a profit center, and the company shut down the factory that made the antivenom in 2003. Wyeth worked with the FDA to produce a five-year supply of the medicine to provide a stopgap while other options were pursued. After that period, the FDA extended the expiration date on existing stock from 2008 to 2009, and then again from 2009 to 2010. But as of press time, no new manufacturer has stepped forward.
Antivenom shortages are a surprisingly common occurrence. The entire state of Arizona ran out of antivenom for scorpion stings after Marilyn Bloom, an envenomation specialist at Arizona State University, retired in 1999. Bloom had been single-handedly making all the scorpion antivenom for state hospitals. Recently, Merck & Co, the only FDA-licensed producer of black widow antivenom, has cut back distribution because of a production shortage of the drug. In a 2007 report, the World Health Organization listed worldwide envenomations as a "neglected public health issue."
New scorpion and black widow antivenoms are currently in the pipeline, thanks to efforts by several poison-control associations to speed foreign drugs into the market through FDA research programs. There is also a coral snake antivenom produced by Mexican drug manufacturer Instituto Bioclon that researchers believe could be even more effective and safe than the outgoing Wyeth product. But that drug, Coralmyn, is not currently licensed for sale by the FDA. The tests required for licensing would cost millions of dollars, and for such a rare treatment (there are 15 times as many scorpion stings per year as coral snake bites), it could take decades for Bioclon to make its money back.
Envenomation experts express exasperation and disbelief at the situation. "It's ridiculous that we're losing a technology that we already have," says Joe Pittman, a snakebite treatment specialist at the Florida Poison Information Center in Tampa. "It's even more ludicrous that we have a product that's available, and we have to jump through so many hoops to get it approved." In July 2009, an FDA advisory board determined that Coralmyn qualified for an accelerated approval process, but there is still no one with the estimated $3 million to $5 million to pay for the required studies.
"Nobody in this situation is being a bad actor," says Eric Lavonas of the Rocky Mountain Poison and Drug Center. "We just don't have a system set up to deal with it." With no adequate replacement for coral snake antivenom, hospitals are likely to appeal to local zoos, many of which maintain small stocks for their staff. But zoos are under no obligation to provide the medicine.
If and when shortages do occur, many hospitals will have no other option but to intubate coral snake bite victims on ventilators for weeks until the effects of the toxin wear off--potentially costing hundreds of thousands of dollars per bite. "It's probably going to end up costing us far more not to deal with this than to deal with it," Lavonas says, "both in human suffering, and in dollars and cents."
Tuesday, April 6, 2010
Parkinson's patient's cycling ability stuns doctors
BY GINA KOLATA
NEW YORK TIMES
Monday, Apr. 05 2010
Dr. Bastiaan R. Bloem of the Radboud University Nijmegen Medical Center in the
Netherlands thought he had seen it all in his years of caring for patients with
Parkinson's disease. But the 58-year-old man who came to see him recently was a
total surprise.
The man had had Parkinson's disease for 10 years, and it had progressed until
he was severely affected. Parkinson's, a neurological disorder in which some of
the brain cells that control movement die, had made him unable to walk. He
trembled and could walk only a few steps before falling. He froze in place, his
feet feeling as if they were bolted to the floor.
But the man told Bloem something amazing: He said he was a regular exerciser —
a cyclist, in fact — something that should not be possible for patients at his
stage of the disease, Bloem thought.
"He said, 'Just yesterday I rode my bicycle for 10 kilometers' — six miles,"
Bloem said. "He said he rides his bicycle for miles and miles every day.
"I said, 'This cannot be,'" Bloem, a professor of neurology and medical
director of the hospital's Parkinson's Center, recalled in a telephone
interview. "This man has end-stage Parkinson's disease. He is unable to walk."
But the man was eager to demonstrate, so Bloem took him outside where a nurse's
bike was parked.
"We helped him mount the bike, gave him a little push, and he was gone," Bloem
said. He rode, even making a U-turn, and was in perfect control, all his
Parkinson's symptoms gone.
Yet the moment the man got off the bike, his symptoms returned. He froze
immediately, unable to take a step.
Bloem made a video and photos of the man trying to walk and then riding his
bike. The photos appear in the April 1 issue of The New England Journal of
Medicine.
After seeing that man, Bloem asked 20 other severely affected patients about
riding a bike. It turned out that all could do it, though it is not clear why.
Bloem and other Parkinson's specialists were amazed. People with Parkinson's
disease can often dance, run, walk smoothly and do complex movements for a few
minutes if they are given appropriate signals — emotional or visual cues. There
are famous examples, such as a group of Parkinson's patients who were caught in
a fire and managed to run down steps and escape, only to freeze in place when
they got outside.
But this effect, known as the kinesia paradox, does not last long. Riding for
miles and miles is very different from walking for a few minutes. And until
now, Bloem said, it was not known that patients with Parkinson's could ride
bikes.
He said bicycling offers patients an opportunity to be symptom-free while they
are riding, to look and feel normal, and to get some real cardiovascular
exercise.
Bloem said he hoped that perhaps regular exercise might slow the progress of
Parkinson's disease. It does in rats, he said.
NEW YORK TIMES
Monday, Apr. 05 2010
Dr. Bastiaan R. Bloem of the Radboud University Nijmegen Medical Center in the
Netherlands thought he had seen it all in his years of caring for patients with
Parkinson's disease. But the 58-year-old man who came to see him recently was a
total surprise.
The man had had Parkinson's disease for 10 years, and it had progressed until
he was severely affected. Parkinson's, a neurological disorder in which some of
the brain cells that control movement die, had made him unable to walk. He
trembled and could walk only a few steps before falling. He froze in place, his
feet feeling as if they were bolted to the floor.
But the man told Bloem something amazing: He said he was a regular exerciser —
a cyclist, in fact — something that should not be possible for patients at his
stage of the disease, Bloem thought.
"He said, 'Just yesterday I rode my bicycle for 10 kilometers' — six miles,"
Bloem said. "He said he rides his bicycle for miles and miles every day.
"I said, 'This cannot be,'" Bloem, a professor of neurology and medical
director of the hospital's Parkinson's Center, recalled in a telephone
interview. "This man has end-stage Parkinson's disease. He is unable to walk."
But the man was eager to demonstrate, so Bloem took him outside where a nurse's
bike was parked.
"We helped him mount the bike, gave him a little push, and he was gone," Bloem
said. He rode, even making a U-turn, and was in perfect control, all his
Parkinson's symptoms gone.
Yet the moment the man got off the bike, his symptoms returned. He froze
immediately, unable to take a step.
Bloem made a video and photos of the man trying to walk and then riding his
bike. The photos appear in the April 1 issue of The New England Journal of
Medicine.
After seeing that man, Bloem asked 20 other severely affected patients about
riding a bike. It turned out that all could do it, though it is not clear why.
Bloem and other Parkinson's specialists were amazed. People with Parkinson's
disease can often dance, run, walk smoothly and do complex movements for a few
minutes if they are given appropriate signals — emotional or visual cues. There
are famous examples, such as a group of Parkinson's patients who were caught in
a fire and managed to run down steps and escape, only to freeze in place when
they got outside.
But this effect, known as the kinesia paradox, does not last long. Riding for
miles and miles is very different from walking for a few minutes. And until
now, Bloem said, it was not known that patients with Parkinson's could ride
bikes.
He said bicycling offers patients an opportunity to be symptom-free while they
are riding, to look and feel normal, and to get some real cardiovascular
exercise.
Bloem said he hoped that perhaps regular exercise might slow the progress of
Parkinson's disease. It does in rats, he said.
Friday, April 2, 2010
A finch's decoded genome might help us with speech
By Kim McGuire
ST. LOUIS POST-DISPATCH
03/31/2010
When we hear a song for the first time, it often seems like it goes in one ear and out the other, sometimes only few catchy words from a chorus leaving much of an impression.
bullet Hear the sounds of the zebra finch
But when the Australian zebra finch hears its father sing for the first time, those simple melodies activate large, complex gene networks in the bird’s brain, according to new research by an international team of scientists that includes researchers from Washington University and the University of Illinois at Urbana-Champaign.
The findings, published today in the journal Nature, reveal how the team successfully decoded the genome of the zebra finch, only the second bird to have its genetic code completely mapped.
The project provides new insights that will help scientists understand how humans learn language and may someday provide insights into diseases like autism that can inhibit speech, team members say.
"Now we can look deep into the genome, not just at the genes involved in vocal learning, but that the complex ways in which they are regulated," said Richard K. Wilson, the research’s senior author and director of Washington University’s Genome Center. "This information provides clues to how vocal learning occurs at the most basic molecular level in birds and people."
Past research has shown that hundreds of genes light up in the finch’s brain as the bird learns a new song.
The new research show that significantly more genes — about 800 total — are activated by the act of singing.
The team selected the zebra finch for study because songbirds are among few animals that learn how to sing — just like humans. As young birds, the finch "babbles" but eventually learns how to imitate its father.
In contrast, a chicken, the other bird to have its genome sequenced, instinctively knows how cluck. It is not a form of communication learned from other birds.
"There is a functional development parallel between the way a bird learns to sing and a human learns to speak," said David Clayton, a neuroscience professor at the University of Illinois and leader of the group that proposed the genome sequencing project. "The avian brain is quite different in a superficial detail from the mammalian brain or the human brain, but some striking parallels have emerged."
Wes Warren, lead author and genetics professor at Washington University, explained that the zebra finch proved to be the model study organism because they learn to sing in a predictable way over a relatively short span of time and many of their genes are conserved in humans.
Now, scientists can conduct future studies to identify a core set of genes in the finch’s brain and see if any of these are disrupted in people with speech disorders caused stuttering, or stroke and by diseases like autism and Parkinson’s, Warren said.
"It’s just amazing to know that when the finch hears a song, there’s always a gene that corresponds in the brain," he said. "Clearly, that’s going to be even more complex in humans."
Warren said as more animals have their genes sequenced, scientists will be able to draw more comparisons that might yield insight into human development.
Next up for some of the Washington University scientists who participated in the finch project is the sequencing of the parrot genome, which is slated for completion sometime later this year.
ST. LOUIS POST-DISPATCH
03/31/2010
When we hear a song for the first time, it often seems like it goes in one ear and out the other, sometimes only few catchy words from a chorus leaving much of an impression.
bullet Hear the sounds of the zebra finch
But when the Australian zebra finch hears its father sing for the first time, those simple melodies activate large, complex gene networks in the bird’s brain, according to new research by an international team of scientists that includes researchers from Washington University and the University of Illinois at Urbana-Champaign.
The findings, published today in the journal Nature, reveal how the team successfully decoded the genome of the zebra finch, only the second bird to have its genetic code completely mapped.
The project provides new insights that will help scientists understand how humans learn language and may someday provide insights into diseases like autism that can inhibit speech, team members say.
"Now we can look deep into the genome, not just at the genes involved in vocal learning, but that the complex ways in which they are regulated," said Richard K. Wilson, the research’s senior author and director of Washington University’s Genome Center. "This information provides clues to how vocal learning occurs at the most basic molecular level in birds and people."
Past research has shown that hundreds of genes light up in the finch’s brain as the bird learns a new song.
The new research show that significantly more genes — about 800 total — are activated by the act of singing.
The team selected the zebra finch for study because songbirds are among few animals that learn how to sing — just like humans. As young birds, the finch "babbles" but eventually learns how to imitate its father.
In contrast, a chicken, the other bird to have its genome sequenced, instinctively knows how cluck. It is not a form of communication learned from other birds.
"There is a functional development parallel between the way a bird learns to sing and a human learns to speak," said David Clayton, a neuroscience professor at the University of Illinois and leader of the group that proposed the genome sequencing project. "The avian brain is quite different in a superficial detail from the mammalian brain or the human brain, but some striking parallels have emerged."
Wes Warren, lead author and genetics professor at Washington University, explained that the zebra finch proved to be the model study organism because they learn to sing in a predictable way over a relatively short span of time and many of their genes are conserved in humans.
Now, scientists can conduct future studies to identify a core set of genes in the finch’s brain and see if any of these are disrupted in people with speech disorders caused stuttering, or stroke and by diseases like autism and Parkinson’s, Warren said.
"It’s just amazing to know that when the finch hears a song, there’s always a gene that corresponds in the brain," he said. "Clearly, that’s going to be even more complex in humans."
Warren said as more animals have their genes sequenced, scientists will be able to draw more comparisons that might yield insight into human development.
Next up for some of the Washington University scientists who participated in the finch project is the sequencing of the parrot genome, which is slated for completion sometime later this year.
Sunday, March 28, 2010
Sex-Crazed Bugs Unleashed in Israel
One of the great challenges of modern agriculture is how to use technology to mass produce crops while sparing consumers from the harmful chemicals and byproducts of the agricultural process. Though meant to kill harmful insects, pesticides carry a very serious risk to the environment.
While studies have shown that mankind is developing cancer and other diseases at a higher rate due to exposure to pesticides, the crop-killing vermin are only becoming more immune to its effects. At the Hebrew University of Jerusalem, researchers have discovered a way to safely eliminate insects without the need for harmful chemicals.
Professor Boaz Yuval at the university’s Robert H. Smith Faculty of Food, Agriculture and the Environment believes that sex is the key.
If you can sterilize male insects before they copulate with females, these females will be unable to lay eggs. The problem, however, is that males who are sterilized also lose their sex drive, leaving the females to mate with male insects who are not sterilized.
Researchers at the Hebrew University of Jerusalem have created a special, high protein, bacteria-enhanced “breakfast of champions” to sterilize males. By greatly increasing their sex drive and sexual performance, females spend all of their time with these Casanova sex-crazed males and never are able to lay eggs of their own.
While original applications of this research will be for plant and animal pests, many are looking to see how this work can be applied to stop the spread of organisms carrying human diseases.
While studies have shown that mankind is developing cancer and other diseases at a higher rate due to exposure to pesticides, the crop-killing vermin are only becoming more immune to its effects. At the Hebrew University of Jerusalem, researchers have discovered a way to safely eliminate insects without the need for harmful chemicals.
Professor Boaz Yuval at the university’s Robert H. Smith Faculty of Food, Agriculture and the Environment believes that sex is the key.
If you can sterilize male insects before they copulate with females, these females will be unable to lay eggs. The problem, however, is that males who are sterilized also lose their sex drive, leaving the females to mate with male insects who are not sterilized.
Researchers at the Hebrew University of Jerusalem have created a special, high protein, bacteria-enhanced “breakfast of champions” to sterilize males. By greatly increasing their sex drive and sexual performance, females spend all of their time with these Casanova sex-crazed males and never are able to lay eggs of their own.
While original applications of this research will be for plant and animal pests, many are looking to see how this work can be applied to stop the spread of organisms carrying human diseases.
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