By: Clara Moskowitz
If you've ever wanted to be the Bionic Woman or a Terminator, new research may at least let you see with their eyes.
Scientists have taken the first step toward creating digital contact lenses that can zoom in on distant objects and display useful facts.
For the first time, engineers have installed an electronic circuit and lights on a regular contact lens.
The prototype they created does not actually light up or display information. But it proves that it is possible to build an electronic lens that is safe to wear and doesn't obstruct vision.
"Looking through a completed lens, you would see what the display is generating superimposed on the world outside," said Babak Parviz, an electrical engineer at the University of Washington who worked on the project. "This is a very small step toward that goal, but I think it's extremely promising."
The project was led by Harvey Ho, a former graduate student of Parviz's now working at Sandia National Laboratories in Livermore, Calif., who presented the results this week at the Institute of Electrical and Electronics Engineers' international conference on Micro Electro Mechanical Systems in Tucson, AZ.
It was difficult for the researchers to graft the tiny electrical circuits, built from layers of metal only a few nanometers thick (for comparison, the width of a typical human hair is about 80,000 nanometers), onto the contact lenses, which are made of organic materials that are safe for the body.
The engineers tested the finished lenses on rabbits for up to 20 minutes and the animals showed no problems.
Eventually, the technique could yield a plethora of gadgets.
Perhaps drivers and pilots could see their direction and speed projected across their view, or people could surf the Web without looking at an external device's screen.
Video gamers could immerse themselves in game landscapes directly in front of their eyes.
Maybe the technique could even create sight aids for visually-impaired people.
"People may find all sorts of applications for it that we have not thought about," Parviz said. "Our goal is to demonstrate the basic technology and make sure it works and that it's safe."
Saturday, January 19, 2008
Friday, December 7, 2007
Best Treatment Option for Mental Disorders May Come Down to Genes
A dopamine-receptor gene variation is linked to changes in brain function, possibly neurotransmitter signaling
By Nikhil Swaminathan
Scientific American
Alterations in the genetic coding for a nerve cell receptor, which detects a chemical signal that is key to behavioral change, could point the way to designing therapies most effective for patients suffering from schizophrenia, drug addiction and other mental illnesses.
"I don't know if what we just published is a viable biomarker," says Wolfgang Sadee, chair of the Department of Pharmacology at The Ohio State University (O.S.U.) College of Medicine and the co-author of a report on the finding published this week in Proceedings of the National Academy of Sciences USA. "But, I think there's a good chance that this is a biomarker that we will at least test and we will know soon if there is something worthwhile."
A team of scientists from O.S.U. examined 68 samples of postmortem tissue from the brains of people without a history of mental illness in search of the profile of messenger RNA (mRNA) transcribed from a particular gene. (mRNA is the intermediate blueprint between gene and protein.) Researchers were specifically hunting for the mRNA created from the two alleles (copies) of the gene DRD2, which codes for a receptor protein for the neurotransmitter dopamine. D2 dopamine receptor malfunction has been linked to drug addiction, schizophrenia and Parkinson's disease. The team focused its search on the striatum (a midbrain region implicated in planning and movement) and the prefrontal cortex, the brain's central processing area.
In 15 of the brain samples, researchers found that one copy of DRD2 was producing at least 50 percent more mRNA than the other one; in the remaining brains, they discovered that both alleles produced equal amounts. They also identified SNPs (single nucleotide polymorphisms, or alterations to the genetic code created by the addition or deletion of a single nucleotide in a gene's long chain). Two of these changes caused differences in the protein made by the gene; one of them appeared to be the result of DRD2 gene being spliced together differently, resulting in a protein consisting of a slightly longer than normal chain of amino acid building blocks.
The unexpected finding of a splice variant caused some excitement in the lab, Sadee says, because, according to the literature "the short form is more inhibitory and the long form may be facilitating dopaminergic transition. … When dopaminergic input comes in, [individuals with the SNPs on one gene copy] would have a chance of having more transmission" than those with two normal copies of the gene.
Sadee contacted Alessandro Bertolino at the University of Bari in Italy, who was doing research that involved monitoring the brain activity of 117 volunteers with functional magnetic resonance imaging (fMRI) during memory tests. Seventeen of the subjects in Bertolino's pool carried the SNPs on a single allele and showed increased activity in their striata and prefrontal cortices during the mental exercises, yet performed worse on the memory tests and had less attention control than the other study participants.
Sadee speculates that the brains of these subjects may be in "unnecessary hyperdrive. The dopamine stimulates more activity and that relates to more brain activity during a memory task," he says. "That is maybe not as good as memory function. … The brain has to work harder to master the same task, and that's induced by this polymorphism."
He says the study could improve current treatments for patients suffering from mental illnesses. The proper antipsychotic drugs may in the future be determined by genotyping patients to assure the most positive effect. Physicians now often have to try out different drugs to test their effectiveness, because this class of medications is highly varied and targets different brain receptors. Such findings as these could dramatically reduce the guesswork involved, thereby leading to the proper prescription from day one. Currently, Sadee says, antipsychotics are only effective 50 to 60 percent of the time and take five to six weeks to begin working.
"The influence of antipsychotics that inhibit D2 antagonist activity will differ between the two" forms of the protein receptor, he says. "One is facilitating and the other inhibiting, so the net effect of inhibiting the D2 receptor will change. So, we think that is one possible mechanism for differences in antipsychotic response."
By Nikhil Swaminathan
Scientific American
Alterations in the genetic coding for a nerve cell receptor, which detects a chemical signal that is key to behavioral change, could point the way to designing therapies most effective for patients suffering from schizophrenia, drug addiction and other mental illnesses.
"I don't know if what we just published is a viable biomarker," says Wolfgang Sadee, chair of the Department of Pharmacology at The Ohio State University (O.S.U.) College of Medicine and the co-author of a report on the finding published this week in Proceedings of the National Academy of Sciences USA. "But, I think there's a good chance that this is a biomarker that we will at least test and we will know soon if there is something worthwhile."
A team of scientists from O.S.U. examined 68 samples of postmortem tissue from the brains of people without a history of mental illness in search of the profile of messenger RNA (mRNA) transcribed from a particular gene. (mRNA is the intermediate blueprint between gene and protein.) Researchers were specifically hunting for the mRNA created from the two alleles (copies) of the gene DRD2, which codes for a receptor protein for the neurotransmitter dopamine. D2 dopamine receptor malfunction has been linked to drug addiction, schizophrenia and Parkinson's disease. The team focused its search on the striatum (a midbrain region implicated in planning and movement) and the prefrontal cortex, the brain's central processing area.
In 15 of the brain samples, researchers found that one copy of DRD2 was producing at least 50 percent more mRNA than the other one; in the remaining brains, they discovered that both alleles produced equal amounts. They also identified SNPs (single nucleotide polymorphisms, or alterations to the genetic code created by the addition or deletion of a single nucleotide in a gene's long chain). Two of these changes caused differences in the protein made by the gene; one of them appeared to be the result of DRD2 gene being spliced together differently, resulting in a protein consisting of a slightly longer than normal chain of amino acid building blocks.
The unexpected finding of a splice variant caused some excitement in the lab, Sadee says, because, according to the literature "the short form is more inhibitory and the long form may be facilitating dopaminergic transition. … When dopaminergic input comes in, [individuals with the SNPs on one gene copy] would have a chance of having more transmission" than those with two normal copies of the gene.
Sadee contacted Alessandro Bertolino at the University of Bari in Italy, who was doing research that involved monitoring the brain activity of 117 volunteers with functional magnetic resonance imaging (fMRI) during memory tests. Seventeen of the subjects in Bertolino's pool carried the SNPs on a single allele and showed increased activity in their striata and prefrontal cortices during the mental exercises, yet performed worse on the memory tests and had less attention control than the other study participants.
Sadee speculates that the brains of these subjects may be in "unnecessary hyperdrive. The dopamine stimulates more activity and that relates to more brain activity during a memory task," he says. "That is maybe not as good as memory function. … The brain has to work harder to master the same task, and that's induced by this polymorphism."
He says the study could improve current treatments for patients suffering from mental illnesses. The proper antipsychotic drugs may in the future be determined by genotyping patients to assure the most positive effect. Physicians now often have to try out different drugs to test their effectiveness, because this class of medications is highly varied and targets different brain receptors. Such findings as these could dramatically reduce the guesswork involved, thereby leading to the proper prescription from day one. Currently, Sadee says, antipsychotics are only effective 50 to 60 percent of the time and take five to six weeks to begin working.
"The influence of antipsychotics that inhibit D2 antagonist activity will differ between the two" forms of the protein receptor, he says. "One is facilitating and the other inhibiting, so the net effect of inhibiting the D2 receptor will change. So, we think that is one possible mechanism for differences in antipsychotic response."
Thursday, November 15, 2007
MRI tests offer glimpse at brains behind the lies
By Richard Willing,
USA TODAY
Two companies plan to market the first lie-detecting devices that use
magnetic resonance imaging (MRI) and say the new tests can spot liars
with 90% accuracy.
No Lie MRI plans to begin offering brain-based lie-detector tests in
Philadelphia in late July or August, says Joel Huizenga, founder of
the San Diego-based start-up. Cephos Corp. of Pepperell, Mass., will
offer a similar service later this year using MRI machines at the
Medical University of South Carolina in Charleston, says its
president, Steven Laken.
Both rely in part on recent research funded by the federal government
aimed at producing a foolproof method of detecting deception.
The new devices differ from polygraphs in key ways. The polygraph
detects stress brought on by telling a lie. The MRI-based devices
purport to measure the lie itself, and not changes in breathing and
pulse rate brought on by lying or by some other cause.
"We're at the beginning of a technology that's going to become more
and more mature," Huizenga says. "But right now, we can offer
(customers) a chance to show they are telling the truth with a
scientific basis and a high degree of accuracy. That's something they
haven't been able to get before."
Potential customers: law enforcement, accused persons, spouses under
suspicion and job applicants. Huizenga says a 1988 law that bars
private employers from giving polygraphs to potential employees
appears not to apply to MRI tests.
No Lie MRI plans to charge $30 a minute to use its device. Cephos has
not yet set a price.
The new products are being introduced as the polygraph is under fire.
In 2002, a National Academy of Sciences study concluded that polygraph
results are too unpredictable to be used for security screening at
national labs. Yet the Department of Defense, as well as the FBI, CIA
and National Security Agency, continue to administer thousands of
polygraph tests each year to job candidates and others seeking
security clearances.
The Department of Defense administered about 12,000 tests in 2002, the
most recent year in which it made data public.
"They haven't found anything yet that they think can top (the
polygraph)," says Britton Chance, a University of Pennsylvania
researcher who has studied brain-based lie detection.
Some scientists and privacy advocates criticize the new lie detectors.
They note that they haven't yet proved themselves in real-world tests
and face prolonged scrutiny before they are admitted in court.
"They are going to be deployed to read people's thoughts," says Barry
Steinhardt, director of the American Civil Liberties Union's
technology and liberty project. "Little if any attention has been paid
to potential misuse and the devastating impact it would have on our
civil liberties."
The new tests work this way: A subject lies with his head in an MRI
machine and pushes a button to answer yes-no questions as they are
flashed on a screen. The machine measures brain activity, focusing on
areas that are believed to show extra exertion when a lie is
generated. Specially designed software grades the test. The two lie detector companies use similar test techniques, but different software.
Most American courts do not admit polygraph evidence because
differences in examiner skill make it hard to determine accuracy rates.
MRI machines are used by hospitals on a daily basis to diagnose tumors
and other disorders.
After the 9/11 attacks, the FBI, CIA, Department of Defense and other
agencies began funding research into how changes in brain activity
correlate with truth telling.
Daniel Langleben, a physician and professor at the University of
Pennsylvania, and Frank Andrew Kozel, a brain image researcher at the
Medical University of South Carolina, received funding for research
into MRI-based lie detection.
Langleben's research was used by No Lie MRI to help develop its lie
detector. Cephos' lie detector is based in part on Kozel's research.
David Heeger, professor of psychology and neural science at New York
University, opposes using MRI for lie detection until more research is
done. Among the many gaps in the research, he says, is whether a false
or imagined memory will show up as a true response or a lie.
MRI-based lie detection "says changes happen (in the brain of a liar)
but it doesn't say why," says Heeger. "There's a lot more work to be
done ... before we have a deep understanding of what goes on when
people lie."
Gregg Bloche, a medical doctor and a law professor at Georgetown
University, says scientists, lawyers and ethicists should conduct a
"high profile discussion" of the new technology's potential uses and
pitfalls before it is made available to the public.
The start-up companies say the technology is ready now. Both say they
will focus on winning acceptance in court for tests taken by
customers. No Lie MRI already is working with a defendant in a
California criminal case, Huizenga says.
"We understand that there are further ethics conversations (needed)
when science pushes the envelope," says Cephos' Laken. "But we don't
see these (tests) being set up in dressing rooms and shopping malls.
That's not going to happen."
USA TODAY
Two companies plan to market the first lie-detecting devices that use
magnetic resonance imaging (MRI) and say the new tests can spot liars
with 90% accuracy.
No Lie MRI plans to begin offering brain-based lie-detector tests in
Philadelphia in late July or August, says Joel Huizenga, founder of
the San Diego-based start-up. Cephos Corp. of Pepperell, Mass., will
offer a similar service later this year using MRI machines at the
Medical University of South Carolina in Charleston, says its
president, Steven Laken.
Both rely in part on recent research funded by the federal government
aimed at producing a foolproof method of detecting deception.
The new devices differ from polygraphs in key ways. The polygraph
detects stress brought on by telling a lie. The MRI-based devices
purport to measure the lie itself, and not changes in breathing and
pulse rate brought on by lying or by some other cause.
"We're at the beginning of a technology that's going to become more
and more mature," Huizenga says. "But right now, we can offer
(customers) a chance to show they are telling the truth with a
scientific basis and a high degree of accuracy. That's something they
haven't been able to get before."
Potential customers: law enforcement, accused persons, spouses under
suspicion and job applicants. Huizenga says a 1988 law that bars
private employers from giving polygraphs to potential employees
appears not to apply to MRI tests.
No Lie MRI plans to charge $30 a minute to use its device. Cephos has
not yet set a price.
The new products are being introduced as the polygraph is under fire.
In 2002, a National Academy of Sciences study concluded that polygraph
results are too unpredictable to be used for security screening at
national labs. Yet the Department of Defense, as well as the FBI, CIA
and National Security Agency, continue to administer thousands of
polygraph tests each year to job candidates and others seeking
security clearances.
The Department of Defense administered about 12,000 tests in 2002, the
most recent year in which it made data public.
"They haven't found anything yet that they think can top (the
polygraph)," says Britton Chance, a University of Pennsylvania
researcher who has studied brain-based lie detection.
Some scientists and privacy advocates criticize the new lie detectors.
They note that they haven't yet proved themselves in real-world tests
and face prolonged scrutiny before they are admitted in court.
"They are going to be deployed to read people's thoughts," says Barry
Steinhardt, director of the American Civil Liberties Union's
technology and liberty project. "Little if any attention has been paid
to potential misuse and the devastating impact it would have on our
civil liberties."
The new tests work this way: A subject lies with his head in an MRI
machine and pushes a button to answer yes-no questions as they are
flashed on a screen. The machine measures brain activity, focusing on
areas that are believed to show extra exertion when a lie is
generated. Specially designed software grades the test. The two lie detector companies use similar test techniques, but different software.
Most American courts do not admit polygraph evidence because
differences in examiner skill make it hard to determine accuracy rates.
MRI machines are used by hospitals on a daily basis to diagnose tumors
and other disorders.
After the 9/11 attacks, the FBI, CIA, Department of Defense and other
agencies began funding research into how changes in brain activity
correlate with truth telling.
Daniel Langleben, a physician and professor at the University of
Pennsylvania, and Frank Andrew Kozel, a brain image researcher at the
Medical University of South Carolina, received funding for research
into MRI-based lie detection.
Langleben's research was used by No Lie MRI to help develop its lie
detector. Cephos' lie detector is based in part on Kozel's research.
David Heeger, professor of psychology and neural science at New York
University, opposes using MRI for lie detection until more research is
done. Among the many gaps in the research, he says, is whether a false
or imagined memory will show up as a true response or a lie.
MRI-based lie detection "says changes happen (in the brain of a liar)
but it doesn't say why," says Heeger. "There's a lot more work to be
done ... before we have a deep understanding of what goes on when
people lie."
Gregg Bloche, a medical doctor and a law professor at Georgetown
University, says scientists, lawyers and ethicists should conduct a
"high profile discussion" of the new technology's potential uses and
pitfalls before it is made available to the public.
The start-up companies say the technology is ready now. Both say they
will focus on winning acceptance in court for tests taken by
customers. No Lie MRI already is working with a defendant in a
California criminal case, Huizenga says.
"We understand that there are further ethics conversations (needed)
when science pushes the envelope," says Cephos' Laken. "But we don't
see these (tests) being set up in dressing rooms and shopping malls.
That's not going to happen."
Don't Forget to Back Up Your Brain
Thursday , November 15, 2007
By Corinna Underwood
As any Baby Boomer will tell you, Americans have more information to cram into their memories than ever. Yet, as we age, our capacity for recall grows weaker.
But what if you could capture every waking moment of your entire life, store it on your computer and then recall digital snapshots of everything you've seen and heard with just a quick search?
Renowned computer scientist Gordon Bell, head of Microsoft's Media Presence Research Group and founder of the Computer History Museum in Silicon Valley, thinks he might be able to do just that.
He calls it a "surrogate memory," and what he considers an early version of it even has an official name — MyLifeBits.
"The goal is to live as much of life as possible versus spending time maintaining our memory system," Bell explains.
• Click here for FOXNews.com's Personal Technology Center.
Perfect surrogate memory would be supplemental to, but ultimately as good as, your original memory.
It could let you listen to every conversation you had when you were 21 or find that photograph of the obscure date you had on summer vacation.
As Bell says, it would "supplement (and sometimes supplant) other information-processing systems, including people."
MyLifeBits isn't quite there yet, but Bell's nevertheless "gone paperless" for the past decade as part of the project, keeping a detailed, digitized diary that documents his life with photographs, letters and voice recordings.
So that he doesn't miss out on important daily events, Bell wears a SenseCam, developed by Microsoft Research, that takes pictures whenever it detects he may want a photograph.
The camera's infrared sensor picks up on body heat and takes snapshots of anyone else in the room, adjusting itself as available light changes.
Not only does MyLifeBits record your life's digital information, but the software, developed by Bell's researchers Jim Gemmell and Roger Lueder, also can help you retrieve it.
"MyLifeBits is a system aimed at capturing cyber-content in the course of daily life with the goal of being able to utilize it in various ways at work, in our personal life — e.g. finances, family, health and for our future memory," Bell says.
Simply enter a keyword such as "pet," for example, and the search engine will find all available information on your childhood puppy.
It also can run more intricate searches, allowing you to cross-reference all associations linked to certain people or places.
If you're having difficulty remembering where you were and who you were with on a certain day, MyLifeBits would remind you.
And just how much data is needed on a day-to-day basis?
"All the bits that we can that will likely have value for our memory in the near and long-term future, a few bits just for the hell of it," Bell says. "We end up with more bits because we need them for relationships."
Still, is recalling every single detail of an entire lifetime too much? How can anyone guess what's going to be important 20 years from now?
"It is impossible to know what will be required in the future," says Bell. "Furthermore, recording everything allows one item to be used to find another item that may have been created at the same time."
Bell says MyLifeBits could have another important benefit: It may actually improve your real memory.
According to Bell, being reminded of someone in a photograph or screensaver strengthens our recollections.
We constantly are reminded of other events when we delve into our past to find snippets for which we are looking. This reinforces a whole host of links to other memories we otherwise may have forgotten.
But since all this is digitally recorded, what if hackers find it? Couldn't MyLifeBits be a threat to privacy and a boon to identity thieves?
Bell doesn't seem overly concerned.
"MLB introduces no new problems that aren't present in modern computer systems," he said, "except that we present a larger cross-section that makes all the content potentially more valuable."
Additional passwords are being built into the most sensitive documents, he explains.
An even bigger hurdle for the project is cost-efficiency.
The Microsoft team predicts that by 2010, a 1-terabyte (1,000-gigabyte) hard drive will cost less than $300.
That could easily hold all text documents, voice files and photographs of a person's complete life experience — but if it came to video, it would be only enough for four hours per day for an entire year.
On a somewhat smaller level, Sunil Vemuri, co-founder and chief product officer of Hyderabad, India-based QTech, Inc., has been working to develop a "memory prosthesis" that can help people with common, day-to-day memory problems.
QTech's "reQall" service provides a toll-free number that allows clients to use any phone to record reminders of events, appointments or thoughts as and when needed.
It then saves and organizes the recordings and sends daily reminders as needed.
"ReQall is meant for anyone who forgets, for anyone with a day-to-day memory problem," Vemuri says. "The aim of reQall is to provide a long-term service that is available to everyone right now."
Vemuri sees great growth potential for reQall. He wants his team to refine the service to suit users' individual memory needs, whether that involves helping patients remember doctors' appointments, friends remember birthdays or even journalists remember specific quotes.
More ambitious is Vemuri's "What Was I Thinking," a project he worked on while a graduate student at MIT.
That centered around software running on a Compaq iPaq personal digital assistant, similar to a Palm Pilot, which then synced to PCs running Mac OS X, Windows or Linux. It was capable of recording data and using a number of search tools to help the user find forgotten memories, using a range of built-in triggers.
"Many things can serve as good memory triggers: the smell or taste of homemade cooking, the smile on a child's face, a good joke, the roar of the crowd when your sports team scores, etc," Vemuri explained on his MIT Web page.
"In our case, the device records audio from conversations and happenings, analyzes and indexes the audio in an attempt to identify the best memory triggers, and provides a suite of retrieval tools to help the wearer access memories when a forgetting incident occurs."
The device's retrieval tools included an analysis of audio recordings to determine if conversations were heated, calm or humorous and a transcription of audio files to text files by means of a speech-recognition program.
In this way, the text files could be searched for specific words or speech patterns that can trigger those elusive memories.
In the future, some variation on these memory prostheses could change our lives on many levels, from settling a squabble over last week's football scores to assisting an elderly patient remember if she has taken her medication.
We rely on our hard drives for saving our music, photographs, e-mails and videos — so perhaps life-logging software and memory prosthetics are simply the next stage in the evolution of our relationship to the computer.
By Corinna Underwood
As any Baby Boomer will tell you, Americans have more information to cram into their memories than ever. Yet, as we age, our capacity for recall grows weaker.
But what if you could capture every waking moment of your entire life, store it on your computer and then recall digital snapshots of everything you've seen and heard with just a quick search?
Renowned computer scientist Gordon Bell, head of Microsoft's Media Presence Research Group and founder of the Computer History Museum in Silicon Valley, thinks he might be able to do just that.
He calls it a "surrogate memory," and what he considers an early version of it even has an official name — MyLifeBits.
"The goal is to live as much of life as possible versus spending time maintaining our memory system," Bell explains.
• Click here for FOXNews.com's Personal Technology Center.
Perfect surrogate memory would be supplemental to, but ultimately as good as, your original memory.
It could let you listen to every conversation you had when you were 21 or find that photograph of the obscure date you had on summer vacation.
As Bell says, it would "supplement (and sometimes supplant) other information-processing systems, including people."
MyLifeBits isn't quite there yet, but Bell's nevertheless "gone paperless" for the past decade as part of the project, keeping a detailed, digitized diary that documents his life with photographs, letters and voice recordings.
So that he doesn't miss out on important daily events, Bell wears a SenseCam, developed by Microsoft Research, that takes pictures whenever it detects he may want a photograph.
The camera's infrared sensor picks up on body heat and takes snapshots of anyone else in the room, adjusting itself as available light changes.
Not only does MyLifeBits record your life's digital information, but the software, developed by Bell's researchers Jim Gemmell and Roger Lueder, also can help you retrieve it.
"MyLifeBits is a system aimed at capturing cyber-content in the course of daily life with the goal of being able to utilize it in various ways at work, in our personal life — e.g. finances, family, health and for our future memory," Bell says.
Simply enter a keyword such as "pet," for example, and the search engine will find all available information on your childhood puppy.
It also can run more intricate searches, allowing you to cross-reference all associations linked to certain people or places.
If you're having difficulty remembering where you were and who you were with on a certain day, MyLifeBits would remind you.
And just how much data is needed on a day-to-day basis?
"All the bits that we can that will likely have value for our memory in the near and long-term future, a few bits just for the hell of it," Bell says. "We end up with more bits because we need them for relationships."
Still, is recalling every single detail of an entire lifetime too much? How can anyone guess what's going to be important 20 years from now?
"It is impossible to know what will be required in the future," says Bell. "Furthermore, recording everything allows one item to be used to find another item that may have been created at the same time."
Bell says MyLifeBits could have another important benefit: It may actually improve your real memory.
According to Bell, being reminded of someone in a photograph or screensaver strengthens our recollections.
We constantly are reminded of other events when we delve into our past to find snippets for which we are looking. This reinforces a whole host of links to other memories we otherwise may have forgotten.
But since all this is digitally recorded, what if hackers find it? Couldn't MyLifeBits be a threat to privacy and a boon to identity thieves?
Bell doesn't seem overly concerned.
"MLB introduces no new problems that aren't present in modern computer systems," he said, "except that we present a larger cross-section that makes all the content potentially more valuable."
Additional passwords are being built into the most sensitive documents, he explains.
An even bigger hurdle for the project is cost-efficiency.
The Microsoft team predicts that by 2010, a 1-terabyte (1,000-gigabyte) hard drive will cost less than $300.
That could easily hold all text documents, voice files and photographs of a person's complete life experience — but if it came to video, it would be only enough for four hours per day for an entire year.
On a somewhat smaller level, Sunil Vemuri, co-founder and chief product officer of Hyderabad, India-based QTech, Inc., has been working to develop a "memory prosthesis" that can help people with common, day-to-day memory problems.
QTech's "reQall" service provides a toll-free number that allows clients to use any phone to record reminders of events, appointments or thoughts as and when needed.
It then saves and organizes the recordings and sends daily reminders as needed.
"ReQall is meant for anyone who forgets, for anyone with a day-to-day memory problem," Vemuri says. "The aim of reQall is to provide a long-term service that is available to everyone right now."
Vemuri sees great growth potential for reQall. He wants his team to refine the service to suit users' individual memory needs, whether that involves helping patients remember doctors' appointments, friends remember birthdays or even journalists remember specific quotes.
More ambitious is Vemuri's "What Was I Thinking," a project he worked on while a graduate student at MIT.
That centered around software running on a Compaq iPaq personal digital assistant, similar to a Palm Pilot, which then synced to PCs running Mac OS X, Windows or Linux. It was capable of recording data and using a number of search tools to help the user find forgotten memories, using a range of built-in triggers.
"Many things can serve as good memory triggers: the smell or taste of homemade cooking, the smile on a child's face, a good joke, the roar of the crowd when your sports team scores, etc," Vemuri explained on his MIT Web page.
"In our case, the device records audio from conversations and happenings, analyzes and indexes the audio in an attempt to identify the best memory triggers, and provides a suite of retrieval tools to help the wearer access memories when a forgetting incident occurs."
The device's retrieval tools included an analysis of audio recordings to determine if conversations were heated, calm or humorous and a transcription of audio files to text files by means of a speech-recognition program.
In this way, the text files could be searched for specific words or speech patterns that can trigger those elusive memories.
In the future, some variation on these memory prostheses could change our lives on many levels, from settling a squabble over last week's football scores to assisting an elderly patient remember if she has taken her medication.
We rely on our hard drives for saving our music, photographs, e-mails and videos — so perhaps life-logging software and memory prosthetics are simply the next stage in the evolution of our relationship to the computer.
Wednesday, November 7, 2007
Bipolar Disorder: In the Genes?
Wednesday, October 10, 2007
By Tina Benitez
Bipolar disorder runs in the family. However, scientists still cannot pinpoint it to one specific gene since there are many other factors that may lead to the manic-depressive illness.
The disorder is 75 to 80 percent hereditary, according to Dr. Candida Fink, a child and adolescent psychiatrist and author of Bipolar Disorder for Dummies and The Ups and Downs of Raising a Bipolar Child. Stress, family life, emotional and psychological stresses should also be taken into account.
“It runs a pretty broad range,” said Fink. “Different stresses are likely contributors. Vulnerability and emotional and psychological stress is partly related, but it isn’t always one, and this is important to know. One can develop bipolar with stress or other things combined. We don’t know if it’s something biological or a mixture of developmental, hormonal imbalances.”
Fink said that some hereditary factors are strong indicators of whether someone will develop bipolar disorder or not. Identical twins have a 70 percent higher chance of developing bipolar disorder. If one parent is bipolar, there is a 7 to 10 percent higher risk of getting bipolar disorder. If there are two parents, there is a 20 percent chance of developing bipolar in the offspring because of the multiple genes.
“It’s a huge issue when getting family history and sitting with someone,” said Fink. “Does bipolar run in the family? Particularly, sometimes the further back you go, the family was not diagnosing it, or no one talked about it. It was kind of like, did you have an aunt Sally that never left the house? The most relevant indicator is the immediate family, which is typical of most mental illnesses, but there’s not just one thing that is going to give us the answer.”
Individuals who are bipolar will present signs of depression first, said Fink, but experts must look for the red flags in the different types of depression when diagnosing it. Was it onset at a young age or not? Were there some brief or discreet episodes in their past?
Dr. Francis McMahon, chief of the Genetics Unit of the Mood Anxiety Disorders Program at the National Institute of Mental Health (NIMH) in Bethesda, Md., said that it has been known for a long time that bipolar disorder and manic depression are the most genetic of all illnesses. There have been three kinds of studies, including family studies that show that bipolar disorder definitely runs in families. The other studies were conducted on twins, identical and fraternal.
“If you have a close family member, you have a 10-fold chance of getting bipolar disorder,” said McMahon. “If you do the math, there is about an 80 percent difference of risk of bipolar, which leaves about a 20 percent chance for other factors, and we know even less about what those are.”
Who Gets It — and Why?
For parents, Fink wants to develop a handbook for parents with children who may be bipolar, because there are so many different mood disturbances throughout childhood. “In studies of kids, there may be depression, but you have to ask if they really do look like the classic bipolar disorder,” Fink said. “There’s also attention deficit disorder, or other illnesses brought on by huge trauma. They have to understand the neurobiology component.”
There’s even a division between men and women when it comes to acquiring bipolar, because more women suffer from depression. Bipolar dramatic episodes may show up in the early 30s with more manic episodes later in life in the 40s. “A lot of bipolar disorder is struggling with depression, mostly reported in childhood. Manic episodes show up later, and that’s when you’re hit over the head with bipolar,” said Fink.
Life experiences, use of abusive drugs can also play a role in developing bipolar disorder, but any one of these can cause anxiety or depression, which may exacerbate bipolar episodes, according to McMahon. “Assuming that you are already susceptible, since it is in the family, there may be more of a chance of getting bipolar.”
McMahon added that if people are bipolar, they have to be aware of several things to control episodes including, but not limited, to:
— Missing nights of sleep
— Trans-meridian travel, which causes stress on the body
— Whether they have stress in the family
“Stress in general is not a good thing,” he said. “But in and of itself some people with bipolar have to watch out for stresses that may come from jet lag as well as occupational stress.
Work stress can lead to manic or depressive episodes, often in the case of someone getting a promotion or getting more responsibilities at work, which can tip them over into being susceptible. Bipolar also tends to be something people get early on in life, and according to McMahon, 80 percent of people who are bipolar will see signs of the illness when they are 24, but it doesn’t mean they will be diagnosed.
Once a psychiatrist goes over the family history with them, there may have been some illness that occurred in adolescence. People can go months and years being undiagnosed and continue to get a number of episodes down the line. “Bipolar is episodic,” he said. “A lot of studies are about what triggers the episode, but there’s very little evidence of why people get it.”
Med Alerts
Some of the bigger challenges with new medications used for treating bipolar disorders, according to McMahon is that there are a lot of drugs that treat the episodes, or prevent the episodes, but there’s nothing available to cure the illness. He added that the big challenge for big treatments in the next decade lie in genetic studies.
One group of studies that has made strides in linking bipolar, major depression and other diseases to the genes is the Bipolar Disorder Phenome Database, a collaboration of institutional research from NIMH, Johns Hopkins University, the University of Colorado’s Health Sciences Center, and the University of Heidelberg in Germany. The database includes 20 years of studies on bipolar individuals and those with a related illness and their family history.
He said that there is one gene, which has been clearly identified as influencing bipolar and other diseases, as well as two other genes that need to be reviewed more deeply.
McMahon said that researchers are seeing more and more linkage between specific genes and diseases, specifically bipolar disorder and depression, but it’s still not clear what happens to this genetic makeup, whether it is brought on hereditarily or from outside factors.
“It sounds like a big achievement, and it has had contradictory results, but it still feels like a big step forward,” he said. “We have a long way forward. We have to figure out how and what they do that goes wrong. If we talk six months from now, we may clearly have found specific genes that link between bipolar and depression.”
By Tina Benitez
Bipolar disorder runs in the family. However, scientists still cannot pinpoint it to one specific gene since there are many other factors that may lead to the manic-depressive illness.
The disorder is 75 to 80 percent hereditary, according to Dr. Candida Fink, a child and adolescent psychiatrist and author of Bipolar Disorder for Dummies and The Ups and Downs of Raising a Bipolar Child. Stress, family life, emotional and psychological stresses should also be taken into account.
“It runs a pretty broad range,” said Fink. “Different stresses are likely contributors. Vulnerability and emotional and psychological stress is partly related, but it isn’t always one, and this is important to know. One can develop bipolar with stress or other things combined. We don’t know if it’s something biological or a mixture of developmental, hormonal imbalances.”
Fink said that some hereditary factors are strong indicators of whether someone will develop bipolar disorder or not. Identical twins have a 70 percent higher chance of developing bipolar disorder. If one parent is bipolar, there is a 7 to 10 percent higher risk of getting bipolar disorder. If there are two parents, there is a 20 percent chance of developing bipolar in the offspring because of the multiple genes.
“It’s a huge issue when getting family history and sitting with someone,” said Fink. “Does bipolar run in the family? Particularly, sometimes the further back you go, the family was not diagnosing it, or no one talked about it. It was kind of like, did you have an aunt Sally that never left the house? The most relevant indicator is the immediate family, which is typical of most mental illnesses, but there’s not just one thing that is going to give us the answer.”
Individuals who are bipolar will present signs of depression first, said Fink, but experts must look for the red flags in the different types of depression when diagnosing it. Was it onset at a young age or not? Were there some brief or discreet episodes in their past?
Dr. Francis McMahon, chief of the Genetics Unit of the Mood Anxiety Disorders Program at the National Institute of Mental Health (NIMH) in Bethesda, Md., said that it has been known for a long time that bipolar disorder and manic depression are the most genetic of all illnesses. There have been three kinds of studies, including family studies that show that bipolar disorder definitely runs in families. The other studies were conducted on twins, identical and fraternal.
“If you have a close family member, you have a 10-fold chance of getting bipolar disorder,” said McMahon. “If you do the math, there is about an 80 percent difference of risk of bipolar, which leaves about a 20 percent chance for other factors, and we know even less about what those are.”
Who Gets It — and Why?
For parents, Fink wants to develop a handbook for parents with children who may be bipolar, because there are so many different mood disturbances throughout childhood. “In studies of kids, there may be depression, but you have to ask if they really do look like the classic bipolar disorder,” Fink said. “There’s also attention deficit disorder, or other illnesses brought on by huge trauma. They have to understand the neurobiology component.”
There’s even a division between men and women when it comes to acquiring bipolar, because more women suffer from depression. Bipolar dramatic episodes may show up in the early 30s with more manic episodes later in life in the 40s. “A lot of bipolar disorder is struggling with depression, mostly reported in childhood. Manic episodes show up later, and that’s when you’re hit over the head with bipolar,” said Fink.
Life experiences, use of abusive drugs can also play a role in developing bipolar disorder, but any one of these can cause anxiety or depression, which may exacerbate bipolar episodes, according to McMahon. “Assuming that you are already susceptible, since it is in the family, there may be more of a chance of getting bipolar.”
McMahon added that if people are bipolar, they have to be aware of several things to control episodes including, but not limited, to:
— Missing nights of sleep
— Trans-meridian travel, which causes stress on the body
— Whether they have stress in the family
“Stress in general is not a good thing,” he said. “But in and of itself some people with bipolar have to watch out for stresses that may come from jet lag as well as occupational stress.
Work stress can lead to manic or depressive episodes, often in the case of someone getting a promotion or getting more responsibilities at work, which can tip them over into being susceptible. Bipolar also tends to be something people get early on in life, and according to McMahon, 80 percent of people who are bipolar will see signs of the illness when they are 24, but it doesn’t mean they will be diagnosed.
Once a psychiatrist goes over the family history with them, there may have been some illness that occurred in adolescence. People can go months and years being undiagnosed and continue to get a number of episodes down the line. “Bipolar is episodic,” he said. “A lot of studies are about what triggers the episode, but there’s very little evidence of why people get it.”
Med Alerts
Some of the bigger challenges with new medications used for treating bipolar disorders, according to McMahon is that there are a lot of drugs that treat the episodes, or prevent the episodes, but there’s nothing available to cure the illness. He added that the big challenge for big treatments in the next decade lie in genetic studies.
One group of studies that has made strides in linking bipolar, major depression and other diseases to the genes is the Bipolar Disorder Phenome Database, a collaboration of institutional research from NIMH, Johns Hopkins University, the University of Colorado’s Health Sciences Center, and the University of Heidelberg in Germany. The database includes 20 years of studies on bipolar individuals and those with a related illness and their family history.
He said that there is one gene, which has been clearly identified as influencing bipolar and other diseases, as well as two other genes that need to be reviewed more deeply.
McMahon said that researchers are seeing more and more linkage between specific genes and diseases, specifically bipolar disorder and depression, but it’s still not clear what happens to this genetic makeup, whether it is brought on hereditarily or from outside factors.
“It sounds like a big achievement, and it has had contradictory results, but it still feels like a big step forward,” he said. “We have a long way forward. We have to figure out how and what they do that goes wrong. If we talk six months from now, we may clearly have found specific genes that link between bipolar and depression.”
Tuesday, November 6, 2007
How A Stressful Life Can Contribute To The Development Of Alzheimer’s Disease
Scientific Blogging
Tuesday, November 06, 2007
Tuesday, November 06, 2007
Research about to published in the journal Molecular Psychiatry, resulting from a collaboration between scientists in Germany, Portugal and the UK, suggests that stress contribute directly to the development of Alzheimer’s disease (AD).
According to the results now published, stress induces the production of amyloid beta (Ab) peptide – the molecule associated with the neural plaques characteristic of the disease – and also makes neurons more vulnerable to Ab toxicity. Administration of glucocorticoids (GC) - the production of which is the first physiological response to stress – was shown to have the same effect, confirming the role of stress in AD. This last result is particularly important as GC are used to treat Alzheimer’s patients and according to this research instead of helping they might be, instead, contributing to the disease.
Alzheimer’s disease is part of a group of illnesses called amyloidoses, which result from protein failure to fold and work properly (proteins’ shape is directly related to their functionality) leading, instead, to their accumulation as toxic insoluble plaques (or amyloids). In Alzheimer’s the misfolded protein is called Ab and is found as insoluble plaques in the diseased neurons of patients.
It is known that AD patients can have higher anxiety and GC levels than those found on normal individuals and, in rodent models of AD, it has been found that stress can exacerbate the disease. Furthermore, high stressful conditions leads to cognitive impairments very similar to those found in AD patients. These observations have led researchers C Catania, N Sousa, OFX Almeida and colleagues in Germany, Portugal and the UK to wonder if there could be a causal relationship between stress and AD.
In order to investigate this possible link the researchers tested middle-aged rats in different stressful situations looking into Ab peptide (and also another molecule called C99) levels in the hippocampus and the prefrontal cortex areas of the rats’ brain.
In fact, the first signs of AD do not correlate with the insoluble plaques of Ab protein found in the diseased brain, but instead, with the levels of soluble Ab peptide, while the hippocampus and the prefrontal cortex are the first brain areas affected in AD. Furthermore the Ab peptide is formed from the breakdown of the amyloid precursor protein APP in a series of consecutive steps that originate a molecule called C99, which, when further degraded/cleaved, creates the Ab peptide (APP –… – C99 – Ab). And while Ab peptide is well known to be neurotoxic, recent reports have indicated that C99 – besides being the precursor of Ab - has a similar toxicity with both molecules affecting neural function and also cognitive behaviour. This has led Catania, Sousa, Almeida and colleagues to use the brain levels of both Ab and C99 as a measure of potential neuro-damage and AD development in their experiments. Additionally, the researchers also looked into the consequences of glucocorticoids administration in order to confirm the specific effects of stress in AD, since GC secretion is the first physiological response to stress.
The team of researchers found that stressful situations or injections of GC (which mimic stress) led to an increase of both C99 and, eventually, of Ab, in both the hippocampus and the prefrontal cortex of the rats’ brain. Furthermore, rats with a history of stress were more susceptible to the effects of stress or GC administration, showing bigger increases in C99 levels. It was also observed that administration of soluble Ab led to a similar increase in C99 in the rats’ brain, supporting results by others that have shown that Ab can induce its own production, but also suggesting that Ab, stress and GC induced the same biochemical responses.
Next, Catania and colleagues looked at the animals’ behaviour - as behavioural changes are the hallmark of AD - more specifically, at their learning and memory abilities, as these are the two first cognitive functions affected in the disease. They also looked into the rats’ anxiety levels since AD patients are known to be abnormally anxious.
For the analysis of spatial memory abilities, stressed and non-stressed rats were tested in a maze over 4 days while their emotional state was accessed by looking into anxiety levels, locomotion patterns and exploratory behaviour.
Their first conclusion was that, like AD patients, rats put into stressful situations or receiving GC were much more anxious than controls. It was also shown that these rats showed had less exploratory interest than control animals. Spatial reference memory – which is involved in learning with repeated experiences, such as those experienced in the maze – was similarly impaired by stress or administration of GC or Ab. This last result again supports the conclusion that the GC and Ab act on DA through the same biochemical mechanism. When stress and GC were applied together, spatial reference memory impairment increased revealing a cumulative effect of the various factors.
In conclusion, Catania, Sousa, Almeida and colleagues show that stress can contribute to Alzheimer’s disease in two ways: by inducing the production of known neurotoxic molecules - C99 and Ab - that affect neural function and cognitive behaviour, but also – in the case of existing a previous history of stress – by making animals more susceptible to the C99-inducing effects of GC and Ab. These results – if further confirmed – have important implications for the understanding of the mechanisms behind Alzheimer’s disease and its predisposing factors and, consequently, also for possible therapeutic approaches.
Catania, Sousa, Almeida and colleagues’ research elucidates the mechanism behind stress and GC direct effect on the brain, and can also be important to understand how stress-mediated diseases, such as depression, affect brain function. The research also alert to the need of investigating further the use of GC in AD therapy and calls for the importance of, when treating AD patients, access previous history of stress or GC therapy.
From:Molecular Psychiatry 2007 advance online publication
“The amyloidogenic potential and behavioral correlates of stress”
Thursday, November 1, 2007
Drug May Counteract Down Syndrome
By JR Minkel
Scientific American
February 25, 2007
Formerly approved drug imparts lasting learning and memory improvements to impaired mice
Researchers may have finally found a drug candidate for reducing the mental retardation caused by Down syndrome, which afflicts more than 350,000 people in the U.S. Researchers gave low doses of a human drug to mice bred to mimic the learning and memory problems in people with Down syndrome. After as little as two weeks, the impaired mice performed as well as normal ones in learning tests, and the improvement lasted for up to two months after treatment ended.
But there is a catch: the drug was taken off the market 25 years ago after being found to cause dangerous seizures in some people. And many compounds that boost learning in mice fail in human trials.
Nevertheless, "anyone studying Down's is going to have their socks blown off by this," says geneticist Roger Reeves, a Down syndrome specialist at the Johns Hopkins School of Medicine in Baltimore, who was not involved in the study. "There hasn't been anything out there that we really could take to patients or that we had a strong possibility of taking into the clinic."
Researchers tested the drug, pentylenetetrazole (PTZ), as well as two other compounds—picrotoxin and a gingko biloba extract called bilobalide—because they all interfere with tiny ion channels on brain cells (neurons). When activated, the channels, known as GABAA receptors, inhibit the cells, making it harder for them to form new synapses, or connections, with neighboring neurons.
The deficits of Down syndrome may occur because the brain contains too many such inhibitory signals, says Stanford University neurobiologist Craig Garner, whose group performed the experiments. "In order to learn, you have to have a period during which synapses can get stronger or weaker," he says. "This changing is what's not possible when you have too much inhibition."
So Garner, his student Fabian Fernandez, and their colleagues gave their mice either low doses of PTZ mixed with milk, or low-dose injections of picrotoxin or bilobalide, daily for two to four weeks to slightly raise the level of excitation in the brain. Immediately after treatment, the animals' scores on two memory tests—for recognizing objects they had seen before or remembering how they last entered a maze—were on par with normal mice; two months later, they still did much better than they normally would, the researchers report in a paper appearing online February 25 in Nature Neuroscience.
The treatment "is allowing the normal properties of neurons to work," Garner says. "This slowly over time leads to an improved circuit."
Reeves says there may be other ways to treat Down syndrome, but "you can see your way to clinical testing most easily from here," because researchers identified specific chemicals. "It's hugely promising," he says. "Maybe it will have a big effect, but we don't know that." The inhibition model is plausible, but still unproved in people, he notes, and until researchers better understand the mechanisms by which the compounds work, "I'm wary of rushing into the clinic."
Garner says clinical trials of PTZ could begin in the next year or two, and evaluating them might take five to 10 years. He notes that although PTZ is nearly 100 years old and was used to treat psychiatric disorders and later dementia, researchers never concluded it was effective. It also caused seizures (at doses 100-fold higher than those given to the mice), so the FDA revoked its approval in 1982.
In Down syndrome, chromosome 21 is present in three copies instead of two. Similarly, the mice used in the study have a duplicated piece of chromosome 16. As in Down syndrome, these animals have malformed facial bones and problems forming new memories.
Reeves notes that many researchers have long considered Down syndrome too complex to crack, but the study "serves as notice to the neuroscience community that there are a lot of interesting things to do here. This is not some vague, mega complex issue."
Scientific American
February 25, 2007
Formerly approved drug imparts lasting learning and memory improvements to impaired mice
Researchers may have finally found a drug candidate for reducing the mental retardation caused by Down syndrome, which afflicts more than 350,000 people in the U.S. Researchers gave low doses of a human drug to mice bred to mimic the learning and memory problems in people with Down syndrome. After as little as two weeks, the impaired mice performed as well as normal ones in learning tests, and the improvement lasted for up to two months after treatment ended.
But there is a catch: the drug was taken off the market 25 years ago after being found to cause dangerous seizures in some people. And many compounds that boost learning in mice fail in human trials.
Nevertheless, "anyone studying Down's is going to have their socks blown off by this," says geneticist Roger Reeves, a Down syndrome specialist at the Johns Hopkins School of Medicine in Baltimore, who was not involved in the study. "There hasn't been anything out there that we really could take to patients or that we had a strong possibility of taking into the clinic."
Researchers tested the drug, pentylenetetrazole (PTZ), as well as two other compounds—picrotoxin and a gingko biloba extract called bilobalide—because they all interfere with tiny ion channels on brain cells (neurons). When activated, the channels, known as GABAA receptors, inhibit the cells, making it harder for them to form new synapses, or connections, with neighboring neurons.
The deficits of Down syndrome may occur because the brain contains too many such inhibitory signals, says Stanford University neurobiologist Craig Garner, whose group performed the experiments. "In order to learn, you have to have a period during which synapses can get stronger or weaker," he says. "This changing is what's not possible when you have too much inhibition."
So Garner, his student Fabian Fernandez, and their colleagues gave their mice either low doses of PTZ mixed with milk, or low-dose injections of picrotoxin or bilobalide, daily for two to four weeks to slightly raise the level of excitation in the brain. Immediately after treatment, the animals' scores on two memory tests—for recognizing objects they had seen before or remembering how they last entered a maze—were on par with normal mice; two months later, they still did much better than they normally would, the researchers report in a paper appearing online February 25 in Nature Neuroscience.
The treatment "is allowing the normal properties of neurons to work," Garner says. "This slowly over time leads to an improved circuit."
Reeves says there may be other ways to treat Down syndrome, but "you can see your way to clinical testing most easily from here," because researchers identified specific chemicals. "It's hugely promising," he says. "Maybe it will have a big effect, but we don't know that." The inhibition model is plausible, but still unproved in people, he notes, and until researchers better understand the mechanisms by which the compounds work, "I'm wary of rushing into the clinic."
Garner says clinical trials of PTZ could begin in the next year or two, and evaluating them might take five to 10 years. He notes that although PTZ is nearly 100 years old and was used to treat psychiatric disorders and later dementia, researchers never concluded it was effective. It also caused seizures (at doses 100-fold higher than those given to the mice), so the FDA revoked its approval in 1982.
In Down syndrome, chromosome 21 is present in three copies instead of two. Similarly, the mice used in the study have a duplicated piece of chromosome 16. As in Down syndrome, these animals have malformed facial bones and problems forming new memories.
Reeves notes that many researchers have long considered Down syndrome too complex to crack, but the study "serves as notice to the neuroscience community that there are a lot of interesting things to do here. This is not some vague, mega complex issue."
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