[press release October 27, 2008]
Jerome P. McDonough says an unintended consequence of our rapidly digitizing world is the potential of a “digital dark age.”
What stands a better chance of surviving 50 years from now, a framed photograph or a 10-megabyte digital photo file on your computer’s hard drive?
The framed photograph will inevitably fade and yellow over time, but the digital photo file may be unreadable to future computers – an unintended consequence of our rapidly digitizing world that may ultimately lead to a “digital dark age,” says Jerome P. McDonough, assistant professor in the Graduate School of Library and Information Science at the University of Illinois at Urbana-Champaign.
According to McDonough, the issue of a looming digital dark age originates from the mass of data spawned by our ever-growing information economy – at last count, 369 exabytes worth of data, including electronic records, tax files, e-mail, music and photos, for starters. (An exabyte is 1 quintillion bytes; a quintillion is the number 1 followed by 18 zeroes.)
The concern for archivists and information scientists like McDonough is that, with ever-shifting platforms and file formats, much of the data we produce today could eventually fall into a black hole of inaccessibility.
“If we can’t keep today’s information alive for future generations,” McDonough said, “we will lose a lot of our culture.”
Contrary to popular belief, electronic data has proven to be much more ephemeral than books, journals or pieces of plastic art. After all, when was the last time you opened a WordPerfect file or tried to read an 8-inch floppy disk?
“Even over the course of 10 years, you can have a rapid enough evolution in the ways people store digital information and the programs they use to access it that file formats can fall out of date,” McDonough said.
From a cultural perspective, McDonough said, there’s a “huge amount of content that’s only being developed or is available in a digital-only format. Magnetic tape, which stores most of the world's computer backups, can degrade within a decade."
“E-mail is a classic example of that,” he said. “It runs both the modern business world and government. If that information is lost, you’ve lost the archive of what has actually happened in the modern world. We’ve seen a couple of examples of this so far.”
McDonough cited the missing White House e-mail archive from the run-up to the Iraq War, a violation of the Presidential Records Act.
“With the current state of the technology, data is vulnerable to both accidental and deliberate erasure,” he said. “What we would like to see is an environment where we can make sure that data does not die due to accidents, malicious intent or even benign neglect.”
McDonough also cited Barack Obama’s political advertising inside the latest editions of the popular videogames “Burnout Paradise” and “NBA Live” as an example of something that ought to be preserved for future generations but could possibly be lost because of the proprietary nature of videogames and videogame platforms.
“It’s not a matter of just preserving the game itself. There are whole parts of popular and political culture that we won’t be able to preserve if we can’t preserve what’s going on inside the gaming world.”
McDonough believes there would also be an economic effect to the loss of data from a digital dark age.
“We would essentially be burning money because we would lose the huge economic investment libraries and archives have made digitizing materials to make them accessible,” he said. “Governments are likewise investing huge sums to make documents available to the public in electronic form.”
To avoid a digital dark age, McDonough says that we need to figure out the best way to keep valuable data alive and accessible by using a multi-prong approach of migrating data to new formats, devising methods of getting old software to work on existing platforms, using open-source file formats and software, and creating data that’s “media-independent.”
“Reliance on open standards is certainly a huge part, but it’s not the only part,” he said. “If we want information to survive, we really need to avoid formats that depend on a particular media type. Commercial DVDs that employ protection schemes make it impossible for libraries to legally transfer the content to new media. When the old media dies, the information dies with it.”
Enthusiasm for switching from proprietary software such as Microsoft’s Office suite to open-source software such as OpenOffice has only recently begun to gather momentum outside of information technology circles.
“Software companies have seen the benefits of locking people into a platform and have been very resistant to change,” McDonough said. “Now we are actually starting to see some market mandates in the open direction.”
McDonough cites Brazil, the Netherlands and Norway as examples of countries that have mandated the use of non-proprietary file formats for government business.
“There has been quite a movement, particularly among governments, to say: ‘We’re not going to buy software that uses proprietary file formats exclusively. You’re going to have to provide an open format so we can escape from the platform,’ ” he said. “With that market demand, you really did see some more pressure on vendors to move to something open.”
Press release: http://news.illinois.edu/news/08/1027data.html
Sunday, November 2, 2008
Saturday, November 1, 2008
Learning How Not to Be Afraid
[press release: October 08, 2008]
Why do some people have the ability to remain calm and relaxed even in the most stressful situations? New experiments in mice by Howard Hughes Medical Institute (HHMI) researchers are providing insight into how the brain changes when the animals learn to feel safe and secure in situations that would normally make them anxious.
HHMI investigator Eric R. Kandel and Daniela D. Pollak conducted experiments in which they conditioned mice to feel safe in stressful situations. Their experiments showed that the mice developed a conditioned inhibition of fear, which Kandel calls "learned safety."
The behavioral changes observed in the mice squelched anxiety as effectively as antidepressant drugs such as Prozac, said Kandel, who is at Columbia University. "It's a little bit like psychotherapy," he noted. "This shows that behavioral intervention works."
The research is reported on October 9, 2008, in the journal Neuron. Kandel conducted the study with Pollak, who will soon leave Kandel's lab to assume a position at the Medical University of Vienna.
The new study is noteworthy because it reveals in elegant detail how behavioral conditioning can affect the brain. According to Kandel, knowing how behavioral intervention works at the molecular and cellular levels may prove to be an interesting route to identifying new ways to treat depression and anxiety disorders.
Kandel, who trained as a psychiatrist, is intrigued by the new discoveries. "I've always been interested in how psychoanalysis works," he said. "Since it is a learning experience, there must be a biological basis in the brain."
Two types of fear, instinctive and learned, have deep evolutionary roots and are essential for survival. But in some people, pathological forms of learned fear can lead to debilitating anxiety disorders, post-traumatic stress syndrome, or depression. Learned safety, on the other hand, reduces chronic stress, one of the hallmarks of depression and other psychopathologies. "The ability to identify, develop, and exploit conditions of safety and security is central to survival and mental health," said Kandel, "but little is known of the neurobiology of these processes."
In previous research, Kandel's group taught mice to associate a specific audible tone with protection from an impending averse event. Over time, the mice became conditioned to take advantage of sources of safety and security in their environments. In the new Neuron study, Pollak and Kandel sought to tease out the behavioral and molecular characteristics of learned safety in mice.
In their experiments, mice were trained to associate safety or fear with specific auditory stimuli (tones). For fear conditioning, the auditory stimulus was paired with a mild shock to the mouse's foot. For safety conditioning, the auditory stimulus was not followed by a shock. The experiments showed that the safety-conditioned mice learned to associate the tone with the absence of danger and displayed less anxiety in the presence of this safety signal.
Moving to a stress test, Kandel's team placed the safety-conditioned mice into a pool of water for a swim test. The forced-swim test is commonly used by researchers to measure how antidepressant drugs affect the behavior of mice. "In this seemingly desperate situation - where the mice have no option to escape from the water — they start to show signs of behavioral despair that are ameliorated by antidepressant medications. We found that the mice trained for safety could overcome their sense of hopelessness in the swim test," Kandel explained. The antidepressant effect in the safety-conditioned mice was similar and comparable in magnitude to treatment with the drug fluoxetine (Prozac), Kandel noted.
Pollak and Kandel then looked at how learned safety influenced the development of newborn cells in the dentate gyrus, a structure located in a region of the brain called the hippocampus. The dentate gyrus is notable because it is one of the few structures in the brain that spawns new neurons - even in adult animals.
The researchers found that mice that had been conditioned for safety had a greater number of newborn cells in the dentate gyrus. When Kandel's team used radiation to blunt the birth of new cells in the dentate gyrus, they discovered that their interventions both slowed safety learning and stunted the antidepressant effects of learned safety.
Pollak and Kandel also found that safety learning ramped up expression of brain-derived neurotrophic factor or BDNF in the dentate gyrus. BDNF is a growth factor that promotes the growth and differentiation of new neurons and their connections.
Intriguingly, genetic analyses revealed that in the amygdala, the brain's fear center, learned safety tunes the expression of key components of the dopamine neurotransmitter system and the neuropeptide system. Both systems are thought to influence learning, mood, and cognition.
Kandel said his group was intrigued to find that learned safety did not influence serotonin, the neurotransmitter typically targeted by antidepressant drugs. Learned safety appears to influence levels of both dopamine and neuropeptide neurotransmitters, suggesting new avenues for antidepressant drug development, he said.
"This has given us several interesting insights and led us to a number of potential targets for new drugs," Kandel explained, noting there are already agents in development that influence the dopamine and neuropeptide pathways.
Press release: http://www.hhmi.org/news/kandel20081008.html
Why do some people have the ability to remain calm and relaxed even in the most stressful situations? New experiments in mice by Howard Hughes Medical Institute (HHMI) researchers are providing insight into how the brain changes when the animals learn to feel safe and secure in situations that would normally make them anxious.
HHMI investigator Eric R. Kandel and Daniela D. Pollak conducted experiments in which they conditioned mice to feel safe in stressful situations. Their experiments showed that the mice developed a conditioned inhibition of fear, which Kandel calls "learned safety."
The behavioral changes observed in the mice squelched anxiety as effectively as antidepressant drugs such as Prozac, said Kandel, who is at Columbia University. "It's a little bit like psychotherapy," he noted. "This shows that behavioral intervention works."
The research is reported on October 9, 2008, in the journal Neuron. Kandel conducted the study with Pollak, who will soon leave Kandel's lab to assume a position at the Medical University of Vienna.
The new study is noteworthy because it reveals in elegant detail how behavioral conditioning can affect the brain. According to Kandel, knowing how behavioral intervention works at the molecular and cellular levels may prove to be an interesting route to identifying new ways to treat depression and anxiety disorders.
Kandel, who trained as a psychiatrist, is intrigued by the new discoveries. "I've always been interested in how psychoanalysis works," he said. "Since it is a learning experience, there must be a biological basis in the brain."
Two types of fear, instinctive and learned, have deep evolutionary roots and are essential for survival. But in some people, pathological forms of learned fear can lead to debilitating anxiety disorders, post-traumatic stress syndrome, or depression. Learned safety, on the other hand, reduces chronic stress, one of the hallmarks of depression and other psychopathologies. "The ability to identify, develop, and exploit conditions of safety and security is central to survival and mental health," said Kandel, "but little is known of the neurobiology of these processes."
In previous research, Kandel's group taught mice to associate a specific audible tone with protection from an impending averse event. Over time, the mice became conditioned to take advantage of sources of safety and security in their environments. In the new Neuron study, Pollak and Kandel sought to tease out the behavioral and molecular characteristics of learned safety in mice.
In their experiments, mice were trained to associate safety or fear with specific auditory stimuli (tones). For fear conditioning, the auditory stimulus was paired with a mild shock to the mouse's foot. For safety conditioning, the auditory stimulus was not followed by a shock. The experiments showed that the safety-conditioned mice learned to associate the tone with the absence of danger and displayed less anxiety in the presence of this safety signal.
Moving to a stress test, Kandel's team placed the safety-conditioned mice into a pool of water for a swim test. The forced-swim test is commonly used by researchers to measure how antidepressant drugs affect the behavior of mice. "In this seemingly desperate situation - where the mice have no option to escape from the water — they start to show signs of behavioral despair that are ameliorated by antidepressant medications. We found that the mice trained for safety could overcome their sense of hopelessness in the swim test," Kandel explained. The antidepressant effect in the safety-conditioned mice was similar and comparable in magnitude to treatment with the drug fluoxetine (Prozac), Kandel noted.
Pollak and Kandel then looked at how learned safety influenced the development of newborn cells in the dentate gyrus, a structure located in a region of the brain called the hippocampus. The dentate gyrus is notable because it is one of the few structures in the brain that spawns new neurons - even in adult animals.
The researchers found that mice that had been conditioned for safety had a greater number of newborn cells in the dentate gyrus. When Kandel's team used radiation to blunt the birth of new cells in the dentate gyrus, they discovered that their interventions both slowed safety learning and stunted the antidepressant effects of learned safety.
Pollak and Kandel also found that safety learning ramped up expression of brain-derived neurotrophic factor or BDNF in the dentate gyrus. BDNF is a growth factor that promotes the growth and differentiation of new neurons and their connections.
Intriguingly, genetic analyses revealed that in the amygdala, the brain's fear center, learned safety tunes the expression of key components of the dopamine neurotransmitter system and the neuropeptide system. Both systems are thought to influence learning, mood, and cognition.
Kandel said his group was intrigued to find that learned safety did not influence serotonin, the neurotransmitter typically targeted by antidepressant drugs. Learned safety appears to influence levels of both dopamine and neuropeptide neurotransmitters, suggesting new avenues for antidepressant drug development, he said.
"This has given us several interesting insights and led us to a number of potential targets for new drugs," Kandel explained, noting there are already agents in development that influence the dopamine and neuropeptide pathways.
Press release: http://www.hhmi.org/news/kandel20081008.html
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