intellectual vanities… about close to everything

Archive for June 2007

Get a First Life… i love it

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Living in a Virtual World

Living in a Virtual World

By Matt Gibson

Since the publication of Neal Stephenson’s landmark SF novel Snow Crash, people have been trying to recreate his “Metaverse”, the interactive virtual world described in the book.

The Metaverse replaces the Internet. You log in, and become a three-dimensional model of your own self, wandering around just like in real life. Instead of going to a company’s website, you walk down to their virtual headquarters. To give someone a phone number, you hand them a virtual business card.Second Life also has a dark side. Researchers from Nottingham University Business School are currently looking into the problem of bullying in the virtual world. Newer, more vulnerable residents have been shot at, physically thrown around, and had their houses fall victim to virtual arsonists. Second Life bullies can use new techniques which aren’t possible in real life, like creating noisy virtual objects that follow people around to intimidate them.

On a larger scale, the Australian Broadcasting Corporation’s Second Life presence, an island formed in the shape of the company’s logo, was recently bombed by virtual vandals, destroying an amphitheatre and other features.

Second Life, created by Linden Research, Inc, is probably the closest anyone has come to realising the Metaverse. After downloading some free software, you pick yourself a new name and dive into the virtual Second Life world. There you can meet anyone else who’s playing the game at the same time, literally bumping into them if you’re not careful.

Some experiences for beginners are very familiar; others are anything but. As well as picking your virtual clothes (you’re strongly advised not to run around naked in “public”, although there are several virtual nudists’ groups), you get to adjust your entire appearance, from the size of your feet to the angle of your nose. And while walking about feels quite natural, flying can take some time to get used to.

So, what’s Second Life for? It’s not a game. There are no dragons to slay, and no concept of “winning”. The point of Second Life is to build an online community in a way that’s never been seen before. People can interact more realistically: gathering together in an arena for a concert; looking at paintings in a gallery; sitting in a Zen garden to listen to a virtual monk (see picture below). People can buy land, join clubs, or just set off to explore a world that’s getting bigger all the time.

It’s not just private citizens, though, but companies who are coming to Second Life. Retailers are selling both virtual and real goods, from Second Life startups making T-shirts for people to wear in the shared hallucination, to multinationals like IBM, which holds client conferences on private islands. Turn up to the Second Life Pontiac dealership and you can go for a virtual test-drive in any of their range of cars.

In September last year, Penguin Books UK announced that they would be establishing a presence in Second Life. Their first move? The virtual publication of one of their most popular novels: Neal Stephenson’s Snow Crash. Yes, you can now read a virtual copy of a book that inspired a universe within the virtual universe it inspired, and my head hurts.

Second Life also has a dark side. Researchers from Nottingham University Business School are currently looking into the problem of bullying in the virtual world. Newer, more vulnerable residents have been shot at, physically thrown around, and had their houses fall victim to virtual arsonists. Second Life bullies can use new techniques which aren’t possible in real life, like creating noisy virtual objects that follow people around to intimidate them.

On a larger scale, the Australian Broadcasting Corporation’s Second Life presence, an island formed in the shape of the company’s logo, was recently bombed by virtual vandals, destroying an amphitheatre and other features.

Earlier bombings in Second Life include attacks on retail stores by The Second Life Liberation Army. The SLLA is a “national liberation movement working towards establishing citizens’ rights within Second Life.” Uneasy walking around in a world where God could just turn off the gravity if He felt like it, the SLLA want to overthrow the Linden Research oligarchy and institute democracy.

Is this taking virtual life too seriously? Perhaps. The parody
website Get a First Life” pokes fun at Second Life users. “Go outside,” it urges. “Membership is free.”

Author Matt meditates in a virtual Zen garden

More virtual shenanigans:

Copping a virtual feel
Playing the cyber field
PCs: our new best friends?
Play Sim City for real


‘Sicko’ subject faces criminal charges

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MAYWOOD, N.J., June 24 (UPI) — A man who helped at Ground Zero after the Sept. 11, 2001, terrorist attacks is being investigated for traveling to Cuba with filmmaker Michael Moore.

Bill Maher of Maywood, N.J., traveled with Moore to seek health treatment in Cuba, where universal healthcare is in place, The New Jersey Star-Ledger reported Sunday.

Maher — who has suffered more than five years with health problems brought on from his volunteer work at Ground Zero — said he was not aware he was breaking any laws by visiting Cuba.

His medical treatment is depicted in Moore’s new documentary, “Sicko.”

Maher reportedly learned last week that he faces charges for violating travel restrictions. He and two other Ground Zero volunteers featured in the documentary are under investigation by the Treasury Department.

Maher told the Star-Ledger he thinks the government is pursuing them for political purposes.

“The reason they have a bug up their butt is about Michael,” said Maher. “It’s ridiculous. What about paying attention to the (Sept. 11) responders who are dying, who can’t get any help? If we wind up going to jail, it’s going to send another message out. Instead of helping (sick Ground Zero volunteers), they’re locking them up.”


Written by huehueteotl

June 25, 2007 at 12:25 pm

Report: Ideal breakfast has ham, cheese

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ciabatta.gifciabatta.gifA scientific study of British students’ eating habits has found eating ham and cheese for breakfast can significantly improve cognitive functioning.

The study headed up by psychology professor David Benton of Wales’ Swansea University found the traditional German breakfast can aid in cognitive functions like memory and attention levels, The Sunday Times of London said.

“It is all down to the glucose release of the breakfast into the bloodstream. The slower the release, the better the pupils performed,” Benton said of his study’s findings.

Benton’s group monitored the eating habits and cognitive performance of 6- and 7-year-olds to determine the effect of a well-balanced breakfast.

Benton’s group also found meals with slow-releasing glucose levels helped children stay physically fit and curbed obesity by limiting one’s appetite.

“The high protein in the breakfast will release into the system slowly, and therefore it will suppress the appetite for longer, and prevent children from snacking,” he told the newspaper.

…done with breakfast. Call for papers on scientific lunch and dinner research now 😉


see also:

Nutr Neurosci. 2006 Jun-Aug;9(3-4):161-8.

The effect of the interaction between glucose tolerance and breakfasts varying in carbohydrate and fibre on mood and cognition.

Nabb SL, Benton D. – Department of Psychology, University of Wales Swansea, Swansea, UK.

As a glucose containing drink has been reported to improve memory, and missing breakfast has been reported to adversely influence memory late in the morning, meals designed to differ in their ability to release glucose into the blood stream were contrasted. Using a factorial design, breakfasts containing 15, 30 or 50 g of carbohydrate and 1.5, 6 or 13 g of fibre were compared. The glucose tolerance of participants proved to be an important factor. Those with better tolerance reported better mood. Those eating breakfasts containing greater amounts of carbohydrate reported feeling tired rather than energetic. The amount of carbohydrate did not negatively affect memory in those with better glucose tolerance, however, the consumption of more carbohydrate resulted in more forgetting in those with poorer glucose tolerance. The effect with reactions times differed from memory in that a greater intake of carbohydrate resulted in faster responses later in the morning.

PMID: 17176639 [PubMed – indexed for MEDLINE]

Written by huehueteotl

June 25, 2007 at 12:03 pm

Posted in Arts, Science

Yawning Saves Your Brain From Overheating

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The next time you “catch a yawn” from someone across the room, you’re not copying their sleepiness, you’re participating in an ancient, hardwired ritual that might have evolved to help groups stay alert as a means of detecting danger. That’s the conclusion of University at Albany researchers Andrew C. Gallup and Gordon G. Gallup, Jr. in a study outlined in the May 2007 issue in Evolutionary Psychology.

The psychologists, who studied yawning in college students, concluded that people do not yawn because they need oxygen, since experiments show that raising or lowering oxygen and carbon dioxide in the blood fails to produce the reaction.  Rather, yawning acts as a brain-cooling mechanism. The brain burns up to a third of the calories we consume, and as a consequence generates heat. 

According to Gallup and Gallup, our brains, not unlike computers, operate more efficiently when cool, and yawning enhances the brain’s functioning by increasing blood flow and drawing in cooler air.

To research the theory that yawning evolved to cool the brain, the UAlbany psychologists had students watch videotapes of people yawning and counted the number of contagious yawns.  In one experiment they found that 50 percent of the people who were instructed to breathe normally or through their mouths yawned while watching other people yawn, while those told to breathe through their nose did not yawn at all. 

In another experiment they found that subjects who held a cold pack to their forehead acted similarly to those who were instructed to breathe through their nose — they, too, did not yawn, while those who held a warm pack or a room temperature pack to their forehead yawned normally. 

Evidence shows that blood vessels in the nasal cavity and face send cool blood to the brain, and by breathing through the nose or by cooling the forehead, the brain is cooled, eliminating the need to yawn.   Recent evidence has linked multiple sclerosis, a demyelinating disease, to thermoregulatory dysfunction.  Excessive yawning is a common symptom of multiple sclerosis, and some MS patients report brief symptom relief after they yawn.

The UAlbany researchers also suggest, again contrary to popular opinion, that yawning does not promote sleep but helps mitigate the need to sleep.  Since yawning occurs when brain temperature rises, sending cool blood to the brain serves to maintain optimal levels of mental efficiency.  Therefore, the psychologists say, when mental processing slows and someone yawns, the tendency for other people to yawn contagiously might have evolved to promote group vigilance as a means of detecting danger.

So the next time you are telling a story and a listener yawns there is no need to be offended — yawning, a physiological mechanism designed to maintain attention, turns out to be a compliment.

Evolutionary Psychology – 2007. 5(1): 92-101

Yawning as a Brain Cooling Mechanism: Nasal Breathing and Forehead Cooling Diminish the Incidence of Contagious Yawning

Andrew C. Gallup, Department of Psychology, State University of New York at Albany, Albany, NY 12222, USA.

Gordon G. Gallup Jr., Department of Psychology, State University of New York at Albany. Email: (Corresponding author)

Abstract: We conducted two experiments that implicate yawning as a thermoregulatory mechanism. The first experiment demonstrates that different patterns of breathing influence susceptibility to contagious yawning. When participants were not directed how to breathe or were instructed to breathe orally (inhaling and exhaling through their mouth), the incidence of contagious yawning in response to seeing videotapes of people yawning was about 48%. When instructed to breathe nasally (inhaling and exhaling through their nose), no participants exhibited contagious yawning. In a second experiment, applying temperature packs to the forehead also influenced the incidence of contagious yawning. When participants held a warm pack (460C) or a pack at room temperature to their forehead while watching people yawn, contagious yawning occurred 41% of the time. When participants held a cold pack (40C) to their forehead, contagious yawning dropped to 9%. These findings suggest that yawning has an adaptive/functional component that it is not merely the derivative of selection for other forms of behavior.

Written by huehueteotl

June 25, 2007 at 9:42 am

Posted in Arts, Psychology, Science

‘Viral Fossil’ May Help Explain Our Vulnerability To HIV

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Human resistance to a retrovirus that infected chimpanzees and other nonhuman primates 4 million years ago ironically may be at least partially responsible for the susceptibility of humans to HIV infection today. These findings provide a better understanding of this modern pandemic infection through the study of an ancient virus called Pan troglodytes endogenous retrovirus, or PtERV1.
“This ancient virus is a battle that humans have already won. Humans are not susceptible to it and have probably been resistant throughout millennia,” said senior author Michael Emerman, Ph.D., a member of the Human Biology and Basic Sciences divisions at the Hutchinson Center. “However, we found that during primate evolution, this innate immunity to one virus may have made us more vulnerable to HIV.”

Evidence of human immunity to this ancient retrovirus first emerged with the sequencing of the chimpanzee genome. “When the chimp genome was sequenced, a team of scientists at the University of Washington led by Evan Eichler found the largest difference overall between the chimp and human genomes was the presence or absence of PtERV1,” Emerman said. “Chimps have 130 copies of PtERV1 and humans have none.”

It is believed that retroviruses have been entering the genome for many millions of years, and so humans share many retroviral DNA fragments with their primate cousins. Such vestiges of primitive infection, rendered inactive by eons of genetic mutation, make up about 8 percent of the human genome.

Innate protection against PtERV1 in humans could be credited, the researchers believe, to the presence of an ancient, rapidly evolving antiviral defense gene called TRIM5a, which produces a protein that binds to and destroys the virus before it can replicate within the body.

“We know that PtERV1 infected chimps, gorillas and old-world monkeys 4 million years ago but left no traces of having infected humans. Our theory is that this is because humans had this innate viral defense system,” Emerman said.

To test their hypothesis, Emerman and co-authors Harmit Singh Malik, Ph.D., an evolutionary biologist and an assistant member of the Center’s Basic Sciences Division, and Shari Kaiser, a graduate student in Emerman’s laboratory, used DNA sequences from the chimp genome to reconstruct a small part of the PtERV1 virus.

They reassembled about one-fifth of the virus by taking dozens of PtERV1 sequences and aligning them to create an “ancestral” sequence, teasing out areas of commonality between them. They then used this information to make a partial viral genome. During reconstruction the viral segment was debilitated, enabling only one round of infection in cells. Working with cells in the laboratory, the researchers found that the human antiviral protein TRIM5a effectively neutralizes this extinct retrovirus, which never successfully fixed into the human genome. 

“However, while TRIM5a may have served humans well millions of years ago, the antiviral protein does not seem to be good at defending against any of the retroviruses that currently infect humans, such as HIV-1,” Emerman said. “In the end, this drove human evolution to be more susceptible to HIV.” For example, the researchers found that changes in TRIM5a that make it better at fighting HIV actually inhibit its ability to stop PtERV1 and vice versa, which indicates that this antiviral gene may only be good at fighting off one virus at a time.

Uncovering the story of TRIM5a’s role in battling one ancient retrovirus while increasing human susceptibility to modern-day HIV “is a lot like doing archaeology — figuring out how humans have become who we are today and why we are or are not susceptible to modern viruses that presently circulate,” Emerman said.

In fact, this emerging area of research, which seeks to better understand modern infections by studying ancient viruses, is known as “paleovirology.” “Ultimately,” said co-author Malik, “if we want to understand why our defenses are the way they are, the answers inevitably lie in these ancient viruses more so than the ones that have affected us only recently, such as HIV.”

These findings were reported by a team of researchers at Fred Hutchinson Cancer Research Center in the June 22 issue of Science.

Polavarapu N, Bowen NJ, McDonald JF. 

Identification, characterization and comparative genomics of chimpanzee endogenous retroviruses.
Genome Biol. 2006;7(6):R51.
PMID: 16805923 [PubMed – indexed for MEDLINE]

Yohn CT, Jiang Z, McGrath SD, Hayden KE, Khaitovich P, Johnson ME, Eichler MY, McPherson JD, Zhao S, Paabo S, Eichler EE.

Lineage-specific expansions of retroviral insertions within the genomes of African great apes but not humans and orangutans.
PLoS Biol. 2005 Apr;3(4):e110. Epub 2005 Mar 1.
PMID: 15737067 [PubMed – indexed for MEDLINE]

Written by huehueteotl

June 25, 2007 at 9:01 am

Posted in Arts, HIV, Science, what I read

Sleeping Pattern Biologically determined

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Individual Differences In Sleep Structure Are Biologically Determined

Sleeping pattern variability has long been attributed to differences in several non-biological factors. Now a study from the Sleep and Performance Research Center at Washington State University Spokane, Wash., has shown that these individual differences are in large part biologically determined and may even prove to be genetic in origin.

Researchers have long observed significant differences in normal people’s sleep. Some are light sleepers, whereas others sleep deeply. Some fall asleep right away, while others take their time.

Such sleeping pattern variability has long been attributed solely to differences in circumstances, habits, and other non-biological factors. But now a study led by Hans Van Dongen, associate research professor and assistant director of the Sleep and Performance Research Center at Washington State University Spokane, has shown that these individual differences constitute traits—that is, they are in large part biologically determined and may even prove to be genetic in origin.

“This is the first study to reveal that substantial differences in sleep patterns exist even among healthy adults who are good sleepers,” said Van Dongen, who emphasized that normal sleep covers a wide terrain and that many different sleep patterns qualify as good sleep. “How much sleep people need and what the structure of their sleep looks like depends in large measure on their biology.”

The results of the NIH-funded research study were published in the June 2007 issue of the Journal of Sleep Research, with WSU graduate student Adrienne Tucker as the lead author. The study, which was conducted in large part at the University of Pennsylvania and was recently continued at Washington State University, assessed the presence and magnitude of biologically determined individual differences in the structure of sleep for a group of 21 carefully screened healthy young adults, and compared these individual differences to the effect of prior sleep deprivation on the structure of their sleep.

Over 11 consecutive days and nights, study participants were monitored continuously in a strictly controlled laboratory environment. They spent eight nights sleeping for up to 12 hours. These nights were interspersed with three 36-hour sleep deprivation periods—that is, three nights without any sleep. During the eight nights when sleep was allowed, polysomnographic recordings—which show brain waves, eye movements, and muscle tone—were done.

The researchers assessed 18 standard sleep parameters, including sleep duration, time to fall asleep, and the amount of time in each sleep stage (stages 1 through 4 and REM sleep). They found large individual differences in these sleep parameters, which showed up consistently across the eight nights with sleep—regardless of whether or not there had been sleep deprivation in the night before. This meant that the individual differences were not driven by circumstance, but were at least partially biologically determined. For deep sleep (stages 3 and 4) in particular, the individual differences were overwhelmingly biological in nature.

“In this group of healthy young adults, the wide variation in the duration and structure of their sleep was, to a large extent, biological in nature. The next logical step is to look for genes that may be responsible for these large individual differences,” Van Dongen said.

The physiological or functional significance of these sleep traits remains a mystery. The fact that all subjects were healthy, young adults and good sleepers seems to rule out any immediate clinical relevance of the differences among them. However, Van Dongen thinks that the sleep differences may be predictive of future clinical conditions.

“Recognition of trait individual differences in sleep may help to understand the increasing evidence for a functional link between sleep and health,” he said.

J Sleep Res. 2007 Jun;16(2):170-80

Trait interindividual differences in the sleep physiology of healthy young adults.

Tucker AM, Dinges DF, Van Dongen HP.

Sleep and Performance Research Center, Washington State University, Spokane, WA 99210-1495, USA.

Despite decades of sleep research by means of polysomnography (PSG), systematic interindividual differences in PSG-assessed sleep parameters have been scarcely investigated. The present study is the first to quantify interindividual variability in standard PSG-assessed variables of sleep structure in terms of stability and robustness as well as magnitude. Twenty-one carefully screened healthy young adults were studied continuously in a strictly controlled laboratory environment, where their PSGs were recorded for eight nights interspersed with three separate 36 h sleep deprivation periods. All PSG records were scored blind to subject and condition, using conventional criteria, and delta power in the non-REM sleep EEG was computed for four electrode derivations. Interindividual differences in sleep variables were examined for stability and robustness, respectively, by comparing results across equivalent nights (e.g. baseline nights) and across experimentally differentiated nights (baseline nights versus recovery nights following sleep deprivation). Among 18 sleep variables analyzed, all except slow-wave sleep (SWS) latency were found to exhibit significantly stable and robust–i.e. trait-like–interindividual differences. This was quantified by means of intraclass correlation coefficients (ICCs), which ranged from 36% to 89% across physiologic variables, and were highest for SWS (73%) and delta power in the non-REM sleep EEG (78-89%). The magnitude of the trait interindividual differences was considerable, consistently exceeding the magnitude of the group-average effect on sleep structure of 36 h total sleep deprivation. Notably, for non-REM delta power–a putative marker of sleep homeostasis–the interindividual differences were from 9.9 to 12.8 times greater than the group-average increase following sleep deprivation relative to baseline. Physiologic sleep variables did not vary among subjects in a completely independent manner–61.1% of their combined variance clustered in three trait dimensions, which appeared to represent sleep duration, sleep intensity, and sleep discontinuity. Any independent functional significance of these sleep physiologic phenotypes remains to be determined.

Written by huehueteotl

June 25, 2007 at 8:44 am

Posted in Arts, Science

Internet Is Addictive, And You Are A Victim Too

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AMA might label Internet as an addiction

ORLANDO, Fla., June 21 (UPI) — The American Medical Association plans to vote on a recommendation to classify Internet and video-game addiction as a formal diagnosis.

The AMA said the heaviest game players are those who play MMORPGs — massive multiplayer online role-playing games — such as World of Warcraft. Those players are more likely to be socially isolated and probably addicted, The Orlando Sentinel said Thursday.

Steve Jones — a communications professor at the University of Illinois and a research fellow with the Pew Internet and American Life Project — said he is skeptical about calling it an addiction.

“Just because any activity might interfere with other activities is not enough to call it an addiction,” he told the newspaper.

Jones said there have been concerns about technology dating back to the 1920s, when people were worried movies were causing children to spend too much time inside

 Hence cautions are to be taken before recklessly creating formal diagnostic categories. Recent medical history is abundant in terms like ADHS or Fibromyalgia, that are so hazy in their delineation, that they might apply two half of the nation or won’t suite anybody, depending on the diagnostician’s rigour. In 2006, the American Medical Association decided to do its part to contribute to the body of knowledge associated with “gaming addiction,” violence and “Internet addiction.” The report — which doesn’t rise to any traditional academic standard for peer-reviewed research, such as a formal literature review — was just published (AMA Report on Internet and Video Game Addiction – PDF).

“Internet adddiction” is a term that was coined in 1996 in a poster at the annual American Psychological Association convention. The term came from a small study that simply changed the word “gambling” in the criteria of “pathological gambling” to “Internet use” and found, not surprising, that a self-selected sample of people identified with the criteria. (The researcher could’ve easily done the same thing with the words, “shopping,” “watching TV,” or “eating chocolate,” and found similar results. This, in itself, is neither an argument pro nor contra non-substance related addiction, though.)

What does the report say about this “disorder”?

“This term seems to have been coined in the 1990s when researchers were attempting to describe a constellation of behaviors observed in persons using the Internet to such an extent that it began to cause other aspects of their lives to become dysfunctional. The DSM-IV disorder most similar to the pattern of behaviors observed with overuse of video games is pathological gambling. “

But unlike the criteria for pathological gambling, which were empirically constructed, the criteria for “Internet addiction” were simply derived from the existing pathological gambling criteria. Hence heavy video game playing is referred to as “video game overuse”, whereas “overuse” certainly is difficult to define.

This is exactly the problem for research. There is no universally accepted definition of “overuse” — of the Internet, of video games, of TV watching, etc. As such, the report states:

“However, as with findings on long-term aggression, there is currently insufficient research to definitively conclude that video game overuse is an addiction. “

Note, AMA does not publish the DSM, the American Psychiatric Association does. The AMA is issuing simply a recommendation. This recommendation, anyway, is welcome to stimulate systematic research as to the boundaries of pathological internet use and gambling as nosological entities.

Written by huehueteotl

June 22, 2007 at 9:10 am

Posted in Psychology