If you need to trust people in a job then hire the least imaginative. Creative people are more likely to cheat for money when they are deceived into thinking they can get away with it.
WASHINGTON -- Creative people are more likely to cheat than less creative people, possibly because this talent increases their ability to rationalize their actions, according to research published by the American Psychological Association.
Creative rationalizations. Yes, if you are going to do something you are going to need to rationalize it is best to be good at rationalizing. Of course, an employer with a lot of money could hire a few creative types to come up with rationalizations.
Sure, creative people are great at coming up with new solutions to problems. But can you trust them?
"Greater creativity helps individuals solve difficult tasks across many domains, but creative sparks may lead individuals to take unethical routes when searching for solutions to problems and tasks," said lead researcher Francesca Gino, PhD, of Harvard University.
Gino and her co-author, Dan Ariely, PhD, of Duke University, conducted a series of five experiments to test their thesis that more creative people would cheat under circumstances where they could justify their bad behavior. Their research was published online in APA's Journal of Personality and Social Psychology.
The researchers used a series of recognized psychological tests and measures to gauge research subjects' creativity. They also tested participants' intelligence. In each of the five experiments, participants received a small sum for showing up. Then, they were presented with tasks or tests where they could be paid more if they cheated. For example, in one experiment, participants took a general knowledge quiz in which they circled their answers on the test paper. Afterward, the experimenter told them to transfer their answers to "bubble sheets" – but the experimenter told the group she had photocopied the wrong sheet and that the correct answers were lightly marked. The experimenters also told participants they would be paid more for more correct answers and led them to believe that they could cheat without detection when transferring their answers. However, all the papers had unique identifiers.
So then giving people the opportunity to cheat on low stakes games is a way to discover who you can rely on when you really need no cheating.
You don't need to fear cheating from people just because they are smart. As long as an intelligent person isn't creative they are just as trustworthy as a dumb person isn't creative.
The results showed the more creative participants were significantly more likely to cheat, and that there was no link between intelligence and dishonesty – i.e., more intelligent but less creative people were not more inclined toward dishonesty.
But surely some creative people are honest and good. What additional element of personality determines whether smart creative people will cheat?
Bright light arouses us. Bright light makes it easier to stay awake. Very bright light not only arouses us but is known to have antidepressant effects. Conversely, dark rooms can make us sleepy. It's the reason some people use masks to make sure light doesn't wake them while they sleep.
So I wonder: Should we use light alarm clocks rather than sound alarm clocks? Seriously, anyone reading this use a clock tied to a light source that either suddenly or gradually grows brighter to wake yourself up in the morning? Sound seems like an unnatural thing to use to wake up. Light at least is causing signals to be sent to the brain that trigger hormonal changes that ready your body to waken. So why not use light to wake up? Seems healthier.
The hypothalamus is key to waking up. It is also key to regulation of hunger, thirst, and body temperature. Hey, have your body warm up before you wake up and then wake up thirsty and feeling really ready to get going. Can light do that for us?
Now researchers at UCLA have identified the group of neurons that mediates whether light arouses us — or not. Jerome Siegel, a professor of psychiatry at the Semel Institute for Neuroscience and Human Behavior at UCLA, and colleagues report in the current online edition of the Journal of Neuroscience that the cells necessary for a light-induced arousal response are located in the hypothalamus, an area at the base of the brain responsible for, among other things, control of the autonomic nervous system, body temperature, hunger, thirst, fatigue — and sleep.
Mice without enough of the neurotransmitter hypocretin can't stay away in the light. Lack of hypocretin causes narcolepsy in humans and also people with Parkinson's don't have enough of it.
These cells release a neurotransmitter called hypocretin, Siegel said. The researchers compared mice with and without hypocretin and found that those who didn't have it were unable to stay awake in the light, while those who had it showed intense activation of these cells in the light but not while they were awake in the dark.
This same UCLA research group earlier determined that the loss of hypocretin was responsible for narcolepsy and the sleepiness associated with Parkinson's disease. But the neurotransmitter's role in normal behavior was, until now, unclear.
Suppose one has a smart phone with a speaker jack. Could the alarm on a smart phone be used to somehow trigger a light? How to make the alarm sound on a headset jack feed into triggering a light switch? Anyone know of off-the-shelf parts available do this?
Cigarettes and alcohol serve as gateway drugs, which people use before progressing to the use of marijuana and then to cocaine and other illicit substances; this progression is called the "gateway sequence" of drug use. An article in Science Translational Medicine by Amir Levine, MD, Denise Kandel, PhD; Eric Kandel, MD; and colleagues at Columbia University Medical Center provides the first molecular explanation for the gateway sequence. They show that nicotine causes specific changes in the brain that make it more vulnerable to cocaine addiction -- a discovery made by using a novel mouse model.
So teens smoking because they think its cool are putting themselves at greater risk of a long assortment of degenerative diseases (cancer, heart disease, stroke, arthritis, and a huge number of others) plus greater risk of becoming a coke fiend.
Don't let nicotine tweak your brain's striatum and inhibit your histone deacetylase.
Alternate orders of exposure to nicotine and cocaine were examined. The authors found that pretreatment with nicotine greatly alters the response to cocaine in terms of addiction-related behavior and synaptic plasticity (changes in synaptic strength) in the striatum, a brain region critical for addiction-related rewards. On a molecular level, nicotine also primes the response to cocaine by inhibiting the activity of an enzyme -- histone deacetylase -- in the striatum. This inhibition enhances cocaine's ability to activate a gene called FosB gene, which promotes addiction.
The relationship between nicotine and cocaine was found to be unidirectional: nicotine dramatically enhances the response to cocaine, but there is no effect of cocaine on the response to nicotine. Nicotine's ability to inhibit histone deacetylase thus provides a molecular mechanism for the gateway sequence of drug use.
Most coke heads were smokers before cokers.
Nicotine enhances the effects of cocaine only when it is administered for several days prior to cocaine treatment and is given concurrently with cocaine. These findings stimulated a new analysis of human epidemiological data, which shows that the majority of cocaine users start using cocaine only after they have begun to smoke and while they are still active smokers. People who begin using cocaine after they've started smoking have an increased risk of cocaine dependency, compared with people who use cocaine first and then take up smoking.
We need drugs that will reverse the effects of cocaine and nicotine on the brain.
The researchers are interested to find out whether alcohol and marijuana cause similar changes to the brain.
Too often with medical services you don't find out what costs you are incurring until you get the bill. In fact, you can end up getting multiple bills from different organizations (e.g. testing labs) from a single visit to a medical provider. So it is not always clear when the final bill has arrived. Comparison shopping on price is made even more difficult since each provider offers a wide array of services and you end up paying for some services before moving on to later stages in diagnosis and treatment where more services are proposed. Into this anti-competitive environment a company named Castlight Health has been collecting price information on medical tests and procedures to provide as an information service.
This lack of transparency has contributed to huge disparities in the cost of procedures. According to Castlight Health, a startup based in San Francisco, a colonoscopy costs anywhere from $563 to $3,967 within a single zip code. EKGs can range from $27 to $143, while the price for a set of three spinal x-rays varies from as little as $38 to as high as $162.
When someone else is picking up the tab, mystery pricing is not much of a problem. But these days, even the 59.5 million Americans who get health benefits through large self-insured employers are increasingly expected to pay a percentage of the costs for their medical care.
Castlight sells this service to employers who then let their employees access it to compare costs. If you've got a high co-pay or high deductible and want to get access to comparative medical services cost information in your area then you could let your employer know this service exists.
Where we need to get to: Your medical history should reside on some cloud service that is linked to diagnostics and treatment advisory software. Test results should flow into your cloud repository and then run through diagnostics apps. When real doctors recommend tests you should be able to instantly find out your options for getting the testing done with pricing, schedule openings, and directions. So what Castlight Health is doing is a valuable piece of a much larger puzzle that I expect will come together over the next 10 to 15 years.
The bulldog has more health problems than just about any breed. An excellent New York Times piece entitled "Can the Bulldog be Saved?" looks at why humans created and continue to perpetuate this suffering and short-lived breed and just how many health problems it suffers.
“We have, to some extent, accentuated physical characteristics of the breed to make it look more human, although essentially more like caricatures of humans, and specifically of children,” he told me. “We’ve bred bulldogs for their flat face, big eyes, huge mouth in relation to head size and huge smiling face.” (Advertisers and animators have long recognized that giving an animal big eyes and a big head is a surefire way to endear it to humans. When Walt Disney created Bambi, the studio wanted the character to be an accurate depiction of a deer. But when the original Bambi sketches were deemed not “cute” enough, Disney shortened Bambi’s muzzle and made his head and eyes bigger.)
In an essay in the anthology “Thinking With Animals: New Perspectives on Anthropomorphism,” Serpell wrote that “if bulldogs were the product of genetic engineering by agripharmaceutical corporations, there would be protest demonstrations throughout the Western world, and rightly so. But because they have been generated by anthropomorphic selection, their handicaps are not only overlooked but even, in some quarters, applauded.”
Read the full article and appreciate what human-guided selection has wrought. Most bulldogs can't have sex on their own or give birth unassisted. They are that messed up. Their live expectancy averages just 6 years. How sad. They suffer more than their owners recognize. The article quotes breeders who are in total denial. My advice: Override your instincts and choose a very healthy breed that hasn't been severely damaged by the show breeders. In the 19th century Charles Darwin called the bulldog a monstrosity. It has gotten worse since then. Don't contribute to the creation of monstrosities.
The tragedy of the bulldog and the denial of its breeders makes me wonder what humans will do when they gain the ability to choose offspring genetic variants. Obviously the potential benefits are huge. But I'm reminded of the parents who dress up their 6 year old daughters for fashion shows. Will they opt for genes that maximize cuteness? Will they even go for genes that delay puberty and keep the kids looking very young into adulthood?
How about the parents who want their kids to become various kinds of athletic stars? How extreme will they go? I think we'll witness something akin to a series of arms races. Imagine lots of parents going for genes to make 7 foot tall basketball players. I even expect the genes of the best basketball players will be stolen for procreative purposes. Ditto football players and athletes for other games.
Will parents choose genes that create more extremes in personality? One can imagine some parents aiming for offspring minds that are perfect to become a calculating, driven, domineering, and charismatic CEO while other parents aim for cognitive attributes that make a great scientist or iconoclastic inventor or musician. Will psychopathy become more or less common as a result of parental control of offspring brain genes? Will genetically engineered women be more or less feminine?
When a physician at a U.S. Department of Veterans Affairs hospital in the Seattle noticed a blood pressure drug was preventing recurring nightmares a UC Berkeley researcher got interested in why. Turns out the drug suppresses the neurotransmitter norepinephrine and that during REM sleep norepinephrine goes down so that the brain can process painful memories in order to take the edge off them the next day. So in the REM sleep state it appears the brain processes emotionally difficult experiences to enable you to better handle these memories the next day.
They say time heals all wounds, and new research from the University of California, Berkeley, indicates that time spent in dream sleep can help.
UC Berkeley researchers have found that during the dream phase of sleep, also known as REM sleep, our stress chemistry shuts down and the brain processes emotional experiences and takes the painful edge off difficult memories.
The findings offer a compelling explanation for why people with post-traumatic stress disorder (PTSD), such as war veterans, have a hard time recovering from painful experiences and suffer reoccurring nightmares.They also offer clues into why we dream.
"The dream stage of sleep, based on its unique neurochemical composition, provides us with a form of overnight therapy, a soothing balm that removes the sharp edges from the prior day's emotional experiences," said Matthew Walker, associate professor of psychology and neuroscience at UC Berkeley and senior author of the study to be published this Wednesday, Nov. 23, in the journal Current Biology.
A good night's sleep is probably of great enduring value after an emotionally painful day. Make it a point to go to sleep earlier after traumatic experiences.
Stress neurochemicals are suppressed during the REM phase while the brain processes emotionally laden memories.
"During REM sleep, memories are being reactivated, put in perspective and connected and integrated, but in a state where stress neurochemicals are beneficially suppressed," said Els van der Helm, a doctoral student in psychology at UC Berkeley and lead author of the study.
If you can avoid seeing or dealing with the same disturbing images twice while awake you'll be better able to handle the images after you have gotten some sleep.
Thirty–five healthy young adults participated in the study. They were divided into two groups, each of whose members viewed 150 emotional images, twice and 12 hours apart, while an MRI scanner measured their brain activity.
Half of the participants viewed the images in the morning and again in the evening, staying awake between the two viewings. The remaining half viewed the images in the evening and again the next morning after a full night of sleep.
Those who slept in between image viewings reported a significant decrease in their emotional reaction to the images. In addition, MRI scans showed a dramatic reduction in reactivity in the amygdala, a part of the brain that processes emotions, allowing the brain's "rational" prefrontal cortex to regain control of the participants' emotional reactions.
In addition, the researchers recorded the electrical brain activity of the participants while they slept, using electroencephalograms. They found that during REM dream sleep, certain electrical activity patterns decreased, showing that reduced levels of stress neurochemicals in the brain soothed emotional reactions to the previous day's experiences.
Sleep is therapeutic. Drugs can enhance the therapeutic effect. Good to know.
Cost, noise, and ruination of scenic views are among the reasons windmills are losing their attraction in the Netherlands.
Arguments over the high cost and maintenance of sea-based turbines, as well as complaints from residents about unsightly land-based models, have brought the Dutch to an impasse.
Offshore wind farms produce more electricity than onshore ones but it costs twice as much as onshore wind power due to the higher cost of materials, more expensive drilling methods, and more complex maintenance.
The Netherlands is a densely populated country. The United States can much more easily build lots of wind farms across the plains states without encroaching on the lives of a large number of people. The Dutch can only do that my building offshore. But offshore wind power costs twice as much.
The continued financial crisis and resulting fiscal austerity in many European countries has undermined political support for renewable energy subsidies. For example, Germany's Economy Ministry has just proposed a large reduction in solar subsidies. While solar panel prices are already down 30% in 2011 demand cuts due to slashing of subsidies could result in much lower prices in 2012. Will the same happen for wind? Or will the wind turbine makers just slash production?
Spain's new government, under heavy pressure from high bond interest rates, may entirely eliminate solar and wind power subsidies. It is hard to see how the Southern European countries can afford to continue any renewable energy subsidies. This may lead to even lower prices for photovoltaics. If you are thinking about putting PV on your house you might want to wait for even cheaper prices next year.
A Wall Street Journal article reports on accumulating evidence that particulates from car and truck exhausts damage brain cells.
As roadways choke on traffic, researchers suspect that the tailpipe exhaust from cars and trucks—especially tiny carbon particles already implicated in heart disease, cancer and respiratory ailments—may also injure brain cells and synapses key to learning and memory.
This is an argument for accelerating the development of batteries for electric vehicles. It is also an argument for working from home or living closer to work to reduce the time you spend breathing vehicle exhaust in your car. Ditto for driving to work very early.
Parenthetically, the amount of smoke I've seen gushing out of a diesel commuter passenger train is disgusting. Are train emissions regulations less strict than truck emissions regulations?
One problem with diesel trucks: they last a long time. So while in recent years emissions regulations for trucks have gotten much tighter we are going to have to wait decades for the older and higher polluting trucks to wear out. Outfitting the older trucks with newer emissions control equipment would be money well spent.
One thing you can do: See if your car has a cabin air filter (note, that PDF is only thru 2007 models and might not be complete) and replace it when dirty. Some filters are easy to replace, others require skill and time. Here's a Prius owners chat on cabin air filter replacement. Note that these filters are not HEPA level. So they are limited but better than nothing.
You can find portable HEPA filters that can plug into ashtray power. If you don't mind basically giving up a seat for an air filter you can get more benefit. But I've read online discussions about the rate of turn-over of cabin air per hour (Air Changes per Hour or ACH) where one participant says the portable HEPA filters can't pump air thru fast enough to keep up in the rate at which air comes in from the outside. But when stuck in traffic the air comes in more slowly and at a lower air quality. Such a filter might work better when it is most needed.
Does any OEM offer a HEPA filter option or some other claim to better air quality thru filtering?
A report by Emily Singer for Technology Review brings a whole new twist to the open access movement for information. Needed: a heart defibrillator maker who will let you capture sensor data from the implanted device.
Hugo Campos is a man on a mission. He wants access to the data being collected inside his body by an implanted cardiac defibrillator. He believes that having this information could help him take control of his health—for example, by helping him figure out what triggers his frequent attacks of abnormal heart rhythms. While not life-threatening, they cause dizziness, fainting, and chest pain. But he says device makers are reluctant to make that information available, mostly for commercial reasons.
More data pooled together means more insights. Just as some people (e.g. Razib Khan) have released their genetic testing data into the public domain so could people with sensors embedded in their bodies. In fact, this will happen. Lots of people will stream real time sensor streams from their bodies to the internet for anyone to capture, watch in real-time, and analyze.
Collection of biological data used to be the sole preserve of scientists doing research. But with sensors and communications networks getting so cheap bottom-up biological and biomedical research is already starting as a result of increasing numbers of individuals uploading their test data web sites. Already this trend is yielding published research with valuable findings.
I expect we will be able to watch live feeds of assorted beating hearts all over the world. Gamers will let spectators watch their hearts beat and their brain waves change as they compete in online game tournaments. People will put sensors on their pets just as they put video cameras on them.
Since a great sense of smell enriches enjoyment of foods and many natural settings a declining sense of smell with age is just another reason to favor the development of rejuvenation therapies.
AURORA, Colo. -- Scientists studying how the sense of smell changes as people age, found that olfactory sensory neurons in those 60 and over showed an unexpected response to odor that made it more difficult to distinguish specific smells, putting them at greater risk from dangerous chemicals and poor nutrition.
"We found clear changes in olfactory sensory neuron responses to odors for those 60 and up," said Professor Diego Restrepo, Ph.D., director of the Center for NeuroScience at the University of Colorado School of Medicine who led the researchers. "When we presented two different odors to the olfactory sensory neurons of younger people they responded to one or the other. The sensory neurons from the elderly responded to both. This would make it harder for the elderly to differentiate between them."
Its like becoming color blind. Old people can't distinguish between as many different scents. I can heart Mick Jagger singing "What a drag it is getting old".
Losing sensitivity to scents is a health hazard. Growing old is dangerous. So lets just not grow old.
According to the study published in the latest issue of Neurobiology of Aging, those losing their sense of smell are at a higher risk of malnutrition since taste and smell are closely related, they may also be unable to detect spoiled food, leaking gas or toxic vapors.
Do taste buds age too? Do old people also get less taste signaling from their tongues?
Imagine someone 70 years old getting some cell therapies combined with perhaps a gene therapy to kill senescent cells on the tongue and nasal passages. They could potentially regain scent and smell sensitivity that they had decades earlier. Throw in similar therapies for their eyes and eyes and their sensory experience could be greatly enhanced.
A cosmic one-two punch of colossal volcanic eruptions and meteorite strikes likely caused the mass-extinction event at the end of the Cretaceous period that is famous for killing the dinosaurs 65 million years ago, according to two Princeton University reports that reject the prevailing theory that the extinction was caused by a single large meteorite.
Princeton-led researchers found that a trail of dead plankton spanning half a million years provides a timeline that links the mass extinction to large-scale eruptions of the Deccan Traps, a primeval volcanic range in western India that was once three-times larger than France. A second Princeton-based group uncovered traces of a meteorite close to the Deccan Traps that may have been one of a series to strike the Earth around the time of the mass extinction, possibly wiping out the few species that remained after thousands of years of volcanic activity.
Researchers led by Princeton Professor of Geosciences Gerta Keller report this month in the Journal of the Geological Society of India that marine sediments from Deccan lava flows show that the population of a plankton species widely used to gauge the fallout of prehistoric catastrophes plummeted nearly 100 percent in the thousands of years leading up to the mass extinction. This eradication occurred in sync with the largest eruption phase of the Deccan Traps — the second of three — when the volcanoes pumped the atmosphere full of climate-altering carbon dioxide and sulfur dioxide, the researchers report. The less severe third phase of Deccan activity kept the Earth nearly uninhabitable for the next 500,000 years, the researchers report. A substantially weaker first phase occurred roughly 2.5 million years before the second-phase eruptions.
Imagine something on the order of the Deccan Traps eruptions occurred today. Would there be any way to do climate engineering to partially ameliorate the effects? I suspect we could not command enough energy in a short enough period of time to do fundamental alterations on the scale necessary.
But suppose we had 100 years to prepare. What could we do? If we had a sufficient amount of nuclear fusion power we could move civilization underground and use the fusion energy to power the synthesis of artificial foods or underground farms. But what could we do on the surface to take the carbon and sulfur out of the atmosphere as fast as a massive volcano would inject it? How to clean the atmosphere?
A study in teenagers showed the "reward hub", which is involved in addiction, was larger in regular players.
A report in Translational Psychiatry said it was unknown if games changed the brain or if brain differences made people more likely to play.
What I wonder: have video games shifted people from drug addiction to game addiction? If so, video games might actually be reducing brain damage by giving people something less harmful to get addicted to. On the other hand, since video games are illegal and have less of a stigma about them more people can become addicted to them more easily.
People who are alcohol-dependent and who also carry a particular variant of a gene run an increased risk of premature death. This is a recent finding from the interdisciplinary research at the Department of Psychology and the Sahlgrenska Academy at the University of Gothenburg, Sweden.
Researchers in the longitudinal project Göteborg Alcohol Research Project (GARP) have been investigating the dopamine D2 receptor gene and found that a variant of this gene is overrepresented in people with severe alcohol dependency, and that it is linked to a number of different negative consequences that can be of vital significance to the person affected.
"Our research shows that alcohol-dependent individuals, who are also carriers of this gene variant, run 10 times the risk of dying prematurely, compared with the average population," says Claudia Fahlke, a representative from the research team.
What genetic variants make for a bigger ventral striatum?
Does someone choose to be understanding and sympathetic? Or do genetic variants for an oxytocin receptor in the brain make people more or less empathetic in very easily recognizable ways? Read below and guess which variants of the oxytocin receptor gene you carry.
CORVALLIS, Ore. – Scientists have discovered that a gene that influences empathy, parental sensitivity and sociability is so powerful that even strangers observing 20 seconds of silent video identified people with a particular genetic variation to be more caring and trusting.
In the study, 23 romantic couples were videotaped while one of the partners described a time of suffering in their lives. The other half of the couple and their physical, non-verbal reactions were the focal point of the study. Groups of complete strangers viewed the videos. The observers were asked to rate the person on traits such as how kind, trustworthy, and caring they thought the person was, based on just 20 seconds of silent video.
"Our findings suggest even slight genetic variation may have tangible impact on people's behavior, and that these behavioral differences are quickly noticed by others," said Aleksandr Kogan, a postdoctoral fellow at the University of Toronto and the study's lead author.
The study builds on previous research conducted by Sarina Rodrigues Saturn, an assistant professor of psychology at Oregon State University. In that study, Saturn and her colleagues linked a genetic variation that affects hormone/neurotransmitter oxytocin's receptor to empathy and stress reactivity. Saturn is senior author on the new study, which is in the latest issue of Proceedings of the National Academy of Sciences (PNAS).
The standard question I always wonder when I read reports about genes causing cognitive differences: Which genetic variants will people choose for their offspring when they become able to make such choices? Will the world become a more or less empathetic place once people can choose which genes their kids can get? Will humanity diverge into very empathetic and very not empathetic groups? Will the empathetic empathize even with the turbo unempathetic?
Perhaps the GGs and AAs should form their own social media social circles.
"It was amazing to see how the data aligned so strongly by genotype," Saturn said. "It makes sense that a gene crucial for social processing would yield these findings; other studies have shown that people are good at judging people at a distance and first impressions really make an impact."
Before the videos were recorded, the scientists tested the couples and identified their genotype as GG, AG, or AA. Individuals homozygous for the G allele (carrying two copies of the G version of the gene) of the oxytocin receptor tend to be more "prosocial," defined by researchers as the ability to behave in a way that benefits another person. In contrast, the carriers of the A version of the gene (AG or AA genotypes) tend to have a higher risk of autism, as well as self-reported lower levels of positive emotions, empathy and parental sensitivity.
The carriers of the AA variants are least trusted.
Oxytocin has already been significantly linked with social affiliation and reduction in stress. It is a peptide made in the hypothalamus and has targets all over the body and the brain. It is best known for its role in female reproduction and is associated with social recognition, pair bonding, dampening negative emotional responses, trust and love.
Out of the 10 people who were marked by the neutral observer as "most prosocial, six carried the GG genotype associated with the oxytocin receptor; of the 10 people who were marked as "least trusted," nine were carriers of the A version of the gene. The people carrying an A version of the gene were viewed as less kind, trustworthy and caring toward their partners in the video.
Possibly the neutral observers are also responding to genetic variants of other genes that tested for in this study.
Imagine you are hiring nurses. Do you want AA or GG nurses? I'm thinking GG since patients want to feel their nurses care about their well-being. On the other hand, kindness is probably a risk factor for a prison guard and probably isn't a desirable trait in a loan officer either.
The scientists say it is for people with diseases. But of course the gamers will eventually be the biggest users. Of course, if virtual game playing is an addiction the scientists are right anyhow.
PHILADELPHIA - A team of researchers co-led by the University of Pennsylvania has developed and tested a new high-resolution, ultra-thin device capable of recording brain activity from the cortical surface without having to use penetrating electrodes. The device could make possible a whole new generation of brain-computer interfaces for treating neurological and psychiatric illness and research. The work was published in Nature Neuroscience.
When will the first person get their skull sawed open to implant an interface to play video games faster? Which country will they have to travel to in order to get this surgery done? Seriously. Also, will humans ever drive cars with implanted interfaces? Or will cars be shifted to pure robotic operation before that happens?
There is of course scientific value to a higher resolution way to measure brain activity.
"The new technology we have created can conform to the brain's unique geometry, and records and maps activity at resolutions that have not been possible before," says Brian Litt, MD, the study's senior author and Associate Professor of Neurology at the Perelman School of Medicine and Bioengineering at the University of Pennsylvania. "Using this device, we can explore the brain networks underlying normal function and disease with much more precision, and its likely to change our understanding of memory, vision, hearing and many other normal functions and diseases." For our patients, implantable brain devices could be inserted in less invasive operations and, by mapping circuits involved in epilepsy, paralysis, depression and other 'network brain disorders' in sufficient detail, this could allow us to intervene to make patients better, Litt said.
Want a brain implant that distracts you from negative thoughts? No, I'm not talking about emotional depression. I'm talking about the sorts of resentful negative thoughts people develop when the financial system nearly crashes. An implant could help you become comfortably numb.
A 360 channel array. No doubt future models will come with even higher capacity.
Composed of 720 silicon nanomembrane transistors in a multiplexed 360-channel array, the newly designed ultrathin, flexible, foldable device can be positioned not only on the brain surface but also inside sulci and fissures or even between the cortical hemispheres, areas that are physically inaccessible to conventional rigid electrode arrays. Current arrays also require separate wires for each individual sensor, meaning that they can sample broad regions of the brain with low resolution or small regions with high resolution, but not both. The multiplexed nanosensors of the new device can cover a much large brain area with high resolution, while using almost ten times fewer wires.
As we age lots of our parts wear out and malfunction. What we need: replacement parts. So every time yet another research group reports success growing replacement organs it is time for cheer. Some lucky Japanese mice have already benefited. Keep an eye out for mice trying to sneak on Japan-bound airplanes.
Last spring, a research team at Japan's RIKEN Center for Developmental Biology created retina-like structures from cultured mouse embryonic stem cells. This week, the same group reports that it's achieved an even more complicated feat—synthesizing a stem-cell-derived pituitary gland.
Click thru to read the details.
Tissue engineering to create the most complex glands and organs requires presenting a dynamically changing 3-dimensional environment to the cells that make up the organ being grown. The cells need to get shifting gradients of chemical signals that attempt to replicate the chemical environment of a developing fetus. A very difficult challenge both because the changing local fetal chemical environment has to be identified and also then replicated.
Growth of organ replacements is one of the most radical forms of rejuvenation. Rather than try to send in repair cells or gene therapies to do, at best, partial fixes the complete replacement of an organ effectively turns the biological clock on it back to complete youthfulness. I expect some reading this will live to see the day when whole organ replacement with vat-grown organs becomes routine - at least for those who can afford the treatment.
Inflammation from chronic bacterial infections is a suspected risk factor for heart disease and stroke. Therefore it is of interest that more frequent teeth cleaning might cut heart disease and stroke risk.
Professional tooth scaling was associated with fewer heart attacks and strokes in a study (Abstract 17704) from Taiwan presented at the American Heart Association's Scientific Sessions 2011.
Among more than 100,000 people, those who had their teeth scraped and cleaned (tooth scaling) by a dentist or dental hygienist had a 24 percent lower risk of heart attack and 13 percent lower risk of stroke compared to those who had never had a dental cleaning. The participants were followed for an average of seven years.
Scientists considered tooth scaling frequent if it occurred at least twice or more in two years; occasional tooth scaling was once or less in two years.
The study included more than 51,000 adults who had received at least one full or partial tooth scaling and a similar number of people matched with gender and health conditions who had no tooth scaling. None of the participants had a history of heart attack or stroke at the beginning of the study.
Getting your teeth cleaned regularly is a good idea anyway since it cuts the risk of loss of teeth and avoids the development of an interest in TV commercials about dentures.
A separate study found a big difference in heart and stroke risk based on the number of remaining teeth.
In a separate study (abstract 10576), researchers found that the value of markers for gum disease predict heart attack, congestive heart failure and stroke in different ways and to different degrees.
Anders Holmlund, D.D.S., Ph.D. Centre for Research and Development of the County Council of Gävleborg, Sweden, and senior consultant; Specialized Dentistry, studied 7,999 participants with periodontal disease and found people with:
- Fewer than 21 teeth had a 69 percent increased risk of heart attack compared to those with the most teeth.
- A higher number of deepened periodontal pockets (infection of the gum around the base of the tooth) had a 53 percent increased risk of heart attack compared to those with the fewest pockets.
- The least amount of teeth had a 2.5 increased risk of congestive heart failure compared to those with the most teeth.
- The highest incidence of gum bleeding had a 2.1 increased risk of stroke compared to those with the lowest incidence.
Haven't gotten your teeth cleaned lately? Time to make an appointment. Also, get out that floss and use it.
Mitochondria are organelles within cells which break down sugar to release energy. Their healthy functioning is key to health. Accumulation of damage in mitochondria is suspected to contribute to aging. In at least some cases Parkinson's Disease is thought to be caused by damaged mitochondria.
Boston, Mass. - Current thinking about Parkinson's disease is that it's a disorder of mitochondria, the energy-producing organelles inside cells, causing neurons in the brain's substantia nigra to die or become impaired. A study from Children's Hospital Boston now shows that genetic mutations causing a hereditary form of Parkinson's disease cause mitochondria to run amok inside the cell, leaving the cell without a brake to stop them. Findings appear in the November 11 issue of Cell.
Mitochondrial movement is often a good thing, especially in neurons, which need to get mitochondria to cells' periphery in order to fuel the axons and dendrites that send and receive signals. However, arresting this movement is equally important, says senior investigator Thomas Schwarz, PhD, of Children's F.M. Kirby Neurobiology Center, since it allows mitochondria to be quarantined and destroyed when they go bad.
"Mitochondria, when damaged, produce reactive oxygen species that are highly destructive, and can fuse with healthy mitochondria and contaminate them, too," Schwarz says. "It's the equivalent of an environmental disaster in the cell."
Damaged mitochondria accumulate in us as we age. The ability to either repair or more reliably eject them would slow the aging process. Combined with other rejuvenation therapies treatments aimed at ridding us of damaged mitochondria will eventually enable us to reverse aging.
To the extent that Parkinson's is caused by damaged mitochondria that's actually good news for the rest of us who do not have Parkinson's. Why? Because Parkinson's provides motives for medical researchers to develop therapies targeting destruction or repair of toxic damaged mitochondria. Such therapies will be beneficial the rest of us. So future treatments developed to fix the root cause of Parkinson's will also help those without Parkinson's.
Biomass energy: the government energy policy disaster that keeps on giving. Yet another reason why biofuel subsidies and biofuel legislated requirements are a bad idea.
A new study on greenhouse gas emissions from oil palm plantations has calculated a more than 50% increase in levels of CO2 emissions than previously thought – and warned that the demand for 'green' biofuels could be costing the earth.
The study from the University of Leicester was conducted for the International Council on Clean Transportation, an international think tank that wished to assess the greenhouse gas emissions associated with biodiesel production. Biodiesel mandates can increase palm oil demand directly (the European Biodiesel Board recently reported big increases in biodiesel imported from Indonesia) and also indirectly, because palm oil is the world's most important source of vegetable oil and will replace oil from rapeseed or soy in food if they are instead used to make biodiesel.
The palm oil plantations let more light hit the ground, heating up the soil, drying it out, and causing the peatlands to break down.
There is more carbon stored in tropical peatlands than in tropical forests.
Dr Sue Page, Reader in Physical Geography at the University of Leicester, added: "Tropical peatlands in Southeast Asia are a globally important store of soil carbon – exceeding the amount stored in tropical forest vegetation. They are under enormous pressure from plantation development. Projections indicate an increase in oil palm plantations on peat to a total area of 2.5Mha by the year 2020 in western Indonesia alone –an area equivalent in size to the land area of the United Kingdom."
Calorie restriction is the only reliable way across a wide range of species to increase life expectancy. So the mechanism by which a low calorie diet extends life is a question which many researchers are pursuing. Since very few of us are willing to live in a state of perpetual hunger we need a drug that would give us the benefit of calorie restriction without the gaunt look and hunger pangs. So a report from a German group on an enzyme in a yeast model that appears to be key to life extension for calorie-restricted yeast merits some attention. The researchers are able to show that turning up the enzyme Srx1 protects an enyzme called Prx1 and the Prx1 is key to preventing aging damage. The result is more Prx1 activity, less damage, and longer life - at least in yeast.
By consuming fewer calories, ageing can be slowed down and the development of age-related diseases such as cancer and type 2 diabetes can be delayed. The earlier calorie intake is reduced, the greater the effect. Researchers at the University of Gothenburg have now identified one of the enzymes that hold the key to the ageing process.
"We are able to show that caloric restriction slows down ageing by preventing an enzyme, peroxiredoxin, from being inactivated. This enzyme is also extremely important in counteracting damage to our genetic material," says Mikael Molin of the Department of Cell and Molecular Biology.
This makes sense from a theoretical perspective. Turning up repair enzymes will reduce the rate at which permanent debilitating (and eventually fatal) damage accumulates. Whether more activity of these particular enzymes would extend life in humans remains to be seen. But it seems very likely that if not these enzymes then some other repair enzymes could extend our lives if we could find safe ways to turn them up to higher levels in our cells.
Prx1 breaks down hydrogen peroxide, a toxic by-product of normal human metabolism.
They are able to show that active peroxiredoxin 1, Prx1, an enzyme that breaks down harmful hydrogen peroxide in the cells, is required for caloric restriction to work effectively.
More Srx1 by itself extends yeast cell life without calorie restriction.
The results, which have been published in the scientific journal Molecular Cell, show that Prx1 is damaged during ageing and loses its activity. Caloric restriction counteracts this by increasing the production of another enzyme, Srx1, which repairs Prx1. Interestingly, the study also shows that ageing can be delayed without caloric restriction by only increasing the quantity of Srx1 in the cell. Repair of the peroxiredoxin Prx1 consequently emerges as a key process in ageing.
A drug that mimics the effects of calorie restriction will only slow down the rate of aging and probably not by a large amount. But slowed aging could give some of us enough time to live until rejuvenation therapies become available.
New York, November 2, 2011 -- A woman goes into labor, and gives birth. The newborn is swaddled and placed to sleep in a nearby bassinet, or taken to the hospital nursery so that the mother can rest. Despite this common practice, new research published in Biological Psychiatry provides new evidence that separating infants from their mothers is stressful to the baby.
It is standard practice in a hospital setting, particularly among Western cultures, to separate mothers and their newborns. Separation is also common for babies under medical distress or premature babies, who may be placed in an incubator. In addition, the American Academy of Pediatrics specifically recommends against co-sleeping with an infant, due to its association with Sudden Infant Death Syndrome, or SIDS.
Humans are the only mammals who practice such maternal-neonate separation, but its physiological impact on the baby has been unknown until now. Researchers measured heart rate variability in 2-day-old sleeping babies for one hour each during skin-to-skin contact with mother and alone in a cot next to mother's bed. Neonatal autonomic activity was 176% higher and quiet sleep 86% lower during maternal separation compared to skin-to-skin contact.
How many easily avoidable ways have we changed our environments that have increased our stress and made us less healthy?
In a small scale study endoscopists appeared to do better at detecting pre-cancerous adenomas when they listened to Mozart. So take along a smart phone with Mozart on it and some speakers and offer their use to your endoscopist when you are getting wheeled in for a colonoscopy.
Washington, DC -- Physicians who listen to Mozart while performing colonoscopy may increase their detection rates of precancerous polyps, according to the results of a new study unveiled today at the American College of Gastroenterology's (ACG) 76th Annual Scientific meeting in Washington, DC.
The study, "The 'Mozart Effect' and Adenoma Detection," by Catherine Noelle O'Shea, DO and David Wolf, MD, of the University of Texas Health Science Center at Houston, found adenoma detection rate—the proportion of patients undergoing screening colonoscopy in whom an adenomatous polyp is found and an important measure of a high quality endoscopic exam --increased from baseline values with music compared to without for two endoscopists whose baseline adenoma detection rates were calculated over a one-year period prior to the start of the study. The "Mozart Effect" refers to a set of research results that found listening to Mozart's music may result in significant short-term improvement in spatial temporal reasoning. Researchers used this previous theory to determine whether or not listening to Mozart while performing a colonoscopy had any impact on an endoscopist's adenoma detection rate.
In this randomized controlled trial, two endoscopists each with experience completing at least 1000 colonoscopies performed screening colonoscopies randomly assigned to music -- where Mozart was played -- or no music. Each endoscopist was unblinded to music exposure. Adenoma detection rates from this study were than calculated and compared to the baseline rates.
"Both endoscopists had higher adenoma detection rates listening to music when compared with their baseline rates," said lead researcher Dr. O'Shea.
Endoscopist #1, who was blinded to outcome, had an adenoma detection rate of 66.7 percent listening to Mozart and 30.4 percent without the music. Endoscopist #2, who was unblinded to the outcome, had an adenoma detection rate of 36.7 percent with Mozart and 40.5 percent without the music. Baseline detection rates were 21.25 percent (Endoscopist #1) and 27.16 percent (Endoscopist #2).
So endoscopist productivity varies all over the map. I wish there was a way to choose an endoscopist based on adenoma detection rate. Ditto for other docs doing other kinds of early stage cancer detection.
Any readers tried different kinds of music when writing software? I'd love to see a software coding productivity study comparing different forms of music, no sounds, normal office sounds, and assorted kinds of white noise.
Got a favorite white noise for enabling the mind to concentrate? I'm looking to try some different forms of sound background to see whether I can up brain productivity by doing so.
When cells get old some of them die. But unfortunately other cells live on what's called a senescent state in which they produce toxins that harm neighboring cells and the whole body. Got some aches and pains? You can probably at least partially blame them on senescent cells. Mayo Clinic researchers working with genetically engineered mice showed that by killing off senescent cells they delayed the development of age-related diseases such as muscle loss and cataracts. Killing off bad cells enabled the good cells in muscles to function better. I want this treatment in a human-usable form. The sooner the better.
ROCHESTER, Minn. — Researchers at Mayo Clinic have shown that eliminating cells that accumulate with age could prevent or delay the onset of age-related disorders and disabilities. The study, performed in mouse models, provides the first evidence that these "deadbeat" cells could contribute to aging and suggests a way to help people stay healthier as they age. The findings appear in the journal Nature, along with an independent commentary on the discovery.
These mice were genetically engineered to make their senescent cells more vulnerable. For us adults perhaps gene therapy could add the genetic mechanism needed to kill off our old cells. But it will be a big challenge to get genes delivered into all the cells in the body.
It is hard to selectively kill off just certain types of cells as cancer treatment side effects and failures have shown. Though in some ways killing senescent cells is easier than killing cancers. First off, to cure cancer the dead rate of cancer cells has to be near 100%. By contrast, the killing of just half of all senescent cells would cut the toxin load to the body in half and leave room for healthier cells to divide and take the place of sicker cells. Second, since a single course of treatment doesn't have to kill all senescent cells there's a lot more time in which to do successive waves of treatments to kill off the surviving senescent cells.
A co-author of this study talks in terms of potential benefits in terms that begin to approach the radical rhetoric of biogerontologist Aubrey de Grey. Aubrey advocates the outright defeat of aging (reversal of aging with youth lasting thousands of years). One of the major planks in Aubrey's platform for aging defeat is the killing off of senescent cells.
"By attacking these cells and what they produce, one day we may be able to break the link between aging mechanisms and predisposition to diseases like heart disease, stroke, cancers and dementia," says co-author James Kirkland, M.D., Ph.D., head of Mayo's Robert and Arlene Kogod Center on Aging and the Noaber Foundation Professor of Aging Research. "There is potential for a fundamental change in the way we provide treatment for chronic diseases in older people."
Human bodies become more inflamed as they get old in large part due to senescent cells.
Five decades ago, scientists discovered that cells undergo a limited number of divisions before they stop dividing. At that point the cells reach a state of limbo — called cellular senescence — where they neither die nor continue to multiply. They produce factors that damage adjacent cells and cause tissue inflammation. This alternative cell fate is believed to be a mechanism to prevent runaway cell growth and the spread of cancer. The immune system sweeps out these dysfunctional cells on a regular basis, but over time becomes less effective at "keeping house."
Note the point about the immune system becoming less able to sweep away dysfunctional cells. Immune system rejuvenation would reduce the incidence of cancer. If we can kill off both cancer cells and senescent cells we could add decades to our life expectancies.
The scientists genetically engineered the mice to cause their senescent cells to die in the presence of a compound that is non-toxic to normal cells.
Dr. van Deursen and colleagues genetically engineered mice so their senescent cells harbored a molecule called caspase 8 that was only turned on in the presence of a drug that has no effect on normal cells. When the transgenic mice were exposed to this drug, caspase 8 was activated in the senescent cells, drilling holes in the cell membrane to specifically kill the senescent cells.
The great result: killing off senescent cells delayed the onset of age-related diseases.
The researchers found that lifelong elimination of senescent cells delayed the onset of age-related disorders such as cataracts and muscle loss and weakness. Perhaps even more importantly, they showed that removing these cells later in life could slow the progression of already established age-related disorders.
The findings support a role of senescent cells in the aging process and indicate that chemicals secreted by these cells contribute to age-related tissue dysfunction and disease.
This is a very exciting report.
This report reminds me of work done by Thomas Rando and Irina Conboy at Stanford (and Conboy later elsewhere) showing that blood from old mice suppresses cell growth in young mice. This suggests that stem cell therapies would work far better if senescent cells were killed off since they are probably (I am guessing) the source of the growth-suppressing blood chemicals in the old. Other work earlier this year by Tony Wyss-Coray at Stanford found a chemokine secreted by cells was at least partially responsible for suppressing neurogenesis (the creation of new neurons).
Blood cells from one mouse cannot travel into the brain of the other because of the blood-brain barrier, so the team concluded that free-floating molecules in the blood, capable of passing through, must be responsible for the effects. By comparing more than 60 chemokines—chemical messengers secreted by cells that circulate in the blood—the researchers identified several associated with the detrimental effect of old blood. Administering one of these chemicals, called CCL11, to young mice dampened neurogenesis and impaired learning and memory.
The ability to kill off senescent cells will probably boost brain function as well as other parts of the body. Gotta love that.
Update: Nicholas Wade looks at the benefits and harm from cells becoming senescent.
And despite being termed senescent, the cells are very active: They convert themselves into factories that churn out 100 different kinds of growth factors, along with cytokines, the inflammatory agents that stimulate the immune system. The evolutionary reason for this activity may be to provoke the immune system to attack patches of premalignant and malignant cells.
It is not certain that wiping out senescent cells will provide an unalloyed blessing. Killing them might up cancer risk. Effective cures for cancer would therefore reduce the risk of treatments that kill senescent cells.
BLOOMINGTON, Ind. -- Just as the Occupy Wall Street movement has brought more attention to financial disparities between the haves and have-nots in American society, researchers from Indiana University and the University Medical Center Utrecht in The Netherlands are highlighting the disproportionate influence of so called "Rich Clubs" within the human brain.
Not all regions of the brain, they say, are created equal.
"We've known for a while that the brain has some regions that are 'rich' in the sense of being highly connected to many other parts of the brain," said Olaf Sporns, professor in the Department of Psychological and Brain Sciences in IU's College of Arts and Sciences. "It now turns out that these regions are not only individually rich, they are forming a 'rich club.' They are strongly linked to each other, exchanging information and collaborating."
Is part of your brain trying to protest? Is it trying to do a sit-down strike against other parts? Which parts of your brain win out in power struggles? Do some parts of your brain get their desires satisfied while other parts go wanting?
Think about it this way: When it becomes possible to connect brains to each other with elaborate embedded interfaces is there any doubt that not all parts of the brain will be connected up into virtual realms? I'm thinking the frontal cortex will make sure it is well connected and other parts of the brain will get short shrift.