what the science is?

"Ability of differentiation is the basic of Science"

........ankur

Risks of Global Warming Rising: Is It Too Late to Reverse Course?

The risk of catastrophic climate change is getting worse, according to a new study from scientists involved with the United Nations Intergovernmental Panel on Climate Change (IPCC). Threats—ranging from the destruction of coral reefs to more extreme weather events like hurricanes, droughts and floods—are becoming more likely at the temperature change already underway: as little as 1.8 degree Fahrenheit (1 degree Celsius) of warming in global average temperatures."Most people thought that the risks were going to be for certain species and poor people. But all of a sudden the European heat wave of 2003 comes along and kills 50,000, [Hurricane] Katrina comes along and there's a lot of data about the increased intensity of droughts and floods. Plus, the dramatic melting of Greenland that nobody can explain certainly has to increase your concern," says climatologist Stephen Schneider of Stanford University, who co-authored the research published this week in the Proceedings of the National Academy of Sciences as well as in several IPCC reports. "Everywhere we looked, there was evidence that what was believed to be likely has happened. Nature has been cooperating with [climate change] theory unfortunately."Schneider and his colleagues updated a graph, dubbed the "burning embers," that is designed to map the risks of damage from global warming. The initial version of the graph [left] drawn in 2001 had the risks of climate change beginning to appear after 3.6 or 5.4 degrees F (2 to 3 degrees C) of warming, but the years since have shown that climate risks kick in with less warming.According to the new graph, risks to "unique and threatened systems" such as coral reefs and risks of extreme weather events become likely when temperatures rise by as little as 1.8 degrees F from 1990 levels, which is on course to occur by mid-century given the current concentrations of atmospheric greenhouse gases. In addition, risks of negative consequences such as increased droughts and the complete melting of ice caps in Greenland and Antarctica definitively outweigh any potential positives, such as longer growing seasons in countries such as Canada and Russia. "We're definitely going to overshoot some of these temperatures where we see these very large vulnerabilities manifest," says economist Gary Yohe of Wesleyan University in Middletown, Conn., another co-author. "We're going to have to learn how to adapt."Adaptation notwithstanding, Yohe and Schneider say that scientists must also figure out a way to reduce greenhouse gas emissions to reverse the heating trend to prevent further damage.Several bills pending in Congress would set a so-called cap-and-trade policy under which an overall limit on pollution would be set—and companies with low output could sell their allowances to those that fail to cut emissions as long as the total stays within the total pollution cap. Any such federal policy would put a price on carbon dioxide pollution, which is currently free to vent into the atmosphere, Yohe note. He, however, favors a so-called carbon tax that would set a fixed price for such climate-changing pollution rather than the cap-and-trade proposals favored by the Obama administration. "It's a predictable price, not a thing that bounces around."But even with such policies in place—not only in the U.S. but across the globe—climate change is a foregone conclusion; global average temperatures have already risen by at least 1.1 degrees Fahrenheit (0.6 degree C) and further warming of at least 0.7 degree F (0.4 degree C) is virtually certain, according to the IPCC. And a host of studies, including a recent one from the Massachusetts Institute of Technology, have shown that global warming is already worse than predicted even a few years ago. The question is: Will it be catastrophic or not? "We've dawdled, and if we dawdle more it will get even worse," Schneider says. "It's time to move."

source:http://www.sciam.com/article.cfm?id=risks-of-global-warming-rising

Optical Illusions and the Illusion of Love!

This is the seventh article in the Mind Matters series on the neuroscience behind visual illusions.
It’s Valentine’s season, which means that everywhere you look there are heart-shaped balloons, pink greeting cards and candy boxes filled with chocolate. But what is true love? Does it exist? Or is it simply a cognitive illusion, a trick of the mind? Let us count the ways. Contrary to the anatomy referenced in all of our favorite love songs, love (as with every other emotion we feel) is not rooted in the heart, but in the brain. (Unfortunately, Hallmark has no plans to mass-produce chocolate-covered arrow-pierced brains in the near future.) By better understanding how the brain falls in love, we can learn about why the brain can get so obsessed with this powerful emotion. In fact, some scientists even see love as a sort of addiction. For instance, neuroscientist Thomas Insel and colleagues at Emory University in Atlanta discovered that monogamous pair bonding has its basis in the same brain reward circuits that are responsible for addiction to drugs such as cocaine and heroin. Their study was conducted in the prairie vole, a small rodent that mates for life. But the conclusions are probably true for humans, too, which may explain why it is so hard to break up a long-term romantic relationship. Losing someone you love is like going through withdrawal.
This month’s slide show features a number of visual illusions with a romantic motif. We hope that you and your special one will enjoy them. And remember, even if love is an illusion, that doesn’t mean it’s not meaningful and real (to our brains, anyway).

Pop! Goes My Heart
Nothing is more romantic than curling up in front of a fire with your loved one on Valentine’s Day, as you lovingly whisper, “chromostereopsis.” Okay, maybe it’s not as passionate as a sonnet—unless you are a vision scientist. Look at the red and blue hearts and examine their depth with respect to the background. Most people find that the red heart pops in front of the blue background whereas the blue heart sinks beneath the red background. This illusion comes about because our eyes’ lenses refract blue light more than red. This phenomenon is called a chromatic aberration; another example of this effect is seeing a rainbow when you shine white light through a prism. When both eyes view the red and blue images simultaneously, the cornea and lens of the eyes refract different amounts of the colors, which results in their systematic and symmetric binocular mislocalization. The brain deals with this sensory aberration by imagining depth—the red heart is in front of the blue background and vice versa—even though none actually exists.

Illusions That Move the Heart
Your wandering eyes pull at your lover’s heartstrings. In this illusion, the heart appears to move and even pulsate as you look around the image. When your eyes move, they shift the retinal images of the white/black edges in the pattern, activating the motion-sensitive neurons in your visual cortex. This neural activation leads to the perception of illusory motion. Note that if you focus your gaze on a single point, the illusory motion slows or stops.

Illusory Neon Heart
Notice that the yellow fields inside of the heart appear paler than the fields forming the contour of the heart, which appear to be a darker shade of yellow/orange. Right? Wrong. Actually, all of the yellow fields in the figure are identical. Any differences that you see are all in your mind. This effect is called “neon color spreading,” because it resembles the effect of the light spreading from a neon lamp. The neural underpinnings of this effect are not yet understood.

Love and Hate
Even more ambivalent is this mirror-symmetric ambigram of love and hate. Talk about mixed feeling—we hope she brings a mirror on her Valentine’s Day date. There’s even a T-shirt available at http://www.madeindesign.com/prod-Psyshirt-love-femme-Pa-Design-refpa85t1l.html.

For Coffee and Tea Lovers
“Yuan yang" is a typical Hong Kong beverage mix of tea and coffee, and also a symbol of marriage and love. Sculptor Tsang Cheung-shing has united both concepts in a beautiful ceramic work, in which tea and coffee poured from two stylish cups meet and kiss each other.

Love Is All Around
Romance is not just a concept for humans and voles. This slide shows that love, and illusions, surround us all.

Source:http://www.sciam.com/article.cfm?id=optical-illusions-and-love

Toyota announcing a plug-in Prius in the future...

Dear EarthTalk: I understand that Toyota is planning to sell a plug-in Prius that will greatly improve the car’s already impressive fuel efficiency. Will I be able to convert my older (2006) Prius to make it a plug-in hybrid vehicle? -- Albert D. Rich, Kamuela, HI
Toyota is readying a limited run of a plug-in Prius, which can average 100 miles per gallon, for use in government and commercial fleets starting in 2009. Toyota will monitor how these cars, which will have high efficiency lithium ion batteries that haven’t been fully tested yet, will hold up under everyday use.
Essentially, a plug-in version of the Prius reverses the roles of the two motors under the hood. The regular Prius relies more on its gas engine, switching to (or combining) use of the electric motor in slow traffic, to maintain cruising speed, and when idling or backing up. The car doesn’t need to plug in because its battery stays charged by the gas motor and by the motion of the wheels and brakes. The plug-in will primarily use its electric motor, allowing commuters to go to and from work every day fully on the electric charge, saving the gas engine for longer trips that exceed the distance the car can go on electricity alone.
Toyota has made no announcement yet as to when consumers will be able to buy a plug-in; that depends largely on the results of the field test of the fleet version. But owners of a current or past model don’t need to wait. Those with automotive mechanical skills can convert their Priuses to plug-ins themselves.
“The conversion is an easy DIY [do-it-yourself] project that you can do for about $4,000, if you choose to use sealed lead acid batteries,” says Houston-based Jim Philippi, who converted his Prius last year, using instructions he downloaded for free from the Electric Auto Association’s PriusPlus.org website. Philippi recommends that DIYers consult Google’s RechargeIT.org as well for useful background information.
For those less inclined to a DIY, several companies now sell readymade kits (some also have kits for converting Ford Escape Hybrid SUVs). Ontario-based Hymotion sells plug-in kits for Prius model years 2004-2008 for around $10,000 via contracted distributors/installers in San Francisco, Seattle and elsewhere. Other providers include Plug-In Conversions Corp., Plug-In Supply, EDrive Systems, Energy Control Systems Engineering Inc. and OEMtek. All typically work with select garages that specialize.
One potential worry about conversions is whether or not Toyota will honor the warranty that came with the original vehicle. The California Cars Initiative (CCI), which has converted several hybrids to plug-ins for research and demonstration purposes (sorry, they’re not for sale), says the carmaker needs to clarify the matter, since hybrid cars typically have four or five separate warranties. There is legal precedent, CCI says, that modifications cannot completely void warranties—only the part(s) affected by a retrofit.
If you’re looking to convert, keep in mind that such a move is not about cost-savings, as it will take some time for fuel savings to justify the upfront cost of even a DIY. Most people interested in such a conversion are doing it for the sake of the environment, not their pocketbooks।

CONTACTS: PriusPlus, www.priusplus.org; Plug-In Conversions Corp., www.pluginconversions.com; Plug-In Supply, www.pluginsupply.com; EDrive Systems, www.edrivesystems.com; Energy Control Systems Engineering, www.energycs.com; OEMtek, www.oemtek.com; CCI, www.calcars.org।

सोर्स:-http://www.sciam.com/article.cfm?id=can-you-plug-in-your-prius

Brain Pacemakers.....

Brain cells, called neurons, communicate with one another through electrical impulses.
In deep-brain stimulation, a battery implanted in a person’s chest delivers steady pulses of electricity to a targeted area of the brain. The artificial current interrupts or corrects dysfunctional electrical activity that is causing medical problems. Doctors can tailor the speed, strength and length of the pulses to get the desired result.
Well established as a way of quelling the tremors that can afflict people with Parkinson’s disease, deep-brain stimulation is showing promise for a host of other ailments, including chronic pain and depression.
The video is brief, just a couple of minutes, but it’s reality TV as riveting as anything you’ll ever see. A man in his mid-50s, affable, articulate, faces the camera and talks a bit about a medical procedure he’s had. He holds in his hand what looks like a remote control. “I’ll turn myself off now,” he says mildly. The man presses a button on the controller, a beep sounds, and his right arm starts to shake, then to flap violently. It’s as if a biological hurricane has engulfed him, or perhaps it’s that his arm is made of straw and some evil sprite is waving it about. With effort, the man grasps the malfunctioning right arm with his left hand and slowly, firmly, subdues the commotion, as if he were calming a child in the throes of a temper tantrum. He’s breathing hard, and it’s clear he can’t keep it up much longer. With an almost desperate gesture, he reaches out for the controller and manages to press the button again. There’s a soft beep, and suddenly it’s over. He’s fine.
Composed, violently afflicted, then composed again. All with the flick of a switch. As before-and-after moments go, this one is potent, verging on the miraculous. It’s the kind of thing you’d expect to witness under a revival tent, not in the neurology ward of a British hospital. Once you’ve seen it, you’ll have an indelible image of Parkinson’s disease. The word “tremor” doesn’t convey what can happen to people—the way they are thrashed and harassed by their own bodies. But this scene, involving a patient of ours, informs viewers about more than a disease; it’s a vivid window onto a powerful medical technology known as deep-brain stimulation (you can watch the video at www.kringelbach.dk/nrn).
Sudden, radical transformation is the hallmark of deep-brain stimulation. The treatment, essentially a pacemaker for the brain, consists of a deceptively simple two-part device. A surgeon threads one or two thin wires into carefully selected locations deep within the brain, then inserts a small battery just underneath the skin near the collarbone. Pulses of electricity travel from the battery to four electrodes situated at the tip of each wire. The effects are instantaneous, usually appearing while the patient is still on the operating table—the quieting of a tremor, the ability to walk again or, in some patients with otherwise treatment-resistant depression, a renewed energy for life.
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Deep-brain stimulation came into its own in the 1990s, and since then surgeons have performed it on more than 35,000 people, mostly to quell Parkinson’s disease and other movement-related disorders. It is not a cure, but it can keep symptoms at bay for years. Recently, as the electrodes have become safer and the batteries smaller and longer- lasting and as advances in brain-imaging techniques such as magnetic resonance imaging have made it possible to place electrodes with greater precision, neurosurgeons have begun investigating the technology as a way to ease a host of other health problems.
The technique has made it possible for children with a disabling movement disorder called dystonia to leave their wheelchairs and lead nearly normal lives. It has brought immediate relief to people suffering from cluster headaches and other kinds of unremitting pain. It has shown tantalizing promise for some psychiatric disorders, including severe cases of depression, obsessive-compulsive disorder and Tourette’s syndrome. It has been attempted as a cure for anorexia and obesity. Some neuroscientists speculate that it could help stem the memory loss brought on by Alzheimer’s disease. The brain is an electrical organ, so there is little that goes wrong with it that could not, hypothetically, benefit from finely calibrated pulses of electricity. Clinical trials of deep-brain stimulation—preliminary testing on small groups of patients—are multiplying at hospitals around the world, from Cleveland and Toronto to Bristol, Grenoble and Milan.
Despite the recent advances, technologically speaking, deep-brain stimulation is not yet fully mature. Today’s devices are programmed to deliver steady, unchanging pulses of electricity. Over the next decade we expect to see a much “smarter” device, one that would turn itself on and off as needed, tailoring its therapy to what is happening moment to moment in the patient’s brain.
The Body ElectricOften when people want to make a difficult task seem easier, they say, “After all, it’s not brain surgery.” And for good reason. Although we know a lot about the brain, there is still a lot of mystery packed into the three pounds of wrinkled tissue that house a human consciousness, and we neuroscientists must proceed with a combination of humility and hubris.
But deep-brain stimulation has an advantage over most other kinds of neurosurgery—namely, it is reversible. If the electrodes malfunction or if they are simply ineffective, they can be turned off or removed. The procedure is not without risk—1 to 3 percent of patients experience bleeding that leads to a stroke, and a slightly larger number develop treatable infections. Unlike most surgeries, however, deep-brain stimulation does not change the physical structure of the brain; electricity does all the work.
Awareness of the role of electricity in the body dates to A.D. 43, when Scribonius Largus, court physician to the ancient Roman emperor Claudius, wrote that headaches and gout could be soothed by the touch of the torpedo fish, which emits an electrical charge when startled. In 1774 Benjamin Franklin noted that static electricity can lead to muscle contraction, and a decade later Italian physician Luigi Galvani observed that by applying electricity to the sciatic nerve he could make the leg of a dead frog twitch in a lifelike manner. His breakthrough inspired Mary Shelley’s Frankenstein, in which a monster cadged together from parts of dead people was animated by a massive electrical charge.
Galvani’s discovery did more than ignite sci-fi fantasies; it ushered in a host of medical advances. In 1870 German neuropsychiatrist Eduard Hitzig and anatomist Gustav Fritsch selectively manipulated the limbs of a live dog by stimulating specific areas of the brain region now known as the motor cortex—in other words, they showed that each muscle of the body, every finger and toe, is controlled by electrical impulses from a dedicated patch of brain tissue. In the 20th century researchers had the tools to investigate the cellular level. They deciphered how electricity travels through a single brain cell, or neuron, and from there to its neighbor, creating the complex networks that dictate our thoughts, actions, memories and desires.
Before long, investigators asked: But what happens when those neural networks short-circuit? In the 1950s and 1960s neurosurgical pioneers, including Natalia Bechtereva in the U.S.S.R., Robert Heath of Tulane University and J. Lawrence Pool of the Neurological Institute of New York, began experimentally applying electricity to the brains of people suffering from chronic pain, depression and movement disorders. The batteries then available were much too large to be implanted, so the devices were kludgy and the relief, sporadic. Still, these investigations established a medical precedent for targeted electrical pulses.
Parkinson’s disease turned out to be an ideal proving ground. In this disorder, neurons die off in a brain area that coordinates movement, the basal ganglia. In a healthy brain, neurons in the basal ganglia communicate in an intricate call-and-­response with groups of neurons in other areas, including the thalamus and the motor cortex. For movements to be quick and fluid, these parts of the brain must work together. Messages traveling between them are called oscillations. They bounce back and forth, moving at different frequencies, some serving to initiate movement, others, to moderate it. But what is key is that the sender and recipient neurons, like two girls rhythmically swinging a jump rope for a third to hop over, must be in sync. In Parkinson’s, diseased neurons lose their ability to keep up, and the oscillations become unbalanced. Neurons fire wildly, and a person moves in a chaotic way or is unable to initiate movement at all.
In the late 1980s surgeons found that if they stimulated either the thalamus or the globus pallidus (a part of the basal ganglia) with fast pulses—up to 180 times per second—they could override the faulty connections. Scientists do not completely understand how deep-brain stimulation works, but we do know that the pulses sent to the electrode sometimes drive and sometimes inhibit the natural activity of neurons. Faster pulses, such as those used in Parkinson’s patients, tend to overwhelm and thus inhibit activity, whereas slower pulses tend to drive it by creating a tempo that the neurons strive to meet.
Working with monkeys that had been given parkinsonian symptoms, one of us (Aziz), as well as other teams led by neuroscientists Mahlon R. DeLong of Emory University and Abdelhamid Benazzouz of the Bordeaux Neuroscience Institute in France, helped to establish that another part of the basal ganglia, the subthalamic nucleus, can be an even more effective implantation spot (it has since become the most popular stimulation target). More recently, Aziz discovered a fourth target for the 20 percent of Parkinson’s patients who do not respond to medication or to stimulation in the three established brain regions. After observing that a part of the brain stem called the pedunculopontine nucleus was underactive in a parkinsonian monkey, Aziz showed that stimulating this area brought stunning results to human patients for whom until recently nothing could be done. Many people who would otherwise be freezing in mid-step or falling over find themselves suddenly able to walk again.
Thanks to this kind of research and to the fact that the requisite batteries are now as small as the ones in cell phones, more than 250 hospitals in the U.S. alone perform deep-brain stimulation for movement disorders. Although other applications are considered experimental, in part because they are not yet approved by the Food and Drug Administration, strong evidence is mounting in their favor. Take, for example, the treatment of pain. Over the past 30 years more than 700 people have had deep-brain stimulation for otherwise treatment-resistant pain; the average long-term success rate is 60 to 70 percent, and when doctors are skilled in patient selection, the success rate approaches 100 percent.
A Sudden Calm Descends In May 2001 a man named Robert Matthews fell and broke his left leg. The fracture did not heal properly, and the leg developed a stubborn antibiotic-resistant infection. Fearing that it would spread, doctors amputated his leg above the knee, but Matthews’s problems did not end there. Although his leg was gone, he felt as if it were still there and in excruciating pain. He tried medications, hypnosis and stimulation of the spinal cord nerve, but nothing helped.
When Matthews was referred to us, he was 58 years old and had been suffering from phantom-limb pain for four years. He was taking large daily doses of opiates and, understandably, felt anxious and depressed. We had previously shown that stimulation of the brain stem, the most ancient part of the brain, can ease otherwise treatment-resistant pain; Matthews seemed an ideal candidate.
On the day of the surgery, our team clamped Matthews into a stereotactic frame—a metal rectangle that surrounds the head and provides three-dimensional coordinates for any point within the brain. We scanned his brain twice—with MRI before the frame was attached (metal objects are unsafe in an MRI machine) and with computed tomography afterward—and used software to merge the images. Like a nose or a foot or any other body part, the brain varies slightly from person to person, so structures deep within it will not always be found in exactly the same location. Now Aziz had a personalized map he could use to plot his trajectory with millimeter precision.
Matthews received an injection of local anesthesia so that he would not feel Aziz drill a small hole in his skull. There are no nerve endings in the brain itself, though, which meant Matthews could be fully awake—and we would need his participation to make the hour-long operation come off. Aziz gently guided a wire tipped with four platinum-­iridium electrodes through the jellylike brain tissue and into the area known as the periventricular gray/periaqueductal gray (PAG). While methodically electrifying first one, then another, of the four electrode prongs, Aziz asked Matthews to describe out loud what he felt.
This is one of the trickiest moments in deep-brain stimulation—banishing the symptom without causing side effects by accidentally activating the wrong spot. The electrode is only about a millimeter and a half wide, but it straddles up to a million neurons. Packed tightly within the PAG are cells that communicate with each part of the body; we wanted to affect only those related to Matthews’s left leg. If he reported feeling tingling or warmth in his hands, arms, face or other leg, Aziz would move the electrode, stimulate a different prong or change the pulses. Moreover, we were prepared for reactions even further afield. The PAG is the seat of the so-called fight-or-flight response, and in the past we have had a patient suffer an anxiety attack on the table. Side effects that can result from imperfect electrode placement in other parts of the brain include eye bobbing, inappropriate laughter and depression.
We gave Matthews a relatively mild amount of current: 1.5 volts—the strength of an AA battery. As for the speed, or frequency, of the pulses, we knew that fast pulses make pain worse, so we started him at about 10 per second and ultimately settled on seven. When we stimulated two of the prongs at these specifications, Matthews felt a sudden calm descend—a comfortable feeling of warmth in his phantom leg. After four years, finally, relief.
Aziz affixed the electrode-tipped wire to Matthews’s skull and implanted a battery over his right pectoral muscle. The battery connects to the electrode by a lead that runs under the skin of Matthews’s chest and neck and behind his ear to his scalp. Matthews has a magnetic remote control to turn the deep-brain stimulator on or off—but he rarely uses it, because as soon as he does, the agony returns. He reports that his pain is 75 percent reduced, and he has been able to resume his life.
Good as that outcome is, in the future we should be able to do better, using technology similar to that of today’s cardiac pacemakers. Computer software in these devices monitors the patient’s heart, sending a jolt of electricity only when it recognizes that the heart is not beating properly. When brain pacemakers become this precise, they will not have to be on all the time, which means, among other things, that the batteries will not have to be changed as often (they currently typically require surgical replacement every six months to five years, although rechargeable batteries are also starting to become available). Before deep-brain stimulation can advance, however, scientists must decode the language of neurons. We need to learn the details of how brain regions communicate, such as which electrical patterns might signify an oncoming tremor, headache or epileptic seizure. Then we can program the device to recognize when a problem is coming on and to deliver the specific pattern of pulses that will short-circuit it. Our team has made an intriguing advance toward discovering just such a “brain signature”, and other studies are under way.
The Hype and the PotentialThe transformative power of deep-brain stimulation is especially striking in the psychiatric realm. Investigators in Toronto, Leuven, Bonn and elsewhere have been enthusiastically reporting results from small trials. There is the report of a 31-year-old man who had such violent tics from Tourette’s syndrome that he could not get a decent job or go out in public without being snickered at, whose body suddenly relaxed. There is the story of a woman whose world literally became brighter—looked newly washed—as soon as the electrode was activated. Other depressed patients said their sensations of “painful emptiness” disappeared. These changes abruptly vanished when patients’ electrodes were switched off.
This is heady stuff, given that we do not understand exactly how deep-brain stimulation works nor do we know for sure what goes wrong in depression, Tourette’s or many of the other syndromes for which stimulation is being attempted, such as obsessive-compulsive disorder, anorexia, overeating and drug addiction. There is potential here—the work on depression in particular seems promising. But some scientists are getting ahead of themselves, and the media have been delighted to assist. In August 2007 neuroscientists at New York–Presbyterian Hospital/Weill Cornell Medical College and the Cleveland Clinic Foundation received lots of attention when they reported using deep-brain stimulation to wake a 38-year-old man from a minimally conscious state. Six years after a brutal beating, the man can eat without a feeding tube and speak a few words, an undeniable improvement. But the fact is that Japanese neurosurgeons have experimented for decades with deep-brain stimulation for just this kind of patient and found that such revivals are rare.
In another recent incident, a man undergoing experimental deep-brain stimulation to treat obesity incidentally retrieved a long-forgotten memory, whose clarity intensified when doctors turned up the voltage. Consequently, some have expressed optimism about brain implants for Alzheimer’s. The problem is that deep-brain stimulation is a relatively blunt tool—it either inhibits or excites a brain region (and in turn, the other brain structures that region talks to). That is fine for Parkinson’s, in which an overactive brain area may need quieting. But in Alzheimer’s what we see are neurons that lose their connections to one another and can no longer store memories. It is unlikely that deep-brain stimulation could repair such intricate connections.
Perhaps contributing to all the excitement about deep-brain stimulation is the fact that it is more than a promising therapy. It is a powerful tool neuroscientists can use to gain insights into the fundamental structure and function of the brain.
Until now our best view of the living human brain has been through imaging studies such as MRI and positron-emission scans, but what we get from them is vague, along the lines of “When a person does such-and-such or thinks such-and-such, there are changes in blood flow or oxygenation in certain parts of the brain that are likely related to changes in neural activity.” With deep-brain stimulation, on the other hand, what you essentially have is an on-off switch located in a specific part of the brain. By observing what happens to the brain as a whole when that switch is activated, you can glean detailed information about how various brain structures interconnect. One particularly exciting avenue that we have pioneered is to combine deep-brain stimulation with an imaging technique called magnetoencephalography (MEG). MEG tracks neural activity on the scale of milliseconds (MRI, in contrast, gives average brain activity over a six-second period and PET over a scale of minutes), providing an exceedingly accurate, moment-to-moment report.
When we used this technique on Matthews, the phantom-limb patient, we saw that the electrode in his brain stem appeared to drive activity in many other brain regions. Among the most active when he felt pain relief was the midanterior orbitofrontal cortex. This structure, located just above the eyes, has been shown in other studies to play a pivotal role in pleasurable (or rewarding) activities such as eating, using drugs and sex. Thus, cessation of pain is an intense form of pleasure, along the lines of snorting a line of cocaine or devouring a delicious pastry. This finding confirms that the orbitofrontal cortex might be an effective new stimulation target for people suffering from anhedonia, a lack of pleasure, which is common to depression and other mental illness.
We expect more revelations. By studying people with brain implants, we might answer questions such as how the brain coordinates learning a new language or solving an algorithm. We might even get new big-picture perspectives, such as how something as elusive as subjective experience can arise from electrical activity. Perhaps most important, we will be able to identify the brain areas where electrical stimulation will be most effective, further helping patients in dire need.

source:http://www.sciam.com/article.cfm?id=sparking-recovery-with-brain-pacemakers&page=1

Insulating Paint Powder Turns Every Color 'Green'

Remember that grade-school riddle, "What's black, white, and red all over?" Depending on who gave you the punch line, the answer was "a sunburned zebra" or "a newspaper." 

Here's an updated version: What's every color in the world, but still always green? 

The answer is paint that includes an insulating powder that originated at NASA. Widely used on commercial and residential structures, it transforms any color of paint into an environmentally friendly insulation barrier that saves energy and cost. 

The solution is simple: mix the powder into any color of interior or exterior paint, then break out the brushes. When spread on walls, ceilings, and roofs, it creates a barrier that deflects the sun's heat away from the house, plus it helps keep heating and air conditioning where they belong. This reduced need for energy is not only cost-effective, but also a kindness to the environment -- an easy way to create your own "green house effect." 

Many businesses use insulating paint to coat air-conditioning ducts, steam pipes and fittings, metal buildings, and cold storage facilities, such as walk-in coolers and freezers. For example, Purina Feeds uses a version of the insulating powder to cover storage silos, helping to prevent feed spoilage. The poultry industry uses it to help regulate the climate inside its hatcheries. Samsung applies it on military vehicles, and Hyundai Corporation's shipbuilding division paints it onto ships. It's even been used to insulate electrical switch boxes on the outside of fighters jets to prevent overheating. 

This simple but powerful solution all began with space shuttle launches. During a launch, heat generated by wind resistance and engine exhaust can potentially be very damaging. In the 1980s, engineers at the Marshall Center developed a spray-on process to apply an insulating mixture to help protect the shuttle. The process involved mixing nine different chemicals into an adhesive that was applied to the boosters' forward assembly, systems tunnel covers, and aft skirt. 

But there were challenges. Once the insulating material was mixed, it had to be applied within five hours. Any delay meant a batch of expensive materials was lost, requiring the time and cost to mix a new batch. The strength of the insulating material was also difficult to regulate, meaning it could chip during the shuttle's flight and splashdown of its reusable booster rockets. Adding to the downside, two of the nine ingredients in the insulating mix weren't environmentally friendly. 

In 1993, Marshall created a solution by atomizing epoxy and other filler materials to create a fine, environmentally friendly insulation powder. The material -- known as MCC-1, or Marshall Convergent Coating-1 -- contained tiny, hollow glass spheres and particles of cork and epoxy. The application process was also changed. Instead of mixing the insulating powder directly into the paint, it was shot from a spray gun at the same time the paint was applied. This change in process eliminated the five-hour "time clock" to complete the painting. 

The improved, eco-friendly insulation powder was first flight tested in 1996 on the STS-79 mission. It was so successful that it was adopted for all subsequent shuttle flights, with virtually no observed missing or chipped paint on the spent boosters during post-flight inspections. 

Bringing the NASA insulation powder to the public market resulted in an innovative partnership with Tech Traders, Inc. Months of testing and development created Insuladd®, a safe, non-toxic powder that can be added to any interior or exterior paint to transform it into a layer of insulation. 

The powder contains hollow, microscopic ceramic spheres, and a unique process applies a coating to these "microspheres." When the paint dries, it forms a radiant heat barrier, converting ordinary house paint into heat-reflecting thermal paint. 

You might say that NASA's contributions to insulating paint can keep green in your world AND in your wallet. That's a good reason to be tickled pink. 

Source:http://www.nasa.gov/topics/nasalife/green_paint.html

Reverse Mathematical Objects!

Newton’s third law: For every reaction there is a reaction, this is a Universal law! Today I will try to prove it mathematically. But still I am not sure of that how it exactly will be applicable practically. During normal thinking hours some seconds proved to be useful and productive which I would like to share with you through my blog! Only the great Almighty knows that whether I would be able to solve the riddle of life or not in my life time. May the Almighty enlighten me!
First draw a circle on x and y axis:-

Here we are analyzing that how the points on the perimeter of the circle behave wrt x and y coordinates! We start from (r,0) and finishes at (r,0) after taking a full anti-clockwise round. Here we intend to analyze the points on perimeter from minimum to maximum wrt to x and y coordinates.
Tabulating this:-

Now if we try to draw the points on any axis as (Min,Max) from first quadrangle to IV quadrangle then we find the flow of the coordinates as Clockwise.
Initially we have drawn the circle in a anticlockwise direction or we have drawn the circle from minimum to maximum in anticlockwise direction. But during mathematical analysis we found that minimum to maximum wrt to any of the coordinates do lies in clockwise direction. It is very interesting to note here that there exists a mathematical drama(U-Turn) here. It may be a reality too!
The same will apply to z and t axis also.
So, behind our every move it is proved at least mathematically that there exists a parallel negative factor also.
If we say the Universe is expanding then there would exist negative volumes also in the Universe. Or we also can’t deny the assumption that Universe is expanding with a rate of –dv/dt creating black holes if v is substantially almost equal to infinity or vice versa.
The derivation is quite simple but gives birth to a very interesting theory of “Reverse Mathematical Objects”.

....ankur

Invention: Infrared lie detector

Although security services the world over have used lie detectors to lock many people up over the years, they are not very reliable. However, a new way of scanning brain activity may change that.

The long-established polygraph test measures a person's respiration rate, heart rate, and perspiration. The idea is to detecting anxiety associated with guilt or lying.

But simply being anxious – about, say, being interrogated – can produce similar signals, and some people may be able to learn to beat the test. By some accounts, the results from such tests are no more accurate than guesswork.

Bouncing light
Measuring brain activity directly is though to be a more promising approach. This is currently achieved using technologies such as functional magnetic resonance imaging or EEGs.

But these methods have disadvantages of their own. For example, EEGs provide only a very low resolution picture of brain function, and fMRIs are hugely expensive, while scans are ruined by small movement of the subject.

Scott Bunce, at Drexel University's College of Medicine in Philadelphia, thinks a better solution is to send near-infrared light through the scalp and skull into the brain and see how much is reflected back. And he has designed a special headband that does just that

Blood simple
The amount of reflected light is dependent on the levels of oxygen in the blood, which in turn depends on how active the brain is at that point.

This, he says, gives a detailed picture of real-time activity within the brain that can be used to determine whether the subject is lying. The technique is both cheaper and easier to apply than fMRI and gives a higher resolution than an EEG.

A similar approach is being used to investigate Alzheimer's disease.

Of course, nobody knows whether brain activity can reliably be decoded to reveal deception, but that's another question.

Source:http://technology.newscientist.com/article/dn14778-invention-infrared-lie-detector.html?DCMP=ILC-tabViewArt&nsref=dn14778

Gender differences seen in brain connections!

Human brains appear to come in at least two flavours: male and female. Now variations in the density of the synapses that connect neurons may help to explain differences in how men and women think.

Even when intelligence levels are equal, women and men excel at different cognitive tasks. But although brain size and neuron density differ between the sexes, these don't seem to correlate with cognitive differences. So, Javier DeFelipe at Complutense University in Madrid, Spain, and colleagues counted the number of synapses instead.

The brain tissue they analysed came from the left temporal cortex, a region of the brain involved in emotional and social processing, of four women and four men with epilepsy. The tissue itself was healthy, having been removed to allow doctors to access underlying damaged areas.

The men had up to 52% more synapses per brain "layer" in this region than the women. While the effect of high synaptic density in this region is unknown, the team suspects that there may be other regions where women out-synapse men.

In any case, says DeFelipe, although different synaptic densities indicates different circuitry between men and women, men shouldn't get too cocky: the density of synapses in mice is greater than in humans.

Journal reference: Proceedings of the National Academy of Sciences (DOI: 10.1073.pnas/0803652105)

Source:http://www.newscientist.com/channel/being-human/brain/dn14685-gender-differences-seen-in-brain-connections.html

Sweet smells lead to sweet dreams

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Can smells sweeten your dreams? Certain aromas, such as lavender, are known to have soporific effects, but once you’re asleep, can smells influence what you dream about?

To find out, Boris Stuck of University Hospital Mannheim, Germany, exposed 15 sleeping volunteers to chemicals that mimicked the smell of either rotten eggs or roses.

"Most everyday smells have two components: the actual smell and a component that irritates your nose," says Stuck. "By exposing the patients to chemicals chosen to only incorporate the smelly component, we were able to stimulate them with really high doses of the smell without them waking up."

Stuck's team waited until their subjects had entered the REM phase of sleep, the stage at which most dreams occur, and then exposed them to a high dose of smelly air for 10 seconds before waking them up one minute later. The volunteers were then quizzed about the content of their dreams and asked how it made them feel.

Rose-tinted dreams
All subjects reported a positive dream experience when stimulated by the rose smell, and most experienced the opposite when exposed to the rotten eggs. Stuck says the smells influence the "emotional colouration" of the dream.

The team are now looking to recruit people who suffer from nightmares to see if exposure to smells can help make their dreams more pleasant.

"The relationship between external stimuli and dreaming is something we are all at some level aware of," says Irshaad Ebrahim of The London Sleep Centre. "This initial research is a step in the direction towards clarifying these questions and may well lead to therapeutic benefits."

Stuck is presenting his work on Sunday at the American Academy of Otolaryngology's annual meeting in Chicago

Source:http://www.newscientist.com/article/dn14773-sweet-smells-lead-to-sweet-dreams.html?DCMP=ILC-tabViewArt&nsref=dn14773

Did the Romans destroy Europe's HIV resistance?

THE hand of history has a very long reach. It appears that the Roman Empire left a legacy that may still affect modern Europe - those living within its conquered lands are more susceptible to HIV. It could explain why a gene that confers resistance to HIV varies in frequency across the continent.

The gene in question codes for a protein receptor called CCR5. The HIV virus binds to this receptor before entering cells. One gene variant, called CCR5-Delta32, has 32 DNA base pairs missing and produces a receptor that HIV cannot bind to, which prevents the virus from entering the cells. People with this variant have some resistance to HIV infection and also take longer to develop AIDS.

Generally, only people in Europe and western Asia carry the variant, and it becomes less and less frequent as you move south. For example, more than 15 per cent of people in some areas of northern Europe carry CCR5-Delta32, compared with fewer than 4 per cent of Greeks (see map). It is not clear why this is so, since the HIV pandemic - which began in the early 1980s - is too recent to have influenced the distribution of the variant.

However, the changing frequency of the variant reflects the changing boundary of the Roman Empire from 500 BC to AD 500, says Eric Faure at the University of Provence in Marseille, France. When Faure and colleague Manuela Royer-Carenzi investigated possible links between Roman colonisation and the frequency of the CCR5-Delta32 variant in nearly 19,000 DNA samples from across Europe, they found that the gene variant seemed to dwindle in regions conquered by the Romans (Infection, Genetics and Evolution, DOI: 10.1016/j.meegid.2008.08.007).

Alternative theories include the idea that the protective variant originated in Scandinavia, and was spread north and east by the Vikings. But the pattern of Viking migration does not match the current distribution of the variant. Another theory is that a major disease, such as plague or smallpox, created a selection pressure on the gene variant which increased its frequency. But its distribution does not match that of disease outbreaks, either.

So how did the Romans lower resistance across Europe? Some studies suggest that they and other southern Europeans had lower levels of CCR5-Delta32. But Faure does not think that the Romans spread the regular version of the gene into their colonies by breeding with indigenous people. "Gene flow between the two was extremely low," he says.

Instead, he reckons the Romans introduced a disease to which people carrying the CCR5-Delta32 variant were particularly susceptible. As the Romans moved north, this disease killed off people with the variant.

Faure notes that the Romans introduced cats and donkeys into Europe which may have carried pathogens that spread to humans.

What's more, the Romans inadvertently brought with them disease-carrying mosquitoes. Intriguingly, modern people with the CCR5-Delta32 variant are more susceptible to the mosquito-borne West Nile virus.


Source:http://www.newscientist.com/channel/health/hiv/mg19926723.900-did-the-romans-destroy-europes-hiv-resistance.html

Minding Mistakes: How the Brain Monitors Errors and Learns from Goofs

Key Concepts
The brain contains neural machinery for recognizing errors, correcting them, and optimizing behavior.
The neurotransmitter dopamine plays a major role in our ability to learn from our mistakes. Genetic variants that affect dopamine signaling may partly explain differences between people in the extent to which they learn from errors or negative consequences.
Certain patterns of cerebral activity often foreshadow errors, opening up the possibility of preventing blunders with portable devices that can detect error-prone brain states.
April 26, 1986: During routine testing, reactor number 4 of the Chernobyl nuclear power plant explodes, triggering the worst catastrophe in the history of the civilian use of nuclear energy.
September 22, 2006: On a trial run, experimental maglev train Transrapid 08 plows into a maintenance vehicle at 125 mph near Lathen, Germany, spewing wreckage over hundreds of yards, killing 23 passengers and severely injuring 10 others.
Human error was behind both accidents. Of course, people make mistakes, both large and small, every day, and monitoring and fixing slipups is a regular part of life. Although people understandably would like to avoid serious errors, most goofs have a good side: they give the brain information about how to improve or fine-tune behavior. In fact, learning from mistakes is likely essential to the survival of our species.
In recent years researchers have identified a region of the brain called the medial frontal cortex that plays a central role in detecting mistakes and responding to them. These frontal neurons become active whenever people or monkeys change their behavior after the kind of negative feedback or diminished reward that results from errors.
Much of our ability to learn from flubs, the latest studies show, stems from the actions of the neurotransmitter dopamine. In fact, genetic variations that affect dopamine signaling may help explain differences between people in the extent to which they learn from past goofs. Meanwhile certain patterns of cerebral activity often foreshadow miscues, opening up the possibility of preventing blunders with portable devices that can detect error-prone brain states.
Error DetectorHints of the brain’s error-detection apparatus emerged serendipitously in the early 1990s. Psychologist Michael Falkenstein of the University of Dortmund in Germany and his colleagues were monitoring subjects’ brains using electroencephalography (EEG) during a psychology experiment and noticed that whenever a subject pressed the wrong button, the electrical potential in the frontal lobe suddenly dropped by about 10 microvolts. Psychologist William J. Gehring of the University of Illinois and his colleagues confirmed this effect, which researchers refer to as error-related negativity, or ERN.

An ERN may appear after various types of errors, unfavorable outcomes or conflict situations. Action errors occur when a person’s behavior produces an unintended result. Time pressure, for example, often leads to misspellings while typing or incorrect addresses on e-mails. An ERN quickly follows such action errors, peaking within 100 milliseconds after the incorrect muscle activity ends.
A slightly more delayed ERN, one that crests 250 to 300 milliseconds after an outcome, occurs in response to unfavorable feedback or monetary losses. This so-called feedback ERN also may appear in situations in which a person faces a difficult choice—known as decision uncertainty—and remains conflicted even after making a choice. For instance, a feedback ERN may occur after a person has picked a checkout line in a supermarket and then realizes that the line is moving slower than the adjacent queue.
Where in the brain does the ERN originate? Using functional magnetic resonance imaging, among other imaging methods, researchers have repeatedly found that error recognition takes place in the medial frontal cortex, a region on the surface of the brain in the middle of the frontal lobe, including the anterior cingulate. Such studies implicate this brain region as a monitor of negative feedback, action errors and decision uncertainty—and thus as an overall supervisor of human performance.
In a 2005 paper, along with psychologist Stefan Debener of the Institute of Hearing Research in Southampton, England, and our colleagues, I showed that the medial frontal cortex is the probable source of the ERN. In this study, subjects performed a so-called flanker task, in which they specified the direction of a central target arrow in the midst of surrounding decoy arrows while we monitored their brain activity using EEG and fMRI simultaneously. We found that as soon as an ERN occurs, activity in the medial frontal cortex increases and that the bigger the ERN the stronger the fMRI signal, suggesting that this brain region does indeed generate the classic error signal.

Learning from LapsesIn addition to recognizing errors, the brain must have a way of adaptively responding to them. In the 1970s psychologist Patrick Rabbitt of the University of Manchester in England, one of the first to systematically study such reactions, observed that typing misstrikes are made with slightly less keyboard pressure than are correct strokes, as if the typist were attempting to hold back at the last moment.
More generally, people often react to errors by slowing down after a mistake, presumably to more carefully analyze a problem and to switch to a different strategy for tackling a task. Such behavioral changes represent ways in which we learn from our mistakes in hopes of avoiding similar slipups in the future.
The medial frontal cortex seems to govern this process as well. Imaging studies show that neural activity in this region increases, for example, before a person slows down after an action error. Moreover, researchers have found responses from individual neurons in the medial frontal cortex in monkeys that implicate these cells in an animal’s behavioral response to negative feedback, akin to that which results from an error.
In 1998 neuroscientists Keisetsu Shima and Jun Tanji of the Tohoku University School of Medicine in Sendai, Japan, trained three monkeys to either push or turn a handle in response to a visual signal. A monkey chose its response based on the reward it expected: it would, say, push the handle if that action had been consistently followed by a reward. But when the researchers successively reduced the reward for pushing—a type of negative feedback or error signal—the animals would within a few trials switch to turning the handle instead. Meanwhile researchers were recording the electrical activity of single neurons in part of the monkeys’ cingulate.
Shima and Tanji found that four types of neurons altered their activity after a reduced reward but only if the monkey used that reduction as a cue to push instead of turn, or vice versa. These neurons did not flinch if the monkey did not decide to switch actions or if it did so in response to a tone rather than to a lesser reward. And when the researchers temporarily deactivated neurons in this region, the monkey no longer switched movements after a dip in its incentive. Thus, these neurons relay information about the degree of reward for the purpose of altering behavior and can use negative feedback as a guide to improvement.
In 2004 neurosurgeon Ziv M. Williams and his colleagues at Massachusetts General Hospital reported finding a set of neurons in the human anterior cingulate with similar properties. The researchers recorded from these neurons in five patients who were scheduled for surgical removal of that brain region. While these neurons were tapped, the patients did a task in which they had to choose one of two directions to move a joystick based on a visual cue that also specified a monetary reward: either nine or 15 cents. On the nine-cent trials, participants were supposed to change the direction in which they moved the joystick.
Similar to the responses of monkey neurons, activity among the anterior cingulate neurons rose to the highest levels when the cue indicated a reduced reward along with a change in the direction of movement. In addition, the level of neuronal activity predicted whether a person would act as instructed or make an error. After surgical removal of those cells, the patients made more errors when they were cued to change their behavior in the face of a reduced payment. These neurons, therefore, seem to link information about rewards to behavior. After detecting discrepancies between actual and desired outcomes, the cells determine the corrective action needed to optimize reward.
But unless instructed to do so, animals do not generally alter their behavior after just one mishap. Rather they change strategies only after a pattern of failed attempts. The anterior cingulate also seems to work in this more practical fashion in arbitrating the response to errors. In a 2006 study experimental psychologists Stephen Kennerley and Matthew Rushworth and their colleagues at the University of Oxford taught rhesus monkeys to pull a lever to get food. After 25 trials, the researchers changed the rules, dispensing treats when the monkeys turned the lever instead of pulling it. The monkeys adapted and switched to turning the lever. After a while, the researchers changed the rules once more, and the monkeys again altered their behavior.

Each time the monkeys did not immediately switch actions, but did so only after a few false starts, using the previous four or five trials as a guide. After damage to the anterior cingulate, however, the animals lost this longer-term view and instead used only their most recent success or failure as a guide. Thus, the anterior cingulate seems to control an animal’s ability to evaluate a short history of hits and misses as a guide to future decisions.
Chemical IncentiveSuch evaluations may depend on dopamine, which conveys success signals in the brain. Neurophysiologist Wolfram Schultz, now at the University of Cambridge, and his colleagues have shown over the past 15 years that dopamine-producing nerve cells alter their activity when a reward is either greater or less than anticipated. When a monkey is rewarded unexpectedly, say, for a correct response, the cells become excited, releasing dopamine, whereas their activity drops when the monkey fails to get a treat after an error. And if dopamine quantity stably altered the connections between nerve cells, its differential release could thereby promote learning from successes and failures.
Indeed, changes in dopamine levels may help to explain how we learn from positive as well as negative reinforcement. Dopamine excites the brain’s so-called Go pathway, which promotes a response while also inhibiting the action-suppressing “NoGo” pathway. Thus, bursts of dopamine resulting from positive reinforcement promote learning by both activating the Go channel and blocking NoGo. In contrast, dips in dopamine after negative outcomes should promote avoidance behavior by inactivating the Go pathway while releasing inhibition of NoGo.
In 2004 psychologist Michael J. Frank, then at the University of Colorado at Boulder, and his colleagues reported evidence for dopamine’s influence on learning in a study of patients with Parkinson’s disease, who produce too little of the neurotransmitter. Frank theorized that Parkinson’s patients may have trouble generating the dopamine needed to learn from positive feedback but that their low dopamine levels may facilitate training based on negative feedback.
In the study the researchers displayed pairs of symbols on a computer screen and asked 19 healthy people and 30 Parkinson’s patients to choose one symbol from each pair. The word “correct” appeared whenever a subject had chosen an arbitrarily correct symbol, whereas the word “incorrect” flashed after every “wrong” selection. (No symbol was invariably correct or incorrect.) One of them was deemed right 80 percent of the time, and another 20 percent. For other pairs, the probabilities were 70:30 and 60:40. The subjects were expected to learn from this feedback and thereby increase the number of correct choices in later test runs.
As expected, the healthy people learned to prefer the correct symbols and avoid the incorrect ones with about equal proficiency. Parkinson’s patients, on the other hand, showed a stronger tendency to reject negative symbols than to select the positive ones—that is, they learned more from their errors than from their hits, showing that the lack of dopamine did bias their learning in the expected way. In addition, the patients’ ability to learn from positive feedback outpaced that from negative feedback after they took medication that boosted brain levels of dopamine, underscoring the importance of dopamine in positive reinforcement.
Dopamine-based discrepancies in learning ability also appear within the healthy popu­lation. Last December, along with psychology graduate student Tilmann A. Klein and our colleagues, I showed that such variations are partly based on individual differences in a gene for the D2 dopamine receptor. A variant of this gene, called A1, results in up to a 30 percent reduction in the density of those receptors on nerve cell membranes.

We asked 12 males with the A1 variant and 14 males who had the more common form of this gene to perform a symbol-based learning test like the one Frank used. We found that A1 carriers were less able to remember, and avoid, the negative symbols than were the participants who did not have this form of the gene. The A1 carriers also avoided the negative symbols less often than they picked the positive ones. Noncarriers learned about equally well from the good and bad symbols.
Thus, fewer D2 receptors may impair a person’s ability to learn from mistakes or negative outcomes. (This molecular quirk is just one of many factors that influence such learning.) Accordingly, our fMRI results show that the medial frontal cortex of A1 carriers generates a weaker response to errors than it does in other people, suggesting that this brain area is one site at which dopamine exerts its effect on learning from negative feedback.
But if fewer D2 receptors leads to impaired avoidance learning, why do drugs that boost dopamine signaling also lead to such impairments in Parkinson’s patients? In both scenarios, do­pa­mine signaling may, in fact, be increased through other dopamine receptors; research indicates that A1 carriers produce an unusually large amount of do­pa­­mine, perhaps as a way to compensate for their lack of D2 receptors. Whatever the reason, insensitivity to unpleasant consequences may contribute to the slightly higher rates of obesity, compulsive gambling and addiction among A1 carriers than in the general population.
Foreshadowing FaultsAlthough learning from mistakes may help us avoid future missteps, inexperience or inattention can still lead to errors. Many such goofs turn out to be predictable, however, foreshadowed by telltale changes in brain metabolism, according to research my team published in April in the Proceedings of the National Academy of Sci­ences USA.
Along with cognitive neuroscientist Tom Eichele of the University of Bergen in Norway and several colleagues, I asked 13 young adults to perform a flanker task while we monitored their brain activity using fMRI. Starting about 30 seconds before our subjects made an error, we found distinct but gradual changes in the activation of two brain networks.
One of the networks, called the default mode region, is usually more active when a person is at rest and quiets down when a person is engaged in a task. But before an error, the posterior part of this network—which includes the retrosplenial cortex, located near the center of the brain at the surface—became more active, indicating that the mind was relaxing. Meanwhile activity declined in areas of the frontal lobe that spring to life whenever a person is working hard at something, suggesting that the person was also becoming less engaged in the task at hand.
Our results show that errors are the product of gradual changes in the brain rather than unpredictable blips in brain activity. Such adjustments could be used to foretell errors, particularly those that occur during monotonous tasks. In the future, people might wear portable devices that monitor these brain states as a first step toward preventing mistakes where they are most likely to occur—and when they matter most.
Editor's Note: This story was originally published with the title "Minding Mistakes"
ABOUT THE AUTHOR(S)

Markus Ullsperger is a physician and head of the cognitive neurology research group at the Max Planck Institute for Neurological Research in Cologne, Germany.

Source:http://www.sciam.com/article.cfm?id=minding-mistakes&page=4

A Natural Log: Our Innate Sense of Numbers is Logarithmic, Not Linear

We humans seem to be born with a number line in our head. But a May 30 study in Science suggests it may look less like an evenly segmented ruler and more like a logarithmic slide rule on which the distance between two numbers represents their ratio (when ­di­vided) rather than their difference (when subtracted).
The mathematical idea of a number line—a line of numbers placed in order at equal intervals—is a simple yet surprisingly powerful tool, useful for everything from taking measure­ments to geometry and calculus.
Previous studies of Westerners showed that people tend to map numbers on a linear scale, with the numerals evenly spaced along the line. But if the numbers are presented as hard-to-count groups of dots, people will logarithmically group the larger numbers closer together on one end of the scale in what researchers call a “compression effect.” Preschoolers also group numbers this way before they begin their formal education in math.

To investigate which number-line concept is innate, neuroscientist Stanislas Dehaene of the College of France in Paris worked with the Mundurukú, an Amazonian culture with little exposure to modern math or measuring devices. The Mundurukú were immediately able to place numbers on a line when asked, but they grouped them logarithmically.
Dehaene says the research suggests that a logarithmic number line might be an intuitive mathematical concept, whereas the idea of a linear number line might have to be learned.
Editor's Note: This story was originally printed with the title "A Natural Log"

Source:http://www.sciam.com/article.cfm?id=a-natural-log