No, it's not just you. According to studies recently conducted by the University of California, Berkeley, the viewing of stereoscopic 3D displays does indeed cause visual discomfort, fatigue and headaches. The problem appears to come from the fact that the viewers' eyes are simultaneously trying to focus on the screen, and on objects that appear to be located either in front of or behind that screen.
The studies involved 24 adult subjects, who viewed 3D content both on small, consumer electronics-style screens, and on larger, theater-style screens. With the smaller screens, which are viewed at a closer distance, content that appeared to be located in front of the screen caused the most discomfort. Interestingly, however, viewing of the larger, more distant screens was most uncomfortable when content appeared to be located behind the screen.
"When watching stereo 3D displays, the eyes must focus - that is, accommodate - to the distance of the screen because that's where the light comes from," said Martin S. Banks, professor of optometry and vision science. "At the same time, the eyes must converge to the distance of the stereo content, which may be in front of or behind the screen."
Further studies are planned, which would include a larger number of test subjects, including children. The U Berkeley researchers hope that their findings could be used to establish guidelines for the positioning of viewers relative to 3D displays.
"Discomfort associated with viewing Stereo 3D is a major problem that may limit the use of technology," said Banks. "We hope that our findings will inspire more research in this area."
The research was recently published in The Association for Research and Vision in Ophthalmology's Journal of Vision.
If you’re like me and you have a visceral reaction to the image above—if it makes your skin crawl, your hair hurt, and your stomach turn—you can count yourself among the trypophobic. According to its Facebook page, which is more than 4,000 members strong, trypophobia is fear of clustered holes. It is usually small holes in organic objects, such as lotus seed heads or bubbles in batter, that give trypophobics the extreme willies, triggering reactions like itchy skin, nausea and a general feeling of discomfort.
Although this may be of no comfort to those who suffer from it, trypophobia is simply one of an infinite number of fears that people experience, some more idiosyncratic than others. The onlinePhobia List, run by an amateur etymologist, contains the names of hundreds of fears, from the well-known (fear of heights: acrophobia) to the fringe (fear of the great mole rat: zemmiphobia). Trypophobia hasn’t made the list yet.
According to Martin Anthony, a psychologist at Ryerson University in Toronto, past-president of the Canadian Psychological Association and author of The Anti-Anxiety Workbook, with the exception of a few terms (agoraphobia, claustrophobia and arachnophobia among them), professionals who study and treat phobias tend not to use all the Latin and Greek names that get tossed around on message boards and in the press.
Anthony wasn’t surprised to hear that some people have an intense aversion to clustered holes because “people can be afraid of absolutely anything.” The factors that contribute to fears and phobias include traumatic experiences (getting bitten by a dog leading to a fear of dogs, for example), observational learning (watching others be afraid of heights), information and instruction (learning to fear being alone in the dark after watching too many horror movies), and various biological factors (like an inherited predisposition to anxiety). “Although the studies on causes of fears have all focused on more common ones, such as spiders and snakes, there is no reason to think that different factors would be responsible for more unusual fears, Anthony says.
Trypophobia may also be catching. An element of so-called emotional contagion seems to be at work on Facebook, where some group members say they didn’t realize they were trypophobic until they started reading others’ comments and clicking on the pictures. “It’s not unusual to laugh harder at a funny movie if others around you are laughing,” Antony explains. “In the same way, we may be more likely to experience fear in a particular moment if others around us are fearful.” For me, however, all it took was a verbal mention of a “fear of small holes” to illicit a shudder. I became disgusted before looking at a single gnarly image of a skin graft or lamprey eel (look ’em up) or reading an online comment. I also immediately assumed that we were talking about biologic objects—holes in wood, in particular. Clearly, in me the fear was preexisting.
One trypophobic reported on Facebook that her fear stems back to childhood, when she had a Renaissance Faire dagger with a handle covered in little holes. Another member wrote: “I was stung by a bee in high school on my outer thigh. I had an allergic reaction, and my skin started to swell. The swelling was so bad, I could see each individual pore on my leg and I freaked out. Since then, I have not been able to look at clusters of holes without getting the heebie-jeebies.” Just. Gross.
Fear and disgust often go hand in hand, Anthony says. “Evolutionarily speaking, almost all of the things that arouse a strong disgust-reaction--spiders, mice, blood, vomit--are things that could have been triggers for fear of illness.” Perhaps the same could be true for little holes, especially in natural objects where they seem particularly out of place. I suspect that we’re disgusted by pockmarked objects because they don’t look quite “right”; these perceived deformities signal danger, which we manifest as revulsion. But then again, a fear of asymmetry (another form of things looking not quite right) in some people with obsessive-compulsive disorder is not associated with disgust, Antony says. Perhaps holes, particularly in organic objects, subconsciously remind us of the symptoms of contagious illnesses that affect the skin, such as the rash or blisters associated with measles and chicken pox, respectively. All of this, of course, is speculation, and just goes to show how little we know about trypophobia.
Masai Andrews hopes that will change. Andrews, who runs Trypophobia.com, founded the Facebook group page in 2009 when he was a sociology minor at SUNY-Albany. “I started the website and Facebook page because I suspected this was a very common phobia and I wanted a place where people could compile information,” Andrews says. “It is my hope that one day the academic and scientific communities will, at the very least, acknowledge the aversion to holes and certain patterns.”
When that happens, a Wikipedia page dedicated to the fear should follow. Surprisingly, one doesn’t exist today. “I can barely keep a page up on the subject without it getting taken down,” Andrews says. In March 2009 the powers that be at Wikipedia determined trypophobia to be a “likely hoax and borderline patent nonsense.” The deletion page also says that Wikipedia is “not for things made up one day.” As for who actually made the word up, that distinction probably belongs to a blogger in Ireland named Louise, Andrews says. According to an archived Geocities page, Louise settled on “trypophobia” (Greek for “boring holes” + “fear”) after corresponding with a representative at the Oxford English Dictionary. Louise, Andrews and trypophobia Facebook group members have petitioned the dictionary to include the word. The term will need to be used for years and have multiple petitions and scholarly references before the dictionary accepts it, Andrews says. I, for one, would prefer to forget about it forever.
Want to find out if you’re trypophobic? Take this quick visual test. But beware: You may be skipping lunch today.
One of the things that our brains excel at is the ability to recognize what things are, even when presented with an incomplete set of data. If we know only that an animal is sold in pet stores and stuffs food in its cheeks, for instance, we can be pretty certain that the animal in question is a hamster. Now, for the first time ever, researchers at the California Institute of Technology (Caltech) have created a DNA-based artificial neural network that can do the same thing ... albeit on a very basic level. They believe that it could have huge implications for the development of true artificial intelligence.
The neural network is made up of just four artificial neurons, as opposed to the human brain's 100 billion real ones.
To test the network, the scientists played a game with it. That game started with the network being trained to "know" four scientists, each one identifiable by a unique combination of yes/no answers to the same four questions (such as "Is the scientist British?"). Human players then chose one of those scientists, and provided the network with an incomplete set of the identifying answers. They did this by dropping DNA strands that were programmed to correspond to those answers, into water in a test tube that contained the neurons.
Communicating through fluorescent signals, the network would then either correctly identify the chosen scientist, it would indicate that it didn't have enough data to identify just one scientist, or it would state that the data didn't match any of the scientists.
This was possible because of the manner in which the added strands of DNA paired with the strands already present in the network. This, in turn, was determined by whether or not the sequences programmed into both strands complimented one another.
It should be noted that the network took eight hours to come up with each of its responses, and that new DNA strands had to be created for each game. Still, theCaltech team state that the technology could ultimately be used for creating biochemical systems with artificial intelligence, which could revolutionize fields such as medicine, chemistry, and biological research.
The research was recently published in the journal Nature.
It's often during those early stages of learning to play a new instrument that many people give up in despair. Even though you swear that you're hitting the right notes, everything still sounds like an old gramophone recording played at the wrong speed. If only you could let someone take control of your hands to fast forward through the arduous repetition phase before muscle memory kicks in and the piece you're trying to play begins to sound more like it should. That's precisely the kind of potential offered by the PossessedHand project. Electrode-packing armbands placed on a user's forearm send electrical pulses through the muscles to take control of the movement of the hand - with fledgling Koto players testing the system having demonstrated greater accuracy and speedier progress.
The goal of the PossessedHand project was to develop a support system for playing musical instruments where users could quickly learn the gestures, positioning and timing needed for a piece of music without having to wear glove-type devices that digitally control the movement of their fingers. By positioning two belts on the forearm of a user - each containing a number of non-invasive electrode pads - researchers were able to effectively take control of five independent and 11 linked joints in the hand to electrically control the movement of individual fingers of the wearer's hand.
Many of the muscles used to move fingers - like the superficial flexor muscle, deep flexor muscle, long flexor muscle of the thumb, common digital extensor muscle, flexor carpi radialis muscle, long palmar muscle, and flexor carpi ulnaris muscle - are located in the forearm. Movement of the joints can be controlled by stimulating these muscles with electrical pulses. The researchers also discovered that muscles at different depths in the forearm respond to different strengths of voltage, resulting in the system being able to take over control of a total of 16 joints in the user's hand.
The PossessedHand prototype consists of a battery, a condenser, a timing volume, a switching board (Photo-MOS Relays Series AQV221), a microcontroller, and solid gel electrode pads on two belts. One armband is positioned on the upper part of the forearm and the other lower down and then connected to PC via USB and controlled by a specially-developed graphical user interface. The pulse width is 0.2 ms and the voltage range is 17 - 29 V.
To overcome difficulties in precise positioning of the electrodes over specific muscles in different users, the researchers crammed 14 electrodes into each of the two armbands and then developed an automated calibration system. The system estimates the relationship between the 28 electrodes, the level of stimulation and the amount of muscle movement required.
Volunteers were blindfolded and asked to identify which joints were being moved by the system and reactions to PossessedHand ranged from Scary, just scary to I felt like my forearm was pushed by someone to I felt like my body was hacked.
The team then transcribed Japanese Koto scores into PossessedHand scores, which included information on which finger should be moved and when. Two beginners then alternated between system supported and non-supported playing of the music, with arm positioning over the 13-stringed instrument being undertaken by the user in both cases. The team noted a significant reduction in timing errors and fewer fingering mistakes when PossessedHand was active.
It's also important when playing a musical instrument to apply the correct amount of force at the appropriate time. Sadly, the PossessedHand experiments could not electrically stimulate enough force to actually grasp an object or play an instrument. As such, this would seem to fit in with learning systems like Piano Hands and Piano Maestro.
Such technology might also find application in the treatment of folks who suffer from impaired muscle control or be used by professionals looking to quickly improve dexterity, such as surgeons.
The paper entitled PossessedHand: Techniques for controlling human hands using electrical muscles stimuli by Emi Tamaki, Takashi Miyaki, and Jun Rekimoto was presented at the ACM CHI Conference on Human Factors in Computing Systems in Vancouver, Canada in May 2011.
The PossessedHand system was recently demonstrated at the World Haptics Conference in Istanbul, Turkey.
In the future, people who are prone to seizures may get an array of electrodes implanted in their brains. These electrodes would be capable of detecting the onset of a seizure, and then releasing medication to prevent it from happening. While it might sound far-fetched, scientists at the University of Pittsburgh have already demonstrated the technology on lab rats.
Multielectrode arrays (MEAs) are capable of recording or controlling the electrical activity in neurons, and are used in devices such as ear implants and pacemakers. The Pittsburgh team coated MEAs with the polymer Polypyrrole (PPy), which is known for its electrical conductivity. Mixed in with the PPy were anti-convulsive neurochemicals.
The coated MEAs were then placed on a rat's brain, and electrically stimulated. This caused the neurochemicals to dissociate from the PPy, and diffuse into the adjacent regions of the brain. Testing indicated that after dissociation, the drugs still remained effective.
Similar technologies have involved implants with built-in drug reservoirs, although these would be larger than the coated MEAs, and could cause tissue damage.
"By directly loading a drug of interest onto an individual electrode site and using an electrical signal to trigger its release, we can precisely control the drug delivery site with ease," said the study's co-author, Prof. X Tracy Cui. "Additionally, our technology can be used for a combination of exogenous chemicals such as subtype-specific receptor antagonists, thus potentially allowing for more precise dissection of neural circuit function at the molecular level."
That doughnut shape decorated with bright green spots, some connected by red pathways, amidst sky blue neighbors could be an artist's creation, but is the result of a creative scientific attempt to grow an active brain in a dish, complete with memories. Really.
Researchers at the University of Pittsburgh published this stunning study in the journal Lab on a Chip {the full paper can be accessed here.} When I first learned how to grow cells in a lab, the technique of tissue culture, the idea of even growing brain cells was a far-fetched dream, much less brain cells capable of forming networks, complete with biological signals.
How did they do it?
To produce the models, the Pitt team stamped adhesive proteins onto silicon discs. Once the proteins were cultured and dried, cultured hippocampus cells from embryonic rats were fused to the proteins and then given time to grow and connect to form a natural network. The researchers disabled the cells' inhibitory response and then excited the neurons with an electrical pulse.
Zeringue and his colleagues were able to sustain the resulting burst of network activity for up to what in neuronal time is 12 long seconds. Compared to the natural duration of .25 seconds at most, the model's 12 seconds permitted an extensive observation of how the neurons transmitted and held the electrical charge, Zeringue said.
From the paper's Abstract: {excerpted for clarity}
Persistent activity in the brain is involved in working memory and motor planning. The ability of the brain to hold information 'online' long after an initiating stimulus is a hallmark of brain areas such as the prefrontal cortex. Recurrent network loops such as the thalamocortical loop and reciprocal loops in the cortex are potential substrates that can support such activity. However, native brain circuitry makes it difficult to study mechanisms underlying such persistent activity. Here we propose a platform to study synaptic mechanisms of such persistent activity by constraining neuronal networks to a recurrent loop like geometry. Using a polymer stamping technique, adhesive proteins are transferred onto glass substrates in a precise ring shape. Primary rat hippocampal cultures were capable of forming ring-shaped networks containing 40-60 neurons. Calcium imaging of these networks show evoked persistent activity in an all-or-none manner. Blocking inhibition leads to an increase in the duration of persistent activity. These persistent phases were abolished by blockade of asynchronous neurotransmitter release by ethylene glycol tetraacetic acid.
This is amazing. I wonder what the "memory" could be - could be a good subject for a science fiction story.
In a move that gives cautious hope to the millions of people suffering some form of paralysis, a team of researchers from UCLA, Caltech and the University of Louisville has given a man rendered paralyzed from the chest down after a hit-and-run accident in 2006 the ability to stand and take his first tentative steps in four years. The team used a stimulating electrode array implanted into the man's body to provide continual direct electrical stimulation to the lower part of the spinal cord that controls movement of the hips, knees, ankles and toes, to mimic the signals the brain usually sends to initiate movement.
Instead of bypassing the nervous system to directly stimulate the leg muscles, the electrical signals provided by the array stimulate the spinal cord's own neural network so it can use the sensory input derived from the legs to direct muscle and joint movements. The stimulation therefore doesn't induce movement, but taps into a network of spinal cord nerves that are capable of initiating movement on their own without the help of the brain, which then work together with cues from the legs to direct muscle movement.
The research team's work builds on previous research at UCLA that showed animals with spinal-cord injuries could stand, balance, bear weight and take coordinated steps while the outermost part of the spinal canal - or epidural space - is stimulated.
Thanks to the breakthrough the test subject, 25 year old Rob Summers, is able to supply the muscular push required to stand up and remain standing for up to four minutes at a time. With periodic assistance, Summers is able to stand for up to an hour, and with the aid of a harness support and some assistance from a therapist he is able to take steps on a treadmill.
Prior to implantation with the epidural stimulating array, Summers, who suffered a complete motor injury at the C7/T1 level of the spinal cord, was unable to move even his toes. But after implantation he was able to not only stand and make repeated stepping motions on a treadmill with the assistance of a harness, but also regained the ability to voluntarily move his toes, ankles, knees, and hips on command. However, once the stimulation is turned off, Summers loses the voluntary control of his limbs.
Over time, Summers also experienced improvements in several types of autonomic function, including bladder and bowel control and temperature regulation. The researchers say these autonomic functions began to return before there was any sign of voluntary movement, which took around seven months after he began receiving epidural stimulation to emerge.
Although the researchers still aren't yet fully sure how these autonomic functions were regained, the results indicate the treatment could help improve the quality of life of spinal cord injury sufferers other than those with the strength to undergo the rigorous physical training Summers did as part of his treatment. The researchers say the relief from secondary complications of complete spinal cord injury - including impairment or loss of bladder control, sphincter control and sexual response - could even prove to be ultimately as, or more important in terms of improving the quality of life of such patients.
While obviously encouraged by the results, the researchers are quick to point out that the study represents just one case and that there's no way to tell how other patients may react. They also point out that Summers, who was an athlete in comparatively excellent physical condition before his accident, retained some sensation in his lower extremities after his injury indicating his spinal cord was not completely severed, which may have played a part in the level of success he was able to attain.
However, the researchers are hopeful that their work could one day provide some individuals suffering spinal cord injuries with the ability to stand independently, maintain balance and take effective steps through the use of a portable stimulation unit and the assistance of a walker. Additionally, the researchers believe the approach could potentially also help in the treatment of stroke, Parkinson's, and other disorders affecting motor function.
The team has received approval from the FDA to test five spinal-cord injury patients and will next try and replicate their initial results with a patient that matches Summers in terms of age, injury, and physical ability. They will then turn to patients who have no sensation to see how that influences the outcome.
Interestingly, the device implanted into Summers is FDA-approved for back pain only and its use was meant only as a test to see if the researcher's concepts would work. As a result, the researchers say the current implants have many limitations and that further advances in the technology should lead to better control of the standing and stepping process. They are also looking at whether it might be possible to move the array higher up on the spinal column to see if it could also be used to affect the arms and hands.
Building a synthetic brain is no easy undertaking, but researchers working on the problem have to start somewhere. In doing so, engineers at the University of Southern California have taken a huge step by building a synthetic synapse from carbon nanotubes.
In tests, their synapse circuit functions very much like a real neuron--neurons being the very building blocks of the brain. Tapping the unique properties of carbon nanotubes, their lab was able to essentially recreate brain function in a very fractional way.
Of course, duplicating synapse firings in a nanotube circuit and creating synthetic brain function are two very different things. The human brain, as we well know, is very complex and hardly static like the inner workings of a computer. Over time it makes new connections, adapts to changes, and produces new neurons.
But while a functioning synthetic brain may be decades away, the synthetic synapse is here now, which could help researchers model neuron communications and otherwise begin building, from the ground up, an artificial mimic of one of biology’s biggest mysteries.
When your sweetheart dumps you, there's a reason why it hurts so much. It turns out your brain registers the psychological hell in exactly the same way it registers physical pain.
A group of scientists used fMRI scans to study the brains of people dealing with being rejected, and compared them to the brains of people experiencing physical pain. They found that the exact same regions of the brain are involved in processing both experiences. For humans, social rejection is tantamount to literal injury.
Write the authors in a paper published this week in the Proceedings of the National Academy of Sciences:
We tested this hypothesis by recruiting 40 individuals who felt intensely rejected as a result of recently experiencing an unwanted romantic relationship break-up (see Methods). Participants performed two counterbalanced tasks during functional MRI (fMRI) scanning: a Social Rejection task and a Physical Pain task (for design, see Fig. 1). Briefly, the Social Rejection task compared Ex-partner trials, in which participants viewed a headshot of their former partner and thought about their specific rejection experience, and Friend trials, in which participants viewed a headshot of a friend who was the same sex as their ex-partner and thought about a recent positive experience they shared with that person. The Physical Pain task also consisted of two types of trials: Hot trials, in which participants experienced noxious thermal stimulation on their left forearm, and Warm trials, in which participants experienced nonnoxious thermal stimulation in the same area. Participants rated how they felt after each task trial using a five-point scale, with lower numbers reflecting more distress.
And indeed, they saw the same regions of the brain lighting up during both physical and mental tasks - specifically, "areas that support the sensory components of physical pain (secondary somatosensory cortex; dorsal posterior insula)." The researchers say that their work could shed light on why different kinds of social rejection can lead to physical pain and other ailments. Ultimately, they say, our brains reveal an intensely strong connection between emotions and physical sensations. An interesting area for future research would be whether witnessing somebody else's distress also affects our brains the same way physical pain does - in other words, do we literally feel the pain of others?
Bees can become mentally young again with just a few simple alterations to their otherwise fixed routines. Because the brains of bees are surprisingly like our own, this trick could help fight dementia and keep human minds young and flexible.
Norwegian researcher Gro Amdam had groups of older bees take part in learning and memory tests. The bees were challenged to associate a particular scent with a particular reward, and then be able to remember that association later on. Most of the older bees were able to make the connection, but more slowly than their younger counterparts, and those bees that had symptoms equivalent to human dementia were unable to make the connection at all, suggesting their short-term memory and ability to learn were both in sharp decline.
Here's where it gets interesting. Bee hives have a fairly strict social structure - the older bees leave the hive to collect food, while the younger bees remain inside and care for larvae. Amdam flipped this by creating a hive where the older bees were again in charge of larvae. This simple alteration caused an instant surge in the older bees' cognitive abilities, with half of the bees showing marked improvement in their learning and memory.
Even better, Amdam has been able to zero in on the physical alterations engendered by this social change. She discovered that eight different proteins associated with growth, repair, and maintenance of the brain cells had undergone massive with growth, with some reaching levels twice that of normal. Many of these proteins have direct human equivalents, which raises the distinct possibility that similar results could be produced in humans.
Amdam explains:
"This is evidence of a certain flexibility in the bee brain, and it is conceivable that the brains of other animals and humans could have a similar potential. If so, the question is whether we would be able to figure out how to tap into this flexibility. Another approach would be to try to figure out how the relevant bee proteins work, and then create substances that trigger similar effects."
One of humanity's most incredible abilities is being able to remember things that happened many years, perhaps even many decades ago. But it's only now that neuroscience is able to really explain how we can form such long-lasting memories.
Scientists have long suspected that the key to remembering things from long ago is what's known as long-term potentiation, or LTP. This basically involves a long-lasting increase in the signals sent along the connections between particular brain cells, which in turn allows us to keep recalling things we experienced decades after they first occurred. But what actually causes LTP had eluded scientists...until now.
Duke researchers have discovered a cascade of special molecules that make an otherwise very short-lived signal last for tens of minutes. That might not seem like a very long time, and yet that's the likely building block on which all our long-term memories rest. Over time, these minutes-long connections, or synapses, would be reinforced and strengthened into connections that can rest months, years, and even decades.
Lead researcher Ryohei Yasuda explains the team's findings:
"We found that a biochemical process that lasts a long time is what causes memory storage," said Yasuda, who is a Howard Hughes Medical Institute Early Career Scientist. The signaling molecules could help to rearrange the framework, and give more volume and strength to the synapses. We reasoned that a long-lasting memory could possibly come from changes in the building block assemblies."
Two of the crucial molecules in strengthening these connections - and, by extension, maintaining the long-term plasticity of the synapses and our continued ability to learn new things - are known as Rho and Cdc42. We already know that mental diseases including Alzheimer's disease are linked to abnormal signals from these molecules, and Yasuda is optimistic that this new research will help us understand more about the underpinnings of the conditions.
Macotakara reports that it has received information indicating that Apple will be introducing the iPad 3 and "iPhone 4S" sometime early next month, with availability set for "late October". The source offered no information, however, on plans for the iPhone 5, although rumors have suggested that Apple will introduce both a revamped iPhone 5 and tweaked iPhone 4 next month.
A breakthrough therapy to modify T-cells into potent tumor-killing agents wiped out leukemia in three patients and allowed two of them to stay cancer-free for a year, US researchers said Wednesday.
The new post-shuttle NASA has said it aims to work more cooperatively with private space industry and outside sources of innovation in writing the next chapter in space exploration and science, and the agency is putting its money where its mouth is. After selecting 30 future technology proposals for funding earlier this week
