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By Hanae Armitage Cataracts cloud the eyes of tens of millions of people around the world and nearly 17.2% of Americans over the age of 40. Currently, the only treatment is surgery—lasers or scalpels cut away the molecular grout that builds in the eye as cataracts develop, and surgeons sometimes replace the lens. But now, a team of scientists and ophthalmologists has tested a solution in dogs that may be able to dissolve the cataract right out of the eye’s lens. And the solution is itself a solution: a steroid-based eye drop. Though scientists don’t fully understand how cataracts form, they do know that the “fog” often seen by patients is a glob of broken proteins, stuck together in a malfunctioning clump. When healthy, these proteins, called crystallins, help the eye’s lens keep its structure and transparency. But as humans and animals alike get older, these crystallin proteins start to come unglued and lose their ability to function. Then they clump together and form a sheathlike obstruction in the lens, causing the signature “steamy glass” vision that accompanies cataracts. Coming up with a solution other than surgery has been tough. Scientists have been hunting for years for mutations in crystallin proteins that might offer new insights and pave the way to an alternate therapy. Now, it looks like a team led by University of California (UC), San Diego, molecular biologist Ling Zhao may have done just that. Her team came up with the eye drop idea after finding that children with a genetically inherited form of cataracts shared a mutation that stopped the production of lanosterol, an important steroid in the body. When their parents did not have the same mutation, the adults produced lanosterol and had no cataracts. © 2015 American Association for the Advancement of Science.
It’s a good combination. Gene therapy to reverse blindness repairs damaged cells in the eye and also rearranges the brain to help process the new information. Visual pathways in the brain are made up of millions of interconnected neurons. When sensory signals are sent along them, the connections between neurons become strong. If underused – for example, as people lose their sight – the connections become weak and disorganised. Over the past few years, a type of gene therapy – injecting healthy genes into the eye to repair mutations – has emerged as a promising way to treat congenital and degenerative blindness. One of the first successful trials began in 2007. It involved 10 blind volunteers with a hereditary disease called Leber’s congenital amaurosis. The condition causes the retina to degenerate and leaves people completely blind early in life. Mutations in at least 19 genes can cause the disease, but all of the people in the trial had mutations in a gene called RPE65. The participants got an injection of a harmless virus in one of their eyes. The virus inserted healthy copies of RPE65 into their retina. Some of the volunteers went from straining to see a hand waving half a metre from their face to being able to read six lines on a sight chart. Others were able to navigate around an obstacle course in dim light – something that would have been impossible before the therapy. © Copyright Reed Business Information Ltd.
Spider-like cells inside the brain, spinal cord and eye hunt for invaders, capturing and then devouring them. These cells, called microglia, often play a beneficial role by helping to clear trash and protect the central nervous system against infection. But a new study by researchers at the National Eye Institute (NEI) shows that they also accelerate damage wrought by blinding eye disorders, such as retinitis pigmentosa. NEI is part of the National Institutes of Health. “These findings are important because they suggest that microglia may provide a target for entirely new therapeutic strategies aimed at halting blinding eye diseases of the retina,” said NEI Director, Paul A. Sieving, M.D. “New targets create untapped opportunities for preventing disease-related damage to the eye, and preserving vision for as long as possible.” The findings were published in the journal EMBO Molecular Medicine. Retinitis pigmentosa, an inherited disorder that affects roughly 1 in 4,000 people, damages the retina, the light-sensitive tissue at the back of the eye. Research has shown links between retinitis pigmentosa and several mutations in genes for photoreceptors, the cells in the retina that convert light into electrical signals that are sent to the brain via the optic nerve. In the early stages of the disease, rod photoreceptors, which enable us to see in low light, are lost, causing night blindness. As the disease progresses, cone photoreceptors, which are needed for sharp vision and seeing colors, can also die off, eventually leading to complete blindness.
by Michael Le Page It is perhaps the most extraordinary eye in the living world – so extraordinary that no one believed the biologist who first described it more than a century ago. Now it appears that the tiny owner of this eye uses it to catch invisible prey by detecting polarised light. This suggestion is also likely to be greeted with disbelief, for the eye belongs to a single-celled organism called Erythropsidinium. It has no nerves, let alone a brain. So how could it "see" its prey? Fernando Gómez of the University of São Paulo, Brazil, thinks it can. "Erythropsidinium is a sniper," he told New Scientist. "It is waiting to see the prey, and it shoots in that direction." Erythropsidinium belongs to a group of single-celled planktonic organisms known as dinoflagellates. They can swim using a tail, or flagellum, and many possess chloroplasts, allowing them to get their food by photosynthesis just as plants do. Others hunt by shooting out stinging darts similar to the nematocysts of jellyfishMovie Camera. They sense vibrations when prey comes near, but they often have to fire off several darts before they manage to hit it, Gómez says. Erythropsidinium and its close relatives can do better, Gómez thinks, because they spot prey with their unique and sophisticated eye, called the ocelloid, which juts out from the cell. "It knows where the prey is," he says. At the front of the ocelloid is a clear sphere rather like an eyeball. At the back is a dark, hemispherical structure where light is detected. The ocelloid is strikingly reminiscent of the camera-like eyes of vertebrates, but it is actually a modified chloroplast. © Copyright Reed Business Information Ltd.
Related chapters from BP7e: Chapter 10: Vision: From Eye to Brain; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 21058 - Posted: 06.16.2015
By Stephen L. Macknik, Susana Martinez-Conde and Bevil Conway This past February a photograph of a dress nearly broke the Internet. It all started when a proud mother-in-law-to-be snapped a picture of the dress she planned to wear to her daughter's wedding. When she shared her picture with her daughter and almost-son-in-law, the couple could not agree on the color: she saw white and gold, but he saw blue and black. A friend of the bride posted the confusing photo on Tumblr. Followers then reposted it to Twitter, and the image went viral. “The Dress” pitted the opinions of superstar celebrities against one another (Kanye and Kim disagreed, for instance) and attracted millions of views on social media. The public at large was split into white-and-gold and blue-and-black camps. So much attention was drawn, you would have thought the garment was conjured by a fairy godmother and accessorized with glass slippers. To sort out the conundrum, the media tapped dozens of neuroscientists and psychologists for comment. Pride in our heightened relevance to society gave way to embarrassment as we realized that our scientific explanations for the color wars were not only diverse but also incomplete. Especially perplexing was the fact that people saw it differently on the same device under the same viewing conditions. This curious inconsistency suggests that The Dress is a new type of perceptual phenomenon, previously unknown to scientists. Although some early explanations for the illusion focused on individual differences in the ocular structure of the eye, such as the patterning and function of rod and cone photoreceptor cells or the light-filtering properties internal to the eye, the most important culprit may be the brain's color-processing mechanisms. These might vary from one person to the next and can depend on prior experiences and beliefs. © 2015 Scientific American
by Penny Sarchet Simon Sponberg of Georgia Institute of Technology in Atlanta and his team have figured out the secret to the moths' night vision by testing them with robotic artificial flowers (see above). By varying the speed of a fake flower's horizontal motion and changing brightness levels, the team tested moths' abilities under different conditions. It has been theorised that the moth brain slows down, allowing their visual system to collect light for longer, a bit like lengthening a camera's exposure. But the strategy might also introduce blur, making it hard to detect fast movement. If the moths were using this brain-slowing tactic, they would be expected to react to fast flower movements more slowly in darker conditions. The team found that there was indeed a lag. It helped them see motion in the dark while still allowing them to keep up with flowers swaying at normal speeds. The size of the lags matched the expected behaviour of a slowed nervous system, providing evidence that moths could be slowing down the action of neurons in their visual system. Previously, placing hawkmoths in a virtual obstacle courseMovie Camera revealed that they vary their navigation strategies depending on visibility conditions. Journal reference: Science, DOI: 10.1126/science.aaa3042 © Copyright Reed Business Information Ltd
Related chapters from BP7e: Chapter 10: Vision: From Eye to Brain; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 7: Vision: From Eye to Brain; Chapter 5: The Sensorimotor System
Link ID: 21041 - Posted: 06.13.2015
Carl Zimmer Octopuses, squid and cuttlefish — a group of mollusks known as cephalopods — are the ocean’s champions of camouflage. Octopuses can mimic the color and texture of a rock or a piece of coral. Squid can give their skin a glittering sheen to match the water they are swimming in. Cuttlefish will even cloak themselves in black and white squares should a devious scientist put a checkerboard in their aquarium. Cephalopods can perform these spectacles thanks to a dense fabric of specialized cells in their skin. But before a cephalopod can take on a new disguise, it needs to perceive the background that it is going to blend into. Cephalopods have large, powerful eyes to take in their surroundings. But two new studies in The Journal Experimental Biology suggest that they have another way to perceive light: their skin. It’s possible that these animals have, in effect, evolved a body-wide eye. When light enters the eye of a cephalopod, it strikes molecules in the retina called opsins. The collision starts a biochemical reaction that sends an electric signal from the cephalopod’s eye to its brain. (We produce a related form of opsins in our eyes as well.) In 2010, Roger T. Hanlon, a biologist at the Marine Biological Laboratory in Woods Hole, Mass., and his colleagues reported that cuttlefish make opsins in their skin, as well. This discovery raised the tantalizing possibility that the animals could use their skin to sense light much as their eyes do. Dr. Hanlon teamed up with Thomas W. Cronin, a visual ecologist at the University of Maryland Baltimore County, and his colleagues to take a closer look. © 2015 The New York Times Company
Related chapters from BP7e: Chapter 10: Vision: From Eye to Brain; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 20966 - Posted: 05.21.2015
By Camille Bains, Imagine being able to see three times better than 20/20 vision without wearing glasses or contacts — even at age 100 or more — with the help of bionic lenses implanted in your eyes. Dr. Garth Webb, an optometrist in British Columbia who invented the Ocumetics Bionic Lens, says patients would have perfect vision and that driving glasses, progressive lenses and contact lenses would become a dim memory as the eye-care industry is transformed. Dr. Garth Webb says the bionic lens would allow people to see to infinity and replace the need for eyeglasses and contact lenses. (Darryl Dyck/Canadian Press) Webb says people who have the specialized lenses surgically inserted would never get cataracts because their natural lenses, which decay over time, would have been replaced. Perfect eyesight would result "no matter how crummy your eyes are," Webb says, adding the Bionic Lens would be an option for someone who depends on corrective lenses and is over about age 25, when the eye structures are fully developed. "This is vision enhancement that the world has never seen before," he says, showing a Bionic Lens, which looks like a tiny button. "If you can just barely see the clock at 10 feet, when you get the Bionic Lens you can see the clock at 30 feet away," says Webb, demonstrating how a custom-made lens that folded like a taco in a saline-filled syringe would be placed in an eye, where it would unravel itself within 10 seconds. He says the painless procedure, identical to cataract surgery, would take about eight minutes and a patient's sight would be immediately corrected. ©2015 CBC/Radio-Canada.
By Angus Chen Jumping spiders are the disco dancers of the arachnid world. The males thump and throb their brightly patterned legs and abdomens at the ladies like in the video above. Yet most of these bright colors should be impossible for the arachnids to see. That’s because their eyes have only two types of color-sensitive cone cells, which are designed to detect just ultraviolet and green light. Now, researchers report today in Current Biology that the North American genus of jumping spiders sees extra colors via a small, thin layer of red-pigmented cells partially covering the center of their retinas. The layer acts as a filter, allowing only red light to pass through and activate retinal cells just below the layer. This essentially converts a few of their green-sensitive cells into red-sensitive cells, allowing the spiders to build palates from three colors much the same way humans do—we have blue, green, and red cone cells. These jumping spiders have some limitations, though. Because their red filter is a small dot over the center of their retinas, they can see red only if they look directly at it. And because the filter blocks out any light that’s not red, anything that they look at has to be pretty bright before they can see any redness on it. Luckily for them, they like to spend time dancing in the sun. © 2015 American Association for the Advancement of Science
By Tina Hesman Saey A man who had been blind for 50 years allowed scientists to insert a tiny electrical probe into his eye. The man’s eyesight had been destroyed and the photoreceptors, or light-gathering cells, at the back of his eye no longer worked. Those cells, known as rods and cones, are the basis of human vision. Without them, the world becomes gray and formless, though not completely black. The probe aimed for a different set of cells in the retina, the ganglion cells, which, along with the nearby bipolar cells, ferry visual information from the rods and cones to the brain. No one knew whether those information-relaying cells still functioned when the rods and cones were out of service. As the scientists sent pulses of electricity to the ganglion cells, the man described seeing a small, faint candle flickering in the distance. That dim beacon was a sign that the ganglion cells could still send messages to the brain for translation into images. That 1990s experiment and others like it sparked a new vision for researcher Zhuo-Hua Pan of Wayne State University in Detroit. He and his colleague Alexander Dizhoor wondered if, instead of tickling the cells with electricity, scientists could transform them to sense light and do what rods and cones no longer could. The approach is part of a revolutionary new field called optogenetics. Optogeneticists use molecules from algae or other microorganisms that respond to light or create new molecules to do the same, and insert them into nerve cells that are normally impervious to light. By shining light of certain wavelengths on the molecules, researchers can control the activity of the nerve cells. © Society for Science & the Public 2000 - 2015
by Rachel Ehrenberg It was the dress that launched a million tweets. In February, a mother-in-law-to-be sent a picture of a dress she was considering wearing to her daughter’s Grace’s wedding to Grace and her fiancé. The couple couldn’t agree on the dress’s color: was it blue and black or white and gold? (White and gold, obviously.) The disagreement prompted the daughter to post the picture on social media, recruiting other opinions. That post caused such a stir that BuzzFeed picked it up, asking the masses to weigh in. And then the Internet went haywire. Within a few days, the original BuzzFeed article had more than 37 million hits. Serious news outlets interviewed neuroscientists and psychologists about color perception and optical illusions. Bevil Conway, a neuroscientist at Wellesley College, was one of those scientists. At the time, he thought the hullabaloo was interesting mostly because it showed how passionately people feel about color (as in, insanely riled-up and deeply offended by alternative views). He joked with NPR’s Robert Siegel, off air, that the story was “fluff,” Conway told me. Well, there’s nothing like a little research to turn fluff into gold (or blue or black). Conway, coauthor of a study appearing online May 14 in Current Biology that explores people’s perceptions of the dress, now calls the phenomenon “profound.” “I think it will go down as one of the most important discoveries in color vision in the last 10 years,” Conway says. “And all because of a crazy photograph.” In those February interviews, Conway (and some other scientists) explained the disparity of opinions on the dress in terms of “color constancy,” a feature of perception that allows us to identify colors under different lighting conditions. If we see a red poisonous snake or a red delicious apple, we need to be able to identify it as red (and dangerous or delicious), whether in bright sunlight or the gloom of clouds. © Society for Science & the Public 2000 - 2015
By C. CLAIBORNE RAY Q. I heard that people can’t look at a color in one room and then pick it out of a set of similar colors in the next room. But there are people with perfect pitch, so are there people with “perfect hue”? A. “The short answer is no,” said Mark D. Fairchild, director of the program of color science at the Munsell Color Science Laboratory of Rochester Institute of Technology. “Color is almost always judged relative to other colors,” Dr. Fairchild said, and the human ability to remember colors over any period of time, or even from room to room, is extremely poor. “Based on memory alone, we can probably reliably identify tens of colors, with some people perhaps able to study hard and get up to a hundred or so,” he said. “If we were to learn a systematic way to scale colors, we might be able to get up to several hundred.” If colors are compared side by side, however, “then we can easily distinguish several thousand colors, and some estimate more than a million,” Dr. Fairchild said. Such ability is somewhat analogous to differentiating tones in hearing, he said. Almost everyone can distinguish tones when they are compared in close succession, he said, but only a very small percentage of people have what is called perfect pitch or absolute pitch: the ability to recall and identify tones after a considerable period of time, without a reference tone for comparison. “Unfortunately, color appearance seems to be even more difficult to remember,” Dr. Fairchild said, “to the point that we don’t speak of anyone as having perfect hue.” © 2015 The New York Times Company
By Jocelyn Kaiser One of the most heralded successes of gene therapy may not be the permanent fix that many had hoped. Leaders of two clinical trials report this week that a treatment that restored some vision to blind patients begins to fade within a few years. A third group, however, says their patients, who received a different version of the therapy, are retaining their improved vision, and a company is moving ahead with efforts to gain regulatory approval for their treatment. It is not a huge surprise that the treatment effects may not last, says eye disease researcher Mark Pennesi of Oregon Health & Science University in Portland, who is running a similar trial. “These are complex diseases and everything that’s been done is sort of first generation,” he says. “The fact that there was biological activity at all is a milestone.” At issue is gene therapy for a rare form of inherited blindness known as Leber’s congenital amaurosis (LCA) that results in complete vision loss by about age 40. About 10% of cases are due to a mutation in retinal pigment epithelium 65 (RPE65), a gene that codes for an enzyme that helps retinal cells make rhodopsin. The pigment is needed by photoreceptor cells—the retina’s light-sending rods and cones—and when RPE65 is mutated, the photoreceptor cells gradually die. In 2007, in the first-ever effort to use gene therapy to treat people with blindness, three separate teams in the United States and the United Kingdom launched clinical trials for the RPE65 type of LCA. A surgeon injected one eye of each patient with a solution containing a harmless virus that ferried a good copy of RPE65 into retinal cells. © 2015 American Association for the Advancement of Science
by Andy Coghlan These neon cells may be blinding, but targeting them could also help preserve sight. In this close-up image of blood vessels – shown in blue – that supply blood to the retina of a one-week-old mouse, the nuclei of cells lining their walls appear in fluorescent colours. The bright-yellow cells are the ones of interest: they could be targeted to help prevent blindness in ageing eyes. Age-related macular degeneration, or AMD, often strikes in middle age, causing a person's vision to deteriorate. A key driver of the disease is excessive growth of obtrusive blood vessels in the retina. A team led by Alain Chédotal of the Institute of Vision in Paris has now discovered that a protein called Slit2 contributes to the rapid increase in offending blood vessels. The yellow cells in the picture are the ones that are dividing. When this activity occurs in middle age, it triggers the excessive increase in blood vessels that results in AMD. By blocking Slit2, it might be possible to reduce this effect, says Chédotal. When the team genetically altered mice so that they couldn't produce Slit2, the animals no longer overproduced the blood vessels that lead to blindness. The researchers think that drugs targeting Slit2 could generate new treatments for AMD. © Copyright Reed Business Information Ltd
By LISA FELDMAN BARRETT and JOLIE WORMWOOD THE Justice Department recently analyzed eight years of shootings by Philadelphia police officers. Its report contained two sobering statistics: Fifteen percent of those shot were unarmed; and in half of these cases, an officer reportedly misidentified a “nonthreatening object (e.g., a cellphone) or movement (e.g., tugging at the waistband)” as a weapon. Many factors presumably contribute to such shootings, ranging from carelessness to unconscious bias to explicit racism, all of which have received considerable attention of late, and deservedly so. But there is a lesser-known psychological phenomenon that might also explain some of these shootings. It’s called “affective realism”: the tendency of your feelings to influence what you see — not what you think you see, but the actual content of your perceptual experience. Affective realism illustrates a common misconception about the working of the human brain. In everyday life, your brain seems to be a reactive organ. You stroll past a round red object in the produce section of a supermarket and react by reaching for an apple. A police officer sees a weapon and reacts by raising his gun. Stimulus is followed by response. But the brain doesn’t really work this way. The brain is a predictive organ. A majority of your brain activity consists of predictions about the world — thousands of them at a time — based on your past experience. These predictions are not deliberate prognostications like “the Red Sox will win the World Series,” but unconscious anticipations of every sight, sound and other sensation you might encounter in every instant. These neural “guesses” largely shape what you see, hear and otherwise perceive. © 2015 The New York Times Company
Related chapters from BP7e: Chapter 10: Vision: From Eye to Brain; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 7: Vision: From Eye to Brain; Chapter 11: Emotions, Aggression, and Stress
Link ID: 20819 - Posted: 04.20.2015
By Jan Hoffman As adults age, vision deteriorates. One common type of decline is in contrast sensitivity, the ability to distinguish gradations of light to dark, making it possible to discern where one object ends and another begins. When an older adult descends a flight of stairs, for example, she may not tell the edge of one step from the next, so she stumbles. At night, an older driver may squint to see the edge of white road stripes on blacktop. Caught in the glare of headlights, he swerves. But new research suggests that contrast sensitivity can be improved with brain-training exercises. In a study published last month in Psychological Science, researchers at the University of California, Riverside, and Brown University showed that after just five sessions of behavioral exercises, the vision of 16 people in their 60s and 70s significantly improved. After the training, the adults could make out edges far better. And when given a standard eye chart, a task that differed from the one they were trained on, they could correctly identify more letters. “There’s an idea out there that everything falls apart as we get older, but even older brains are growing new cells,” said Allison B. Sekuler, a professor of psychology, neuroscience and behavior at McMaster University in Ontario, who was not involved in the new study. “You can teach an older brain new tricks.” The training improved contrast sensitivity in 16 young adults in the study as well, although the older subjects showed greater gains. That is partly because the younger ones, college students, already had reasonably healthy vision and there was not as much room for improvement. Before the training, the vision of each adult, young and older, was assessed. The exercises were fine-tuned at the beginning for each individual so researchers could measure improvements, said Dr.G. John Andersen, the project’s senior adviser and a psychology professor at the University of California, Riverside. © 2015 The New York Times Company
Related chapters from BP7e: Chapter 10: Vision: From Eye to Brain; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 7: Vision: From Eye to Brain; Chapter 13: Memory, Learning, and Development
Link ID: 20763 - Posted: 04.07.2015
by Andy Coghlan Who needs sight to get around when you've got a digital compass in your head? A neuroprosthesis that feeds geomagnetic signals into the brains of blind rats has enabled them to navigate around a maze. The results demonstrate that the rats could rapidly learn to deploy a completely unnatural "sense". It raises the possibility that humans could do the same, potentially opening up new ways to treat blindness, or even to provide healthy people with extra senses. "I'm dreaming that humans can expand their senses through artificial sensors for geomagnetism, ultraviolet, radio waves, ultrasonic waves and so on," says Yuji Ikegaya of the University of Tokyo in Japan, head of the team that installed and tested the 2.5-gram implant. "Ultrasonic and radio-wave sensors may enable the next generation of human-to-human communicationMovie Camera," he says. The neuroprosthesis consists of a geomagnetic compass – a version of the microchip found in smartphones – and two electrodes that fit into the animals' visual cortices, the areas of the brain that process visual information. Whenever the rat positioned its head within 20 degrees either side of north, the electrodes sent pulses of electricity into its right visual cortex. When the rat aligned its head in a southerly direction, the left visual cortex was stimulated. The stimulation allowed blind rats to build up a mental map of their surroundings without any visual cues. During training, blind rats equipped with digital compasses improved at finding food rewards in a five-pronged maze, despite being released from one of three different arms of the maze at random each time. © Copyright Reed Business Information Ltd
Related chapters from BP7e: Chapter 10: Vision: From Eye to Brain; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain; Chapter 5: The Sensorimotor System
Link ID: 20757 - Posted: 04.04.2015
Jon Hamilton A biotech company and two scientists hope to change that. On Wednesday, Avalanche Biotechnologies in Menlo Park and the University of Washington in Seattle announced a licensing agreement to develop the first treatment for colorblindness. The deal brings together a gene therapy technique developed by Avalanche with the expertise of vision researchers at the University of Washington. "Our goal is to be treating colorblindness in clinical trials in patients in the next one to two years," says Thomas Chalberg, the founder and CEO of Avalanche. Dalton the squirrel monkey during the color vision test. i Dalton the squirrel monkey during the color vision test. Courtesy of Neitz Laboratory The agreement has its roots in a scientific breakthrough that occurred six years ago. That's when two vision researchers at the University of Washington used gene therapy to cure a common form of colorblindness in squirrel monkeys. "This opened the possibility of ultimately getting this to cure colorblindness in humans," says Jay Neitz, who runs the Color Vision Lab at UW along with his wife, Maureen Neitz. The couple knew that transferring their success from monkey to man would be a challenge. But they were determined, says Maureen Neitz. "We've spent our entire careers writing NIH grants where we say our goal is to improve human health." © 2015 NPR
By Rachel Feltman I'm not usually one for heartstring-tugging ads, but this collaboration between Valspar Paint and EnChroma, a company that makes color-boosting sunglasses for the color-blind, is pretty cool. And the coolest thing about the glasses in the above video is that they weren't designed to help the color-blind at all. Smithsonian Magazine reports that EnChroma Labs founder Don McPherson (a materials scientist) had originally engineered the glasses with surgeons in mind. The lenses contained rare earth iron and absorbed a ton of light to protect surgeons performing laser eye surgery. The boosted absorption also made colors pop more vibrantly, allowing them to more easily distinguish among different tissues during surgery. But the stellar eye protection and vibrant colors meant that many surgeons wanted to wear them outside the operating room. McPherson himself started using them as regular sunglasses. And when a color-blind friend tried them on, he was amazed: He could distinguish orange traffic cones from the grass and pavement around them. He was perceiving color in a way he never had before. Now EnChroma sells the glasses (which have been specifically tailored for color blindness since the accidental discovery) for a few hundred bucks a pop. McPherson explains that all people have three photopigments in the eye, also known as cones, which are sensitive to blue, green and red. Blue operates fairly independently, while the red and green cones, in most humans, overlap, affecting the perception of certain colors. For example, if 10 photons landed on the red cone and 100 landed on the green cone, the object viewed would appear more green. Whereas if an equal number of photons landed on the red and green cones, the color perceived would be yellow.
|By Susana Martinez-Conde and Stephen L. Macknik All visual art is illusory in that it involves a departure from reality, a filtering through the mind of the artist. This subjectivity applies not only to abstract works but also to representational art, in which the artist translates his or her perception into a physical object capable of inducing a similar perception in the viewer. Painters render the three-dimensional world on a flat surface. These representations are enough to suspend our visual system's disbelief and trigger barrages of neuronal firing that become visions of bathers, bridges and water lilies. It is never about reality but about how the artist sees and wants to portray it. This artistic vision is a mishmash of expectations, memories, assumptions, imagination and intent. It is also, in a sense, a reflection of neural shortcuts and basic visual processes. The picture becomes even more complicated when painters suffer from pathologies of the eyes or brain that force them to see their surroundings in ways that diverge from standard experience. The artwork produced by such artists allows us to participate in their perception—and misperception—of the world. For example, failing vision can translate into an eerie loss of precision and detail in paintings. The pictures of American artist Georgia O'Keeffe became flatter and less intricate as she developed bilateral age-related macular degeneration, a retinal disease that affects central, high-resolution vision. The later works of American painter Mary Cassatt similarly show an uncharacteristic absence of delicacy in faces as she developed cataracts. French impressionist Claude Monet also had cataracts, which rendered his paintings imprecise and muted in color. After he underwent successful cataract surgery, his paintings regained definition and vibrancy. As the examples in this column attest, the effects of vision or brain diseases can sometimes be traced in great works of art. © 2015 Scientific American