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By Mitch Leslie Some microbes that naturally dwell in our intestines might be bad for our eyes, triggering autoimmune uveitis, one of the leading causes of blindness. A new study suggests that certain gut residents produce proteins that enable destructive immune cells to enter the eyes. The idea that gut microbes might promote autoimmune uveitis “has been there in the back of our minds,” says ocular immunologist Andrew Taylor of the Boston University School of Medicine, who wasn’t connected to the research. “This is the first time that it’s been shown that the gut flora seems to be part of the process.” As many as 400,000 people in the United States have autoimmune uveitis, in which T cells—the commanders of the immune system—invade the eye and damage its middle layer. All T cells are triggered by specific molecules called antigens, and for T cells that cause autoimmune uveitis, certain eye proteins are the antigens. Even healthy people carry these T cells, yet they don't usually swarm the eyes and unleash the disease. That's because they first have to be triggered by their matching antigen. However, those proteins don't normally leave the eye. So what could stimulate the T cells? One possible explanation is microbes in the gut. In the new study, immunologist Rachel Caspi of the National Eye Institute in Bethesda, Maryland, and colleagues genetically engineered mice so their T cells recognized one of the same eye proteins targeted in autoimmune uveitis. The rodents developed the disease around the time they were weaned. But dosing the animals with four antibiotics that killed off most of their gut microbes delayed the onset and reduced the severity of the disease. © 2015 American Association for the Advancement of Science.

Related chapters from BP7e: Chapter 10: Vision: From Eye to Brain; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 7: Vision: From Eye to Brain; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 21317 - Posted: 08.19.2015

By CLAIRE MARTIN The eyeglass lenses that Don McPherson invented were meant for surgeons. But through serendipity he found an entirely different use for them: as a possible treatment for colorblindness. Mr. McPherson is a glass scientist and an avid Ultimate Frisbee player. He discovered that the lenses he had invented, which protect surgeons’ eyes from lasers and help them differentiate human tissue, caused the world at large to look candy-colored — including the Frisbee field. At a tournament in Santa Cruz, Calif., in 2002, while standing on a grassy field dotted with orange goal-line cones, he lent a pair of glasses with the lenses to a friend who happened to be colorblind. “He said something to the effect of, ‘Dude, these are amazing,’ ” Mr. McPherson says. “He’s like, ‘I see orange cones. I’ve never seen them before.’ ” Mr. McPherson was intrigued. He said he did not know the first thing about colorblindness, but felt compelled to figure out why the lenses were having this effect. Mr. McPherson had been inserting the lenses into glasses that he bought at stores, then selling them through Bay Glass Research, his company at the time. Mr. McPherson went on to study colorblindness, fine-tune the lens technology and start a company called EnChroma that now sells glasses for people who are colorblind. His is among a range of companies that have brought inadvertent or accidental inventions to market. Such inventions have included products as varied as Play-Doh, which started as a wallpaper cleaner, and the pacemaker, discovered through a study of hypothermia. To learn more about color vision and the feasibility of creating filters to correct colorblindness, Mr. McPherson applied for a grant from the National Institutes of Health in 2005. He worked with vision scientists and a mathematician and computer scientist named Andrew Schmeder. They weren’t the first to venture into this industry; the history of glassmakers claiming to improve colorblindness is long and riddled with controversy. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 21303 - Posted: 08.17.2015

When the owl swooped, the “blind” mice ran away. This was thanks to a new type of gene therapy to reprogramme cells deep in the eye to sense light. After treatment, the mice ran for cover when played a video of an approaching owl, just like mice with normal vision. “You could say they were trying to escape, but we don’t know for sure,” says Rob Lucas of the University of Manchester, UK, co-leader of the team that developed and tested the treatment. “What we can say is that they react to the owl in the same way as sighted mice, whereas the untreated mice didn’t do anything.” This is the team’s best evidence yet that injecting the gene for a pigment that detects light into the eyes of blind mice can help them see real objects again. This approach aims to treat all types of blindness caused by damaged or missing rods and cones, the eye’s light receptor cells. Most gene therapies for blindness so far have concentrated on replacing faulty genes in rarer, specific forms of inherited blindness, such as Leber congenital amaurosis. Deep down The new treatment works by enabling other cells that lie deeper within the retina to capture light. While rod and cone cells normally detect light and convert this into an electrical signal, the ganglion and bipolar cells behind them are responsible for processing these signals and sending them to the brain. By giving these cells the ability to produce their own light-detecting pigment, they can to some extent compensate for the lost receptors, or so it seems.

Related chapters from BP7e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 21298 - Posted: 08.15.2015

Despite virtual reality’s recent renaissance, the technology still has some obvious problems. One, you look like a dumbass using it. Two, the stomach-churning mismatch between what you see and what you feel contributes to “virtual reality sickness.” But there’s another, less obvious flaw that could add to that off-kilter sensation: an eye-focusing problem called vergence-accommodation conflict. It’s only less obvious because, well, you rarely experience it outside of virtual reality. At SIGGRAPH in Los Angeles this week, Stanford professor Gordon Wetzstein and his colleagues are presenting a new head-mounted display that minimizes the vergence-accommodation conflict. This isn’t just some esoteric academic problem. Leading VR companies like Oculus and Microsoft know all too well their headsets are off, and Magic Leap, the super secret augmented reality company in Florida, is betting the house on finding a solution first. “It’s an exciting area of research,” says Martin Banks, a vision scientist at the University of California, Berkeley. “I think it’s going to be the next big thing in displays.” Okay okay, so what’s the big deal with the vergence-accommodation conflict? Two things happen when you simply “look” at an object. First, you point your eyeballs. If an object is close, your eyes naturally converge on it; if it’s far, they diverge. Hence, vergence. If your eyes don’t line up correctly, you end up seeing double. The second thing that happens is the lenses inside your eyes focus on the object, aka accommodation. Normally, vergence and accommodation are coupled. “The visual system has developed a circuit where the two response talk to each other,” says Banks. “That makes perfect sense in the natural environment. They’re both trying to get to the same distance, so why wouldn’t they talk to one another?” In other words, your meat brain has figured out a handy shortcut for the real world.

Related chapters from BP7e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 21287 - Posted: 08.12.2015

Nell Greenfieldboyce Take a close look at a house cat's eyes and you'll see pupils that look like vertical slits. But a tiger has round pupils — like humans do. And the eyes of other animals, like goats and horses, have slits that are horizontal. Scientists have now done the first comprehensive study of these three kinds of pupils. The shape of the animal's pupil, it turns out, is closely related to the animal's size and whether it's a predator or prey. The pupil is the hole that lets light in, and it comes in lots of different shapes. "There are some weird ones out there," says Martin Banks, a vision scientist at the University of California, Berkeley. Cuttlefish have pupils that look like the letter "W," and dolphins have pupils shaped like crescents. Some frogs have heart-shaped pupils, while geckos have pupils that look like pinholes arranged in a vertical line. Needless to say, scientists want to know why all these different shapes evolved. "It's been an active point of debate for quite some time," says Banks, "because it's something you obviously observe. It's the first thing you see about an animal — where their eye is located and what the pupil shape is." For their recent study, Banks and his colleagues decided to keep things simple. They looked at just land animals, and just three kinds of pupils. "We restricted ourselves to just pupils that are elongated or not," Banks explains. "So they're either vertical, horizontal or round." © 2015 NPR

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: 21277 - Posted: 08.08.2015

By Rachel Feltman Ever wondered what the world looks like to nonhuman animals? Scientists do, too. It can actually be a really important question. Sometimes humans can't see things -- like skin markings designed to attract mates or flower colors meant to draw pollinators -- that are incredibly important in the life and behavior of an animal. That's why researchers at the University of Exeter have developed a software that converts photos to "animal vision." The software, which is available for free online, is described in a recent paper in the journal Methods in Ecology and Evolution. Its creators have already used it extensively themselves to perform studies on animals who see light outside the spectrum visible to humans. They've also used it to track imperceptible color changes that occur in women's faces during ovulation. The software works by integrating photos taken using ultraviolet filters with those taken using regular color filters, a process that scientists used to have to dial in manually for whatever species they were studying. By meshing the visible light spectrum with information from a full-spectrum image, the software can replicate the visual experience of animals who see more colors than humans, including light in the ultraviolet range.

Related chapters from BP7e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 21272 - Posted: 08.08.2015

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.

Related chapters from BP7e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 21205 - Posted: 07.23.2015

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.

Related chapters from BP7e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 21185 - Posted: 07.18.2015

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.

Related chapters from BP7e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 21130 - Posted: 07.04.2015

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

Related chapters from BP7e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 21053 - Posted: 06.15.2015

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.

Related chapters from BP7e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 20950 - Posted: 05.19.2015

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

Related chapters from BP7e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 20947 - Posted: 05.19.2015

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

Related chapters from BP7e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 20938 - Posted: 05.16.2015

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

Related chapters from BP7e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 20937 - Posted: 05.16.2015

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

Related chapters from BP7e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 20916 - Posted: 05.13.2015

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

Related chapters from BP7e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 20892 - Posted: 05.05.2015

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

Related chapters from BP7e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 20839 - Posted: 04.23.2015