Links for Keyword: Vision
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
By John Bohannon It may sound like a bird-brained idea, but scientists have trained pigeons to spot cancer in images of biopsied tissue. Individually, the avian analysts can't quite match the accuracy of professional pathologists. But as a flock, they did as well as trained humans, according to a new study appearing this week in PLOS ONE. Cancer diagnosis often begins as a visual challenge: Does this lumpy spot in a mammogram image justify a biopsy? And do cells in biopsy slides look malignant or benign? Training doctors and medical technicians to tell the difference is expensive and time-consuming, and computers aren't yet up to the task. To see whether a different type of trainee could do better, a team led by Richard Levenson, a pathologist and technologist at the University of California, Davis, and Edward Wasserman, a psychologist at the University of Iowa, in Iowa City, turned to pigeons. In spite of their limited intellect, the bobble-headed birds have certain advantages. They have excellent visual systems, similar to, if not better than, a human's. They sense five different colors as opposed to our three, and they don’t “fill in” the gaps like we do when expected shapes are missing. However, training animals to do a sophisticated task is tricky. Animals can pick up on unintentional cues from their trainers and other humans that may help them correctly solve problems. For example, a famous 20th century horse named Clever Hans was purportedly able to do simple arithmetic, but was later shown to be observing the reactions of his human audience. And although animals can perform extremely well on tasks that are confined to limited circumstances, overtraining on one set of materials can lead to total inaccuracy when the same information is conveyed slightly differently. © 2015 American Association for the Advancement of Science
Related chapters from BP7e: Chapter 17: Learning and Memory; Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 7: Vision: From Eye to Brain
Link ID: 21652 - Posted: 11.21.2015
Susan Milius Certain species of the crawling lumps of mollusk called chitons polka-dot their armor-plated backs with hundreds of tiny black eyes. But mixing protection and vision can come at a price. The lenses are rocky nuggets formed mostly of aragonite, the same mineral that pearls and abalone shells are made of. New analyses of these eyes support previous evidence that they form rough images instead of just sensing overall lightness or darkness, says materials scientist Ling Li of Harvard University. Adding eyes to armor does introduce weak spots in the shell. Yet the positioning of the eyes and their growth habits show how chitons compensate for that, Li and his colleagues report in the November 20 Science. Li and coauthor Christine Ortiz of MIT have been studying such trade-offs in biological materials that serve multiple functions. Human designers often need substances that multitask, and the researchers have turned to evolution’s solutions in chitons and other organisms for inspiration. Biologists had known that dozens of chiton species sprinkle their armored plates with simple-seeming eye spots. (The armor has other sensory organs: pores even tinier than the eyes.) But in 2011, a research team showed that the eyes of the West Indian fuzzy chiton (Acanthopleura granulata) were much more remarkable than anyone had realized. Their unusual aragonite lens can detect the difference between a looming black circle and a generally gray field of vision. Researchers could tell because chitons clamped their shells defensively to the bottom when a scary circle appeared but not when an artificial sky turned overall shadowy. © Society for Science & the Public 2000 - 2015
Angus Chen If you peek into classrooms around the world, a bunch of bespectacled kids peek back at you. In some countries such as China, as much as 80 percent of children are nearsighted. As those kids grow up, their eyesight gets worse, requiring stronger and thicker eyeglasses. But a diluted daily dose of an ancient drug might slow that process. The drug is atropine, one of the toxins in deadly nightshade and jimsonweed. In the 19th and early 20th centuries, atropine was known as belladonna, and fancy Parisian ladies used it to dilate their pupils, since big pupils were considered alluring at the time. A few decades later, people started using atropine to treat amblyopia, or lazy eye, since it blurs the stronger eye's vision and forces the weaker eye to work harder. As early as the 1990s, doctors had some evidence that atropine can slow the progression of nearsightedness. In some countries, notably in Asia, a 1 percent solution of atropine eyedrops is commonly prescribed to children with myopia. It's not entirely clear how atropine works. Because people become nearsighted when their eyeballs get too elongated, it's generally thought that atropine must be interfering with that unwanted growth. But as Parisians discovered long ago, the drug can have some inconvenient side effects. © 2015 npr
A clinical trial funded by the National Institutes of Health has found that the drug ranibizumab (Lucentis) is highly effective in treating proliferative diabetic retinopathy. The trial, conducted by the Diabetic Retinopathy Clinical Research Network (DRCR.net) compared Lucentis with a type of laser therapy called panretinal or scatter photocoagulation, which has remained the gold standard for proliferative diabetic retinopathy since the mid-1970s. The findings demonstrate the first major therapy advance in nearly 40 years. “These latest results from the DRCR Network provide crucial evidence for a safe and effective alternative to laser therapy against proliferative diabetic retinopathy,” said Paul A. Sieving, M.D., Ph.D., director of NIH’s National Eye Institute (NEI), which funded the trial. The results were published online today in the Journal of the American Medical Association. Treating abnormal retinal blood vessels with laser therapy became the standard treatment for proliferative diabetic retinopathy after the NEI announced results of the Diabetic Retinopathy Study in 1976. Although laser therapy effectively preserves central vision, it can damage night and side vision; so, researchers have sought therapies that work as well or better than laser but without such side effects. A complication of diabetes, diabetic retinopathy can damage blood vessels in the light-sensitive retina in the back of the eye. As the disease worsens, blood vessels may swell, become distorted and lose their ability to function properly. Diabetic retinopathy becomes proliferative when lack of blood flow in the retina increases production of a substance called vascular endothelial growth factor, which can stimulate the growth of new, abnormal blood vessels.
By Kelli Whitlock Burton More than half of Americans over the age of 70 have cataracts, caused by clumps of proteins collecting in the eye lens. The only way to remove them is surgery, an unavailable or unaffordable option for many of the 20 million people worldwide who are blinded by the condition. Now, a new study in mice suggests eye drops made with a naturally occurring steroid could reverse cataracts by teasing apart the protein clumps. “This is a game changer in the treatment of cataracts,” says Roy Quinlan, a molecular biologist at Durham University in the United Kingdom who was not part of the study. “It takes decades for the cataracts to get to that point, so if you can reverse that by a few drops in the eye over a couple of weeks, that’s amazing.” The proteins that make up the human lens are among the oldest in the body, forming at about 4 weeks after fertilization. The majority are crystallins, a family of proteins that allow the eye to focus and keep the lens clear. Two of the most abundant crystallins, CRYAA and CRYAB, are produced in response to stress or injury. They act as chaperones, identifying and binding to damaged and misfolded proteins in the lens, preventing them from aggregating. But over the years, as damaged proteins accumulate in the lens, these chaperones become overwhelmed. The mutated proteins then clump together, blocking light and producing the tell-tale cloudiness of cataracts. © 2015 American Association for the Advancement of Science
By Christof Koch Artificial intelligence has been much in the news lately, driven by ever cheaper computer processing power that has become effectively a near universal commodity. The excitement swirls around mathematical abstractions called deep convolutional neural networks, or ConvNets. Applied to photographs and other images, the algorithms that implement ConvNets identify individuals from their faces, classify objects into one of 1,000 distinct categories (cheetah, husky, strawberry, catamaran, and so on)—and can describe whether they see “two pizzas sitting on top of a stove top oven” or “a red motorcycle parked on the side of the road.” All of this happens without human intervention. Researchers looking under the hood of these powerful algorithms are surprised, puzzled and entranced by the beauty of what they find. How do ConvNets work? Conceptually they are but one or two generations removed from the artificial neural networks developed by engineers and learning theorists in the 1980s and early 1990s. These, in turn, are abstracted from the circuits neuroscientists discovered in the visual system of laboratory animals. Already in the 1950s a few pioneers had found cells in the retinas of frogs that responded vigorously to small, dark spots moving on a stationary background, the famed “bug detectors.” Recording from the part of the brain's outer surface that receives visual information, the primary visual cortex, Torsten Wiesel and the late David H. Hubel, both then at Harvard University, found in the early 1960s a set of neurons they called “simple” cells. These neurons responded to a dark or a light bar of a particular orientation in a specific region of the visual field of the animal. © 2015 Scientific American
By Jessica Schmerler Young brains are plastic, meaning their circuitry can be easily rewired to promote learning. By adulthood, however, the brain has lost much of its plasticity and can no longer readily recover lost function after, say, a stroke. Now scientists have successfully restored full youthful plasticity in adult mice by transplanting young neurons into their brain—curing their severe visual impairments in the process. In a groundbreaking study published in May in Neuron, a team of neuroscientists led by Sunil Gandhi of the University of California, Irvine, transplanted embryonic mouse stem cells into the brains of other mice. The cells were primed to become inhibitory neurons, which tamp down brain activity. Prior to this study, “it was widely doubted that the adult brain would allow these cells to disperse, integrate and reactivate plasticity,” says Melissa Davis, first author of the study. Scientists have been attempting such a feat for years, refining their methods along the way, and the Irvine team finally saw success: the cells were integrated in the brain and caused large-scale rewiring, restoring the high-level plasticity of early development. In visually impaired mice, the transplant allowed for the restoration of normal vision, as demonstrated by tests of visual nerve signals and a swimming maze test. The scientists have not yet tested the transplanting technique for other neurological disorders, but they believe the technique has potential for many conditions and injuries depending on how, exactly, the new neurons restore plasticity. It is not yet known whether the proliferation of the transplanted cells accounts for the restored plasticity or if the new cells trigger plasticity in existing neurons. If the latter, the treatment could spur the rewiring and healing of the brain following traumatic brain injury or stroke. © 2015 Scientific American
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: 21572 - Posted: 10.27.2015
By Karen Weintraub The short answer is: not yet, but treatments are getting better. Getting older is the leading risk factor for age-related macular degeneration, the leading cause of vision loss in the United States. Macular degeneration comes in two forms: dry and wet. The dry form is milder and usually has no symptoms, but it can degenerate into the wet form, which is characterized by the growth of abnormal blood vessels in the back of the eye, potentially causing blurriness or vision loss in the center of the field of vision. The best treatment for wet macular degeneration is prevention, said Dr. Rahul N. Khurana, a clinical spokesman for the American Academy of Ophthalmology and a retina specialist practicing in Mountain View, Calif. Not smoking, along with eating dark green vegetables and at least two servings of fish a week, may help reduce the risk of macular degeneration, he said. An annual eye exam can catch macular degeneration while it is still in the dry form, Dr. Khurana said, and vitamins can help prevent it from progressing into the wet form, the main cause of vision loss. Dr. Joan W. Miller, chief of ophthalmology at Massachusetts Eye and Ear, said anyone with a family history of the disease should get a retina check at age 50. People should also get an eye exam if they notice problems like trouble adjusting to the dark or needing more light to read. The federally funded Age-Related Eye Disease Study, published in 2001 and updated in 2013, found that people at high risk for advanced age-related macular degeneration could cut that risk by about 25 percent by taking a supplement that included 500 milligrams of vitamin C, 400 I.U.s of vitamin E, 10 milligrams of lutein, 2 milligrams of zeaxanthin, 80 milligrams of zinc, and 2 milligrams of copper. © 2015 The New York Times Company
By Hanae Armitage CHICAGO, ILLINOIS—Aside from a few animals—like pythons and vampire bats—that can sense infrared light, the world of this particular electromagnetic radiation has been off-limits to most creatures. But now, researchers have engineered rodents to see infrared light by implanting sensors in their visual cortex—a first-ever feat announced here yesterday at the annual meeting of the Society for Neuroscience. Before they wired rats to see infrared light, Duke University neuroscientist Miguel Nicolelis and his postdoc Eric Thomson engineered them to feel it. In 2013, they surgically implanted a single infrared-detecting electrode into an area of the rat’s brain that processes touch called the somatosensory cortex. The other end of the sensor, outside the rat’s head, surveyed the environment for infrared light. When it picked up infrared, the sensor sent electrical messages to the rats’ brains that seemed to give them a physical sensation. At first, the rats would groom and rub their whiskers repeatedly whenever the light went on. But after a short while, they stopped fidgeting. They even learned to associate infrared with a reward-based task in which they followed the light to a bowl of water. In the new experiment, the team inserted three additional electrodes, spaced out equally so that the rats could have 360 degrees of infrared perception. When they were primed to perform the same water-reward task, they learned it in just 4 days, compared to 40 days with the single implant. “Frankly, this was a surprise,” Thomson says. “I thought it would be really confusing for [the rats] to have so much stimulation all over their brain, rather than [at] one location.” © 2015 American Association for the Advancement of Science.
By Kerry Grens Eric Altschuler has been staring at mirrors. Specifically, those of van Eyck, Caravaggio, Parmigianino, Escher, and other painters. The Temple University professor and his colleague V.S. Ramachandran of the University of California, San Diego, are on the hunt for novel ways that artists have presented reflections, as a means of seeking out potentially new modes of therapy. Ramachandran and Altschuler have pioneered methods of using a mirror to alleviate phantom limb pain and other conditions. A patient sits at the side of the mirror with, say, his right arm reflected in front of the glass. The patient peeks around the corner to view the reflection as if he were looking at his left arm—a setup Ramachandran and Altschuler call the parasagittal reflection. In their cataloging of mirrors in art, presented as a poster at the Society for Neuroscience (SfN) meeting held in Chicago this week, Altschuler and Ramachandran found that for 500 or more years, painters presented frontal plane reflections (a straight-on view in the mirror). It wasn’t until 1946 that something different—the parasagittal view, in particular—appeared in fine art: in M.C. Escher’s lithograph, “Magic Mirror,” Altschuler and Ramachandran reported at SfN. The viewer has an angled view at a ball reflected in a mirror, with an identical ball positioned symmetrically behind the mirror—very similar to the concept of mirror therapy. “Magic Mirror” was produced 50 years before Ramachandran first published on mirror therapy, and even then Ramachandran was unaware of the artwork. “Escher was very clever,” Altschuler told The Scientist, noting that perhaps there are other novel approaches just waiting to be discovered in paintings. © 1986-2015 The Scientist
Gene therapy preserved vision in a study involving dogs with naturally occurring, late-stage retinitis pigmentosa, according to research funded by the National Eye Institute (NEI), part of the National Institutes of Health. The findings contribute to the groundwork needed to move gene therapy forward into clinical trials for people with the blinding eye disorder, for which there is currently no cure. Scientists from the University of Pennsylvania and the University of Florida, Gainesville also determined for the first time that gene therapy may be of potential benefit even after there has been significant loss of cells in the eye. Up to this point, animal studies had shown benefits from gene therapy only when it was used in the earliest stages of the disease. “The study shows that a corrective gene can stop the loss of photoreceptors in the retina, and provides good proof of concept for gene therapy at the intermediate stage of the disease, thus widening the therapeutic window,” said Neeraj Agarwal, Ph.D., a program director at NEI. Retinitis pigmentosa is the most common inherited disease that causes degeneration of the retina, the light-sensitive tissue lining the back of the eye. Roughly 1 in 4,000 people are affected and about 10 to 20 percent have a particularly severe form called X-linked retinitis pigmentosa, which predominately affects males, causing night blindness by age 10 and progressive loss of the visual field by age 45. About 70 percent of people with the X-linked form carry mutations that cause loss of function of the retinitis pigmentosa GTPase Regulator (RPGR) gene, which encodes a protein important for maintaining the health of photoreceptors.
By Ariana Eunjung Cha When it comes to studies on birth order, first-borns tend to make out pretty well. Research says they tend to be smarter, more outgoing, and exhibit more leadership qualities. Unfortunately, it's not all good news. A new paper published in JAMA Ophthalmology shows that first-borns also tend to be 10 percent more likely to be near-sighted and 20 percent more likely to have severe myopia than their siblings. In fact, the risk for myopia appeared to be progressively lower the later you were born in terms of your birth order. The researchers from Cardiff University suggested that the cause was “parental investment in education” because parents may have a tendency to put more pressure on first-borns. They theorized that parents may be more demanding that first-borns do more "near" activities, such as reading, which may impact their eyesight. Previous studies have shown a strong link between time spent outdoors and a diminished risk of myopia, and it may stand to reason that children who spend more time on studies may be spending less time outdoors. Jeremy Guggenheim, a doctoral student, and colleagues wrote that while there's no way to make a definitive causal link, their study found that when they adjusted for a proxy for educational exposure — the highest educational degree or age at completion of full-time education — they saw a less dramatic association between near-sightedness and birth order.
By ANDREW POLLACK What could become the first gene therapy to win approval in the United States moved closer to market on Monday, when its developer announced that the medicine had succeeded in a late-stage clinical trial in treating an inherited eye disease that can cause blindness. The developer, Spark Therapeutics, said the treatment had allowed people with certain so-called inherited retinal dystrophies to more easily maneuver in dimmer light than they could before. The company said it planned to apply to the Food and Drug Administration next year for approval to sell the product. “We saw substantial restoration of vision in patients who were progressing toward complete blindness,” Dr. Albert M. Maguire, a professor of ophthalmology at the University of Pennsylvania and a lead researcher in the study, said in a news release being issued by Spark. Dr. Katherine High, Spark’s president and chief scientific officer, said this was the first successful randomized, controlled trial for any gene therapy aimed at an inherited disease. “I’ve been working in gene therapy for most of my career,” she said. “It’s been a long time coming, and I’m delighted.” Besides encouraging the once beleaguered field of gene therapy, the results — if interpreted positively by investors — could help lift biotechnology stocks, which have been battered recently by concerns over a backlash against high drug prices. Still, much remains unknown. Spark did not provide the actual trial data, saying only that the treatment achieved the main goal of the study as well as two out of three of its secondary goals. It is also unclear what the F.D.A. will deem sufficient for approval of the product. Spark’s stock had slumped in the last two months as it changed how it would measure the results of the trial. © 2015 The New York Times Company
For primary school children in China, spending an extra 45 minutes per day outside in a school activity class may reduce the risk of nearsightedness, or "myopia," according to a new study. In some parts of China, 90 per cent of high school graduates have nearsightedness, and rates are lower but increasing in Europe and the Middle East, the authors write. "There were some studies suggesting the protective effect of outdoor time in the development of myopia, but most of this evidence is from cross-sectional studies [survey] data that suggest 'association' instead of causality," said lead author Dr. Mingguang He of Sun Yat-sen University in Guangzhou. "Our study, as a randomized trial, is able to prove causality and also provide the high level of evidence to inform public policy." Intense levels of schooling and little time spent outdoors may have contributed to the epidemic rise of nearsightedness in China, he told Reuters Health by email. The researchers divided 12 primary schools in China into two groups: six schools continued their existing class schedule, while six were assigned to include an additional 40 minutes of outdoor activity at the end of each school day. Parents of children in the second group were also encouraged to engage their children in outdoor activities on the weekends. In total, almost 2,000 first-graders, with an average age of almost seven years old, were included. After three years, 30 per cent of the outdoor activity group had developed nearsightedness, compared to almost 40 per cent of kids in the control group, according to the results in JAMA. ©2015 CBC/Radio-Canada.
When we move our head, the whole visual world moves across our eyes. Yet we can still make out a bee buzzing by or a hawk flying overhead, thanks to unique cells in the eye called object motion sensors. A new study on mice helps explain how these cells do their job, and may bring scientists closer to understanding how complex circuits are formed throughout the nervous system. The study was funded by the National Institutes of Health, and was published online in Nature. “Understanding how neurons are wired together to form circuits in the eye is fundamental for advancing potential new therapies for blinding eye diseases,” said Paul A. Sieving, M.D., Ph.D., director of NIH’s National Eye Institute (NEI). “Research aimed at regenerating photoreceptors, for example, is enriched by efforts to understand the circuitry in the eye.” Object motion sensors are one of about 30 different types of retinal ganglion cells (RGCs) in the retina, the light-sensitive tissue at the back of the eye. These cells are unique because they fire only when the timing of a small object’s movement differs from that of the background; they are silent when the object and the background move in sync. Researchers believe this is critical to our ability to see small objects moving against a backdrop of complex motion. The cells in the retina are wired up like an electrical circuit. Vision begins with photoreceptors, cells that detect light entering the eye and convert it into electrical signals. Middleman neurons, called interneurons, shuttle signals from photoreceptors to the RGCs. And each RGC sends the output visual information deeper into the brain for processing. This all takes place within fractions of a second, so the scientists were surprised to discover that before it reaches object motion sensors, visual information about object motion takes a detour through a unique type of interneuron. Their results represent an ongoing effort by scientists to map out complex circuits of the nervous system.
By SINDYA N. BHANOO The human eye has a blind spot, though few of us realize it. Now, a new study suggests that it is possible to reduce the spot with training. The optic nerve, which carries visual signals to the brain, passes through the retina, a light-sensitive layer of tissue. There are no so-called photoreceptors at the point where the optic nerve intersects the retina. The right eye generally compensates for the left eye’s blind spot and vice versa, so the spot is hardly noticed. Researchers trained 10 people using a computer monitor and an eye patch. The participants were shown a waveform in the visual field of their blind spot day after day. After 20 days of this repeated stimulation, the blind spot shrunk by about 10 percent. The researchers believe that neurons at the periphery of the blind spot became more responsive, effectively reducing the extent of functional blindness. The findings add to a growing body of research suggesting that the human eye can be trained, said Paul Miller, a psychologist at the University of Queensland in Australia and an author of the study, which appeared in the journal Current Biology. This kind of training may help researchers develop better treatments for visual impairments like macular degeneration. “This is the leading cause of blindness in the western world,” Mr. Miller said. © 2015 The New York Times Company
Related chapters from BP7e: Chapter 10: Vision: From Eye to Brain; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 7: Vision: From Eye to Brain; Chapter 13: Memory, Learning, and Development
Link ID: 21367 - Posted: 09.01.2015
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
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.
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.