RETINA INDIA

Ultrasonic Bracelet Helps Blind People Navigate

2015-11-21T00:03:00.000+05:30

Based on the resonance location system (echo) used by bats and dolphins to navigate, Marco Antonio Trujillo Tejeda and Cuauhtli Padilla Arias, mechatronic engineers from the Tec de Monterrey in Mexico, devised a bracelet that makes mobility simpler and safer for the blind.

"Mobility is a tool that complements objects like the traditional cane, as it is used at ground level and locates objects just two steps away, meanwhile the bracelet has a range of four and a half meters," says Trujillo Tejeda.

Sunu band bracelet emits high-frequency sound waves (30 pulses per second) that bounce after hitting an object and are recorded by a proximity sensor that calculates the distance, which translates into vibrations directly into the wearer's wrist; as the person get closer to the objects, the pulses will be more frequent.

The bracelet is based on the resonance location system (echo) used by bats and dolphins to navigate.

The device registers objects from two centimeters wide. Operating indoors, where the width of sound waves is thinner to record more details and where obstacles are closer, as well as outdoors where the wavelength range is wider.

"The person scans its surroundings by moving the wrist back and forth, to anticipate and to dodge objects. Sunu band is activated when the wearer performs some movement on foot, giving 14 hours of continuous use, but can last up to a week without having to recharge."

Marco Trujillo explains that along with the bracelet a tag is offered to locate lost objects, and it works just by placing the small device to anything like keys or other objects susceptible of being lost; it communicates via Bluetooth with a smartphone or bracelet, which will vibrate to indicate proximity to the tag, and emits an alarm for easy location.

Creativity and sensitivity were two constants in Marco Trujillo from his childhood, which he shared with a deaf cousin, his best friend at the time, and with who he created a communication system that only they could decode.

As part of his career plans he developed technologies that help people with disabilities, for example, an interface for a computer mouse that could facilitate communication for people with cerebral palsy, a device to help the blind cook and inform them time and temperature, or a mechanism that recorded images and translated them into Braille on a display for a blind person to appreciate. His social service was performed in a welfare institution for blind girls, which further opened his sensitivity.

Sunu band bracelet emits high-frequency sound waves (30 pulses per second) that bounce after hitting an object and are recorded by a proximity sensor that calculates the distance.

"Blindness is a disability that takes away people’s independence, and makes them stand aside in activities they could perform. The investments made in science to help the blind are mostly on surgeries or treatments to restore vision, and still there is little for developments that involve adaptation.

Sunu band allowed Marco Trujillo, and his partner Cuauhtli Padilla, participate in various technology competitions and the creation of the company Sunu, which has enrolled in a couple of Mexican accelerators of technology-based companies and one in Boston (USA). One of the most important awards received by the development is as one of 10 innovators under 35 delivered by the MIT Tech Review.

The bracelet is protected by an international patent and is in the process of being internationally produced thanks to the interest of a company manufacturing medical devices in Guadalajara, Mexico. The development will go on pre-sale through a crowdfunding campaign on indiegogo.com starting this month.

Source

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Ocular treatment likely to become first Gene Therapy approved in US

2015-10-05T23:43:00.000+05:30

(c) nature.com

Spark Therapeutics has announced positive results from the Phase 3 pivotal trial of its lead gene therapy product candidate, SPK-RPE65, for the treatment of RPE65-mediated inherited retinal dystrophies (IRDs). These results represent the first successful randomized, controlled Phase 3 trial ever completed in gene therapy for a genetic disease.

The pivotal trial met its primary endpoint (p = 0.001), demonstrating improvement of functional vision in the intervention group compared to the control group, as measured by the change in bilateral mobility testing between baseline and one year. In addition, subjects who received SPK-RPE65 outperformed control subjects across the first two secondary endpoints: full-field light sensitivity threshold testing (p < 0.001) and the mobility test change score for the first injected eye (p = 0.001). The third secondary endpoint, visual acuity, did not show statistically significant evidence of benefit (p = 0.17). All reported p-values reflect results from the intent-to-treat (ITT) population, the most stringent efficacy analysis population described in the statistical analysis plan (SAP).

The multicenter, pivotal phase 3 trial randomized 31 subjects with confirmed RPE65 gene mutations. The ITT population included 21 subjects in the intervention group and 10 in the control group. For the primary endpoint, subjects were evaluated at multiple time points over the course of one year for their performance in navigating a mobility course under a variety of light levels ranging from one lux (equivalent to a moonless summer night) to 400 lux (a brightly lit office) using the bilateral testing condition. Each attempt was recorded, and the videos were sent to independent, centralized, masked graders to assign a pass/fail score based on speed and accuracy with which the subjects navigated the course.

In addition to the primary endpoint, the SAP included three secondary endpoints tested statistically in the following hierarchical order:

Full-field light sensitivity threshold testing (FST), which reflects underlying physiological function by measuring light sensitivity of the entire visual field.
Change in mobility test score for the first eye injected, which compares the mobility test performance between baseline and year one for the first eye injected for the intervention group and, for the control group during the control year, the first eye injected after they crossed over.
Visual acuity testing, which measures changes in central vision by assessing the ability of the subject to read a standard eye chart.

A summary of top-line efficacy results follows:

Primary outcome (ITT):

Mobility test (MT) change score, bilateral (p = 0.001)

Secondary outcomes (ITT):

FST, averaged over both eyes (p < 0.001)
MT change score, first injected eye (p = 0.001)
Visual acuity, averaged over both eyes (p = 0.17)

There were no serious adverse events related to SPK-RPE65 or deleterious immune responses observed in the trial. Overall, adverse events related to the administration procedure were consistent with observations in earlier studies of SPK-RPE65.

Additional data from this clinical trial will be presented in a series of scientific meetings in the coming months, beginning with a presentation at the Retina Society Annual Scientific Meeting on October 10th in Paris by Principal InvestigatorStephen R. Russell, MD, of the Stephen A. Wynn Institute for Vision Research at the University of Iowa.

Based on these results, Spark intends to file a Biologics License Application with the U.S. Food and Drug Administration in 2016.

Quotes:

Albert M. Maguire, MD, principal investigator in the trial and professor of ophthalmology at the Perelman School of Medicine of the University of Pennsylvania: “We saw substantial restoration of vision in patients who were progressing toward complete blindness. The majority of the subjects given SPK-RPE65 derived the maximum possible benefit that we could measure on the primary visual function test, and this impressive effect was confirmed by a parallel improvement in retinal sensitivity. If approved, SPK-RPE65 should have a positive, meaningful impact on the lives of patients with this debilitating condition.”

Jean Bennett, MD, PhD, professor of ophthalmology and director of the Center for Advanced Retinal and Ocular Therapeutics at the Perelman School of Medicine of the University of Pennsylvania: “These results are the culmination of more than a decade of work of many dedicated individuals to correct the underlying cause of RPE65-mediated blindness through the one-time administration of a gene therapy. We are excited about the potential impact that the results will have on the treatment of this and other blinding conditions.”

Gordon Gund, Chairman of the Foundation Fighting Blindness: “This is a watershed moment in the long-time pursuit of innovative gene therapy solutions for a range of blinding retinal degenerative diseases. Spark, The Children’s Hospital of Philadelphia, the Foundation Fighting Blindness and a long list of collaborators in the non-profit, academic and government sectors are to be commended for diligently persevering over many years in their aim to realize the potential of gene therapy in the fight against blindness.”

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AMD likely to be more in people with deficient vitamin D status

2015-08-29T05:47:00.000+05:30

A multi-institutional team reports that vitamin D may play a significant role in eye health, specifically in the possible prevention of age-related macular degeneration, or AMD, among women who are more genetically prone to developing the sight-damaging disease.

In a paper published in JAMA Ophthalmology online, the team found that women who are deficient in vitamin D and have a specific high-risk genotype are 6.7 times more likely to develop AMD than women with sufficient vitamin D status and no high risk genotype.

(c) foodandhealth.com

“Most people have heard that you should eat carrots to help your vision. However, there appear to be many other ways that adequate nutrition can support eye health. Having adequate vitamin D status may be one of them,” says Amy Millen, PhD, the study’s lead author. “This is not a study that can, alone, prove a causal association, but it does suggest that if you’re at high genetic risk for AMD, having a sufficient vitamin D status might help reduce your risk.”

“To our knowledge, this is the first study that’s looked at the interaction between genetic risk and vitamin D status in the context of age-related eye disease,” adds Millen.

Researchers analyzed data compiled on 1,230 women ages 54 to 74 who participated in the Carotenoids in Age-related Eye Disease Study (CAREDS), which is an ancillary study of the Women’s Health Initiative (WHI) Observational Study (OS). The WHI OS is a major National Institutes of Health-funded research program, at 40 centers nationwide, aimed at addressing the most common causes of death, disability and poor quality of life in postmenopausal women. CAREDS was conducted among participants at three of the centers: University of Wisconsin (Madison), the University of Iowa (Iowa City) and the Kaiser Center for Health Research (Portland, Oregon).
Researchers were able to determine participants’ vitamin D status by analyzing serum samples for a vitamin D biomarker, 25-hydroxyvitamin D [25(OH)D], which provided a glimpse into vitamin D intake through all sources: diet, supplements and sunlight.

Amy Millen, (c) buffalo.edu

Human skin can synthesize vitamin D when exposed to ultraviolet light, Millen explains. However, for many people, 15 to 30 minutes a day with 10 percent of their skin exposed might be sufficient. In winter months, when there is a lower solar angle, sun exposure may not be not sufficient to maintain blood level for people who live north of a line from about Washington, D.C., to Los Angeles. At these times and locations, dietary intake may be needed. Dietary sources of vitamin D include fortified foods such as milk and foods that naturally contain vitamin D such as fatty fish like salmon and mackerel.

Among many genes linked to AMD, one of the strongest is a specific genetic variant (Y402H) in the complement factor H gene, called CFH for short. This gene codes for the CFH protein that is involved in the body’s immune response to destroy bacteria and viruses.

Inflammation is believed to be involved in the development of macular degeneration.

(c) NEI

“People who have early stage AMD develop drusen, lipid and protein deposits that build up in the eye. Your body sees this drusen as a foreign substance and attacks it, in part via the complement cascade response,” explains Millen. “CFH is one of the proteins involved in this response. We see more AMD in people who have certain variants in the gene which encodes a form of this CFH protein that is associated with a more aggressive immune response.”

Vitamin D shows promise for protecting against macular degeneration because of its anti-inflammatory and antiangiogenic properties.

The study, as per the authors, suggests that being deficient for vitamin D may increase one’s risk for AMD, and that this increased risk may be most profound in those with the highest genetic risk for this specific variant in the CFH protein.

The study results, however, shouldn’t prompt people to run to the nearest grocery store to purchase vitamin D supplements. The message is not that achieving really high levels of vitamin D are good for the eye, but that having deficient vitamin D levels may be unhealthy for your eyes, as per the researchers.

Although the odds of having AMD was higher in women who were deficient for vitamin D, with 25(OH)D levels below 12 ng/mL (30 nmol/L), increasing vitamin D levels beyond 12 ng/mL did not further lower the odds of AMD to any meaningful extent.

The study was funded by the National Eye Institute of the National Institutes of Health.

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Clinical Trial utilizing optogenetics to start for Retinitis Pigmentosa soon

2015-08-26T01:11:00.000+05:30

(c) nature.com

RetroSense Therapeutics’ Investigational New Drug (IND) application for gene therapy based clinical trial for their product RST-001 has received clearance from the US Food and Drug Administration. RetroSense is developing RST-001 for the treatment of retinitis pigmentosa, a genetic condition that leads to the progressive degeneration of rod and cone photoreceptors (cells found in the retina that sense light), resulting in severe vision loss and blindness. With its IND now in effect, RetroSense expects to initiate a Phase I/II clinical trial by year-end in order to evaluate the safety and, potentially, efficacy of RST-001.

(c) bu.edu

RetroSense Therapeutics is developing RST-001 as a first-in-class gene therapy application of optogenetics. Optogenetics refers broadly to means of conferring light sensitivity to cells that were not previously, or natively, light sensitive. By applying optogenetics to retinas in which rod and cone photoreceptors have degenerated, RetroSense is working to confer new light sensitivity to the retina, with the expectation of some degree of improved or restored vision for affected patients.

In 2014, the FDA granted Orphan Drug designation for RST-001 based on its development as a treatment of RP, a rare disease that affects an estimated 100,000 people in the United States. As a designated Orphan Drug, RST-001 is eligible for various development incentives under the Orphan Drug Act, including a potential waiver from FDA’s application user fees, certain tax incentives and Orphan Drug exclusivity.

Source

Featured image on top (c) bu.edu

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Microglia - a potential therapeutic target in Retinitis Pigmentosa

2015-07-04T21:50:00.001+05:30

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.

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.

A microglial cell (green) extends
spider-like arms to capture and
consume rod photoreceptor cells (blue).
Credit: Dr. Wai Wong, NEI.

Lead investigator, Wai T. Wong M.D., Ph.D., chief of the Unit on Neuron-Glia Interactions in Retinal Disease at NEI, and his team studied mice with a mutation in a gene that can also cause retinitis pigmentosa in people. The researchers observed in these mice that very early in the disease process, the microglia infiltrate a layer of the retina near the photoreceptors, called the outer nuclear layer, where they don’t usually venture. The microglia then create a cup-like structure over a single photoreceptor, surrounding it to ingest it in a process called phagocytosis. Wong and his team caught this dynamic process on video. The whole feast, including digestion, takes about an hour.

Phagocytosis is a normal process in healthy tissues and is a key way of clearing away dead cells and cellular debris. However, in retinitis pigmentosa the researchers found that the microglia target damaged but living photoreceptors, in addition to dead ones. To confirm that microglia contribute to the degeneration process, the researchers genetically eliminated the microglia, which slowed the rate of rod photoreceptor death and the loss of visual function in the mice. Inhibiting phagocytosis with a compound had a similar effect. The microglia seem to ignore cone photoreceptors, which fits with the known early course of retinitis pigmentosa.

The researchers feel that the findings suggest therapeutic strategies that inhibit microglial activation may help decelerate the rate of rod photoreceptor degeneration and preserve vision.

What triggers microglia to go on this destructive feeding frenzy? Wong and colleagues found evidence that photoreceptors carrying mutations undergo physiological stress. The stress then triggers them to secrete chemicals dubbed “find me” signals, which is like ringing a dinner bell that attracts microglia into the retinal layer. Once there, the microglia probe the photoreceptors repeatedly, exposing themselves to “eat me” signals, which then trigger phagocytosis. In response to all the feasting, the microglia become activated. That is, they send out their own signals to call other microglia to the scene and they release substances that promote inflammation.

Other potential treatments for retinitis pigmentosa, such as gene therapy, are progressing, but are not without challenges. Gene therapy requires replacing defective genes with functional genes, yet more than 50 distinct genes have been linked to the disease in different families, so there’s no one-size-fits-all gene therapy. A therapy targeting microglia might complement gene therapy because it’s an approach that’s independent of the specific genetic cause of retinitis pigmentosa.

A clinical trial (NCT02140164) is already underway at NEI to see if the anti-inflammatory drug minocycline can block the activation of microglia and help slow the progression of retinitis pigmentosa. The trial is currently recruiting participants.

This research was supported by the National Eye Institute Intramural Research Program and grant NS087198 from NIH’s National Institute of Neurological Disorders and Stroke.

Source: NEI

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World's first-ever braille tablet has been developed

2015-06-27T04:28:00.002+05:30

The first-ever braille tablet has been developed, using a new liquid-based technology to create tactile relief outputting braille, graphics and maps for the blind and partially sighted.

(c) ibtimes.co.uk

Austria-based startup Blitab Technology claims the "revolutionary" technology could be used to open up the digital era to the visually impaired, with plans to develop a braille smartphone.

"We are creating the first tactile tablet for blind and visually impaired people," Slavi Slavev, chief technology officer and co-founder of Blitab Technology, told IBTimes UK at the Hello Tomorrow Conference in Paris. "What we are doing is creating a completely new technology which outputs braille in a completely new and innovative way without any mechanical elements.

(c) ibtimes.co.uk

"This is revolutionary and we want to solve a great issue, and that's the literacy of blind people. The technology is quite scalable so we can output images and put any tactile relief representation like maps and graphics, such as geometric figures, in order to serve as an educational tool for blind people."

Other devices currently on the market are mechanical and only allow for one line of braille to be generated at any one time. They also cost about three-times the price of the €2,500 (£1,778, $2,802) Blitab. More recent refreshable braille concepts, such as the Anagraph e-reader, have run out of funds before being able to bring the product to market.

The Blitab tablet uses liquid bubbles to instantly generate braille text or relief images, while the corresponding technology allows text files to be instantly converted into braille from USB sticks, web browsers or NFC tags.

"Currently there are some solutions which are extremely expensive and they represent only one line [of braille]," Slavev said. "These devices were developed 40 years ago and because no one has offered any new innovations since then, that's still all that's on the market."

In the UK, interest in the Blitab has been shown by the Royal National Institute for the Blind (RNIB) and Barclays bank, due to its potential for helping blind and partially-sighted customers instore.

Blitab is currently in the prototyping stage but if the ongoing investment round is successful, the startup is hoping to bring the first product to market by September 2016.

Slavev added: "We think blind people should be included in the digital era in which we live, with all of the smartphones and tablets, but also ensure that they have a proper way to do everything that sighted people do, like web browsing, reading books and downloading books.

"Only 1% of all books worldwide are available in printed braille, as it's very expensive to produce printed braille. Some people are even saying that braille is decreasing among blind people but we want to get to the point where we can actually change this."

Ed: It is currently not available for purchase, though the company website is taking pre-orders.

Source: International Business Times

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Berkeley Architect sustains his vision despite blindness

2015-06-27T00:01:00.000+05:30

Oh, that we could see as clearly as blind architect Chris Downey. Leading his UC Berkeley seminar students to equitable, barrier-eliminating design solutions or consulting on a 170,000-square-foot blind rehab center at the Veterans Affairs center in Palo Alto or filling the stroke seat on his East Bay Rowing Club team, the 52-year-old Piedmont architect and teacher says he lacks sight, but is not without vision.

Recognizing Downey's contributions to the field, in the 20 years' experience he had before losing sight in 2008 and in the years following, the American Institute of Architects created a short documentary about his story. The AIA's "#ILookUp campaign" is aimed at educating the general public about the profession and inspiring the next generation of architects through film.

Downey says a consultant for the AIA called "out of the blue" to ask if he'd participate in the documentary. The AIA's sudden intrusion is rather like the manner in which Downey lost his sight. At age 45 -- his father had died at 36 from complications from brain surgery -- Downey began having blurry vision and trouble tracking a baseball while playing catch with his son, Renzo. Tests revealed a benign tumor wrapped around his optic nerve. Downey underwent a nine-hour surgery and woke able to see, if imperfectly.

"The sight started to fail in the second day and the third day it was gone. The last things I saw were half things," he recalls. "The water mark across my vision was black above and blurry below. I could see color splotches but not detail, like my wife's face."

Remarkably, acceptance was swift. "It came together in a 24-hour period that this was a new normal. It was a heavy day. It was like falling down a hole or a wall being built up around me. Family situations went through my mind," he says.

A grandmother with severe rheumatoid arthritis who had beautiful handwriting and recited joyous scripture to start every day reminded him that being miserable or being happy was a choice.

His surgeon challenged him to "get on with training, have a full, robust life, and not look for miracle cures." Nurses brought him a cell phone with oversized tactile buttons that he still owns. His son made jokes. A friend arrived, having researched tandem bike riding that would allow him to continue climbing Oakland's hills.

"I was still there, I realized. My dad died when I was 9. Sure, I was blind, but my son still had a father," Downey says.

And Downey still had a passion for architecture and the social and cultural issues the profession encompasses.

Other sensory mechanisms awakened. Downey discovered hearing is more physical than sight ("You can feel sound," he says) and an embossed printer allows him to "read" PDF's.

He developed a way of drawing with wax sticks that leaves raised lines he can feel and allows him to share sketches with team members by photographing the images. An iPad-like sketch pad with a rubber sheet that senses a drawing and raises a line has a USB reader that converts the sketch to a graphic file and enables Downey to continue the rapid digital interface his sighted colleagues enjoy.

"Chris has taught me that I'm my greatest limitation if I don't go after my dreams," says Sana Jahani, 21, a recent architecture UC Berkley graduate. Jahani appears in the documentary and says Downey tells students there are no limits, only breakthroughs to be made.

"He emphasizes the reasons why you and I should care about ADA compliant design," Jahani says. "We'll all age and, at some time, we'll need these things. My interactions with people with disabilities has changed. He taught me not to be uncomfortable and to start thinking about these issues now."

Downey says he's "incredibly lucky" to have lost his sight in the Bay Area. Public transit and wide sidewalks, along with streets that aren't too broad to cross allow him to live independently and spontaneously. "I learned to make it to a train, the ferry, a bus. I can navigate all over the Bay Area and beyond. Other big cities like Atlanta, you're dependent on paratransit. That requires reservations and there are no cancellations with para transit."

Downey says multi-sensory design perspectives apply to any building, but especially to homes. "In California, a home's close relationship to the land allows us to focus on space as sensual, alive. It's profound to feel wind or hear children at play and bring that quality inside."

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Tablet computers for the blind in development

2015-06-23T23:03:00.002+05:30

Is Braille on the way out? Do we have enough interest in teaching Braille to visually impaired students? Considering some of the subject matter cannot be explained to them by voice, are there any attempts to make this means of communication more accessible via smartphones and technology in the current age? Surprising to some, there are attempts being made to develop this technology to help the visually impaired students.

In 1970, more than half of blind American schoolchildren could read Braille. Now, only about 10% can. (We guess the numbers shouldn't be very different in India.) That decline is mostly a consequence of a change of policy, where visually impaired children are being taught, as far as possible, alongside their sighted peers. Since most people in a class of both the sighted and the blind will have no use for Braille, and most teachers no knowledge of it, its neglect is hard to avoid. Moreover, as the number of those who can read Braille declines, so does demand for books written in it. That, in turn, means fewer such books are being embossed - reducing yet further any incentive to learn the system in the first place.

Louis Braille’s patterns of raised dots, detectable by the fingertips and used to signify letters, numerals, punctuation marks, musical notation and mathematical symbols, which he invented in 1821, may be on the way out.

In a world of recorded sound, text-to-voice translators and voice-activated software, the withering of Braille might not be thought to matter much. But it does. Only a quarter of blind Americans of working age actually have jobs, and it is surely no coincidence that almost all of them can read Braille.

Braille may, however, be about to enjoy a comeback. Until now, technology has been its enemy. But it could become its friend, as a new generation of tablet computers with specially designed Braille displays is developed.

One route, being explored by the Braille Press itself, in conjunction with the Massachusetts Institute of Technology, is to make screens out of a ceramic that changes shape when exposed to electric currents.

(c) NBP, Boston, MA, USA

National Braille Press, in Boston, MA, USA, is developing b2g (Braille to Go), which is a portable, refreshable braille computer and optional smart phone, designed specifically for blind people. It weighs 20 ounces, has good processing speed, and 32GB of internal memory.Slightly larger than a 7 inch tablet, the b2g is a small but powerful computer that has our own originally designed ergonomic braille keyboard for data entry, with a 20 cell braille display for output.It is based on an electro-mechanical approach that uses Nitinol, a shape memory alloy, as the actuation method. This version will have five rows of braille, 40 cells across, plus a graphic array comprised of closely spaced pins that will render graphics and images on demand.

A second, developed by Disney as part of a wider project and known as electrostatic haptics, is to generate vibrations in parts of the screen. These trick the fingers into perceiving those areas to be raised or textured, when they are not.

(c) Disnery Research

The most developed approach, though—a prototype of which will go on show on June 23rd at the World Haptics Conference in Chicago—is the brainchild of Sile O’Modhrain and Brent Gillespie at the University of Michigan, Ann Arbor. It uses a pleasingly 19th-century technology, pneumatics, to generate Braille symbols.

The screen of the device includes a grid of pins the diameter of Braille dots. Normally, the tops of these pins are flush with the screen’s surface. When needed, though, they can be pushed upwards to create patterns representing Braille symbols. This is possible because each pin rests on a silicone-rubber membrane that sits above a small cavity. The cavity is, in turn, connected to a tiny pneumatic line and valve. When air is blown through the valve into the cavity, the membrane balloons up, pushing the pin above the screen’s surface. When the valve is opened and the air released, the pin returns to its hidey-hole.

The prototype on show in Chicago has a grid of 56 pins (eight across and seven down), which lets it display two rows of characters, with spaces between them. But Dr O’Modhrain reckons it should be possible to scale it up to the size of a normal tablet, which would mean it could have 12,500 pins and thus display 26 lines, each 40 characters long. A device this size would weigh about twice as much as a conventional tablet and might cost, Dr O’Modhrain reckons, $1,000.

Bringing Braille into the information-technology era in this way could give it a new lease of life. And that is only right, for it was, in effect, the first method of digital communication.

Source: The Economist

Intas launches RAZUMAB, the first biosimilar to Lucentis (ranibizumab)

2015-06-23T02:00:00.000+05:30

Intas Pharmaceuticals has launched RAZUMAB, its biosimilar to Lucentis (ranibizumab).

Intas is the first company globally to develop and launch a biosimilar version of ranibizumab. RAZUMAB is manufactured under strict guidelines for sterile use in the eye and is offered as single dose vial, thus reducing the risk of contamination during use.

Ranibizumab is a therapeutic antibody fragment designed specifically for treating degenerative conditions of the eye. It blocks the production of vascular endothelial cell growth factor A (VEGF-A), a protein which when over expressed leads to abnormal blood vessel growth in the retina, that can cause leaks and vision loss.

Ranibizumab is indicated for the treatment of neovascular (wet) Age-related Macular Degeneration (AMD), a common degenerative condition of the eyes in the elderly. It is also indicated for Macular Edema following Retinal Vein Occlusion (RVO), Diabetic Macular Edema (DME), Diabetic Retinopathy in patients with Diabetic Macular Edema and vision loss resulting from choroidal neovascularization in pathologic myopia (mCNV).

RAZUMAB, as per the company, will be about 25 per cent cheaper than the imported Lucentis. This would lead to an annual saving of about Rs 35,000 or more in the cost of treatment to the patient, depending on the number of injections used and the clinical condition of the patient.

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Students in Birmingham develop a smart cane for the blind

2015-05-09T01:01:00.001+05:30

A revolutionary ‘smart’ cane enabling the visually impaired to instantly identify friends and family could be available soon, thanks to students at Birmingham City University.

The ‘XploR’ mobility cane, being developed by ICT students Steve Adigbo, Waheed Rafiq and Richard Howlett, uses smartphone technology to recognize familiar faces from up to 10 meters away. The cane also features GPS functionality to aid navigation.

The device has added importance for one of its developers, Steve Adigbo, whose grandfather is blind. The smart cane incorporates facial recognition technology to alert the user when they are approaching a relative or friend.

The Birmingham City University team have already presented the XploR cane to medical and science professionals in Luxembourg and France, and plan to visit organizations in Germany later this year.

The students have designed the XploR cane to detect faces up to 10 meters away, vibrating when detecting a recognizable individual from a bank of images stored on an internal SD memory card.

The device will guide users towards friends and family members using an ear piece and audio guidance, with the information being relayed through Bluetooth technology.

The students conducted market research at the Beacon Centre for the Blind in Wolverhampton, West Midlands, to determine key features that the visually impaired would find useful in a mobility cane. They found that high-spec technology features were essential requirements for users, as well as the cane needing to be fairly lightweight and easy to use. They will return to the Beacon Centre later this year for people to test the product and also to highlight the training and security features of the cane.

The student project forms part of LILA, a European initiative encouraging entrepreneurship and fostering internationalization.

Source for text & picture

Scleral thinning seen following intravitreal anti-VEGF injections

2015-04-23T05:02:00.000+05:30

Research conducted at the University Hospital in Bern, Switzerland suggests that scleral changes may occur in patients following repeated intravitreal injections of anti-VEGF agents in the same quadrant.

The research, carried out among 35 patients under-going anti-VEGF treatment, indicated a potential association between the total number of intravitreal injections and changes in the scleral thickness in the inferotemporal quadrant. The authors of the study recommend that alternating the injection site should be considered in patients requiring multiple intravitreal injections.

Anti-VEGF medications such as ranibizumab (Lucentis), bevacizumab (Avastin) and aflibercept (Eylea) have been highly successful in tackling a number of retinal pathologies however, the requirement for regular injections over a number of years can present new challenges which have the potential to cause co-morbidities over time. While the standard needle for intravitreal injection is small (30-gauge) and the injection is usually performed in the same infero- or superotemporal quadrant, approximately 3 mm from the limbus, the continuing number of injections has the potential to alter the mechanical structure of the retina at the injection site.

To determine the impact of such injections a retrospective controlled study was designed to record changes in the scleral architecture of patients that had received 30 or more intravitreal ranibizumab injections in the inferior temporal quadrant. The study used enhanced depth imaging anterior segment spectral domain optical coherence tomography (AS SD-OCT) to detect changes in the sclera in the study population.

The mean age of the 35 patients studied was 76 years of age and ranged from 61–87 years, with an approximate male-to-female ratio of 3:4. Twenty-seven (27) of the patients had received intravitreal anti-VEGF treatment in one eye for exudative AMD, seven were treated for cystoid macular edema (CME) due to central retinal vein occlusion (CRVO), and one patient was treated for diabetic macular edema (DME). Of the patients studied, each had at least 30 injections in one eye in the inferotemporal quadrant and 10 or less injections in the fellow eye.

The research findings – the only report known to evaluate the effects of repeat injections on the sclera – showed that in the study eyes with more than 30 injections, the average scleral thickness in the inferotemporal quadrant was 568.4 μm (SD6 66 μm) and 590.6 μm (SD6 75 μm) in the fellow eyes with 10 or less injections (P. 0.003). The mean average scleral thickness in the other three quadrants (inferonasal, superotemporal, and superonasal) was 536.6 μm in the study eyes (SD 6 100 μm) and 545.2 μm (SD 6 109 μm) in the fellow eyes (P. 0.22).

The authors concluded that there was a borderline association which may be relevant to clinicians caring for patients requiring anti-VEFG treatment.

Source
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Converting rods into cones in a model of retinitis pigmentosa (RP) rescues retinal degeneration

2015-04-22T23:59:00.000+05:30

Heritable retinal degeneration is a common cause of visual impairment and blindness, affecting millions of people worldwide. Many research groups have focused on targeted gene therapy as a treatment for these diseases. However, inherited retinal diseases can be caused by mutations in any one of more than 200 genes, and the pathogenic mechanisms of various mutations differ greatly. This was the motivating factor in the work by Dr James C Corbo and his team at the Washington University School of Medicine to develop gene-independent therapies that would be more widely applicable. This work has been published in the Proceedings of the National Academy of Sciences.

It is estimated that almost 200 distinct genes are the causative agent behind one or more inherited retinal pathologies. Retinitis pigmentosa (RP) accounts for approximately 50% of known inherited retinal degeneration cases. RP is probably one of the most heterogeneous diseases recorded to date, arising from mutations in more than 50 genes with over 3,000 mutations reported by mid-2013. In addition, many syndromic forms of RP also exhibit genetic heterogeneity which, when combined with incomplete penetrance and clinical heterogeneity, result in a significant medical challenge in terms of devising optimized clinical care strategies.

While RP can be initiated (literally) in thousands of different ways, the course of disease generally progresses through an increasing level of rod photoreceptor cell loss followed by cone photoreceptor degeneration. Retinitis pigmentosa is a subtype of retinal degeneration that might be particularly amenable to a gene-independent approach. Here, mutations in rod-enriched genes initiate a progressive sequence of rod cell death followed by cone loss. Cone dysfunction is particularly debilitating for patients, yet it appears to be secondary to rod death; studies in animal models suggest that collapse of the outer nuclear layer (ONL) during rod degeneration may generate an oxidative, nutrient-deficient environment that is toxic to cones. In this case, preservation of rod cell bodies may be sufficient to forestall secondary cone death. the researchers hypothesized that converting adult rods into cones could make the cells resistant to the effects of mutations in rod-specific genes, thereby preventing ONL collapse and secondary cone loss. Although conversion of rods into cones would be expected to result in a loss of rod function and consequent night blindness, this disability is generally well tolerated by patients and might be considered an acceptable risk if coupled with significant cone rescue.

The researchers (headed by Dr Joseph C Corbo (left in pic), credit: Washington Univ School of Medicine) report the rescue of retinal degeneration by the reprogramming of rods into cones (photo on top credit: Corbo Lab). The study used a well-characterized retinal transcription factor to re-direct rods to a cone cell fate. The principle itself of course is not new. Conversion of one differentiated cell type into another has been carried out in other contexts, including the conversion of pancreatic exocrine cells into β-cells or, auditory endothelial cells into hair cells and fibroblasts into neurons. Of course rod reprogramming is quite different in that the conversion itself would result in a loss of rod function followed by consequent night blindness. However, most individuals might agree that night blindness is an acceptable risk in the context of maintaining a healthy cone cell population and functional photopic vision. The result of the cellular reprogramming in this case reduced rod photoreceptor cell death in a rhodopsin knock-out model of retinitis pigmentosa (RP). The loss of the rod cell population has a deleterious impact on the cones which subsequently degenerate leaving patients with both reduced or absent photopic and scotopic vision. The results of the research suggest that maintaining a rod photoreceptor cell architecture may be sufficient to slow or halt cone cell degeneration.

To achieve their results, the research team exploited the biology of the neural retina-specific leucine zipper (Nrl) transcription factor, known from many previous studies to determine photoreceptor cell fate in the retina. Under normal conditions, photoreceptor precursors expressing Nrl become rods whereas those without Nrl progress to a cone photoreceptor lineage. To knock out Nrl in a model of retinitis pigmentosa the research team generated a conditional Nrl knock out controlled through a tamoxifen inducible promoter. A daily injection of 4-hydroxyl-tamoxifen (4-OHT), between postnatal day 42 and 44, caused inactivation of the Nrl transcription factor resulting in the reprogramming of rods to a cone cell fate. Assays of the reprogrammed pseudo-cones demonstrated a significant decrease in the scotopic ERG response suggesting a loss of rod function, while genetic analysis indicated a loss of expression of rod-specific genes, including rhodopsin, with a parallel activation of cone specific genes.

The work resulted in partial reprogramming of rods into cells with a variety of cone-like molecular, histologic, and functional properties. While the reprogramming was dependent on the timing of Nrl knock-out, the strategy nevertheless rescued the cone cell population within a model of RP. Keeping the rod cells alive, even dysfunctional rods harboring mutations that cause RP, appeared to be sufficient to maintain the retinal architecture and thereby support cone cell survival. In concluding their research, the authors commented that apart from providing insights into the plasticity and maintenance of rod photoreceptor identity, the study demonstrated that partial rod-to-cone reprogramming can forestall retinal degeneration in the Rho−/− model of retinitis pigmentosa. Although these cells are not true cones, they exhibit sufficient down-regulation of rod-specific genes to resist the deleterious effects of a rod-specific mutation. Thus, rod reprogramming may represent a unique therapeutic strategy for retinal disease caused by mutations in rod-enriched genes.

In addition, the research team suggests that the re-programming approach may also be employed to generate a novel cone cell population that could serve to rescue other retinal degenerative conditions, including age-related macular degeneration. While the results indicate the potential for this strategy in the rhodopsin knock-out model, other models of RP, including dominant forms, will need to be tested.

Source

Blind candidates to get extra 20 minutes per hour in HPSC exams

2015-04-22T09:03:00.003+05:30

Coming to the aid of a blind candidate, the state commissioner for persons with disabilities has directed the Haryana Public Service Commission (HPSC) to give additional 20 minutes per hour to blind candidates appearing in competitive examinations conducted by the Commission.

In his April 8 court order, commissioner for persons with disabilities, Haryana, Phool Chand Yadav said the complainant, Chirag Mittal of Hisar, a blind candidate has contended that HPSC was providing only 10 minutes per hour to the blind candidates appearing for competitive examinations which is not suitable as the blind person has to get help for reading the question paper as well as giving dictation.

The complainant relied on the August 19, 2014 judgment of Delhi high court in this regard. “In my opinion the present case is fit for issuance of directions to HPSC to comply with the judgments/orders because of the fact that action of the Commission is discriminatory towards persons with disabilities. Mentally retarded and those having locomotor disabilities ( disability of muscles, bones and joints causing restriction of movement of the limbs or any form of Cerebral Palsy) are given 20 minutes per hour whereas the blind are given 10 minutes,’’ the order said.

It further said that the HPSC is directed to provide every blind candidate appearing for competitive examination 20 minutes per hour as per law laid down by the Delhi high court and Supreme Court and guidelines issued by the chief commissioner for persons with disabilities.

Source

Study challenges conventional wisdom that sight-based brain sensory network is impaired with blindness

2015-04-14T05:32:00.000+05:30

Is visual input essential to how the topographical map of the visual cortex develops in the human brain? In a new research, scientists at the Hebrew University of Jerusalem, and those from in Germany and USA, show that the way in which the brain organizes its visual sense remains intact even in people who are blind from birth.

The scientists also note that at least the pattern of functional connectivity between the visual area and the topographical representation of space (up/down, left/right, etc.) can develop on its own without any actual visual experience. The findings, reported in the journal Brain, dispel the nearly half-century belief that the visual cortex — the area of the brain concerned with the sense of sight — completely fails to develop properly in people who are blind at birth, suggesting it might not be completely correct.

Though the 'blind brain' wiring may change greatly in the blind in its frontal language related parts, it still retains the most fundamental topographical and functional connectivity organizational principles of the visual cortex, known as 'retinotopic mapping' — the processing of two-dimensional visual images through the eye, as per the co-lead researcher Amir Amedi, Associate Professor of Medical Neurobiology at the Hebrew University's Edmond and Lily Safra Center for Brain Sciences and IMRIC, the Institute for Medical Research Israel-Canada.

The researchers found that the same "mapping" divisions-of-labor present in the normally sighted brain are also present in the brains of people born blind as reflected from their resting state connectivity patterns. This fundamental organization of the visual cortex was even found in people whose eyes did not develop normally, suggesting normal eye development may not be necessary for the establishment of large-scale functional connectivity network mapping in the most fundamental visual areas like V1, the primary visual cortex. Contrary to conventional wisdom, the latest findings reported by Prof. Amir Amedi, Dr. Ella Striem-Amit and Smadar Ovadia-Caro suggest that some key features and properties of visual cortex organization do not require visual experience to progress. The study further adds that the brain's visual cortex does not lose all of its properties even when completely deprived of vision.

The authors add that some of the brain’s connectivity maps is hardwired, possibly dependent on genetically-driven processes that do not need any external sensory information for their activation, while other process might indeed need visual input to specialize, The visual brain resting-state connectivity networks separated to up vs. down, right vs. left, front vs. back are also present in the brain of those born blind.

Previous research by neurophysiologists David Hubel and Torsten Wiesel, which earned them a Nobel Prize in 1981, suggested that sight restoration could not be attempted on people blind from birth. Therefore, they surmised, the blinded cortex could not enable the blind-from-birth to have sight.

This latest research, combined with other research conducted in the Amedi Lab for Multisensory Research, suggests that it may be possible to successfully teach blind people to 'see with sounds and touch.' Using tools of sensory substitution, it may be possible to aid people born blind (or late blind) in a variety of new ways in the future, including restoring high-order functional pattern recognition for objects, localization, shape and even numbers and text, as previously reported in the journal Nature Communications.

Useful content:

Amedi Lab allows any interested person, including people with visual impairment, to download and train themselves on using such technologies for free. Please click here.
Videos and images are available here. If you plan to use it anywhere, please attribute it to Amedi lab.

Source

New clinical trial utilizing stem cells for retinitis pigmentosa

2015-04-14T05:20:00.000+05:30

ReNeuron has announced that it has filed application with the US FDA to commence Phase I/II clinical trial in the US with its stem cell therapy candidate for the blindness-causing disease, retinitis pigmentosa. The clinical trial will be evaluating its human Retinal Progenitor Cell therapy candidate for retinitis pigmentosa.

ReNeuron has worked with collaborators and academic institutions in the retinal disease field to successfully take its retinitis pigmentosa programme through pre-clinical development. These include the Schepens EyeResearch Institute/Massachusetts Eyeand Ear (an affiliate of Harvard Medical School), UCL Institute of Ophthalmology, MoorfieldsEye Hospital and the US-based Foundation Fighting Blindness.

The pre-clinical program has also benefited from UK Government funding under a BioMedical Catalyst grant, awarded in 2013. Pre-clinical studies carried out in disease models by the Company’s academic collaborators have demonstrated that, when transplanted into the retina, the retinal progenitor cell technology has the potential to preserve existing photoreceptors, potentially reducing or halting further deterioration of vision. In addition, the progenitor cells have been shown to mature into functional photoreceptors that engraft into the photoreceptor layer, bringing the possibility of restored vision.

The proposed Phase I/II clinical trial will be conducted at Massachusetts Eye and Ear, Boston, with Dr Eric Pierce, Director, Retinal Degenerations Service at Massachusetts Eye and Ear, will be the Principal Investigator for the clinical trial.

The trial design is an open-label, dose escalation study to evaluate the safety, tolerability and preliminary efficacy of the hRPC stem cell therapy candidate in up to 15 patients with advanced RP. The method of administration of the hRPCs will be a single sub-retinal injection. The primary endpoint of the study is safety, with patients being followed up for 12 months post-treatment with monitoring including measurements of visual acuity. Subject to regulatory and local ethics approvals, ReNeuron expects to be able to commence the clinical trial in the second half of this year.

Source

New development in the race to bring bionic eye closer to patients

2015-01-28T04:47:00.002+05:30

A French company called Pixium Vision is testing a system called Iris that promises to improve the vision of the blind.

More than half a century ago, when he was just 18 years old, Georges (not the real name) learned that he had retinitis pigmentosa. He was told that his vision would progressively deteriorate until he was blind. As predicted, when Georges reached his early fifties, his world went completely dark. Last year, at the push of a button, Georges suddenly saw light again.


Electrode array placed on the retinal surface

Iris is currently undergoing a pilot testing program. The company’s founder, Bernard Gilly, is a scientist-turned-entrepreneur with a network of businesses focused on using technologies to improve human health, mostly around the nervous system.

Technological advances such as microbiology and microelectronics are creating new opportunities to restore sight and scientists are making enormous strides in understanding the workings of the brain. It’s long been known that electricity can stimulate the nervous system, and a technique called “neuromodulation” is being used to address everything from Parkinson’s disease to chronic pain. Now, it can treat blindness, too.

Iris consists of three different parts: one, the retinal implant implanted in the patient’s eye. It
comprises an electrode array affixed surgically to the surface of the retina (epi-retinal position). This electrode is connected to an electronic circuit (ASIC) containing a radio antenna for controlling the transmission of final information to each of the electrodes and for receiving power, which is transmitted by RF induction; two, the visual interface takes the form of a pair of glasses that have an integrated mini-camera with a biomimetic sensor (ATIS) and an infra-red transmitter, and three, a pocket computer connected to the visual interface by a cable. This computer replaces the signal processing function of the retina through a high-speed processor and proprietary customizable software. The image is captured by the biomimetic camera and sent to the computer
where it is analyzed and converted into a digital signal. This digital signal is then transmitted to the IR emitter integrated in the glasses, which transfers the information to an IR receiver located on the implant. The signal is then sent to the ASIC, which distributes different stimulation signals to each of the electrodes.

Epiretinal implant (c) Pixium Vision

An IRIS implant with an array of approximately 50 electrodes is currently being tested in a clinical study; and IRIS-150 with a 150-electrode array is expected to be commercialized in Europe this year.
The best candidates for Iris are patients with degenerative eye conditions. A surgeon implants a tiny silicon chip with 150 electrodes on the retina. Afterwards, the patient wears a pair of dark glasses with an integrated video camera that sends images to a portable mini-computer. This computer transforms the pictures into digital signals, which are sent back to the glasses, then transmitted wirelessly to a receiver on the implant. Pulses activate the electrodes, and the optic nerve carries the images to the brain.

After surgery, patients follow a program of rehabilitation to teach their brains how to interpret these new images. What they see is basic shapes in variations of black, white, and gray. (The resolution is still too low for them to distinguish facial features or read.)

Dr Yannick Le Mer, the surgeon who implanted the system in three of Pixium’s test subjects, says it is impossible to know beforehand how anyone will react, since it depends on each brain’s adaptability—like learning to play the piano or speak Japanese. Some catch on immediately, while others struggle.

One recent autumn day, Georges, a small, soft-spoken man, traveled from his home in Brittany to the Quinze-Vingts hospital in eastern Paris. A young therapist named Alexandre Leseigneur was waiting for him, and the two spent the day together practicing using the system in the corridors. (The glasses were not yet available for practice at home.)

Georges put the glasses on and hung a strap with the computer over his shoulder. The first time they went into the hallway, he moved hesitantly, shuffling sideways and reaching out his hand. The flashes appeared to be too bright and George felt lost. Leseigneur plugged the glasses into a laptop computer, adjusted the settings, and they went out again. This time was better. Following a black band on the floor, Georges walked the length of a corridor and even managed to avoid an obstacle blocking his path.

Gilly estimates that when the Iris arrives on the European market in late 2015, the cost to each patient will be around 100,000 euros, plus surgery. Though that might sound expensive, he says it’s a bargain compared to the price of blindness. A study at the University of Chicago forecasts that in the United States alone, costs related to eye disease and vision problems will reach $717 billion by 2050.

Last June, Pixium made an initial public offering, raising nearly 40 million euros (more than $53 million) from European investors. It is not the only company working in this field. Various permutations of what is commonly called a “bionic eye” are being developed from Germany to Australia. The pioneer is an American company, Second Sight Medical, which earned European approval for its Argus II system in 2011 and FDA approval in 2013. In November, Second Sight had its own successful IPO, raising some $32 million.

While the Iris is very similar to the Argus II, Gilly mentions a few key differences. Iris's camera captures only the changes in the environment, so that the overall view is continuous, closer to the way the human eye actually sees. The implant can also be easily removed and replaced with upgrades as they become available.

The company’s next generation product, Prima, will start clinical trials in 2016. With at least 10 times as many electrodes, it should enable people to read and to see facial features.

Prima is a miniaturized retinal prostheses (PRIMA) based on sub-retinal implant technology that is being developed in partnership with Stanford University. The PRIMA system is designed to enable greater physiological signal processing, while simplifying the surgical procedure. It will include a sub-retinal implant composed of a micro-sized wireless electrode array, featuring over 150 pixels each made of a micro-photovoltaic diode feeding a central stimulatory electrode. These arrays are fully autonomous (no wires) enabling the possibility of implanting multiple tiles in the sub-retinal space to achieve direct stimulation at the photoreceptor layer from a matrix of up to several 1,000 electrodes; the visual interface similar to that used for IRIS, consisting of a pair of glasses and an integrated biomimetic
mini-camera sensor (ATIS), and also includes a digital micromirror device to convey the visual information signal and light (power) to the micro-photovoltaic diodes, and a pocket computer is connected to the visual interface and will process the visual information into electrical signals. The Company plans to begin clinical trials of PRIMA in Europe during 2016.

Since these products lead to synthetic vision, the possibilities are vast. Soon the technology will permit users to see as clearly at night as during the day. A future device might be able to transmit the contents of an e-book or a movie directly to the retina. For now, the goal is simply to help someone locate a door in a room.

Georges agrees. He tells about how not long ago, he was taking a walk near his home, when his cane slipped under a truck. Since he didn't know it, he tried to reach out for the cane and unfortunately smacked my head against the truck. He left that if he had been using this system, he would have been able to see it.

* All pictures in this article are copyrighted of Pixium Vision

Pixium Vision & Fortune

A major advance in gene therapy for Retinitis Pigmentosa

2015-01-27T12:58:00.000+05:30

A paper published in Nature Communications sheds light on why, until now, it has not been possible to effectively restore vision in rd1 mice – the world’s major model for retinitis pigmentosa (RP). This research also demonstrates how a particular type of mutation in this mice was the cause of failure of previous gene therapy attempts.

The rd1 mouse is a model of retinitis pigmentosa caused by defects in the PDE6B gene. The model was first described back in 1924 and is the oldest and most widely used model of retinal degeneration in the world. When light enters the eye and hits the rod cells (a type of photoreceptor – the light sensing cells of the eye), PDE6B is required to help turn this stimulus into electrical signals that can be understood by the brain and translated into an image. In rd1 mice, the defect in PDE6B leads to a rapid degeneration of the retina within the first four weeks of life, which is characterised by the death of rod cells and a complete loss of vision.

Numerous attempts have been made to preserve and restore function to rod cells in rd1 mice in the hope that an approach towards developing a treatment for RP patients could be identified. Past attempts to restore vision in these mice using gene therapy (where the normal gene is put back into the effected cells by means of a harmless virus known as a vector) has had limited success. In this model, retinal degeneration happens appears to happen so quickly that there aren’t enough, if any, healthy rod cells left to treat.

In other animal models (such as dogs) where progression of retinal degeneration caused by defects in PDE6B is somewhat slower, a restoration of vision has been possible and has led to the conclusion that in rd1 mice, the degeneration happens too quickly to allow for a window of opportunity to treat. This has confused the issue around whether a gene therapy approach to treating this form of RP in people could be effective.

Recent work from the group in UCL in other more severe forms of retinal degeneration, specifically that of Leber Congenital Amaurosis Type 4 (LCA4 [caused by a defect in the gene AIPL1]), however, has cast doubts on this explanation of previous findings in rd1 mice. Using an AIPL1 gene therapy, the scientists in UCL have been able to rescue vision loss in an LCA4 mouse model, which experiences a complete loss of vision in the first three weeks of life; faster than in rd1 mice.

Using the latest in gene therapy vector technology, the team has successfully created a more efficient and rapid acting PDE6B gene therapy then had previously been possible to address the short window of opportunity to treat. This approach was able to not only preserve the rod cells but restore their function as well. However, despite this, the team found that these mice were still not responding to a light stimulus suggesting that somewhere in the pathway that carries signals from the rod cells to the brain there must be a second and currently unreported defect blocking the signal.

An analysis of the genetic code of rd1 mice has indeed identified a defect in a gene called GPR179 that had not previously been found in the rd1 mouse strain. This defect affects the retinal bipolar cells – specialised cells that help transmit signals from the photoreceptors of the eye to the nerve cells that carry signals up to the brain. This defect is likely to be found in most of the rd1 mice around the world today and could have been present in this mouse strain for as long as 65 years. Through a process of selective breeding of different mouse models the team have successfully removed the GPR179 defect from rd1 mice and been able to demonstrate that PDE6B gene therapy does indeed lead to the preservation and restoration of rod cell function and that these mice can still sense and respond to light a year after treatment.

This study provides strong evidence to support the potential of gene therapy for RP caused by defects in the PDE6B gene and future studies will be required to assess further the potential. This study by no means suggests that previous work in rd1 mice is not valid but instead highlights the need, where appropriate, to reassess past findings and ensure that future work considers if the presence of a GPR179 defect may be a contributing factor to the results.

Source: UCL Eyetherapy Blog, Nature Communications

Legally Blind Mom Sees New Baby With Special Eyewear

2015-01-23T12:00:00.002+05:30

A specialized piece of eyewear gave a legally blind woman from Ontario, Canada, the opportunity to do something that new parents may take granted — see her baby hours after his birth.

Kathy Bietz, 29, was diagnosed with Stargardt disease, a genetic condition that causes macular degeneration, when she was 11. While she has some peripheral vision, she developed a blind spot in the centre of her field of vision and is legally blind.

She has had a big change in her life since using a device produced by the firm eSight, highlighted by the moment she first saw Aksel, who is now a few weeks old.

After wearing them for the first time, Kathy said she could notice that the baby had her husband’s feet and toes, while he has her lips. The glasses made it possible for her and her husband to have the family experience of looking at their brand new baby, and bonding with him.

The eSight device is equipped with a video camera that sits over the bridge of the wearer’s nose. The images captured from the camera are enhanced and projected onto high definition screens in front of the eyes.

According to Taylor West, a spokesperson for eSight, the patient's eyes perceive more when they look at the screen than they can with their natural eyesight. While the device would not be able to help people who have no vision, it can be customized to suit a variety of eye impairments. A user can adjust contrast, brightness and shadow depending on his or her preferences.

The device, launched in 2013, sells for $15,000. The company has a fundraising department that helps people purchase the eyewear. Those efforts include helping people with crowdfunding efforts, grant applications and a new campaign centred on Beitz's story, dubbed #MakeBlindnessHistory.

Source: CBC News

Results from AREDS-2 clinical trial & what it means for you

2015-01-22T14:21:00.000+05:30

Age-Related Eye Disease Study (AREDS) and Age-related Eye Diseases Study-2 (AREDS-2) were landmark studies in providing a clue to show benefit from nutritional supplements. The article below, from Retina India's newsletter from 2013, is still relevant today to patients of Age-related macular degeneration.

Age-Related Eye Disease Study (AREDS) had reported in 2001 that a nutritional supplement of daily high doses of vitamins C and E, beta-carotene, and the minerals zinc and copper—called the AREDS formulation—can help slow the progression to advanced AMD. American Academy of Ophthalmology has recommended use of the AREDS formulation to reduce the risk of advanced AMD.

However, beta-carotene use has been linked to a heightened risk of lung cancer in smokers. And there have been concerns that the high zinc dose in AREDS could cause minor side effects, such as stomach upset, in some people.

from NEI

In 2006, the National Eye Institute (NEI) launched AREDS2, a five-year study designed to test whether the original AREDS formulation could be improved by adding omega-3 fatty acids; adding lutein and zeaxanthin; removing beta-carotene; or reducing zinc. The study also examined how different combinations of the supplements performed. Omega-3 fatty acids are produced by plants, including algae, and are present in oily fish such as salmon. Lutein and zeaxanthin are carotenoids, a class of plant-derived vitamins that includes beta-carotene; both are present in leafy green vegetables and, when consumed, they accumulate in the retina. Prior studies had suggested that diets high in lutein, zeaxanthin, and omega-3 fatty acids protect vision.

Adding omega-3 fatty acids did not improve a combination of nutritional supplements commonly recommended for treating age-related macular degeneration (AMD), a major cause of vision loss among older people. The plant-derived antioxidants lutein and zeaxanthin also had no overall effect on AMD when added to the combination; however, they were safer than the related antioxidant beta-carotene. This study has been published in the Journal of the American Medical Association.

Apparently, even before the AREDS2 study was finished, manufacturers began marketing supplements based on the study design.

In AREDS2, participants took one of four AREDS formulations daily for five years. The original AREDS included 500 milligrams vitamin C, 400 international units of vitamin E, 15 milligrams beta-carotene, 80 milligrams zinc, and two milligrams copper. Other groups took AREDS with no beta-carotene, AREDS with low zinc (25 milligrams), or AREDS with no beta-carotene and low zinc. Participants in each AREDS group also took one of four additional supplements or combinations: these included lutein/zeaxanthin (10 milligrams/2 milligrams), omega-3 fatty acids (1,000 milligrams), lutein/zeaxanthin and omega-3 fatty acids, or placebo. Progression to advanced AMD was established by examination of retina photographs or treatment for advanced AMD.

AMD breaks down cells in the layer of tissue called the retina in the back of the eye that provide sharp central vision, which is necessary for tasks such as reading, driving, and recognizing faces. Advanced AMD can lead to significant vision loss.

Ed: To read more about the disease AMD, please read the article by Dr Mallika Goyal, Hyderabad, in the December issue of inSIGHT.

In the first AREDS trial, participants with AMD who took the AREDS formulation were 25 percent less likely to progress to advanced AMD over the five-year study period, compared with participants who took a placebo. In AREDS2, there was no overall additional benefit from adding omega-3 fatty acids or a 5-to-1 mixture of lutein and zeaxanthin to the formulation. However, the investigators did find some benefits when they analyzed two subgroups of participants: those not given beta-carotene, and those who had very little lutein and zeaxanthin in their diets.

Those who took an AREDS formulation with lutein and zeaxanthin but no beta-carotene were found to have a reduced risk of developing advanced AMD over the five years of the study by about 18 percent, compared with participants who took an AREDS formulation with beta-carotene but no lutein or zeaxanthin. Further analysis also showed that participants with low dietary intake of lutein and zeaxanthin at the start of the study, but who took an AREDS formulation with lutein and zeaxanthin during the study, were about 25 percent less likely to develop advanced AMD compared with participants with similar dietary intake who did not take lutein and zeaxanthin.

Removing beta-carotene from the AREDS formulation did not curb the formulation’s protective effect against developing advanced AMD, an important finding because several studies have linked taking high doses of beta-carotene with a higher risk of lung cancer in smokers. Although smokers were not given a formulation with beta-carotene in AREDS2, the study showed an association between beta-carotene and risk of lung cancer among former smokers.

Adding omega-3 fatty acids or lowering zinc to the AREDS formulation also had no effect on AMD progression.

The study included more than 4,000 subjects at 82 clinical sites around the US, aged 50 to 85 years, who were at risk for advanced AMD. Eye care professionals assess risk of developing advanced AMD in part by looking for yellow deposits called drusen in the retina. The appearance of small drusen is a normal part of aging, but the presence of larger drusen indicates AMD and a risk of associated vision loss. Over time, the retina begins to break down in areas where large drusen are present during a process called geographic atrophy. AMD can also spur the growth of new blood vessels beneath the retina, which can leak blood and fluid, resulting in sudden vision loss. These two forms of AMD are often referred to as dry AMD and wet AMD respectively.

The AREDS2 study results provide physicians and patients with new information about preventing vision loss from AMD. People over 60 years old should get a dilated eye exam at least once a year and should discuss with their doctor whether taking AREDS supplements is appropriate for them.

Who should consider taking a combination of antioxidants and zinc like those examined in AREDS and AREDS2? People at high risk for developing advanced AMD should consider taking the antioxidant-zinc combinations examined in AREDS and AREDS2. These people are defined as having either:

Intermediate AMD in one or both eyes. It usually involves little or no vision loss.
Advanced AMD in one eye, which may lead to significant visual loss, but not the other eye.

Note for patients: Queries pertaining to retinal disorders (along with scanned relevant copies of the medical reports) can be e-mailed to doctor@retinaindia.org. Retina India’s medical team will try to answer the queries as soon as possible.

Students build sonar based watch for helping the blind to navigate

2015-01-22T06:11:00.000+05:30

When a biologist who studies bats and a computer scientist cross paths, amazingly cool things can happen. Cool things such as a sonar device to assist the visually impaired.

(c) Wake Forest Univ

The idea came from biology professor William Conner of Wake Forest University in the US, who for decades has been studying echolocation in bats and moths to learn more about the evolution of animal communication. Conner, who also is the David and Lelia Farr Professor of Innovation, Creativity, and Entrepreneurship, teaches a class called “Bio-inspiration and Biomimetics,” which looks at how animals and plants can inspire the design of new technologies.

Prof Conner talked with Paul Pauca, an associate professor of computer science, who was immediately interested. A collaborative project was born. The pair assembled an interdisciplinary team of students to figure out how to put Conner’s idea into action.

Student-driven project Jack Janes, a senior computer science major; Dominic Prado, a senior biology major; and Ran Chang, a sophomore computer science major, began brainstorming during the first STEM incubator meeting of the Fall 2014 semester.

The students questioned about how to use this concept in a creative way to help blind people navigate better. They eventually focused on developing a device that could be worn like a watch by a visually-impaired person as a supplement to other aids like a cane or dog. Ultimately, they decided on the watch because of it’s small profile and dimensions. Prado, one of the students, came up with a clever name for it: HELP, the Human Echo Location Partner.

How does it work?

(c) Wake Forest Univ

The prototype is made up of several components. It is powered by an Arduino Lilypad microprocessor, runs JAVA-like code written by Janes, and is combined with the sonar distance sensors and two cellphone vibrating motors. It measures the distance of objects and provides feedback via vibrations to the user. The frequency of vibrations is proportional to the distance from the detected object, allowing the user to accurately discern an obstacle’s proximity; they get faster as it draws near.

To test their device, the team turned to sophomore Kathryn Webster, a blind student who navigates campus with her guide dog, Enzo. One of Webster’s difficulties on campus is dealing with whether doors into buildings or classrooms are open or closed. She tested the device without Enzo and found that it vibrated as she approached a closed door and stopped when it was opened.

What’s Next?

Next steps include fine-tuning the device to make it smaller and more aesthetically pleasing. And they want to keep it affordable – all of their parts and materials cost less than $60. They are also trying to figure out ways to minimize the amount of power it uses because they would like to make it run off a watch battery.

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Does a full vision restoration happen after treatment from being blind from birth?

2015-01-21T05:30:00.000+05:30

A partial restoration of sight is possible in individuals blind from birth, thanks to the most recent advances in research. However, a group of researchers of the Mind/Brain Center of the University of Trento and of the University of Montréal in Canada have discovered that the functional reorganization of the brain happens in individuals who, for a long period, experienced a long sense deprivation, which could potentially impede complete sight restoration.

The researchers, including were able to study a case of a patient, visually impaired since birth, whose sight was restored during her adult life, following an artificial corneal implant (Boston Keratoprothesis) surgery in one eye. It is known that visual cortex maintains a certain degree of plasticity, with the capacity of the brain to tune its activity according to the experience it perceives, even in individuals visually impaired since birth. But the authors of the paper that describes this results discovered that, even months after the surgery, the visual cortex* does not restore its complete normal functioning.

* The visual cortex is the part of the occipital lobe responsible for the processing of the electric inputs coming from the eye.

In blind individuals, the occipital cortex responds to stimuli coming from other sense organs, such as hearing and touching, thus partially compensating the loss of sight. This challenges the sight restoration of individuals who undergo a transplantation, because the cortex - after its reorganization - may not be able to process visual inputs any longer, as per the researchers.

To better understand the importance of this phenomenon researchers examined the 50-year-old Canadian female patient through a set of behavioural and neurophysiological tests. They monitored, before and after the surgery, the changes of the sight and the brain anatomy, as a response to visual and sound stimuli. Therefore the team of researchers used the functional MRI to record the brain activations of the patient during the performance of specific visual and hearing tasks and then compared them with the activations of individuals with normal sight and individuals blind since birth, while performing the same tasks.

Before the surgery, the patient presented a structural and functional reorganization of the occipital areas typical of individuals with a long sense deprivation. Therefore the possibility of a partial recovery of the previous functions, after the sight restoration in adult age was proved. Considering the significant recent advances in the technological solutions that allow for the sight restoration, these results play a significant role in the clinical implications to foresee the possible results of transplantations in patients to be operated.

The study suggests that the eye surgery may achieve good results, also in adults severely visually impaired since childhood. However, it is important to warn that the observed restoration in the visual cortex, in terms of minor response to sound stimuli and the gradual increase of response to visual stimuli and the density of the brain, is not complete. Indeed seven months after the surgery, some areas continue to respond weakly to sound stimuli, despite the simultaneous response to visual inputs. This overlap may be the reason why some features of sight, in spite of the gradual improvements, still remain below standard seven months after the transplantation.

The clinical implications are twofold: The results of this research pave the way for the systematic clinical use of the pre-surgery MRI as a prognosis tool regarding the efficacy of the transplantation. Further, they open up ways for specific rehabilitation programmes after sight-restoration surgery.

The research “Tracking the evolution of cross modal plasticity and visual functions before and after sight-restoration” by Giulia Dormal, Olivier Collignon et. al. was published in the Journal of Neurophysiology.

The study was financed by the Canada Research Chair Program, Canadian Institutes of Health Research, Saint-Justine Foundation, the European Research Council, Veronneau Troutman Foundation, Fonds de recherche en ophtalmologie de l’Université de Montréal, PAI/UIAP grant PAI/33 and the Belgian National Fund for Scientific Research.

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Delhi University developing mathematical kits for visually impaired kids

2015-01-12T05:30:00.000+05:30

To make solving numerical problems less taxing for visually-impaired students, Delhi University is developing specialised 'mathematical kits' which will make it much easier for them to study the subject. The varsity plans to carry out a campaign across the country during which students and teachers will visit various blind schools where it will distribute the kits to the students and conduct workshops to teach them how to use it.

In the second phase, after receiving feedback from various quarters, DU plans to recommend to HRD Ministry for inclusion of the tools in the curriculum.

The kits have been developed by four DU students pursuing M.Sc Maths Education in consultation with experts and two professors, Prof. Jyoti Sharma and Prof. Pankaj Tyagi.

The team conducted a survey at various blind schools in Delhi and found out that the only specialised technique available for their teaching is Braille. Few schools use audio mediums too. Madan Chaturvedi of DU's Cluster Innovation Centre mentioned to PTI that the current technology can only be helpful in teaching literature or other subjects but not maths, which is very complex. He continued that the kit has been divided into three parts. The first one contains geometry tools which include specially-designed scale, protractor, compass, and a board. Braille technology has also been used to make the tools. The second part of development includes shape-based abacus, which is different from a routine abacus. The third segment is braille designed board for multiples and factors. Apart from this, they will also include a snakes and ladders game, especially designed to suit the needs of the blind. The game will help the users get a hang of how to use other tools.

The tools have been tested by students of three blind schools, and the team plans to validate the tools by seeking feedback from a large sample size and then approach experts for advice on any room for improvement. They have also been careful about details such as the material used, the size, whether it can be used for classes, etc.

After completion of the first phase, the varsity also plans to introduce the product commercially in the market. DU, which boasts of a well-stocked Braille library, had last year installed a special technology in all its libraries to enable visually-challenged students to also access the books. The technology called 'Inclusive Print Access Project' can scan books and automatically transcribe the text to speech.

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Poor Avastin responders in AMD & DME may have increased risk to obstructive sleep apnea

2015-01-03T09:23:00.003+05:30

from Wikipedia

Poor responders to Bevacizumab (Avastin) in patients with age-related macular degeneration (AMD) and diabetic macular edema (DME) may have increased risk to obstructive sleep apnea (OSA). To read more, click here.

Nanotechnology breakthrough will lead to a better bionic eye for the blind

2014-12-25T05:59:00.000+05:30

(c) American Chemical Society

Scientists from Hebrew University of Jerusalem researchers, in collaboration with colleagues from Tel Aviv University and Newcastle University, have developed a new light-sensitive film that could one day form the basis of a bionic eye (or an artificial retina) that could help people suffering from retinal damage or degeneration.

The retina, a thin cellular layer in the back of the eye composed of light-sensitive rods and cones, converts images to electrical impulses and sends the information to the brain. Damage to the retinal cells from conditions such as macular degeneration, retinitis pigmentosa and others leads to visual impairment or even total blindness. In India, it is estimated that about 3 million people suffer from dry age-related macular degeneration (AMD), with about 10% of them (about 3,00,000) suffering from wet-type of AMD.

Scientists around the world are currently designing a variety of medical devices to counter the effects of retinal disorders by sending visual signals to the brain, usually referred to as bionic eyes. One of them, the ARGUS-II, is an approved device for use in patients with advanced retinitis pigmentosa, in the United States and in Europe. But these silicon-chip based solutions are typically hampered by their size, use of rigid parts, or requirement of external wiring such as to energy sources.

In this new study, the scientists developed a novel approach for retina stimulation, with their device being able to absorb light and stimulate neurons without using wires or external power sources. The researchers combined semiconductor nanorods and carbon nanotubes to create a wireless, light-sensitive, flexible implantable film. The film transforms visual cues to electric signals, mimicking the function of the photo-sensitive cells in the retina. Therefore, it could potentially form part of a future prosthetic device that will replace the damaged cells in the retina.

The researchers tested the new device on light-insensitive retinas from embryonic chicks and observed a neuronal response triggered by light. According to the researchers, the new device is compact, capable of higher resolution than previous designs, and is also more effective at stimulating neurons. While much work remains until this can provide a practical solution, with additional research, the researchers hope their carbon nanotube-semiconductor nanocrystals film will one day effectively replace damaged retinas in humans.

The researchers received funding from the Israel Ministry of Science and Technology, the European Research Council and the Biotechnology and Biological Sciences Research Council.

The research was published in Nano Letters.

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Eye drops for treatment of macular edema in Retinitis Pigmentosa and Usher's syndrome

2014-12-16T09:33:00.000+05:30

A study published in Ophthalmologica by researchers from the Hospital de São João, Porto in Portugal has looked at the effect of dorzolamide versus ketorolac eye drops on macular edema in patients with Retinitis Pigmentosa (RP) and Usher's syndrome (US).

A total of 28 eyes of 18 patients (5 eyes had US, 23 had RP) were studied, with 15 eyes allocated to ketorolac tromethamine 0.5% (4 drops daily regimen), while 13 eyes to dorzolamide hydrochloride 2% (3 drops daily regimen) treatment groups.

Snellen's best-corrected visual acuity (BCVA), foveal thickness (FT) and foveal zone thickness (FZT) measured by Stratus® optical coherence tomography (OCT) were evaluated at baseline, 1, 3, 6 and 12 months after treatment.

Patients assigned to ketorolac had a baseline BCVA of 0.37 ± 0.17 logMAR which improved at the end of 1 year to 0.28 ± 0.16 (p = 0.02). Three eyes (20%) of 2 patients improved by 7 letters or more. Mean FT and FZT did not change significantly during the study follow-up. After 1 year of treatment, 4 eyes (27%) of 3 patients showed an improvement of at least 16% of FT and 11% of FZT. Patients assigned to dorzolamide had a baseline BCVA of 0.48 ± 0.34 logMAR which improved in the first 6 months (0.40 ± 0.30; p = 0.01), with a decrease at 1 year (0.42 ± 0.27; p = 0.20). Seven eyes (54%) of 5 patients had an improvement of 7 letters or more. Mean FT and FZT did not change significantly either. After 1 year of treatment, 3 eyes (23%) of 2 patients showed an improvement of at least 16% on FT and 11% on FZT.

The researchers suggest that dorzolamide and ketorolac improves visual acuity in selected cases.