Cornell Scientists develop 'bionic eye'

Cornell University Researchers have dramatically boosted the performance of retinal implants by cracking a “code” that communicates visual signals to the brain.

The code consists of specific patterns of electrical pulses.

By incorporating it into their device, the scientists came close to restoring normal vision in totally blind mice lacking any light-sensitive cells.

Tests showed that the animals were able to discern facial features and track images with their eyes.

A reconstruction based on electrical signals from the implant showed recognisable features of a baby’s face.

In contrast, a standard retinal implant without the new encoder produced a confused pattern of bright and dark spots.

The results, published in the journal Proceedings of the National Academy of Sciences, could pave the way to life-changing retinal prosthetics, the scientists believe.

Even the best retinal implants currently restore only very limited vision, allowing patients to see spots of light and high-contrast edges.

The US team led by Dr Sheila Nirenberg, from Cornell University in New York, wrote: “Our results show that incorporation of the code dramatically increases prosthetic performance, well beyond what can be achieved just by increasing resolution.

“Moreover, they show that the combination of the code and high-resolution stimulation is able to bring prosthetic capabilities up to the level of normal or near-normal image presentation.”

Scientists around the world are exploring the potential of retinal implants to help people with degenerative blinding diseases such as retinitis pigmentosa.

More than 20 million people around the world are blind or at risk of blindness due to the diseases. Typically, they destroy the light-sensitive photoreceptors of the retina but leave nerve connections intact.

By replacing natural photoreceptors with artificial ones, it is hoped that some degree of sight can be restored. However, results to date have been disappointing. Although some sight can be restored, serious visual impairment remains.

The new study shows that boosting resolution - effectively the number of “pixels” the eye can see - is not enough on its own. For the image to be relayed successfully to the brain, the light signals must first be translated into the right patterns of electrical impulses.

Retinal Ganglion cells, a type of nerve cell within the retina, are responsible for communicating the visual messages.

In congenitally blind mice fitted with the new implant, the ganglion cells fired correctly almost 90% of the time, said the scientists.

Behavioural and eye-tracking experiments suggested that a high level of vision had been restored to the mice.

In one striking test, an image of a baby’s face was reconstructed from the “spike trains” - electrical signals - produced by blind mouse retinas with standard and encoder implants.

Features that could not be seen at all in the “standard” reconstruction were clearly visible from the new implant.

“Not only is it possible to discern that the image is a baby’s face, but also it is possible to tell that it is this particular baby,” the scientists wrote.

They concluded: “In sum, our results show that incorporating the code dramatically increases prosthetic capabilities. Although increasing resolution also improves performance, there is an inherent ceiling on the quality of image this can produce; adding the code breaks through this barrier. The coded output combined with high-resolution stimulation makes natural vision restoration possible.”

Dyslexia, Blindness and braille?

1) Can a person who reads Braille visually be dyslexic?
2) Can a person who reads Braille by touch be dyslexic?
3) Can a person who is written-language dyslexic also be dyslexic in Braille?
4) Will a person who is written-language dyslexic necessarily be dyslexic in Braille?

The answer to questions 1-3 is an unqualified yes. The answer to 4 is extremely complicated.

Dyslexia is a processing disorder and has, in theory, nothing to do with vision. A dyslexic reader does not "see" words incorrectly. The eyes correctly capture the information, but somewhere in the brain the information is "decoded" (or recoded) improperly, resulting in inaccurate phonological signals.

The stereotypical backwards letters or misordered letters (a symptom that actually occurs in only a very small percentage of dyslexics) is a symptom of incorrect language decoding, not visual decoding. In fact, dyslexia may be more commonly associated with auditory processing issues than visual ones.

This means that a person can in fact be "Braille dyslexic". The same coding and decoding difficulties that impede reading in English could impede coding and decoding of language in Braille.

This applies regardless of whether the Braille is processed visually or by touch. Once the brain is trained to recognize a symbol as language, whether that language is the Latin alphabet, Japanese logograms, or Braille patterns, there is a potential for improper coding and decoding.

Some people even experience dyslexia issues with fingerspelling in sign language. On the other hand, non-linguistic signals are unaffected, so a dyslexic person is unlikely to have difficulty recognizing pictures of things and properly identifying them. (Because dyslexia is often an underlying cause of, or accompanied by, aphasia and other speech disorders, it can create the impression of a visual disorder where there is none.)

Here is where it gets complicated; because there is no identifiable "language centre" of the brain, language processes are distributed across different sections of the brain. It is unclear exactly "where" and how the processing issues associated with dyslexia arise.

What we do know, is that dyslexia is not an "across the board" disorder,difficulty with one language does not imply difficulty with all languages. Orthographically "deep" languages, which have complex and varied relationships between letters and phonemes, such as English, pose different problems from those in orthographically "shallow" languages, which have more straightforward and consistent relationships between letters and phonemes, such as German, which are in turn different from logograms, where images, or graphemes, are not related to phonemes.

Dyslexia can occur in any, or all, or any combination, but difficulty in one does not necessarily imply difficulty in all. A language that takes advantage of a different "pathway" might "route around" the processing disorder, or it might be affected by it to a different, greater or lesser degree.

Braille, however, is not a "different language". Braille is a different script, but basic "uncontracted Braille" is a transliteration of the written language (let's assume for the moment we are talking about English).

In Braille, the pattern for a corresponds to the letter a, the pattern for b corresponds to the letter b, etc. Since dyslexia is not a visual disorder but rather a disorder in the coding / decoding of the linguistic patterns themselves, it is highly likely that the same linguistic difficulties would be encountered. That is, inputting the same letters by a different sense is unlikely to "route around" the coding malfunction.

Contracted Braille
That would be too easy an answer, though, so here's another wrinkle: most Braille texts are not printed in "uncontracted Braille". Because Braille is not nearly as compact as the written Latin alphabet, most Braille uses a set of contractions, substituting letters and letter combinations for words and letter combinations.

Contracted Braille has single-character contractions for letter combinations such as "sh" and "ch" and even some words such as "and" and "but". Additionally, longer words are frequently significantly contracted, such as "ll" for the word "little" and "xs" for "itself". So even though English Braille is in fact the English language, many words are spelled differently in printed Braille.

There are three "grades" of Braille spelling: Grade 1, uncontracted (a direct transliteration of English spelling); Grade 2, contracted (a large number of contracted spellings); and Grade 3, shorthand (an extremely contracted version used as shorthand, much like journalistic shorthand).

It is unlikely that contracted Braille would "route around" all of a dyslexic's processing problems. It could, however, mitigate some of them or it could actually exacerbate them by adding even more orthographic depth. In addition, because dyslexics often develop coping mechanisms to mitigate their own processing problems, learning Braille might pose difficulties related to a dyslexic's secondary functions, not the actual coding and decoding itself.

So here is the part where your particular question is important. If you just need to know whether a character could be dyslexic in Braille because you want to write a dyslexic Braille reader into your story, the answer is definitely, Yes.

If your character normally reads standard written English and is learning to read Braille, and you want to know how the dyslexia would translate over, it's not really clear.

It could mitigate the condition; if your character is only mildly dyslexic, this could be a huge advantage, although for anything other than only borderline dyslexia it is unlikely to mitigate it entirely.

Or the dyslexia could be just as bad, or even worse, in the new writing system. On the other hand, the process of learning to read Braille could provide the dyslexic character with some new coping strategies that allow him to function at a higher level.

Stargardt Disease: The Leading cause of Macular Degeneration in childhood Blidness

Stargardt disease is a rare yet life devastating condition. It is the most common form of inherited macular degeneration, and affects about one in 10,000 people (about 30,000 people in the United States).

There is currently no cure or treatment for Stargardt disease but clinical trials using gene and cell therapies are currently undergoing.

Patients with Stargardt most often start experiencing significant vision loss during their childhood and teenage years (60% of the patients are diagnosed before 20 years of age).

This vision loss cannot be corrected by glasses, and diagnosis had been traditionally delayed due to the young age of the patients and the rareness of the disease.

After diagnosis, and depending on age at onset, vision deteriorates progressively to levels below 20/200 (legal blindness).

The disease affects mostly the central vision and spares some of the peripheral vision, although there are very severe forms that lead to complete blindness.

Almost all of those affected by Stargardt disease will live legally blind during their adult lives, although patients with late onset may retain some visual acuity.

Loss of central vision leads to impossibility to perform tasks such as reading, writing, driving or recognizing faces.

In 1997, scientists discovered that Stargardt disease results from a defective gene, the ABCA4, responsible for the synthesis of an important protein called Rim protein.

A normally functioning Rim protein transports vitamin A molecules from the photoreceptors (the molecules sensitive to light) back into specialized cells (called RPE), where vitamin A molecules are recycled to be reused for vision.

In Stargardt, the defects in the ABCA4 gene lead to partial or full dysfunction of this protein. As a result, vitamin A transport is affected and vitamin A molecules tend to accumulate in the photoreceptors.

This accumulation leads to the formation of toxic pigments (known as "vitamin A dimers") believed to be partly responsible for vision loss.

Although normal individual also form vitamin A dimers, this process usually takes decades, explaining why age-related macular degeneration (AMD) occurs later in life of normal people, while the same process takes only a few years in Stargardt explaining vision loss from childhood.

Read more of this article here at Alkeus - Stargardt disease

BrailleTouch App: Helps blind to send text messages

Researchers at Georgia Tech produced the app - to be made available on Apple and Android devices - based on the Braille writing system.

It is claimed typing with the app is up to six times faster than existing methods for texting without sight.

Access to technology for the visually-impaired is a growing issue due to the proliferation of touchscreens.

Experts say currently available tools, such as Apple's Voiceover technology, are functional but too slow to be used effectively.

Brailletouch, which the team hope to release in the next couple of weeks, uses a system that is controlled with six fingers and, crucially, does not require any movement of the hands.

"Users who know how to type Braille well never move their hands," explained Mario Romero, lead researcher on the project.

"When users hold the phone they hold the phone with the screen facing away from them in landscape mode.

"They wrap the index, middle and ring finger in each hand around the phone.

"It's not like the Qwerty keyboard where you move up and down. That's why this thing works - we can get away with only six keys."

"This is not for texting and driving” Mario Romero Lead researcher

Eyes-free kit

Brailletouch will be free and open-source, its makers say, and it is hoped it could even become an "eyes-free" solution for fully-sighted people who want to text while visually pre-occupied with something else.

"Learning to type Braille is learning to memorise where the the dots fall," Mr Romero said.

"It took me and my colleagues a few hours to memorise things so we could start typing at around 10 words per minute. It's not something that takes years.

"We're hoping that, if not Braille, a similar system may solve the issue of having too many keys that are too small that force everybody to look at the screen when they're typing."

However, Mr Romero was quick to dampen any possible hopes that the software could be used to text while behind the wheel.

"They need to concentrate on what they're doing. This is not for texting and driving," he said.

'Truly blind'
Mr Romero highlighted a growing anxiety shared among the blind community that the widespread adoption of touchscreens for many machines and devices is making them "truly blind".

"There is extreme concern about this new trend.

"A lot of equipment today - from copying machines to machines at the gym - is all coming with touch screens."

He added that while research into tactile screens, which give users feedback by moulding, is taking place, we are still some way from having touchscreens which adequately cater for the visually-impaired.

"Blind people say I 'see' things with my fingers," Mr Romero said.

"But on touchscreens they are truly blind."

Seeing Things That Aren’t There? Charles Bonnet Syndrome

One woman saw a fully dressed Royal Canadian mountie in her living room. Another saw the same red brick building in every part of town, as well as in the country. One man saw monkeys with red hats and blue coats playing in his yard.

They were all experiencing Charles Bonnet (“bo-nay”) Syndrome.

“Do you ever see something you know is not there, but it looks real?” It’s a question that Lylas G. Mogk, M.D., and Raman Deol, O.D., of the Henry Ford Center for Vision Rehabilitation and Research in metropolitan Detroit, always ask their low-vision patients.

Low vision that cannot be improved through corrective lenses or surgery can be the result of macular degeneration, glaucoma, diabetes, stroke, or other causes.

Some of their patients respond that they see purple flowers everywhere, even in winter. Others see animals, people, buildings, or geometric, quilt-like patterns. They rarely share their experience with their families, for fear of being misunderstood. Some wonder whether the visions suggest early dementia.

In 1789, Swiss naturalist Charles Bonnet described the visions of his father-in-law, who had low vision and saw people, animals and other objects that he knew were not real.

Bonnet himself experienced phantom visions later in his life, similar to those of his father-in-law. Bonnet’s discovery went largely unnoticed for 150 years until the 1930s, when doctors rediscovered his files and named the syndrome after him.

The frequently undiagnosed Charles Bonnet Syndrome is very common, affecting 20 – 30 percent of those with low vision. Some may experience it for a few months, others for several years.

The images can occur daily or only occasionally, with the same image appearing to the same person. There is no cure, but most people are not bothered by the images, and many find them interesting or amusing, especially once they understand it’s just their eyes playing tricks on them.

Although the cause is not known, the images can be compared to the “phantom pain” that can be felt by people who have had a limb amputated.

The nerves that were connected to the missing limb still send signals to the brain. In our visual system, the nerves no longer receiving visual messages can cause the brain to “see” realistic images, while recognizing they are not real.

Many physicians are not yet aware of Charles Bonnet Syndrome, and may mistake it for psychotic hallucinations. Patients with the syndrome have been misdiagnosed and prescribed anti-psychotic medications.

To identify Charles Bonnet Syndrome, ophthalmologists use these criteria:
• The person has low vision.
• The images occur when the person is conscious, with open eyes.
• The person recognizes the images are not real.
• The same image appears repeatedly, superimposed on the real world. For example, the person sees a room normally, but the wall appears to have flowers on it and only that same image of flowers recurs to that same person.
• Images are only visual; they may move, but there are no sounds or smells. It’s like seeing a picture, or watching a silent movie.
• Images are common, familiar objects. They may be amusing or mildly annoying, but not frightening.
People with low vision who believe they may be experiencing Charles Bonnet Syndrome should discuss it with their ophthalmologist.

Gene Therapy Researchers develop correction for blindness

A new gene therapy method developed by University of Florida researchers has the potential to treat a common form of blindness that strikes both youngsters and adults. 

The technique works by replacing a malfunctioning gene in the eye with a normal working copy that supplies a protein necessary for light-sensitive cells in the eye to function. The findings are published today (Monday, Jan. 23) in the Proceedings of the National Academy of Sciences online.

Several complex and costly steps remain before the gene therapy technique can be used in humans, but once at that stage, it has great potential to change lives.

"Imagine that you can't see or can just barely see, and that could be changed to function at some levels so that you could read, navigate, maybe even drive — it would change your life considerably," said study co-author William W. Hauswirth, Ph.D., the Rybaczki-Bullard professor of ophthalmology in the UF College of Medicine and a professor and eminent scholar in department of molecular genetics and microbiology and the UF Genetics Institute.

"Providing the gene that's missing is one of the ultimate ways of treating disease and restoring significant visual function."

The researchers tackled a condition called X-linked retinitis pigmentosa, a genetic defect that is passed from mothers to sons. Girls carry the trait, but do not have the kind of vision loss seen among boys.

About 100,000 people in the U.S. have a form of retinitis pigmentosa, which is characterized by initial loss of peripheral vision and night vision, which eventually progresses to tunnel vision, then blindness.

In some cases, loss of sight coincides with the appearance of dark-colored areas on the usually orange-coloured retina.

The UF researchers previously had success pioneering the use of gene therapy in clinical trials to reverse a form of blindness known as Leber's congenital amaurosis. About 5 percent of people who have retinitis pigmentosa have this form, which affects the eye's inner lining.

"That was a great advance, which showed that gene therapy is safe and lasts for years in humans, but this new study has the potential for a bigger impact, because it is treating a form of the disease that affects many more people," said John G. Flannery, Ph.D., a professor of neurobiology at the University of California, Berkeley who is an expert in the design of viruses for delivering replacement genes. Flannery was not involved in the current study.

Aiding the Blind: Kinecthesia - Oct 2011 - YouTube

Two Students from the University of Pennsylvania have modified a Kinect to help the vision impaired to become more aware of their environment. The project is called Kinecthesia and functions as a radar-like device, but instead of using sound, the device uses the Kinect's cameras to map out the environment and translate it into a sensation the blind can understand.

Eric Berdinis and Jeff Kiske, juniors of the University of Pennsylvania majoring in Computer Engineering, has garnered attention in the 2011 Google's Zeitergeist Young Minds Conference with their application of the gaming peripheral. The project was born from both student's final project for Rahul Mangharam's embedded systems class. The resulting device can be likened to a high-tech walking cane.

The Kinect is a motion detecting gaming peripheral produced by Microsoft. The device is used for the Xbox 360 which can interpret specific gestures and track movement of individuals or objects. The device is composed of an RGB camera, an infrared sensor acting as a depth sensor and multiple-array microphone. It can perform facial recognition, voice recognition and gesture recognition.

Using the Kinect's multiple cameras, Berdinis and Kiske have made a harness that produces vibrations to notify the wearer of coming obstacles. The Kinect is connected to a BeagleBoard, a whole computer in a single board, and fitted in a waistband or belt. The device is ran in Linux and 16 AAA batteries. Since it was still in development the device is not made to run for hours. There are six vibrating motors to guide the user and weighs 1349g as of now.

There are already a number of people hacking their Kinect devices for other applications besides gaming like 3D modeling, controlling robots and using motion capture to automate devices, augment reality, and even produce a low-budget CGIs for amateur movies. Remember the movie Total Recall with the virtual wife? It would be a surprise if no one made one already. The Kinect has made motion capture reachable to consumers and they are very much willing to experiment.

It is great that people are experimenting and applying on technologies readily available for them. Will this open doors on new innovators? Does Microsoft see a new market for their devices?

The project's development can be tracked on their own website at kinecthesia.com. The website also contains the project source code, parts list and assembly instructions.

Daily drug restores sight to hereditary blind

A hereditary form of blindness has been delayed or reversed for the first time by a daily drug treatment. The drug is the first to benefit people with a disease of their mitochondria, the energy powerhouses of cells.

There had been no way to halt the rapid onset of blindness in people with the most common mitochondrial disease, called Leber's hereditary optic neuropathy. It strikes men in their twenties, leading to total blindness within three to six months of the first symptoms appearing.

But after receiving a drug called idebenone for six months, some people whose sight had begun to deteriorate reported drastic improvements in their vision that continued after the trial ended.

In the trial, 55 people received idebenone and 30 were given a placebo. After six months, 11 people who received idebenone could read an extra two lines on a standard vision chart – and nine people who could not read any letters at the outset could by the end.

"This is not a cure, but it's a significant effect," says team leader Patrick Chinnery of Newcastle University in the UK.

Successful treatment

It is also the first time that an inherited mitochondrial disease has been successfully treated. "This trial tells us there's hope for this and other mitochondrial diseases," says Chinnery.

The drug didn't work for everyone. The beneficiaries were those who, at the outset, had better vision in one eye than the other. Chinnery thinks this disparity means the disease is only just beginning to progress, and so is more treatable.

The disease strikes retinal ganglion cells that connect the light-sensitive cells of the retina to the brain via the optic nerve. Damage results from failure of mitochondrial enzymes to deliver electrons efficiently through the chain of reactions that generate energy. Idebenone is thought to deputise for these defective enzymes.

Chinnery says there were no serious side effects to the drug, and suggests that if carriers of the mutations can be identified through genetic testing, it might be possible to prevent blindness by giving the drug before symptoms develop.

He adds that it may be possible to use idebenone to treat other mitochondrial diseases. One possible candidate is Melas syndrome, a disorder resulting from defects in the ability of mitochondrial enzymes to clear lactic acid "waste" from cells, leading to brain swelling, heart and muscle weakness and a variety of other symptoms.

"It's a great first step, and the suggestion that some patients benefit justifies further trials," says Robin Ali of University College London, who is head of an ongoing gene therapy study in 12 people with Leber's congenital amaurosis, a non-mitochondrial congenital form of childhood blindness.

Journal reference: Brain, DOI: 10.1093/brain/awr170

'Sighted' wheelchair for the Blind

The introduction of the white cane early in the last century gave blind and visually-impaired users a mobility tool that not only helped them to get around, but also allowed them to be seen by others.

Now researchers from Sweden's Luleå University of Technology – the same place that designed the autonomous wheelchair – have developed and publicly tested a system which could potentially give wheelchair-bound blind people a virtual white stick to help them detect and avoid obstacles.

An electric wheelchair has been fitted with a navigational laser scanner which provides virtual 3D maps of the surroundings, and sends feedback about any obstructions to the user via a haptic interface.

Using the time of flight technique, a pioneering navigational laser scanner developed by professor Kalevi Hyyppä of the University's EISLAB sweeps the area around the wheelchair to produce a virtual 3D map of the surroundings.

This information is sent to a haptic interface, which allows the user to "see or feel" obstacles such as open doors, or pedestrians, and use the joystick to navigate past them without so much as a bump.

The first public test run was undertaken by the project's prospective PhD student Daniel Innala Ahlmark (who is himself visually-impaired), along one of the busy corridors of the University's Computer Science, Electrical and Space Engineering Department. He remarked afterward that he felt safe when using the system, and that it was just "like using a white cane."

The team – which also includes assistant professor Håkan Fredriksson and PhD student Fredrik Broström – admits that there are a few limitations to overcome before such a mobility tool could go into commercial production.

The current laser scanning system, for instance, cannot register anything above and below the beam, so plans are underway to develop a 3D camera that will be able to produce multi-level virtual maps.

It is estimated that a more sensitive, production-ready system could be available within the next five years.

New Brain Structure Explains Willful Blindness

The article in today's NYT by Nancy Koehn titled “Why Red Flags Can Go Unnoticed” was chiefly concerned with the effects of willful blindness in humans. It did not answer the primary question: WHY do people ignore clear warnings of impending problems.

Bruce Nappi, in his new novel LIARS! provides a profound explanation: two human species coexist on earth today, and one of them is not able to broadly understand or apply logical reasoning, and no, it's not males and females!

The new discovery came when he first determined what creates consciousness in the human brain. Step one was recognising a new physiological brain model that revises Sigmund Freud's Id, ego and super-ego brain structure.

The second was sorting out what makes humans different from animals. In fact, contrary to common belief, that difference does not occur at the homo sapiens level but further back down the evolutionary tree. Differences in awareness for humans and animals are described and labeled A2 and A1 respectively, but, the characteristics listed for humans (A2) raised a big problem: they didn’t describe all known human abilities.

He categorised the additional abilities with a new label A3. The implication was both amazing and unsettling! Both A3 and A2 had human traits, but they were as distinct as A2 (humans) and A1 (animals). The solution required that each be considered a different species - amazing for sure.

However, if the discovery was true, it would have huge ramifications for human social structures. He tested the theory against more and more of the great social questions. The new A3 model produced so many logical answers that he is convinced he has stumbled onto a profound discovery.

New Brain Structure Explains Willful Blindness In Humans And Why Red Flags Go Unnoticed

Mobile Accessibility for Poorly Sighted - Demo UK - Android Market

This application has been designed for people who are blind or partly sighted but it could equally work with people with word or number blidness.



Mobile Accessibility Demo UK - Android Market

This application has been designed for people who are blind.

This is a fully functional 30 days evaluation version of Mobile Accessibility.

Mobile Accessibility is a screen-access application which allows people who are blind or have low vision to use an Android phone in an intuitive, easy and simple way.

Mobile Accessibility is two products in one:

- It is a suite of 10 accessible applications (Phone, Contacts, SMS, Alarm, Calendar, Email, Web, Where am I, Apps and Settings) which have been especially designed for the blind and visually impaired. They all have a simplified interface whose textual information is spoken using Nuance Vocalizer® voice synthesis.

- It is also a screen reader which allows you to get out of the suite and navigate the standard interface of your phone.
Please note that if you want to use the screen reader functionality of Mobile Accessibility you will need a phone with physical navigational controls such as a trackball or trackpad.

Inside the Mobile Accessibility suite of accessible applications you can do the following:

- Phone: Make calls, answer calls, hear the caller ID and manage your call log.
- Contacts: Manage your contacts, even those from social networks such as Facebook.
- SMS: Compose and read short messages. Manage conversations.
- Alarms: Set your alarms.
- Web: Full web browser experience, similar to what you can find on your PC. Jump by the control of your choice (links, paragraphs, headings, forms, etc.) to navigate faster to the information of your interest. Bookmark your favourite webpages.
- Calendar: Create, edit and delete a calendar entry. View all events per day, week or month.
- Email: Full access to your Gmail account.
- Where am I? : GPS application that gives you updates on your current location.
- Apps: Access the list of apps installed on your Android phone.
- Settings: Change ringtone. Configure feedback and notifications (vibration or audio). Configure keyboard echo, punctuation verbosity, speech pitch and rate, etc.
- Quick access to date and time, phone status information such as battery level and network coverage, number of missed calls and unread messages, etc.

Main Highlights:

- Touch navigation: You can use Mobile Accessibility not only with the trackball or the physical keyboard of your phone, but also with its touchscreen! Simply move your finger around the screen and the voice synthesis will read the text located under your finger. Or if you prefer, you can also swipe up/down/right/left and tap on the screen to navigate through the interface. And if you wish you can enable sound and vibration feedback.

- Easy to input text: In or outside the Mobile Accessibility suite you can use the touch qwerty keyboard as well as the speech recognition to write text quickly and easily. Imagine writing an SMS or an Email using your voice only... just great!

- Voice synthesis: Code Factory has been making mobile phones accessible to the blind and visually impaired for many years now, and we know that the voice matters... and a lot! For Mobile Accessibility Code Factory has partnered with Nuance® and Vocalizer® is therefore the voice of Mobile Accessibility.

Leading cause of blindness identified - Age-related macular degeneration (AMD)

The mechanism behind a leading cause of blindness has been discovered, which could result in new treatments for a disease that causes 50 per cent of all blindness in the western world.

Age-related macular degeneration (AMD) is caused by damage to the macula – part of the retina at the back of the eye – and is thought to be linked to alterations in the gene resonsible for CFH, a protein involved in the body's immune response.

To work out how this might cause AMD, Paul Bishop at the University of Manchester, UK, and colleagues applied normal and diseased forms of CFH to macula obtained from donated eyes. Abnormal CFH seemed unable to bind to the macula, probably as a result of not being able to bind to two specific carbohydrates.

If there is not enough functional CFH bound to the macula, the immune system does not recognise the tissue as its own and so will attack it, says Bishop. "Now that we know the mechanism, we can think about treatments, such as injecting CHF into the bloodstream."

First human trials for stem cell blindness therapy

The pioneering treatment could help people losing their sight due to Stargardt, a currently untreatable disease that is one of the most common forms of youth blindness

Photo: GETTY

The first human trials of a stem cell therapy for an eye disease that causes blindness in young people could start next year (2010).

The pioneering treatment could help people losing their sight due to Stargardt, a currently untreatable disease that is one of the most common forms of youth blindness.

Studies on rats and mice have found that the therapy prevents further vision loss without adverse side effects, and the firm behind the breakthrough has now applied to US authorities to test it on humans.

The treatment would consist of a single injection of retinal cells derived from embryonic stem cells left over from IVF treatment.

"After years of research and political debate, we're finally on the verge of showing the potential clinical value of embryonic stem cells," said Robert Lanza, the chief scientific officer at Advanced Cell Technology, the firm which developed the therapy. "The field desperately needs a big clinical success."

The trials would involve 12 Stargardt patients currently losing their sight, and could begin early in 2010 if the Food and Drug Administration grants approval.

Embryonic stem cell research has been controversial because human embryos are destroyed in order to obtain the cells capable of developing into almost every tissue of the body but it also holds great promise for treating cancer, diabetes, Alzheimer's and other diseases.

Gene therapy cures colour-blind monkeys - health - New Scientist

Gene therapy cures colour-blind monkeys - health - 16 September 2009 - New Scientist

Two colour-blind monkeys nicknamed Dalton and Sam have been "cured" through gene therapy.

The breakthrough could be a prelude to new gene treatments for human vision disorders that currently result in blindness. And because the treated monkeys were "middle aged", it challenges the assumption that gene therapies cannot work in adults because their brain connections are too set in their ways to change beneficially.

A human gene injected into the monkeys' eyes enabled them for the first time to produce Clong-wavelength opsin" the pigment sensitive to red and green light. "That gave them a retina like that of a normal person with full colour vision," says Jay Neitz at the University of Washington in Seattle.

The team used squirrel monkeys because the males are known to be colour-blind, whereas females have full colour vision. Males do have a full set of colour-sensing "cone" cells in their eyes, but they only make pigments for detecting blue and yellow light, making them blind to red and green.

Shared via AddThis

Vision through Retina Implants

The Argus II is a minuscule artificial eye that attaches to the retina via 60 electrodes. Stephen Rose, chief research officer at the Foundation Fighting Blindness, says it has “great potential for giving vision to people with the most advanced retinal disease.” With the second phase of human trials underway, expect production models this year.