Wednesday, January 27, 2010

Google has a search engine specifically for those with Low Vision

Did you know google had a search page for those with low vision?  It is only in its preliminary stages but it could be helpful.  It responds to hot keys, magnifies the results you have selected, and beeps when you change the focus on the page.

Give it a try

Google Accessible Web Search for the Visually Impaired

Friday, January 22, 2010

Should your eye doctor sell supplements?

This article raises a good point.  Doctors should not be in the position of selling you products.  And supplements benefits are inconsistent at best.  Here is an excerpt from the article.

There's something fishy about this, besides the fish oil, in my opinion. If a doctor wants to suggest that this product may help, show me the research and tell me that I can buy it in places besides your office. I later discovered that a similar formula with Lutein, Zeaxanthin and fish oil is available at Sam's Club for half the cost. I suspect it's available at any retailer that sells a lot of supplements and vitamins.

What do you thing?  Click the title for the full article.

Thursday, January 21, 2010

Brian Mckeever will compete and make history!

I posted earlier that Brian Mckeever was attempting to compete in both the Olympic and Paralympic games this winter.  Well it is now official he has quallified to be a part of the Canadian Cross Country Olympic team.  Brian is 30 years old and suffers from Stargardts disease.  Here is an excerpt from the article.


The 30-year-old Canmore, Alta., resident will be selected to Canada's Olympic cross-country ski team on Friday, making him the first athlete to compete at both the Olympic and Paralympic Winter Games.

Mr. McKeever, who suffers from Stargardt's disease and is legally blind, stamped his double pass to Whistler by winning an able-bodied 50-kilometre Haywood NorAm race last month in Canmore. The race was one of four Olympic trials established by Cross Country Canada.

We'll be rooting for him, (even though he's Canadian).

Click the title for the full article.

Low vision aides show to have a drastic difference in reading speeds

I know it sounds obvious but reading the numbers is interesting to me.  Here is the short article.


Low vision aids can significantly improve reading speed and reading ability in patients with age-related macular degeneration, but better overall visual acuity still correlates with better reading ability.
According to a retrospective study of 530 patients with AMD who were provided either optical visual aids or closed-circuit TV systems as a low-vision aid, the added magnification of the system helped improved words read per minute.
For the entire group of patients, mean reading speed improved from 20 ± 33 words per minute (wpm) to 72 ± 35 wpm. However, among patients with a visual acuity less than 0.1, reading speed improved from 0.4 ± 3.8 wpm to 40 ± 13 wpm compared with 20 ± 28 wpm to 84 ± 30 wpm among patients with a visual acuity score of 0.1 or better.
Still, in the study, low vision aids had a marked impact on reading ability: Only 16% of patients were able to read before receiving a low vision aid compared with 94% after.

Click the title for full story

Wednesday, January 6, 2010

Macular Degeneration Cause discovered on a molecular level

Researchers at University College London have discovered the chemical proccess that causes Macualr Degeneration.  They state it is caused by the interaction of two protiens blood protein Factor H, and C-reactive protein.  These proteins work together to clear out the debris of dead cells in the retina, but if the levels are not optimal or if someone has a genetically different form of Factor H then dead cells are not cleaned up properly and for a deposite called drusen.  These deposits take the place of new cells and also restrict the bloodflow to neighboring cells causing them to die.  At least that is how I understood it.  here is the article in full.

Researchers at University College London say they have gleaned a key insight into the molecular beginnings of age-related macular degeneration, the No. 1 cause of vision loss in the elderly, by determining how two key proteins interact to naturally prevent the onset of the condition.

In a paper to be published in a forthcoming issue of the Journal of Biological Chemistry, the team reports for the first time how a common blood protein linked to the eye condition reins in another protein that, when produced in vastly increased amounts in the presence of inflammation or infection, can damage the eye.

"By starting to understand these interactions in greater detail, we can begin to devise methods that will ultimately prevent the development of blindness in the elderly," said Zuby Okemefuna, the lead author of the paper to be published Jan. 8.

Age-related macular degeneration, or AMD, is painless but affects the macula, the part of the retina that allows one to see fine detail. One form of the debilitating condition, known as "wet" AMD, occurs when abnormal and fragile blood vessels grow under the macula, leaking blood and fluid and displacing and damaging the macula itself. The second form, "dry" AMD, occurs when light-sensitive cells in the macula slowly break down.

It is believed that both forms start on a common molecular route and then deviate into dry or wet AMD, explained the research leader, Steve Perkins.

"The earliest hallmark of AMD is the appearance of protein, lipid and zinc deposits under the retinal pigment epithelial cells," he said, adding that the yellowish deposits, usually discovered by an ophthalmologist, are commonly known as "drusen."

The researchers studied two proteins involved in drusen formation -- blood protein Factor H and a second blood protein known as C-reactive protein -- and showed that Factor H binds to C-reactive protein when C-reactive protein is present in large amounts, as in the case of infection, to reduce the potentially damaging effects of an overactive immune system.

"In the eye, during the normal processes of aging, cells will die naturally for all sorts of reasons," Okemefuna said. "The blood supply to the eye will bring C-reactive protein with it, and a low level of C-reactive protein activity will enable the normal processes of clearance of dead cells at the retina through mild inflammation. In conditions of high inflammation, the levels of C-reactive protein in the retina will increase dramatically."

Uncontrolled C-reactive protein activity causes damage to the retina, which is followed by more inflammation and then even more damage to the retina, and so forth.

"It's the debris of broken up retinal cells, some of which is caused by this cycle, that is deposited as drusen," Okemefuna said.

The team also found that a genetically different form of Factor H does not bind to the C-reactive protein quite as well as the normal one, making people who carry the modified protein more vulnerable to an immune system attack in the eye and, thus, drusen buildup.

"In normal individuals, further damage to the retina by prolonged exposure to high levels of C-reactive protein is prevented by Factor H. C-reactive protein also prevents Factor H from clumping together and initiating the processes that lead to drusen formation," Perkins said. "Both these 'good' activities of Factor H are much reduced in the genetically different form of Factor H."

While there is no known cure for AMD, existing therapies aim to treat the symptoms and delay progression.

"It is interesting how the interaction of these two blood proteins protects the eye during crisis," Perkins said. "The two proteins also can be involved in a rare and often fatal cause of kidney failure in children. We now are better positioned to begin to work out preventative strategies for these diseases."

Ruodan Nan, Ami Miller and Jayesh Gor also were co-authors on the study, which was funded over the past three years by University College London, the Biotechnology and Biological Sciences Research Council, the Mercer Fund of the Fight for Sight Charity and the Henry Smith Charity.

Click the title to read the full article.