A study conducted by Johnson & Johnson Vision Care has measured, for the first time ever, a coefficient of friction value on human corneal donor tissue.

 

The coefficient of friction is dependent on the type of buffer solution, but may not be dependent on donor age or on the time of death when measuring fresh corneal tissue, according to the study.

 

The study found that the coefficient of friction were 0.0134 in tear-mimicking solution, 0.0060 in tear-mimicking solution with phosphate buffer saline solution, 0.0144 in tear-mimicking solution with HEPES buffer and sodium chloride and 0.0153 in tear-like fluid with phosphate buffer saline solution.

 

“Now that we’ve measured the coefficient of friction value, additional investigation into the frictional behaviour of cornea tissue and its relation to contact lenses can be studied,” says Dr. Tawnya Wilson, principal research optometrist at VISTAKON^®. “This knowledge will ultimately lead to the development of better contact lenses that can mimic corneal properties and that can address end-of-day comfort for our patients.”

 

Source:

www.jnjvc.com

 

Researchers from Germany recently discovered the activation mechanism of one of the proteins that protect the eye against cataracts, laying the foundation for the development of new therapies.

 

The refractive power of the human eye depends on a highly concentrated protein solution. Two proteins in particular, ɑA-cristallin and ɑB-cristallin, ensure that other proteins do not turn into clumps over time. When this protective mechanism fails, the patient develops a cataract. 

 

“The great challenge in the analysis of these two crystallin types lies in their inordinate variety,” explains Johannes Buchner, professor for biotechnology at the Technical University of Munich. “These proteins exist as a mixture of very different forms, each comprising a variable number of subunits. This makes it very difficult to distinguish the individual structures from one to the other.”

 

In 2009, the German team had deciphered part of ɑB-cristallin, a molecule comprising 24 subunits, but found that in its idle form, it contributes little to the protection of the eye. It needed a trigger mechanism to activate it. This mechanism has now been uncovered.

 

These new insights provide a solid foundation for developing new therapeutic approaches. For instance, medication to treat cataracts could activate ɑB-cristallin, which would be in charge of clearing up cloudy lenses. This could eventually replace the need for surgery.

Source:

http://www.sciencedaily.com/releases/2013/10/131023141130.htm

 

Just 13 days in space may be enough to cause profound changes in eye structure and in the expression of some genes, according to researchers from the United States.

 

The study looked at how low gravity and radiation and oxidative damage affect mice after time spent in space. This study is the first to examine eye-related gene expression and cell behaviour after spaceflight.

 

“We found several changes in the expression of genes that help cells cope with oxidative stress in the retina, possibly caused by radiation exposure,” said Patricia Chévez-Barrios, the study’s principal investigator. “These changes were partially reversible upon return to Earth. We also saw optic nerve changes consistent with mechanical injury, but these changes did not resolve. And we saw changes in the expression of DNA damage repair genes and in apoptotic pathways, which help the body destroy cells that are irreparably damaged.”

 

The damage to the eyes is a problem for some astronauts back on Earth. It could also make it difficult for them to complete long missions, such as round-trip travel to Mars (12 to 16 months) or to the moons of Jupiter (two years). “We don’t know if damage caused by longer periods of oxidative stress will be more severe. Only more studies with longer exposure times may help answer this question.”

Source:

http://www.sciencedaily.com/releases/2013/10/131024121156.htm

 

The company which pioneered electronic focusing eyewear emPower has just announced it is filing for Chapter 7. According to information publicly disclosed, PixelOptics ran into severe financial difficulties several weeks ago and burdened with significant debt, has exhausted all of its options to remain viable.

 

The Canadian company Aspex Eyewear was a partner of PixelOptics in this endeavour both as a manufacturer and exclusive distributor of the eyewear which was never distributed in Canada.

 

The first-ever electronic focusing eyewear emPower attracted worldwide attention when it was launched in the US in 2011. However, in mid-2012, problems with robustness of the first-generation emPower were encountered and the company stopped distributing them last March after having sold, it seems, approximately 1 000 pairs. The company developed a second generation, but was unable to commercialize it due to its financial situation.

 

A number of key employees left the company in the past few weeks including Brett Craig, a former president of Transitions Optical.  

 

The company closed its doors last Friday. The court will appoint an executor who will oversee liquidation of the company’s assets, most notably an intellectual property portfolio of over 400 patents and patent applications, many of which involve electronic focusing eyewear.

 

Researchers from the University of Pennsylvania took their first step toward a gene therapy that could prevent vision loss or even restore vision in individuals suffering from Best disease.

 

Also known as vitelliform macular dystrophy, the hereditary disease affects one in every 10,000 people. It especially affects children and young adults, and can cause severe central vision loss.

 

“Step one in designing a gene therapy for these conditions is to make sure that we can target the cells that are affected, and this is what our study has done,” says investigator Gustavo Aguirre. His team conducted experiments on dogs with canine multifocal retinopathy, which is similar to Best disease.

 

The researchers injected a health copy of the Best1 gene into the retina to replace the malfunctioning copy using a vector, a harmless virus. They used vectors rAAV2/1 and rAAV2/2 by loading them with either the human version or the dog version of the Best1 gene. They found that the gene went to the right place and remained stable for six months, indicating that the therapy is lasting.

 

However, the rAAV2/1 gene seems to have damaged the cones, which disqualifies it as a delivery vector for now. The rAAV2/2 vector did not produce this side effect.  

Source:

http://www.medicalnewstoday.com/releases/267507.php