An international team of scientists led by King’s College London has identified 24 new genes that cause refractive errors and short-sightedness.

 

The researchers published their findings in the journal Nature Genetics. Until now, the scientific community knew that short-sightedness was hereditary, but did not fully understand the genetic baggage involved. To learn more, the researchers analysed genetic and refractive error data of over 45,000 people from 32 different studies. They found 24 new genes for this trait, and confirmed 2 previously reported genes. People with these genes are 10 times more likely to develop short-sightedness.

 

“Currently myopia is corrected with glasses or contact lenses, but now that we understand more about the genetic triggers for the condition, we can begin to explore other ways to correct it or prevent progression,” says Professor Chris Hammond, of King’s College. “It is an extremely exciting step forward which could potentially lead to better treatments or prevention in the future for millions around the world.”

 

Source: http://www.kcl.ac.uk/newsevents/news/newsrecords/2013/02-Feb/24-new-genes-for-short-sightedness-identified.aspx

Almost 43,000 visitors attended the most recent Mido exhibition, held March 2 to 4, which is an increase of more than 3% in a still difficult economic context in Italy and several European countries.

 

Sixty percent of visitors came from 40 different countries, with Italian opticians making up the rest of the visitors. Over 600 of the Italian visitors took advantage of the new initiative, “A Train for Mido,” which enabled them to take the Frecciarossa train free of charge from Rome to Mido and back.

 

The number of exhibitors also increased by 3% this year. Among newcomers was Quebec eyewear maker Zig Eyewear. “This was our first time at Mido, and we plan on repeating the experience next year,” said Cendrine Obadia, designer and founder of Zig Eyewear. Others, like Alain Mikli and Vuarnet, were back after a few years away.

 

The next Mido is scheduled for March 1–3, 2014. In the meantime, on April 11–14, 2013, Out of Mido will invite well-known eyewear manufacturers to showcase their creations at the NHOW hotel’s gallery, as part of the design-oriented Milan Furniture Fair.

How does our brain organize thousands of images that flood our retinas each day? That’s the question that scientists from the University of California, Berkeley, sought to answer by creating the first interactive map of how the brain organizes these groupings. 

 

The result is what researchers are calling “a continuous semantic space.” Up to now, the scientific community thought that each category of object or action humans see (people, animals, vehicles, movements) is represented in a separate region of the visual cortex. The study by the Berkeley team, however, shows that these categories are actually represented in highly organized, overlapping maps that cover almost 20% of the brain, including the somatosensory and frontal cortices.

 

A clearer understanding of how the brain organizes visual input could help with the diagnosis and treatment of brain disorders. It could also help create brain-machine interfaces.

“Our discovery suggests that brain scans could soon be used to label an image that someone is seeing, and may also help teach computers how to better recognize images,” said doctoral student Alexander Huth.

 

Source: http://newscenter.berkeley.edu/2012/12/19/semanticspace

A researcher in ophthalmology and neuroscience at the LSU Health Sciences Center New Orleans Neuroscience Center of Excellence has discovered a protein that protects retinal photoreceptor cells from degeneration caused by light damage.

 

The protein, called FATP4 (for fatty acid transport protein) could become the target of new treatments for retinal degenerative disease or age-related macular degeneration, according to the article published in the Journal of Neuroscience.

 

The researchers were trying to understand what could impede the proper functioning of the RPE65 enzyme, the mutations of which have been linked to various kinds of vision loss, retinal degeneration, and blinding eye diseases. They found that the FATP4 protein was inhibiting RPE65.

 

Recently, mutations in the human FATP4 gene have been identified in patients with a certain recessive disorder which also features one of the toxic by-products associated with abnormal visual cycles. This by-product, called A2E, accumulates in retinal pigment epithelial cells with age. This means additional studies are needed to determine whether the FATP4 mutations cause age-related disorders and retinal degeneration.

 

Source: http://www.sciencedaily.com/releases/2013/02/130212172207.htm