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And why do you have your messages turned off, sunniman? 
Take prosthetic arms, for example: We dont have a clue about the calculations that occur in the brain to trigger arm muscle motor neurons, but that doesnt stop us from slapping some electrodes onto a subjects bicep muscles and measuring the electric pulses that occur when you tell him to think about moving your arm. By the same logic, a brain-computer interface can measure what our general cranial activity looks like when were thinking something and react accordingly, but it can only do this through training; it cant actually understand our thoughts. Taking this one step further, though, Sheila Nirenberg of Cornell University has been trying to work out how the retina in your eye communicates with your brain and judging by a recent talk at TEDMED (embedded below), it seems like shes actually cracked it.
Now, reading the brains output (as in a prosthetic arm) is one thing, but feeding data into the brain is something else entirely and understanding the signals that travel from the retina, through the optic nerve, to the brain is really about as bleeding edge as it gets. Nirenberg still used a brute force technique, though: By taking a complete animal eye and attaching electrodes to the optic nerve, she measured the electric pulses the coded signal that a viewed image makes. You might not know what the code means, but if a retina always generates the same electric code when looking at a lion, and a different code when looking at a bookcase, you can then work backwards to derive the retinas actual encoding technique.
Nirenberg did this until she produced mathematical equations that, with startling accuracy, encode images into neuron pulses that can be understood by an animal brain. In the image below, the far left picture represents the pre-Nirenberg state of the art prosthetic eye, and the mid two images are what her prosthetic are capable of. Not quite as good as the real thing, but when you imagine that this is a silicon chip being implanted into the eye of a blind animal and then wired into the optic nerve, you really ought to be awestruck. In case youre wondering, the transducer that the image references is a piece of hardware that converts the output from the silicon chip into signals that are ready to travel along the optic nerve to the brain.
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Several years ago I worked for a very large company that had thousands of employees. Our insurance package one year came out and said that it would play for correcting eye surgery for employees and their families. I personally knew dozens of fellow co-workers and their spouses who had the surgery done. I never knew anyone who had a negative experience with the surgery.
My ex-wife was one of the people who had the surgery. She was severely near sighted and had to wear thick glasses to see beyond 10 feet. After the surgery she was 20/20 vision and never had any problems.
I just thought of something while reading your posts.
women wear burkas so the men cant get all sex riled by seeing their forms and want another mans wife.
Why dont we just fix all the eyes of muslim men so they cant see more than a few feet?
Then women would not have to bear the burden of men being unable to control their thoughts.
Its the mans sin you are trying to prevetn right?
Then lets make the men bare the burden of their own sin instead of the ladies having to bear the burden of anothers sin.
Injections of the cells produced only modest changes in the animals eyesight, but the results have raised hopes that a similar therapy might one day help reverse some forms of human blindness, such as age-related macular degeneration, the most common cause of blindness, which affects up to 15 percent of people over 75. In the study, researchers at University College Londons Institute of Ophthalmology injected the precursors of light-sensitive cells taken from newborn mice into the eyes of adult mice with a genetic form of night blindness.
Each jab delivered about 200,000 photoreceptor cells, of which 20,000 to 30,000 attached to the animals retinas and made working neural connections. Although the newly wired-up cells accounted for less than 1 percent of the rods in the retinas, the mice still showed an improvement in eyesight. This is the first proof of principle for restoring vision by transplanting photoreceptor cells. Until now its been assumed, and hoped for, but not actually proven, said Rachael Pearson, a neuroscientist at the institute, who led the study published in Nature. The retina contains two broad kinds of light sensitive cells, rods and cones. In mice and humans, more than 95 percent are rods. These work well in the dark and are good at spotting movement, but see the world in black and white. Cones are less numerous, but give a sharp, color view of the world in good lighting conditions.
The scientists used only rods in the latest experiments, as they are easier to transplant, but they are now pushing ahead with plans to repeat the work with cone cells. In humans, about 200,000 cones are concentrated in a small, central part of the retina called the fovea. In a series of tests, including one that measured the animals ability to distinguish varying shades of gray, and another that timed how quickly mice found a submerged platform in a water tank under low lighting conditions, the animals vision was 10 to 20 percent as good as healthy mice. The animals that performed best had the most newly connected rod cells.
Untreated, the mice were effectively blind in dim light. Now weve discovered we can restore vision, it gives us impetus to go on and make the process better, said Robin Ali, a senior author on the study. Scientists need to clear several major hurdles before considering rod and cone transplants for human clinical trials. One crucial step is to make suitable donor cells, either from established stores of embryonic stem cells, or by converting patients skin cells into photoreceptor cells. Another question is whether donor cells last for long when transplanted, or are rejected by the bodys immune system.
Mice eye research raises hopes of cure for blindness - Taipei Times
Researchers are warning about a dangerous parasite found in dust, as well as sea, pool and tap water, that could cause blindness to contact lens users. The acanthamoeba parasite has the potential to gnaw through the eyeball of an exposed contact lens wearer, which results in blindness, the Belfast Telegraph reports. The Centers for Disease Control refers to the ocular infection as acanthamoeba keratitis on its official website. [The parasite] is a microscopic, free-living [amoeba], or amoeba that can cause rare, but severe infections of the eye, skin, and central nervous system, the site states. The [amoeba] is found worldwide in the environment in water and soil [and] can be spread to the eyes through contact lens use, cuts, or skin wounds or by being inhaled into the lungs.
Symptoms reportedly include itchy, watery eyes, sensitivity to light, swelling in the upper eyelid, blurred vision, and extreme pain. Additionally, the damage to a sufferers vision could become permanent within a week of infection, optician Graeme Stevenson told the Daily Mail. Generally it leaves you with scarring. Your cornea is your window on life and if the infection penetrates in towards the third layer you are left with scarring, with a kind of frosty windscreen, he explained to the Daily Mail, adding that approximately 75 reported infections per year could be prevented by patients following instructions from their doctors. Stevenson added, Usually a lot of it is non-compliance. Its patients rinsing their case out in tap water or rinsing their lenses out in tap water. Potentially something as simple as swimming or showering while wearing their lenses increases the risk significantly.
Regular lens care and cleaning is recommended for those wishing to avoid infection. Treatment options reportedly include eye drops every 20 minutes, day and night, or time in the hospital. Cornea transplants have also been given in extreme cases, the Daily Mail learned. Though research has most recently come from the United Kingdom, scientists warn that the problem is international. Fiona Henriquez, researcher at the University of the West of Scotland, told the Daily Mail that it could be a potential problem for every single contact lens wearer.
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A chemical was shown to clear cataracts in mice and human eye lens tissue in lab experiments, and researchers have already licensed it to a company to develop for human use. The chemical is soluble enough to be used as an eye drop, researchers said, making for a far easier -- and cheaper -- method of treating the blinding condition, referred to as the "holy grail in ophthalmology." Cataracts is a degenerative condition caused by the misfolding and clumping of proteins in the eye called crystallins, causing the eye's lens to lose transparency. Researchers have been searching for ways to prevent the proteins from clumping, and to dissipate the clumps, called amyloids, that have already formed.
In July, researchers at the University of California San Diego reported a chemical compound, lanosterol, cleared cataracts in rabbit and dog eye lenses. In that study, lanosterol had to be injected into the eye because it was not soluble enough to for an eye-drop formulation. Researchers at the University of California San Francisco and the University of Michigan continued working with similar compounds, settling on compound 29, which in the lab dissolved amyloids that had already formed and stabilized crystallins, preventing them from clumping into amyloids.
Researchers identified a chemical that dissolves cataracts, a clouding of the eye's lens as proteins clump on its surface, and is soluble enough to be used in eye drops -- the "holy grail of ophthalmology."
In the new study, published in the journal Science, the researchers tested the compound on mice with mutations that made them predisposed to cataracts and mice with naturally developed age-related cataracts, finding that drops containing compound 29 improved transparency in the rodents' eye lenses. The same was seen in human lens tissue clouded by cataracts that had been removed during surgery. The compound has been licensed by the University of Michigan to a company formed in the incubator program at UC San Francisco called ViewPoint Therapeutics to develop it for human use.
Based on the similarity between amyloids formed in the eye that cause cataracts and those formed in other parts of the body causing other degenerative diseases, Gestwicki thinks the research could lead to treatments for other diseases. "If you look at an electron micrograph at the protein aggregates that cause cataracts, you'd be hard-pressed to tell them apart from those that cause Alzheimer's, Parkinson's, or Huntington's diseases," said Dr. Jason Gestwicki, an associate professor of pharmaceutical chemistry at UC San Francisco, in a press release. "By studying cataracts we've been able to benchmark our technologies and to show by proof-of-concept that these technologies could also be used in nervous system diseases, to lead us all the way from the first idea to a drug we can test in clinical trials."
Eye drops clear cataracts in human lens tissue, mice - UPI.com
Researchers found a combination of chemotherapy and a protein inhibitor improves the outcome of children with retinoblastoma, according to a recent study. Inhibiting the protein YM155, which prevents the process of cell death, made chemotherapy more effective against cancer cells in the lab and when treating mice with the cancer, researchers at the Children's Hospital of Los Angeles report in the study.
Retinoblastoma is the most common eye cancer among children, and is often treated with chemotherapy depending on the size and location of tumors. "Our study shows proof of concept, that we can enhance chemotherapeutic approaches to retinoblastoma while using the same dosage," Dr. Charles Gomer, a researcher at Children's Hospital Los Angeles and a professor at the University of Southern California, in a press release.
For the study, published in the journal PLOS ONE, researchers tested the effects of YM155 on cancer cells that had been treated with either of the chemotherapy drugs carboplatin or topotecan, or radiation. In cells exposed to any of the three chemotherapies, the protein survivin, which inhibits apoptosis -- the process of cell death -- was unaffected. After researchers combined cancer treatment with YM155 to inhibit the protein's expression, signs of apoptosis could be detected in the cells.
The combination therapy was then tested on tumors in mouse eyes, with YM155 enhancing cell death and prolonging the effects of cancer treatments on the tumors. "We're hopeful that following additional preclinical studies that this combination therapy will offer better outcomes to children with retinoblastoma and perhaps the possibility of reduced chemotherapy, reducing long-term adverse effects," Gomer said.
Study: Combination therapy improves retinoblastoma outcome
