Tag Archive blindness

Mother’s Milk May Help Prevent Blindness In Preemies

Mother’s Milk May Help Prevent Blindness In Preemies

Originally posted at npr.org / by Tara Haelle / @tarahaelle

Babies born prematurely are at risk of eye damage and, in severe cases, permanent blindness. Treatments can help. And human milk looks like it helps, too.
Babies born prematurely are at risk of eye damage and, in severe cases, permanent blindness. Treatments can help. And human milk looks like it helps, too. iStockphoto

If Stevie Wonder had been born three decades later, we might never have gotten “Superstition” and “Isn’t She Lovely” — but the musician might never have gone blind, either. Born premature, Wonder developed retinopathy of prematurity, an eye disease that afflicts more than half of babies born before 30 weeks of gestation.

Though treatments were developed in the 1980s, about 400 to 600 U.S. children and50,000 children worldwide still go blind every year from the condition. Now a study suggests that number could be slashed by more than half if all those preemies received their mothers’ milk.

“It makes sense that human milk can be protective against retinopathy of prematurity because we know it’s protective against abnormal neurological outcomes in tiny babies,” said Susan Landers, a neonatologist in Austin, Texas, and a member of the American Academy of Pediatrics Section on Breastfeeding Executive Committee. “Retinal tissue is just like neural tissue embryologically; it grows from the same immature cells.”

Stevie Wonder, seen here performing in 2014, was born prematurely and lost his sight due to retinopathy of prematurity. Jim Ross/Invision/AP

The study, actually a combined analysis of five studies from 2001 through 2013, found that preemies receiving human milk from their mothers had 46 to 90 percent lower odds of retinopathy of prematurity (ROP), depending on how much milk they received and how severe the ROP was. The studies were observational, so they cannot show that breast milk directly caused the lower risk.

“This is a very provocative study, and it does open new questions in new areas for research, but I think it’s too early to conclude that breast milk prevents ROP,” said Michael Chiang, a professor of ophthalmology and medical informatics at Oregon Health & Science University’s Casey Eye Institute who was not involved in the study. It was published online Monday in the journalPediatrics.

Of the infants who develop ROP, most recover and develop well without treatment, but about 10 percent develop severe ROP, increasing their risk of blindness, Chiang said. About half of those infants need treatment, which will prevent blindness in 80 to 90 percent of them.

The new research analyzed the outcomes of 2,208 preterm infants based on whether they received exclusive human milk, any human milk, mainly human milk (more than 50 percent), exclusive formula, any formula or mainly formula. The study did not include donor milk, so all the milk was the mother’s pumped or hand-expressed breast milk.

Infants who exclusively received breast milk had 89 percent reduced odds of severe ROP compared to infants who received any formula. Infants who received a mixture of breast milk and formula had roughly half the odds of developing severe ROP compared to infants exclusively receiving formula. The analysis included a very large older study that had found no reduced risk for ROP from breast milk, but most infants in that study received less than 20 percent breast milk.

“Despite including a negative study with large numbers, the results are still very, very significant,” said Landers, who was not involved in the study. “That strengthens this study considerably.”

Until the 1940s and 1950s, ROP did not exist because infants born prematurely rarely survived, Chiang said. As doctors learned to how to keep these tiny babies, usually little more than 3 pounds at birth, alive, they discovered that the blood vessels in their retinas would often start to grow out of control. If the abnormal growth continued, their retinas detached, causing blindness.

The first treatment developed in the 1980s was cryotherapy, which slowed blood vessel growth. Laser treatments later replaced cryotherapy and have remained the standard of care since. The newest treatment is bevacizumab, a drug made from humanized antibodies that slows the growth of new blood vessels.

The cause of ROP isn’t entirely understood, but scientists believe oxidative stress can stimulate the abnormal growth of the blood vessels. Providing preemies with oxygen is often key to their survival, but that oxygen exposure might lead to ROP, according to Jianguo Zhou, a neonatologist in Shanghai, and lead author of the study.

The antioxidants in breast milk offer one possible way that breast milk could prevent ROP, Zhou explained in an email. But the preventive mechanism could be indirect as well.

“Breast milk, specifically maternal breast milk, has been shown to be associated with reduced risk of many severe complications of prematurity, including a severe gastrointestinal disease called necrotizing enterocolitis,” said Tarah Colaizy, an associate professor of pediatrics and neonatology at the University of Iowa Carver College of Medicine. “It has also been shown to decrease the risk of potentially life-threatening blood infections, and there is some evidence that the severity of lung disease due to prematurity is reduced in infants fed maternal milk.”

Infants without these complications may receive less oxygen therapy, thus lowering the incidence of ROP, Zhou pointed out. Among 2 million infants born before 32 weeks each year worldwide, Zhou estimates that a tenth of them could develop severe ROP.

“Theoretically, exclusive human milk feeding could potentially prevent 8 percent (160,000) very preterm infants from severe ROP globally,” Zhou wrote. “That is an enormous influence and prevents thousands of preterm infants from blindness or visual impairment.”

ROP is still rare in places with the poorest health infrastructure because very premature infants still do not survive, but in China, India, Latin America and Eastern Europe, the problem is growing as doctors keep the infants alive but lack the neonatology and ophthalmology expertise to screen for and treat ROP. Even in the US where treatment is more available, screening may not be.

“Especially in rural and medically underserved areas, there’s not enough supply of ophthalmologists to do these exams,” Chiang said. “It’s a huge problem in the US and internationally.”

But providing exclusive maternal milk to preemies is easier said than done, Landers said. The biggest barrier is adequate lactation support for mothers in the NICU as well as the psychological complexity of the issue for mothers themselves.

“It’s a very stressful time, and expressing milk is the only thing that moms can do, so we put a lot of pressure on them,” Landers said. Some mothers don’t fare well under that pressure. The mothers need to start pumping within 12 hours of birth, as well as instruction in expressing milk and support and encouragement over the three or so months she will need to pump before her baby can breast-feed. “As hard as it is to get them started on pumping, it’s harder still to keep them going,” Landers said.

Even greater cultural obstacles exist among poor and African-American mothers, Landers said, but donor milk may not offer the same benefits, possibly because of its processing and storage needs.

“To give these mothers the best chance of providing milk, the health care system needs to provide them with professional help in the form of lactation consultants with specific expertise in preterm infant-mother pairs, the appropriate breast pumps and supplies to collect and store milk and assistance in transportation to get the milk to the NICU for the baby,” Colaizy said. “For these extremely fragile infants, maternal breast milk is a potentially life-saving intervention, and we should do everything possible for mothers to help them provide it.”

Tara Haelle is a freelance health and science writer based in Peoria, Ill. She’s on Twitter: @tarahaelle

Thank you npr.org / Tara Haelle

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A Cure for Blindness Just Might Come From Algae

Originally posted at wired.com
A Cure for Blindness Just Might Come From Algae

THE ALGAE THAT could cure blindness doesn’t even see, technically. Chlamydomonas reinhardtii are simple, single-cell green algae that live in water and in dirt. They have a round body, two whip-like tails, and a single primitive eye—not even an eye, really, an eyespot—that they use to seek out sunlight for photosynthesis.

Chlamydomona reinhardtii green algae.

Like human eyes, though, that eyespot makes use of light-sensitive proteins. One of them is called channelrhodopsin-2, and it’s this algal protein, transplanted into the human retina, that could one day restore sight to the blind. And this isn’t just some far-out dream: Last month, the FDA approved human clinical trials for the Ann Arbor-based company RetroSense to do just that.

Take a breath. Yes, this sounds pretty crazy—but not totally voodoo-far-out crazy. Channelrhodopsin-2, you see, is a rock star of the neuroscience world. For the past decade, neuroscientists have been using this protein to make neurons react to light. Neurons don’t typically respond to light—given they’re stuck inside skulls and all—but genetically encode the protein into neurons, and scientists can easily probe brain circuits with light, a technique known as optogenetics.

If channelrhodopsin-2 works in brain cells, why not eye cells? And so RetroSense is planning to use optogenetics in humans for the first time ever, recruiting 15 patients blinded by the genetic eye disease retinitis pigmentosa for its clinical trial. “We are looking to get it off the ground this year in the fall,” says CEO Sean Ainsworth.

RetroSense will use a virus to insert copies of the channelrhodopsin-2 gene into neurons of the inner retina, which normally are not sensitive to light. (Rods and cones are the usual light-sensitive cells.) This is gene therapy, and gene therapy to cure genetic eye disease is not radically new idea. In several clinical trials, researchers have injected viruses carrying a normal copy of a gene to make up for a patient’s faulty copy to restore sight. Herein lies the difference though: RetroSense isn’t inserting a gene from another human, another mammal, or even another animal, but from an alga. Forget cross-species—this is cross-domain.

It didn’t start out with algae. RetroSense is licensing its technology from Zhuo-Hua Pan, a vision researcher at Wayne State University who studies how to restore sight when the rods and cones of the eye die off. That’s what happens in diseases like retinitis pigmentosa or age-related macular degeneration. The obvious solution fixes human deficiencies with human genes: Encode the light-sensitive proteins from human rods in the other, functional cells in the diseased retina. But those proteins are finicky, and they have to work in concert with several other proteins—meaning scientists need to insert several genes. “We thought that would be almost impossible to do,” says Pan.

In 2003, Pan came across a paper on channelrhodopsin-2 from Chlamydomonas reinhardtii. Scientists started putting it into mammalian cells—and all they needed was one gene and one protein. “It worked perfectly, even in the very beginning,” says Pan. “That basically was just really, really lucky.” The hundreds of neuroscience labs relying on optogenetics might say the same.

Putting channelrhodopsin-2 into inner retinal neurons circumvents a lot of the eye’s complexity. The first thing you need to know about how the eye works is that it doesn’t make sense. For one, it appears to be wired backwards: Light has to pass through several layers of neurons before reaching the light-sensitive rods and cones at the back of the retina, which then has to send electric signals back through all those the layers of neurons on the way to the brain. (In the diagram, the back of the retina is at the top.) The rods and cones have it backwards, too—they fire in darkness, not in light, and inverting that code is part of the work of those neurons. If the human eye was the work of an intelligent designer, he was a mad one.

Retrosense targets only that last layer of neurons, called retinal ganglion cells. Make them light sensitive, the logic goes, and you can bypass the damaged or dead neurons that come before it. It’s a simpler eye.

The FDA-approved Argus II, a bionic eye, also stimulates the non-light-sensitive neurons in the retina. With only 60 electrodes to stimulate neurons, though, its resolution is poor. If gene therapy can get channelrhodopsin-2 into just 10 percent of the million retinal ganglion cells in each eye, says Pan, that’s equivalent to 100,000 electrodes. One challenge for human trials will making sure channelrhodopsin-2 gets into enough retinal ganglion cells. Pan says that’s easy in rodents, but his primate experiments seems to show some sort of barrier that prevents easy insertion of channelrhodopsin-2.

If channelrhodopsin-2 does make it into the cells, will patients have anything resembling normal vision? Channelrhodopsin-2 is 1,000 times less sensitive to light than cones. And retinal ganglion cells don’t normally deal with raw light signals; they’re usually receiving input from multiple rods or cones. The brain is plastic, but is it plastic enough to make sense of these new signals? Mice that undergo the treatment appear to see bars of light, which is encouraging. As the clinical trial progresses, humans may soon be able to report what they see in far greater detail.

Channelrhodopsin-2 has revolutionized how neuroscientists study neurons in mice, rats, zebrafish, and fruit flies. Getting optogenetics into humans was always going to be far trickier. A decade later, RetroSense is finally going to try.

Originally posted at wired.com

Thank you wired.com

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Researchers Developing Innovative Gene Therapy for Cone-Rod Dystrophy

Published first at blindness.org




April 17, 2014 – At first blush, completely shutting down both copies of a gene might not seem like the best way to treat an inherited retinal disease. That’s because genes and the proteins they express are thought to be essential to the health and well-being of all cells in the body.

But the approach was used successfully in a Foundation-funded gene-therapy study of mice with autosomal dominant cone-rod dystrophy (adCORD) caused by mutations in the gene GUCA1A, also known as GCAP1. It is one of 10 genes that can cause adCORD, a retinal degenerative disease characterized by reduced visual acuity and color perception, as well as loss of central and daytime vision. Affected individuals are often legally blind by the age of 40.

Led by Wolfgang Baehr, Ph.D., and Li Jiang, Ph.D., at the University of Utah, the study provided a proof-of-concept for an approach they hope to use in humans. Results were published in Frontiers in Molecular Science.

The scientists shut down the normal and the mutated copy of GCAP1, because the approach was simpler than trying to target only the defective copy, and the investigators determined that vision wasn’t compromised when the healthy copy was also shut down.

GCAP1 is a gene that leads to the production of a protein involved in phototransduction, the biochemical process in photoreceptors that converts light to electrical signals, which are sent back to the brain and interpreted as vision. However, if one of the two GCAP1 copies is defective, a toxic protein is produced and adCORD develops.

To be effective in most cases, a gene therapy for an autosomal dominant retinal disease must either shut down the defective gene copy and leave the normal copy intact, or deliver a copy of the normal gene after shutting done both copies. In some cases, scientists can override the defective copy by only delivering a normal copy.

However, Dr. Baehr’s team found that in the case of GCAP1, shutting down both copies successfully halted retinal degeneration in mice; even with no normal copy, the phototransduction process worked well and vision was preserved.

Dr. Baehr believes that the protein expressed by GCAP1 is not essential for normal vision or retinal health. However, the defective protein is toxic.

To shut down the GCAP1, Dr. Baehr developed a gene therapy which produces messages known as short-hairpin RNA (shRNA). The shRNA block GCAP1’s naturally occurring RNA messaging system, rendering the gene inactive.

“What is most impressive about this gene therapy approach is its simplicity,” says Stephen Rose, Ph.D., chief research officer of the Foundation Fighting Blindness. “The strategy of shutting down the gene altogether will not work for a vast majority of other retinal degenerations, but for GCAP1, it is the most straightforward therapeutic path, so it makes sense to take it.”

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Telemedicine Initiative To Treat, Prevent Blindness






University of California, Davis (UCD) And Orbis International Partner

5/23/2014 9:07:19 AM

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 May 22, 2014 /PRNewswire/ — Today, UC Davis Health System and Orbis International, a leading global non-governmental organization (NGO) that works to eliminate avoidable blindness, signed an agreement of cooperation that will expand the use of telemedicine technology to help treat and prevent blindness in the developing world.

Orbis operates the Flying Eye Hospital (FEH), a fully equipped mobile teaching hospital. UC Davis telemedicine, information technology and eye specialists will work with Orbis to expand training efforts including through Orbis Flying Eye Hospital programs.

The new alliance, which features the expertise of the UC Davis Center for Health and Technology and the UC Davis Eye Center, paves the way for developing new research, education and telehealth collaborations to advance vision science and eye care on a global scale.

The World Health Organization estimates that 285 million people are visually impaired worldwide. This includes 39 million individuals who are blind and 246 million who have low vision. About 90 percent of the world’s visually impaired live in developing countries, and 80 percent of all cases of visual impairment can be avoided or cured. These include refractive errors, cataracts and glaucoma, the leading causes of visual impairment worldwide.

Through the agreement, UC Davis specialists in telemedicine, information technology, ophthalmology, anesthesiology and nursing will work with Orbis on initiatives such as staff development, fellowships and programs on the Orbis Flying Eye Hospital — a fully equipped mobile teaching hospital on board a DC-10 jet. Trainees will have opportunities for hands-on training in the UC Davis Center for Health and Technology simulation center and Orbis’s telehealth program for real-time surgical demonstrations.

“Orbis is honored to join in this agreement with the UC Davis Eye Center,” said Jenny Hourihan, president and chief executive officer of Orbis. “UC Davis is such an impressive partner and dedicated in helping to make quality eye health accessible while advancing programs and technology used in eye health worldwide. We are excited to collaborate and share tools and resources to expand the reach and influence that telehealth has in preventing and treating avoidable blindness.”

The project includes establishing telehealth links that will transmit live broadcasts of eye surgeries at UC Davis to virtual classrooms in remote regions in the developing world with the opportunity for trainees thousands of miles away to ask questions of surgeons in real time. It also will explore live e-consultations with partners around the world and further Orbis’s ongoing efforts to establish an open-source ophthalmic electronic medical record system, which will help develop a more robust e-health infrastructure, provide access to increased decision-making support and offer researchers a wealth of global data.

“Advances in telecommunications technologies and broadband capacity in developing countries has created new opportunities to improve training for physicians, nurses and other members of the health-care team and expanded access to health-care services among the world’s most vulnerable populations,” said Thomas Nesbitt, associate vice chancellor for strategic technologies and alliances at UC Davis. “By partnering with Orbis, a recognized pioneer in establishing sustainable, quality eye health care worldwide, we are leveraging UC Davis’ expertise in telehealth and distance learning to have a profound impact on global health.”

Orbis works to bring quality eye care to communities by building capacity with local partners to develop infrastructure, trained staff and, ultimately, sustainable eye care services. Since 1982, Orbis has carried out programs in 92 countries, enhanced the skills of more than 325,000 eye care professionals, and provided medical and optical treatments to more than 23.3 million adults and children. Since 2006, nearly 20 UC Davis faculty and staff have participated in 14 medical missions, traveling to ChinaVietnam,PeruIndonesiaIndiaEl SalvadorEthiopiaZambia and Panama.

About UC Davis Health System

UC Davis Health System improves lives by providing excellent patient care, conducting groundbreaking research, fostering innovative, interprofessional education and creating dynamic, productive community partnerships. It encompasses one of the country’s best medical schools, a 619-bed acute-care teaching hospital, a 1,000-member physician practice group and the Betty Irene Moore School of Nursing. It is also home to the UC Davis Center for Health and Technology, a global leader in using telehealth and distance learning to meet the needs of populations in remote and underserved regions, and the UC Davis Eye Center, which conducts collaborative vision research, provides world-class eye care, trains the next generation of ophthalmologists and vision scientists, and develops cures for blinding eye diseases, from cornea to cortex.Together, they make UC Davis a hub of innovation that is transforming health for all. For information, visit healthsystem.ucdavis.edu.

About Orbis
Orbis prevents and treats blindness through hands-on training, public health education, improved access to quality eye care, advocacy and partnerships with local health care organizations. By building long-term capabilities, Orbis helps its partner institutions take action to reach a state where they can provide, on their own, quality eye care services that are affordable, accessible, and sustainable. To learn more about Orbis, please visit www.orbis.org.

Related Links
UC Davis Health System

A glaucoma teaching case operation in progress on board the Orbis Flying Eye Hospital in Jinan, China being conducted by Dr. James Brandt, Orbis Volunteer Faculty member from UC Davis. A new partnership with UC Davis will include establishing telehealth links that will transmit live broadcasts of eye surgeries at UC Davis to virtual classrooms in remote regions in the developing world with the opportunity for trainees thousands of miles away to ask questions of surgeons in real time.
Orbis Volunteer Faculty Member Dr. James Brandt of UC Davis gives a lecture in the classroom on board the Flying Eye Hospital in Jinan, China in April. UCD Health System, UCD Center for Health and Technology, the UCD Eye Center and Orbis have signed an agreement of cooperation to expand the use of telemedicine technology to treat and prevent avoidable blindness globally.

Thank you Orbis


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Stem Cells Cure Blindness

Stem Cells Cure Blindness

Simone Biow's picture

Submitted by Simone Biow on Mon, 11/20/2006 – 8:11pm

The Controversy

Earlier this November, scientists from the University College London Institutes of Ophthalmology and Child Health and Moorfields Eye Hospital were able to restore vision to blind lab mice. This scientific breakthrough signifies that millions of people with optical conditions such as macular degeneration (loss of sight experienced by the elderly), diabetic retinopathy, and a variety of other forms of blindness could be able to regain sight through a remarkably simple procedure. However, the fact that the procedure requires stem cells from foetuses—currently viewed as a highly controversial method by many politicians—has prevented this procedure from becoming more publicized in the U.S. (1).

The Breakthrough

Researchers have identified certain cells on the margin of adult retinas that are similar to stem cells. Additionally, retinal cell replacement may be the most effective method of “cell transplant therapy because photoreceptor loss initially leaves the rest of the wiring to the brain intact” (1). In other words, major surgical reconstruction is not necessary. Any surgical procedure would only involve the superficial layer of the retina and not the particularly sensitive optic nerve wiring at the back of the eye. However, in order to attain human retinal cells at the necessary stage of development, stem cells would need to be extracted from a foetus during the second trimester of pregnancy (1). Because stem cells are able to proliferate and develop into many other types of cells within the human body, they can be extracted from any part of the foetus. However, the timing is imperative if the procedure is to work.

Three Blind Mice… See How the Procedure Works...

1. Early stage retinal stem cells were extracted from a 3 to 5 day old newborn mouse (1).

2. The retinal cells were transplanted onto the retinal surface of a blind mouse whose condition was genetically programmed to resemble the gradual loss of sight characteristic to the human disease retinitis pigmentosa or age-related macular degeneration (1).

3. The cells embed themselves and connected with other cells on the retina of blind mouse. Within 30 minutes the photoreceptors from the retinal stem cells implanted themselves and fused electrical connections with the animals’ existing retinal nerve cells (3). As a result, the formerly blind mice’s pupils began to respond to light and there was activity in the optic nerve (indicating that the eye was transmitting signals to the brain) (1).

Anatomy & Physiology of the Eye: Photoreceptors

The retina (around 0.5 mm thick) lines the back of the eye. It is lined with a network vascular blood vessels and neurons that gradually channel towards the optic nerve which contains the ganglion cell axons that connect the ganglion cells to the brain. The ganglion cells—the neurons of the retina that transmit images to the brain—are located in the innermost region of the retina and extend toward the lens, or anterior portion of the eye (2). The photoreceptors—the rod and cone shaped cells—are situated toward the outermost portion of the retina and are closer to the back of the eye (5). As a result, light must penetrate the nerve cells within the retina before reaching and activating the rods and cones. Once reached, the rods and cones absorb photons through their visual pigments and translate the photons into a biochemical message and then into an electrical message that stimulates all of the succeeding neurons of the retina. Consequently, “the retinal message concerning the photic input and some preliminary organization of the visual image into several forms of sensation are transmitted to the brain [by] the spiking discharge pattern of the ganglion cells” (2). From then on the brain is responsible for identifying, processing and interpreting the visual image (2).

Candidates for retinal cell replacement surgery must have some retinal cone and rod photoreceptors intact (1) . The retinal cell replacement surgery primarily serves to repair the nerve synapses in the retina, the macula lutea, and the fovea. The surgery cannot generate new photoreceptors.

The surgery mainly repairs the macula and the fovea. The macula functions as a short wavelength filter while the fovea, characterized by a dark circular area towards the back of the eye, is considered to be the most vital portion of the retina. Like the lens, it functions as “a protective mechanisms for avoiding bright light and especially ultraviolet irradiation damage” (2). The fovea is entirely composed of a mosaic cone photoreceptors that are arranged in a hexagonal structure. Outside of the foveal pit, the density of cone photoreceptors becomes increasingly more balanced with that of rod photoreceptors. There is a peak in the density of rod photoreceptors at about 4.5mm (or 18 degrees) from the foveal pit where the rod photoreceptors arrange themselves in a ring around the fovea (5). (Naturally, the optic nerve (the blindspot) is entirely free of photoreceptors) (5). If the macula or fovea cones are damaged (as happens gradually over many years), instant blindness results (2). However, macular degeneration could be easily remedied since stem cells take only about half an hour to develop into photoreceptors.

Repairing the Cornea

In August of 2003, Mike May, a Californian man who had been left blind for 40 years as the result of an accident that happened when he was three years old had his vision restored. Though the vision in his left eye was permanently lost, he could still sense light with his right eye. Researchers implanted corneal and limbal stem cells into his right eye. Five months after the surgery, May was able to sense movements and recognize simple shapes. After two years, he was able to see forms, color, and motion nearly accurately. His 3D perception and face and object recognition remained impaired, though his ability to sense motion was the best restored visual faculty (4).

Like photoreceptors, the cornea is responsible for channelling light through the eye’s surface. The corneal surface refracts to provide 2/3 of the eye’s focusing power. he corneal surface is entirely transparent and not lined with blood vessels, so the uniformity of cells may contribute to its ability to regenerate more rapidly than other cells in the human body. On the other hand, it is extremely sensitive. There are more nerve endings on the cornea than anywhere else on the human body (6). The cells that compose the layers of the cornea are found to regenerate at a rapid pace, though less rapid than photoreceptor cells. Again, a simple surgical procedure, most of which is processed by human mechanisms, could restore sight to millions of people if only the procedure were to be legalized.

Anatomy of the Eye

courtesy of U.S. National Library of Medicine

(1) “Cell transplants ‘restore sight.'” BBC International News Online. (http://news.bbc.co.uk/2/hi/health/6120664.stm)

(2) Simple Anatomy of the Retina. (http://webvision.med.utah.edu/sretina.html)

(3) “Cell Transplants Restore Vision in Mice.” Live Science. (http://www.livescience.com/healthday/535968.html)

(4) “Cell Transplant Restores Vision.” BBC International News Online. (http://news.bbc.co.uk/2/hi/health/3171993.stm)

(5) Photoreceptors. (http://webvision.med.utah.edu/photo1.html)

(6) “Cornea.” Eye Anatomy. (http://www.stlukeseye.com/anatomy/Cornea.asp)


Serendip Visitor's picture

Stem Cells

Submitted by Mr. T (not verified) on Sun, 06/13/2010 – 3:35pm.

This woman was at the hospital at the same time as Frank.
I want to send you all my e mail adress but It wont work here because we should not advertise

Hello guys,

Well, has it really been 3 months and 1 week since we came home, WOW WOW WOW and WOW! Well, I am doing pretty well. I had my tests the other day in Dublin and I have my visual fields and visual acuity check this wednesday so I will update when I get results.

Since my last post my left and right eye are now at around 5 meters!! Big difference from 1 meter??!! I notice a lot more little things like I could see the goal posts at a match last week and every day things. My improvements have slowed down a lot, maybe its because when i first cam home i was seeing everything for the first time! But I am still thrilled as I have gained 4 meters of sight this year, something I thought would never happen.

Other then that I am keeping really well, still smiling and enjoying watching the world cup!! Its strange watching soccer properly!! the players all have legs and all 🙂

Anyway, I will be sure to let ye know how my results go and please keep me in yere thoughts and prayers! There working!!

Lots of love and enjoy the world cup 2010!!

Lots of irish hugs and kisses


Add comment June 14th, 2010
1 Month home….

Hi there,

I cant believe we are home 4 weeks already. The time flew. It feels almost like a dream that we were even there!! Everything is going really well. I have noticed a few improvements since my last post. Little things really, like shopping, I can make out clothes sizes, on certain items, my finger counting has improved amazingly!! I watched a hurling match on my tv and I could actually make out the 2 different teams!! I even knew no 15 jersey!! Its almost as if my little jigsaw pieces are fewer.

I know I have a long way to go but hopefully I will get there. I am continuing my accupuncture, herbs etc and I really hope they help. Someday I WILL drive…..

Thanks for helping me through the past few months.


Thank you http://serendip.brynmawr.edu/exchange/node/50


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