Women Have Bigger Pupils Than Men

ScienceDaily (Apr. 26, 2012) - From an anatomical point of view, a normal, non-pathological eye is known as an emmetropic eye, and has been studied very little until now in comparison with myopic and hypermetropic eyes. The results show that healthy emmetropic women have a wider Pupil diameter than men.

Normal, non-pathological emmetropic eyes are the most common type amongst the population (43.2%), with a percentage that swings between 60.6% in children from three to eight years and 29% in those older than 66.

Therefore, a study determines their anatomical pattern so that they serve as a model for comparison with eyes that have refractive defects (myopia, hypermetropia and stigmatism) pathological eyes (such as those that have cataracts).

"We know very little about emmetropic eyes even though they should be used for comparisons with myopic and hypermetropic eyes" Juan Alberto Sanchis-Gimeno, researcher at the University of Valencia and lead author of the study explained.

The project, published in the journal 'Surgical and Radiologic Anatomy' shows the values by gender for the central corneal thickness, minimum total corneal thickness, white to white distance and Pupil diameter in a sample of 379 emmetropic subjects.

"It is the first study that analyses these anatomical indexes in a large sample of healthy emmetropic subjects" Sanchis-Gimeno states. In recent years new technologies have been developed, such as corneal elevation topography, which allows us to increase our understanding of in vivo ocular anatomy.

Although the research states that there are no big differences between most of the parameters analysed, healthy emmetropic women have a wider Pupil diameter than men.

"It will be necessary to investigate as to whether there are differences in the anatomical indexes studied between emmetropic, myopic and hypermetropic eyes, and between populations of different ethnic origin" the researcher concludes.

How the human eye works

Light penetrates through the Pupil, crosses the crystalline lens and is projected onto the retina, where the photoreceptor cells turn it into nerve impulses, and it is transferred through the optic nerve to the brain. Rays of light should refract so that they can penetrate the eye and can be focused on the retina. Most of the refraction occurs in the cornea, which has a fixed curvature.

The Pupil is a dilatable and contractile opening that regulates the amount of light that reaches the retina. The size of the Pupil is controlled by two muscles: the Pupillary sphincter, which closes it, and the Pupillary dilator, which opens it. Its diameter is between 3 and 4.5 millimetres in the human eye, although in the dark it could reach up to between 5 and 9 millimetres.

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Study Links Genes to Common Forms of Glaucoma

ScienceDaily (Apr. 26, 2012) - Results from the largest genetic study of Glaucoma, a leading cause of blindness and vision loss worldwide, showed that two genetic variations are associated with primary open angle Glaucoma (POAG), a common form of the disease. The identification of genes responsible for this disease is the first step toward the development of gene-based disease detection and treatment.

About 2.2 million people in the U.S. have Glaucoma. POAG is often associated with increased eye pressure but about one-third of patients have normal pressure Glaucoma (NPG). Currently, no curative treatments exist for NPG.

Researchers including lead author Janey Wiggs, M.D., Ph.D., and Lou Pasquale, M.D., Co-Directors of the Harvard Glaucoma Center of Excellence, analyzed DNA sequences of 6,633 participants, half of whom had POAG. Participants were part of two NIH-funded studies: GLAUGEN (Glaucoma Genes and Environment) and NEIGHBOR (NEI Glaucoma Human genetics collaBORation), conducted at 12 sites in the United States. Dr. Pasquale is Director of the Glaucoma Service at Mass. Eye and Ear.

The results, reported online in PLoS Genetics (April 26, 2012), found that two variations were associated with POAG, including NPG. These are the first variants commonly associated with NPG. One variant is in a gene located on chromosome 9 called CDKN2BAS whereas the other variant is in a region of chromosome 8 where it may affect the expression of genes LRP12 or ZFPM2. These genes may interact with transforming growth factor beta (TGF-beta), a molecule that regulates cell growth and survival throughout the body. Previous studies have also implicated TGF-beta in Glaucoma.

"This research has provided important new insights into the disease pathogenesis and will make future studies focused on translating this information into the clinic possible. Ultimately we hope to prevent blindness caused by this very common eye disease," said lead author Dr. Wiggs.

"This study has identified an important molecular pathway in the development of POAG. Control of TGF-beta might lead to more effective therapies for this blinding disease," said Dr. Hemin Chin, associate director for Ophthalmic Genetics at the National Eye Institute.

Funding sources for this research include the National Eye Institute, National Human Genome Research Institute, Lions Eye Research Fund, Glaucoma Center of Excellence, the Margolis Fund, and Research To Prevent Blindness.

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How Does Nearsightedness Develop in Children?

ScienceDaily (Mar. 1, 2012) - Myopia (Nearsightedness) develops in children when the lens stops compensating for continued growth of the eye, according to a study in the March issue of Optometry and Vision Science, official journal of the American Academy of Optometry.

The journal is published by Lippincott Williams & Wilkins, a part of Wolters Kluwer Health.

Using detailed information on eye growth and vision changes in children over time, the new research shows "decoupling" of lens adaptation from eye growth about a year before myopia occurs. Donald O. Mutti, OD, PhD, of The Ohio State University College of Optometry, is lead author of the new study.

Growth Imbalance Leads to Myopia…

The researchers analyzed repeated measurements of vision and eye growth performed over several years in children aged 6 to 14. The study focused on the growth of the two key parts of the eye affecting normal vision: the cornea, the transparent front part that lets light into the eye; and the lens, located behind the cornea, which focuses light rays on the retina at the back of the eye.

Myopia or Nearsightedness -- difficulty seeing objects at a distance -- develops in about 34% of American children as they grow. Vision professionals and scientists typically think of myopia as a problem occurring when the eyeball becomes too long (front to back) for the optical power of the cornea and lens.

However, it has been unclear how this imbalance develops in children who previously had normal vision. To answer this question, Dr. Mutti and colleagues compared changes in eye growth for children who developed myopia at different ages versus those whose vision remained normal.

They found that, in children without myopia, the lens grew thinner and flatter to maintain normal vision as the eye grew. This adaptation maintained a normal balance between the optical power of the lens and the increasing length of the eyeball. From age nine months to nine years, eyeball length increased by an average of three millimeters.

...As Lens Stops Responding to Increasing Eye Length

However, in children who developed myopia, the lens stopped changing in response to eye growth. Nearsightedness developed not just because of increases in the length of the eyeball, but rather because the optical power of the lens no longer changed as the eye grew.

The imbalance occurred rather suddenly: about one year before the children became Nearsighted. For at least five years after the development of myopia, the eye kept becoming longer but the lens stopped flattening and thinning.

In contrast to the lens, changes in corneal growth showed little or no relation to the development of myopia. The cornea is responsible for about two-thirds of the optical power of the eye, and the lens for the remaining one-third.

The study provides vision professionals with an important new piece of information on why some children develop myopia. However, what's still unclear is why the lens suddenly stops adapting to continued growth of the eye. More research will be needed to answer that question -- one possibility is that an abnormally thick ciliary muscle within the eye forms a mechanical restriction preventing the stretching that thins and flattens the lens as the eye continues to grow.

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Vitamin B-Based Treatment for Corneal Disease May Offer Some Patients a Permanent Solution

ScienceDaily (Oct. 24, 2011) - Patients in the United States who have the Cornea-damaging disease keratoconus may soon be able to benefit from a new treatment that is already proving effective in Europe and other parts of the world. The treatment, called collagen crosslinking, improved vision in almost 70 percent of patients treated for keratoconus in a recent three-year clinical trial in Milan, Italy. The treatment is in clinical trials in the United States and is likely to receive FDA approval in 2012.

The results of the Milan study are being presented Oct. 24, 2011 at the 115th Annual Meeting of the American Academy of Ophthalmology in Orlando, Florida.

In a session titled Long-term Results of Corneal Crosslinking for Keratoconus, Paolo Vinciguerra, MD will describe the treatment and three-year follow up of more than 250 keratoconus patients who received collagen crosslinking at his clinic. Sixty-eight percent of the 500 eyes treated gained significant visual acuity, with their results remaining stable at the end of the follow-up period. Patients over age 18 were most likely to improve.

In the collagen crosslinking procedure, riboflavin (vitamin B) is applied to the Cornea, which is then exposed to a specific form of ultraviolet light. Collagen fibers regenerate with new bonds forming between them, increasing Corneal stiffness and strength. The treatment also combats the causes of keratoconus, reducing the chance that it will recur. The rest of the eye receives only minimal UV exposure during treatment. Dr. Vinciguerra's new study confirms that adverse effects are rare. Previous research by his team indicated no loss of Corneal endothelial cell, a measurement used to assess the safety of Corneal treatments, in patients who received collagen crosslinking.

"For many people with keratoconus, collagen crosslinking can provide a better and more permanent solution to their vision problems," said Dr. Vinciguerra. "Given that no current treatment in use in the U.S. offers permanent correction, this effective option represents a significant advance for Corneal medicine."

One in 2,000 people in the United States and worldwide are diagnosed with keratoconus, a disease that damages the collagen fibers that form the structure of the Cornea, which is the outer surface of the eye. The Cornea's crucial task is to focus, or "refract," incoming light toward the eye's lens. To perform properly, the Cornea needs to be rounded, like the surface of a ball. As keratoconus worsens and the Cornea becomes thinner, it may bulge outward in a cone shape, causing nearsightedness and/or astigmatism, making clear vision impossible. As the number of fibers and links between them decline, the Cornea loses up to 50 percent of its normal stiffness.

Standard treatments in the U.S., such as specialized eyeglasses, contact lenses, or implanted lenses, cannot permanently correct keratoconus, and none of these treatments address the underlying causes. Severe keratoconus often requires Corneal transplant.

The 115th Annual Meeting of the American Academy of Ophthalmology is in session October 23 through 25 at the Orange County Convention Center in Orlando, Fla. It is the world's largest, most comprehensive ophthalmic education conference. Approximately 25,000 attendees and more than 500 companies gather each year to showcase the latest in ophthalmic technology, products and services. To learn more about the place Where All of Ophthalmology Meets visit www.aao.org/annual_meeting.

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Detecting Glaucoma Before It Blinds

Early detection and diagnosis of open angle Glaucoma important so that treatment can be used in the early stages of the disease developing to prevent or avoid further vision loss. Writing in a forthcoming issue of the International Journal of Medical Engineering and Informatics, researchers in the US have analyzed and ranked the various risk factors for open angle Glaucoma so that patients can be screened at an earlier stage if they are more likely to develop the condition.

Glaucoma is one of the main leading causes of blindness; it is a progressive and irreversible disease. Of the various forms of Glaucoma, open angle Glaucoma (OAG) is the most common and can cause the most damage. Unfortunately, unless a patient is undergoing regular screening from about the age of 40 years because of a family history, it is otherwise difficult to detect until substantial and irreversible vision loss has occurred. Glaucoma is the third leading cause of blindness worldwide and the second leading cause of blindness in the USA.

Now, Duo Zhou and colleagues at the University of Medicine and Dentistry of New Jersey, Newark, have used statistical collinearity analysis to evaluate risk factors for OAG, and logistic regression models to identify a minimum set of such risk factors for prognosis and diagnosis of the disease. Their study was based on more than 400 patients with subtle or severe vision problems who attended hospital. It reveals the relative risk of being a smoker, age, visual "field test" results, presence of a localized notch or thinning of the neuroretinal rim identified during standard eye examination, cup to disk ratio (a measure of restriction of the optic nerve at the back of the eye) and other factors.

The data are complex and separating out predictors from diagnostic factors was difficult, the team admits. However, they suggest that family history, medical history, current medications, geographic location, visual field test and ocular examination must all be considered in diagnosis and prognosis for OAG. They have excluded certain factors from the OAG prognosis: gender, race, family history of Glaucoma, diabetes mellitus, hypercholesterolemia, thyroid disease, migraine, Reynaud's disease and myopia as these have no direct effect on OAG development.

As revealed in the analyses, the odds of developing OAG will be increased by 91% with an increase in the Cup-to-Disc ratio of 0.1. Risk increases by 3% annually by age but decreases by 31% for every dB increase of mean deviation of Humphrey visual field. The odds of developing OAG will be 4.36 higher for patients with abnormal Humphrey visual filed overall test, 7.19 higher in patients with localized notch or thinning of the neuroretinal rim. Interestingly, patients with a smoking history seem to be less likely to develop OAG as compared to those with smoking history; although there are many smokers with OAG. Oddly, because of the location of the study, the team can also say that patients living in Atlantic/Quebec will be 73% less likely to develop OAG compared to their fellow Canadians in Ontario.

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Cornea Gene Discovery Reveals Why Humans See Clearly

ScienceDaily (Dec. 12, 2011) — A transparent Cornea is essential for vision, which is why the eye has evolved to nourish the Cornea without blood vessels. But for millions of people around the world, diseases of the eye or trauma spur the growth of blood vessels and can cause blindness.

A new Northwestern Medicine study has identified a gene that plays a major role in maintaining clarity of the Cornea in humans and mice -- and could possibly be used as gene therapy to treat diseases that cause blindness. The paper is published in the Proceedings of the National Academy of Sciences.

"We believe we've discovered the master regulator gene that prevents the formation of blood vessels in the eye and protects the clarity of the Cornea," said lead author Tsutomu Kume, associate professor of medicine at Northwestern University Feinberg School of Medicine and a researcher at Feinberg Cardiovascular Research Institute.

The existence of the gene, FoxC1, was previously known, but its role in maintaining a clear Cornea is a new finding. Working with a special breed of mice that are missing this gene, Kume and colleagues found abnormal vascular formations, or blood vessels, streaking their Corneas and blocking light.

When Kume discovered the Corneal blood vessels in the mutant mice, he called a collaborator at the University of Alberta in Canada, Ordan Lehmann, MD, professor of ophthalmology and medical genetics.

Lehmann found that his patients who have a single copy of this mutated FoxC1 gene -- and who have congenital glaucoma -- also have abnormal blood vessel growth in their eyes.

"The exciting thing is by showing the loss of FoxC1 causes vascularization of the cornea, it means increasing levels of the gene might help prevent the abnormal growth of blood vessels, potentially in multiple eye disorders that cause blindness," said Lehmann, a coauthor on the paper. "That's the hope." One possible use might be in corneal transplants, he said, where the growth of new blood vessels onto the transplanted cornea is a major problem.

Kume next plans to test the gene therapy in mice to see if injecting FoxC1 inhibits the formation of blood vessels in the cornea.

The research is funded by National Institutes of Health and Canadian Institutes of Health Research.

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New Treatment For Age-Related Macular Degeneration Within Sight

With 8 million people at high risk for advanced age-related Macular Degeneration, researchers from Harvard and Japan discovered that the experimental drug, endostatin, may be the cure. A research report describes how giving endostatin to mice significantly reduced or eliminated abnormal blood vessel growth within the eye, which is ultimately why the disease causes blindness.

"Our study provides intriguing findings that may lead to a better treatment of age-related Macular Degeneration," said Alexander Marneros, the first author of the report, "but clinical studies in patients with age-related Macular Degeneration are still necessary."

In this study, researchers describe testing the effects of endostatin on mice lacking this naturally occurring substance. The mice without endostatin were about three times more likely to develop advanced age-related Macular Degeneration (AMD) than normal mice. Then the researchers administered endostatin to both sets of mice. In the mice lacking endostatin, the number of abnormal blood vessels that cause AMD were reduced to normal levels. In control mice with normal levels of endostatin, the number of abnormal blood vessels were practically undetectable.

"With Baby Boomers reaching advanced ages, new treatments are desperately needed to keep age-related Macular Degeneration from becoming a national epidemic," said Gerald Weissmann, MD, Editor-in-Chief of The FASEB Journal. "This research provides hope for those at risk for blindness, and it gives everyone another glimpse of how investments in molecular biology will ultimately pay off in terms of new treatments and cures."

AMD is a progressive disease that affects the part of the eye that allows people to see fine details. The disease gradually destroys sharp, central vision, and in advanced stages ultimately leads to total blindness. Abnormal blood vessel growth, also known as angiogenesis, is a hallmark of advanced AMD. These faulty blood vessels leak fluids and blood, causing catastrophic vision loss.

As the name implies, risk for age-related Macular Degeneration increases with age, and 8 million people are considered to be at high risk for the disease. Of these individuals, approximately 1 to 1.3 million will develop advanced AMD within the next five years. Endostatin is an experimental drug, which is currently being tested to stop cancer in people by restricting the formation of abnormal blood vessels supply blood to tumors. Endostatin is a protein in collagen, and while collagen is used in a range of products for skin care to gelatin desserts, consumption or use of these products does not have any effect on tumors or AMD.

Weissmann added, "This research proves once and for all that endostatin functions as the body's own natural inhibitor of new blood vessel growth as Judah Folkman of Harvard predicted."

This research was published in the December 2007 issue of The FASEB Journal.

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The Pupils Are the Windows to the Mind

The eyes are the window into the soul -- or at least the mind, according to a new paper published in Perspectives on Psychological Science, a journal of the Association for Psychological Science. Measuring the diameter of the Pupil, the part of the eye that changes size to let in more light, can show what a person is paying attention to. Pupillometry, as it's called, has been used in social psychology, clinical psychology, humans, animals, children, infants -- and it should be used even more, the authors say.

The Pupil is best known for changing size in reaction to light. In a dark room, your Pupils open wide to let in more light; as soon as you step outside into the sunlight, the Pupils shrink to pinpricks. This keeps the retina at the back of the eye from being overwhelmed by bright light. Something similar happens in response to psychological stimuli, says Bruno Laeng of the University of Oslo, who cowrote the paper with Sylvain Sirois of Université du Québec à Trois-Rivières and Gustaf Gredebäck of Uppsala University in Sweden. When someone sees something they want to pay closer attention to, the Pupil enlarges. It's not clear why this happens, Laeng says. "One idea is that, by essentially enlarging the field of the visual input, it's beneficial to visual exploration," he says.

However it works, psychological scientists can use the fact that people's Pupils widen when they see something they're interested in.

Laeng has used Pupil size to study people who had damage to the hippocampus, which usually causes very severe amnesia. Normally, if you show one of these patients a series of pictures, then take a short break, then show them another series of pictures, they don't know which ones they've seen before and which ones are new. But Laeng measured patients' Pupils while they did this test and found that the patients did actually respond differently to the pictures they had seen before. "In a way, this is good news, because it shows that some of the brains of these patients, unknown to themselves, is actually capable of making the distinction," he says.

Pupil measurement might also be useful for studying babies. Tiny infants can't tell you what they're paying attention to. "Developmental psychologists have used all kinds of methods to get this information without using language," Laeng says. Seeing what babies are interested in can give clues to what they're able to recognize -- different shapes or sounds, for example. A researcher might show a child two images side by side and see which one they look at for longer. Measuring the size of a baby's Pupils could do the same without needing a comparison.

The technology already exists for measuring Pupils -- many modern psychology studies use eye-tracking technology, for example, to see what a subject is looking at, and Laeng and his coauthors hope to convince other psychological scientists to use this method.

http://www.sciencedaily.com/releases/2012/01/120127162800.htm

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BACK-TO-SCHOOL CHECKLIST SHOULD INCLUDE TRIP TO EYE DOCTOR
Parents and students throughout the country are crossing items off their back-to-school checklists, but most are missing an important task to ensure learning success : a visit to the eye doctor for a comprehensive eye exam!
As classrooms adopt more technologically advanced tools, such as interactive blackboard presentations, the dependence on adequate visual capabilities will increase.
Studies indicate that some children with undetected vision problems can be misdiagnosed with attention deficit disorder (ADD) or attention deficit hyperactivity disorder (ADHA). The American Optometric Association (AOA) survey revealed that 64 percent of teachers witnessed a direct improvement in a child’s academic performance and/or classroom behavior after an eye or vision problem was diagnosed and treated! If your child experiences any of the following, an optometrist should be consulted about a possible vision problem:

Loses place while reading
Avoids close work
Tends to rub eyes
Has headaches
Turns or tilts head
Makes frequent reversals when reading or writing
Uses finger to maintain place when reading
Omits or confuses small words when reading
Consistently performs below potential
Struggles to complete homework
Squints while reading or watching television
Has behavioral problems
Holds reading material closer than normal.


Early detection and treatment are key in correcting vision problems and helping children see clearly. The AOA recommends that a child’s first eye examination by an eye doctor take place at 6 months of age. Comprehensive eye exams should be conducted beginning at age 3, before a child enters school, and then every two years, unless otherwise advised by an optometrist. In between exams, parents and teachers should monitor children for the more prevalent signs that a student’s vision may be impaired.