Month: March 2014

The Center for Vision Restoration of UPMC and the University of Pittsburgh today announced a $3 million gift from Louis J. Fox, a Pennsylvania native and Pitt graduate. UPMC has pledged to match Mr. Fox’s donation to the Center.

Mr. Fox, a retired commodity merchant banker and trader, has embraced the Center’s mission to discover cures for blindness and vision impairment through a joint program of the UPMC Eye Center and McGowan Institute for Regenerative Medicine.

“His generous gift will aid us in our efforts to pioneer comprehensive, patient-driven research and clinical therapies to treat people who through disease, accident or injury have limited sight. To honor his generosity, the Center will now be known as the Louis J. Fox Center for Vision Restoration,” said Center executive director Maj. Gen. (retired) Gale Pollock, who, as former Deputy Surgeon General of the U.S. Army, recognized the need to find ways to restore lost vision.

More than one in 10 of all combat wounds during the conflicts in Iraq and Afghanistan have been eye injuries and, in some cases, have left service members with impaired vision, Gen. Pollock noted. Unfortunately, there often is very little that can be done to restore sight after severe eye trauma. In addition, the World Health Organization estimates that about 120 million people worldwide are visually impaired due to cataracts, corneal scarring, glaucoma, macular degeneration, diabetic retinopathy and other conditions.

Those figures hit home for Mr. Fox, who was diagnosed 10 years ago with central retinal vein occlusion (CRVO), an incurable condition caused by blood vessel obstruction. It rapidly left him with life-changing vision loss, first in his right eye and then in his left three years later. More than 100,000 Americans are estimated to have CRVO.

“Before my situation, I knew very little about vision loss,” said Mr. Fox, who is married with two grown children and currently resides in Ft. Lauderdale, Fla. and Taconic, Conn. “As an avid pilot and sailor, I had taken my good vision for granted. Losing it has been extremely difficult. I learned of the Center for Vision Restoration at UPMC soon after it was established in September 2008, and of the promising work being done here.”

“My heartfelt desire is that my contribution speeds the discovery and development of therapies that will make it possible for people to see again,” he added.

Source
The University of Pittsburgh

Using the tools and techniques of soft condensed matter physics, a research team in Switzerland has demonstrated that a finely tuned balance of attractions between proteins keeps the lens of the eye transparent, and that even a small change in this balance can cause proteins to aggregate and de-mix. This leads to cataract formation, the world’s leading cause of blindness. This work could shed light on other protein aggregation diseases (such as Alzheimer’s disease), and may one day lead to methods for stabilizing protein interactions and thus preventing these problematic aggregations from occurring.

The eye lens is made up of densely packed crystallin proteins, arranged in such a way that light in the visible wavelength range can pass through. But for a variety of reasons including UV radiation exposure and age, the proteins sometimes change their behavior and clump together. As a result, light is scattered once it enters the lens, resulting in cloudy vision or blindness. There is currently no known way to reverse the protein aggregation process once it has begun. Nearly 5 million people every year undergo cataract surgery in which their lenses are removed and replaced with artificial ones.

Previous research has shown that the interactions between the three major crystallin proteins that make up the concentrated eye lens protein solution are key to cataract formation. A team of scientists from the University of Fribourg, EPFL and the Rochester Institute of Technology (USA) studied the interactions between two of these proteins, at concentrations similar to those found in the eye lens, using a combination of neutron scattering experiments and molecular dynamics computer simulations. They found that a finely tuned combination of attraction and repulsion between the two proteins resulted in an arrangement that was transparent to visible light. “By combining experiments and simulations it became possible to quantify that there had to be a weak attraction between the proteins in order for the eye lens to be transparent,” explains EPFL postdoctoral researcher Giuseppe Foffi, a member of the Institut Romand de Recherche Numerique en Physique des Materiaux (IRRMA). “Our results indicate that cataracts may form if this balance of attractions is disrupted, and this opens a new direction for research into cataract formation.”

“Lots of studies have been done on individual proteins in the lens,” adds University of Fribourg physicist and lead author Anna Stradner, “But none on their mixtures at concentrations typically found in the eye. We modeled these proteins as colloidal particles, and found there was a very narrow window in which the protein solution remained stable, and this was a necessary condition for lens transparency.”

In addition to unveiling important new information about the interactions of the proteins in the eye lens, this benchmark study provides a framework for further study into the molecular properties and interactions of proteins. The results suggest that these properties could perhaps be manipulated to prevent aggregation or reverse the aggregation process once it has begun.

The results are reported in the November 9 issue of Physical Review Letters. The neutron scattering experiments were done at the Paul Scherrer Institute in Villigen, Switzerland, and the research was supported by grants from the Swiss National Science Foundation, the Marie Curie Network and the National Institutes of Health (USA).

Source: Mary Parlange

Ecole Polytechnique F?�d?�rale de Lausanne

Leaders in the fight to eliminate curable corneal blindness that brings unnecessary misery to 10 million people worldwide have joined forces from opposite sides of the globe.

“An extreme shortage of cornea tissue available for transplant is a worldwide problem”

In a move that builds on a legacy of innovation in treatment of corneal blindness, the Singapore Eye Bank and the Singapore National Eye Centre will engage consulting services from SightLife eye bank in Seattle, WA (United States) to achieve these three local and regional objectives:

1) Increase long-term capacity of the Singapore Eye Bank to recover enough tissue to meet 100% of local need for sight-restoring transplants, and to further develop its education and training initiatives as a centre for excellence in eye banking in Asia.

2) Build on the already proud tradition of cornea donation in Sri Lanka by establishing a model national eye bank in that country, the National Eye Bank of Sri Lanka. The Sri Lankan people are known throughout the world for their service to others through faith-based cornea donation at the end of life.

3) Grow the Association of Eye Banks of Asia (an association formed with the Asia Cornea Society) in its ability to offer services that support member needs and reduce corneal blindness in Asia.

“An extreme shortage of cornea tissue available for transplant is a worldwide problem,” said Professor Donald Tan, Medical Director of both the Singapore Eye Bank and the Singapore National Eye Centre, internationally acclaimed for its corneal transplantation program, and for leadership in corneal blindness prevention through the stewardship of the Asia Cornea Society.

“SightLife is a global leader in eye banking with a dedicated team of experts to support eye bank development around the world. We want to work with the best partners in building local and regional capacity to meet this crucial need.” Professor Tan is also the President of both Asia Cornea Society and the Association of Eye Banks of Asia.

“We are honored at this opportunity to join efforts with the Singapore Eye Bank and the Singapore National Eye Centre, and with colleagues of such international reputation in the ophthalmology field as Professor Tan,” said Monty Montoya, President of SightLife. “Partnerships like this are by far the most effective way to end unnecessary corneal blindness for 10 million people worldwide.”

Source:

SightLife

Asia Cornea Society (ACS)

Association of Eye Banks of Asia (AEBA)

A comprehensive drug development strategy that starts with extensive screening of potential targeting agents and then narrows down to a small-molecule prototype has yielded two potential drugs that block cancer-promoting pathways in novel ways, a team led by scientists at The University of Texas M. D. Anderson Cancer Center reports in two papers published back-to-back online at the Proceedings of the National Academy of Sciences.

“The conceptual advance here is to demonstrate how to go rapidly from screening to structural-functional analysis to drug prototype in a few years,” said co-senior author Wadih Arap, M.D., Ph.D., of the David H. Koch Center at M. D Anderson.

“The practical outcome is a pair of new drug candidates, one that acts as a decoy to inhibit a cancer-promoting pathway and another that blocks angiogenesis, the development of new blood vessels, which has the potential to treat both cancer and retinopathies that cause blindness,” said co-senior author Renata Pasqualini, Ph.D., also of the David H. Koch Center.

The strategy begins with the screening of millions of peptides – short combinations of at least two amino acids, the building blocks of proteins. Once a peptide is found that binds the target, a durable drug called a peptidomimetic is made from short combinations of non-natural amino acids.

For proof of concept, the team targeted the epidermal growth factor receptor pathway (EGFR) and the vascular endothelial growth factor receptor pathway (VEGFR).

EGFR is overexpressed on the cell surfaces of a number of cancers, including lung, colon, and head and neck. Epidermal growth factor binds to the receptor and causes cells to divide. It is currently treated with two types of drugs, antibodies that block the receptor and small kinase inhibitors. VEGFR is overexpressed in the cancer vascular system and is central to the formation of new blood vessels (angiogenesis) that accompany tumor growth

Drugs reduce tumor volume, blood vessel growth in mice

The researchers created a decoy that lures EGF away from its receptor. In a mouse model of head and neck cancer, mice that received the decoy had a median tumor size half that of those in control groups.

They also demonstrated that the drug prototype could also serve as a decoy for cetuximab, an antibody drug that blocks the pathway by plugging into the EGFR. When the peptidomimetic and cetuximab were introduced into human colon and head and neck cancer cell lines, the small drug inhibited the antibody’s action.

For VEGFR, the team discovered a peptide that binds to the receptor, inhibiting angiogenesis. In a series of mouse model experiments, treated mice showed reductions in the number of blood vessels ranging from 37 percent to 72 percent.

In an animal model of retinopathy – overgrowth of blood vessels in the eye that can cause blindness – mice treated with the peptide had a 59 percent reduction in angiogenesis compared to control mice. A separate test of the peptidomimetic in an eye drop formulation resulted in a 53 percent reduction in abnormal retinal blood vessel growth.

This raises the possibility of developing an easily administered treatment for diabetic retinopathy or retinopathy of prematurity, Arap said. Preclinical studies continue for both cancer and retinopathy applications. Using small molecules to bind to the receptor site is a new approach to inhibiting VEGFR.

Screening, winnowing and developing the peptides

The group’s approach begins by screening the target receptors with a phage display library used by Arap and Pasqualini. This method screens billions of viral particles that each display a different peptide on its outer coat to find those that fit into the receptor like a key goes into a lock.

Candidate peptides are next winnowed by using structural and functional analysis. Once a peptide is identified and tested, the researchers take an additional step to synthesize a new version of the peptide more suited for use as a drug.

L-amino acids and proteins are the building blocks of life but are easily degraded by cellular protein recycling machinery, making peptide-based drugs more vulnerable to destruction. Through a process called retro-inversion, the group chemically synthesizes a mirror image peptidomimetic using D amino acids along with a reversed peptide sequence. The resulting products are more durable but still target the receptor.

For example the peptide that targets VEGFR is called RPL, letters that represent three natural amino acids that make up the peptide. The retro-inverted D-peptidomimetic is D(LPR). For the EGFR decoy, the natural peptide CVRAC becomes the D-peptidomimetic D(CARVC).

The two prototype drugs will need to be further refined in preclinical models and later tested in clinical trials before they can become available for general use.

Both studies were funded by grants from the U.S. Department of Defense and the National Institutes of Health, and awards from the Gillson-Longenbaugh Foundation, the Marcus Foundation and AngelWorks. Marina Card??-Vila, Ph.D., first author of the EGFR paper, is a fellow of the Susan G. Komen for the Cure. Ricardo J. Giordano, Ph.D., the first author of the VEGFR paper, is currently an Assistant Professor of Biochemistry at the Chemical Institute, University of S??o Paulo, Brazil.

Co-authors of the VEGFR paper with first author Giordano, Pasqualini and Arap are Card??-Vila and Ahmad Salameh, Ph.D., of M. D. Anderson’s David H. Koch Center; Christiane Anobom, Ph.D., Ana Valente, Ph.D., and Fabio Almeida, Ph.D. of the National NMR Center, Rio de Janeiro Federal University, Rio de Janeiro, Brazil; Benjamin Zeitlin, Ph.D., and Jacques N?�r, D.D.S., Ph.D., of the Angiogenesis Research Laboratory at the University of Michigan School of Dentistry; David Hawke, Ph.D., of M. D. Anderson’s Center for Targeted Therapy; and Richard Sidman, M.D., of Harvard Medical School and the Department of Neurology at Beth Israel Deaconess Medical Center.

Co-authors on the EGFR paper with first author Card??-Vila, Arap and Pasqualini are Giordano; Sidman of Harvard; and Zhen Fan, M.D., and John Mendelsohn, M.D., M. D. Anderson’s president, both of the Department of Experimental Therapeutics.

Source
University of Texas M. D. Anderson Cancer Center

Researchers at University College London say they have gleaned a key insight into the molecular beginnings of age-related macular degeneration, the No. 1 cause of vision loss in the elderly, by determining how two key proteins interact to naturally prevent the onset of the condition.

In a paper to be published in a forthcoming issue of the Journal of Biological Chemistry, the team reports for the first time how a common blood protein linked to the eye condition reins in another protein that, when produced in vastly increased amounts in the presence of inflammation or infection, can damage the eye.

“By starting to understand these interactions in greater detail, we can begin to devise methods that will ultimately prevent the development of blindness in the elderly,” said Zuby Okemefuna, the lead author of the paper to be published Jan. 8.

Age-related macular degeneration, or AMD, is painless but affects the macula, the part of the retina that allows one to see fine detail. One form of the debilitating condition, known as “wet” AMD, occurs when abnormal and fragile blood vessels grow under the macula, leaking blood and fluid and displacing and damaging the macula itself. The second form, “dry” AMD, occurs when light-sensitive cells in the macula slowly break down.

It is believed that both forms start on a common molecular route and then deviate into dry or wet AMD, explained the research leader, Steve Perkins.

“The earliest hallmark of AMD is the appearance of protein, lipid and zinc deposits under the retinal pigment epithelial cells,” he said, adding that the yellowish deposits, usually discovered by an ophthalmologist, are commonly known as “drusen.”

The researchers studied two proteins involved in drusen formation — blood protein Factor H and a second blood protein known as C-reactive protein — and showed that Factor H binds to C-reactive protein when C-reactive protein is present in large amounts, as in the case of infection, to reduce the potentially damaging effects of an overactive immune system.

“In the eye, during the normal processes of aging, cells will die naturally for all sorts of reasons,” Okemefuna said. “The blood supply to the eye will bring C-reactive protein with it, and a low level of C-reactive protein activity will enable the normal processes of clearance of dead cells at the retina through mild inflammation. In conditions of high inflammation, the levels of C-reactive protein in the retina will increase dramatically.”

Uncontrolled C-reactive protein activity causes damage to the retina, which is followed by more inflammation and then even more damage to the retina, and so forth.

“It’s the debris of broken up retinal cells, some of which is caused by this cycle, that is deposited as drusen,” Okemefuna said.

The team also found that a genetically different form of Factor H does not bind to the C-reactive protein quite as well as the normal one, making people who carry the modified protein more vulnerable to an immune system attack in the eye and, thus, drusen buildup.

“In normal individuals, further damage to the retina by prolonged exposure to high levels of C-reactive protein is prevented by Factor H. C-reactive protein also prevents Factor H from clumping together and initiating the processes that lead to drusen formation,” Perkins said. “Both these ‘good’ activities of Factor H are much reduced in the genetically different form of Factor H.”

While there is no known cure for AMD, existing therapies aim to treat the symptoms and delay progression.

“It is interesting how the interaction of these two blood proteins protects the eye during crisis,” Perkins said. “The two proteins also can be involved in a rare and often fatal cause of kidney failure in children. We now are better positioned to begin to work out preventative strategies for these diseases.”

Ruodan Nan, Ami Miller and Jayesh Gor also were co-authors on the study, which was funded over the past three years by University College London, the Biotechnology and Biological Sciences Research Council, the Mercer Fund of the Fight for Sight Charity and the Henry Smith Charity.

Source:
Angela Hopp

American Society for Biochemistry and Molecular Biology

As Glaucoma Research Foundation moves into the first year of a comprehensive new Strategic Plan setting Strategic Imperatives through 2011, a gift of $1,550,000 from Melza and F.T. Barr has kicked off GRF’s new $12 million capital campaign in support of the plan, announced GRF President and CEO Thomas M. Brunner.

“This is an extraordinary gift and sets an inspiring example that beating glaucoma must be everyone’s top priority,” said Brunner. “An epidemic of blindness from glaucoma may be coming if we don’t act now to get ahead of this dreaded disease. Following the Barr’s wonderful lead, increased giving from all of us will enable GRF to fund the innovative research that gives genuine hope we will prevail.”

“I feel so strongly that GRF is on the right track,” said F.T. Barr, a GRF board member from Houston, “I have increased my gift by 50% from our last capital campaign.” The new capital campaign builds on the momentum of a three-year campaign completed last summer. The goal of $7.5 million was surpassed with total giving of $8.3 million.

That campaign had been originally motivated by the need to extend GRF’s Catalyst For a Cure research consortium into a second three-year cycle after its start-up phase. The Barrs had anchored that campaign with a gift of $1 million, which in turn inspired other members of the Board to increase their own personal giving collectively by 200%.

GRF’s first major gift program, The Catalyst Circle, was also born in that campaign, bringing in more than 100 donors at the $1,000 level and above.

“Gifts like the Barrs’, and the others it will inspire, are essential if we are to fund the kind of innovative research needed to unlock the mysteries of glaucoma,” explained Brunner. “During the due diligence phase of our planning, we were very concerned to learn that sight-stealing threat presented by glaucoma is simply not a priority of our national health institutions.” In fact, Brunner said, GRF is among the few national leaders (outside of academia, industry and the government) providing grant funds to stimulate innovative glaucoma research.

GRF’s capacity to make those grants relies almost totally on the generosity of individuals across the country. GRF receives no government funding.

Strategic Plan Sets Imperatives through 2011

Strategic Imperatives in the plan include:

– In research, reinforcing GRF’s commitment to innovative research, emphasizing the need for the multi-year collaborations aimed at funding a cure, and the expansion of the number of grants awarded in the Shaffer Fund for Glaucoma Breakthroughs to engage new minds and ideas;

– In Patient Education , seeking partnerships with affiliate agencies to maximize patient resources and minimize duplication of efforts, and offering wide distribution of all these materials at minimal cost to eye care professionals and their patients everywhere;

– In finance and administration , a continuation of efficiencies that allow 85 cents of every dollar raised to go to research and patient education programs.

About The Glaucoma Research Foundation

Glaucoma is the leading cause of preventable blindness. Founded in 1978 in San Francisco, the Glaucoma Research Foundation works to prevent vision loss from glaucoma by investing in innovative research, education, and support with the ultimate goal of finding a cure.

Glaucoma Research Foundation

1. Intersubunit Anesthetic Binding on GABAA Receptors

Guo-Dong Li, David C. Chiara, Gregory W. Sawyer, S. Shaukat Husain, Richard W. Olsen, and Jonathan B. Cohen

Anesthesia has revolutionized medicine since its introduction in 1846. But the molecular workings of the responsible agents have remained surprisingly elusive. This week, Li et al. tackled the problem using photoaffinity labeling, a technique for labeling binding sites on proteins. Because most general anesthetics enhance the activity of GABAA receptors, the authors photolabeled GABAA receptors, purified from bovine cortex, with a photoreactive analog of the intravenous anesthetic etomidate. By protein microsequencing, they identified two labeled methionines. GABAA receptors are heteromers of five subunits each having extracellular domains and four membrane-spanning domains (M1-4). One photolabeled methionine was in the M1 region of the a subunit and the other was in M3 of the ?? subunit. Structural models predict that the anesthetic site is a water-filled pocket located in the same subunit interface as the GABA binding site in the extracellular domain, some 50 A away. The perfect place for an allosteric modulatory site, it would seem.

2. Transcranial Imaging of Visual Cortical Plasticity

Manavu Tohmi, Hiroki Kitaura, Seiji Komagata, Masaharu Kudoh, and Katsuei Shibuki

Several tricks have been used to map brain activity noninvasively, thus avoiding potentially toxic dyes and manipulation of the tissue. This week, Tohmi et al. report on a noninvasive imaging technique that is powered by mitochondria. The authors compared the well studied intrinsic optical imaging method to that of endogenous flavoprotein fluorescence, the latter of which relies on activity-induced changes in the fluorescence of mitochondrial flavoproteins. The authors measured transcranial fluorescence in the visual cortex of anesthetized mice before and after one eye had been sewn shut for days or weeks. As expected, monocular deprivation led to decreased light responses from the deprived eye, whereas responses from the nondeprived eye increased in the binocular, but not the monocular, zone of the cortex. Imaging by endogenous flavoprotein fluorescence proved to be superior to imaging of intrinsic signals both in terms of signal-to-noise ratio and temporal resolution.

3. Probing Cerebellar Granule Cell Function In Vivo

Henrik Jorntell and Carl-Fredrik Ekerot

Often the simplest explanation can be the best one. Jorntell and Ekerot argue that this is the case for the way in which cerebellar granule cells process somatosensory information. A granule cell has about four dendrites, each receiving input rom a single excitatory mossy fiber synapse, which in turn transmits signals from a specific site (or eceptive field) on the skin. The authors recorded synaptic activity in granule cells in the forelimb area of the cerebellar C3 zone in decerebrate/unanesthetized cats after different types of skin stimulation. Each mossy fiber input to a granule cell contributed to spiking. There was little evidence of convergence from different types of inputs or from different receptive fields. In other words, these granule cells did not integrate different types of inputs, as has been proposed in sparse-coding theories, but rather acted as signal-to-noise-enhancing threshold detectors for a single, specific type of input.

4. Altered AMPA Receptor Trafficking and ALS

Chen Lai, Chengsong Xie, Stefanie G. McCormack, Hsueh-Cheng Chiang, Marta K. Michalak, Xian Lin, Jayanth Chandran, Hoon Shim,Mika Shimoji, Mark R. Cookson, Richard L. Huganir, Jeffrey D. Rothstein, Donald L. Price, Philip C. Wong, Lee J. Martin, J. Julius Zhu, and Huaibin Cai

Loss-of-function mutations in the ALS2 gene cause a juvenile form of amyotrophic lateral sclerosis, resulting in a progressive loss of motor neurons. This week, Lai et al., using a combination of molecular and electrophysiological approaches, found that loss of the ALS2 gene product alsin in ALS2-/- mice causes defects in AMPA receptor trafficking. When Lai et al. looked for proteins that interact with alsin, they fished out the glutamate receptor interacting protein 1 (GRIP1), whose role is to shuttle the AMPA receptor subunit GluR2 to the postsynaptic membrane. In neurons from ALS2-/- mice, neither GRIP1 nor GluR2-containing AMPA receptors made their way to the synapse. This is not inconsequential because AMPA receptors lacking GluR2 subunits are more permeable to calcium, which rendered neurons more vulnerable to excitotoxicity. Thus, impaired AMPA trafficking in the absence of normal alsin could contribute to motor neuron degeneration.

Contact: Sara Harris

Society for Neuroscience

Glaucoma appears to be associated with slower spoken reading and increased reading impairment in older adults, according to a report in the January issue of Archives of Ophthalmology, one of the JAMA/Archives journals.

“Glaucoma [a common eye condition, which can damage the eye and cause loss of vision] affects 2 percent of U.S. adults older than 40 years, and as many as 10 percent have suspected glaucoma,” according to background information in the article. “Determining who should be treated requires that we understand when and how glaucoma produces disability.”

Pradeep Y. Ramulu, M.D., Ph.D., and colleagues at the Wilmer Eye Institute, Johns Hopkins University, Baltimore, tested 1,154 individuals (average age 79.7) to evaluate the relationship between glaucoma and spoken reading speed. Participants were asked to read non-scrolling text aloud. Those who read slower than 90 words per minute were defined as having impairment. Glaucoma status was determined by testing participants’ visual fields, optic nerve images and medical records. Demographic information was also noted.

A total of 1,017 (95.6 percent) of participants did not have glaucoma. An additional 73 had unilateral glaucoma (glaucoma in one eye) and 64 had bilateral glaucoma (glaucoma in both eyes). “Univariate analysis demonstrated reading impairment in 16 percent of subjects without glaucoma, 21.1 percent of subjects with unilateral glaucoma and 28.4 percent of subjects with bilateral glaucoma,” the authors write. “Subjects with unilateral glaucoma showed similar reading speeds and odds of reading impairment when compared with subjects without glaucoma. Subjects with bilateral glaucoma read 29 words per minute slower than those without glaucoma and had roughly twice the odds of reading impairment.”

“Lower levels of education were associated with slower reading speeds, and race persisted as a significant predictor of reading speed even after adjusting for education,” the authors write.

“As reading out loud was necessary to measure reading speed, racial differences in speaking rates could account for the difference in the measured reading rate ??�,” the authors conclude. “Future work should evaluate reading in subjects with glaucoma under more realistic conditions to further explore if reading impairment is more prevalent than reported herein.”

Arch Ophthalmol. 2009;127[1]:82-87.

This study was supported by National Institutes of Health grants. Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.

Archives of Ophthalmology

Chances are you or someone you know has had laser eye surgery to
correct blurry vision. Now, doctors are using the procedure in a new way. In some cases,
they’re not just helping patients see better, they’re actually preventing them from going blind.

Mike Samogala says he’s never taken time with his kids for granted. Lately, those moments
have meant even more. Just a few months ago, Mike was diagnosed with eye cancer. It came
with no warning or symptoms.

“There was nothing. I mean, you just, every year you get your eyes examined and you can tell
when you need your glasses or contacts changed, and that’s what it was like,” says Samogala.

Because there are so few treatment options, Mike lost his eye to cancer. But doctors hope to
prevent that in other patients by using a very common, very proven approach.

“Laser may be used for very early, very thin melanomas that are not near the optic nerve.
These patients require closer follow up, but if the laser is used they can preserve 100% of their
vision in many cases,” says Tom Olencki, MD, with Ohio State University’s James Cancer
Hospital.

Dr. Olencki says that’s a vast improvement over some of the options in the past. Most patients
either lost the eye, or underwent more extensive radiation treatments. Catching the tumor early
could mean something as simple as a few minutes under the laser. And it could mean more
than just saving a patient’s eyesight, it could save their lives.

“Many times if the eye melanoma is discovered while it’s still small and thin, we can almost
assure patients long-term survival,” says Olencki.

Doctors aren’t sure what causes eye cancer, but it may have something to do with eye color. His
pale blue eyes may have put Mike more at risk.* Eye cancer is rare, affecting only about 2,000
people each year.** Doctors believe exposing the eyes to direct, bright sunlight and smoking
may be risk factors. Experts say you should get your eyes checked by age 50, especially if you
notice a change in your vision.

*Risk Factors for Primary Intraocular Melanoma, American Cancer Society. Retrieved April 2008 from cancer
**Cancer Facts & Figures 2008, American Cancer Society. Retrieved April 2008 from cancer keywords:
cancer rates 2008

Ohio State University

Early-stage age-related macular degeneration appears to be related to modifiable risk factors, including smoking and low levels of high-density lipoprotein (HDL or “good” cholesterol), according to a report in the June issue of Archives of Ophthalmology, one of the JAMA/Archives journals. The condition appears uncommon before age 55 but the risk increases with age thereafter.

Most studies assessing the prevalence of age-related macular degeneration (AMD) have focused on middle- and older-age adults, according to background information in the article. “To our knowledge, accurate estimates of prevalence of AMD among adults younger than 40 years are lacking,” the authors write. “Such information is important for understanding the relationships of risk factors to AMD across the age spectrum and for identifying factors that might affect this disease earlier in life.”

Ronald Klein, M.D., M.P.H., of the University of Wisconsin, Madison, and colleagues assessed 2,810 individuals age 21 to 84 participating in the Beaver Dam Offspring Study. The presence and severity of drusen-yellow or white deposits in the retina, an early sign of AMD-was determined, along with that of other characteristics of AMD.

Early AMD was present in 3.4 percent of the participants, with rates varying from 2.4 percent in those age 21 to 34 to 9.8 percent in those age 65 years and older. Besides age, other factors associated with increased risk for AMD included being male, smoking more heavily for a longer period of time, and being hearing impaired, whereas having higher levels of HDL cholesterol was associated with reduced risk.

Factors not associated with early AMD included blood pressure, body mass index, physical activity level, history of heavy drinking, white blood cell count or total cholesterol level.

Drusen were present in the macula-the area in the retina responsible for sharp vision-in 63.3 percent of the participants, and the frequency of drusen increased with age. When age was considered, men and women had approximately the same number of drusen.

“In summary, the Beaver Dam Offspring Study data provide precise estimates of the prevalence of various signs of AMD (soft drusen, pigmentary abnormalities) over a wide spectrum of ages from the third to the ninth decade of life,” the authors write. “They demonstrate that early AMD onset may occur in midlife. Some modifiable factors (smoking status and serum HDL cholesterol level) associated with AMD in older cohorts were associated with early AMD in this cohort of middle-aged adults.”

“The higher frequency of AMD in people aged 65 or older in an aging population makes this an important public health problem,” they conclude. “Further information regarding the natural history of AMD and its risk factors, especially early in life, is important for developing preventive approaches to it.”

Archives of Opthalmology. 2010;128[6]:750-758.

Source
Archives of Opthalmology