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Archive - Nov 14, 2015

Programmable Electronic Glasses with Digital Eye Patch May Provide Better-Tolerated Treatment for “Lazy Eye”--New Glasses Approved by FDA and Now Available from Eye Care Professionals in United States

A new study on lazy eye found that programmable electronic glasses help improve vision in children just as well as the more traditional treatment using eye patches. This "digital patch" is the first new effective treatment for lazy eye in half a century. Results from the first U.S. trial of this device will be presented at AAO 2015, the 119th Annual Meeting of the American Academy of Ophthalmology. Lazy eye, also called amblyopia, remains the most common cause of visual impairment in children. Amblyopia is poor vision in an eye that did not develop normally during early childhood. This can occur when one eye is much more nearsighted than the other, or when one eye wanders or strays inward. The child needs to receive treatment by the age of 8 or so while their eyes and brain are still developing, or he or she could become blind in the weaker eye. Unfortunately, getting children to comply with lazy eye treatments like eye patches or medicated drops remains a significant challenge for both ophthalmologists and parents alike. A recent study found that 1 in 4 kids feel anxiety before using eye drops. Nearly 15 percent refuse to take eye drops at all. Both drops and eye patches work based on the occlusion method. This method blocks vision in the eye with the best sight, forcing the brain to rely on the so-called “lazy eye.” During the process, vision improves though many children will still need glasses to correct their eyesight. In comparison, the electronic glasses used in this study combine vision correction and occlusion. The lenses can be filled to fit a child's vision prescription. Because the lenses are liquid crystal display (LCD), they can also be programmed to turn opaque, occluding vision in the left or right eye for different time intervals, acting like a digital patch that flickers on and off.

In Addition to Telomerase, ATM Kinase Also Shown to Control Telomere Length; New Study from Johns Hopkins; Nobel Laureate Led Work

Since the discovery of the enzyme telomerase in 1984 (recognized by the 2009 Nobel Prize in Physiology or Medicine), identifying other biological molecules that lengthen or shorten the protective caps on the ends of chromosomes has been slow going. Now, researchers at Johns Hopkins, led by one of the three telomerase 2009 Nobel Laureates, report uncovering the role of an enzyme crucial to telomere length and say the new method they used to find this enzyme should speed discovery of other proteins and processes that determine telomere length. Their results were published online on November 12, 2015 in an open-access article in Cell Reports. The article is titled “ATM Kinase Is Required for Telomere Elongation in Mouse and Human Cells.” "We've known for a long time that telomerase doesn't tell the whole story of why chromosomes' telomeres are a given length, but with the tools we had, it was difficult to figure out which proteins were responsible for getting telomerase to do its work," says Carol Greider, Ph.D., the Daniel Nathans Professor and Director of Molecular Biology and Genetics at the Johns Hopkins Institute for Basic Biomedical Sciences. Dr. Greider shared the 2009 Nobel Prize in Physiology or Medicine jointly with Dr. Elizabeth Blackburn and Dr. Jack Szostak, "for the discovery of how chromosomes are protected by telomeres and the enzyme telomerase." ( Figuring out exactly what's needed to lengthen telomeres has broad health implications, Dr. Greider notes, because shortened telomeres have been implicated in aging and in diseases as diverse as lung and bone marrow disorders, while overly long telomeres are linked to cancer.

Anti-VEGF Drug (Lucentis) Injections Highly Effective in Treating Proliferative Diabetic Retinopathy, Joslin Diabetes Center & Harvard Medical School Scientists Report

A clinical trial among more than 300 patients has found that the drug ranibizumab (Lucentis) is highly effective in treating proliferative diabetic retinopathy (PDR), a complication of diabetes that can severely damage eyesight. The results, published by the Journal of the American Medical Association (JAMA) (see article link below), demonstrate the first major therapy advance for the condition in nearly 40 years. A different report of the same study was previously described in a BioQuick News article ( based on a JAMA news release ). Funded by the National Eye Institute (NEI) and conducted by the Diabetic Retinopathy Clinical Research Network (, the JAMA-reported trial compared Lucentis injections with a type of laser therapy called panretinal photocoagulation, which has remained the gold standard for PDR since the mid-1970s. Although laser therapy preserves central vision, it can damage night vision and side vision, so researchers have sought therapies that lack these side-effects. The new trial results "provide crucial evidence for a safe and effective alternative to laser therapy against PDR," said NEI Director Paul A. Sieving, M.D., Ph.D. "Patients who received Lucentis showed a little bit better central vision, much less loss of their side vision, and substantially less risk for surgery than patients who received laser treatment," said Lloyd Paul Aiello, M.D., Ph.D., Director of the Beetham Eye Institute at Joslin Diabetes Center and Professor of Ophthalmology at Harvard Medical School. "These findings will change the available treatment options for patients with PDR." Diabetic retinopathy damages blood vessels in the light-sensitive retina in the back of the eye. As the disease worsens, blood vessels can swell and lose their ability to function properly.

Anti-VEGF Drug (Lucentis) Injections Yield Results Comparable to Those of Laser Panretinal Photocoagulation, with Fewer Side-Effects, in 2-Year Study of Proliferative Diabetic Retinopathy Treatments, JAMA Article Reports

Among patients with proliferative diabetic retinopathy PDR), treatment with an injection in the eye of the drug ranibizumab (Lucentis) resulted in visual acuity that was not worse than panretinal photocoagulation at 2 years, according to a study appearing in an open-access article published online on November 13, 2015 in the Journal of the American Medical Association (JAMA), and intended to coincide with the study’s presentation at the American Academy of Ophthalmology 2015 Annual Meeting (November 14-17, Las Vegas, Nevada) ( The JAMA article is titled “Panretinal Photocoagulation vs Intravitreous Ranibizumab for Proliferative Diabetic Retinopathy: A Randomized Clinical Trial.” PDR is a leading cause of vision loss in patients with diabetes mellitus, resulting in 12,000 to 24,000 new cases of blindness each year in the United States. Pan-retinal photocoagulation (PRP), a laser procedure is currently the standard treatment for reducing severe visual loss from PDR. However, PRP can cause permanent peripheral visual field loss and decreased night vision and may exacerbate diabetic macular edema (DME), which is swelling of the retina in diabetes mellitus due to leaking of fluid from blood vessels within the macula of the eye). These negative effects make alternative treatments desirable, according to background information provided in the JAMA article. When used as treatment of DME, intra-vitreous anti-vascular endothelial growth factor (anti-VEGF) agents reduce the risk of diabetic retinopathy worsening and increase the chance of improvement, making these agents a potentially viable PDR treatment. Adam R.

Small Organic Compound (NT157) Inhibits IGF1R-IRS1/2 & STAT3 Signaling Pathways; May Be Effective As “Double-Agent” Against Both Melanoma & Colon Cancer; NT157 Is Licensed by Israel’s TyrNovo Onco-Pharma Company

Cancer is a highly complex disease in which the tumor recruits its surrounding tissue, as well as the immune system, to support and promote its own growth. This explains why tumor therapy has been difficult for physicians. Researchers now realize that, not only does the tumor need to be targeted, but also its microenvironment and the immune system, which are both subverted by the tumor to support its growth. Two studies published recently in Oncogene focus on new potential-drug-treatment research through a careful study of, and link between, colorectal cancer (CRC) and melanoma. In one article, published online on September 14, 2015, long-time cancer researcher Alexander Levitzki (photo), Ph.D., Wolfson Family Professor Emeritus of Biochemistry at the Hebrew University of Jerusalem, and his senior colleagues, Efrat Flashner-Abramson, Ph.D., and Hadas Reuveni, Ph.D., together with additional colleagues, described a small organic molecule known as NT157 and its action against metastatic human melanoma. Professor Levitzki and his team showed that NT157 acts as a dual-targeting agent that blocks two different signal transduction pathways that are central to the development and maintenance of multiple human cancers. They showed that NT157 targets, not only the IGF1R-IRS1/2 signaling pathway, as previously reported, but also the Stat3 signaling pathway, and that the compound demonstrates remarkable anti-cancer characteristics in A375 human melanoma cells and in a metastatic melanoma model in mice.

TITAN Technology with Functionalized “Dendrimers” Used to Analyze Endocytosis

Purdue researchers have devised a way to capture the finer details of complex cell processes by using tiny synthetic particles known as dendrimers, in a method that could lead to more targeted treatment for cancer. In particular, they have developed a novel proteomic strategy named TITAN (Tracing Internalization and TrAfficking of Nanomaterials) to reveal real-time protein–dendrimer interactions using a systems biology approach. Dendrimers are symmetrically branched nanoparticles, similar in size to naturally occurring proteins. Dendrimers are similar in size to naturally occurring proteins. A dendrimer's small size and its branched structure make it an ideal courier for transporting a variety of molecules via its many branches into a cell. A precise understanding of how cells engulf small particles, in a process known as endocytosis, could help researchers improve drug delivery and reveal the mechanisms of viruses. But the particles "eaten" by cells and the proteins that control cell entry pathways are too small for conventional technologies to detect. W. Andy Tao, Ph.D., Professor of Biochemistry, Purdue University, and his Purdue collaborators, have developed the TITAN method that sends “dendrimers” into cells to track, capture, and isolate the proteins that regulate the cell internalization process, identifying 809 proteins involved in cell entry pathways. The TITAN method "helps us understand how cells internalize extracellular particles and how they move these particles around," Dr. Tao said. The Purdue group’s article was originally published online on October 1, 2015 in the Journal of the American Chemical Society (JACS). The JACS article is titled “Time-Resolved Proteomic Visualization of Dendrimer Cellular Entry and Trafficking.”