Pocket-sized retina camera, no dilating required

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Posted on 2nd May 2017 by Pacific ClearVision Institute in General |Retina

It’s the part of the eye exam everyone hates: the pupil-dilating eye drops. The drops work by opening the pupil and preventing the iris from constricting in response to light and are often used for routine examination and photography of the back of the eye. The drops sting, can take up to 30 minutes to work, and cause blurry vision for several hours afterwards, often making them inconvenient for both patient and doctor.

Now, researchers at the University of Illinois at Chicago College of Medicine and Massachusetts Eye and Ear/Harvard Medical School have developed a cheap, portable camera that can photograph the retina without the need for pupil-dilating eye drops. Made out of simple parts mostly available online, the camera’s total cost is about $185.

“As residents seeing patients in the hospital, there are often times when we are not allowed to dilate patients — neurosurgery patients for example,” said Dr. Bailey Shen, a second-year ophthalmology resident at the UIC College of Medicine. “Also, there are times when we find something abnormal in the back of the eye, but it is not practical to wheel the patient all the way over to the outpatient eye clinic just for a photograph.”

The prototype camera can be carried in your pocket, Shen said, and can take pictures of the back of the eye without eye drops. The pictures can be shared with other doctors, or attached to the patient’s medical record.

The camera is based on the Raspberry Pi 2 computer, a low-cost, single-board computer designed to teach children how to build and program computers. The board hooks up to a small, cheap infrared camera, and a dual infrared- and white-light-emitting diode. A handful of other components — a lens, a small display screen and several cables — make up the rest of the camera.

The camera works by first emitting infrared light, which the iris — the muscle that controls the opening of the pupil — does not react to. Most retina cameras use white light, which is why pupil-dilating eye drops are needed.

The infrared light is used to focus the camera on the retina, which can take a few seconds. Once focused, a quick flash of white light is delivered as the picture is taken. Cameras exist that use this same infrared/white light technique, but they are bulky and often cost thousands of dollars.

Shen’s camera photos show the retina and its blood supply as well as the portion of the optic nerve that leads into the retina. It can reveal health issues that include diabetes, glaucoma and elevated pressure around the brain.

Shen and his co-author, Dr. Shizuo Mukai, associate professor of ophthalmology at Harvard Medical School and a retina surgeon at Massachusetts Eye and Ear, describe their camera and provide a shopping list of parts, instructions for assembly, and the code needed to program the camera in the Journal of Ophthalmology.

“This is an open-source device that is cheap and easy to build,” said Mukai. “We expect that others who build our camera will add their own improvements and innovations.”

“The device is currently just a prototype, but it shows that it is possible to build a cheap camera capable of taking quality pictures of the retina without dilating eye drops, ” Shen said. “It would be cool someday if this device or something similar was carried around in the white-coat pockets of every ophthalmology resident and used by physicians outside of ophthalmology as well.”

Myopia cell discovered in retina: Dysfunction of cell may be linked to amount of time a child spends indoors

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Posted on 2nd May 2017 by Pacific ClearVision Institute in General |Retina

Northwestern Medicine scientists have discovered a cell in the retina that may cause myopia when it dysfunctions. The dysfunction may be linked to the amount of time a child spends indoors and away from natural light.

“This discovery could lead to a new therapeutic target to control myopia,” said Greg Schwartz, lead investigator and assistant professor of ophthalmology at Northwestern University Feinberg School of Medicine.

More than a billion people in the world have myopia, whose incidence is rising and is linked to how much time people spend indoors as children.

The newly discovered retinal cell — which is highly sensitive to light — controls how the eye grows and develops. If the cell instructs the eye to grow too long, images fail to be focused on the retina, causing nearsighted vision and a lifetime of corrective glasses or contact lenses.

“The eye needs to stop growing at precisely the right time during childhood,” Schwartz said.

It has long been long known the retina contains a signal to focus the image in the eye, and this signal is important for properly regulating eye growth during childhood.

“But for years no one knew what cell carried the signal,” Schwartz said. “We potentially found the key missing link, which is the cell that actually does that task and the neural circuit that enables this important visual function.”

Schwartz named the cell, “ON Delayed,” in reference to its slow responses to lights becoming brighter. The cell was unique among many other cell types tested in its exquisite sensitivity to whether an image was in focus.

He described the neural circuit as the diagram that reveals how this cell is wired to other cells in the retina to acquire this unique sensitivity.

How too much time indoors may trigger myopia

The indoor light spectrum has high red/green contrast, which activates these clusters of photoreceptors in the human eye, creating the equivalent of an artificial contrast image on the retina. It’s likely the human version of the ON Delayed retinal ganglion cell would be overstimulated by such patterns, causing aberrant over-growth of the eye, leading to myopia, Schwartz said.

The study will appear in the Feb. 20 print issue of Current Biology. It was published online Jan. 26.

To conduct the study, Schwartz and co-author Adam Mani, a postdoctoral fellow in ophthalmology at Feinberg, used microscopic glass electrodes to record electrical signals from cells in a mouse retina while presenting patterns of light on a digital projector.

The next goal is to find a gene specific to this cell. Then scientists can turn its activity up or down in a genetic mouse model to try to induce or cure myopia.

The study is part of Schwartz’s larger body of research to reverse engineer the retina by identifying new retinal cell types in mice. The retina has about 50 types of retinal ganglion cells, which together convey all the information we use to perceive the visual world. Each of these cells provides different visual information — such as color or motion — about any point in space.

Schwartz, who is funded by the National Institutes of Health (NIH), wants to identify the new cells by their specific function, analyze their genetic signatures and understand how the cells are interconnected within the retina and to their targets in the brain. His research could lead to gene therapy to treat blindness and to improve the function of artificial retinal prosthetics.

The article is titled “Circuit Mechanisms of a Retinal Ganglion Cell with Stimulus-Dependent Response Latency and Activation Beyond Its Dendrites.”

Fish oil component helps damaged brain, retina cells survive, shows research

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Posted on 2nd May 2017 by Pacific ClearVision Institute in General |Retina

A team of researchers led by Nicolas Bazan, MD, PhD, Boyd Professor and Director of the Neuroscience Center of Excellence at LSU Health New Orleans School of Medicine, has shown for the first time that NDP1, a signaling molecule made from DHA, can trigger the production of a protective protein against toxic free radicals and injury in the brain and retina. The research, conducted in an experimental model of ischemic stroke and human retinal pigment epithelial (RPE) cells, is available in Advance Publication Online in Nature Research’s Cell Death and Differentiation.

Neuroprotectin D1 (NPD1) is a lipid messenger made from the omega-3 fatty acid docosahexaenoic acid (DHA) made on demand when cell survival is compromised. NPD1 was discovered and named in 2004 by Dr. Bazan and colleagues. Oxidative stress, resulting from the constant production of damaging free radicals, lays the groundwork for cell death. Cell death is accelerated by catastrophic events, like ischemic stroke, as well as neurodegenerative and blinding-eye diseases. The research team found that when systematically administered one hour after two hours of experimental stroke, NPD1 increased the production and availability of ring finger protein 146, which has been named Iduna. Iduna facilitates DNA repair and protects against a form of programmed cell death in stroke known as parthanatos by suppressing the production of a destructive protein called PARP. Their findings also include that NDP1 enhanced the production of Iduna and protection in two types of human RPE cells (ARPE-19 and primary RPE) undergoing uncompensated oxidative stress. The researchers found that the effect of NDP1 on Iduna activity peaked at six hours after the onset of the oxidative stress, A dose-dependent curve showed an increase of Iduna activity starting as 25 nM NPD1 in both types of human RPE cells. These results suggest that NDP1 selectively induces Iduna activity when uncompensated oxidative stress triggers the formation of NPD1 that in turn activates Iduna.

“These findings are significant because they show how NPD1, a lipid mediator made ‘on demand,’ modulates the abundance of a critically important protein (Iduna) toward cell survival,” notes Nicolas Bazan, MD, PhD, Boyd Professor and Director of the Neuroscience Center of Excellence at LSU Health New Orleans School of Medicine. “This protein, relatively little studied, turns out to be key for cell functional re-programing and subsistence.” DHA, found in fish oil, is an essential omega-3 fatty acid and is vital for proper brain function. It is also necessary for the development of the nervous system, including vision. A study from the Bazan laboratory published in 2011 found that DHA triggered the production of Neuroprotectin D1, a naturally occurring neuroprotective molecule in the brain derived from DHA. NDP1 bioactivity governs key gene interactions decisive in cell survival when threatened by disease or injury.

“The further unraveling of the molecular details of DHA-NPD1-Iduna expression signaling may contribute to possible therapeutic interventions for retinal degenerations and ischemic stroke.” says Bazan.

Research on retinal pigment epithelial cells promises new future treatment for glaucoma patients

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Posted on 2nd May 2017 by Pacific ClearVision Institute in General |Retina

Scientific research builds its own momentum as one discovery triggers another, building an ongoing wave of unexpected possibilities. In the world of glaucoma, such a surge began when advances in stem cell research opened doors experts had never imagined.

With this new perspective, they began to consider innovative ways to use specialized cells in the eye, like retinal pigment epithelial cells and ganglion cells. Today researchers continue to follow that path, knowing that each small step they take may lead to future glaucoma treatments.

What Are Retinal Pigment Epithelium (RPE) Cells?

Most people know at least a little about the retina. The retina is a thin tissue that’s about an inch in diameter, yet it contains all the photoreceptor cells responsible for beginning vision and their circuits that produce signals that become vision.

If you could look beneath the retina, you’d find a sheet of black cells called the retinal pigment epithelium, (RPE). The easiest way to describe the RPE is to say it supports the retina, but that doesn’t begin describe its value. These cells help by renewing the light-absorbing pigments contained in the rod and cone photoreceptors on a daily basis. They also enhance vision by absorbing scattered light. They ensure survival of photoreceptor cells by delivering nutrients, while also serving as a barrier that blocks damaging substances from getting into the retina. The RPE also stops free radicals before they can damage the retina.

The retinal pigment epithelial cells are shaped like a six-sided hexagon, so they fit together as tight as a puzzle. Tiny projections extend from RPE cells, reach out to cover photoreceptor cells and carry nutrients into the cells. When RPE cells are damaged, photoreceptor cells die, ultimately leading to blindness.

What do RPE Cells Have to do Glaucoma?

Glaucoma doesn’t typically damage RPE cells, but thanks to advances in stem cell research, it looks like RPE cells may play a crucial role in finding a cure to the degenerative disease. Experts have been studying stem cells for the last seven decades, but their time and effort is beginning to pay off.

Researchers discovered that mature stem cells from various places in the body can be removed and injected with a combination of genes that reprogram the adult cells back into their fresh embryonic state. These cells are called induced pluripotent stem cells. This has been put into practice in the lab, where adult stem cells taken from bone marrow were reprogrammed to grow into various eye cells.

When certain induced pluripotent stem cells are grown together with RPE cells, they can be reprogrammed to turn into photoreceptor cells and other retinal cells. It may even be possible to develop a group of protective nerve cells in the retina — retinal ganglion cells — that are damaged by glaucoma. While these amazing discoveries have yet to take shape as a viable treatment option for glaucoma, they certainly make it possible to believe that research using RPE cells may one day lead to a novel stem cell-based treatment that could stop or even reverse the progression of glaucoma.

A closer look at the eye: New retinal imaging technique

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Posted on 2nd May 2017 by Pacific ClearVision Institute in General |Retina

Researchers at the University of Rochester Medical Center have developed a new imaging technique that could revolutionize how eye health and disease are assessed. The group is first to be able to make out individual cells at the back of the eye that are implicated in vision loss in diseases like glaucoma. They hope their new technique could prevent vision loss via earlier diagnosis and treatment for these diseases.

In a study highlighted in the Proceedings of the National Academy of Sciences, Ethan A. Rossi, Ph.D., assistant professor of Ophthalmology at the University of Pittsburgh School of Medicine, describes a new method to non-invasively image the human retina, a layer of cells at the back of the eye that are essential for vision. The group, led by David Williams, Ph.D., Dean for Research in Arts, Sciences, and Engineering and the William G. Allyn Chair for Medical Optics at the University of Rochester, was able to distinguish individual retinal ganglion cells (RGCs), which bear most of the responsibility of relaying visual information to the brain.

There has been a longstanding interest in imaging RGCs because their death causes vision loss in glaucoma, the second leading cause of acquired blindness worldwide. Despite great efforts, no one has successfully captured images of individual RGCs, in part because they are nearly perfectly transparent.

Instead of imaging RGCs directly, glaucoma is currently diagnosed by assessing the thickness of the nerve fibers projecting from the RGCs to the brain. However, by the time retinal nerve fiber thickness has changed detectably, a patient may have lost 100,000 RGCs or more.

“You only have 1.2 million RGCs in the whole eye, so a loss of 100,000 is significant,” said Williams. “The sooner we can catch the loss, the better our chances of halting disease and preventing vision loss.”

Rossi and his colleagues were able to see RGCs by modifying an existing technology — confocal adaptive optics scanning light ophthalmoscopy (AOSLO). They collected multiple images, varying the size and location of the detector they used to gather light scattered out of the retina for each image, and then combined those images. The technique, called multi-offset detection, was performed at the University of Rochester Medical Center in animals as well as volunteers with normal vision and patients with age-related macular degeneration.

Not only did this technique allow the group to visualize individual RGCs, but structures within the cells, like nuclei, could also be distinguished in animals. If Rossi can achieve that level of resolution in humans, he hopes to be able to assess glaucoma before the retinal nerve fiber thins — and even before any RGCs die — by detecting size and structure changes in RGC cell bodies.

While RGCs were the main focus of Rossi’s investigations, they are just one type of cell that can be imaged using this new technique. In age-related macular degeneration, cone photoreceptors that detect color and are important for central vision are the first to die. AOSLO has been used to image cones before, but these cells were difficult to see in areas near Drusen, fatty deposits that are the most common early sign of the disease. Using their multi-offset technique in age-related macular degeneration patients, Rossi was able to assess the health of cones near Drusen and in areas where the retina had been damaged.

“This technique offers the opportunity to evaluate many cell classes that have previously remained inaccessible to imaging in the living eye,” said Rossi. “Not only RGCs, but potentially other translucent cell classes and cellular structures.”

Rossi and his colleagues warn that their study included a small number of volunteers and an even smaller number of age-related macular degeneration patients. More studies will be needed to improve the robustness of the technique and ensure their results are reproducible before it can be widely used in the clinic. Rossi is now setting up his own laboratory at the University of Pittsburgh and plans to continue working with Williams’ group in studying this technique and its ability to detect changes in retinal cells over the course of retinal diseases.