New Eye Monitoring Device Spots Early Signs of Diabetes

New Eye Monitoring Device Spots Early Signs of Diabetes

Originally posted by medgadget.com

by  on  • 4:23 pm

diabetic autonomic neuropathy New Eye Monitoring Device Spots Early Signs of DiabetesAutonomic neuropathy is a common complication arising from diabetes, causing side effects like gastroparesis, erectile dysfunction, and other conditions due to damaged autonomic nerves. Early detection of diabetic autonomic neuropathy can have substantial benefits to patients thanks to treatment commencing sooner than it does now. Now researchers at National Taiwan University Hospital and National Chiao-Tung University in Taiwan developed an optical sensor that hangs off a pair of glasses and helps spot autonomic neuropathy by monitoring the activity of the eye for a half hour.

diabetic neuropathy detector New Eye Monitoring Device Spots Early Signs of DiabetesThe device shines light from four color LEDs into the eye in order to stimulate the pupil to change size. It does this repeatedly, changing certain parameters, while a camera watches the pupil dilate in response to the light. By measuring the size of the pupil, its response time, and response speed, the researchers have shown that the new pupillometer may be a new modality for spotting autonomic neuropathy much earlier than what doctors are currently able to do. There are more extensive clinical trials planned to confirm the efficacy of the technology, with the hope that in a few years we’ll have convenient glasses that a patient can wear during a regular checkup to check for early signs of diabetes.

From the Optical Society:

Currently doctors rely on observing changes in digestive speed, heart rate and blood pressure to detect diabetic autonomic neuropathy, but this limits their ability to make a diagnosis early on, said Mang Ou-Yang, who led the research with colleagues at National Chiao-Tung University. Now they have shown that monitoring the pupils of people with diabetes may be a better approach.

“Compared to the existing diagnostic techniques, the pupillometer is a more reliable, effective, portable and inexpensive solution for diagnosing diabetic autonomic neuropathy in its early stages,” said Ou-Yang.

The pupil is useful for detecting diabetic autonomic neuropathy due to the neurological conditions caused by the disease. Like many organs, the eyes and pupil are dually innervated, receiving signals from both the parasympathetic and sympathetic divisions of the autonomic nervous system. These divisions control the pupil’s circular and radial muscles, respectively.
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Will

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What role does your brain play in “seeing” the world?

Originally posted at Serendip Studio.

Seeing more than your eye does

Most people (even many who work on the brain) assume that what you see is pretty much what your eye sees and reports to your brain. In fact, your brain adds very substantially to the report it gets from your eye, so that a lot of what you see is actually “made up” by the brain.


Some special features of the anatomy of the eyeball make it possible to demonstrate this to yourself. The front of the eye acts like a camera lens, differently directing light rays from each point in space so as to create on the back of the eye a picture of the world. The picture falls on a sheet of photoreceptors (red in the diagram), specialized brain cells (neurons) which are excited by light.

The sheet of photoreceptors is much like a sheet of film at the back of a camera. But it has a hole in it. At one location, called the optic nerve head, processes of neurons collect together and pass as a bundle through the photoreceptor sheet to form the optic nerve (the thick black line extending up and to the left in the diagram), which carries information from the eye to the rest of the brain. At this location, there are no photoreceptors, and hence the brain gets no information from the eye about this particular part of the picture of the world. Because of this, you should have a “blind spot” (actually two, one for each eye), a place pretty much in the middle of what you can see where you can’t see.


Look around. Do you see a blind spot anywhere? Maybe the blind spot for one eye is at a different place than the blind spot for the other (this is actually true), so you don’t notice it because each eye sees what the other doesn’t. Close one eye and look around again. Now do you see a blind spot? Hmm. Maybe its just a little TINY blind spot, so small that you (and your brain) just ignore it. Nope, its actually a pretty BIG blind spot, as you’ll see if you look at the diagram below and follow the instructions.

Close your left eye and stare at the cross mark in the diagram with your right eye. Off to the right you should be able to see the spot. Don’t LOOK at it; just notice that it is there off to the right (if its not, move farther away from the computer screen; you should be able to see the dot if you’re a couple of feet away). Now slowly move toward the computer screen. Keep looking at the cross mark while you move. At a particular distance (probably a foot or so), the spot will disappear (it will reappear again if you move even closer). The spot disappears because it falls on the optic nerve head, the hole in the photoreceptor sheet.

So, as you can see, you have a pretty big blind spot, at least as big as the spot in the diagram. What’s particularly interesting though is that you don’t SEE it. When the spot disappears you still don’t SEE a hole. What you see instead is a continuous white field (remember not to LOOK at it; if you do you’ll see the spot instead). What you see is something the brain is making up, since the eye isn’t actually telling the brain anything at all about that particular part of the picture.


Alright, you say, that’s kind of neat, but maybe the brain isn’t “making it up.” It just knows to put white where the blind spot is. Let’s try another situation and see what happens.

Table of Contents:

Blindspot Home Page
More Blind Spots
Switching Colors
Lines
Final Blindspot and Further Reading
Map Your Own Blindspot

Resources Elsewhere:

MD Support, a website serving the Macular Degeneration Community, adapted this exhibit for diagramming vision: http://www.mdsupport.org/map/map.html.

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Ocular gene therapy: current progress and future prospects

As gene therapy begins to produce its first clinical successes, interest in ocular gene transfer has grown owing to the favorable safety and efficacy characteristics of the eye as a target organ for drug delivery. Important advances also include the availability of viral and non-viral vectors that are able to efficiently transduce various ocular cell types, the use of intraocular delivery routes and the development of transcriptional regulatory elements that allow sustained levels of gene transfer in small and large animal models after a single administration. Here, we review recent progress in the field of ocular gene therapy. The first experiments in humans with severe inherited forms of blindness seem to confirm the good safety and efficacy profiles observed in animal models and suggest that gene transfer has the potential to become a valuable therapeutic strategy for otherwise untreatable blinding diseases.These two authors contributed equally to this work.

Link to purchase this material from Trends in Molecular Medicine

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Cone-Rod Dystrophy Gene Therapy Rescues Vision in Canines

First published at blindness.org

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Oct. 10, 2013 – A French research team led by Fabienne Rolling, Ph.D., of INSERM, has used gene therapy to restore vision in a canine model of cone-rod dystrophy caused by mutations in the gene RPGRIP1. Reported in the journal Molecular Therapy, the advancement marks the first time RPGRIP1 gene therapy has been used successfully in a large-animal model of cone-rod dystrophy. Demonstration of safety and efficacy in a large animal is an important step in moving the therapy into human studies. Dr. Rolling says that her team is now adapting the RPGRIP1 for evaluation in humans.

In humans and the canine model, cone-rod dystrophy affects cones first, leading to loss of visual acuity and color vision in childhood. Loss of peripheral and night vision follow as the disease progresses and affects rods.

In the RPGRIP1 gene therapy study, cone function was significantly rescued in the canines while rod function was preserved. The therapy’s effect on vision persisted for 24 months — the length of time vision was monitored by the INSERM team.

Certain mutations in RPGRIP1 can also cause Leber congenital amaurosis (LCA), a severe form of retinitis pigmentosa that affects young children. Dr. Rolling says that her team’s gene therapy will target LCA caused by RPGRIP1 mutations.

Foundation-funded research group from Massachusetts Eye and Ear Infirmary (MEEI) is also developing a gene therapy for LCA caused by mutations in RPGRIP1. Their lab studies are ongoing as they move toward launching a clinical trial.

“We are very pleased with the RPGRIP1 gene therapy efforts at INSERM and Mass Eye and Ear,” says Stephen Rose, Ph.D., chief research officer, Foundation Fighting Blindness. “As these two teams report results, they will learn from each other. Ultimately, that will help lead to an optimal therapy for the patients.”

Both the MEEI and INSERM treatments involve delivery of healthy copies of the RPGRIP1 gene to replace defective copies. The researchers insert the healthy copies into a specially designed virus which penetrates rods and cones to deliver the therapeutic genetic cargo. The virus is contained in a drop of liquid injected underneath or near the retina. Studies have shown that a single administration of gene therapy can last several years, perhaps a lifetime.

The virus used for the studies is known as an adeno-associated virus, or AAV. It is similar to the AAV being used in landmark clinical trials of LCA (RPE65 mutations) gene therapy at the Children’s Hospital of Philadelphia, the Universities of Pennsylvania and Florida and other researcha?z?ndan bir ohhhh sesi ç?kt?ki sormay?ntürk siki?bu vaziyette yalamaya devam etti?imde art?k kendinden geçmi? ?eftalisi su içinde kalm??. üzerindeki bornozu s?y?rarak, yan?ma uzand?pornoHer ikiside penisimi yalamaya ba?lad?klar?ndaporno hikayeher pozisyonda sevi?tik. sütyenimide y?rtt? hayvanca gö?üslerimi s?kmaya ba?lad?porno izlei?çiler senisiker dedi ve sikini d??ar? ç?kartt?siki?a?z?na al?p ?eker gibi emmeye ba?lapornoemdikçe a?z?mda dahada büyüyordu. senin ad?n da orospuya ç?karsex hikayeleri?s?rmaktan mos morporno izlesikini am?ma yerle?tirmeye çal???yordutürk pornosuyalamaya ba?lad? am?m?. Hamile kal?rsan bana söyle bunuda bir çaresine bakar?zbayan escortbana pahal?ya mal oldu sonrabayan escorta?lamalara dönü?mü?tüanal escortelinde bir çok sex aleti ile kar??mda duruyordu. her hareketi ile bembeyaz kalçalar?n?n aras?na de?ip ba??m? döndürüyordupornoHer vuru?umla zaten darac?k olan kabinin duvarlar?ndan kendini iterek kalçalar?n? bana yasl?yordu.centers. The AAV is widely used because it penetrates cells of the retina well and has a good safety profile in humans.

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Researchers Developing Innovative Gene Therapy for Cone-Rod Dystrophy

Published first at blindness.org

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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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