21 Feb 2009
Macular degeneration in the elderly (“age-related macular degeneration”, AMD) is a major cause of blindness. Its prevalence increases to 30% in patients 75 to 85 years of age. AMD occurs in two forms: dry and wet AMD. Central geographic atrophy, the “dry” form of advanced AMD, results from atrophy to the retinal pigment epithelial layer below the retina, which causes vision loss through loss of photoreceptors (rods and cones) in the central part of the eye. While no treatment is available for this condition, vitamin supplements appear to slow the progression of dry macular degeneration and, in some patients, improve visual acuity. Neovascular or exudative AMD, the “wet” form of advanced AMD, causes vision loss due to abnormal blood vessel growth in the choriocapillaries, ultimately leading to blood and protein leakage below the macula. Bleeding, leaking, and scarring from these blood vessels eventually cause irreversible damage to the photoreceptors and rapid vision loss if left untreated. It is only recently that new drugs have been approved for wet AMD which halt progression of the visual loss or even lead to improvement. The humanized antibody fragment ranibizumab (Lucentis) directed against vascular endothelial growth factor (VEGF) was developed by Genentech and Novartis has been approved in more than 70 countries worldwide since 2006 and posted record sales of US$ 1.76 bln in 2008.
The proven effectiveness and commercial success of the anti-VEGF treatment of wet AMD has encouraged many companies to develop new treatments of wet AMD based on the proven target VEGF as well as on other experimental approaches (anti-angiogenic, anti-proliferative, anti-inflammatory). More than 20 different approaches are in clinical development and more than 20 preclinical stage projecs are under evaluation for wet AMD. Among the projects are many biologics (antibodies, peptides, proteins, antisense, DNA, cells) facilitated by the topical (intravitreal administration). Small molecule approaches may confer the convenience of oral administration but efficacy still has to be demonstrated. Fewer projects are in clinical development for dry AMD, but the most prominent ones have reached advanced clinical testing, but definitive results are still lacking.
Wednesday, February 25, 2009
Tuesday, February 17, 2009
Protect Your Eyes with Sunglasses
Protect your eyes with sunglasses that offer ultraviolet protection. The second strategy is to wear 'blue blocking' glasses.
The color that blocks blue is yellow, so blue blockers must contain a yellow tint. There are ready-made "NOIR" sunglasses that block blue and UV light with a variety of tints, including:
light yellow,
dark yellow, amber, and
plum.
NOIR glasses are available as clip-ons, and as large plastic frames that fit over your regular glasses.
The color that blocks blue is yellow, so blue blockers must contain a yellow tint. There are ready-made "NOIR" sunglasses that block blue and UV light with a variety of tints, including:
light yellow,
dark yellow, amber, and
plum.
NOIR glasses are available as clip-ons, and as large plastic frames that fit over your regular glasses.
Thursday, February 12, 2009
Avastin is inexpensive for Macular Degeneration therapy
Implications:
Ophthalmologists around the country use Avastin intravitreally for wet macular degeneration in doses far smaller than those used for systemic cancer. Although it is an "off-label" use of the drug, the cost for using Avastin is 1/6oth of Lucentis, a very similar drug, also made by Genentech, that IS FDA approved for macular degeneration. Yet, Avastin works just as well as Lucentis for far less cost. I am able to get the Avastin for $50 per dose, whereas Lucentis is $3,000 per dose. So, where Avastin is expensive for a small benefit in cancer therapy, it is quite inexpensive and highly effective in the treatment of macular dengeneration.
Analysis:
Avastin, while an expensive drug, has other uses that are currently "off-label" according to the FDA. Yet the doses are small and the cost is much less than the comparable FDA approved drug. The cost issue of Avastin is an artificial one, caused by the FDA's regulatory methods. It's efficacy in both metastatic colon cancer and macular degeneration has been well shown, and the FDA is responsible for the cost differential (see "Key Implications" above). The New York Times article does not adequately address the real reasons behind the high cost of Avastin for systemic use. The FDA regulatory process is also responsible for the high cost of any medicine that carries the FDA stamp of approval. The FDA process is flawed, not the prescribers of the drug, makers of the drug, or the recipients who get substantial benefits.
Ophthalmologists around the country use Avastin intravitreally for wet macular degeneration in doses far smaller than those used for systemic cancer. Although it is an "off-label" use of the drug, the cost for using Avastin is 1/6oth of Lucentis, a very similar drug, also made by Genentech, that IS FDA approved for macular degeneration. Yet, Avastin works just as well as Lucentis for far less cost. I am able to get the Avastin for $50 per dose, whereas Lucentis is $3,000 per dose. So, where Avastin is expensive for a small benefit in cancer therapy, it is quite inexpensive and highly effective in the treatment of macular dengeneration.
Analysis:
Avastin, while an expensive drug, has other uses that are currently "off-label" according to the FDA. Yet the doses are small and the cost is much less than the comparable FDA approved drug. The cost issue of Avastin is an artificial one, caused by the FDA's regulatory methods. It's efficacy in both metastatic colon cancer and macular degeneration has been well shown, and the FDA is responsible for the cost differential (see "Key Implications" above). The New York Times article does not adequately address the real reasons behind the high cost of Avastin for systemic use. The FDA regulatory process is also responsible for the high cost of any medicine that carries the FDA stamp of approval. The FDA process is flawed, not the prescribers of the drug, makers of the drug, or the recipients who get substantial benefits.
Thursday, February 5, 2009
EXPERIMENTAL THERAPY MAY LEAD TO MACULAR DEGENERATION, RESEARCHERS CAUTION
Johns Hopkins Medicine
Media Relations and Public Affairs
Media Contacts: Maryalice Yakutchik; 443-287-2251; myakutc1@jhmi.edu
Audrey Huang; 410-614-5105; audrey@jhmi.edu
August 27, 2008
Having discovered a genetic trigger for age-related macular degeneration, the leading cause of vision loss in people over 50, researchers report that an experimental state-of-the-art therapy for treating eye disease could adversely affect the vision of some patients with the "wrong" genetic makeup.
In the August 28 online issue of the New England Journal of Medicine, a multi-institutional team, including an interdisciplinary contingent from Johns Hopkins, reports that a mutation in toll-like receptor 3 (TLR3), a protein known to help cells fight some types of infection, is associated with protection from geographic atrophy. Geographic atrophy, also known as the "dry" form of macular degeneration, is the progressive shriveling of retinal cells in the central part of the tissue called the macula where cell loss equates to irreversible vision loss.
The new study implies that there could, in fact, be adverse consequences in some individuals who undergo a new treatment using a method called RNA interference to silence genes in the wet form of age-related macular degeneration (AMD), where growth of abnormal blood vessels causes vision loss.
RNA interference (RNAi) can be used in some cases to turn off disease-causing genes. Human trials using RNAi therapy already are under way for a host of diseases, including AMD. In theory, turning off a disease gene is a good idea, but it may not be good for everyone because everyone differs in their genetic makeup, cautions Nicholas Katsanis Ph.D., an associate professor of ophthalmology, molecular biology and genetics and member of the Institute of Genetic Medicine at the Johns Hopkins School of Medicine.
"The problem is that if you happen to be an individual who has the 'wrong' genetic code in TLR3, you might inadvertently trigger a detrimental effect in your retina," he explains. "You might cure the individual of one thing and increase their risk in something else." In this case, it's possible to cure the wet form of AMD but at the same time increase risk for the other form.
"This discovery has significant implications for diagnosing the dry form of (AMD), which is the most prevalent form, affecting more than 8 million Americans," says Kang Zhang, M.D., Ph.D., a professor of ophthalmology and human genetics and member of the Shiley Eye Center at the University of California San Diego. "It also allows us to develop new drugs to treat the dry form of AMD, for which there currently is no treatment."
In the current report, the team describes experiments on mouse and human genes showing that the activity of your TLR3 can determine whether or not you're afforded a degree of protection from geographic atrophy. TLR3 is activated in response to viral infection; it causes infected cells to die. Based on one's genetic code, some people have more active TLR3 while others, less active.
"What TLR3 does in the case of infection is sacrifice an infected cell to protect the neighborhood," Zhang explains.
Biologically well-intentioned though the sacrifice may be, it can lead to blindness.
Based on previous reports hinting to TLR3 involvement in macular degeneration, Katsanis, Zhang and colleagues first set out to determine whether that link was real.
By analyzing the DNA of patients in a case-control study, the researchers not only verified previously published reports indicating an association between TLR3 and macular degeneration, but also went on to show a specific association between one "fairly common" variant of TLR3 and geographic atrophy. They found that people with specific chemical difference in the TLR3 protein were less likely to have geographic atrophy.
To test the assumption that the chemical difference rendered TLR3 less active, the researchers next used cells from human eyes containing either a "normal" or variant version of TLR3. To activate TLR3, they infected these cells with fake RNA mimicking genetic material common to many viruses, and measured how many cells died. Fifty percent fewer cells with the variant version of TLR3 died compared to cells containing the normal version, leading the researchers to conclude that the variant version of TLR3 must be less active and therefore kills fewer cells.
Finally, to be sure that differences in TLR3 activity cause similar differences in cell death in whole eyes (and not just isolated eye cells), they teamed up with the team of Jayakrishna Ambati, M.D., a professor of physiology, ophthalmology and visual sciences at University of Kentucky and injected RNA into mice, one set of which was genetically engineered to have no TLR3. Two weeks later, researchers examined their eyes and found that those mice with TLR3 exhibited 61 percent more dead eye cells than mice without TLR3, further indicating that TLR3 activity triggers cells to die, which in turn can lead to geographic atrophy.
"You and me, we have a good 20 to 30 percent chance of getting macular degeneration," Katsanis says. "So when the time comes for us to start thinking about intervention, we might want to get genotyped first, and then decide what kind of therapeutic paradigm might be most appropriate for us."
The researchers envision a day when vaccines might protect us from the viruses that trigger the pathways that are inappropriately activated or repressed in models of macular degeneration: "If we can figure out which viruses might be acting as triggers, we might be able to find a way to combat them. This would be a far more effective therapy, in my view, than trying to design a gene therapy approach," says Zhang.
The TLR3 discovery bolsters a growing body of research that illustrates how genetic information stratifies individuals for responses to particular therapies; it is the first involving the retina.
"Clearly, the statement that we're not all the same is not exactly novel, and yet, I'm still struck by how homogenized people become when it comes to clinical trials," Katsanis says. "It baffles me, frankly."
The research was funded by the National Institutes of Health, the Foundation Fighting Blindness and the Macula Vision Research Foundation, Veterans Affairs Merit Award, the Ruth and Milton Steinbach Fund, Research to Prevent Blindness, Burroughs Wellcome Fund, Clinical Scientist Award in Translational Research, and the American Health Assistance Foundation.
Other participating researchers are from Johns Hopkins University, University of California San Diego, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, Chengdu, China, University of Utah School of Medicine, Oregon Health & Science University, University of Kentucky, Greater Baltimore Medical Center, Keck School of Medicine of the University of Southern California, and Rockefeller University.
On the Web:
http://www.hopkinsmedicine.org/geneticmedicine/
http://content.nejm.org/
Media Relations and Public Affairs
Media Contacts: Maryalice Yakutchik; 443-287-2251; myakutc1@jhmi.edu
Audrey Huang; 410-614-5105; audrey@jhmi.edu
August 27, 2008
Having discovered a genetic trigger for age-related macular degeneration, the leading cause of vision loss in people over 50, researchers report that an experimental state-of-the-art therapy for treating eye disease could adversely affect the vision of some patients with the "wrong" genetic makeup.
In the August 28 online issue of the New England Journal of Medicine, a multi-institutional team, including an interdisciplinary contingent from Johns Hopkins, reports that a mutation in toll-like receptor 3 (TLR3), a protein known to help cells fight some types of infection, is associated with protection from geographic atrophy. Geographic atrophy, also known as the "dry" form of macular degeneration, is the progressive shriveling of retinal cells in the central part of the tissue called the macula where cell loss equates to irreversible vision loss.
The new study implies that there could, in fact, be adverse consequences in some individuals who undergo a new treatment using a method called RNA interference to silence genes in the wet form of age-related macular degeneration (AMD), where growth of abnormal blood vessels causes vision loss.
RNA interference (RNAi) can be used in some cases to turn off disease-causing genes. Human trials using RNAi therapy already are under way for a host of diseases, including AMD. In theory, turning off a disease gene is a good idea, but it may not be good for everyone because everyone differs in their genetic makeup, cautions Nicholas Katsanis Ph.D., an associate professor of ophthalmology, molecular biology and genetics and member of the Institute of Genetic Medicine at the Johns Hopkins School of Medicine.
"The problem is that if you happen to be an individual who has the 'wrong' genetic code in TLR3, you might inadvertently trigger a detrimental effect in your retina," he explains. "You might cure the individual of one thing and increase their risk in something else." In this case, it's possible to cure the wet form of AMD but at the same time increase risk for the other form.
"This discovery has significant implications for diagnosing the dry form of (AMD), which is the most prevalent form, affecting more than 8 million Americans," says Kang Zhang, M.D., Ph.D., a professor of ophthalmology and human genetics and member of the Shiley Eye Center at the University of California San Diego. "It also allows us to develop new drugs to treat the dry form of AMD, for which there currently is no treatment."
In the current report, the team describes experiments on mouse and human genes showing that the activity of your TLR3 can determine whether or not you're afforded a degree of protection from geographic atrophy. TLR3 is activated in response to viral infection; it causes infected cells to die. Based on one's genetic code, some people have more active TLR3 while others, less active.
"What TLR3 does in the case of infection is sacrifice an infected cell to protect the neighborhood," Zhang explains.
Biologically well-intentioned though the sacrifice may be, it can lead to blindness.
Based on previous reports hinting to TLR3 involvement in macular degeneration, Katsanis, Zhang and colleagues first set out to determine whether that link was real.
By analyzing the DNA of patients in a case-control study, the researchers not only verified previously published reports indicating an association between TLR3 and macular degeneration, but also went on to show a specific association between one "fairly common" variant of TLR3 and geographic atrophy. They found that people with specific chemical difference in the TLR3 protein were less likely to have geographic atrophy.
To test the assumption that the chemical difference rendered TLR3 less active, the researchers next used cells from human eyes containing either a "normal" or variant version of TLR3. To activate TLR3, they infected these cells with fake RNA mimicking genetic material common to many viruses, and measured how many cells died. Fifty percent fewer cells with the variant version of TLR3 died compared to cells containing the normal version, leading the researchers to conclude that the variant version of TLR3 must be less active and therefore kills fewer cells.
Finally, to be sure that differences in TLR3 activity cause similar differences in cell death in whole eyes (and not just isolated eye cells), they teamed up with the team of Jayakrishna Ambati, M.D., a professor of physiology, ophthalmology and visual sciences at University of Kentucky and injected RNA into mice, one set of which was genetically engineered to have no TLR3. Two weeks later, researchers examined their eyes and found that those mice with TLR3 exhibited 61 percent more dead eye cells than mice without TLR3, further indicating that TLR3 activity triggers cells to die, which in turn can lead to geographic atrophy.
"You and me, we have a good 20 to 30 percent chance of getting macular degeneration," Katsanis says. "So when the time comes for us to start thinking about intervention, we might want to get genotyped first, and then decide what kind of therapeutic paradigm might be most appropriate for us."
The researchers envision a day when vaccines might protect us from the viruses that trigger the pathways that are inappropriately activated or repressed in models of macular degeneration: "If we can figure out which viruses might be acting as triggers, we might be able to find a way to combat them. This would be a far more effective therapy, in my view, than trying to design a gene therapy approach," says Zhang.
The TLR3 discovery bolsters a growing body of research that illustrates how genetic information stratifies individuals for responses to particular therapies; it is the first involving the retina.
"Clearly, the statement that we're not all the same is not exactly novel, and yet, I'm still struck by how homogenized people become when it comes to clinical trials," Katsanis says. "It baffles me, frankly."
The research was funded by the National Institutes of Health, the Foundation Fighting Blindness and the Macula Vision Research Foundation, Veterans Affairs Merit Award, the Ruth and Milton Steinbach Fund, Research to Prevent Blindness, Burroughs Wellcome Fund, Clinical Scientist Award in Translational Research, and the American Health Assistance Foundation.
Other participating researchers are from Johns Hopkins University, University of California San Diego, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, Chengdu, China, University of Utah School of Medicine, Oregon Health & Science University, University of Kentucky, Greater Baltimore Medical Center, Keck School of Medicine of the University of Southern California, and Rockefeller University.
On the Web:
http://www.hopkinsmedicine.org/geneticmedicine/
http://content.nejm.org/
Wednesday, January 28, 2009
Finding macular degeneration treatments
Susan Slobac asked about: Finding macular degeneration treatments.
Vision problems due to the onset of macular degeneration are quite prevalent, especially in the elderly. Macular degeneration occurs when the macula, located in the central portion of the retina in the eye, becomes weakened or damaged. The result is a loss of central vision. Central vision is used to read and drive, so it is crucial to save as much of a patient’s vision as possible as soon as possible. Although this medical condition has no cure at this time, there are some promising new macular degeneration treatments that have shown to alleviate and slow down some of the symptoms of age-related macular degeneration.
There is a range of vision loss that can occur depending on the severity and type of age-related macular degeneration a patient has. Because it affects the macula located in the center of the retina, a patient’s peripheral vision is usually not adversely affected by the condition. With the onset of the condition, a patient’s vision might still be quite good, but the situation can worsen over time. There are two different types of age-related macular degeneration that often result in the greatest loss of central vision, and they are called wet and dry. The dry form of advanced macular degeneration is caused by the reduction of the rods and cones located in the retina, while wet advanced macular degeneration occurs due to leakage of excessive blood vessels and the resulting scarring under the macula.
One thing that retinal specialists might tell their patients with macular degeneration is to take certain vitamins as part of a spectrum of macular degeneration treatment s. Patients in the initial onset stages of this condition sometimes benefit from taking vitamins C, E, zinc, lutein, zeaxanthin and eating foods that are high in beta-carotenes, such as dark green leafy vegetables, corn and peas.
Another macular degeneration treatment can be found in cholesterol reducing drugs. People in the early stages of this medical condition often develop drusen, or yellow deposits, in the macula. The development and increase in the number of drusen seems to be related to the patient’s cholesterol level, with drusen more prevalent in those with higher cholesterol. Medications, such as statins, which reduce cholesterol, and aspirin, which reduces inflammation, may have a significant impact on reducing the size and number of drusen in the macula and thus lessen the chances of someone developing age-related macular degeneration.
A couple of wet advanced macular degeneration treatments, Macugen and Lucentis, have been approved by the FDA. Macugen is useful because it helps to reduce the number of excessive blood vessels that can grow under the retina. These can become inflamed and eventually burst, causing vision problems. Lucentis also reduces the growth of too many blood vessels. Lucentis is administered as an injection under the eye, and offers a great new treatment option for some patients with these kinds of vision problems.
The future is looking brighter with these emerging new macular degeneration treatments.
Vision problems due to the onset of macular degeneration are quite prevalent, especially in the elderly. Macular degeneration occurs when the macula, located in the central portion of the retina in the eye, becomes weakened or damaged. The result is a loss of central vision. Central vision is used to read and drive, so it is crucial to save as much of a patient’s vision as possible as soon as possible. Although this medical condition has no cure at this time, there are some promising new macular degeneration treatments that have shown to alleviate and slow down some of the symptoms of age-related macular degeneration.
There is a range of vision loss that can occur depending on the severity and type of age-related macular degeneration a patient has. Because it affects the macula located in the center of the retina, a patient’s peripheral vision is usually not adversely affected by the condition. With the onset of the condition, a patient’s vision might still be quite good, but the situation can worsen over time. There are two different types of age-related macular degeneration that often result in the greatest loss of central vision, and they are called wet and dry. The dry form of advanced macular degeneration is caused by the reduction of the rods and cones located in the retina, while wet advanced macular degeneration occurs due to leakage of excessive blood vessels and the resulting scarring under the macula.
One thing that retinal specialists might tell their patients with macular degeneration is to take certain vitamins as part of a spectrum of macular degeneration treatment s. Patients in the initial onset stages of this condition sometimes benefit from taking vitamins C, E, zinc, lutein, zeaxanthin and eating foods that are high in beta-carotenes, such as dark green leafy vegetables, corn and peas.
Another macular degeneration treatment can be found in cholesterol reducing drugs. People in the early stages of this medical condition often develop drusen, or yellow deposits, in the macula. The development and increase in the number of drusen seems to be related to the patient’s cholesterol level, with drusen more prevalent in those with higher cholesterol. Medications, such as statins, which reduce cholesterol, and aspirin, which reduces inflammation, may have a significant impact on reducing the size and number of drusen in the macula and thus lessen the chances of someone developing age-related macular degeneration.
A couple of wet advanced macular degeneration treatments, Macugen and Lucentis, have been approved by the FDA. Macugen is useful because it helps to reduce the number of excessive blood vessels that can grow under the retina. These can become inflamed and eventually burst, causing vision problems. Lucentis also reduces the growth of too many blood vessels. Lucentis is administered as an injection under the eye, and offers a great new treatment option for some patients with these kinds of vision problems.
The future is looking brighter with these emerging new macular degeneration treatments.
Saturday, January 24, 2009
Seeing Machine Helps Blind See Pictures
A seeing machine developed at MIT helps people with visual impairments see pictures.
Nick Barber, IDG News Service
Friday, January 23, 2009 12:00 PM PST
Using her prototype "seeing machine," Elizabeth Goldring can take pictures and see them -- with her blind eye.
After more than 20 years of work, Goldring, a senior fellow at MIT's Center for Advanced Visual Studies and her colleagues have designed a portable device that allows people with visual impairments to watch videos, access the internet, view photographs, or just see the face of a friend.
Her work started when she lost the vision in both of her eyes and doctors at the Schepens Eye Research Institute in Boston used a scanning laser ophthalmoscope, or SLO, to determine if she had any healthy retina left. The machine, which costs over US$100,000, projected images directly onto the retina of the eye, bypassing the hemorrhages contributing to her blindness.
"Technicians projected stick figures onto my retinas and I could see some of those stick figures," she said of the experience. Goldring then asked them if they could write the word "sun," which she could also see. "I was amazed. It was the first word I'd seen for months."
After her visit, she contacted and worked with the inventor of the SLO, hoping to reduce the size and cost of the device. That research yielded a $4,000 desktop model that allowed the blind to see black-and-white images. Soon after, a desktop model was created that allowed for color images to be seen. Goldring admits that version doesn't work well, but it paved the way for the current prototype.
Once a video signal is plugged into the 5-inch square box, it is then fed to an LCD panel on the inside, according to Quinn Smithwick, a postdoctoral associate at the MIT Media who has been working with Goldring on the seeing machine. The connection to the box is for a standard RCA video jack so almost anything with a video output can be plugged in. The LCD panel inside is illuminated by a bright bank of LEDs behind it, which are collimated, or traveling in the same direction. As the light passes through the LCD screen, the image pattern is "imprinted" onto the light. A lens at the back of the box focuses the light into a single point, which then enters the pupil of the eye and passes onto the retina.
"It's not that we're taking the camera image and blowing it up so you can see something big," said Smithwick. "We're trying to bypass any bad optics you may have and then get enough light and enough contrast onto the back of your retina and then you can use what little bits of retina you may have left to view it."
Goldring thinks the seeing machine could help people with macular degeneration and proliferative retinal diseases, two of the main causes of blindness in the U.S., according to Goldring. Using the device, Goldring said she can see faces and general details of people such as the color of their hair and what they are wearing. Without it, she would only know that someone is standing close to her.
Brandon Taylor, a graduate student at the MIT Media Lab, said the next step for the seeing machine is to test it with a wider population.
"We've received positive results with Elizabeth and there have been a couple other people who have used it and its been very encouraging, but what we really want to do for this testing phase is figure out what types of eye conditions this is beneficial for ... and how much improvement this machine can achieve," said Taylor. Goldring noted that there does need to be some working retina for the machine to work.
"People aren't interested in what blind people see and we have a lot of pent-up desire to express ourselves visually and this is the first step to that," said Goldring.
She and her team already have plans under way to test the seeing machine at the Low Vision Clinic at the Joslin Diabetes Center's Beetham Eye Institute in Boston. After refining the device, they would also like to make it commercially available, though are not sure when it will be or for how much. Their prototype, not including the digital camera, cost under $500 because "everything in it is already mass-produced for other purposes," Taylor said.
"Keeping the visual sense alive is something good, even if you don't use it to cross the street," Goldring said.
Nick Barber, IDG News Service
Friday, January 23, 2009 12:00 PM PST
Using her prototype "seeing machine," Elizabeth Goldring can take pictures and see them -- with her blind eye.
After more than 20 years of work, Goldring, a senior fellow at MIT's Center for Advanced Visual Studies and her colleagues have designed a portable device that allows people with visual impairments to watch videos, access the internet, view photographs, or just see the face of a friend.
Her work started when she lost the vision in both of her eyes and doctors at the Schepens Eye Research Institute in Boston used a scanning laser ophthalmoscope, or SLO, to determine if she had any healthy retina left. The machine, which costs over US$100,000, projected images directly onto the retina of the eye, bypassing the hemorrhages contributing to her blindness.
"Technicians projected stick figures onto my retinas and I could see some of those stick figures," she said of the experience. Goldring then asked them if they could write the word "sun," which she could also see. "I was amazed. It was the first word I'd seen for months."
After her visit, she contacted and worked with the inventor of the SLO, hoping to reduce the size and cost of the device. That research yielded a $4,000 desktop model that allowed the blind to see black-and-white images. Soon after, a desktop model was created that allowed for color images to be seen. Goldring admits that version doesn't work well, but it paved the way for the current prototype.
Once a video signal is plugged into the 5-inch square box, it is then fed to an LCD panel on the inside, according to Quinn Smithwick, a postdoctoral associate at the MIT Media who has been working with Goldring on the seeing machine. The connection to the box is for a standard RCA video jack so almost anything with a video output can be plugged in. The LCD panel inside is illuminated by a bright bank of LEDs behind it, which are collimated, or traveling in the same direction. As the light passes through the LCD screen, the image pattern is "imprinted" onto the light. A lens at the back of the box focuses the light into a single point, which then enters the pupil of the eye and passes onto the retina.
"It's not that we're taking the camera image and blowing it up so you can see something big," said Smithwick. "We're trying to bypass any bad optics you may have and then get enough light and enough contrast onto the back of your retina and then you can use what little bits of retina you may have left to view it."
Goldring thinks the seeing machine could help people with macular degeneration and proliferative retinal diseases, two of the main causes of blindness in the U.S., according to Goldring. Using the device, Goldring said she can see faces and general details of people such as the color of their hair and what they are wearing. Without it, she would only know that someone is standing close to her.
Brandon Taylor, a graduate student at the MIT Media Lab, said the next step for the seeing machine is to test it with a wider population.
"We've received positive results with Elizabeth and there have been a couple other people who have used it and its been very encouraging, but what we really want to do for this testing phase is figure out what types of eye conditions this is beneficial for ... and how much improvement this machine can achieve," said Taylor. Goldring noted that there does need to be some working retina for the machine to work.
"People aren't interested in what blind people see and we have a lot of pent-up desire to express ourselves visually and this is the first step to that," said Goldring.
She and her team already have plans under way to test the seeing machine at the Low Vision Clinic at the Joslin Diabetes Center's Beetham Eye Institute in Boston. After refining the device, they would also like to make it commercially available, though are not sure when it will be or for how much. Their prototype, not including the digital camera, cost under $500 because "everything in it is already mass-produced for other purposes," Taylor said.
"Keeping the visual sense alive is something good, even if you don't use it to cross the street," Goldring said.
Wednesday, January 14, 2009
Improve your peripherical circulation
Simon - one of my regular clients for massage - has a problem with his peripherical circulation: his feet are always cold, no matter if it is summer or winter. So, I decided to make a research in order to give him some advice on how to reduce the symptoms and I thought to share the results with you.
FOOD
Many herbal remedies such as ginkgo biloba can help improve blood circulation but so too can much of the food we eat. Five of the most effective circulation boosting foods are as follows:
1) Pumpkin seeds: they are a good source of vitamin E which research has shown can help reduce the stickiness of blood and therefore lower the likelihood of blood clots forming.
2) Oranges: the high levels of vitamin C and bioflavonoids in oranges help the flow of blood through your body by strengthening the capillary walls.
3) Nuts: they contain niacin, or vitamin B3 as it is sometimes referred to, which essentially gives your blood a boost and therefore can prevent circulation problems.
4) Watermelon and tomatoes: they are rich in lycopene which can help prevent a buildup of plaque (a substance that can interfere with blood flow) in the arteries and therefore ensure healthy blood circulation.
5) Garlic: blood circulation is another of the many strings to garlic’s bow. It can help prevent the accumulation of plaque and in some cases actively reduce it.
6) Bilberry: it has been used for centuries, both medicinally and as a food in jams and pies. It is related to the blueberry and is native to Northern Europe. Bilberry fruit contains some chemicals that have excellent antioxidant properties. They scavenge damaging particles in the body known as free radicals, helping to prevent or reverse damage to cells. Antioxidants have been shown to help prevent a number of long-term illnesses such as heart disease, cancer, and an eye disorder called macular degeneration.
EXERCISE
Regular exercise can help to reduce the symptoms of reduced peripherical circulation.
SMOKING
Stop smoking, if you smoke.
LOWER YOUR BLOOD PRESSURE
If it is too high.
REGULAR MASSAGE
Can help increase the blood flow going into the muscles.
Roberto Bocchetti is an experienced and qualified Personal Trainer and Massage Terapist in London, UK. To contact Roberto, please call +44 7508 250 126.
FOOD
Many herbal remedies such as ginkgo biloba can help improve blood circulation but so too can much of the food we eat. Five of the most effective circulation boosting foods are as follows:
1) Pumpkin seeds: they are a good source of vitamin E which research has shown can help reduce the stickiness of blood and therefore lower the likelihood of blood clots forming.
2) Oranges: the high levels of vitamin C and bioflavonoids in oranges help the flow of blood through your body by strengthening the capillary walls.
3) Nuts: they contain niacin, or vitamin B3 as it is sometimes referred to, which essentially gives your blood a boost and therefore can prevent circulation problems.
4) Watermelon and tomatoes: they are rich in lycopene which can help prevent a buildup of plaque (a substance that can interfere with blood flow) in the arteries and therefore ensure healthy blood circulation.
5) Garlic: blood circulation is another of the many strings to garlic’s bow. It can help prevent the accumulation of plaque and in some cases actively reduce it.
6) Bilberry: it has been used for centuries, both medicinally and as a food in jams and pies. It is related to the blueberry and is native to Northern Europe. Bilberry fruit contains some chemicals that have excellent antioxidant properties. They scavenge damaging particles in the body known as free radicals, helping to prevent or reverse damage to cells. Antioxidants have been shown to help prevent a number of long-term illnesses such as heart disease, cancer, and an eye disorder called macular degeneration.
EXERCISE
Regular exercise can help to reduce the symptoms of reduced peripherical circulation.
SMOKING
Stop smoking, if you smoke.
LOWER YOUR BLOOD PRESSURE
If it is too high.
REGULAR MASSAGE
Can help increase the blood flow going into the muscles.
Roberto Bocchetti is an experienced and qualified Personal Trainer and Massage Terapist in London, UK. To contact Roberto, please call +44 7508 250 126.
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