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09/Oct/2020

New insight on how people with retinal degenerative disease can maintain their night vision for a relatively long period of time has been published today in the open-access eLife journal.

The study suggests that second-order neurons in the retina, which relay visual signals to the retinal ganglion cells that project into the brain, maintain their activity in response to photoreceptor degeneration to resist visual decline — a process known as homeostatic plasticity. Rod photoreceptors are the cells responsible for the most sensitive aspects of our vision, allowing us to see at night, but can be lost during retinal degenerative disease.

The new findings pave the way for further research to understand how our eyes and other sensory systems respond and adapt to potentially compromising changes throughout life.

“Neuronal plasticity of the inner retina has previously been seen to occur in response to photoreceptor degeneration, but this process has been mostly considered maladaptive rather than homeostatic in nature,” explains co-first author Henri Leinonen, a postdoctoral researcher at the University of California, Irvine, US. “Our study was conducted at a relatively early stage of disease progression, while most previous studies focused on severe disease stages, which may account for the discrepancy. Very recently, several studies using triggered photoreceptor loss models have shown adaptive responses in bipolar cells — cells that connect the outer and inner retina. But whether such adaptation occurs during progressive photoreceptor degenerative disease, and whether it helps to maintain visual behavior, was unknown.”

To address this question, Leinonen and colleagues studied a mouse model of retinitis pigmentosa. This is the name given to a group of related genetic disorders caused by the P23H mutation in rhodopsin, a protein that enables us to see in low-light conditions. Retinitis pigmentosa causes the breakdown and loss of rod-shaped photoreceptor cells in the retina, leading to difficulties seeing at night.

The team combined whole-retinal RNA-sequencing, electrophysiology and behavioral experiments in both healthy mice and those with retinitis pigmentosa as the disease progressed. Their experiments showed that the degeneration of rod photoreceptors triggers genomic changes that involve robust compensatory molecular changes in the retina and increases in electrical signalling between rod photoreceptors and rod bipolar cells. These changes were associated with well-maintained behavioural night vision despite the loss of over half of the rod photoreceptor cells in mice with retinitis pigmentosa.

“This mechanism may explain why patients with inherited retinal diseases can maintain their normal vision until the disease reaches a relatively advanced state,” says co-first author Nguyen Pham, Graduate Research Assistant at the John A. Moran Eye Center, University of Utah Health, Salt Lake City, US. “It could also inspire novel treatment strategies for diseases that lead to blindness.”

“Our results suggest retinal adaptation as the driver of persistent visual function during photoreceptor degenerative disease,” concludes senior author Frans Vinberg, PhD, Assistant Professor at the John A. Moran Eye Center, University of Utah Health. “Additional research is now needed to discover the exact homeostatic plasticity mechanisms that promote cellular signalling and visual function. This could help inform the development of potential new interventions to enhance homeostatic plasticity when needed.”


28/Jun/2019

The Digital Gap Between Rich and Poor Kids Is Not What We Expected

America’s public schools are still promoting devices with screens — even offering digital-only preschools while the rich are banning screens from class altogether.

It wasn’t long ago that the worry was that rich students would have access to the internet earlier, gaining tech skills and creating a digital divide. But now, as Silicon Valley’s parents increasingly panic over the impact screens have on their children and move toward screen-free lifestyles, worries over a new digital divide are rising. It could happen that the children of poorer and middle-class parents will be raised by screens, while the children of Silicon Valley’s elite will be going back to wooden toys and the luxury of human interaction.

And parents say there is a growing technological divide between public and private schools even in the same community. As more screens appear in the lives of the poor, screens are disappearing from the lives of the rich. The richer you are, the more you spend to be offscreen.

At the private Waldorf School, which promises a back-to-nature, nearly screen-free education popular with Silicon Valley executives, time on screens is increasingly seen as unhealthy and intentionally avoided. While the nearby public Hillview Middle School promotes its 1:1 iPad program.

WordPsychologist Richard Freed, who wrote a book about the dangers of screen-time for children and how to connect them back to real world experiences, divides his time between speaking before packed rooms in Silicon Valley and his clinical practice with low-income families in the far East Bay, where he is often the first one to tell parents that limiting screen-time might help with attention and behavior issues.

“There’s a message out there that your child is going to be crippled and in a different dimension if they’re not on the screen,” said Pierre Laurent, a former Microsoft and Intel executive now on the board of trustees at Silicon Valley’s Waldorf School. “That message doesn’t play as well in this part of the world.”

“For a lot of kids in low income communities, schools don’t have the resources for extracurricular activities, and their parents can’t afford nannies,” Dr. Freed said. The knowledge gap around tech’s danger is enormous.

Dr. Freed and 200 other psychologists petitioned the American Psychological Association in August to formally condemn the work psychologists are doing with persuasive design for tech platforms that are designed for children.

Screen exposure starts young. And children who spent more than two hours a day looking at a screen got lower scores on thinking and language tests, according to early results of a landmark study on brain development in more than 11,000 children, supported by the National Institutes of Health. Most disturbing, the study is finding that the brains of children who spend a lot of time on screens are different. For some kids, there is premature thinning of their cerebral cortex. In adults, one study found an association between screen time and depression.

A toddler who learns to build with virtual blocks in an iPad game gains no ability to build with actual blocks, according to Dimitri Christakis, a pediatrician at Seattle Children’s Hospital and a lead author of the American Academy of Pediatrics’ guidelines on screen time.

Wealthy families do not live like this. They have grown afraid of screens. They want their children to play with blocks, and tech-free private schools are booming. Humans are more expensive, and the wealthy are willing and able to pay for them. Conspicuous human interaction — living without a phone for a day, quitting social networks and not answering email — has become a status symbol.

All of this has led to a curious new reality: Human contact is becoming a luxury good. So as wealthy kids are growing up with less screen time, poor kids are growing up with more. How comfortable someone is with human engagement could become a new class marker.


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24/Jun/2019

Eyes hold clues for treating severe autism more effectively

Vocabulary tests for individuals with the severest forms of autism spectrum disorder, or ASD, are notoriously inaccurate. They commonly ask the test-taker to point to an illustration after hearing a spoken word, measuring the ability to understand and perform a task as much as word knowledge.

The implications are significant. Poor assessments result not only in teaching strategies that are ineffective but also make researchers wary, leading to a shortage of research on individuals with Level 3 ASD, the diagnosis given to the most severe forms of autism, that could help improve their quality of life.

That’s according to Emily Coderre, lead author of a new study in the journal Cognitive and Behavioral Neurology and a faculty member in the University of Vermont’s Department of Communication Science and Disorders.

In the new study, Coderre and colleagues at Johns Hopkins Medicine demonstrate that assessment tools capturing implicit signs of word knowledge like eye movement among those with Level 3 ASD — tools that have rarely been used with this group — offer the potential to be more accurate than traditional behavioral assessments, closely matching the reports of parents and caregivers, the current “gold standard” for determining an individual’s vocabulary knowledge.

“Children and adults with severe ASD often score much lower than they should on traditional language assessments,” Coderre said. “They may not understand the instructions or be unable to point to a picture after hearing the spoken word. Or they may be frightened by the equipment or simply not care to participate. The new study points the way toward a much better approach.”

Three implicit measures of word knowledge

To assess vocabulary knowledge among five adults with Level 3 ASD, researchers in the study used what are called implicit measures of word knowledge.

In one test researchers used a technique called eye movement monitoring. After hearing a spoken word, which matched one of four illustrations on a computer screen, the researchers tracked the subjects’ eye movements. If their eyes quickly chose the matching visual and stayed with it, that signaled knowledge of the word. If the eyes flitted from one object to the next, it demonstrated the word was probably not known.

In a second test called pupillary dilation, subjects again heard a spoken word and were shown four visuals. If the pupils dilated, that signaled cognitive effort, and the probability that the word was not known. If pupils did not dilate, that likely demonstrated knowledge of the word.

In a third test, researchers used electroencephalography to measure brain activity in the research subjects. Subjects heard a word and were shown an image that either matched or did not match it. Earlier research has shown there are typical brain patterns for congruent and incongruent pairs of words and images, enabling the researchers to infer whether the word was known based on these electrical signatures.

The three measures had varying degrees of accuracy with each of the five research subjects. Although the researchers concluded that these implicit measures show promise in providing estimates of vocabulary knowledge, this variability suggests that these assessments should be tailored to each individual.

An earlier study by the research team offered further validation of the research findings. That study found that the three implicit measures were highly accurate in assessing word knowledge among a group of adults who did not have ASD.

Better interventions, more knowledge

Given the small research sample, the research findings are preliminary. But their potential implications are significant, Coderre said.

Implicit measures of vocabulary could result in more effective interventions that are tailored to the true language knowledge of the individual.

“Language is often one of the areas where individuals with autism struggle, especially at the more severe end of the spectrum, where a large percentage have little to no functional language,” Coderre said. “Anything we can do to improve their language outcomes will improve their quality of life.”

The new tools could also result in more research into those with severe ASD, she said, not only in language acquisition but in other areas of cognition.

Nonverbal intelligence testing often relies on visual clues, for instance, she said. Subjects might be shown an image of a puzzle with a missing piece and be asked to find the piece among several options, a task well suited to the EM and PD testing.

“These techniques could very well be extended to other domains,” Coderre said.

That could help address a challenge in the field — the huge lack of literature on individuals with Level 3 ASD.

“There’s so much focus on the milder end of the spectrum, the people who are more functionally verbal, that people on the more severe end of the spectrum tend to be overlooked,” Coderre said.

“With measures like these, we can do not only more interventions-based research, but also work with this population in general, so we can better understand how their strengths and weaknesses are similar to or different from other individuals on the spectrum. The more understanding we have, the more help we can offer.”


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06/May/2019

Cases of herpes zoster ophthalmicus tripled in 12-year time span, highest among older adults

Source:

Michigan Medicine – University of Michigan

 

More Americans are being diagnosed with eye complications of shingles, but older adults can call the shots on whether they are protected from the painful rash that can cost them their eyesight.

Among a group of 21 million adults, occurrences of herpes zoster ophthalmicus (HZO), when shingles gets in the eyes, tripled during a 12-year-period, according to Kellogg Eye Center research presented at the 2019 Association for Research in Vision and Ophthalmology annual meeting in Vancouver.

Study author Nakul Shekhawat, M.D., MPH, says it’s important to figure out which patients are at greatest risk for HZO and how to prevent it “because of the severity of the disease and potential sight-threatening complications.”

Even though caused by the same virus, shingles is different than chickenpox.

Years after recovering from chickenpox, the virus can become active again, causing shingles, a painful, debilitating infection that can lead to corneal scarring and blindness.

Kellogg researchers found that incidence of herpes zoster ophthalmicus across the United States rose substantially between 2004 and 2016, occurring in 9.4 cases per 100,000 people at the beginning of the study period and growing 3 fold to 30.1 cases per 100,000 by the end of the study period.

Shingles affecting the eye may be more of a problem for women and adults over age 75 (53 cases per 100,000), two groups with the highest rates of infection, the study showed.

While shingles has been cropping up in young adults, it is still considered one of the perils of old age.

“Older patients were at far greater risk for HZO, highlighting just how important it is for older adults to get the shingles vaccination,” says Shekhawat, a comprehensive ophthalmologist at the University of Michigan Department of Ophthalmology and Visual Sciences.

Whites, more so than other racial groups, were diagnosed with HZO, with rates lower among blacks (23.4), Asians (21.0) and Latinos (14.6). Among whites, the rate was 30.6 cases per 100,000.

That female (29.1 cases per 100,000 persons) and white patients had such high infection rates raises interesting questions, Shekhawat says, about their community exposure and whether their immune systems uniquely place them at risk.

The shingles vaccination provides strong protection from shingles and its complications, but the vaccine is not widely used. Two doses of Shingrix are more than 90% effective at preventing shingles and are recommended for those age 50 and older.

Even if an adult has had shingles in the past, Shingrix can help prevent future occurrences, according to the U.S. Centers for Disease and Protection.

The Kellogg team of vision and health services researchers included statistician Nidhi Talwar and Joshua D. Stein, M.D., a member of the U-M Institute for Healthcare Policy and Innovation and the U-M Center for Eye Policy and Innovation. They studied demographics and variations in herpes zoster ophthalmicus in the United States with support from Eversight Eye Bank and the Blue Cross Blue Shield of Michigan Foundation.

The findings were based on health claims data for patients enrolled in a large nationwide managed care plan.


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24/Apr/2019

Antioxidants key to lowering risk of age-related cataracts

A $5.7 billion global medical bill to restore sight for the estimated 45 million people with cataracts could be slashed in half by a diet rich in colorful fruits and vegetables, according to an international study.

Researchers from China and the University of South Australia have published the first study of its kind to verify the link between foods high in antioxidants and a lower risk of age-related cataracts (ARC).

UniSA Senior Research Fellow Dr. Ming Li and colleagues from Xi’an Jiaotong University analyzed 20 studies from around the world looking at the impact of vitamins and carotenoids on cataract risk.

Despite some inconsistencies, the findings overwhelmingly support the benefits of eating citrus fruits, capsicum, carrots, tomatoes and dark green vegetables such as spinach, broccoli and kale to delay the onset of ARC.

Their paper has been published in the American Journal of Clinical Nutrition ahead of World Optometry Week (March 26-30).

“Age-related cataracts are the leading cause of visual impairment among the elderly throughout the world, with unoperated cataracts contributing to 35 percent of all blindness,” Dr. Li says. “Although cataract extraction surgery is an effective method to restore vision, it will have cost society more than $5.7 billion by 2020.”

With the population aging dramatically and an increasing number of people needing surgery, urgent action is needed, the researchers say.

“If we could delay the onset of ARC by 10 years it could halve the number of people requiring surgery.”

Improvements would rely on global changes to most of the world’s diet, however, with current consumption of antioxidants well below the recommended level to prevent age-related cataracts.

 


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19/Apr/2019

In studies with lab-grown human cells and in mice, Johns Hopkins Medicine researchers have found that an experimental drug may be twice as good at fighting vision loss as previously thought.

In studies with lab-grown human cells and in mice, Johns Hopkins Medicine researchers have found that an experimental drug may be twice as good at fighting vision loss as previously thought.

The new research shows that the compound, named AXT107, stops abnormal blood vessels in the eye from leaking vision-blocking fluids. These results build on previous research that showed the same compound stopped the growth of abnormal vessels in animal studies of the blinding disease diabetic macular edema and wet age-related macular degeneration.

Diabetic macular edema and wet age-related macular degeneration are the leading causes of vision loss in the U.S. Approximately 750,000 Americans age 40 and older have diabetic macular edema, and wet age-related macular degeneration affects over 1.6 million Americans age 50 and older. Both diseases can eventually cause blindness if untreated.

Current drugs for diabetic macular edema and wet age-related macular degeneration focus on halting the growth of these abnormal vessels to preserve what vision is left. The current standard of treatment is monthly injections directly into the eye to suppress new blood vessel growth. These frequent visits can be a burden for patients due to the discomfort, a small risk for each injection and, for some patients, difficulty getting to the appointment because their vision is not good enough to drive.

“Our findings give us a better understanding of how this potential treatment stops the disease from progressing and does it more quickly, efficiently, and has a longer duration than current drugs used in people with vision loss of this kind,” says Aleksander Popel, Ph.D., professor of biomedical engineering at the Johns Hopkins University School of Medicine.

The study was published in the Feb. 21 issue of the Journal of Clinical Investigation Insight.

In healthy eyes, the cells that make up blood vessels are bound together by proteins residing on the surface of the cell that are directed into place by Tie 2, another protein. Tie2 proteins pack tightly together where cells meet their neighbors and act like Velcro to create a fluid-tight connection between cells in the blood vessel’s wall. In diabetic macular edema, the Tie2 proteins disperse across the cell and no longer can maintain the fluid-tight barrier between the inside of a blood vessel and the outside. Gaps form between the cells, allowing fluids to permeate into the surrounding tissue.

To understand how the drug they developed could strengthen these connections, the researchers designed a series of experiments to explore how AXT107 affects the control of Tie2 and the Velcro-like proteins.

In their first experiment, the researchers used cells derived from human blood vessels grown in the lab that mimicked those seen in wet age-related macular degeneration. When they added the AXT107 drug to these cells, the researchers found that AXT107 initiated a series of changes to cellular proteins. Using a technique to measure protein changes, the researchers found that Tie2 proteins seemed to migrate across the cell. Groups of Tie2 proteins began to congregate where cells met their neighbors, and began rebuilding connections with other blood vessel cells.

The researchers note that when observed under a microscope, the cells went from jagged-looking around the edges to having smooth and continuous outer edges that could be better suited for one cell to fit snugly against another. “It was like zipping them up with a zipper,” says Popel.

The researchers further tested whether these smooth cells could create a watertight barrier, which would be necessary to create a blood vessel that doesn’t leak. So they grew the cells in a single layer and tested whether fluid could pass through by pouring a fluorescent liquid on top of the cells and checking to see if any of the glowing liquid ended up underneath. The researchers observed that cells treated with 100 ?M of the AXT107 drug allowed 2.5 times less dye through the cell layer than control cells receiving no drug. This showed the researchers that the drug helped blood vessel cells create a watertight seal between them.

The researchers next wanted to see if the same effect could be achieved in living blood vessels. They used a fluorescent dye to observe the blood vessels in the eyes of normal mice and mice genetically engineered to mimic human macular degeneration. In the healthy mice, the researchers observed glowing blood vessels with crisp edges and very little fluorescence outside of the vessel. However, in the mice with macular degeneration, glowing liquids passed through the blood vessels, blurring the barrier between blood vessels and the surrounding tissues.

The researchers treated the engineered mice with leaky blood vessels, like those seen in macular degeneration, with injections of the AXT107 peptide into the animals’ eyes. After four days, the researchers found that in mice treated with AXT107, about half as much of the fluorescent dye leaked from their vessels as in animals that received saline injections containing no drug. These results, say researchers, show that the AXT107 drug was able to seal up leaking vessels and prevent vision-blocking fluids from permeating into the surrounding tissue.

Popel says previous studies of AXT107 in animal models showed the drug lasted longer than current treatments by forming a small clear gel of slow-releasing drug in the eye. If proved effective in humans, patients might need only one or two injections to the eye per year, instead of the monthly injections that are the current standard of care.

Popel says AXT107 provides a new therapeutic approach that targets two clinically validated pathways for retina diseases while the anti-VEGF agents only target one aspect of the disease. “In addition to potentially improving the response for patients, the longer duration of AXT107 may allow for less frequent dosing, thus reducing the treatment burden for patients,” says Popel.

The researchers say they plan to test the AXT107 peptide for safety and efficacy in clinical trials of people with diabetic macular edema next year.

Story Source:

Materials provided by Johns Hopkins Medicine. Note: Content may be edited for style and length.


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22/Mar/2019

New Treatment could improve and prolong sight in those suffering vision loss

Millions of Americans are progressively losing their sight as cells in their eyes deteriorate, but a new therapy developed by researchers at the University of California, Berkeley, could help prolong useful vision and delay total blindness.

The treatment — involving either a drug or gene therapy — works by reducing the noise generated by nerve cells in the eye, which can interfere with vision much the way tinnitus interferes with hearing. UC Berkeley neurobiologists have already shown that this approach improves vision in mice with a genetic condition, retinitis pigmentosa, that slowly leaves them blind.

Reducing this noise should bring images more sharply into view for people with retinitis pigmentosa and other types of retinal degeneration, including the most common form, age-related macular degeneration.

“This isn’t a cure for these diseases, but a treatment that may help people see better. This won’t put back the photoreceptors that have died, but maybe give people an extra few years of useful vision with the ones that are left,” said neuroscientist Richard Kramer, a professor of molecular and cell biology at UC Berkeley. “It makes the retina work as well as it possibly can, given what it has to work with. You would maybe make low vision not quite so low.”

Kramer’s lab is testing drug candidates that already exist, he said, though no one suspected that these drugs might improve low vision. He anticipates that the new discovery will send drug developers back to the shelf to retest these drugs, which interfere with cell receptors for retinoic acid. Many such drug candidates were created by pharmaceutical companies in the failed hope that they would slow the development of cancer.

“There has been a lot of excitement about emerging technologies that address blinding diseases at the end stage, after all of the photoreceptors are lost, but the number of people who are candidates for such heroic measures is relatively small,” Kramer said. “There are many more people with impaired vision — people who have lost most, but not all, of their photoreceptors. They can’t drive anymore, perhaps they can’t read or recognize faces, all they have left is a blurry perception of the world. Our experiments introduce a new strategy for improving vision in these people.”

Kramer and his UC Berkeley colleagues reported their results this week in the journal Neuron.

‘Ringing in the eyes’

WordResearchers have known for years that the retinal ganglion cells, the cells that connect directly with the vision center in the brain, generate lots of static as the light-sensitive cells — the photoreceptors — begin to die. This happens in inherited diseases such as retinitis pigmentosa, which afflicts about one in 4,000 people worldwide, but it may also occur in the much larger group of older people with age-related macular degeneration, a disease that affects the crucial part of the retina needed for precise vision. The sharp edges of an image are drowned in such static, and the brain is unable to interpret what’s seen.

Kramer focused on the role of retinoic acid after he heard that it was linked to other eye changes resulting from retinal degeneration. The dying photoreceptors — the rods, sensitive to dim light, and the cones, needed for color vision — are packed with proteins called opsins. Each opsin combines with a molecule of retinaldehyde, to form a light-sensitive protein called rhodopsin.

“There are 100 million rods in the human retina, and each rod has 100 million of these sensors, each one sequestering retinaldehyde,” he said. “When you start losing all those rods, all that retinaldehyde is now freely available to get turned into other things, including retinoic acid.”

Kramer and his team found that retinoid acid — well-known as a signal for growth and development of embryos — floods the retina, stimulating the retinal ganglion cells to make more retinoic acid receptors. It’s these receptors that make ganglion cells hyperactive, creating a constant buzz of activity that submerges the visual scene and prevents the brain from picking out the signal from noise.

“When we inhibit the receptor for retinoic acid, we reverse the process and shut off the hyperactivity. People who are losing their hearing often get tinnitus, or ringing in the ears, which only makes matters worse. Our findings suggest that retinoic acid is doing something similar in retinal degeneration — essentially causing ‘ringing in the eyes,'” Kramer said. “By inhibiting the retinoic acid receptor, we can decrease the noise and unmask the signal.”

The researchers sought out drugs known to block the receptor and showed that treated mice could see better, behaving much like mice with normal vision. They also tried gene therapy, inserting into ganglion cells a gene for a defective retinoic acid receptor. When expressed, the defective receptor bullied out the normal receptor in the cells and quieted their hyperactivity. Mice treated with gene therapy also behaved more like normal, sighted mice.

Ongoing experiments suggest that the brain, too, responds differently once the receptor is blocked, showing activity closer to normal.

While Kramer continues experiments to determine how retinoic acid makes the ganglion cells become hyperactive and how effective the inhibitors are at various stages of retinal degeneration, he is hopeful that the research community will join the effort to repurpose drugs originally developed for cancer into therapies for improving human vision.


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18/Jan/2019

A study has found that CBD — a major chemical component in marijuana — appears to increase the pressure inside the eye of mice, suggesting the use of the substance in the treatment of glaucoma may actually worsen the condition.

FULL STORY

One of the most commonly proposed uses of medical marijuana is to treat glaucoma.

But a study from researchers at Indiana University has found that a major chemical component in the substance appears to worsen the primary underpinning of the disease: a rise in pressure inside the eye.

The chemical that causes this rise in pressure is cannabidiol, or CBD, a non-psychoactive ingredient in cannabis that is increasingly marketed to consumers in products such as oil, gummies, creams and health food. It is also approved in many states as a treatment for conditions such as pediatric epilepsy.

The study was reported Dec. 14 in the journal Investigative Ophthalmology & Visual Science.

“This study raises important questions about the relationship between the primary ingredients in cannabis and their effect on the eye,” said Alex Straiker, an associate scientist in the IU Bloomington College of Arts and Sciences’ Department of Psychological and Brain Sciences, who led the study. “It also suggests the need to understand more about the potential undesirable side effects of CBD, especially due to its use in children.”

The study, which was conducted in mice, specifically found that CBD caused an increase in pressure inside the eye of 18 percent for at least four hours after use.

Tetrahydrocannabinol, or THC, the primary psychoactive ingredient of marijuana, was found to effectively lower pressure in the eye, as has been previously reported. But the study found that the use of CBD in combination with THC blocked this effect.

Specifically, the study found that male mice experienced a drop in eye pressure of nearly 30 percent eight hours after exposure to THC alone. A lower pressure drop of 22 percent was also observed after four hours in male mice.

The effect was weaker in female mice. This group experienced a pressure drop of only 17 percent after four hours. No difference in eye pressure was measured after eight hours.

The results suggest that females may be less affected by THC, though it isn’t clear whether this extends to the substance’s psychoactive effects.

“This difference between males and females — and the fact that CBD seems to worsen eye pressure, the primary risk factor for glaucoma — are both important aspects of this study,” Straiker said. “It’s also notable that CBD appears to actively oppose the beneficial effects of THC.”

By comparing the effect of these substances on mice without specific neuroreceptors affected by THC and CBD, the IU researchers were also able to identify the two specific neuroreceptors — named CB1 and GPR18 — by which the first substance lowered pressure inside the eye.

“There were studies over 45 years ago that found evidence that THC lowers pressure inside the eye, but no one’s ever identified the specific neuroreceptors involved in the process until this study,” Straiker said. “These results could have important implications for future research on the use of cannabis as a therapy for intraocular pressure.”

 


03/Jan/2019

It’s a new year, and many of us are looking to make positive changes in our lives.

The best way to do that is not by making resolutions, but by creating habits that will stick for the long term. If you want to run a marathon, form the habit of running. If you want to write a novel, form the writing habit. If you want to be more mindful, form the habit of meditation.

Of course, that’s easier said than done — just form new habits, no problem! So, in this guide, I’m going to lay out the key steps to forming the habits that will change your life.

Steps to Creating a Habit

Pick a positive habit. I recommend you find new, positive habits to form, rather than starting with quitting a bad habit. If you want to quit eating junk food … focus instead on creating the habit of eating more vegetables. Good positive habits to start with: meditation, reading, writing, exercise, eating vegetables, journaling, flossing.

One habit at a time. We all have a list of a dozen habits we’d like to change — and all right now! But in my experience, the more habits you do at once, the less likely your chances of success. Even one habit at a time takes focus and energy! Trust me on this: doing one habit at a time is the best strategy, by far, for any but the best habit masters.

Small steps are successful. People underestimate the importance of this, but along with one habit at a time, it’s probably the most important thing you can do to ensure success. Start really small. Meditate for 2 minutes a day the first week (increase by 2-3 minutes a week only if you’re consistent the previous week). Start running for 5-10 minutes a day, not 30 minutes. Eat a small serving of vegetables for one meal, don’t try to change your entire diet at once. Start as small as you can and increase in small steps, only as long as you stay consistent. Small steps allow your mind to adjust gradually and are the best method by far.

Set up reminders. The thing that trips people up in the beginning is remembering to do the habit. Don’t let yourself forget! Set up visual reminders around where you want to remember (ex: in the kitchen, for the veggies habit, or a note on your bathroom mirror for flossing), along with digital reminders on your phone and calendar.

Set up accountability. How will you hold yourself to this habit change when you feel like quitting? Accountability. Join a community or small team to hold yourself accountable.

Find reward in the doing. You won’t stick to any change for long if you really hate doing it. Instead, find some pleasure in the doing of the habit. For example, if you go running, don’t think of it as torture, but as a way to enjoy the outdoors, to feel your body moving, to feel alive. Bring mindfulness to each moment of doing the habit and find gratitude and joy as you do it. The habit will become the reward, and you’ll look forward to this nice oasis of mindfulness.

Try to be as consistent as possible. The more consistent you are, the better. Resist putting off the habit and make it your policy to just get started when you have said you’ll do it, rather than indulging in the old pattern of, “I’ll do it later.” That’s an old habit that you want to retrain by doing it immediately.

Review & adjust regularly. I like to review how I did with my habits at the end of each day, before I sleep. It helps me get better and better at habits. But at the minimum, review once a week (and do a check-in with your accountability team) and adjust as needed. For example, if you forgot to do the habit, adjust by creating new reminders. If you aren’t consistent, maybe set up a challenge with your team so that you pay them $10 each day you miss (for example). Adjusting each week means you’ll get better and better at doing this habit. If you fall down, keep coming back.


21/Aug/2018

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People Are Flushing Contact Lenses Down the Toilet … And It’s a Huge Problem for the Environment

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Contact lens wearers often dispose of the products by washing them down the drain or flushing them down the toilet — and that’s bad news for the environment, new research suggests.

Contact lenses recovered from treated sewage sludge could harm the environment. Credit: Charles Rolsky

Lenses that are washed down the drain ultimately end up in wastewater treatment plants, according to a team that presented its findings at the 256th National Meeting & Exposition of the American Chemical Society. The scientists estimate that anywhere from six to 10 metric tons of plastic lenses end up in wastewater in the U.S. alone each year.

Contacts tend to be denser than water, which means they sink, and this could ultimately pose a threat to aquatic life, especially bottom feeders that may ingest the contacts, according to a press release from the American Chemical Society.

“We found that 15 to 20 percent of contact wearers are flushing the lenses down the sink or toilet,” said Charlie Rolsky, a Ph.D. student who presented the work. “This is a pretty large number, considering roughly 45 million people in the U.S. alone wear contact lenses.”

Rolsky, Rolf Halden, and Varun Kelkar are at the Biodesign Institute’s Center for Environmental Health Engineering at Arizona State University.

To help address the fate of contact lenses during treatment, the researchers exposed five polymers found in many manufacturers’ contact lenses to anaerobic and aerobic microorganisms present at wastewater treatment plants for varying times and performed Raman spectroscopy to analyze them.

“We found that there were noticeable changes in the bonds of the contact lenses after long-term treatment with the plant’s microbes,” Kelkar said.

The team concluded that microbes in the wastewater treatment facility actually altered the surface of the contact lenses, weakening the bonds in the plastic polymers.

“When the plastic loses some of its structural strength, it will break down physically,” Kelkar said. “This leads to smaller plastic particles which would ultimately lead to the formation of microplastics.”

Aquatic organisms can mistake microplastics for food and since plastics are indigestible, this dramatically affects the marine animals’ digestive system. The animals are part of a long food chain. Some eventually find their way to the human food supply, which could lead to unwanted human exposures to plastic contaminants and pollutants that stick to the surfaces of the plastics.

The team hopes the industry will take note of the research and, at a minimum, provide a label on the packaging describing how to properly dispose of contact lenses, which is by placing them with other solid waste.

“Ultimately, we hope that manufacturers will conduct more research on how the lenses impact aquatic life and how fast the lenses degrade in a marine environment,”

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