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Mouse Study Hints at Hope Against Blindness

By Dennis Thompson
HealthDay Reporter

MONDAY, July 11, 2016 (HealthDay News) — Researchers report they have regenerated parts of damaged optic nerves in a handful of blind mice, a breakthrough that might lead to a human cure for glaucoma and other nerve-related blindness.

A combination of gene therapy and visual stimulation prompted partial regrowth of the optic nerves, restoring some communication between the brain and the eye in these mice, said study senior researcher Andrew Huberman.

“We didn’t regenerate every cell from the eye to the brain,” said Huberman, an associate professor of neurobiology at Stanford University School of Medicine, in Palo Alto, Calif. “It was a small fraction of the total number of cells.

“Nonetheless,” he added, “the mice could use that limited number of regenerated cells to see certain things. They went from being blind mice to being mice that could see a number of things.”

Nerve cells attached to the central nervous system normally do not regenerate, Huberman said. People blinded by glaucoma — in which increasing eye pressure damages the optic nerve — never regain the sight they lost.

Eye doctors typically put all their effort into preventing further loss of vision in people with glaucoma, said Dr. Andrew Iwach, chair of the Glaucoma Research Foundation.

“This data shows that there is a bridge to get to the other side of this, to go from being on defense to being on offense, where we can help people see,” said Iwach, an associate clinical professor of ophthalmology at the University of California, San Francisco. “That would be a game-changer for many patients.”

But Dr. Harry Quigley, director of the Glaucoma Center at the Johns Hopkins’ Wilmer Eye Institute in Baltimore, warned that people blinded due to nerve damage should not get their hopes up for an impending cure based on these results.

“It isn’t anything that could be turned into therapy in a human anytime soon, and I don’t think they’re suggesting that,” Quigley said.

For this study, Huberman and his colleagues used forceps to crush the optic nerve leading to one eye in a group of laboratory mice. They then set about trying to repair the nerve they’d damaged, using different therapies.

Simply regrowing the connection between the eye and the brain wasn’t enough — the researchers also had to make sure that the connection would rewire itself correctly. “If neurons don’t wire up correctly, you get failures of the brain to function properly,” Huberman explained.

Partial regeneration of the optic nerve occurred when researchers used gene therapy to stimulate the mTOR pathway, a process in the body that promotes growth of nerve tissue.

The research team also had some success in promoting optic nerve regeneration through visual stimulation. Placed in a “mouse IMAX theater,” the mice used only their damaged eye to watch a series of high-contrast moving bars. That therapy promoted some nerve regrowth, the researchers said.

But neither approach alone could re-establish the link between brain and eye. “We found that the neurons would regrow, but not very far,” Huberman said. “They would grow towards the brain, but they couldn’t reconnect with the brain.”

However, combining both gene therapy and visual stimulation caused a small part of the optic nerve to fully regenerate a connection between the eye and the brain, the researchers found.

“When we did that, we saw an incredible synergistic effect,” Huberman said. “The axons not only regrew, but they grew very fast and they regrew all the way back into the brain.”

Vision tests performed after the therapy showed that the connection had wired up properly.

One test projected an expanding dark circle onto the damaged eye, meant to give the impression of a bird of prey’s approach. The mice responded to the stimulation, scrambling for shelter to avoid the threat.

Huberman hopes to begin human experiments soon. “We are going directly from this into human studies,” he said. “We’re very quickly trying to move this towards technology that would allow stimulation of neurons, to test whether that would enhance regeneration.”

However, curing glaucoma-created blindness in a human will be much more complex than partially restoring sight in lab mice, Quigley said. Research with animals often doesn’t pan out in humans.

And Quigley noted that the optic nerve sustains chronic long-term damage from glaucoma, which presents a much messier problem than that faced by the lab mice.

The experiment “is not a model of glaucoma. This is a model of optic nerve injury by crushing,” Quigley explained. “Glaucoma is not as clean and easy as crushing the nerve, which is quick and dirty and all the nerve cells die at once.”

In addition, the researchers destroyed 50,000 optic nerve cells in the mice, but only were able to regenerate about 200, he noted.

“Would that really give rise to a functional improvement over blindness?” Quigley asked. “There’s no question you can do something to improve the regrowth of some few nerve cells in the eye. The difficulty is that for the many, many people who have eye diseases who are already visually impaired or blind, they’re going to think, ‘Oh, great! This is a treatment that’s going to help me.’ “

The study findings were published online July 11 in the journal Nature Neuroscience.

More information

For more on glaucoma, visit the U.S. National Eye Institute.





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Mouse Study Hints at Hope Against Blindness

By Dennis Thompson
HealthDay Reporter

MONDAY, July 11, 2016 (HealthDay News) — Researchers report they have regenerated parts of damaged optic nerves in a handful of blind mice, a breakthrough that might lead to a human cure for glaucoma and other nerve-related blindness.

A combination of gene therapy and visual stimulation prompted partial regrowth of the optic nerves, restoring some communication between the brain and the eye in these mice, said study senior researcher Andrew Huberman.

“We didn’t regenerate every cell from the eye to the brain,” said Huberman, an associate professor of neurobiology at Stanford University School of Medicine, in Palo Alto, Calif. “It was a small fraction of the total number of cells.

“Nonetheless,” he added, “the mice could use that limited number of regenerated cells to see certain things. They went from being blind mice to being mice that could see a number of things.”

Nerve cells attached to the central nervous system normally do not regenerate, Huberman said. People blinded by glaucoma — in which increasing eye pressure damages the optic nerve — never regain the sight they lost.

Eye doctors typically put all their effort into preventing further loss of vision in people with glaucoma, said Dr. Andrew Iwach, chair of the Glaucoma Research Foundation.

“This data shows that there is a bridge to get to the other side of this, to go from being on defense to being on offense, where we can help people see,” said Iwach, an associate clinical professor of ophthalmology at the University of California, San Francisco. “That would be a game-changer for many patients.”

But Dr. Harry Quigley, director of the Glaucoma Center at the Johns Hopkins’ Wilmer Eye Institute in Baltimore, warned that people blinded due to nerve damage should not get their hopes up for an impending cure based on these results.

“It isn’t anything that could be turned into therapy in a human anytime soon, and I don’t think they’re suggesting that,” Quigley said.

For this study, Huberman and his colleagues used forceps to crush the optic nerve leading to one eye in a group of laboratory mice. They then set about trying to repair the nerve they’d damaged, using different therapies.

Simply regrowing the connection between the eye and the brain wasn’t enough — the researchers also had to make sure that the connection would rewire itself correctly. “If neurons don’t wire up correctly, you get failures of the brain to function properly,” Huberman explained.

Partial regeneration of the optic nerve occurred when researchers used gene therapy to stimulate the mTOR pathway, a process in the body that promotes growth of nerve tissue.

The research team also had some success in promoting optic nerve regeneration through visual stimulation. Placed in a “mouse IMAX theater,” the mice used only their damaged eye to watch a series of high-contrast moving bars. That therapy promoted some nerve regrowth, the researchers said.

But neither approach alone could re-establish the link between brain and eye. “We found that the neurons would regrow, but not very far,” Huberman said. “They would grow towards the brain, but they couldn’t reconnect with the brain.”

However, combining both gene therapy and visual stimulation caused a small part of the optic nerve to fully regenerate a connection between the eye and the brain, the researchers found.

“When we did that, we saw an incredible synergistic effect,” Huberman said. “The axons not only regrew, but they grew very fast and they regrew all the way back into the brain.”

Vision tests performed after the therapy showed that the connection had wired up properly.

One test projected an expanding dark circle onto the damaged eye, meant to give the impression of a bird of prey’s approach. The mice responded to the stimulation, scrambling for shelter to avoid the threat.

Huberman hopes to begin human experiments soon. “We are going directly from this into human studies,” he said. “We’re very quickly trying to move this towards technology that would allow stimulation of neurons, to test whether that would enhance regeneration.”

However, curing glaucoma-created blindness in a human will be much more complex than partially restoring sight in lab mice, Quigley said. Research with animals often doesn’t pan out in humans.

And Quigley noted that the optic nerve sustains chronic long-term damage from glaucoma, which presents a much messier problem than that faced by the lab mice.

The experiment “is not a model of glaucoma. This is a model of optic nerve injury by crushing,” Quigley explained. “Glaucoma is not as clean and easy as crushing the nerve, which is quick and dirty and all the nerve cells die at once.”

In addition, the researchers destroyed 50,000 optic nerve cells in the mice, but only were able to regenerate about 200, he noted.

“Would that really give rise to a functional improvement over blindness?” Quigley asked. “There’s no question you can do something to improve the regrowth of some few nerve cells in the eye. The difficulty is that for the many, many people who have eye diseases who are already visually impaired or blind, they’re going to think, ‘Oh, great! This is a treatment that’s going to help me.’ “

The study findings were published online July 11 in the journal Nature Neuroscience.

More information

For more on glaucoma, visit the U.S. National Eye Institute.





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Why Being Cold Might Foster a Cold

MONDAY, July 11, 2016 (HealthDay News) — Scientists may be proving Mom right: Your odds of avoiding a cold get better if you bundle up and stay warm.

Warmer body temperatures appear to help prevent the cold virus from spreading, in multiple ways, researchers at Yale University found.

For the study, a team led by immunology professor Akiko Iwasaki examined human airways cells. These cells produce essential immune system proteins called interferons that respond to a cold virus.

The cells were infected with the virus in a lab and incubated at either a core body temperature of 98.6 degrees Fahrenheit or a cooler temperature of 91.4 degrees Fahrenheit.

Using mathematical models, the researchers found that when infected cells were exposed to healthy core body temperatures, the virus died off more quickly and wasn’t able to replicate as well.

Warmer body temperatures also seemed to help on another front. Iwasaki’s group reported that the activity of an enzyme called RNAseL — which attacks and destroys viral genes — was also enhanced at higher temperatures.

This new work adds to prior research by the Yale team. In that study, conducted in mice, Iwasaki’s group found that at several degrees below core body temperature, virus-fighting interferons were less able to do their job.

The cooler temperatures also enabled the cold virus to spread in the animals’ airway cells, the researchers said.

The combined research suggests that “there are three [immunological] ways to target this virus now,” Iwasaki said in a Yale news release.

Each of the pathways influence the immune system’s ability to fight the virus that causes the common cold. Iwasaki and her team believe the findings could provide new strategies for scientists working to develop treatments against the pesky illness.

The study was published July 11 in the Proceedings of the National Academy of Sciences.

More information

The U.S. Centers for Disease Control and Prevention has more about preventing common colds.





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2nd U.S. Case of Bacteria Resistant to Last-Resort Antibiotic

MONDAY, July 11, 2016 (HealthDay News) — Scientists have identified a second patient in the United States who was infected with a bacteria that is resistant to an antibiotic of last resort.

The new case involved a patient in New York, while the first reported case involved a woman from Pennsylvania. However, the New York patient was actually infected more than a year ago and the resistant bacteria was only spotted recently in lab testing. The Pennsylvania infection occurred last spring, researchers said.

Both patients had E. coli with a gene called mcr-1, which makes bacteria resistant to the antibiotic colistin, the scientists explained.

In the latest study, the researchers tested more than 13,500 strains of E. coli and nearly 7,500 strains of Klebsiella pneumoniae collected from hospitals in North America, Latin America, Europe and the Asia-Pacific region in 2015.

The results showed that almost 2 percent of the E. coli samples were resistant to colistin, and 19 tested positive for mcr-1. Those 19 samples were found in the United States and nine other countries in all of the regions.

The study was published July 11 in the journal Antimicrobial Agents and Chemotherapy, a journal of the American Society for Microbiology.

The findings raise concerns that mcr-1 — first identified in food, animals and people in China in the 1980s — may be able to jump to other types of bacteria that are already resistant to other antibiotics, the researchers said. Because mcr-1 is now present worldwide, it needs to be closely monitored, the study authors stressed.

“The fact that the gene has been detected in food livestock and raw meat is also concerning,” study corresponding author Mariana Castanheira, director of molecular and microbiology at JMI Laboratories in Iowa, said in a journal news release.

But she noted that the samples that tested positive for mcr-1 were still susceptible to several widely used antibiotics.

That means that E. coli and Klebsiella pneumoniae with mcr-1 are unlikely to cause hard-to-treat infections at this time, Castanheira said.

She said she and her colleagues are continuing their research.

In the first U.S. patient found to have colistin-resistant E. coli, the bacteria was also resistant to first-line antibiotics. That case — reported May 26 in a journal of the American Society of Microbiology — triggered alarm bells.

“It is the end of the road for antibiotics unless we act urgently,” Dr. Tom Frieden, director of the U.S. Centers for Disease Control and Prevention, warned at the time.

More information

The U.S. Centers for Disease Control and Prevention has more on antibiotic resistance.





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Heart Failure After Heart Attack Tied to Cancer Risk in Study

By Randy Dotinga
HealthDay Reporter

MONDAY, July 11, 2016 (HealthDay News) — People who develop heart failure after a heart attack may also face a higher risk of cancer, a new study suggests.

And, they may be prone to cancers affecting the lungs or the digestive system, according to the researchers.

“Patients with cardiovascular disease experience a high burden of other diseases and should be followed with that awareness in mind,” said study co-author Dr. Veronique Roger, a professor of medicine and epidemiology at the Mayo Clinic in Rochester, Minn.

The researchers said the new study wasn’t designed to prove a cause-and-effect relationship between heart problems and cancers. Also, the number of heart failure patients diagnosed with cancer in the study was small.

Still, the research shows the importance of closely monitoring cardiac patients, Roger said.

Previous Mayo Clinic research has linked heart failure to a 70 percent higher risk of cancer. Patients with heart failure, a potentially fatal condition, have weakened hearts that can’t pump enough blood to meet the body’s needs. Fluids often build up in the feet and legs, leading to painful swelling.

The new study included more than 1,000 people in Minnesota who’d had a heart attack. Their average age was 65, and 60 percent were male. The researchers tracked the study volunteers’ health for an average of five years.

From that group, 228 developed heart failure (21 percent) and 98 developed types of cancer other than non-melanoma skin cancer. Eight percent of patients without heart failure developed cancer compared to 12 percent of those with heart failure, the study found.

After the researchers adjusted their statistics for factors such as age, gender and other health conditions, they found that heart failure patients had about 71 percent higher odds of getting diagnosed with cancer compared to heart attack survivors who didn’t develop heart failure.

However, the researchers found that cancer death rates were similar for those with heart failure and those without.

Nearly 29 percent of the heart failure patients with cancer had respiratory tumors; the rate was only 17 percent for non-heart failure patients with cancer. There was a similar gap for digestive cancers, the study authors said.

These findings suggest that smoking and alcohol use could be playing major roles in both heart failure and cancer, study co-author Roger said.

The increased risk of cancer probably isn’t due to the extra testing and medical attention given to people with heart failure, said Dr. Gregg Fonarow, a professor of cardiovascular medicine at the University of California, Los Angeles.

“Cancer did not increase until years after the onset of heart failure, suggesting this is not resulting from extra testing that heart failure patients may receive,” said Fonarow, who’s familiar with the study findings.

Fonarow added that heart failure could boost cancer rates by disrupting the workings of cells and increasing inflammation in the body.

“It is unlikely that the medications used to treat heart failure are increasing the cancer risk since randomized clinical trials of these heart failure medications have not detected an increased risk of cancer associated with their long-term use,” he said.

What should heart failure patients do to protect themselves? Fonarow suggested they talk to their physicians about getting all the recommended cancer screenings for their age.

The study appears in the July 19 issue of Journal of the American College of Cardiology.

More information

The Nebraska Comprehensive Cancer Control Program has more on cancer and heart disease .





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Insurance Mandates Boost U.S. Autism Diagnoses

MONDAY, July 11, 2016 (HealthDay News) — More U.S. children are getting diagnosed and treated for autism in states that require commercial health insurers to cover these services, a new study finds.

But countless more kids with undiagnosed autism spectrum disorder still aren’t receiving needed medical attention, said researchers from the University of Pennsylvania Perelman School of Medicine in Philadelphia.

“These are encouraging findings,” said study leader David Mandell, a professor in the department of psychiatry.

“We now know that more children are being served, but we are also acutely aware that these numbers are well below the prevalence of autism spectrum disorder in our society, indicating that the mandates have not had the full effect that advocates desired,” he explained.

“This is merely a step in the right direction. These mandates represent a patch, not a panacea,” Mandell, who is also director of Penn’s Center for Mental Health Policy and Services Research, added in a university news release.

Autism spectrum disorder describes a range of conditions — from mild to severe — that often include repetitive behaviors and difficulties with social communication. U.S. health officials estimate that 1 in 68 children has autism spectrum disorder.

Treatment for the disorder is costly since it may include 25 hours of educational and behavioral therapy a week for several years, the study authors noted.

Studies have shown that intensive behavioral treatments improve learning, communication and social skills in young kids with autism, according to Autism Speaks, an advocacy organization.

Fifteen years ago, Indiana was the first state to mandate that commercial health insurers cover behavioral treatments for autism. Since then, 43 other states have also made autism treatment more accessible to families that couldn’t afford it.

To assess the effectiveness of these mandates, the Penn researchers analyzed inpatient and outpatient health insurance claims from 2008 through 2012 for more than 1 million children aged 21 and younger. The patients were covered by United HealthCare, Aetna and Humana, three of the largest U.S. health insurers.

Over the course of the study, just over 154,000 kids were diagnosed with autism. Overall, the mandates resulted in a 12.7 percent annual increase in diagnoses, the researchers said.

The longer these laws were in place, the more children were identified, with an 18 percent jump noted in the final years of the study.

In states with autism mandates, the rate of diagnosis was 1.8 per 1,000 children compared to 1.6 per 1,000 children in states that lacked such requirements, the findings showed.

The study was published July 11 in JAMA Pediatrics.

More information

The U.S. National Institute of Neurological Disorders and Stroke has more about autism spectrum disorder.





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Study Links Severe Head Injury to Parkinson’s Risk

By Steven Reinberg
HealthDay Reporter

MONDAY, July 11, 2016 (HealthDay News) — A traumatic brain injury with loss of consciousness may increase the risk of developing Parkinson’s disease, new research suggests.

“It could be that the head injury itself initiates a cascade of effects that ultimately lead to Parkinson disease,” said lead researcher Dr. Paul Crane, a professor of medicine at the University of Washington School of Medicine in Seattle.

Or, Crane added, the head injury may not cause Parkinson’s, but make it “more difficult for people who have sustained a head injury to recover, adjust to or deal with the cascade of events leading to Parkinson disease that are separate from the head injury itself.”

However, the study did not prove that a traumatic brain injury causes the risk of Parkinson’s to rise.

Parkinson’s disease is a chronic and progressive movement disorder that affects the central nervous system. Symptoms worsen with time. Nearly 1 million Americans have the disorder. The cause is unknown and there is no cure. But, there are treatment options — such as medication and surgery — to manage symptoms, according to the Parkinson’s Disease Foundation.

For the study, Crane and his colleagues collected data on more than 7,000 older adults, average age 80. Among these individuals, 865 had suffered a head injury and lost consciousness at some point in their lives — some fairly early in life. Of these, 142 were unconscious for more than one hour.

Crane’s team found that more than 1,500 suffered from dementia and 117 had Parkinson’s disease.

They researchers said they uncovered a link between brain injury with loss of consciousness for more than an hour and a greater risk for Parkinson’s disease. There was also a link to greater risk of microscopic stroke, according to the study.

The researchers did not find an association between head injury with loss of consciousness and increased risk for dementia, Crane said.

It’s not clear why a head injury might raise the risk of Parkinson’s disease, Crane said.

The findings were published online July 11 in the journal JAMA Neurology.

Dr. Mill Etienne is a spokesman for the American College of Neurology. He said people should take protective measures when participating in activities where a head injury is likely.

“Any activity you are involved in, you want to do what you can to protect your brain,” he said. “Because, although the head trauma might happen when you are young, it could have a long-lasting impact later in your lifetime.”

Crane agreed, adding that accidental head injuries will happen.

“We already know we should be encouraging the use of bike helmets and so on to limit the chance of a severe head injury. We should also seriously consider eliminating activities with the very highest levels of risk of head injuries,” he said.

More information

For more information on traumatic brain injury, visit the U.S. National Institute of Neurological Disorders and Stroke.





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Global Team Taps Into DNA Behind Type 2 Diabetes

MONDAY, July 11, 2016 (HealthDay News) — An international team of scientists appears to be advancing knowledge about the genetic factors contributing to type 2 diabetes.

The researchers say they have also identified more than 12 genes that directly increase risk for the condition.

“Our study has taken us to the most complete understanding yet of the genetic architecture of type 2 diabetes,” said the study’s co-senior author, Michael Boehnke. He is director of the Center for Statistical Genetics at the University of Michigan School of Public Health in Ann Arbor.

“With this in-depth analysis, we have obtained a more complete picture of the number and characteristics of the genetic variants that influence type 2 diabetes risk,” Boehnke said. He made his comments in a news release from the Wellcome Trust Centre for Human Genetics at the University of Oxford in England, which also contributed to the study.

One in 10 people globally either has type 2 diabetes or is predicted to develop it, according to background research with the study. Environmental factors such as diet and exercise, as well as inherited genetic changes, contribute to your risk of developing the condition, Boehnke and his colleagues explained.

Learning more about how these factors contribute to the blood sugar disease could lead to new ways to prevent or treat it, the researchers said.

For the study, more than 300 scientists from 22 countries analyzed the genetic makeup (genome) of more than 120,000 people whose ancestry can be traced to Europe, South and East Asia, the Americas and Africa. Participants had their entire genome sequenced or just the part that codes directly for proteins (the exome).

By comparing the genetic variations between those who had type 2 diabetes and those who didn’t, the researchers assessed the influence of rare, “private” DNA differences along with common DNA differences that many people share.

Contrary to what some researchers expected, the study revealed that most of the genetic risk for type 2 diabetes is associated with common shared differences in the genetic code, not rare ones.

Each of these differences adds to an individual’s overall risk of disease, the study authors said. Future strategies to develop a personalized prevention or treatment approach should take into account a patient’s genetic profile as well as environmental risk factors, the researchers suggested.

“Our study tells us that genetic risk for type 2 diabetes reflects hundreds, or even thousands, of different genetic variants, most of them shared across populations,” said the study’s co-lead author, Jason Flannick. He is senior group leader at the Broad Institute of Harvard and MIT in Cambridge, Mass. “This large range of genetic effects may challenge efforts to deliver personalized (or precision) medicine.”

In addition, the study identified more than 12 risk genes directly associated with the development of type 2 diabetes. One example, the researchers said, is the TM6SF2 gene, which increases diabetes risk by altering the amount of fat stored in the liver.

Flannick said the data from the study has been made publicly accessible for researchers around the world “in the hope that this will accelerate efforts to understand, prevent and treat this condition.”

The study was published July 11 in the journal Nature.

More information

The American Diabetes Association has more about type 2 diabetes.





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Many Adults Use Antibiotics Without Consulting Doctor, Survey Finds

MONDAY, July 11, 2016 (HealthDay News) — Adding to fears about the overuse of antibiotics, a new Texas study finds that one in every 20 adults has hoarded the drugs and used them without a doctor’s guidance.

For years, health experts have warned that overuse of antibiotics is leading to drug-resistant “superbug” bacteria that could pose dire health problems.

Self-diagnosis and overuse of the drugs could now be adding to the problem, the researchers behind the new study said.

“When people self-diagnose and self-prescribe antibiotics it is likely that the therapy is unnecessary because most often these are upper respiratory infections that are mostly caused by viruses,” said study lead author Dr. Larissa Grigoryan. She an instructor in Family and Community Medicine at Baylor College of Medicine in Houston.

“The most common conditions patients reported self-treating with antibiotics were sore throat, runny nose or cough — conditions that typically would get better without any antibiotic treatment,” Grigoryan said in a news release from the American Society for Microbiology.

One infectious-disease expert expressed alarm at the new findings.

“This report on people using previously prescribed antibiotics, for self-diagnosed reasons, is terribly disturbing, potentially dangerous for the individual and clearly detrimental to society as a whole,” said Dr. Howard Selinger. He is chair of family medicine at Quinnipiac University School of Medicine, in Hamden, Conn.

“Self-diagnosis and treatment with previously prescribed antibiotics puts the patient at risk for potentially dangerous side effects such as disruption of bowel bacteria, diarrhea, etc.,” he noted.

Also, “even if the choice of a previously used antibiotic is appropriate, the quantity will be insufficient to complete the job due to previous use,” Selinger pointed out.

For the study, Grigoryan’s team randomly selected and surveyed 400 adults treated at diverse family practice clinics across the Houston area.

Of these patients, 5 percent said they had used antibiotics without a prescription in the past year. The researchers also found that one in every four patients surveyed admitted that he or she would use any antibiotics on hand — without contacting the doctor first.

Overall, 14 percent of the adults polled said they kept a stash of antibiotics in their home. Most of these drugs were saved from prior prescriptions.

Of the antibiotics obtained without a prescription, 40 percent were purchased in a store or pharmacy; 24 percent were bought outside of the United States; 20 percent were supplied by friends or family members, and 12 percent were left over from previous prescriptions.

The researchers said that in 4 percent of the cases, antibiotics used without a prescription were drugs intended for use in animals, not humans.

“Patients from public primary care clinics, those with less education, and younger patients had a higher risk of [non-prescription] use in our survey,” Grigoryan’s team wrote.

Cost may be driving some of this non-prescription use, the researchers theorized. They pointed out that copays for drugs at public clinics may be $70 or more, so some patients may seek cheaper ways to get antibiotics.

Whatever the cause, the trend could have big implications for the health of individuals, and public health in general, doctors said.

When people use an incomplete series of leftover antibiotics, this can allow germs to develop a dangerous resistance to the drug, Selinger explained.

“That’s resistance that then puts everyone in the population at risk for a future infection that is difficult if not impossible to treat,” he said.

Dr. Len Horovitz is an internist and infectious disease specialist at Lenox Hill Hospital in New York City. He called the overuse of antibiotics a “major health concern.”

“It’s a bad enough practice when doctors overprescribe, but now it’s clear that patients themselves are acquiring antibiotics and are self-prescribing,” Horovitz said. “Inappropriate use is most often for a cold, where antibiotics won’t work.”

The study was published July 11 in the journal Antimicrobial Agents and Chemotherapy.

More information

The U.S. Centers for Disease Control and Prevention provides more information on antibiotic resistance.





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Behold: Kylie Jenner’s Secret to Perfectly Shaped Brows

Photo: Getty Images

Photo: Getty Images

Kylie Jenner may change her hair color several times a week (OK, we’re exaggerating a little bit, but we’re sure that has happened before), but there is one thing that remains a constant in her look. That, of course, would be her perfectly shaped eyebrows.

We have marveled at them many times, and the day has finally come when Kylie and her makeup artist, Mario Tejada, have revealed their brow secrets with us. Cause for celebration? Oh, we think so.

In a video posted on her app, Tejada says that they first like to tint eyebrows for a more defined look.

Then, using a spoolie, he combs Kylie’s brows in an upward position. Next, using light, feather-like strokes, he fills them in with a pencil (for Kylie, he uses Anastasia Beverly Hills in Medium Brown) and then applies foundation at the bridge to define them.

While we love an Anastasia eyebrow pencil with all of our hearts, the one thing that truly stood out was the MUA’s tip for figuring out how long your brow needs to be. He said to take the spoolie pencil and place it from the tip of your nose to your temple. Where it hits on your temple is where your brow should end. Yup, definitely trying that one out!

So while her method does include a lot of steps, her brows are legit.

Now, we’ll leave you with some pics so you can spend some time admiring her makeup.

Instagram Photo

Instagram Photo

Just a suggestion, Kylie… Maybe your next makeup venture should be all about the brow?

This article originally appeared on InStyle.com/MIMI.




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