Spanish researchers are developing bladeless wind turbines .

A Spanish company called Vortex Bladeless has come up with bladeless wind turbine technology that seeks to provide more energy for less, and address the criticisms aimed at traditional wind farms – particularly where wildlife is concerned.

With blades that spin at speeds of more than 320 km/h (200 miles/hour), wind turbines haven’t been the best news for the birds that live around them. While for the most part, the damage is fairly minimal, one wind farm in particular, Altamont Pass in California, US, has drawn the ire of local residents because of the 1,300 birds of prey – including eagles, falcons, hawks – that are killed each year as they try to migrate through it.
And keeping all those heavy blades spinning that fast indefinitely? Well, it’s no easy task, and certainly not cheap, energy-wise. According to Vortex Bladeless, just by ditching the blades – and all moving parts, in fact – they will save around 40 percent of the energy cost of regular wind turbines, largely by cutting down on maintenance costs. “Since the Vortex doesn’t have moving parts or gears, it should last longer and it won’t require periodic lubrication,” Dante D’Orazio from The Verge reports. “The simpler design also means that manufacturing costs are about half that of a traditional wind turbine.”

D’Orazio adds that the bladeless turbines are estimated to harvest approximately 30 percent less energy, but because they’re basically just sticks now, you can cram a whole lot more of them into the space of a regular wind turbine. Plus these things are completely silent, so no one can claim instances of wind turbine syndrome, where the sub-sonic noise generated by traditional wind turbines is blamed for everything from headaches and dizziness to sleepiness and depression.

So how do they work, exactly? Just like traditional wind turbines, the bladeless variety still needs to capture kinetic energy and convert it to electricity, but instead of using a blade, it uses a phenomenon known as vorticity, which produces a series of spinning vortices in the surrounding air. The team at Vortex Bladeless designed their 2.7-metre-high ‘cones’ specifically so that these vortices would accumulate simultaneously all the way up their length. Liz Stinson explains at Wired:

“In its current prototype, the elongated cone is made from a composite of fibreglass and carbon fibre, which allows the mast to vibrate as much as possible (an increase in mass reduces natural frequency). At the base of the cone are two rings of repelling magnets, which act as a sort of nonelectrical motor. When the cone oscillates one way, the repelling magnets pull it in the other direction, like a slight nudge to boost the mast’s movement regardless of wind speed.”

The kinetic energy that’s generated from all this movement is then converted into useable electricity using an electrical generator called an alternator.

Vortex Bladeless have already raised over $1 million in funding, and hope to gather more from investors in the US. They’re planning on installing their first prototype by the end of the year.

Sugar: Eight times more addictive than cocaine – learn how to break the habit now

“The $1 trillion industrial food system is the biggest drug dealer around, responsible for contributing to tens of millions of deaths every year and siphoning trillions of dollars from our global economy through the loss of human and natural capital,” asserted Dr. Mark Hyman in the article “Sweet poison: How sugar, not cocaine, is one of the most addictive and dangerous substances.”

Hyman has plenty of experience in the field, with 20 years as a practicing physician. He’s also chairman of the Institute for Functional Medicine, as well as founder and director of the Ultra Wellness Center in Massachusetts.

Hyman isn’t simply on a campaign against sugar; he’s on a mission to rein in our current health crisis of obesity, autoimmune disease, high blood pressure, inflammation, hormonal imbalance, depression, anxiety and sleep disorders. A monumental task, since he considers the sweet stuff to be as powerfully addictive as alcohol, cocaine or even heroin.

A health disaster

Secreted within a majority of processed and packaged food, sugar is a hidden health destroyer. Americans alone consume a staggering 152 pounds each year. According to Hyman, it’s eight times more addictive than cocaine. As a nation, we are sugar addicts — true junkies in the clutches of an industrial food system.

And it doesn’t matter the type — white, brown or high-fructose corn syrup — it all contributes to cancer, heart disease, diabetes and obesity. Research indicates that when an overabundance of sugar is consumed, the liver converts it to fat, which can lead to plaque in the arteries and tumor growth. As it turns out, certain tumors have insulin receptors that feed on glucose.

Since the 1970s, food manufacturers began stripping products of fat because it was believed to be unhealthy. But the food turned tasteless, so sugar was the go-to replacement. Now, the substance is in everything from Starbucks coffee drinks to salad dressings and bread.

Hyman believes that we “need a big solution that reaches deep into what is offered in our supermarkets, restaurants, schools and workplaces[.] We need a solution that addresses the policy roots in agriculture, food marketing, dietary recommendations and the way doctors are trained to diagnose and treat patients.”

But the first step is to take responsibility for our own health. And one way to do that is to detox from sugar.

How to break the habit

Getting off sugar isn’t just about avoiding desserts and sweets, although that’s an excellent start. We need to dig deep, read labels and give up processed foods as a whole. Dr. Hyman has developed a 10-day detox diet that is a solution for blood sugar disorders. During an episode of The Dr. Oz Show, Hyman recommends eliminating the following foods from the diet:

Wheat and grains, as both are inflammatory and trigger hunger and craving.

Stop drinking “liquid death,” otherwise known as sugary drinks and soda, which drive up insulin and create belly fat. Dr. Hyman personally knows of one patient who dropped 75 pounds simply by removing soda from their diet.

Ditch convenience foods, since they are designed to be addictive with high flavor and sugar.

Finally, avoid dairy — it’s another pro-inflammatory edible that promotes weight gain.

If you are curious about what you can eat to detox from sugar, improve health and shed excess weight, have a look at this handy shopping guide developed by Dr. Hyman.

Learn more:

Human attention span down to just eight seconds .

human attention span, attention span, human attention, microsoft study, human brain research, brain research, human brain research microsoft, microsoft human brain research, microsoft news, science news, world news
A recent Microsoft study revealed that human attention span has reduced to just 8 seconds.

With the rise in digital technology, the human attention span has shortened from 12 seconds to eight seconds in more than a decade, a recent study by Microsoft  Corporation has found.

Humans now have an attention span less than of a goldfish (nine seconds average).

The 54-page study sought to understand what impact technology and today’s digital lives are having on attention spans.

The researchers collected data from surveys of more than 2,000 Canadians over the age of 18.

They played games and interacted online to help scientists determine the impact of smartphones and other digital media on everyday life.

Participants’ brain activity was recorded and behaviour was filmed while they interacted with different social media platforms across devices and in different environments.

The team measured their attention levels and activities to view how attention varied by screen, task, content type and structure.

The findings revealed human attention span has fallen from an average of 12 seconds in the year 2000 to just eight seconds today.

The decrease was seen across all age groups and genders in the study.

Those in the age group of 18 to 34 had a 31 percent high sustained attention span compared to those age 55 and over at 35 percent.

Meanwhile, males (33 percent) had a better attention span than females (31 percent).

Young respondents were more likely to display addiction-like behaviours when it came to their devices.

For example, 77 percent of people aged 18 to 24 responded “yes” when asked “When nothing is occupying my attention, the first thing I do is reach for my phone,” compared with only 10 percent of those over age 65.

“Out of the 18 to 24 age group, more than half admit to checking their phone every 30 minutes or less and over three-fourths used their portable devices while watching TV,” the findings showed.

On a positive note, the researchers found the ability to multitask has significantly improved.

“Heavy multi-screeners find it difficult to filter out irrelevant stimuli a” they are more easily distracted by multiple streams of media,” stated the report posted on the Microsoft website.

Cystic fibrosis drug offers hope to patients .


CF therapy

A “groundbreaking” cystic fibrosis therapy could profoundly improve patients’ quality of life, say doctors.

Patients often die before their 40s as mucus clogs and damages their lungs and leaves them prone to infection.

A major trial on 1,108 patients, in the New England Journal of Medicine, showed a combination of drugs could bypass the genetic errors that cause the disease and may increase life expectancy.

The Cystic Fibrosis Trust said it could “improve the lives of many”.

One in every 2,500 babies in the UK has cystic fibrosis.

Errors in sufferers’ DNA – inherited from their parents – damage the microscopic machinery that controls salt and water levels in the linings of the lungs.

The result is a thick mucus that inexorably damages the lungs.

Antibiotics help prevent infection and drugs can loosen the mucus, but nothing deals with the fundamental problem for most patients.


The combination of drugs – lumacaftor and ivacaftor – were designed to repair that microscopic machinery.

The trial showed that those patients given the cocktail for 24 weeks had better lung function.

Cystic fibrosis also affects the mucus lining in the gut so the doctors were pleased to see the patients also gained weight in the trial.

‘Fundamental treatment’

Prof Stuart Elborn, who led the European part of the trial from Queen’s University Belfast, told the BBC News website: “This is very exciting and it really demonstrates that we can correct the basic defects in cystic fibrosis.

“This is likely to become a fundamental treatment for cystic fibrosis.

“Starting in children may prevent the disease process developing if we correct the basic defect early in life.

“Will this improve survival for people with cystic fibrosis? We would anticipate it would have a really good chance of doing that, but we don’t know for sure yet.”

There are however, many types of error in the DNA that can culminate in cystic fibrosis.

This treatment combination should work on around half of patients, while one of the drugs on its own corrects a small proportion of errors.

New treatments are still required for the remaining patients.


Susanna McColley, professor of paediatrics at Northwestern University, said these were “groundbreaking findings” that showed the future of treating cystic fibrosis.

She told the BBC: “For subjects I’ve cared for, they felt better in ways that are not necessarily measurable.

“One young woman said, and this is a direct quote, her CF ‘is not a problem’.”

Janet Allen, the director of research at the Cystic Fibrosis Trust charity, said: “These results open up a new front in the fight against cystic fibrosis and this combination therapy looks set to be an important additional treatment option that could improve the lives of many.

“As this leading edge of science continues to be explored and better understood, we are hopeful that a future of personalised medicines is increasingly within reach.”

The therapy is being examined by regulators around the world.

Two Large Hadron Collider experiments first to observe rare subatomic process .

Event display from the LHCb experiment on the Large Hadron Collider shows an example of collisions that produced candidates for the rare decay of the Bs particle, predicted and observed to occur only about four times out of a billion.

Two experiments at the Large Hadron Collider at the European Organization for Nuclear Research (CERN) in Geneva, Switzerland, have combined their results and observed a previously unseen subatomic process.

As published in the journal Nature this week, a joint analysis by the CMS and LHCb collaborations has established a new and extremely rare decay of the Bs particle (a heavy composite particle consisting of a bottom antiquark and a strange quark) into two muons. Theorists had predicted that this decay would only occur about four times out of a billion, and that is roughly what the two experiments observed.

“It’s amazing that this theoretical prediction is so accurate and even more amazing that we can actually observe it at all,” said Syracuse University Professor Sheldon Stone, a member of the LHCb collaboration. “This is a great triumph for the LHC and both experiments.”

LHCb and CMS both study the properties of particles to search for cracks in the Standard Model, our best description so far of the behavior of all directly observable matter in the universe. The Standard Model is known to be incomplete since it does not address issues such as the presence of dark matter or the abundance of matter over antimatter in our universe. Any deviations from this model could be evidence of new physics at play, such as new particles or forces that could provide answers to these mysteries.

“Many theories that propose to extend the Standard Model also predict an increase in this Bs decay rate,” said Fermilab’s Joel Butler of the CMS experiment. “This new result allows us to discount or severely limit the parameters of most of these theories. Any viable theory must predict a change small enough to be accommodated by the remaining uncertainty.”

Researchers at the LHC are particularly interested in particles containing bottom quarks because they are easy to detect, abundantly produced and have a relatively long lifespan, according to Stone.

“We also know that Bs mesons oscillate between their matter and their antimatter counterparts, a process first discovered at Fermilab in 2006,” Stone said. “Studying the properties of B mesons will help us understand the imbalance of matter and antimatter in the universe.”

That imbalance is a mystery scientists are working to unravel. The big bang that created the universe should have resulted in equal amounts of matter and antimatter, annihilating each other on contact. But matter prevails, and scientists have not yet discovered the mechanism that made that possible.

“The LHC will soon begin a new run at higher energy and intensity,” Butler said. “The precision with which this decay is measured will improve, further limiting the viable Standard Model extensions. And of course, we always hope to see the new physics directly in the form of new particles or forces.”

This discovery grew from analysis of data taken in 2011 and 2012 by both experiments. Scientists also saw some evidence for this same process for the Bd particle, a similar particle consisting of a bottom antiquark and a down quark. However, this process is much more rare and predicted to occur only once out of every 10 billion decays. More data will be needed to conclusively establish its decay to two muons.

The U.S. Department of Energy Office of Science provides funding for the U.S. contributions to the CMS experiment. The National Science Foundation provides funding for the U.S. contributions to the CMS and LHCb experiments. Together, the CMS and LHCb collaborations include more than 4,500 scientists from more than 250 institutions in 44 countries.

Taking immortality away from cancer .

Lung cancer cells treated with the CNIO TRF1 inhibitor ETP-47037 (right) show less TRF1 bound to the telomeres (green, top), more telomeric DNA damage (pink, bottom), and therefore, an acute telomere uncapping, than non-treated cancer cells (left).

Scientists from the Spanish National Cancer Research Centre (CNIO) have discovered a new strategy to fight cancer, which is very different from those described to date. Their work shows for the first time that telomeres — the structures protecting the ends of the chromosomes — may represent an effective anti-cancer target: by blocking the TRF1 gene, which is essential for the telomeres, they have shown dramatic improvements in mice with lung cancer.

“Telomere uncapping is emerging as a potential mechanism to develop new therapeutic targets for lung cancer,” mention the authors with equal contribution in EMBO Molecular Medicine; Maria Garcia-Beccaria, Paula Martinez and Marinela Mendez, from the CNIO Telomeres and Telomerase Group led by Maria Blasco, who is also an author in the article. The research was also carried out in collaboration with the Experimental Therapeutics Programme, the Experimental Oncology Group and the Histopathology, Molecular Imaging and Microscopy Units at the CNIO, as well as with the Animal Medicine and Surgery Department at the Universidad Complutense de Madrid.

Every time a cell divides, it must duplicate its genetic material, the DNA, which is packed inside the chromosomes. However, given how the mechanism of DNA replication works, the end of each chromosome cannot be replicated completely, and, as a result, telomeres shorten with each cell division. Excessively short telomeres are toxic to cells, which stop replicating, and eventually, the cells are eliminated by senescence or apoptosis.

This phenomenon has been known for decades, as well as the fact that it usually does not occur in tumour cells. Cancer cells proliferate without any apparent limits, and therefore, they are constantly dividing, but their telomeres do not gradually become shorter; the key behind this mechanism is that the telomerase enzyme in cancer cells remains active, while in most healthy cells telomerase is turned off. The constant repair of telomeres by telomerase is, in fact, one of the mechanisms that allows tumour cells to be immortal and divide endlessly.

Hence, an obvious strategy to fight cancer is to inhibit the telomerase enzyme in tumour cells. This approach has been tested before, but with worrisome results: telomeres do shorten, but this shortening is lethal to tumour cells only after a variable number of cell divisions necessary for telomeres to become completely eroded– thus the effects are not instantly seen.

In the study now published, the researchers also target telomeres, but their approach is completely different from the telomerase one.


Telomeres are made up of repeating patterns of DNA sequences that are repeated hundreds of times — this is the structure that shortens with each cellular division. Telomere DNA is bound by a six-protein complex, called shelterin (from the term shelter or protection), which forms a protective covering. The CNIO team strategy consisted of blocking one of the shelterins, namely TRF1, so that that the telomere shield was destroyed.

The idea of targeting one of the shelterins has not been tried so far, due to the fear of encountering many toxic effects caused by acting on these proteins that are present in both healthy and tumour cells.

“Nobody had explored the idea of using one of the shelterins as an anti-cancer target,” explains Blasco. “It is difficult to find drugs that interfere with protein binding to DNA, and the possibility exists that drugs targeting telomere caps could be very toxic. For these reasons, no one had explored this option before, although it makes a lot of sense.”


The present work subtitled ‘Shelterin as a novel target in cancer,’ shows that blocking TRF1 only causes minor toxicities that are well tolerated by mice. “It does however prevent the growth of lung carcinomas already developed in mice,” write the authors in EMBO Molecular Medicine.

“TRF1 removal induces an acute telomere uncapping, which results in cellular senescence or cell death. We have seen that this strategy kills cancer cells efficiently, stops tumour growth and has bearable toxic effects,” explains Blasco.

TRF1 has been inhibited both genetically — in mice where the gene has been removed — and chemically using selected compounds from CNIO’s proprietary collection of active compounds. These compounds, including the inhibitor ETP-470037 developed by the CNIO Experimental Therapeutics Programme, may provide a starting point for the development of new drugs for cancer therapy.

“We’ve shown that we can find potential drugs able to inhibit TRF1 that have therapeutic effects when administered orally to mice,” says Blasco.


The scientists worked with mouse models for lung cancer, the cancer type that has the highest death rates worldwide. Specifically, they used a mouse with a very aggressive type of lung cancer for which no drug targets have been found to date: the tumours have an active K-Ras oncogene and the p53 tumor suppressor is missing. TRF1 is the first target that is able to inhibit the growth of these highly aggressive tumours.

The work process has been long. The researchers first selected TRF1 among the shelterin family. TRF1 is one of the most studied shelterins that is present exclusively at the telomeres and has potential as a good anti-cancer target — its inhibition also affects the so-called cancer stem cells that might be responsible for tumour recurrence over time.

The next aim was to demonstrate that TRF1 is really an anti-cancer target. To do so, the researchers genetically blocked its activity in mice with lung cancer as well as in healthy mice, in order to test the toxicity of the procedure.

Having established the effectiveness and low toxicity of the new target, the researchers searched for chemical compounds that could have activity against TRF1. Two types of compounds have been found. “We are now looking for partners in the pharmaceutical industry to bring this research into more advanced stages of drug development,” says Blasco.

Viagra And Other Erectile Dysfunction Drugs Vary In Effectiveness, Side Effects

viagra side effects
Viagra is the most effective treatment for erectile dysfunction, but it also has a higher rate of side effects than other options. 

Viagra is known generically as sildenafil. Men concerned about possible side effects of Viagra like headaches, flushing, indigestion and nasal congestion may want to start on Cialis, which is known generically as tadalafil, researchers report in European Urology. If that’s not effective, men in some countries can try Zydena (udenafil).

Many men have trouble getting or keeping an erection, especially as they age, but erectile dysfunction – also known as ED – is not a natural part of aging, according to the U.S. National Institutes of Health.

The new review compares seven common ED therapies, all belonging to a class of medications called phosphodiesterase 5 inhibitors (PDE5i’s). They work by inhibiting an enzyme that may reduce the potency of an erection.

Viagra, Cialis, Levitra (vardenafil) and Stendra (avanafil) all work this way and are approved for use in the U.S. The additional drugs Zydena, Helleva (lodenafil) and Mvix (mirodenafil) are only approved for use in other countries.

PDE5i’s are considered the first-choice therapy for ED, but they’re only effective for 60 to 80 percent of men who try them, and many will stop taking them, according to Dr. Alexander W. Pastuszak of Baylor College of Medicine’s urology department in Houston, Texas. He was not part of the new study.

Researchers at the University of Zurich, the Swiss Federal Institute of Technology, and Maastricht University Medical Center in the Netherlands reviewed 82 studies of the drugs’ effectiveness and 72 studies exploring side effects.

These treatments are all more effective than placebo for treating erectile dysfunction, and are generally safe and well tolerated, the authors note.

A 50- or 100-milligram (mg) dose of Viagra appeared to be the most effective treatment. It performed about 50 percent better than a placebo. Smaller doses were less effective. Stendra, in doses ranging from 50 to 200 mg, was among the least effective – only 20 to 30 percent more effective than a placebo.

The 50-milligram dose of Stendra was associated with the lowest rate of side effects of any medication – 8.5 percent of the time. A 20-mg dose of Levitra had the highest rate of side effects: 25 percent. Higher doses of Viagra and Cialis tended to cause side effects between 21 and 22 percent of the time.

“Viagra has an established efficacy and safety profile and remains an important treatment option for men with erectile dysfunction,” a spokesperson for Pfizer, makers of the drug, told Reuters Health in a statement. “Viagra has been studied for more than 15 years in more than 136 completed and ongoing clinical trials involving more than 23,000 men with ED.”

Side effects depend on which drug is used and what other enzymes the drug is able to inhibit, Pastuszak told Reuters Health by email. One of the main side effects of Viagra is visual changes, whereas Cialis more often causes muscle pain.

More generally, these types of ED drugs can cause a drop in blood pressure, because they are vasodilators, which open blood vessels, he said. He added that they should not be used with nitrate-based heart medications since they can cause a steep drop in blood pressure.

“Other common side effects include facial flushing, congestion, headache, and upset stomach,” Pastuszak said.

“Men complain of side effects, but more often of a lack of complete efficacy,” he said. “The drugs are not for everyone, as they won’t necessarily help a man with severe erectile dysfunction as much as they would someone with mild or moderate ED.”

Urologists will already have an understanding of the effectiveness and side effects of the available ED therapies, so the new results will not be a surprise, he said.

Only Cialis is to be taken daily, the other options are all short-acting, so men have the option of trying several to see which one works well, he said.

Doctors should carefully discuss expectations and treatment effects of the various options with patients before choosing a therapy, the authors write.

Some ED patients may want immediate stronger efficacy at the cost of higher side effects, while others may not.

Single vs Bilateral Lung Transplant in IPF and COPD

The use of double-lung transplants has been controversial because, of course, transplanting both lungs when it is not needed wastes a scarce resource. Historically, however, much of the literature has suggested that double-lung transplant outcomes are better, particularly in patients with IPF and COPD, perhaps because of underlying bronchiectasis or the improved functional reserve that comes with two lungs vs one. Many of these studies derived their data from the UNOS (United Network for Organ Sharing) or Lung Transplant Registry, and many of the earlier studies exploring this question were completed before we had the lung allocation score.

Previously, length of time on a waiting list was the main driver in terms of whether a patient received a lung transplant or not, and patients with IPF got a 6-month credit on the waiting list. More recently, the system for lung allocation has moved to one that is very similar to the system used for liver transplants, where the goal is to try to balance the risk for death while waiting for a lung transplant, against the benefit of receiving a lung transplant, to optimize outcomes for everyone in the pool.

Even after applying this lung allocation score, many patients with IPF or COPD receive bilateral lung transplants; however, many also get single transplants. The question is, what is the best way to allocate these scarce resources?

The Study

These investigators went to the UNOS registry to look at outcomes of patients after lung transplant as a function of whether they had IPF or COPD and whether they received a single- or double-lung transplant. They specifically compiled cases during the era of the lung allocation score, where some effort to balance risk and benefit has been integrated into the allocation of these scarce resources.

These authors looked at outcomes in about 4100 patients with IPF and 3100 patients with COPD. In an unadjusted analysis, the overall outcomes were good compared with historical outcomes, with median survivals above 50% at 5 years, regardless of whether patients received a single-lung transplant or a double-lung transplant, and of whether they had COPD or IPF.

When they looked specifically at patients with IPF, the unadjusted analysis found a survival advantage associated with double-lung transplant vs single-lung transplant. The Kaplan-Meier curves remained separated from the moment of transplantation forward. They also conducted an adjusted analysis that was propensity score–matched, to try to “pseudorandomize” the data to take into account the probability of getting one kind of transplant vs another. In addition, they looked at various important confounders such as the presence of pulmonary artery hypertension. This adjusted analysis showed a clear survival benefit associated with the double-lung transplant in patients with IPF: approximately 65-month survival vs about 50 months in IPF patients who received a single-lung transplant. That is a 15-month benefit and was statistically significant.

In the patients with COPD, the story is a bit more nuanced. The unadjusted analysis showed a benefit of double-lung transplant vs single-lung transplant in the population with COPD. However, the adjusted analysis—a careful, very nuanced statistical examination—found that the net benefit of a double- vs single-lung transplant was reduced to only 4 months. This was no longer statistically significant—not even close. It was also clear that there was a major interaction between double- and single-lung transplants, type of underlying disease (IPF or COPD), and eventual outcome.

Practice-Changing Results

These data are quite thought-provoking. It is a large analysis conducted during the lung allocation score era, and the investigators were very careful with their statistical modeling.


I believe that these results should begin to change our lung transplant practices. We need to derive better ways to sort out who needs a single-lung or a double-lung transplant. In patients with IPF, these data suggest clearly that the double-lung transplant is probably the right way to go. For patients with COPD vs historical controls, we do not have good data to show that there is necessarily any survival benefit associated with lung transplantation. For COPD, we need to step back and reevaluate the double- vs single-lung question, and perhaps use datasets similar to this to ascertain which patients benefit from a double- vs a single-lung transplant instead of simply saying that all patients with COPD are the same. Perhaps we should come up with scoring tools that are validated in external and other datasets across the globe to finally say which COPD patients, if any, benefit from double-lung transplant over single-lung transplant.

Infant antibiotic use linked to adult diseases .

Antibiotics are by far the most common prescription drugs given to children.

A new study led by researchers at the University of Minnesota has found a three-way link among antibiotic use in infants, changes in the gut bacteria, and disease later in life. The imbalances in gut microbes, called dysbiosis, have been tied to infectious diseases, allergies and other autoimmune disorders, and even obesity, later in life.

The study, led by Biomedical Informatics and Computational Biology program graduate student fellow Pajau Vangay, also developed a predictive model with potential clinical importance for measuring healthy development of bacteria in the gut of young children. The findings were published today in the scientific journal Cell Host & Microbe.

Antibiotics are by far the most common prescription drugs given to children. They account for about one-fourth of all medications prescribed to children, with a third of these prescriptions considered unnecessary. Other studies have shown profound short- and long-term effects of antibiotics on the diversity and composition of the bacteria in our bodies, called our microbiome.

“Diseases related to metabolism and the immune system are increasing dramatically, and in many cases we don’t know why,” said the study’s senior author Dan Knights, a computational biologist and assistant professor in the University of Minnesota’s Department of Computer Science and Engineering and Biotechnology Institute. “Previous studies showed links between antibiotic use and unbalanced gut bacteria, and others showed links between unbalanced gut bacteria and adult disease. Over the past year we synthesized hundreds of studies and found evidence of strong correlations between antibiotic use, changes in gut bacteria, and disease in adulthood.”

Knights and his colleagues developed a framework to map how antibiotics may be acting in the gut to cause disease later in life. In the case of allergies, for example, the use of antibiotics may eradicate key gut bacteria that help immune cells mature. These cells would have been essential for keeping the immune system at bay when confronted with allergens. Even if these bacteria return, the immune system remains impaired. Related to obesity, antibiotic-induced changes in the gut microbiota resulted in increased levels of short-chain fatty acids that affect metabolism.

The study also examined the development of bacteria in the gut. Researchers demonstrated that an infant’s age could be predicted within 1.3 months based on the maturity of their gut bacteria. This finding could lead to a clinical test and interventions for children whose microbiome is developmentally delayed due to antibiotics or other factors.

“We think these findings help develop a roadmap for future research to determine the health consequences of antibiotic use and for recommendations for prescribing them,” Knights said. “The clinical test we demonstrated would also allow us to think about interventions at an early age.”

In addition to Knights and Vangay, researchers involved in the study include Tonya Ward, a postdoctoral researcher in the University of Minnesota Biotechnology Institute and Jeffery Gerber, a researcher with the Division of Infectious Diseases at the Children’s Hospital of Philadelphia.

Confusing the Retinoic Acids: Mix-ups Between Tretinoin and ISOtretinoin

A 14-year-old girl diagnosed with acute promyelocytic leukemia (APL) was started on oral tretinoin (all-trans retinoic acid [ATRA]) for induction therapy. APL is a medical emergency with a high rate of mortality, so it is critical to start treatment with tretinoin as soon as the diagnosis is suspected. The patient was hospitalized during induction treatment. She was able to finish the treatment course and achieved complete remission. The patient was discharged, and the following month, she returned to the outpatient infusion center to begin 10 cycles of intravenous (IV) chemotherapy. Tretinoin was to continue on an outpatient basis, along with IV chemotherapy per protocol. But instead of administering two 14-day cycles of tretinoin as intended, an oncology clinic nurse enrolled the patient and prescriber in the iPledge program and called in a prescription for Claravis (ISOtretinoin [13-cis retinoic acid]; other brands include Amnesteem, Myorisan, and Sotret) to a local pharmacy. The clinic nurse did not realize that tretinoin and ISOtretinoin were not the same medication. She was probably more familiar with ISOtretinoin because it is prescribed more frequently than tretinoin in many pediatric oncology centers. The pharmacist at the local pharmacy did not have access to the patient’s clinical information, and the physicians continued to use the abbreviation “ATRA” in their office notes, never noting the generic/brand name of the medication on the patient’s profile. Thus, the patient began to take Claravis, not tretinoin, at home. When the patient was admitted to the hospital again about 4 months later, inpatient chemotherapy orders included tretinoin but requested the use of the patient’s home supply. When an inpatient nurse and pharmacist checked the patient’s supply, they realized it was ISOtretinoin, and not tretinoin as intended. The patient’s physicians were contacted, and the family was informed of the error. Fortunately, the patient did not experience any reported adverse effects while taking Claravis or lack of disease control while not taking the correct drug. So far, the patient continues to be in remission. ISOtretinoin can be used in chemotherapy treatment protocols in addition to its use in treating severe recalcitrant nodular acne. The drug has an unlabeled use in children for treating neuroblastoma, with a dosage of 160 mg/m2/day in 2 divided doses. Tretinoin is used almost exclusively for APL. The recommended dosage is 45 mg/m2/day administered as 2 evenly divided doses until complete remission is documented. Therapy should be discontinued 30 days after achievement of complete remission or after 90 days of treatment, whichever occurs first. Both tretinoin and ISOtretinoin are available in liquid-filled, 10-mg capsules, but ISOtretinoin is also available as 20-, 30-, and 40-mg capsules. Patients receiving ISOtretinoin must be enrolled in the iPledge program, but tretinoin does not require enrollment in any registry. Bottom line—this type of medication error associated with similar medication names is best prevented during the prescribing process with the use of a well-designed order set for APL, highlighting that tretinoin (and not ISOtretinoin) should be prescribed. Referring to the drug as all-trans retinoic acid rather than tretinoin may also help differentiate it from ISOtretinoin; however, use of the acronym ATRA alone is discouraged. This error also highlights the importance of requiring the pharmacist filling this prescription to know the patient’s diagnosis and the drug’s clinical indication at the time the prescription is filled.

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