Brain decoder can eavesdrop on your inner voice

brainy_2758840b

Talking to yourself used to be a strictly private pastime. That’s no longer the case – researchers have eavesdropped on our internal monologue for the first time. The achievement is a step towards helping people who cannot physically speak communicate with the outside world.

“If you’re reading text in a newspaper or a book, you hear a voice in your own head,” says Brian Pasley at the University of California, Berkeley. “We’re trying to decode the brain activity related to that voice to create a medical prosthesis that can allow someone who is paralysed or locked in to speak.”

When you hear someone speak, sound waves activate sensory neurons in your inner ear. These neurons pass information to areas of the brain where different aspects of the sound are extracted and interpreted as words.

In a previous study, Pasley and his colleagues recorded brain activity in people who already had electrodes implanted in their brain to treat epilepsy, while they listened to speech. The team found that certain neurons in the brain’s temporal lobe were only active in response to certain aspects of sound, such as a specific frequency. One set of neurons might only react to sound waves that had a frequency of 1000 hertz, for example, while another set only cares about those at 2000 hertz. Armed with this knowledge, the team built an algorithm that could decode the words heard based on neural activity alone (PLoS Biology, doi.org/fzv269).

The team hypothesised that hearing speech and thinking to oneself might spark some of the same neural signatures in the brain. They supposed that an algorithm trained to identify speech heard out loud might also be able to identify words that are thought.

Mind-reading

To test the idea, they recorded brain activity in another seven people undergoing epilepsy surgery, while they looked at a screen that displayed text from either the Gettysburg Address, John F. Kennedy’s inaugural address or the nursery rhyme Humpty Dumpty.

Each participant was asked to read the text aloud, read it silently in their head and then do nothing. While they read the text out loud, the team worked out which neurons were reacting to what aspects of speech and generated a personalised decoder to interpret this information. The decoder was used to create a spectrogram – a visual representation of the different frequencies of sound waves heard over time. As each frequency correlates to specific sounds in each word spoken, the spectrogram can be used to recreate what had been said. They then applied the decoder to the brain activity that occurred while the participants read the passages silently to themselves.

Despite the neural activity from imagined or actual speech differing slightly, the decoder was able to reconstruct which words several of the volunteers were thinking, using neural activity alone (Frontiers in Neuroengineering, doi.org/whb).

The algorithm isn’t perfect, says Stephanie Martin, who worked on the study with Pasley. “We got significant results but it’s not good enough yet to build a device.”

In practice, if the decoder is to be used by people who are unable to speak it would have to be trained on what they hear rather than their own speech. “We don’t think it would be an issue to train the decoder on heard speech because they share overlapping brain areas,” says Martin.

The team is now fine-tuning their algorithms, by looking at the neural activity associated with speaking rate and different pronunciations of the same word, for example. “The bar is very high,” says Pasley. “Its preliminary data, and we’re still working on making it better.”

The team have also turned their hand to predicting what songs a person is listening to by playing lots of Pink Floyd to volunteers, and then working out which neurons respond to what aspects of the music. “Sound is sound,” says Pasley. “It all helps us understand different aspects of how the brain processes it.”

“Ultimately, if we understand covert speech well enough, we’ll be able to create a medical prosthesis that could help someone who is paralysed, or locked in and can’t speak,” he says.

Several other researchers are also investigating ways to read the human mind. Some can tell what pictures a person is looking at, others have worked out what neural activity represents certain concepts in the brain, and one team has even produced crude reproductions of movie clips that someone is watching just by analysing their brain activity. So is it possible to put it all together to create one multisensory mind-reading device?

In theory, yes, says Martin, but it would be extraordinarily complicated. She says you would need a huge amount of data for each thing you are trying to predict. “It would be really interesting to look into. It would allow us to predict what people are doing or thinking,” she says. “But we need individual decoders that work really well before combining different senses.”

http://www.newscientist.com/article/mg22429934.000-brain-decoder-can-eavesdrop-on-your-inner-voice.html

New Study Ties Autism Risk to Creases in Placenta

placenta

After most pregnancies, the placenta is thrown out, having done its job of nourishing and supporting the developing baby.

But a new study raises the possibility that analyzing the placenta after birth may provide clues to a child’s risk for developing autism. The study, which analyzed placentas from 217 births, found that in families at high genetic risk for having an autistic child, placentas were significantly more likely to have abnormal folds and creases.

“It’s quite stark,” said Dr. Cheryl K. Walker, an obstetrician-gynecologist at the Mind Institute at the University of California, Davis, and a co-author of the study, published in the journal Biological Psychiatry. “Placentas from babies at risk for autism, clearly there’s something quite different about them.”

Researchers will not know until at least next year how many of the children, who are between 2 and 5, whose placentas were studied will be found to have autism. Experts said, however, that if researchers find that children with autism had more placental folds, called trophoblast inclusions, visible after birth, the condition could become an early indicator or biomarker for babies at high risk for the disorder.

“It would be really exciting to have a real biomarker and especially one that you can get at birth,” said Dr. Tara Wenger, a researcher at the Center for Autism Research at Children’s Hospital of Philadelphia, who was not involved in the study.

The research potentially marks a new frontier, not only for autism, but also for the significance of the placenta, long considered an after-birth afterthought. Now, only 10 percent to 15 percent of placentas are analyzed, usually after pregnancy complications or a newborn’s death.

Dr. Harvey J. Kliman, a research scientist at the Yale School of Medicine and lead author of the study, said the placenta had typically been given such little respect in the medical community that wanting to study it was considered equivalent to someone in the Navy wanting to scrub ships’ toilets with a toothbrush. But he became fascinated with placentas and noticed that inclusions often occurred with births involving problematic outcomes, usually genetic disorders.

He also noticed that “the more trophoblast inclusions you have, the more severe the abnormality.” In 2006, Dr. Kliman and colleagues published research involving 13 children with autism, finding that their placentas were three times as likely to have inclusions. The new study began when Dr. Kliman, looking for more placentas, contacted the Mind Institute, which is conducting an extensive study, called Marbles, examining potential causes of autism.

“This person came out of the woodwork and said, ‘I want to study trophoblastic inclusions,’ ” Dr. Walker recalled. “Now I’m fairly intelligent and have been an obstetrician for years and I had never heard of them.”

Dr. Walker said she concluded that while “this sounds like a very smart person with a very intriguing hypothesis, I don’t know him and I don’t know how much I trust him.” So she sent him Milky Way bar-size sections of 217 placentas and let him think they all came from babies considered at high risk for autism because an older sibling had the disorder. Only after Dr. Kliman had counted each placenta’s inclusions did she tell him that only 117 placentas came from at-risk babies; the other 100 came from babies with low autism risk.

She reasoned that if Dr. Kliman found that “they all show a lot of inclusions, then maybe he’s a bit overzealous” in trying to link inclusions to autism. But the results, she said, were “astonishing.” More than two-thirds of the low-risk placentas had no inclusions, and none had more than two. But 77 high-risk placentas had inclusions, 48 of them had two or more, including 16 with between 5 and 15 inclusions.

Dr. Walker said that typically between 2 percent and 7 percent of at-risk babies develop autism, and 20 percent to 25 percent have either autism or another developmental delay. She said she is seeing some autism and non-autism diagnoses among the 117 at-risk children in the study, but does not yet know how those cases match with placental inclusions.

Dr. Jonathan L. Hecht, associate professor of pathology at Harvard Medical School, said the study was intriguing and “probably true if it finds an association between these trophoblast inclusions and autism.” But he said that inclusions were the placenta’s way of responding to many kinds of stress, so they might turn out not to be specific enough to predict autism.

Dr. Kliman calls inclusions a “check-engine light, a marker of: something’s wrong, but I don’t know what it is.”

That’s how Chris Mann Sullivan sees it, too. Dr. Sullivan, a behavioral analyst in Morrisville, N.C., was not in the study, but sent her placenta to Dr. Kliman after her daughter Dania, now 3, was born. He found five inclusions. Dr. Sullivan began intensive one-on-one therapy with Dania, who has not been given a diagnosis of autism, but has some relatively mild difficulties.

“What would have happened if I did absolutely nothing, I’m not sure,” Dr. Sullivan said. “I think it’s a great way for parents to say, ‘O.K., we have some risk factors; we’re not going to ignore it.’ ”

Thanks to Dr. Rajadhyaksha for bringing this to the attention of the It’s Interesting community.

Largest psychiatric genetic study in history shows a common genetic basis that underlies 5 types of mental disorders

Protein_CACNA1C_PDB_2be6
Structure of the CACNA1C gene product, a calcium channel named Cav1.2, which is one of 4 genes that has now been found to be genetically held in common amongst schizophrenia, bipolar disorder, autism, major depression and attention deficit hyperactivity disoder. Groundbreaking work on the role of this protein on anxiety and other forms of behavior related to mental illness has previously been established in the Rajadhyaksha laboratory at Weill Cornell Medical Center.
http://weill.cornell.edu/research/arajadhyaksha/

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3481072/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3192195/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3077109/

From the New York Times:
The psychiatric illnesses seem very different — schizophrenia, bipolar disorder, autism, major depression and attention deficit hyperactivity disorder. Yet they share several genetic glitches that can nudge the brain along a path to mental illness, researchers report. Which disease, if any, develops is thought to depend on other genetic or environmental factors.

Their study, published online Wednesday in the Lancet, was based on an examination of genetic data from more than 60,000 people worldwide. Its authors say it is the largest genetic study yet of psychiatric disorders. The findings strengthen an emerging view of mental illness that aims to make diagnoses based on the genetic aberrations underlying diseases instead of on the disease symptoms.

Two of the aberrations discovered in the new study were in genes used in a major signaling system in the brain, giving clues to processes that might go awry and suggestions of how to treat the diseases.

“What we identified here is probably just the tip of an iceberg,” said Dr. Jordan Smoller, lead author of the paper and a professor of psychiatry at Harvard Medical School and Massachusetts General Hospital. “As these studies grow we expect to find additional genes that might overlap.”

The new study does not mean that the genetics of psychiatric disorders are simple. Researchers say there seem to be hundreds of genes involved and the gene variations discovered in the new study confer only a small risk of psychiatric disease.

Steven McCarroll, director of genetics for the Stanley Center for Psychiatric Research at the Broad Institute of Harvard and M.I.T., said it was significant that the researchers had found common genetic factors that pointed to a specific signaling system.

“It is very important that these were not just random hits on the dartboard of the genome,” said Dr. McCarroll, who was not involved in the new study.

The work began in 2007 when a large group of researchers began investigating genetic data generated by studies in 19 countries and including 33,332 people with psychiatric illnesses and 27,888 people free of the illnesses for comparison. The researchers studied scans of people’s DNA, looking for variations in any of several million places along the long stretch of genetic material containing three billion DNA letters. The question: Did people with psychiatric illnesses tend to have a distinctive DNA pattern in any of those locations?

Researchers had already seen some clues of overlapping genetic effects in identical twins. One twin might have schizophrenia while the other had bipolar disorder. About six years ago, around the time the new study began, researchers had examined the genes of a few rare families in which psychiatric disorders seemed especially prevalent. They found a few unusual disruptions of chromosomes that were linked to psychiatric illnesses. But what surprised them was that while one person with the aberration might get one disorder, a relative with the same mutation got a different one.

Jonathan Sebat, chief of the Beyster Center for Molecular Genomics of Neuropsychiatric Diseases at the University of California, San Diego, and one of the discoverers of this effect, said that work on these rare genetic aberrations had opened his eyes. “Two different diagnoses can have the same genetic risk factor,” he said.

In fact, the new paper reports, distinguishing psychiatric diseases by their symptoms has long been difficult. Autism, for example, was once called childhood schizophrenia. It was not until the 1970s that autism was distinguished as a separate disorder.

But Dr. Sebat, who did not work on the new study, said that until now it was not clear whether the rare families he and others had studied were an exception or whether they were pointing to a rule about multiple disorders arising from a single genetic glitch.

“No one had systematically looked at the common variations,” in DNA, he said. “We didn’t know if this was particularly true for rare mutations or if it would be true for all genetic risk.” The new study, he said, “shows all genetic risk is of this nature.”

The new study found four DNA regions that conferred a small risk of psychiatric disorders. For two of them, it is not clear what genes are involved or what they do, Dr. Smoller said. The other two, though, involve genes that are part of calcium channels, which are used when neurons send signals in the brain.

“The calcium channel findings suggest that perhaps — and this is a big if — treatments to affect calcium channel functioning might have effects across a range of disorders,” Dr. Smoller said.

There are drugs on the market that block calcium channels — they are used to treat high blood pressure — and researchers had already postulated that they might be useful for bipolar disorder even before the current findings.

One investigator, Dr. Roy Perlis of Massachusetts General Hospital, just completed a small study of a calcium channel blocker in 10 people with bipolar disorder and is about to expand it to a large randomized clinical trial. He also wants to study the drug in people with schizophrenia, in light of the new findings. He cautions, though, that people should not rush out to take a calcium channel blocker on their own.

“We need to be sure it is safe and we need to be sure it works,” Dr. Perlis said.

Drunk Mice Sober Up Fast After Nanoparticle Injection

enzymes
Enzymes: Three enzymes are combined with a DNA scaffold along with their enzymatic inhibitors, leading to a triple-compound architecture. A thin polymer is grown around the enzymes, encapsulating them in a sort of nano-pill. Enzymes working in close proximity ensures they can clean up after each other’s toxic byproducts.

Multiple enzymes delivered in a nanocapsule could work as an alcohol antidote, reducing blood alcohol levels and preventing liver damage.

A new nanostructured enzyme complex can lower blood alcohol levels in intoxicated mice, according to a new study. The nano-pill, which assembles and encapsulates three types of enzymes, could work as a type of alcohol antidote. It also suggests that this unique protein-tailoring method could be used for lots of ailments.

Enzymes are proteins that spark a whole host of biological processes, but many can only work when they are in specific places in a cell, or when they are accompanied by other enzymes. Proper positioning speeds up chemical reactions, and it mitigates the potentially nasty byproducts of some of those reactions. Researchers have been trying to use enzymes as drugs for a long time, but it has been difficult to produce the right combinations, meaning they might not function properly or they might be rejected by the body.

After you drink alcohol, it loiters in your bloodstream until enzymes produced in the liver can break it down. But this takes the liver some time, and meanwhile, you’re intoxicated. This new enzyme injection does the same job much quicker, helping the liver break down alcohol and thus sobering up a tipsy mouse in a hurry. This also helps protect the hard-working liver from damage.

Researchers in California packed up complementary enzymes in a nano-capsule, producing what basically amounts to a tiny enzyme pill. The capsule coating, made of a superthin polymer, keeps the enzymes together and protects them from breaking down in the body.

Led by Yunfeng Lu, a chemical and biomolecular engineering professor at UCLA, researchers injected mice with three enzymes related to the breakdown of sugars, and after this worked, they tried it with two enzymes related to the breakdown of alcohol, alcohol oxidase (AOx) and catalase. They wanted to test the enzymes as both an intoxication preventive and a treatment.

When mice were fed a diet of alcohol and the nano-capsule at the same time, their blood alcohol concentrations were greatly reduced within 30-minute increments, compared to mice that were fed just alcohol or alcohol plus one of the enzymes. The team also tested it on drunk mice, and found the treatment greatly lowered yet another enzyme, alanine transaminase, which is a biomarker for liver damage.

“Nanocomplexes containing alcohol oxidase and catalase could reduce blood alcohol levels in intoxicated mice, offering an alternative antidote and [preventive treatment] for alcohol intoxication,” the authors write. The paper appears in Nature Nanotechnology.

http://www.popsci.com/science/article/2013-02/drunk-mice-sober-after-nanoparticle-injection

Economic crisis in Greece has lowered their air pollution

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EVEN the darkest cloud may have a silver lining. The sharp drop in air pollution that accompanied Greece’s economic crisis could be a boon to the nation’s health.

Mihalis Vrekoussis of the Cyprus Institute in Nicosia and colleagues used three satellites and a network of ground-based instruments to measure air pollution over Greece between 2007 and 2011. Levels of nitrogen dioxide fell over the whole country, with a particularly steep drop of 30 to 40 per cent over Athens. Nitrogen monoxide, carbon monoxide and sulphur dioxide also fell (Geophysical Research Letters, DOI: 10.1002/grl.50118).

Pollution levels have been falling since 2002, but the rate accelerated after 2008 by a factor of 3.5, says Vrekoussis. He found that the drop in pollution correlated with a decline in oil consumption, industrial activity and the size of the economy. “This suggests that the additional reported reduction in gas pollutant levels is due to the economic recession,” he says.

In Athens, a combination of heavy car use and lots of sunshine have created serious health problems, so city dwellers should see real benefits. Sunlight triggers chemical reactions that make the car exhaust pollution more harmful, for instance by forming small particulates that cause respiratory diseases. “Hospital admissions for asthma should decline,” says Dwayne Heard of the University of Leeds in the UK.

It’s not all good news: despite the drop in pollutants, levels of ground-level ozone – another cause of respiratory disease – have risen. Ozone would normally be suppressed by nitrogen oxides, but those have declined. That will take the edge off the benefit, says Heard.

Greece isn’t the only country where air pollution has dropped. Nitrogen oxide levels fell across Europe after the 2008 financial crisis (Scientific Reports, doi.org/j74). In the US, nitrogen dioxide levels fell between 2005 and 2011, with the sharpest fall at the height of the recession (Atmospheric Chemistry and Physics, doi.org/j75).

Such declines can be one-offs, or governments can help make them permanent, says Ronald Cohen of the University of California, Berkeley, who led the US study. “A time of crisis is a real opportunity to initiate change.” After the 2008 financial downturn, for instance, the US and Europe committed to pollution cuts. “In 10 years, there will be an end to air pollution in the US and Europe,” says Cohen. “It’s an incredible success story.”

Greece, however, is not seizing the current opportunity, says Vrekoussis. “Investments in clean technologies and low-carbon green strategies have been abandoned,” he says. “I’m afraid that in the long run the negative effects will override the positives.”

Global greenhouse gas emissions initially fell in the wake of the financial crisis, but not by much. Emerging economies like China and India continued their economic growth, so a small emissions drop in 2009 was followed by a huge rise in 2010 which continued in 2011.

http://www.newscientist.com/article/mg21729014.300-greek-economic-crisis-has-cleared-the-air.html?cmpid=RSS|NSNS|2012-GLOBAL|online-news

Daily aspirin may increase risk for age-related blindness

ctm_0321_ASPIRIN_620x350

Many people take aspirin to prevent heart attacks, but new research suggests the added benefits may be coming at the expense of pill-takers’ eyesight.

A 15-year-study published Jan. 22 in JAMA Internal Medicine showed that people taking regular aspirin faced a higher risk for age-related macular degeneration (AMD), one of the leading causes of blindness in older adults. The research also suggests the risk may worsen over time.

AMD commonly affects adults 50 and older, gradually destroying their “macula,” which is a part of the eye that provides sharp, central vision that’s required to see objects clearly. There are two types of the disease: “Dry” AMD is most common and occurs when the light-sensitive cells in the macula slowly break down, gradually blurring central vision while “wet” or neovascular AMD occurs when blood vessels under the macula leak blood and fluid, causing damage. Wet AMD is often more severe but also more rare, affecting about 10 percent of patients with AMD.

People at a high risk for having a heart attack — such as those who have heart disease — are encouraged by the American Heart Association and other medical groups to take a daily low-dose of aspirin.

For the study, Australian researchers tracked nearly 2,400 adults who were given four exams during the 15 year study. More than 250 of these individuals took aspirin regularly because aspirin is thought to prevent clots from forming by “thinning” the blood.

The researchers found an increased risk for wet AMD among aspirin takers, with 1.9 percent of patients having the condition at five years, 7 percent at 10 years and 9.3 percent at 15 years. That compares with 0.8 percent of non-aspirin takers at five years, 1.6 percent at 10 years and 3.7 percent at 15 years.

“Regular aspirin use was significantly associated with an increased incidence of neovascular AMD,” concluded the authors, led by Dr. Gerald Liew of the University of Sydney in Australia.

In December, a study published in JAMA also found that people who used aspirin regularly for 10 years were more likely to have wet AMD, but the overall reported risk was still low.

Liew wrote that the decision to stop taking aspirin is a “complex” one and should be decided on an individual basis. For example, those at a higher risk for AMD such as people with a family history or smokers — who are two times more likely to develop AMD than non-smokers — may want to consider changing their aspirin regimen.

In an accompanying editorial published in the same issue, Dr. Sanjay Kaul and Dr. George A. Diamond, cardiologists at Cedars-Sinai Medical Center, Los Angeles, wrote that the study was observational, and could not prove cause and effect. Therefore, it may be too soon to recommend people curb their aspirin intake.

“In the absence of definitive evidence regarding whether limiting aspirin exposure mitigates AMD risk, one obvious course of action is to maintain the status quo,” they wrote.

Dr. Gregg Fonarow, a spokesman for the American Heart Association and professor of cardiology at the University of California, Los Angeles, added to HealthDay that more rigorous randomized controlled trials have yet to demonstrate any increased risk of blindness from people taking aspirin.

“Individuals prescribed aspirin for high-risk primary prevention or secondary cardiovascular prevention should not be concerned or discontinue this beneficial therapy,” he said.

To reduce your risk for AMD, the National Eye Institute recommends exercising, eating a healthy diet rich in leafy greens and fish, maintaining normal blood pressure and cholesterol, and avoiding smoking.

http://www.cbsnews.com/8301-204_162-57565181/daily-aspirin-may-increase-risk-for-age-related-blindness/

In the Flesh: The Embedded Dangers of Untested Stem Cell Cosmetics

original

When cosmetic surgeon Allan Wu first heard the woman’s complaint, he wondered if she was imagining things or making it up. A resident of Los Angeles in her late sixties, she explained that she could not open her right eye without considerable pain and that every time she forced it open, she heard a strange click—a sharp sound, like a tiny castanet snapping shut. After examining her in person at The Morrow Institute in Rancho Mirage, Calif., Wu could see that something was wrong: Her eyelid drooped stubbornly, and the area around her eye was somewhat swollen. Six and a half hours of surgery later, he and his colleagues had dug out small chunks of bone from the woman’s eyelid and tissue surrounding her eye, which was scratched but largely intact. The clicks she heard were the bone fragments grinding against one another.

About three months earlier the woman had opted for a relatively new kind of cosmetic procedure at a different clinic in Beverly Hills—a face-lift that made use of her own adult stem cells. First, cosmetic surgeons had removed some the woman’s abdominal fat with liposuction and isolated the adult stem cells within—a family of cells that can make many copies of themselves in an immature state and can develop into several different kinds of mature tissue. In this case the doctors extracted mesenchymal stem cells—which can turn into bone, cartilage or fat, among other tissues—and injected those cells back into her face, especially around her eyes. The procedure cost her more than $20,000, Wu recollects. Such face-lifts supposedly rejuvenate the skin because stem cells turn into brand-new tissue and release chemicals that help heal aging cells and stimulate nearby cells to proliferate.

During the face-lift her clinicians had also injected some dermal filler, which plastic surgeons have safely used for more than 20 years to reduce the appearance of wrinkles. The principal component of such fillers is calcium hydroxylapatite, a mineral with which cell biologists encourage mesenchymal stem cells to turn into bone—a fact that escaped the woman’s clinicians. Wu thinks this unanticipated interaction explains her predicament. He successfully removed the pieces of bone from her eyelid in 2009 and says she is doing well today, but some living stem cells may linger in her face. These cells could turn into bone or other out-of-place tissues once again.

Dozens, perhaps hundreds, of clinics across the country offer a variety of similar, untested stem cell treatments for both cosmetic and medical purposes. Costing between $3,000 and $30,000, the treatments promise to alleviate everything from wrinkles to joint pain to autism. The U.S. Food and Drug Administration (FDA) has not approved any of these treatments and, with a limited budget, is struggling to keep track of all the unapproved therapies on the market. At the same time, pills, oils, creams and moisturizers that allegedly contain the right combination of ingredients to mobilize the body’s resident stem cells, or contain chemicals extracted from the stem cells in plants and animals, are popping up in pharmacies and online. There’s Stem Cell 100, for example, MEGA STEM and Apple Stem Cell Cloud Cream. Few of these cosmetics have been properly tested in published experiments, yet the companies that manufacture them say they may heal damaged organs, slow or reverse natural aging, restore youthful energy and revitalize the skin. Whether such cosmetics may also produce unintended and potentially harmful effects remains largely unexamined. The increasing number of untested and unauthorized stem cell treatments threaten both people who buy them and researchers hoping to conduct clinical trials for promising stem cell medicine.

So far, the FDA has only approved one stem cell treatment: a transplant of bone marrow stem cells for people with the blood cancer leukemia. Among the increasing number of unapproved stem cell treatments, some clearly violate the FDA’s regulations whereas others may technically be legal without its approval. In July 2012, for example, the U.S. District Court upheld an injunction brought by the FDA against Colorado-based Regenerative Sciences to regulate just one of the company’s several stem cell treatments for various joint injuries as an “unapproved biological drug product.” The decision hinged on what constitutes “minimal manipulation” of cells in the lab before they are injected into patients. In the treatment that the FDA won the right to regulate, stem cells are grown and modified in the lab for several weeks before they are returned to patients; in Regenerative Sciences’s other treatments, patients’ stem cells are extracted and injected within a day or two. Regenerative Sciences now offers the legally problematic treatment at a Cayman Island facility.

Many stem cell cosmetics reside in a legal gray area. Unlike drugs and “biologics” made from living cells and tissues, cosmetics do not require premarket approval from the FDA. But stem cell cosmetics often satisfy the FDA’s definitions for both cosmetics and drugs. In September 2012 the FDA posted a letter on its Web site warning Lancôme, a division of L’Oréal, that the way it describes its Genifique skin care products qualify the creams and serums as unapproved drugs: they are supposed to “boost the activity of genes,” for example, and “improve the condition of stem cells.” Other times the difference between needing or not needing FDA approval comes down to linguistic nuance—the difference between claiming that a product does something or appears to do something.

Personal Cell Sciences, in Eatontown, N.J., sells some of the more sophisticated stem cell–based cosmetics: an eye cream, moisturizer and serum infused with chemicals derived from a consumer’s own stem cells. According to its website and marketing materials, these products help “make skin more supple and radiant,” “reduce the appearance of fine lines and wrinkles around the eyes and lips,” “improve cellular renewal” and “stimulate cell turnover for renewed texture and tone.” In exchange for $3,000, Personal Cell Sciences will arrange for a participating physician to vacuum about 60 cubic centimeters (one quarter cup) of a customer’s fat from beneath his or her skin and ship it on ice to American CryoStem Corp. in Red Bank, N.J., where laboratory technicians isolate and grow the customer’s mesenchymal stem cells to around 30 million strong. Half these cells are frozen for storage; from the other half, technicians harvest hundreds of different kinds of exuded growth factors and cytokines—molecules that help heal damaged cells and encourage cells to divide, among other functions. These molecules are mixed with many other ingredients—including green tea extract, caffeine and vitamins—to create the company’s various “U Autologous” skin care products, which are then sold back to the consumer for between $400 and $800. When the customer wants a refill, technicians thaw some of the frozen cells, collect more cytokines and produce new bottles of cream.

In an unpublished safety trial sponsored by Personal Cell Sciences, Frederic Stern of the Stern Center for Aesthetic Surgery in Bellevue, Wash., and his colleagues monitored 19 patients for eight weeks as they used the U Autologous products on the left sides of their faces. A computer program meant to objectively analyze photos of the volunteers’ faces measured an average of 25.6 percent reduction in the volume of wrinkles on the treated side of the face. Analysis of tissue biopsies revealed increased levels of the protein elastin, which helps keep skin taut, and no signs of unusual or cancerous cell growth.

Supposedly, the primary active ingredients in the U Autologous skin care products are the hundreds of different kinds of cytokines they contain. Cytokines are a large and diverse family of proteins that cells release to communicate with and influence one another. Cytokines can stimulate cell division or halt it; they can suppress the immune system or provoke it; they can also change a cell’s shape, modulate its metabolism and force it to migrate from one location to another like a cowboy corralling cattle. Researchers have only named and characterized some of the many cytokines that stem cells secrete. Some of these molecules certainly help repair damaged cells and promote cell survival. Others seem to be involved in the development of tumors. In fact, some recent evidence suggests that the cytokines released by mesenchymal stem cells can trigger tumors by accelerating the growth of dormant cancer cells. Personal Cell Sciences does not pick and choose among the cytokines exuded by its customers’ stem cells—instead, it dumps them all into its skin care products.

Based on the available evidence so far, topical creams containing cytokines from stem cells pose far less risk of cancer than living stem cells injected beneath the skin. But scientists do not yet know enough about stem cell cytokines to reliably predict everything they will do when rubbed into the skin; they could interact with healthy skin cells in a completely unexpected way, just as the unintended interplay between calcium hydroxylapatite and stem cells produced bones in the Los Angeles woman’s eye. Stern acknowledges that unusual tissue growth is a concern for any treatment based on stem cells and the chemicals they release. “Down the line, we want to continue watching that,” he says. Unlike many other clinics, he and his colleagues have been keeping tabs on their patients through regular follow-ups. John Arnone, CEO of American CryoStem and founder of Personal Cell Sciences, says the fact that U Autologous skin care products contain such a diversity of cytokines does not bother him: “I’ve seen worse things out there. I’ve been putting this formulation for almost a year on myself prior to the study. I’m the best guinea pig here.”

Beyond the considerable risks to consumers, unapproved stem cell treatments also threaten the progress of basic research and clinical trials needed to establish safe stem cell therapies for serious illnesses. By harvesting stem cells, subsequently nourishing them in the lab and transplanting them back inside the human body, scientists hope to improve treatment for a variety of medical conditions, including heart failure, neurodegenerative disorders like Parkinson’s, and spinal cord injuries—essentially any condition in which the body needs new cells and tissues. Researchers are investigating many stem cell therapies in ongoing, carefully controlled clinical trials. Some of the principal questions entail which of the many kinds of stem cells to use; how to safely deliver stem cells to patients without stimulating tumors or the growth of unwanted tissues; and how to prevent the immune system from attacking stem cells provided by a donor. Securing funding for such research becomes all the more difficult if shortcuts taken by private clinics and cosmetic manufacturers—and the subsequent botched procedures and unanticipated consequences—imprint a stigma on stem cells.

“Many of us are super excited about stem cells, but at same time we have to be really careful,” says Paul Knoepfler, a cell biologist at the University of California, Davis, who regularly blogs about the regulation of stem cell treatments. “These aren’t your typical drugs. You can stop taking a pill and the chemicals go away. But if you get stem cells, most likely you will have some of those cells or their effects for the rest of your life. And we simply don’t know everything they are going to do.”

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https://www.scientificamerican.com/article.cfm?id=stem-cell-cosmetics&WT.mc_id=SA_emailfriend

Thanks to Dr. Nakamura for bringing this to the attention of the It’s Interesting community.

Closest Single Star Like Our Sun May Have Habitable Planet

sun

An international team of astronomers led by the University of Hertfordshire has discovered that Tau Ceti, one of the closest and most Sun-like stars, may host five planets — with one in the star’s habitable zone.

At a distance of twelve light years and visible with the naked eye in the evening sky, Tau Ceti is the closest single star that has the same spectral classification as our Sun. Its five planets are estimated to have masses between two and six times the mass of Earth — making it the lowest-mass planetary system yet detected. One of the planets lies in the habitable zone of the star and has a mass around five times that of Earth, making it the smallest planet found to be orbiting in the habitable zone of any Sun-like star.

The international team of astronomers, from the UK, Chile, the USA, and Australia, combined more than six-thousand observations from three different instruments and intensively modelled the data. Using new techniques, the team has found a method to detect signals half the size previously thought possible. This greatly improves the sensitivity of searches for small planets and suggests that Tau Ceti is not a lone star but has a planetary system.

Mikko Tuomi, from the University of Hertfordshire and the first author of the paper, said: “We pioneered new data modelling techniques by adding artificial signals to the data and testing our recovery of the signals with a variety of different approaches. This significantly improved our noise modelling techniques and increased our ability to find low mass planets.”

“We chose Tau Ceti for this noise modelling study because we had thought it contained no signals. And as it is so bright and similar to our Sun it is an ideal benchmark system to test out our methods for the detection of small planets,” commented Hugh Jones from the University of Hertfordshire.

James Jenkins, Universidad de Chile and Visiting Fellow at the University of Hertfordshire, explained: “Tau Ceti is one of our nearest cosmic neighbours and so bright that we may be able to study the atmospheres of these planets in the not too distant future. Planetary systems found around nearby stars close to our Sun indicate that these systems are common in our Milky Way galaxy.”

Over 800 planets have been discovered orbiting other worlds, but planets in orbit around the nearest Sun-like stars are particularly valuable. Steve Vogt from University of California Santa Cruz said: “This discovery is in keeping with our emerging view that virtually every star has planets, and that the galaxy must have many such potentially habitable Earth-sized planets. They are everywhere, even right next door! We are now beginning to understand that Nature seems to overwhelmingly prefer systems that have a multiple planets with orbits of less than one hundred days. This is quite unlike our own solar system where there is nothing with an orbit inside that of Mercury. So our solar system is, in some sense, a bit of a freak and not the most typical kind of system that Nature cooks up.”

“As we stare the night sky, it is worth contemplating that there may well be more planets out there than there are stars … some fraction of which may well be habitable,” remarked Chris Tinney from the University of New South Wales.

Journal Reference:

1.M. Tuomi, H. R. A. Jones, J. S. Jenkins, C. G. Tinney, R. P. Butler, S. S. Vogt, J. R. Barnes, R. A. Wittenmyer, S. O’Toole, J. Horner, J. Bailey, B. D. Carter, D. J. Wright, G. S. Salter, D. Pinfield. Signals embedded in the radial velocity noise. Periodic variations in the tau Ceti velocities. Astronomy & Astrophysics, 2012; DOI: 10.1051/0004-6361/201220509

http://www.sciencedaily.com/releases/2012/12/121219084102.htm

Diuretic Drug Offers Latest Hope for Autism Treatment

sn-autism

 

A drug used for decades to treat high blood pressure and other conditions has shown promise in a small clinical trial for autism. The drug, bumetanide, reduced the overall severity of behavioral symptoms after 3 months of daily treatment. The researchers say that many parents of children who received the drug reported that their children were more “present” and engaged in social interactions after taking it. The new findings are among several recent signs that treatments to address the social deficits at the core of autism may be on the horizon.

Several lines of evidence suggest that autism interferes with the neurotransmitter GABA, which typically puts a damper on neural activity. Bumetanide may enhance the inhibitory effects of GABA, and the drug has been used safely as a diuretic to treat a wide range of heart, lung, and kidney conditions. In the new study, researchers led by Yehezkel Ben-Ari at the Mediterranean Institute of Neurobiology in Marseille, France, recruited 60 autistic children between the ages of 3 and 11 and randomly assigned them to receive either a daily pill of bumetanide or a placebo. (Neither the children’s parents nor the researchers who assessed the children knew who received the actual drug.)

As a group, those who got bumetanide improved by 5.6 points on a 60-point scale that’s often used to assess behaviors related to autism, the researchers report today in Translational Psychiatry. That was enough to nudge the group average just under the cutoff for severe autism and into the mild to medium category. The study did not look directly at whether the drug improved all symptoms equally or some more than others. “We have some indications that the symptoms particularly ameliorated with bumetanide are the genuine core symptoms of autism, namely communication and social interactions,” Ben-Ari says. More work will be needed to verify that impression. Ben-Ari says his team is now preparing for a larger, multicenter trial in Europe.

The current study already looks interesting to some. “It’s enough to make me think about trying it in a few of my autism patients who haven’t responded to other interventions,” says Randi Hagerman, a pediatrician who studies neurodevelopmental disorders at the University of California, Davis. Social interactions tend to be reinforcing, Hagerman adds, so getting an autistic child to start interacting more can have a positive effect on subsequent brain development.

Other drugs have recently shown promise for autism. In September, Hagerman and colleagues reported that arbaclofen, a drug that stimulates a type of GABA receptor, reduced social avoidance in people with fragile X syndrome, a genetic disorder that shares many features with autism. Many researchers are also hopeful about clinical trials under way with drugs that block certain receptors for glutamate, the main neurotransmitter in the brain that excites neural activity. Results from those trials should come out next year.

All of this work, including the new study, suggests that drugs that reduce neural excitation by blocking glutamate or enhance inhibition by boosting GABA may be helpful for treating autism, says Elizabeth Berry-Kravis, a pediatric neurologist at Rush University in Chicago, Illinois, and a collaborator on the recent arbaclofen study. “There seems to be this imbalance between excitation and inhibition in people with autism.”

That’s a potentially game-changing insight. Now doctors can only prescribe drugs that treat individual symptoms of autism rather than the underlying cause of the disorder, Berry-Kravis says. Doctors often prescribe antipsychotic drugs to reduce irritability, for example, but those drugs don’t address the social and communication problems at the heart of the disorder. “It’s exciting that now we’re thinking about the underlying mechanisms and treating those.”

http://news.sciencemag.org/sciencenow/2012/12/diuretic-drug-offers-latest-hope.html

Birds hold funerals for the dead

 

When western scrub jays encounter a dead bird, they call out to one another and stop foraging.

The jays then often fly down to the dead body and gather around it, scientists have discovered.

The behaviour may have evolved to warn other birds of nearby danger, report researchers in California, who have published the findings in the journal Animal Behaviour.

The revelation comes from a study by Teresa Iglesias and colleagues at the University of California, Davis, US.

They conducted experiments, placing a series of objects into residential back yards and observing how western scrub jays in the area reacted.

The objects included different coloured pieces of wood, dead jays, as well as mounted, stuffed jays and great horned owls, simulating the presence of live jays and predators.

The jays reacted indifferently to the wooden objects.

But when they spied a dead bird, they started making alarm calls, warning others long distances away.

The jays then gathered around the dead body, forming large cacophonous aggregations. The calls they made, known as “zeeps”, “scolds” and “zeep-scolds”, encouraged new jays to attend to the dead.

The jays also stopped foraging for food, a change in behaviour that lasted for over a day.

When the birds were fooled into thinking a predator had arrived, by being exposed to a mounted owl, they also gathered together and made a series of alarm calls.

They also swooped down at the supposed predator, to scare it off. But the jays never swooped at the body of a dead bird.

The birds also occasionally mobbed the stuffed jays; a behaviour they are known to do in the wild when they attack competitors or sick birds.

The fact that the jays didn’t react to the wooden objects shows that it is not the novelty of a dead bird appearing that triggers the reaction.

The results show that “without witnessing the struggle and manner of death”, the researchers write, the jays see the presence of a dead bird as information to be publicly shared, just as they do the presence of a predator.

Spreading the message that a dead bird is in the area helps safeguard other birds, alerting them to danger, and lowering their risk from whatever killed the original bird in the first place, the researchers say.

Other animals are known to take notice of their dead.

Giraffes and elephants, for example, have been recorded loitering around the body of a recently deceased close relative, raising the idea that animals have a mental concept of death, and may even mourn those that have passed.

http://www.bbc.co.uk/nature/19421217