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Scientists don’t know all the causes of autism, but they do know that certain genes and environmental factors can play a role in the broad spectrum of developmental disabilities that fall under the term. Gaining additional knowledge isn’t easy, however, because most of the nitty gritty brain research is done in rodents — animals that don’t mimic complex brain disorders well. Now, researchers in China say that they’ve managed to produce monkeys that display autism-like behaviors for the first time, according to a study published in Nature today. Their research, however, raises questions about scientists’ ability to create a non-human primate model of autism that’s actually valid. SCIENTISTS INTRODUCED A HUMAN GENE INTO THE MONKEYS' DNA   To produce the monkeys, the scientists introduced a human gene called MeCP2 in the genome of macaques. The gene caused the monkeys to display behavioral symptoms akin to those seen in children with MeCP2 duplication syndrome — a rare disorder that causes autism-like behaviors. These symptoms include repetitive movements, anxiety, and decreased social interaction. In addition, the monkeys were able to pass the gene and their associated symptoms down to their offspring, which means these monkeys may give researchers a chance to study the genetics of autism spectrum disorders in a much more robust way than they’ve been able to in the past. Scientists might even be able to come up with treatments to reduce symptoms of autism in humans, the authors of the study say. But other researchers have doubts about the effectiveness of using these primates to model human brain disorders. Unlike children who have the MeCP2 duplication syndrome, the monkeys in the experiment weren’t severely developmentally delayed; combined with the high cost of producing these animals, there are big enough problems to put the entire model into question. "In all honesty, I’m not so excited about this study," says Hilde Van Esch, a geneticist at the University of Leuven in Belgium who studies MeCP2 duplication syndrome. Many children who have the duplication syndrome meet the formal criteria for an autism diagnosis, but they also tend to have symptoms that aren’t typical of autism, like "severe developmental delays, seizures, some [can’t] walk without aid," she says. The fact that these monkeys don’t have these problems is "surprising." And because the syndrome is rare in humans, it’s unclear how these monkeys might help autism research as a whole. "MeCP2 duplication syndrome is surely not ‘the’ prototype of autism," she says. "So the clinical utility of this model is, in my opinion, very low." Huda Zoghbi, director of the Jan and Dan Duncan Neurological Research Institute at Texas Children’s Hospital, also thinks that the monkeys’ symptoms put the validity of the animal model into question. The monkeys failed to develop the cardinal features of the MeCP2 duplication syndrome, and only the male monkeys had social interaction deficits — a fact that the authors of the study don’t explain. That means that the monkeys "don’t reproduce the human duplication disorder," she says. Because of these uncertainties, using the monkeys to model autism doesn’t make sense, she says.   THESE MONKEYS "ARE THE FIRST PRIMATE MODELS OF AUTISM." The scientists who produced the monkeys are far more optimistic. These monkeys "are the first primate models of autism," says Zilong Qiu, a neuroscientist at the Chinese Academy of Sciences in Beijing and a co-author of the study. "I’m thrilled by the possibility that we may be able to reverse the genetic causes in the transgenic autism monkey model." In humans, MeCP2 duplication syndrome occurs when humans have extra copies of the MeCP2 genes. To replicate this syndrome in macaques, scientists genetically modified monkey embryos by introducing the MeCP2 gene into the monkey’s DNA. Then, they implanted over 50 embryos into 18 surrogate monkeys. A total of nine female surrogates became pregnant, but only eight baby monkeys were born alive. These macaques displayed some of the symptoms typical of children with MeCP2 duplication syndrome, including anxiety, repetitive behaviors, what Qiu refers to as "defects in social interactions" with other monkeys. In addition, the researchers used sperm from the first generation of monkeys to create a second generation of transgenic monkeys who also displayed autism-like behaviors. Now that the monkeys have been developed, Qiu and his team of researchers have begun to use brain imaging technology to identify brain circuits that play a role in the monkeys’ autism-like behaviors. If the researchers can do that, they might be able to "rescue the affected brain circuits," Qiu says — and alter the monkeys’ autism-like behaviors. As a model for autism, the monkeys "aren’t perfect," but they could be better than mice designed to replicate the syndrome, says Alysson Muotri, a human brain development researcher at the University of California–San Diego. "At least the [monkeys] could mimic autism-like behaviors," he says. Still, it’s unclear if the monkeys "can actually generate novel insights into the human condition," Muotri says. The study published today doesn’t reveal anything new — and that’s a bit of a letdown, he says. "I would expect to learn some new biology here, but I have not." "I WOULD EXPECT TO LEARN SOME NEW BIOLOGY HERE, BUT I HAVE NOT." Even if the researchers can improve their model, the high cost of producing the monkeys will pose an important barrier to further research. "Primate studies are extremely expensive — the animals live a long time and have long gestation periods compared to rodents," Zoghbi says. "I think we should always make sure that our effort produces results worth the investment." Van Esch agrees. "In my opinion, there are easier and cheaper ways to study neurodevelopmental disorders." It’s also worth noting that DNA isn’t the only factor involved in autism spectrum disorders; environmental factors, like pesticides, have been linked to autism as well. So even though there’s a lot of value in studying how human genes lead to autism-like behaviors, DNA is just one piece of the puzzle. The fact that monkeys are more closely related to humans shouldn’t be used to justify using an inadequate model, Zoghbi says. "Decades of research using mice that do not [mimic features of the syndrome as closely as possible] resulted in a lot of research that can’t be translated, so it is important that we hold same standards to non-human primate models." And that means stating the limitations of each new animal model clearly. "We have to be very careful when there is a lot of desperation from human patients for answers to their problem — whether that be autism or Alzheimer’s or cancer or any other dreaded disease."   Credit  Arielle Duhaime-Ross

You see them everywhere, on people’s wrists and in annoyingly contagious adverts but could wearable fitness devices be put to even better use? Yes, they monitor your day to day ‘fitness’, such things as how many steps you’re taking and how much sleep you’re getting but if they are able to gather this sort of information could they not also gather data that tells you there is something seriously wrong? That is certainly the hope and idea behind aparito, an app and wearable device that aims to help children suffering from a variety of diseases. Founder and director of aparito, Dr. Elin Haf Davies, who has worked as a children’s nurse for many years, explains how aparito was born out of a ‘frustration that we were relying on very sterile snapshots of data that tell you how the patient is doing on a hospital visit but which doesn’t actually tell you anything about how they’re coping in day to day life at home.’ I hope our approach will contribute quite significantly to changing the way patients are in control of their own data. The idea behind aparito is simple: to take information gathered by the wearable device, combine it with the patient’s perspective on how they are handling their illness. The data can be accessed by the patient’s doctor in real-time at all times, cutting out the need for all manner of long and arduous tests to get the same results. The key to this is that the app and wearable device are designed to benefit both the patient and the doctor. The patient is able to keep track of their symptoms and therefore better manage their illness as well as knowing when to take medication. Meanwhile, the doctor is able to monitor the everyday activity of the patient.   To read full story Click Here Credit Alex Moss

Researchers at Vanderbilt University have developed a technique to mimic complex systems of capillaries using cotton candy machines. The new technique is used in creating three-dimensional templates of the capillary system and is said to be a huge improvement over other methods. Sugar wouldn't work in creating the threads needed for the template—it was too soluable—so the researchers turned to a special polymer for the job. After spinning a system of polymer threads, the researchers pour a gelatin mixture that includes human cells over the polymer structure. Once the mixture cools, the polymer threads dissolve, leaving behind an elaborate network of tiny passages. "Some people in the field think this approach is a little crazy,” researcher Leon Bellan told Vanderbilt's research news site, “but now we’ve shown we can use this simple technique to make microfluidic networks that mimic the three-dimensional capillary system in the human body in a cell-friendly fashion." Bellan bought his first cotton candy machine from Target for $40—a small price in creating a technique that could help in engineering much-needed livers, kidneys, or bones.   To read full story Click Here Credit NICOLE CARPENTER

If you were wondering why your hair was looking somewhat less lustrous than in previous years, we finally have an answer for you: it's because your thinning hair is turning into skin. For the first time, researchers have pinpointed a mechanism that turns age damaged stem cells in hair follicles into skin. As it happens to more and more stem cells, the hair follicles shrink and eventually disappear -- leaving you hairless. It's the first time such a mechanism has been identified with ageing. Unlike stem cells elsewhere in the body, hair follicle cells regenerate on a cyclical basis -- a growth phase is followed by a dormant phase in which they stop producing hair.  To find out why hair thins, Emi Nishimura and her team at Tokyo Medical and Dental University began looking at follicle stem cell growth cycles in mice. They found that age-related DNA damage triggers the destruction of the protein Collagen 17A1, which in turn triggers the transformation into 'epidermal keratinocytes' -- or skin. When the research was replicated in humans, they found that follicles in people aged over 55 were also smaller, and lower in Collagen 17A1. "We assume that ageing processes and mechanisms explain the human age-associated hair thinning and hair loss," Nishimura said.  Hair follicle stem cells are now likely to be used as a model for studying more general stem cell behaviour. Researchers are keen to point out that stem cell depletion is unlikely to be the only cause of hair loss, but suggest that Collagen 17A1 could be used as a target for hair loss treatments.    To read full story Click Here Credit Emily Reynolds  

New research attempts to shed light on the most common reasons patients are readmitted post-surgery, and how hospitals can nip the issue in the bud.  In a study recently published in the Journal of the American Medical Association (JAMA), a team of researchers looked at readmission rates after surgical procedures overall, as well as rates for several specific surgeries. The goal was to determine what sorts of problems caused complications requiring unexpected readmission. Information was pulled from the American College of Surgeons National Surgical Quality Improvement Program. The program tracks the primary reason for a patient’s readmission, which helped researchers figure out whether the subsequent hospital visit was related to the person’s initial condition. After looking at the data for close to 450 hospitals over a year-long period, researchers found that the number one reason for patients to be readmitted to the hospital after surgery was experiencing a surgical site infection. The second reason: an obstruction or ileus. To read full story Click Here Credit Jess White 

Newswise — Jan. 22, 2016─A diet rich in fiber may not only protect against diabetes and heart disease, it may reduce the risk of developing lung disease, according to new research published online, ahead of print in the Annals of the American Thoracic Society. Analyzing data from the National Health and Nutrition Examination Surveys, researchers report in “The Relationship between Dietary Fiber Intake and Lung Function in NHANES,” that among adults in the top quartile of fiber intake: • 68.3 percent had normal lung function, compared to 50.1 percent in the bottom quartile. • 14. 8 percent had airway restriction, compared to 29.8 percent in the bottom quartile.In two important breathing tests, those with the highest fiber intake also performed significantly better than those with the lowest intake. Those in the top quartile had a greater lung capacity (FVC) and could exhale more air in one second (FEV1) than those in the lowest quartile. “Lung disease is an important public health problem, so it’s important to identify modifiable risk factors for prevention,” said lead author Corrine Hanson PhD, RD, an associate professor of medical nutrition at the University of Nebraska Medical Center. “However, beyond smoking very few preventative strategies have been identified. Increasing fiber intake may be a practical and effective way for people to have an impact on their risk of lung disease.” Researchers reviewed records of 1,921 adults, ages 40 to 79, who participated in NHANES during 2009-2010. Administered by the Centers for Disease Control and Prevention, NHANES is unique in that it combines interviews with physical examinations. Fiber consumption was calculated based on the amount of fruits, vegetables, legumes and whole grains participants recalled eating. Those whose diets included more than 17.5 grams of fiber a day were in the top quartile and represented the largest number of participants, 571. Those getting less than 10.75 grams of fiber a day were in the lower group and represented the smallest number of participants, 360. Researchers adjusted for a number of demographic and health factors, including smoking, weight and socioeconomic status, and found an independent association between fiber and lung function. They did not adjust for physical activity, nor did the NHANES data allow them to analyze fiber intake and lung function over time—limitations acknowledged by the authors. Authors cited previous research that may explain the beneficial effects of fiber they observed. Other studies have shown that fiber reduces inflammation in the body, and the authors noted that inflammation underlies many lung diseases. Other studies have also shown that fiber changes the composition of the gut microbiome, and the authors said this may in turn reduce infections and release natural lung-protective chemicals to the body. If further studies confirm the findings of this report, Hanson believes that public health campaigns may one day “target diet and fiber as safe and inexpensive ways of preventing lung disease.” To read the article in full, please visit: http://www.thoracic.org/about/newsroom/press-releases/resources/White-201509-609OC.PDF