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  • richardmitnick 10:23 am on July 8, 2019 Permalink | Reply
    Tags: 7 Tesla MRI, , , , Medicine,   

    From Science News: “A 100-hour MRI scan captured the most detailed look yet at a whole human brain” 

    From Science News

    July 8, 2019
    Laura Sanders

    A device recently approved by the U.S. FDA made extremely precise images of a postmortem sample.

    CLOSE-UP A 3-D view of the entire human brain, taken with a powerful 7 Tesla MRI and shown here from two angles, could reveal new details on structures in the mysterious organ.

    Over 100 hours of scanning has yielded a 3-D picture of the whole human brain that’s more detailed than ever before. The new view, enabled by a powerful MRI, has the resolution potentially to spot objects that are smaller than 0.1 millimeters wide.

    “We haven’t seen an entire brain like this,” says electrical engineer Priti Balchandani of the Icahn School of Medicine at Mount Sinai in New York City, who was not involved in the study. “It’s definitely unprecedented.”

    The scan shows brain structures such as the amygdala in vivid detail, a picture that might lead to a deeper understanding of how subtle changes in anatomy could relate to disorders such as post-traumatic stress disorder.

    To get this new look, researchers at Massachusetts General Hospital in Boston and elsewhere studied a brain from a 58-year-old woman who died of viral pneumonia. Her donated brain, presumed to be healthy, was preserved and stored for nearly three years.

    Before the scan began, researchers built a custom spheroid case of urethane that held the brain still and allowed interfering air bubbles to escape. Sturdily encased, the brain then went into a powerful MRI machine called a 7 Tesla, or 7T, and stayed there for almost five days of scanning.

    The strength of the 7T, the length of the scanning time and the fact that the brain was perfectly still led to the high-resolution images, which are described May 31 at bioRxiv.org. Associated videos of the brain, as well as the underlying dataset, are publicly available.

    ZOOM IN This video moves from the outer wrinkles to the inner structures and then back out to the wrinkles of a complete human brain at extremely high resolution.

    Researchers can’t get the same kind of resolution on brains of living people. For starters, people couldn’t tolerate a 100-hour scan. And even tiny movements, such as those that come from breathing and blood flow, would blur the images.

    But pushing the technology further in postmortem samples “gives us an idea of what’s possible,” Balchandani says. The U.S. Food and Drug Administration approved the first 7T scanner for clinical imaging in 2017, and large medical centers are increasingly using them to diagnose and study illnesses.

    These detailed brain images could hold clues for researchers trying to pinpoint hard-to-see brain abnormalities involved in disorders such as comas and psychiatric conditions such as depression. The images “have the potential to advance understanding of human brain anatomy in health and disease,” the authors write.

    See the full article here .


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  • richardmitnick 2:08 pm on June 20, 2019 Permalink | Reply
    Tags: "Researchers Call for Personalized Approach to Aging Brain Health", , , Medicine,   

    From University of Arizona: “Researchers Call for Personalized Approach to Aging Brain Health” 

    U Arizona bloc

    From University of Arizona

    June 18, 2019
    Alexis Blue

    UA psychologist Lee Ryan and her collaborators have proposed a precision aging model designed to help researchers better understand and treat age-related cognitive decline on an individual level.

    People are living longer than ever before, but brain health isn’t keeping up. To tackle this critical problem, a team of researchers has proposed a new model for studying age-related cognitive decline – one that’s tailored to the individual.


    There’s no such thing as a one-size-fits-all approach to aging brain health, says Lee Ryan, professor and head of the University of Arizona Department of Psychology. A number of studies have looked at individual risk factors that may contribute to cognitive decline with age, such as chronic stress and cardiovascular disease. However, those factors may affect different people in different ways depending on other variables, such as genetics and lifestyle, Ryan says.

    In a new paper published in the journal Frontiers in Aging Neuroscience, Ryan and her co-authors advocate for a more personalized approach, borrowing principles of precision medicine in an effort to better understand, prevent and treat age-related cognitive decline.

    “Aging is incredibly complex, and most of the research out there was focusing on one aspect of aging at a time,” Ryan said. “What we’re trying to do is take the basic concepts of precision medicine and apply them to understanding aging and the aging brain. Everybody is different and there are different trajectories. Everyone has different risk factors and different environmental contexts, and layered on top of that are individual differences in genetics. You have to really pull all of those things together to predict who is going to age which way. There’s not just one way of aging.”

    Although most older adults – around 85% – will not experience Alzheimer’s disease in their lifetimes, some level of cognitive decline is considered a normal part of aging. The majority of people in their 60s or older experience some cognitive impairment, Ryan said.

    This not only threatens older adults’ quality of life, it also has socioeconomic consequences, amounting to hundreds of billions of dollars in health care and caregiving costs, as well as lost productivity in the workplace, Ryan and her co-authors write.

    The researchers have a lofty goal: to make it possible to maintain brain health throughout the entire adult lifespan, which today in the U.S. is a little over 78 years old on average.

    In their paper, Ryan and her co-authors present a precision aging model meant to be a starting point to guide future research. It focuses primarily on three areas: broad risk categories; brain drivers; and genetic variants. An example of a risk category for age-related cognitive decline is cardiovascular health, which has been consistently linked to brain health. The broader risk category includes within it several individual risk factors, such as obesity, diabetes and hypertension.

    The model then considers brain drivers, or the biological mechanisms through which individual risk factors in a category actually impact the brain. This is an area where existing research is particularly limited, Ryan said.

    Finally, the model looks at genetic variants, which can either increase or decrease a person’s risk for age-related cognitive decline. Despite people’s best efforts to live a healthy lifestyle, genes do factor into the equation and can’t be ignored, Ryan said. For example, there are genes that protect against or make it more likely that a person will get diabetes, sometimes regardless of their dietary choices.

    While the precision aging model is a work in progress, Ryan and her collaborators believe that considering the combination of risk categories, brain drivers and genetic variants is key to better understanding age-related cognitive decline and how to best intervene in different patients.

    Ryan imagines a future in which you can go to your doctor’s office and have all of your health and lifestyle information put into an app that would then help health-care professionals guide you on an individualized path for maintaining brain health across your lifespan. We may not be there yet, but it’s important for research on age-related cognitive decline to continue, as advances in health and technology have the potential to extend the lifespan even further, she said.

    “Kids that are born in this decade probably have a 50% chance of living to 100,” Ryan said. “Our hope is that the research community collectively stops thinking about aging as a single process and recognizes that it is complex and not one-size-fits-all. To really move the research forward you need to take an individualized approach.”

    Ryan is associate director of the Evelyn F. McKnight Brain Institute at the UA, which is one of the foremost universities in the world for researching the aging brain and age-related cognitive changes. Her co-authors on the paper include UA Regents’ Professor of Psychology Carol Barnes, who directs the UA’s Evelyn F. McKnight Brain Institute; UA professors Meredith Hay and Matthias Mehl; and collaborators from the Phoenix-based Translational Genomics Institute, Georgia Institute of Technology, Leonard M. Miller School of Medicine and John Hopkins University.

    See the full article here .

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    U Arizona campus

    The University of Arizona (UA) is a place without limits-where teaching, research, service and innovation merge to improve lives in Arizona and beyond. We aren’t afraid to ask big questions, and find even better answers.

    In 1885, establishing Arizona’s first university in the middle of the Sonoran Desert was a bold move. But our founders were fearless, and we have never lost that spirit. To this day, we’re revolutionizing the fields of space sciences, optics, biosciences, medicine, arts and humanities, business, technology transfer and many others. Since it was founded, the UA has grown to cover more than 380 acres in central Tucson, a rich breeding ground for discovery.

    Where else in the world can you find an astronomical observatory mirror lab under a football stadium?

    U Arizona mirror lab

    An entire ecosystem under a glass dome? Visit our campus, just once, and you’ll quickly understand why the UA is a university unlike any other.

  • richardmitnick 6:36 am on June 7, 2019 Permalink | Reply
    Tags: , Medicine, Physician burnout,   

    From Stanford University – Medicine: “Collaboration aims to battle physician burnout” 

    Stanford University Name
    From Stanford University – Medicine

    Tracie White

    The California Medical Association and Stanford Medicine have launched a multimillion dollar project to reduce physician burnout by providing support to doctors statewide.

    Stanford Medicine is collaborating with the California Medical Association on a project to battle the epidemic of physician burnout by providing support services to doctors across the state.

    “Our goal is to provide support to physicians so that they, in turn, can provide the best health care for all Californians,” said Tait Shanafelt, MD, the Jeanie and Stew Ritchie Professor and director of Stanford’s WellMD Center, which developed the project. “There is nothing like this comprehensive, statewide program anywhere in the country. It’s potentially a game-changing new model.”

    The five-year, multimillion-dollar initiative will tackle the complex problem of burnout through a multipronged approach built on a population health framework. It will include efforts to promote well-being for all physicians; provide tailored support at times of increased risk for burnout, such as when physicians have relocated or are going through malpractice suits; and assistance for physicians experiencing burnout or who are considering leaving the profession. The program also will try to change the culture within the medical community that holds physicians to superhuman expectations, discourages mental health treatment and results in exhausted, cynical physicians.

    “Addressing the systemic issue of physician burnout is essential to not only increasing physician well-being but ultimately delivering better patient care,” said Lloyd Minor, MD, dean of the School of Medicine. “I’m confident that this comprehensive project that incorporates research-driven strategies developed at Stanford Medicine will help get to the core of the problem.”

    The wages of burnout

    Recent studies show that more than 50 percent of U.S. physicians experience symptoms of professional burnout, a syndrome marked by exhaustion, cynicism and feelings of a loss of career purpose. The consequences are dire. Among doctors, they have led to rising suicide rates, substance abuse and addiction, and broken relationships. Burnout has also been shown to erode quality of care, increase medical errors and cause turnover and attrition that threaten to reduce access to care. As a result, Californians, as well as the rest of the country, are facing an inadequate physician workforce as more physicians cope with their distress by reducing patient load, working part-time or leaving the profession altogether, according to studies.

    “In addition to mitigating burnout, we hope to reduce the physician suicide rate in California,” said Mickey Trockel, MD, PhD, project co-leader and clinical associate professor of psychiatry and behavioral sciences at Stanford. “We also hope that by engaging physicians — and their organizations — in preserving physician well-being, they will be more effective in serving those who need them.”

    The project will focus on practical, hands-on methods of prevention and intervention, with programs available to all physicians.It will incorporate a leadership academy to train medical leaders from across the state on leadership behaviors to cultivate professional fulfillment at the work unit and organizational level. It also will include efforts to convene leaders from medical schools and residency programs statewide to work together to help change the culture of medicine and improve well-being for physicians in training.

    “Physician burnout, which is primarily due to problems in the practice environment, has reached a crisis level in the U.S.,” said Sherilyn Stolz, executive director of the WellMD Center. “Bringing Stanford’s expertise in physician wellness together with the resources of the CMA is a powerful force to drive progress.”

    The project also will encourage collegiality and community-building, provide individual coaching programs for physicians and offer access to new professional development opportunities, Shanafelt said.

    In addition, the project will provide support to the WellMD Center for improving wellness among Stanford medical school faculty and staff, as well as serve as a vehicle for other Stanford experts in undergraduate and graduate education as well as leadership development to disseminate their knowledge to benefit physicians statewide, Shanafelt said.

    See the full article here .

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    Stanford Medicine integrates research, medical education and health care at its three institutions – Stanford University School of Medicine, Stanford Health Care (formerly Stanford Hospital & Clinics), and Lucile Packard Children’s Hospital Stanford. For more information, please visit the Office of Communication & Public Affairs site at http://mednews.stanford.edu.

    Stanford University campus. No image credit

    Stanford University

    Leland and Jane Stanford founded the University to “promote the public welfare by exercising an influence on behalf of humanity and civilization.” Stanford opened its doors in 1891, and more than a century later, it remains dedicated to finding solutions to the great challenges of the day and to preparing our students for leadership in today’s complex world. Stanford, is an American private research university located in Stanford, California on an 8,180-acre (3,310 ha) campus near Palo Alto. Since 1952, more than 54 Stanford faculty, staff, and alumni have won the Nobel Prize, including 19 current faculty members

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  • richardmitnick 11:09 am on May 30, 2019 Permalink | Reply
    Tags: "‘I will feel actual rage.’ Unusual responses to kind touches could help explain autism traits", , , Medicine,   

    From Science Magazine: “‘I will feel actual rage.’ Unusual responses to kind touches could help explain autism traits” 

    From Science Magazine

    May. 29, 2019
    George Musser

    Cinyee Chiu and Edwin Tse/Spectrum

    Even the slightest touch can consume Kirsten Lindsmith’s attention. When someone shakes her hand or her cat snuggles up against her, for example, it becomes hard for her to think about anything else. “I’m taken out of the moment for however long the sensation lasts,” she says. Some everyday sensations, such as getting her hands wet, can feel like torture: “I usually compare it to the visceral, repulsive feeling you’d get plunging your hand into a pile of rotting garbage,” says the 27-year-old autistic writer.

    Stephanie Dehennin, an autistic illustrator who lives in Belgium, detests gentle touches but doesn’t mind firm hugs. “I will feel actual rage if someone strokes me or touches me very lightly,” she says. Dehennin seeks out deep pressure to relieve her stress. “I’ll sit between my bed and my nightstand, for example — squeezed between furniture.”

    Strong reactions to touch are remarkably widespread among people who have autism, despite the condition’s famed heterogeneity. “The touch thing is as close to universal as they come,” says Gavin Bollard, an autistic blogger who lives in Australia and writes about his and his autistic sons’ experiences. These responses are often described as a general hypersensitivity, but they are more complex than that: Sometimes autistic people crave touch; sometimes they cringe from it. For many people on the spectrum, these sensations are so intense that they take measures to shape their ‘touchscape.’ Some pile on heavy blankets at night for the extra weight; others cut off their clothing tags.

    The common thread may be an altered perception of ‘affective touch,’ a sense discovered in people only a few decades ago. ‘Discriminative touch’ tells us when something impinges on our skin, with what force and where; affective touch, by contrast, conveys nuanced social and emotional information. The kinds of touch that autistic people may find loathsome, such as a soft caress, are associated with this latter system.

    Research on affective touch is still nascent, but the idea that it is linked to autism is tantalizing, experts say. A growing number of studies indicate that affective touch is at least partly responsible for our ability to develop a concept of self, something long thought to differ in people with autism [Spectrum]. Even newer is the idea that an atypical sense of affective touch may be one of autism’s underlying causes.

    “Maybe this is actually getting at a biological marker that gets us a better understanding of the causes of autism and, at the very least, a very early detection of autism,” says Kevin Pelphrey, a neuroscientist at the University of Virginia in Charlottesville.

    A sixth sense

    Despite the many anecdotes about an altered sense of touch in autistic people, quantifying the differences has proved difficult. In some experiments, autistic people notice a light pressure on their skin that their typical peers are oblivious to. But others show less sensitivity than or no real difference from controls. “There’s all this clinical evidence around, but the actual empirical studies are confused,” says Carissa Cascio, associate professor of psychiatry and behavioral sciences at Vanderbilt University Medical Center in Nashville, Tennessee.

    One reason for this confusion is that not every study or clinical report distinguishes between affective and discriminative touch. Discriminative touch conveys signals about pressure, vibration and stretching of the skin. These signals shoot along thick ‘type A’ nerve fibers, or ‘afferents,’ at speeds of more than 200 miles per hour to the brain’s sensory regions. Affective touch signals, meanwhile, travel slowly via thinner ‘type C’ afferents and communicate pain, itch and temperature; the variety of type C nerve fibers that communicate touch — called C-tactile fibers — register in emotion centers in the brain.

    C-tactile fibers respond only to specific kinds of touch. Researchers use a specialized technique called ‘microneurography’ to find the fibers and measure their activity. The method involves sticking an acupuncture-like needle deep into the skin, typically near the elbow, and then feeding in electrical pulses. As the needle gets closer to a nerve, less current is needed to evoke a tingling sensation. Once the needle is within the nerve, it can begin measuring the nerve’s electrical activity. The system is set up to have nerves produce clicks or light drumrolls on a loudspeaker whenever they fire. The C-tactile fibers crackle loudest when a participant is stroked lightly, no faster than a few inches per second, and at 32 degrees Celsius — the same temperature as human skin. Because the signals propagate slowly, the sound is delayed by about a half a second.

    At first glance, these fibers seems pointless. They don’t help you hold a pencil or feel a vibrating phone. They are found only in skin that has hair — the face and the forearm, for instance — and not in fingertips, palms, soles or genitals, body parts we typically associate with touch. Yet studies show that they give physical contact its emotional timbre; they relay the warm feelings that can come with a friend’s caress, for example, or the icy shivers that can follow a brush with a stranger.

    In this way, the fibers serve as a mode of communication between people, a channel not of physical information but of intimacy. “These fibers are signaling something that isn’t really touch; it’s something we don’t have a name for,” says Håkan Olausson, professor of clinical neuroscience at Linköping University in Sweden, who co-discovered the fibers in people in the 1980s. (For lack of a better word, he still calls it touch.)

    Olausson and others owe much of what they have learned about affective touch to a woman known in the medical literature as ‘Patient G.L.’ In April 1979, this woman checked into a hospital in Montreal with Guillain-Barré syndrome, a rare autoimmune disorder that attacks muscle and sensory neurons. In her case, it had destroyed her type A nerve fibers but spared her type C’s. She was left with the tactile equivalent of ‘blindsight’: Although she no longer felt contact, motion or pressure against her skin, she could still have an emotional reaction to being touched. It was an early clue that these nerve fibers carry emotional freight.

    Cinyee Chiu and Edwin Tse/Spectrum

    To confirm the idea, Olausson and his colleagues turned to brain imaging. In 2002, they scanned G.L. as they touched her skin. Their actions evoked no response [Nature Neuroscience] in her somatosensory cortex, which ordinarily receives input from type A fibers, but her emotion-processing posterior insula did react. She reported feeling a faint, hard-to-place, pleasant sensation. In recent years, her brain seems to have compensated for her lost sense of discriminative touch by repurposing her affective-touch system. “When we last met about a year ago, she said that she has started to feel touch sensations in daily life — for example, when she puts on her stockings,” Olausson says.

    His team has collected additional evidence linking type C nerve fibers to emotional communication by studying about 20 members of a community in remote northern Sweden. These individuals all share a congenital loss of these fibers — in a sense, the inverse of G.L.’s condition. In a study of five of the people, they showed no activity in the insula in response to skin stroking and rated the sensation as less pleasant [Brain] than controls did. In some ways, their experience of touch might resemble that of autistic people, although there is no evidence that autism is particularly prevalent in this community.

    Even when both touch systems are intact, social context can dampen or amplify our perception of affective touch. In a study published in February, researchers scanned the brains of 27 neurotypical adults. When a lab assistant stroked the participants’ forearms, social areas of their brains, such as the superior temporal gyrus, lit up with activity. When the participants stroked their own arms, those regions showed no change in activity — which is to be expected because the task is not social. What was unexpected was that the participants’ basic sensory-processing areas also stayed silent. In stroking their own arms, they had desensitized that part of their body to touch in general.

    In a companion study, the team also tested people’s touch sensitivity by poking their forearms with von Frey fibers — plastic hairs that deliver a calibrated force — while a lab assistant stroked their arms or the participants stroked a pillow or themselves. The pillow had no effect on the participants’ sensitivity to touch: They felt the von Frey fibers just as they would if they weren’t being stroked at all. By contrast, when a lab assistant stroked the participant — a social gesture — the researchers had to poke the participant’s arm harder with the von Frey fibers for the touch to be felt. They had to apply an even stronger force when the participants stroked their own arms. “Touching your own arm numbs this area,” says lead investigator Rebecca Boehme, a researcher also at Linköping. Together, these results suggest that the affective touch system is tuned to recognize human contact [PNAS] and to differentiate self from other.

    Sensing the self

    To many researchers, the affective touch system suggests a compelling mechanism at autism’s roots. Touch is one of the dominant modes of perception and social interaction in the earliest weeks and months of a baby’s life. “A whole lot of your world is coming to you through caregiver touch — there’s a whole lot of cuddling, cradling, rocking,” Cascio says. If babies’ perceptions of these touches are altered in some way, it could transform how they situate themselves in the world and learn to interact with others. Those changes, in turn, could account for autism’s hallmark social challenges.

    Most researchers interviewed for this article subscribe to some version of this idea but admit it is still tentative. “We really don’t have strong evidence for it yet,” Cascio says. What evidence they do have falls somewhere along a three-link chain of logic.

    The first link is the observation that affective touch seems crucial for delineating our sense of ‘self.’ To explore that idea, some researchers have turned to the ‘rubber-hand illusion,’ in which an experimenter strokes a participant’s hand and a stuffed rubber glove at the same time until the participant mistakes the fake hand for her own. In typical people, the illusion is strongest when the stroking speed and textures involved elicit the peak response of C-tactile fibers. “You make an almost unconscious-to-the-individual change, and that makes a big change in their perception,” says Aikaterini Fotopoulou, a cognitive neuroscientist at University College London.

    Yet another hint that affective touch is important to self-definition comes from people who have had a stroke and feel one of their arms is not their own. In a study of seven people who lost the ability to recognize their left arm, Fotopoulou and her colleagues stroked that arm to activate the participants’ C-tactile fibers. The participants then reported reconnecting with their ‘lost’ limbs. “They start saying things like, ‘Well, after you touched it, I said to my arm: Come, I welcome you back,’” Fotopoulou says.

    The second link is more theoretical: If affective touch can redraw a person’s boundaries such that they mistake a fake hand for their own, perhaps it is responsible for drawing those boundaries to begin with. This link in the chain holds that our entire sense of body ownership may be one grand rubber-hand illusion imparted from all that cuddling we got as babies. “I put my leg there, or my fingers there, and then there is a response. I say, ‘Oh, that’s me,’” says Anna Ciaunica, a philosopher of mind at University College London who works with Fotopoulou.

    The third link connects these two ideas to autism. Cascio and others have found that autistic people are less susceptible to the rubber-hand illusion than neurotypical people are, suggesting their sense of self is somehow less flexible. That rigidity might explain the strong response many of them have to touch. “If you have a very clear border of your own body, then of course everything else that touches you will bother you,” Boehme says. Many autistic people also say they relate their feelings about touch directly to their sense of self. Kirsten Lindsmith has written about this in her blog: “When I shake a person’s hand, I feel as though a tiny part of myself — my awareness, my consciousness, my identity — is commandeered by their touch, and I no longer feel fully autonomous.” Dehennin also says she experiences that sensation: “I often feel like I’m not ‘in’ my body; deep pressure helps that.”

    Cinyee Chiu and Edwin Tse/Spectrum

    Several imaging studies also suggest that autistic people have an altered sense of affective touch. In 2012, for example, Cascio led a series of experiments in which a lab assistant stroked autistic and typical adults’ forearms with a soft cosmetics brush, bumpy burlap or scratchy plastic mesh. Both groups described each texture much in the same way, but brain imaging revealed that they processed the sensations differently [PubMed]: The autistic group showed more activity than controls in brain regions associated with discriminative touch and less in those associated with affective touch.

    Most interesting, Cascio says, was that burlap in particular lit up social brain regions in the controls, even though burlap has no obvious social significance. She interprets this activity as subconscious deliberation — that is, the burlap touch could be considered positive or negative depending on social cues. “We’re seeing processing in those regions that would make us think that they’re trying to figure out how pleasant or unpleasant it feels,” she says. The social brain areas of autistic participants, however, don’t seem to show this internal deliberation. Or if they do, as Cascio’s newer work suggests, they do so after a delay.

    In another experiment, autistic people and controls both said they liked the sensation of being stroked rhythmically on the arm or hand with a watercolor paintbrush. “A lot of the field would be like, ‘Well, that’s kind of a dead end; maybe touch isn’t affected in autism,’” says Pelphrey, one of the researchers. But brain scans again showed clear distinctions between the groups. Stroking the forearm, rich in type C afferents, lit up social brain areas in the controls, but stroking the palm, which contains predominantly type A nerve fibers, had no such effect. In autistic participants, location didn’t matter; their social brain activity remained at a constant level in between the extremes shown by the typical participants. “Individuals with autism showed the middle response for everything,” Pelphrey says.

    Autistic people also appear to process pain differently , reflecting possible differences in their type C nerve fibers. In 2017, Cascio’s lab affixed a small heating pad, about 1 inch in diameter, to the calves of autistic and neurotypical volunteers. They then brought the temperature to an agonizing 49 degrees Celsius for 15 seconds. (The pad was not hot enough to burn the skin.) Both groups rated the pain 7 out of 10. But once again brain imaging offered a nuanced picture. In brain areas that respond to pain, such as the anterior cingulate cortex, insula and thalamus, the reaction in the neurotypical people lasted 30 seconds, lingering after the heat was removed. In autistic people, it abated after only 10 seconds, even though heat was still being applied. “It really looks like, when you look at the data, that something’s turning the pain response off,” Cascio says.

    Connecting the dots

    What all this experimental evidence means is still unclear, apart from generally confirming that, in autistic people, something unusual goes on in type C nerve fiber activity and touch perception. Whatever differences exist appear to be present from early in life. Parents often recall that their autistic children, as babies, recoiled from contact and avoided being picked up. “Human beings respond to the act of being picked up either by fighting back or by becoming rigid in ways that actually help you to pick them up,” Pelphrey says. But babies who go on to be diagnosed with autism often do neither, which can make them feel curiously heavier than they are, he says.

    His team is investigating whether unusual touch sensitivity in infants can predict a later autism diagnosis. They are testing ‘baby siblings’ of children with autism, who are at an increased risk of being diagnosed with the condition. The researchers plan to record the babies’ response — at 3, 6, 9 and 12 months of age — to touch on their palms and forearms, looking for differences in their senses of discriminative and affective touch, respectively. “We can hopefully develop something that will serve as a screener,” Pelphrey says.

    Other researchers are working on more sophisticated approaches to study touch in older children and adults with autism. They have their work cut out for them. The emotional quality of touch is difficult to measure, in part because it depends on more than just physical stimulus. Type C nerves are not yet fully understood. And simply asking people how they feel can mask important features of touch perception.

    Researchers will also need to consider how differences in affective touch fit into the broader experience of being autistic. Layered on top of the raw sensations are cultural norms about touch, which vary and can make social situations fraught for people with the condition. A flinch can be read as a rebuff, a declined handshake as disinterest. Many autistic people say they learned as children to suppress their feelings about touch in order to conform to typical expectations — something that leaves them vulnerable to abuse. “‘No’ was trained out of us,” says Ashley Smith-Taylor, an autistic self-advocate and mother of four neurodiverse children.

    Also hanging over the field is an old theory known as the ‘refrigerator mother’ hypothesis. From the 1940s into the 1960s, psychologists attributed autism to parents who made no effort to connect with their children emotionally, including cuddling them. “There was this tendency to blame parents, and particularly mothers,” Cascio says. She and others stress that if autism does originate in the sense of touch, it arises from deep in the nervous system and is entirely unrelated to nurture. It may also begin in the womb. During the first and second trimester, the fetus is covered by ‘lanugo hair’ that may stimulate the type C nerve fibers in utero; at this stage of development, these fibers provide our first sensory input. “That input, according to my theory, is basically the process which is beginning to let that developing brain know it’s got a body,” says Francis McGlone, professor of neuroscience at Liverpool John Moores University in the United Kingdom.

    McGlone admits that there is no solid evidence that connects autism to a dearth of affective touch early in life, but he isn’t waiting for it, either. He is developing a device that could be placed into incubators to stimulate type C nerve fibers in preterm infants. “The C-tactile afferent is the Higgs boson of the social brain. It’s the missing particle that socializes the developing brain. It brings everything else together,” he says. His invention could be useful for many children — even if it turns out that affective touch has little to do with autism’s origins.

    See the full article here .


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  • richardmitnick 9:50 am on May 30, 2019 Permalink | Reply
    Tags: , , Medicine,   

    From University of Washington: “UW, collaborating institutions awarded $9.5 million for detecting autism earlier in childhood” 

    U Washington

    From University of Washington

    May 29, 2019
    Kim Eckart

    Research scientist Tanya St. John works with a baby at the University of Washington Autism Center.

    A multicenter research team that includes the University of Washington Autism Center has received a five-year, $9.5 million grant to determine whether brain imaging can help detect infants who are likely to go on to develop autism spectrum disorder. Led by Washington University and the University of North Carolina at Chapel Hill, the research network of eight institutions received the grant from the National Institutes of Health’s National Institute of Mental Health.

    The new grant supports the continued efforts of researchers in the Infant Brain Imaging Study, or IBIS, network. Scientists will scan the brains of 250 children who have an older sibling with autism, looking for differences that predict which high-risk children are more, and less, likely to develop the condition.

    “Our studies have identified brain alterations in high-risk infants at 6 months of age that can predict a later autism diagnosis,” said Dr. Stephen R. Dager, professor of radiology at the University of Washington School of Medicine and principal investigator at the UW. “Now we are going to work with a new group of families to confirm whether our initial findings can be replicated.”

    Infant siblings of children with autism have a 20 percent chance of developing autism spectrum disorder themselves – a much higher risk than children in the general population. Researchers believe that if brain scans can accurately identify which infants are at highest risk, then careful assessment over the first two years of life could detect behavioral symptoms as soon as they emerge. This would allow interventions to begin sooner and improve those children’s outcomes.

    IBIS researchers published initial findings in 2017 [PubMed], which showed that magnetic resonance imaging (MRI) correctly identified 80% of babies who went on to be diagnosed with autism at age 2. They also correctly predicted more than 90% of babies who subsequently did not receive that diagnosis.

    “These imaging findings are very exciting and, if replicated, can allow much earlier diagnosis of autism,” said Dager.

    The UW Autism Center, part of the Center on Human Development and Disability, has long studied the signs of autism and the effectiveness of intervention strategies, and has been involved with IBIS since its inception.

    “We have learned so much from the children and families in the IBIS studies. We understand much more about the way autism symptoms unfold in infants with autism risk, starting with subtle early sensory-motor signs and developing into social communication and repetitive behavior in the second year of life,” said Annette Estes, director of the UW Autism Center, research professor of speech and hearing sciences, and co-lead investigator of the IBIS study in Seattle. “These brain findings in the first year of life could be game-changers if the findings hold up. They could allow us to approach autism in a new way, before symptoms emerge.”

    As parents from around the country brought younger and younger children to be evaluated at the UW, the UW Autism Center established its Infant and Toddler Clinic in spring 2017. The clinic provides evaluations for infants and toddlers up to 24 months of age, along with psychologists and behavior analysts to create a treatment plan with clinic- and home-based activities — just as would happen with older children.

    “IBIS families told us how valuable it was to have assessments over the first years of life so they could be sure that any signs of autism would be caught as soon as possible,” said Tanya St. John, a clinical psychologist at the UW Autism Center. “It has been gratifying to bring these services to families in the community, including people who may not have a family history of autism but who just have questions about their infant’s development. Our team has been able to see these young children quickly and get their parents the information and support they need.”

    For the new study, babies will undergo MRI scans while asleep. Those tests will be performed when the infants are 6 and 12 months old, to analyze both the brain’s structure and its functional connections. Infants also will be evaluated for language development, repetitive behaviors, social responsiveness and other behaviors that may, in the future, help understand how autism unfolds in the first year of life.

    “Our goal is to improve outcomes for infants at highest risk,” said Estes. “Intervention that starts before children fall far behind in development, and perhaps before symptoms become clear, might prevent many problems faced by families today.”

    Along with the UW, Washington University and the University of North Carolina, other institutions involved are Children’s Hospital of Philadelphia, the University of Minnesota, New York University, the University of Alberta and McGill University. Families participating in the study must travel to the IBIS screening site nearest their hometowns. The imaging sites are located in Seattle, St. Louis, Philadelphia, Chapel Hill, N.C., and Minneapolis-St. Paul.

    To learn more about the IBIS study in Seattle, contact uwautism@uw.edu.

    See the full article here .


    Please help promote STEM in your local schools.

    Stem Education Coalition

    The University of Washington is one of the world’s preeminent public universities. Our impact on individuals, on our region, and on the world is profound — whether we are launching young people into a boundless future or confronting the grand challenges of our time through undaunted research and scholarship. Ranked number 10 in the world in Shanghai Jiao Tong University rankings and educating more than 54,000 students annually, our students and faculty work together to turn ideas into impact and in the process transform lives and our world. For more about our impact on the world, every day.
    So what defines us —the students, faculty and community members at the University of Washington? Above all, it’s our belief in possibility and our unshakable optimism. It’s a connection to others, both near and far. It’s a hunger that pushes us to tackle challenges and pursue progress. It’s the conviction that together we can create a world of good. Join us on the journey.

  • richardmitnick 9:38 am on May 29, 2019 Permalink | Reply
    Tags: "Nerve stimulation could provide new treatment option for most common type of stroke", A new nerve stimulation therapy to increase blood flow could help patients with the most common type of stroke up to 24 hours after onset., , Medicine, Stroke treatments,   

    From UCLA Newsroom: “Nerve stimulation could provide new treatment option for most common type of stroke” 

    From UCLA Newsroom

    May 24, 2019
    Sandy Van

    The treatment uses a small neurostimulator electrode that is temporarily implanted through the roof of the mouth. BrainsGate

    Research [The Lancet] led by a UCLA scientist found that a new nerve stimulation therapy to increase blood flow could help patients with the most common type of stroke up to 24 hours after onset.

    A study of 1,000 patients found evidence that the technique, called active nerve cell cluster stimulation, reduced the patients’ degree of disability three months after they suffered an acute cortical ischemic stroke, which affects the surface of the brain.

    Dr. Jeffrey Saver, director of the UCLA Comprehensive Stroke Center, was the co-principal investigator of the study, which was conducted at 73 medical centers in 18 countries.

    “We believe this represents the advent of an entirely new treatment for patients with acute ischemic stroke,” said Saver, who also is senior associate vice chair for clinical research in neurology at the David Geffen School of Medicine at UCLA. The study is published today in The Lancet.

    Unlike the two currently approved therapies for acute stroke, which open blocked arteries by dissolving or removing a clot, the new approach applies electrical stimulation to nerve cells behind the nose, increasing blood flow in the brain by dilating undamaged arteries and bypassing the blockage to treat the threatened region of the brain.

    In previous studies to understand the mechanism by which the treatment would work, scientists found that the nerve cell cluster stimulation not only increases blood flow, but also preserves the blood-brain barrier, which prevents brain swelling. It also improved neurons’ ability to compensate for injury and form new connections.

    In a study subset of 520 people who had major deficits and confirmed injury to the cerebral cortex, 40% of those who did not have the stimulation had favorable outcomes, versus 50% of those who did have the stimulation. Although those results fell just short of statistical significance, when the data are combined with similar findings from an earlier trial, the cumulative statistics indicate that the therapy is effective when administered eight to 24 hours after the onset of a cortical acute ischemic stroke.

    The treatment uses a small neurostimulator electrode that is temporarily implanted through the roof of the mouth. (The implant requires only local anesthesia.) During the study, the electrode actively stimulated the nerve cell cluster four hours a day for five consecutive days.

    The first treatment for ischemic stroke, the clot-dissolving drug alteplase, was approved by the Food and Drug Administration in 1996. When administered soon after onset, the drug, which is also called tPA, can sometimes clear a blocked artery, restore blood flow and avert stroke damage. However, its effectiveness diminishes if treatment is delayed beyond three hours, it does not work for all patients, and some people have conditions that preclude its use.

    More recently, the FDA has approved clot-retrieval devices that are threaded through arteries to capture and remove blockages. Used alone or in conjunction with tPA, those devices have extended treatment time to 24 hours after the onset of stroke in some patients, although earlier treatment is more effective. But the devices require expertise that may be absent outside of major medical centers.

    “Stroke continues to be a major cause of death and disability in the United States and around the world, making it imperative that we develop new, effective treatments to complement existing therapies, including in the extended treatment window,” Saver said.

    The trial found that the new stimulation treatment can be safe and effective for people who are not eligible for clot-dissolving medication, Saver said. Future studies will determine the effectiveness of the new therapy when it is used with clot-dissolving medications and clot-retrieving devices.

    Saver and Dr. Natan Bornstein of Tel Aviv University and the Shaare Zedek Medical Center in Israel, were the study’s co-first authors.

    The research was funded by device manufacturer BrainsGate Ltd. Saver, Bornstein and other authors were paid by BrainsGate for serving on a steering committee that provided guidance on the study’s design and approach.

    See the full article here .

    Please help promote STEM in your local schools.

    Stem Education Coalition

    UC LA Campus

    For nearly 100 years, UCLA has been a pioneer, persevering through impossibility, turning the futile into the attainable.

    We doubt the critics, reject the status quo and see opportunity in dissatisfaction. Our campus, faculty and students are driven by optimism. It is not naïve; it is essential. And it has fueled every accomplishment, allowing us to redefine what’s possible, time after time.

    This can-do perspective has brought us 12 Nobel Prizes, 12 Rhodes Scholarships, more NCAA titles than any university and more Olympic medals than most nations. Our faculty and alumni helped create the Internet and pioneered reverse osmosis. And more than 100 companies have been created based on technology developed at UCLA.

  • richardmitnick 9:06 pm on May 27, 2019 Permalink | Reply
    Tags: , , , DNA functions, Medicine   

    From COSMOS Magazine: “Autism linked to ‘junk’ DNA mutations” 

    Cosmos Magazine bloc

    From COSMOS Magazine

    28 May 2019
    Andrew Masterson

    Almost all DNA is non-coding, but research shows it is certainly not ‘junk’. Credit Anthony Harvie/Getty Images

    Mutations in so-called “junk” DNA have been tied to the development of autism (ASD) in children who do not have parents or siblings with the condition.

    The research, published in the journal Nature Genetics, provides an important piece of information in the quest to understand ASD, but also has wider significance.

    “This is the first clear demonstration of non-inherited, non-coding mutations causing any complex human disease or disorder,” says lead researcher Olga Troyanskaya of the US Flatiron Institute’s Centre for Computational Biology.

    Less than 2% of human DNA codes for the proteins that enable the critical functions of metabolism. The remaining 98% used to be thought of as effectively ballast, characterised as makeweight “junk”.

    Today, the label is recognised as a misnomer, and has been largely replaced by the term “non-coding”. Research [NIH] has shown that at least some of it plays very important roles in regulating the activity of genes – switching them on and off, and variously enhancing or dampening protein-coding activity.

    Previous studies have tied about 30% of autism cases in families with no prior history of the condition – so-called “simplex” cases – to mutations in particular coding genes.

    Using a machine-learning approach, Troyanskaya and colleagues analysed the genomes of 1790 people, comprising simplex autism cases and their families. Their model was trained to predict how any given DNA sequence would affect gene expression.

    The analysis revealed that cases linked to mutations in non-coding DNA should be of the same magnitude as those tied to coding DNA changes.

    The approach enables the identification of particular targets within the non-coding DNA which can now be the subject of more intense and focussed research.

    A computational biologic approach to DNA function, the researchers say, opens up a broad range of possible avenues for the understanding of conditions driven by genetic function.

    “This enables a new perspective on the cause of not just autism, but many human diseases,” says co-author Jian Zhou.

    See the full article here .

    Please help promote STEM in your local schools.

    Stem Education Coalition

  • richardmitnick 11:06 am on May 27, 2019 Permalink | Reply
    Tags: "'Submarines' small enough to deliver medicine inside human body", , Dr Liang: each capsule of medicine could contain millions of micro-submarines and within each micro-submarine would be millions of drug molecules., , Medicine, Micro-submarines powered by nano-motors, , This is significant not just for medical applications but for micro-motors generally.,   

    From University of New South Wales: “‘Submarines’ small enough to deliver medicine inside human body” 

    U NSW bloc

    From University of New South Wales

    27 May 2019
    Lachlan Gilbert

    UNSW engineers have shown that micro-submarines powered by nano-motors could navigate the human body to provide targeted drug delivery to diseased organs without the need for external stimulus.

    An artist’s representation of ‘micro-submarines’ transporting their medical cargo through capillaries among red blood cells. Picture: UNSW.

    Cancers in the human body may one day be treated by tiny, self-propelled ‘micro-submarines’ delivering medicine to affected organs after UNSW Sydney chemical and biomedical engineers proved it was possible.

    In a paper published in Materials Today, the engineers explain how they developed micrometre-sized submarines that exploit biological environments to tune their buoyancy, enabling them to carry drugs to specific locations in the body.

    Corresponding author Dr Kang Liang, with both the School of Biomedical Engineering and School of Chemical Engineering at UNSW, says the knowledge can be used to design next generation ‘micro-motors’ or nano-drug delivery vehicles, by applying novel driving forces to reach specific targets in the body.

    “We already know that micro-motors use different external driving forces – such as light, heat or magnetic field – to actively navigate to a specific location,” Dr Liang says.

    “In this research, we designed micro-motors that no longer rely on external manipulation to navigate to a specific location. Instead, they take advantage of variations in biological environments to automatically navigate themselves.”

    What makes these micro-sized particles unique is that they respond to changes in biological pH environments to self-adjust their buoyancy. In the same way that submarines use oxygen or water to flood ballast points to make them more or less buoyant, gas bubbles released or retained by the micro-motors due to the pH conditions in human cells contribute to these nanoparticles moving up or down.

    This is significant not just for medical applications, but for micro-motors generally.

    “Most micro-motors travel in a 2-dimensional fashion,” Dr Liang says.

    “But in this work, we designed a vertical direction mechanism. We combined these two concepts to come up with a design of autonomous micro-motors that move in a 3D fashion. This will enable their ultimate use as smart drug delivery vehicles in the future.”

    Dr Liang illustrates a possible scenario where drugs are taken orally to treat a cancer in the stomach or intestines. To give an idea of scale, he says each capsule of medicine could contain millions of micro-submarines, and within each micro-submarine would be millions of drug molecules.

    “Imagine you swallow a capsule to target a cancer in the gastrointestinal tract,” he says.

    “Once in the gastrointestinal fluid, the micro-submarines carrying the medicine could be released. Within the fluid, they could travel to the upper or bottom region depending on the orientation of the patient.

    “The drug-loaded particles can then be internalised by the cells at the site of the cancer. Once inside the cells, they will be degraded causing the release of the drugs to fight the cancer in a very targeted and efficient way.”

    For the micro-submarines to find their target, a patient would need to be oriented in such a way that the cancer or ailment being treated is either up or down – in other words, a patient would be either upright or lying down.

    Dr Liang says the so-called micro-submarines are essentially composite metal-organic frameworks (MOF)-based micro-motor systems containing a bioactive enzyme (catalase, CAT) as the engine for gas bubble generation. He stresses that he and his colleagues’ research is at the proof-of-concept stage, with years of testing needing to be completed before this could become a reality.

    Dr Liang says the research team – comprised of engineers from UNSW, University of Queensland, Stanford University and University of Cambridge – will be also looking outside of medical applications for these new multi-directional nano-motors.

    “We are planning to apply this new finding to other types of nanoparticles to prove the versatility of this technique,” he says.

    See the full article here .


    Please help promote STEM in your local schools.

    Stem Education Coalition

    U NSW Campus

    Welcome to UNSW Australia (The University of New South Wales), one of Australia’s leading research and teaching universities. At UNSW, we take pride in the broad range and high quality of our teaching programs. Our teaching gains strength and currency from our research activities, strong industry links and our international nature; UNSW has a strong regional and global engagement.

    In developing new ideas and promoting lasting knowledge we are creating an academic environment where outstanding students and scholars from around the world can be inspired to excel in their programs of study and research. Partnerships with both local and global communities allow UNSW to share knowledge, debate and research outcomes. UNSW’s public events include concert performances, open days and public forums on issues such as the environment, healthcare and global politics. We encourage you to explore the UNSW website so you can find out more about what we do.

  • richardmitnick 10:02 am on May 26, 2019 Permalink | Reply
    Tags: "Targeting Key Gene Could Help Lead to Down Syndrome Treatment", , , Medicine, ,   

    From Rutgers University: “Targeting Key Gene Could Help Lead to Down Syndrome Treatment” 

    Rutgers smaller
    Our Great Seal.

    From Rutgers University

    May 22, 2019

    Todd Bates

    Rutgers-led team uses stem cell-based disease models to pinpoint gene linked to impaired memory in Down syndrome.

    A living 3D “organoid” model of the brain generated from Down syndrome human stem cells. Photo: Ranjie Xu/Rutgers University-New Brunswick.

    Targeting a key gene before birth could someday help lead to a treatment for Down syndrome by reversing abnormal embryonic brain development and improving cognitive function after birth, according to a Rutgers-led study.

    Using stem cells that can turn into other cells in the brain, researchers developed two experimental models – a living 3D “organoid” model of the brain and a mouse brain model with implanted human cells – to investigate early brain development linked to Down syndrome, according to the study in the journal Cell Stem Cell. The study focused on human chromosome 21 gene OLIG2.

    “Our results suggest the OLIG2 gene is potentially an excellent prenatal therapeutic target to reverse abnormal embryonic brain development, rebalance the two types of neurons in the brain – excitatory and inhibitory, and a healthy balance is critical – as well as improve postnatal cognitive function,” said Peng Jiang, assistant professor in the Department of Cell Biology and Neuroscience at Rutgers University–New Brunswick.

    Usually, a baby is born with 46 chromosomes, but babies with Down syndrome have an extra copy of chromosome 21. That changes how a baby’s body and brain develops, which can lead to mental and physical challenges, according to the U.S. Centers for Disease Control and Prevention. Down syndrome is the most common chromosomal condition diagnosed in the United States, affecting about one in 700 babies, and about 6,000 infants are born each year with the condition.

    The researchers obtained skin cells collected from Down syndrome patients and genetically reprogrammed those cells to human-induced pluripotent stem cells (hiPSCs). Resembling embryonic stem cells, the special cells can develop into many different types of cells, including brain cells, during early life and growth and are useful tools for drug development and disease modeling, according to the National Institutes of Health.

    Using brain cells derived from stem cells with an extra copy of chromosome 21, the scientists developed the 3D brain organoid model, which resembles the early developing human brain. They also developed the mouse brain model, with stem cell-derived human brain cells implanted into the mouse brain within a day after the mice were born. They found that inhibitory neurons – which make your brain function smoothly – were overproduced in both models, and adult mice had impaired memory. They also found that the OLIG2 gene plays a critical role in those effects and that inhibiting it led to improvements.

    The combination of the brain organoid and mouse brain model could be used to study other neurodevelopmental disorders such as autism spectrum disorder. It may also help scientists better understand the mechanisms in Alzheimer’s disease. Down syndrome patients often develop early-onset Alzheimer’s disease, Jiang noted.

    The study’s lead author is Ranjie Xu, a postdoctoral researcher in Jiang’s lab. Other Rutgers co-authors include Hyosung Kim, a former post-doc in Jiang’s lab; Ronald P. Hart, a professor in the Department of Cell Biology and Neuroscience at Rutgers–New Brunswick; Zhiping P. Pang, an associate professor in the Department of Neuroscience and Cell Biology at Rutgers Robert Wood Johnson Medical School, and Jing-Jing Liu, a former post-doc in Pang’s lab. Scientists at the University of Texas Health Science Center, Kent State University, and University of Nebraska Medical Center contributed to the study.

    See the full article here .


    Please help promote STEM in your local schools.

    Stem Education Coalition


    Rutgers, The State University of New Jersey, is a leading national research university and the state’s preeminent, comprehensive public institution of higher education. Rutgers is dedicated to teaching that meets the highest standards of excellence; to conducting research that breaks new ground; and to providing services, solutions, and clinical care that help individuals and the local, national, and global communities where they live.

    Founded in 1766, Rutgers teaches across the full educational spectrum: preschool to precollege; undergraduate to graduate; postdoctoral fellowships to residencies; and continuing education for professional and personal advancement.

    As a ’67 graduate of University college, second in my class, I am proud to be a member of

    Alpha Sigma Lamda, National Honor Society of non-tradional students.

  • richardmitnick 6:46 am on May 23, 2019 Permalink | Reply
    Tags: "Can AI help fight antibiotic-resistant superbugs?", , , , , Medicine   

    From CSIROscope: “Can AI help fight antibiotic-resistant superbugs?” 

    CSIRO bloc

    From CSIROscope

    23 May 2019
    Sian Stringer

    A sample of penicillin mould from Alexander Fleming himself. Image: Science Museum London

    Antibiotics. They’ve been our go-to for treating (and sometimes preventing) bacterial infections ever since Alexander Fleming found mould keeping bacteria in check in his petri dishes almost a century ago and figured it was worth investigating.

    But bacteria are shrewd. They were among the first life forms to inhabit Earth, and the fact they’re still here some 3.5 billion years later means they’re extremely resilient and capable of constant change to adapt to their environment.

    This adaptability, combined with our use of antibiotics, is contributing to a surge of antibiotic-resistant superbugs. And with the surge showing no signs of slowing, the global scientific community is working hard to find new ways to fight the resistance – before it’s too late.

    Antibiotics and what they’re good for

    Many antibiotics work by attacking specific parts of bacteria that human cells don’t have, such as cell walls, and can either stop bacteria from replicating or kill them outright.

    Along with antivirals and antimalarials, antifungals and antibiotics are classed as “antimicrobials”, agents that target microorganisms. Medicine involves an arsenal of antimicrobials critical in fighting a huge range of infections, with antibiotics used against the bugs responsible for infections like pneumonia, food poisoning, and even surgery-related infections.

    For a little light reading, check out the World Health Organization’s list of the most critical antimicrobials for human medicine.


    The rise of antimicrobial-resistant superbugs

    Antimicrobial resistance (or AMR for short) is a resistance that a microorganism can develop against the treatments we use to wipe them out.

    Infections such as tuberculosis, sepsis and pneumonia are becoming harder to treat as bacteria develop resistances to existing treatments and spread themselves globally through their human hosts. Even surgery and cancer chemotherapy would become less successful if we lost the ability to prevent or treat related infections.

    It’s a scary thought.

    Why are bugs getting stronger?

    There is a range of reasons why AMR is spreading. While a certain level of resistance does naturally occur over time, it’s been accelerated by the overuse and misuse of antimicrobials, giving bacteria more opportunity to build up resistance.

    Because of their effectiveness, antibiotics have sometimes become the go-to answer for illness, even when they don’t work (such as for colds and flu) and people sometimes self-medicate with antibiotics from old prescriptions they haven’t used. Even something as seemingly harmless as not finishing the full course of antibiotics can be a problem: this can leave a small leftover bunch of bacteria and give them the opportunity to build up a tolerance to the drug.

    Antibiotics have also been widely used for animal health, including preventing disease in healthy animals. And the problem with AMR microbes is that they’re not fussy about where they live – they can be found in humans, animals, our food, and even in our water, air and dirt – so they’re good at spreading across environments.

    It’s estimated that resistant bugs could kill 10 million people every year by 2050. We’re essentially in a race against AMR superbugs to develop new treatments for life-threatening infections before existing treatments stop working.

    Resistance isn’t useless: The resistance against resistance


    Antimicrobial resistance is a huge and immediate challenge faced not only by Australians but by everyone around the world. So we’re forging ahead in the effort to find ways to manage or overcome it.

    A team of our researchers, specialising in areas including biosecurity, digital health and risk assessments, are all contributing their expertise to a new collaboration called OUTBREAK. It’s funded by the Medical Research Future Fund and led by the University of Technology Sydney, in partnership with other organisations around Australia, the UK and New Zealand.

    Over the next year, the OUTBREAK project will scope out an Australia-wide, artificial intelligence-powered knowledge engine against AMR, based on a “One Health” approach – the interconnection between human, animal and environmental health.

    This knowledge engine would aim to pull together streams of data from people, animals and the environment so we can get real-time information about AMR hotspots, track the spread of superbugs and infectious diseases, and provide early warnings and other critical information to help leaders make informed decisions about public health and biosecurity.

    In the long term, the engine could be a powerful tool for improving our understanding of AMR and finding ways to work around it.

    Big data and biosecurity are key

    We’re harnessing big data to find big solutions in the fight against superbugs

    The amount of information OUTBREAK is hoping to pull together is huge. It could include bacterial genome sequences, land use, location of specific facilities such as waste water recycling plants and hospitals, data about antibiotic prescriptions, and infection data, alongside geospatial mapping to link data to its physical location. We’ll then need some way to make sense of all that data.

    And that’s where transformational bioinformatics comes into the fold! Our Australian e-Health Research Centre’s Dr Denis Bauer and her Transformational Bioinformatics team use AI and machine learning to find new ways to make sense of huge amounts of data.

    “Finding the tell-tale signs of acquired resistance in the genome of micro-organisms is computationally intensive, especially since we don’t want to miss anything or raise a false alarm,” Denis says.

    “It’s like trying to find a specific and unique grain of sand on the beach.”

    So Denis and her team will channel their combined knowledge in helping to analyse the data from OUTBREAK, which ultimately could also be applied to detecting and tracking emerging infectious disease.

    Dr Paul De Barro, our Risk and Evaluation Preparedness Program Director and an infectious disease guru, is also part of the OUTBREAK project and says biosecurity will play a massive role in the resistance against resistance.

    “Strengthening our people, animals and environments against emerging diseases in the face of growing populations, climate change and increased international trade is critically important,” Paul says.

    “Antibiotic resistance threatens to totally up-end our existing medical approaches to managing infectious diseases, so we’re hopeful OUTBREAK has the potential to become an important tool in the race against antimicrobial resistance.”

    See the full article here .


    Please help promote STEM in your local schools.

    Stem Education Coalition

    SKA/ASKAP radio telescope at the Murchison Radio-astronomy Observatory (MRO) in Mid West region of Western Australia

    So what can we expect these new radio projects to discover? We have no idea, but history tells us that they are almost certain to deliver some major surprises.

    Making these new discoveries may not be so simple. Gone are the days when astronomers could just notice something odd as they browse their tables and graphs.

    Nowadays, astronomers are more likely to be distilling their answers from carefully-posed queries to databases containing petabytes of data. Human brains are just not up to the job of making unexpected discoveries in these circumstances, and instead we will need to develop “learning machines” to help us discover the unexpected.

    With the right tools and careful insight, who knows what we might find.

    CSIRO campus

    CSIRO, the Commonwealth Scientific and Industrial Research Organisation, is Australia’s national science agency and one of the largest and most diverse research agencies in the world.

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