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  • richardmitnick 8:15 pm on March 22, 2018 Permalink | Reply
    Tags: , , , New England Is Sitting on a Bed of Hot Rocks, , Scientific American   

    From Rutgers via Scientific American: “New England Is Sitting on a Bed of Hot Rocks” 

    Rutgers smaller
    Our once and future Great Seal.

    Rutgers University

    Scientific American

    April 2018
    Shannon Hall

    Colorful forests fill the landscape in the Berkshires of western Massachusetts.
    Photograph by Berthold Steinhilber, laif, Redux, courtesy of natgeo.com, which also provided the link to the article in Geology, which Scientific American was to lazy to do. Looking for the link is how I found the photo.

    Credit: Thomas Fuchs

    For the past 200 million years New England has been a place without intense geologic change. With few exceptions, there have been no rumbling volcanoes or major earthquakes. But it might be on the verge of awakening.

    Findings published this January in Geology show a bubble of hot rock rising underneath the northern Appalachian Mountains. The feature was first detected in 2016 by EarthScope, a collection of thousands of seismic instruments sprinkled throughout the U.S. Vadim Levin, a geophysicist at Rutgers University, says this wealth of sensors lets earth scientists peer under the North American continent, just as the Hubble Space Telescope has enabled astronomers to gaze deep into the night sky. Should the broiling rock breach the surface—which could happen, though not until tens of millions of years from now—it would transform New England into a burbling volcanic landscape.

    The finding has sparked many questions, given that New England is not located along an active plate margin (where one tectonic plate rubs against another) but sits squarely in the middle of the North American plate. The exact source of the hot rock bubble, for example, is unclear. Because the edge of the North American continent is colder than a plate near an active margin, Levin suspects this edge is cooling the mantle—the layer just below the crust that extends toward the earth’s core. As cold chunks of mantle sink, they may displace hotter segments, which would rise toward the surface. Scientists believe they have now imaged such an ascending piece. Although it sounds simple, this scenario “is a story that at present does not have a place in a textbook,” Levin says.

    Or perhaps pieces of the North American continent are breaking off and sinking into the mantle (which would also push the warmer mantle upward), observes William Menke, a geophysicist at Columbia University, who was not part of the study.

    Scientists do not yet know which model is correct or if an entirely different one may be involved. Levin and his colleagues are eager to collect more data to bring this unusual hotspot into sharper focus and, in doing so, flesh out the theory of plate tectonics. “We know little about the interior of our planet, and every time we look with a new light … we find things we did not expect,” Levin says. “When we do, we need to rethink our understanding of how the planet functions.”

    See the full article here .

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    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.

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  • richardmitnick 1:37 pm on October 9, 2017 Permalink | Reply
    Tags: Anxiety may seem to be a prominent feature of autism but it is not one of the diagnostic criteria, , Autism and Anxiety, Children with autism may be inherently more likely to develop anxiety than their typical peers, Scientific American, Why a fear of the unknown is a strong feature of autism is less clear   

    From SA: “Unmasking Anxiety in Autism” 

    Scientific American

    Scientific American

    October 9, 2017
    Jessica Wright

    Anxiety can assume unusual forms—turning uncertainty, or even a striped couch, into a constant worry.

    Credit: Corey Brickley, Spectrum.

    No one except Gregory Kapothanasis knows exactly what upset him today. On this hot day in July, he went to his day program for adults with developmental disabilities, as he has done without incident five days a week for the past four years. But then things unraveled. According to the program’s report, he grabbed a staff member’s arm hard enough to bruise it. Then, on the bus during the daily outing, he started screaming and hitting his seat. Now, several hours later, he is finally home, but there is a stranger in his living room. Bouncing from one couch to another, clutching a faded beige blanket stolen from his aunt’s dog, Kapothanasis still seems out of sorts.

    His mother, Irene — who has cared for him, with the help of home aides, for all of his 24 years — is playing over the day’s events, trying to figure out what triggered him. His outburst is disturbingly reminiscent of a difficult period that peaked six years ago but is uncharacteristic of the young man today. Kapothanasis loves interacting with other people, going to the beach and dining at DiMillo’s, a floating restaurant in a decommissioned car ferry in Portland, Maine.

    Kapothanasis has autism and speaks only a few words: He can’t explain what happened this morning. Did he have constipation and discomfort, as his doctor suggested? Did he get bored of the day’s program, causing him to act out? Had something occurred on the bus previously that made him fear that part of his day? All his mother can do is wonder — and try to make his evening better.

    Kapothanasis places several pieces of gum in his mouth, something his mother says soothes him. Then he curls up for a nap and dozes off. The time it takes him to calm down is short compared with the protracted meltdowns that routinely overtook him during his teen years. He became aggressive starting in puberty: He would bite and hit himself, or hit and grab other students, teachers and bus drivers. His mother had to supervise his interactions with his siblings, even though, as triplets, they had always been close. In December 2011, when he was 18 years old and over 6 feet tall, his behaviors had escalated so much that his school enrolled him at the inpatient clinic at Spring Harbor Hospital in Maine.

    “Look, we all have scars from Gregory, we’ve all felt his wrath. And it came to the point where he had to be institutionalized,” his mother says. He spent five long weeks at the hospital. “It was probably one of the darkest moments in our lives,” she says.

    When Kapothanasis arrived at the hospital, he didn’t seem sad, cried only on occasion and didn’t respond to things not visible to others — signs he did not have depression or psychosis. But he startled easily, paced and rocked in place, and sweated heavily. “The phrase ‘cat on a hot tin roof’ was pretty descriptive,” recalls Matthew Siegel, director of the developmental disorders program at the hospital.

    After several weeks of close observation, Siegel and his colleagues managed to piece together Kapothanasis’ behaviors into a clear diagnosis, based on criteria outlined in the “Diagnostic and Statistical Manual of Mental Disorders.” In addition to his autism, “he was kind of screaming anxiety — if you’re looking for it,” Siegel says. Until then, it seems no one had been. When Kapothanasis entered the clinic, he was on his third antipsychotic medication. Some are approved to treat aggression as a feature of autism, but none treat anxiety. “It’s fair to say that he was not being treated for anxiety,” Siegel says.

    There are many reasons it took nearly six years for Kapothanasis to get the help he needed. Doctors may have assumed that his aggression and tendency to hurt himself were part of his autism, Siegel says. Traits that characterize autism — including social deficits, stereotyped movements and restricted interests — can mask or mimic symptoms of anxiety. During a visit to an outpatient clinic, for example, Siegel points out a nonverbal young woman with autism who repeatedly traces a pattern in the air with her hands. At first glance, her gestures resemble ‘stimming,’ the repetitive behaviors often seen in autism. But she does it at specific times, Siegel says, suggesting a ritual related to obsessive-compulsive disorder — a form of anxiety.

    Compounding the problem, many people on the spectrum, like Kapothanasis, cannot tell their caregivers or doctors what they are feeling or thinking. Those who can may still struggle to identify and understand their own emotions — a phenomenon called alexithymia — or to articulate them to others. Because of these factors, the clinical questionnaires designed to ferret out anxiety traits in neurotypical individuals are woefully inadequate for many people with autism. The tests may also miss children with autism, who can have unusual phobias, such as a fear of striped couches or exposed pipes.

    “People on the spectrum have really unique, distinct ways of perceiving the world, and also have distinct experiences, which is why we’ll see classic things like social phobia and generalized anxiety, but also maybe these more distinct, more autism-related manifestations,” says psychologist Connor Kerns, assistant research professor at the A.J. Drexel Autism Institute in Philadelphia. Kerns and others are working on new ways to measure both ordinary and unusual forms of anxiety in people with autism. This work could help clinicians better detect the anxiety that hides behind autism, reveal the underlying mechanisms and lead to better treatment.

    Hiding in plain sight:

    Anxiety may seem to be a prominent feature of autism, but it is not one of the diagnostic criteria. “People say, ‘Oh, it’s just part of autism, everyone with autism has anxiety.’ That is 100 percent not true,” Siegel says. “I’ve got 12 kids sitting outside my door at my hospital right now, and several of them do not have anxiety.”

    Studies attempting to pin down the proportion of people with autism who also have clinically significant anxiety have produced a staggeringly broad range, from 11 to 84 percent. The discrepancy in these reported rates is “fundamentally unbelievable,” says Lawrence Scahill, professor of pediatrics at Emory University in Atlanta. “Whenever you see a range like that, you know that it’s driven by the source of the sample, where they got the sample from, the methods used to do the assessment and how quick they were to pull the trigger on a diagnosis.”

    What is believable, he says, is that autism and anxiety are not independent conditions that sometimes co-occur. In fact, children with autism may be inherently more likely to develop anxiety than their typical peers. But the overlap in features between the two conditions makes diagnosing anxiety extremely difficult. “I’m convinced that the measurement of anxiety in children with autism has to be different,” Scahill says.

    The traditional tests for anxiety, such as the Screen for Child Anxiety-Related Emotional Disorders and the Spence Children’s Anxiety Scale, rarely hold up as well in children with autism as they do in the groups they were designed for. In a 2013 study, Scahill and his colleagues investigated one particular test — the 20-item anxiety scale of the Child and Adolescent Symptom Inventory (CASI) — in parents of 415 children with autism.

    How the researchers framed the test’s questions significantly affected how the parents responded. Less than 5 percent of the parents endorsed statements describing anxiety that require a child to express herself — for instance, “worries about physical health” or “complains about feeling sick when separation is expected.” By contrast, parents were most likely to agree with statements that rely on their observations, such as “acts restless or edgy.” This trend was especially true among parents whose children have intellectual disability.

    Based on their findings, Scahill and his colleagues decided to talk to parents as part of their efforts to develop a measure of anxiety specific to children with autism. Over the course of six focus groups, which yielded more than 600 pages of transcripts, the researchers interviewed the parents of 45 children who have both autism and anxiety. They encouraged the parents to describe their child’s behaviors rather than make inferences about what the child was thinking. They then used these observations to formulate 52 questions. The trick to deciding which questions to ask, Scahill says, was not letting features of autism “leak” into them. Many parents talked about meltdowns but, when pressed for more detail, agreed they couldn’t tell the difference between meltdowns caused by anxiety and those that crop up for other reasons related to autism. Using meltdowns to flag anxiety in children with autism would have been a mistake, Scahill says. Instead, the focus group responses pointed to new indicators, including “Gets stuck on what might go wrong” and “Needs a lot of reassurance that things will work out.”

    Credit: Spectrum

    In unpublished data, the researchers combined the 52 new questions with the 20 questions on the CASI and gave them to 990 parents of children with autism. Based on the responses, they weeded out 31 items that were either redundant, seemingly irrelevant or rarely endorsed by the parents. Based on the remaining 41 queries, they found that roughly one-quarter of the children in the study have high levels of anxiety, another quarter have low levels of anxiety, and the rest fall somewhere in between.

    The researchers plan to test whether the measure is reliable over time, evaluating the same children with 10-day breaks between sessions. If the screen proves reliable, Scahill says, it might also be used to assess the efficacy of anxiety treatments in children with autism. “We have more to offer the treatment of anxiety right now than we have for the core features of autism,” he says. “So it behooves us, in my opinion, to be tough-minded about making sure we’re measuring anxiety and not something else.”

    Into the unknown:

    Erik Chaston, a 29-year-old graduate of Brigham Young University in Provo, Utah, works at a credit union, developing detailed workflows for the bank’s employees. Chaston, who has autism, has won awards for his clear and surprisingly entertaining videos that elucidate the supply-chain process. But for years, he was also fixated on the faint clicking noises people make with their saliva when they talk.

    As a student, while working as a sound engineer for the campus sports channel, Chaston began obsessing over fixing these and other sounds in his recordings. “It made me feel like I was constantly worried about things, because everyone talks like this,” he says. He held it together and excelled at work, but would shut down around his family. After he graduated, the problem seeded fears about what kind of job he would be able to hold down. The uncertainty made him especially anxious, he recalls.

    This intolerance of uncertainty is a common refrain among people with autism and their parents. For many people on the spectrum, this feeling may simply be an expression of one of autism’s core features — for instance, it may relate to inflexibility in the need to have enough time for a special interest or a fixation. But if that fixation turns into a source of constant fear or worry, it may in fact be an expression of anxiety, researchers say. “To me, it makes a lot of sense that it’s something about the sticky element of the brains of people on the spectrum that would also lead them to have anxiety about change,” Kerns says.

    In 2014, Kerns and her colleagues developed an adapted version of the Anxiety Disorders Interview Schedule (ADIS) — a one- to two-hour clinical interview with both parents and children, designed to flag anxiety. Based on interviews with 59 children who have autism and their parents, the researchers documented examples of anxiety that don’t fit the standard definition. Although nearly half of the children had traditional forms of anxiety, 18 of them also showed signs of non-traditional anxiety; another 9 children showed only the unusual forms of anxiety, such as an intolerance of uncertainty.

    So Kerns and her colleagues expanded their ‘ASD-specific addendum’ to flag non-traditional anxiety traits that the standard screen might miss: fear of novelty or uncertainty; fear of social situations for reasons other than social ridicule; excessive worry about being able to engage in a special interest; and unusual phobias. The section on fearing change asks, for example, “Does your child react if the change is positive (e.g., getting out of school early)?” The addendum also includes questions about a child’s social skills, sensory sensitivities and repetitive behaviors to help clinicians differentiate anxiety from autism features. For instance, it asks about a child’s history with bullying or social rejection to clarify whether a child is avoiding social events for a good reason — because her bully might attend — or because she is so traumatized by bullying that she fears any social outing. Only the latter would qualify as anxiety. “We want to look for when anxiety has overgrown the actual threat,” Kerns says. Her work solidifies what many clinicians knew anecdotally. “[Kerns] put a description to something that we had been seeing but didn’t have a word for,” Siegel says.

    Why a fear of the unknown is a strong feature of autism is less clear. Some researchers speculate that people with autism have trouble predicting future events, heightening their sense of uncertainty. Other work implicates sensory sensitivities and poor verbal comprehension, suggesting that different aspects of autism feed into this type of anxiety.

    Scientists are also looking for less subjective ways to measure anxiety in autism using various physiological and brain-imaging methods. John Herrington at the Children’s Hospital of Philadelphia and his colleagues are in the midst of a long-term study of 150 children, roughly half of whom have autism, looking at measures of stress, such as heart rate variability and sweat levels. They are also using a technology that tracks where someone is looking to try to distinguish a lack of social interest from social anxiety. Initial findings from their brain-imaging data suggest that the amygdala, a brain region involved in making fearful associations, is smaller in children with autism and anxiety than in those with autism alone.

    Another team is also homing in on the amygdala. Mikle South’s team at Brigham Young University is exploring the theory that instead of having an overactive fear response, people with autism have trouble finding a ‘safe space’ and, as a result, are afraid of everything. To test that idea, he is interviewing some adults with autism about their specific fears and scanning others’ brains. More than half of the people he talks to are consumed with worry, he says. “They worry about so much all of the time, they worry about everything,” South says. “There’s nothing they’re not worrying about.”

    Confronting fears:

    Breaking the cycle of fear is never easy, but it may be especially difficult for someone with autism. For Chaston, help came from what he considered an unexpected source — a self-help book on mindfulness that his mother foisted on him. Practicing mindfulness helped him develop strategies to deal with things that annoyed him. The best-documented approach for treating anxiety in children with autism, cognitive behavioral therapy (CBT), works on similar principles. CBT combines talk therapy with repeated exposures to the source of the fear to change unhelpful thought patterns and behaviors.

    That said, many children with autism may not benefit from traditional forms of CBT, says Eric Storch, professor of psychology at the University of South Florida in Tampa. Storch’s team has found that children with autism who benefit from CBT do not always maintain those gains: Those who improve only a little sometimes do much better one to two years later, whereas some of those who respond well later relapse. “It wasn’t sticking the way we would predict,” Storch says. The findings suggest that children with autism need therapy for longer, and with more follow-up, than their typical peers — “a critical difference in the treatment approach,” he says.

    Children with autism also have trouble generalizing lessons learned in therapy to other aspects of their lives. That means it is especially important to include their caregivers in treatment, because these adults can reinforce the lessons throughout the child’s day, Storch says.

    Credit: Spectrum

    To incorporate some of this extra support, a team at the University of California, Los Angeles developed a modified version of CBT, called the Behavioral Interventions for Children with Autism. The revision recommends, for example, that doctors and parents help a child to master appropriate social behaviors before putting the child in a feared social situation. Confronting situations that make the child anxious is crucial to the therapy’s success, Storch says. The modification also offers extra help for children who may feel socially isolated, having therapists work with schools to give these children peers who can guide them through social situations.

    A small 2009 trial suggested that anxiety levels in most children with autism abate after they receive this modified version of CBT. A follow-up analysis found that another version of CBT adjusted for adolescents with autism is just as effective. A team of researchers, including Storch and Kerns, plans to compare the modified version with other therapies in children with autism in a 16-week trial of 180 children. Children who have autism and clinically diagnosed anxiety will receive either the modified or the traditional form of CBT, or will continue with whatever treatment they received before.

    Their parents will also take the ADIS, along with Kerns’ addendum. It is possible that the children who have non-traditional anxiety will benefit the most from a modified treatment, Kerns says.

    However successful, CBT cannot be the only option for children with autism, notes Roma Vasa, a child and adolescent psychiatrist at the Kennedy Krieger Institute in Baltimore. “There’s a lot of variability in how much they can really report on their internal experience and how connected they are with their thoughts and their feelings,” she says. “There needs to be more trials of effective medication to help these kids.”

    There are no drugs approved for treating anxiety in autism. Last year, Vasa and her colleagues published a set of recommendations for clinicians who prescribe anxiety drugs to children on the spectrum. Among her guidelines: Raise doses slowly, as these drugs may exacerbate irritability.

    In Kapothanasis’ case, drugs to treat his anxiety, including fluoxetine and guanfacine, turned out to be extremely helpful. Still, Siegel’s team didn’t rely on medications alone to treat him. They discovered that Kapothanasis had no real means of communicating. His aides at school had told his mother that he could, for example, ask for a bottle of water by handing over a drawing of it. But the speech-language pathologists in the hospital realized he really had no idea how to use this picture-exchange system. They helped him learn a new system, in which he points to photos of things from his daily life rather than to cartoon depictions of them. They prepared a visual schedule that lets him know what to expect each day. And, perhaps most valuable, according to his mother, is that they found new ways for him to soothe himself: by bouncing on a yoga ball or running his hands through tubs of uncooked rice.

    These tactics are ones that now, years later, can still turn a bad day around. When Kapothanasis wakes from his catnap, he ambles over to the kitchen and makes himself a snack. Back in the living room, he spots a blue fleece blanket his mother has laid out for him in front of the television, a plastic bowl filled with uncooked rice in the center.

    As he walks over to the rice, the tension in the air thins palpably. Contorting his large body into a pretzel shape and leaning close to the blanket, Kapothanasis dumps out the container’s contents. Then, carefully placing the bowl in front of him, he scoops up handfuls of rice and lets them fall through his fingers in soft streams down his forehead. The grains tap out a staccato beat as they land in the bowl. Once it is full, he empties the bowl and begins again. And again … and again. After a while, he looks up, faces the stranger in the room for the first time. And smiles.

    See the full article here .

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  • richardmitnick 12:22 pm on December 29, 2016 Permalink | Reply
    Tags: , , CAR-T therapy, , Scientific American   

    From SA: “Experimental Cancer Therapy Makes Inroads Treating Brain Cancer” 

    Scientific American

    Scientific American

    December 29, 2016
    Meghana Keshavan

    The immunotherapy approach may soon be commercially available for leukemia and lymphoma.

    Credit: Akira Ohgaki Flickr (CC BY 2.0)

    Glioblastoma is one of the deadliest cancers — an illness that responds to few treatment options, and often poorly. But a single case study that uses an experimental immunotherapy to treat these brain tumors might give oncologists a new way to approach the disease.

    The therapy, called CAR-T, is controversial and has faced hurdles in clinical trials. It has shown great promise in treating blood cancers like leukemia and lymphoma — but has proven challenging in treating other forms of the disease, including solid tumors.

    “This is the first example of CAR-T working in solid tumor cancers,” said Dr. Behnam Badie, chief of neurosurgery at City of Hope and a key investigator in the study. “In the initial treatments, I was holding my breath, waiting to get called in the middle of the night to go rescue somebody. But it’s amazing how safe it was.”

    The results are being published this week in the New England Journal of Medicine.

    Researchers at the City of Hope cancer treatment center in the Los Angeles Area tested a CAR-T therapy out on a 50-year-old man with recurrent multifocal glioblastoma — that is, several tumors growing in tandem in his brain. He had failed all other available treatments.

    CAR-T therapy involves extracting a patient’s immune cells, re-engineering them to learn how to target their cancer, and then feeding them back into the body. Surgeons removed the tumors, and then infused the experimental cellular therapy directly to the regions where the cancer had grown (other CAR-T treatment protocols are usually intravenous).

    The patient was in remission for about seven months after the CAR-T infusions began. The tumors did come back — but not in the areas that responded to the T cells, Badie said.

    This experimental therapy may soon be available commercially for certain blood cancers, as two drug makers — Novartis and Kite Pharma — are on the verge of filing for approval with the Food and Drug Administration.

    The glioblastoma therapy targets cells with the IL-13Rα2 antigen, a receptor which is found commonly on cells in brain tumors. City of Hope researchers are testing out a number of other antigens specific to brain cancers, Badie said, though they’re not disclosing which.

    Notably, the treatment was fairly innocuous, Badie said, which was certainly unexpected, since CAR-T therapy is notorious for its adverse events. In particular, Badie said he was bracing himself for neurotoxicity:

    “The results were really dramatic,” Badie said. “My own father passed from glioblastoma 10 years ago — and I never imagined we’d get to this stage so fast.”

    There have been other trials studying CAR-T’s efficacy in glioblastoma, but with intravenous application. The results from this one patient, Badie said, were good initial evidence that delivering CAR-T to the tumor site itself, rather than intravenously, might enhance efficacy. Badie said he believes that, based on this study, CAR-T could prove to be potent in other solid tumor cancers — particularly pediatric brain cancers.

    The results spurred both cautious optimism — and a dose of skepticism.

    “I can’t say this paper’s solved the problem of solid tumors, or this is the way to treat them,” said Dr. Jae Park, a hematologist-oncologist who specializes in CAR-T therapy at Memorial Sloan Kettering Cancer Center. “But it’s the first trial to show an objective response in glioblastoma, and suggests this is one way to get around the limitations of CAR-T.”

    But it’s a “flash in the pan,” according to Dr. Vinay Prasad, a hematologist-oncologist at the Oregon Health and Sciences University.

    “Even though this was a provocative case, even in this one case the cancer has already returned,” Prasad said in an email. “Will CAR-T work for other patients? Will it help most patients? Will it be better than alternatives? And will patients live longer or live better? We don’t know.”

    See the full article here .

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  • richardmitnick 11:51 am on December 29, 2016 Permalink | Reply
    Tags: , Are Giant Sequoia Trees Succumbing to Drought?, , Scientific American   

    From SA: “Are Giant Sequoia Trees Succumbing to Drought?” 

    Scientific American

    Scientific American

    Thayer Walker
    Video and Photographs by Novus Select

    Researchers climb 300 feet to the tops of thousand-year-old trees to analyze how they are faring.


    By the time John Muir and his trusty mule Brownie splashed across the Marble Fork of the Kaweah River in the fall of 1875, the Scottish-born naturalist had already seen his fair share of California grandiosity: Yosemite Valley; the high Sierra; Mariposa Grove. Muir had a thirst for exploration and a talent for storytelling. He founded the Sierra Club and dubbed its eponymous mountains the “Range of Light.” When Muir sauntered upon a montane plateau in what is now known as Sequoia National Park on that autumn day, he found a very large stand of very large trees. Drawing his poetry from the obvious he named it, quite simply, the Giant Forest.

    The dominant feature of the Giant Forest is the giant sequoia (Sequoiadendron giganteum), the biggest tree on Earth. Thousands of them grow in this 2,300-acre grove, including five of the ten largest specimens in the world. They reach heights of nearly 300 feet; their trunks can span more than 30 feet; and they’re nearly impossible to miss if you’re tromping beneath their canopy. “In every direction Sequoia ruled the woods…” Muir waxed in Our National Parks, “a magnificent growth of giants grouped in pure temple groves.” And yet, at 4:00 a.m. on a warm August morning, our hearty group of scientists and climbers is having a tough time finding the damn things.

    “I feel like we’ve gone too far,” says forest ecologist Wendy Baxter, 36, stopping the group. The ivory glow of a full moon offers enough illumination to hike without fear of face-planting, but it makes for a poor navigational beacon.

    It’s the fourth day of two weeks of fieldwork led by Baxter and fellow forest ecologist Anthony Ambrose. Scientists at UC Berkeley’s Dawson Research Lab, the two are part of Leaf to Landscape, a program in collaboration with the United States Geological Survey, the National Park Service, and the Carnegie Airborne Observatory, that is focused on studying and managing the health of the giant sequoias.

    California, of course, is in the middle of a historically punishing drought at a time when there’s never been more demand for water. According to the United States Forest Service, 62 million trees have died in California this year alone. Since 2011, a total of 102 million trees have perished, with tens of millions more on death’s doorstep. California’s forests generate fundamental ecosystem services by creating healthy watersheds, providing wildlife habitat, and sequestering atmospheric carbon, and they’re dying at unprecedented rates. Even the great giant sequoias are showing concerning signs of stress. It’s Ambrose and Baxter’s goal to collect and analyze tree samples to understand how the sequoias are faring under these rapidly changing conditions, and what might be done to protect them. But first we have to find them.

    “Have we come to any intersections at all?” asks Ambrose, 48, whose attention has been focused on answering my questions instead of spotting landmarks.

    “I remember this tree, for sure,” someone chirps, a sentiment that seems more appropriate as an epitaph on a lost hiker’s headstone than as a vote of directional confidence. After a brief parley, we correct our course up a gentle rise, down into a shallow basin, and past a pair of landmarks, unmistakable even at this dark hour.


    The path splits twin sylvan towers standing inches apart and hundreds of feet tall. It’s still too dark to marvel at their height, but the base of each tree inspires awe enough, gnarled and bulbous and swelling with woody knuckles the size of a Toyota Prius. A few hundred yards farther, the trail continues through the hollowed-out center of another sequoia. Fire, the great creator and destroyer, Kali of the Giant Forest, raged here long ago, burning out the tree’s core. The wound is enormous, 40 feet tall or more and nearly the size of the tree’s entire 12-foot diameter. Yet the grand monarch survived the blaze, which also would have cooked off the thick layers of duff that choke seedling growth, offering tiny sequoias a chance to one day touch the sky and survive their own infernos.

    The group splits apart at the meadow, each climber heading to the tree they’ll be sampling. The scientists have targeted 50 sequoias for study—“the biggest, gnarliest trees in the forest,” Ambrose says—and this morning he’ll climb a 241-footer. In most other forests a tree like this would be a star attraction with an honorific name and perhaps even a viewing area. Here, it’s simply known as “tree 271.”

    Ambrose has striking blue eyes and wears a woodsman’s beard with a chinstrap of white whiskers. He slides on his climbing harness and tugs the rope anchored to the crown some 24 stories above. He’s been studying trees for more than two decades, first with a focus on coast redwoods (Sequoia sempervirens) as an undergraduate and master’s student at Humboldt State University, and then on giant sequoias for his doctoral and post-doc work at Berkeley. “From an aesthetic perspective to a biological one, these trees are some of the most spectacular organisms on the planet,” he says with the enthusiasm of a boxing promoter. “They are the pinnacle of what a plant can become. They force you to think about life and your own place in it.”


    He clips on a pair of jumar ascenders—mechanical devices that attach to the rope and allow him to pull himself up. “You can’t really understand the true character of a tree from the ground,” he says. Ambrose turns off his headlamp, cranes his head toward the canopy, and begins the long, dark climb into a world of mystery.

    The giant sequoia has dominated its landscape for millions of years and captivated global imagination since the mid-19th century when rumors of trees the size of fairy-tale beanstalks came roaring out of the Sierras. One of three redwood species, the giant sequoia is not the world’s tallest tree; that crown belongs to its northern cousin, the coast redwood. But in terms of sheer volume of biomass, no living organism ever to walk, swim, fly, or stand on this planet comes close. They are of such stature that people struggle to describe them and so compare them to other very big things: blue whales, 747s, dinosaurs, the Statue of Liberty, elephant herds, space shuttles. Giant sequoias make mice of them all.

    More than 100 million years ago, when the planet was warmer and wetter, the sequoia’s earliest relatives thrived across much of the Northern Hemisphere. Redwood fossils have been found everywhere from Northern Mexico and the Canadian Arctic to England. During the late Miocene, some 10 to 20 million years ago, the closest direct ancestor of the giant sequoia lived in what is now southern Idaho and western Nevada. As the Sierra Nevada Mountain Range continued its uplift and the climate became drier, the giants’ range shrank. Today, the last remaining sequoias are limited to 75 groves scattered along a narrow belt of the western Sierra Nevada, some 15 miles wide by 250 miles long.


    Giant sequoias are among the longest-living organisms on Earth. Though no one knows the trees’ absolute expiry date, the oldest ever recorded is 3,200 years old. Muir claimed to have found a stump with 4,000 tree rings, one per year. During their early years the trees are subject to predation and the volatile whims of nature. Once they reach adolescence after a few centuries, however, sequoias become well-nigh indestructible. Their bark is soft and fibrous and contains very little pitch, qualities that make the trees extremely resistant to fire. The tannins that give their wood a rich cinnamon hue also repel insects and fungi.

    When a mature sequoia does die, mortality is usually a function of its marvelous size. Root rot can deprive a tree of a solid anchor and fire can undermine its base, but rarely will either actually kill a 30-story monarch. Gravity is the ultimate culprit, for a giant sequoia with an uncertain foundation faces a violent and certain end. The persistent tug of gravity can pull an unbalanced tree to the forest floor with such a thunderous crash that the reverberation can be heard miles away. The sequoia’s fate is an Icarian allegory, met not by flying too close to the sun, but by stretching too far from its roots.

    Thanks largely to their ability to withstand disease and drought, it’s extremely rare for a giant sequoia to die standing upright. “You don’t get to be 2,000 years old without surviving a few dry spells,” Ambrose tells me. Which is exactly why United States Geological Survey forest ecologist Nate Stephenson was so alarmed when, in September 2014, he went for a walk in the Giant Forest and saw something unexpected.

    “I had been saying with confidence for decades that if you hit a big drought, the first signs of climatic changes would show up in seedlings,” recalls Stephenson, who has studied trees in Sequoia and Kings Canyon National Parks since 1979. “I was completely wrong.”


    He surveyed an area that had burned a few years prior, where seedlings had taken root. Crawling around on his hands and knees, Stephenson was surprised to see that the seedlings were rigid and full of water, their leaves a vibrant blue-green. This was the third year of drought in California, and the summer of 2014 was particularly brutal. There should be some evidence of drought stress, he thought. Sitting on the ground, he leaned back, craned his head toward the heavens to ponder the mystery, and found his answer.

    Above him stood a grand old monarch. The crown of the tree was almost entirely brown, a scale of dieback he’d never seen. He searched for other trees displaying similar stress and when he found one with branches close to the ground, he touched it. The foliage crumbled off. In more than 30 years of studying these trees Stephenson had only seen two die on their feet. Five years into the current drought, he’s now seen dozens of standing dead.

    Stephenson quickly assembled a team to survey the 2014 dieback before autumn storms could blow away the evidence. The National Park Service (NPS) enlisted Ambrose and Baxter to begin their fieldwork in 2015. While the NPS and scientists working in Montana’s Glacier National Park might already be resigned to a glacier-free future as the climate changes, no one is ready to consider the possibility of Sequoia without its namesake trees.

    “Headache!!!” Ambrose yells.

    His warning, the tree-climbing vernacular for plummeting deadfall, fills the forest moments before a branch whooshes passed, inches from my head. It happens so quickly, the broken limb has already hit the ground before I have a chance to move.

    “And that’s why we wear helmets when we work around trees,” he explains to the small group of us standing at the base of the sequoia.

    The lessons come quickly on our first day of fieldwork. We set up on a steep hillside and Baxter demonstrates how to prepare the rigging for a climb. Tall and lean with a strong jawline and a soft voice, she’s as comfortable doing stable isotope analysis in the lab as she is setting a 600-foot static line in a tree. “I love the combination of physical exertion and intellectual stimulation,” she tells me. “It’s a struggle to get to the top of the tree. You’re sweating and huffing and puffing, but that’s when you start collecting your samples and the science begins.”

    In 2015, Baxter and Ambrose did much of the work themselves, identifying and rigging 50 trees, making six climbs a day, and collecting samples and measurements from each one. Their days began at 2:30 a.m. and ended at 10 p.m.—if they were lucky. “That was brutal,” Baxter recalls.

    They have more help this time around. Over the course of two weeks, more than a dozen volunteers—students, professional arborists, climbing junkies—will rotate in and out. The schedule, while not nearly as frantic as the previous year, is aggressive. We wake up at 3 a.m. and begin our hike from the Crescent Meadow parking lot into the Giant Forest an hour later. After climbing trees and taking and analyzing samples all day, we head back to our campground for some R&R before collapsing into bed.

    The immediate goal is to understand the severity of water stress the trees are facing, the water content in the leaves, and the amount of the stable carbon-13 (13C) isotope the tree uses during photosynthesis, which offers additional insight into how the trees are coping with drought. With that information, scientists and park officials can assess the trees’ health and begin to think about ways to protect giant sequoias through practices like controlled burns, which clear the ground for seedlings and eliminate less fire-resistant trees that compete for water.

    Ambrose’s first exposure to forest management came as a wildland firefighter following his senior year of high school in Chico, California. The experience, he recalls, involved “hours of boredom followed by long stretches of terror,” and gave him a first-hand look at how a policy of aggressive fire suppression can have an adverse effect on forest ecosystems.

    For more than a century, the government’s approach toward forest fire has been one of suppression. But indiscriminately stamping out frequent, less intense, naturally occurring fires disrupts the natural process of consumption and rejuvenation that species like giant sequoias need to thrive. It also allows dangerous levels of fuels to pile up—until one explosive holocaust vaporizes everything. “You get these large landscape conversions, conifer forests turning into brush,” Ambrose says.

    In 2013, the Rim Fire swept through the Sierras, consuming more than 257,000 acres. It was the third largest fire in California’s recorded history and burned for 15 months. It never reached Sequoia National Park, but it did sweep through parts of Yosemite some 100 miles north. As a precautionary measure, officials even set sprinklers around of some of Yosemite’s giant sequoias in case the fire got too close.

    Stretching hundreds of feet into the air presents some very real physical challenges for giant sequoias. See how these massive trees have overcome gravity to become giants of the forest.

    Giant sequoias, like all trees, play a central role in the hydrologic cycle. Storms drop rain and snow, which giant sequoias can chug to the tune of 800 gallons per day—more than any other tree. As the trees draw water out of the ground, the air surrounding the leaves draws water through the trees and, eventually, back into the atmosphere. That process, called transpiration, creates tension within the tree’s water columns. The drier the atmosphere and the less groundwater available, the higher the tension. Under extreme drought conditions, when that tension grows too high, those columns of water can snap like a rubber band. Gas bubbles form, creating an embolism that prevents the flow of water up the trunk. If this happens enough, a tree will shed its leaves and can, eventually, die.

    To measure water tension and other biological processes, climbers sample each tree twice a day, once under cool pre-dawn conditions when the tree is least stressed, and once under the heat of the midday sun. The scientists clip foliage from the lower and upper canopies, which allows them to assess conditions at different parts of the tree.

    After the safety talk and rigging demonstration, Ambrose grabs a laminated map from his pack and assigns the climbers to their trees. Pulling on a forest-green arborist harness, he clips a pouch onto each hip to carry his samples. Then he steps into the foot straps attached to the ascenders and begins the climb.

    His arms, legs, and core work in an assembly line of movement. Hanging on the rope in a crouch, he slides his right arm up, follows with his left, pulls his knees to his chest, and stands up straight in the stirrups, at which point he repeats the routine—scores of times on his way to the top. Climbers call it “jugging,” a process as onomatopoeically laborious as it sounds.

    About 100 feet up, Ambrose stops at the lower canopy, marked by the first significant limbs, which can grow up to six feet in diameter. He clips a handful of tiny branches, puts them into a plastic bag, shoves the bag into his hip pouch, and continues climbing. The tree’s leaves regulate gas exchange through tiny pores called stomata. The stomata take in carbon dioxide and release oxygen and water vapor. When a tree becomes too water-stressed it closes its stomata. This stops water loss through transpiration but also prevents the tree from absorbing atmospheric carbon dioxide and using it for photosynthesis. Sequoias have vast carbon stores to help them weather these lean times, but if the stomata stay closed for too long, the trees will eventually starve to death.

    As Ambrose works in the tree, I take a short hike up to the top of a hill just above the study site, where the cost of California’s drought reveals itself in spectacular panorama. The Middle Fork of the Kaweah River plummets from the high Sierra into the agricultural empire of the San Joaquin Valley. Polished granite swells and the jagged sawtooth mountains of the Great Western Divide dominate the horizon; pine, fir, and cedar trees blanket the river basin. The colors are rich and electric, but they don’t all sit right. In a sea of green, huge islands of red metastasize across the landscape. These ochre forests are not sequoia. They are thousands and thousands and thousands of dead trees.

    Numerically speaking, giant sequoias constitute a small portion of California’s forest. A few weeks before my foray with Ambrose and Baxter, I hopped on a survey flight with Greg Asner, principal investigator at the Carnegie Airborne Observatory (CAO), to get a better understanding of what’s happening to trees across the entire state and what that might indicate for the future of the sequoias.

    Asner, 48, runs a flying laboratory called the Airborne Taxonomic Mapping System, a Dornier 228 airplane tricked out with $12 million of custom-built equipment that allows the CAO to measure the composition, chemistry, and structure of a forest in detail and efficiency that, not long ago, was relegated to the realm of science fiction. “In California,” said Asner, “we have exact numbers on 888 million trees.”

    We met at 7:30 a.m. at Sacramento’s McClellan Air Park. Dressed in snappy black flight suits, Asner and his four-man team were going through last-minute checks and waiting for the sun to climb higher in the sky, which would allow for more accurate measurements. The goal for the day: map a 3,600-square-mile section of northern California forest.

    Collecting such voluminous amounts of detailed data requires a unique toolbox. The plane itself is geared toward special mission work with its high-payload capacity and short takeoff and landing capabilities. An imaging spectrometer, resting atop a hole cut in the belly of the plane, absorbs light across the spectrum, from ultraviolet to short-wave infrared. It allows the CAO to measure 23 different chemicals in the trees, including water, nitrogen, and sugar content. To work properly, internal sensors within the imaging spectrometer are kept at -132 Celsius, atomically cold temperatures.

    A laser system next to the imaging spectrometer fires a pair of lasers from the bottom of the plane 500,000 times per second, creating a three-dimensional image of the terrain below, and every tree on it. A second spectrometer, this one with an enhanced zoom capacity, allows the team to take measurements of individual branches on a tree—from 12,000 feet up. Finally, a piece of equipment known as an Internal Measurement Unit records the X,Y, and Z axes as well as pitch, roll, and yaw of the plane to ensure that its positioning in the air doesn’t compromise the accuracy of the data it collects from the ground. “This unit is the same technology as what’s in the nose of a cruise missile,” Asner explained. “Because of that, the State Department has a say in what countries we visit.” The CAO studies forests all over the world—Peru, Malaysia, Panama, South Africa, Hawaii.

    Once airborne, we dismissed the sprawl of the Central Valley for the coastal mountains. To the naked eye, the Shasta-Trinity National Forest looked splendorous, 2.2 million acres of rivers and mountains. Mount Shasta, a 14,179-foot active volcano, was still holding on to a handsome cap of snow and the landscape was vibrant and green. Asner’s spectrometer shared a different story. “Visual assessment doesn’t tell you much,” he said. On his computer screen, the green trees below were all reading red. They were dead. We just couldn’t see it yet. “A lot of this was not here last year,” he said with the clinical efficiency of a doctor diagnosing a cancer patient. CAO’s statewide findings suggest tens of millions of trees might not survive another dry winter.

    Sugar pine (Pinus lambertiana), a species that grows in large, contiguous groves and can live 500 years, has been hit the hardest, accounting for some 70 percent of the mortality, but cedar, fir, and oak are all suffering as well. It’s not just the lack of precipitation that’s killing these trees; it’s the cascading effect of climate change. Water-stressed trees make easier targets for mountain pine beetles (Dendroctonus ponderosae), which lay their eggs in the trunk and eat the trees.

    Using data collected by and visualizations generated by the Carnegie Airborne Observatory (CAO), scientists and forest managers can see both the current and future impacts of drought on Sequoia National Park. Learn what CAO scientist Greg Asner sees in this image.

    Asner shared a map of the Giant Forest. The sequoias were a cool, comforting shade of blue, demonstrating high water content. Water seeks its low point, Asner explained, and the Giant Forest sits in a plateau cup. “It’s an oasis, a refugio. Right now, those trees are of least concern.” It was bittersweet news, like celebrating the last house standing after a tornado.

    “Drought is a cumulative process,” Asner explained as the plane made a long bank off the western slope of Shasta. “Forests have biological inertia. We don’t know where the physiological tipping point is. Currently, we’re losing carbon from the forest.”

    Forests are supposed to absorb carbon, so I wasn’t sure if I’d heard Asner correctly over the communication system. I tapped my headphones to make sure they were still working. “I’m sorry, did you just say the forests are releasing carbon into the atmosphere?” Automobiles, coal-fired power plants, cattle production—those are all carbon sources. But the mighty forests of California?

    “That’s my guess,” he said. “It’s hard to imagine the forests are still carbon sinks.”

    Of the hundreds of feet it takes to climb to the top of a giant sequoia, the first six are invariably the most difficult.

    After two days on the ground watching the rest of the team sliding up and down the sequoias, I ask Ambrose for a tutorial. Over the years, I’ve spent enough time on rock and rope to scratch my way up a 5.10, but tree climbing—beyond the scampering variety, anyway—is new territory.

    It looks easy enough. Ambrose has been powering into the canopy in minutes, and Baxter has a fancy one-legged technique that looks like she’s hopping on air. I, meanwhile, can barely get 12 inches off the ground. Those charming fire caves that serve as a window to ancient battles? They’re actually hazardous overhangs that cause a climber to pendulum into a cavern of charred pith. The two feet of duff piled up on the root system? That makes it just hard enough to get the clearance from the tree trunk needed to begin a comfortable climb. I’ve never done the splits, but with my feet strapped into the stirrups I find myself spinning, spread-eagled in endless, dizzying circles. Then I sprain my knee.


    If Ambrose and Baxter climb their ropes like graceful inchworms, I look like a marionette having a seizure. Eventually I reach the lower canopy but my knee feels like a water balloon in a pressure cooker and I’m a long way from mastering Baxter’s hop-along trick. I descend in the interest of doing more climbing later in the week.

    Back on the ground, I limp over to Ambrose and tell him of my failed attempt. “It’s tricky the first time. You want to avoid gripping the ascenders too tightly. And really, you shouldn’t be using your upper body very much at all. You mostly want to use knees and core.” Translation: The exact opposite of what I was doing.

    A few days later I get my chance on another pre-dawn climb. The tree is one of the largest individuals in the world—220 feet tall and 20 feet in diameter at the base—all the more impressive considering it’s growing in shallow soil atop a plate of granite. Underground, the tree’s been waging war with its rocky substrate for millennia, its roots probing every crack and fracture in a tireless search for water. I clear the first few feet without issue and begin the long journey to the top.


    The sequoia is shaped like a giant barrel, tall and fat with hardly a taper. For the first ten stories, the trunk is a sheer wall of wood with an uninterrupted profile. I pass the crown of a neighboring 90-foot pine before even reaching the first branch of the sequoia. As I enter the sprawling branch network of lower canopy, the climb shifts from a smooth glide to a bruising slugfest. I work my way over, around, and between branches, each the size of a normal tree. About half way up, a pair of branches five feet thick shoots out from opposite sides of the trunk and up in an L-shape, like two arms flexing in a proclamation of strength.

    Finally, the top. After 40 minutes of climbing, I take a seat to catch my breath. The crown is gargantuan. On one side a half dozen branches converge to create a bench wide enough for a square dance. It’s easy to get lost in the scale, but as my heart slows and the morning brightens, the subtleties stand out. Thousands of green cones the size of ping-pong balls hang from the branches like chandeliers. Unlike the lower sections of the tree, the bark here is smooth and seamless with a purple tint, and etched with fine lines like topographic contours. A menorah of knobby vertical branches, called reiterated trunks, sprouts out of the crown. I scamper up the last 10 feet and perch on the stumpy tip of one of the spires.



    The crowns of sequoias punctuate the tree line like bushy, green exclamation points. Surrounded only by a warm breeze and empty space, I find myself completely exposed and suffering through an emotional paradox. There’s freedom up here with the birds, a glorious release from anything familiar. But it’s a narrow liberty. The laws of gravity and my seismic discomfort of heights dissuade me from any spread-eagle “I’m King of The World” moments. A western tanager (Piranga ludoviciana) lands on a branch and swivels its bright red head toward me, confused by the interloper in its realm. On the forest floor, a black bear (Ursus americanus) lumbers about for breakfast. More people have summited Everest—more people have probably walked on the moon—than have stood atop this noble tree.

    “There is absolutely no limit to its existence,” John Muir wrote of the sequoia in Our National Parks. “Nothing hurts the big tree.” The sunrise, however, reveals an unsettling future. Even here, in the country’s second-oldest national park, the horizon is the sickly yellow of a cigarette butt, a vaporous mixture of Central Valley smog and forest fire smoke from the myriad infernos burning across the state.

    Muir’s hyperbole is understandable. The tree I’m sitting atop probably took root before Athenian democracy sprouted in ancient Greece. It has lived through the rise and fall of many of the world’s great civilizations, from Romans to Mayans to the British Empire. Its long shadow has spread over this forest for three millennia, but that can’t obscure the exhaust of human progress. As I clip my climbing descender onto the rope and begin the journey to the forest floor, I can’t help but wonder: Will this tree stand long enough to witness our own demise? Or will it fall first?

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  • richardmitnick 1:53 pm on December 8, 2016 Permalink | Reply
    Tags: , , Scientific American, Sweeping Health Bill Clears U.S. Senate   

    From SA: “Sweeping Health Bill Clears U.S. Senate” 

    Scientific American

    Scientific American

    December 7, 2016
    Toni Clarke

    Credit: Flickr / (CC BY 2.0)

    The U.S. Senate voted overwhelmingly on Wednesday to support sweeping legislation that will reshape the way the Food and Drug Administration approves new medicines.

    It will also provide funding for cancer and Alzheimer’s research, help fight the opioid epidemic, expand access to mental health treatment and advance research into precision medicine.

    Two years in the making, the 21st Century Cures Act was passed last week by the House of Representatives and will now go to President Barack Obama to sign into law. Supporters say it will speed access to new drugs and devices, in part by allowing clinical trials to be designed with fewer patients and cheaper, easier-to-achieve goals.

    “For the second consecutive year, the Senate is sending the President another Christmas miracle for his signature,” Senator Lamar Alexander, a Republican from Tennessee said in a statement. “Last year, it was the Every Student Succeeds Act, and this time, it’s the 21st Century Cures Act — a bill that will help virtually every American family.”

    Critics of the legislation say it gives massive handouts to the pharmaceutical industry and will lower standards for drug and medical device approvals.

    “This gift – which 1,300 lobbyists, mostly from pharmaceutical companies, helped sell – comes at the expense of patient safety by undermining requirements for ensuring safe and effective medications and medical devices,” consumer watchdog Public Citizen said in a statement.

    Democratic Senator Elizabeth Warren was among the handful of senators who voted against the bill, as was independent senator and former Democratic presidential candidate Bernie Sanders. Each decried what they described as big handouts to the pharma industry. Even so the bill passed 94-5. The House passed it by a vote of 392-26.

    The $6.3 billion act, sponsored by Republican Representative Fred Upton, authorizes $4.8 billion for the National Institutes of Health and $500 million to the Food and Drug Administration.

    It also calls for $1 billion over two years to battle the opioid epidemic. On Tuesday the Drug Enforcement Administration issued a report showing that in 2014 about 129 people died every day as a result of drug poisoning. Of those, 61 percent are opioid or heroin related.

    “Opioids such as heroin and fentanyl – and diverted prescription pain pills – are killing people in this country at a horrifying rate,” Acting Administrator Chuck Rosenberg said. “We face a public health crisis of historic proportions.”

    The bill also calls for $1.8 billion in funding for Vice President Joseph Biden’s Cancer Moonshot initiative designed to bolster cancer research by reducing bureaucracy and promoting research collaboration.

    Critics note that the money described in the bill must be appropriated by separate funding bills and that the money may ultimately never materialize. Yet the changes to the clinical trial process, something long sought by the drug industry, will be set in stone regardless of whether money for the research projects is forthcoming.

    Among those changes: Greater prominence will be given to “real world” evidence gathered outside the framework of a randomized, controlled clinical trial, the gold standard for determining whether a drug is safe and effective. Such evidence could be much easier for drug companies to collect.

    “The passing of 21st Century Cures Act is a show of extraordinary bipartisan unity after a divisive election that should be celebrated,” said Ellen Sigal, chair of the patient advocacy group Friends of Cancer Research.

    Under the Act patient input will be formally incorporated into the FDA’s drug review process.

    Funding for the Act will be offset by reductions in some Medicaid payments and through the sale of oil from the Strategic Petroleum Reserve. The White House supports the bill but said earlier it was concerned that draining the Petroleum Reserve “continues a bad precedent of selling off longer term energy security assets to satisfy near term budget scoring needs.”

    (Reporting by Toni Clarke in Washington; editing by Leslie Adler and Tom Brown)

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  • richardmitnick 1:44 pm on December 8, 2016 Permalink | Reply
    Tags: , Polar Sea Ice the Size of India Reportedly Vanishes in Record Heat, Scientific American   

    From SA: “Polar Sea Ice the Size of India Reportedly Vanishes in Record Heat” 

    Scientific American

    Scientific American

    Alister Doyle

    Credit: David Stanley Flickr (CC BY 2.0)

    Sea ice off Antarctica and in the Arctic is at record lows for this time of year after declining by twice the size of Alaska in a sign of rising global temperatures, climate scientists say.

    Against a trend of global warming and a steady retreat of ice at earth’s northern tip, ice floating on the Southern Ocean off Antarctica has tended to expand in recent years.

    But now it is shrinking at both ends of the planet, a development alarming scientists and to which a build-up of man-made greenhouse gases, an El Nino weather event that this year unlocked heat from the Pacific Ocean and freak natural swings may all be contributing.

    “There are some really crazy things going on,” said Mark Serreze, director of the U.S. National Snow and Ice Data Center (NSIDC) in Boulder, Colorado, saying temperatures in parts of the Arctic were 20 degrees Celsius (36°F) above normal some days in November.

    Worldwide, this year is on track to be the warmest on record.

    Combined, the extent of polar sea ice on Dec. 4 was about 3.84 million square kilometers (1.48 million square miles) below the 1981-2010 average, according to NSIDC satellite measurements. That is roughly the size of India, or two Alaskas.

    Antarctica’s expanding sea ice in many recent years has been a big theme for those who doubt global warming is man-made.

    John Turner of the British Antarctic Survey said chilly westerly winds that sweep around the continent, perhaps insulating it from the effects of global warming, were the weakest for November in two decades. That may have let more heat seep south, he said.

    A recovery of the high-altitude ozone layer over Antarctica, which led to cooler air over the continent when it was damaged by now-banned industrial chemicals, may also be a factor.

    But Turner said it was hard to pinpoint exactly what was happening.

    “When we began getting satellite data from 1979 the sea ice started to decrease. Everyone said it was global warming … but then it started to increase again,” he said.


    Accepting mainstream scientific findings and responding to increases in floods and heat waves and rising sea levels, almost 200 governments last year agreed to phase out fossil fuels this century and limit the global temperature rise above pre-industrial levels to less than two degrees celsius.

    U.S. President-elect Donald Trump, who has called man-made climate change a hoax, has threatened to pull out of that agreement, reached in Paris in December. Last month he however also said he had an “open mind”.

    The polar regions are radically different from each other because the Arctic is an ocean ringed by land and Antarctica is a vast land mass surrounded by water.

    Ice around Antarctica, retreating with a summer thaw, is the smallest for early December at 11.22 million square kilometers (4.33 million square miles), beating a record from 1982, NSIDC data show.

    Arctic sea ice, expanding in winter, is at a record low of 10.25 million square kilometers (3.96 million square miles), below a 2006 record.

    Anders Levermann, a professor at the Potsdam Institute for Climate Impact Research, said the low polar sea ice pointed to man-made warming. “It’s an extraordinary departure from the norm,” he said.

    Serreze at the NSIDC said the twin record lows might be “blind dumb chance”. But the worry was that “Antarctica is the sleeping elephant that is beginning to stir.”

    Scientists say Antarctica’s glaciers could slip more quickly into the ocean, speeding up the pace of sea level rise, if there is less ice floating on the sea to pin them back.

    (For a graphic comparing current polar sea ice levels with record lows, click on tmsnrt.rs/2g0ziIz)

    See the full article here .

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  • richardmitnick 4:05 pm on December 6, 2016 Permalink | Reply
    Tags: Breakthrough awards announce winners in physics, life sciences and mathematics, Scientific American,   

    From SA: “Black-Hole Fireworks Win Big in Multimillion-Dollar Science Prizes” 

    Scientific American

    Scientific American

    December 5, 2016
    Zeeya Merali

    Breakthrough awards announce winners in physics, life sciences and mathematics

    Credit: Kimberly White Getty Images

    Posing problems in science can be just as rewarding as solving them. The discovery of the black-hole firewall paradox — one of the most confounding puzzles to emerge in physics in recent years — has bagged its co-founder a share of one of this year’s US$3-million Breakthrough Prizes, the most lucrative awards in science.

    Joseph Polchinski, at the University of California, Santa Barbara, is one of three string theorists to share the fundamental-physics prize — announced along with the life-sciences and mathematics awards on 4 December at a glitzy ceremony at NASA’s Ames Research Center in Mountain View, California.

    Joseph Polchinski

    Polchinski co-authored an analysis in 2012 that concluded that either black holes are surrounded by a ring of high-energy particles known as a firewall — a possibility that contradicts the general theory of relativity — or physicists’ understanding of quantum theory is wrong. As yet, there is no consensus as to which of these two cornerstones of physics has to give.

    “I made a list of about 11 distinct solutions proposed by some of the biggest names in physics, but none are quite convincing, and none are clearly wrong,” says Polchinski. “I’m completely mystified.”

    Andrew Strominger and Cumrun Vafa, both at Harvard University in Cambridge, Massachusetts, share the physics prize with Polchinski.

    Andrew Strominger

    Cumrun Vafa

    All three have examined black-hole physics from the perspective of string theory, which posits that at the fundamental level, elementary particles are made up of strings that are anchored to higher-dimensional membranes, or ‘branes’.

    Theories without experiments

    The Breakthrough physics prizes have previously been criticized for honouring string theorists because string theory lies beyond the reach of direct experimental testability. But the prize’s founder, Russian billionaire Yuri Milner, argues that this helps to set the prize apart from awards such as the Nobels, which require ideas to be backed up by experiments. “The physics prizes are really recognizing intellectual achievement,” he says. In this case of firewalls, he adds, “this can be in the asking of a question, rather than the finding of an answer”.

    This May, the Breakthrough prizes cemented another distinction from the Nobels by announcing a special collective prize to 1,015 people working on the LIGO project. In February, researchers working at LIGO announced the first detection of gravitational waves, ripples in the fabric of space-time created when two black holes merge. The Nobel prizes honour at most three people in their science categories.

    The three LIGO project leaders — physicists Ronald Drever and Kip Thorne at the California Institute of Technology in Pasadena, and Rainer Weiss of the Massachusetts Institute of Technology in Cambridge — will share $1 million; the remaining $2 million will be distributed among the other 1,012 physicists who worked on the project. This continues a trend set last year, when 1,377 neutrino physicists split the mega-prize. “The physics prize selection committee want to send a clear message here that experimental physics is collaborative,” Milner says.

    Ronald Drever

    Kip Thorne

    Rainer Weiss

    LIGO bloc new
    Caltech/MIT Advanced aLigo Hanford, WA, USA installation
    Caltech/MIT Advanced aLigo Hanford, WA, USA installation

    Caltech/MIT Advanced aLigo detector installation Livingston, LA, USA
    Caltech/MIT Advanced aLigo detector installation Livingston, LA, USA

    Gravitational waves. Credit: MPI for Gravitational Physics/W.Benger-Zib
    Gravitational waves. Credit: MPI for Gravitational Physics/W.Benger-Zib

    Cornell SXS, the Simulating eXtreme Spacetimes (SXS) project
    Cornell SXS, the Simulating eXtreme Spacetimes (SXS) project

    Life-sciences awards

    Harry Noller, a molecular biologist at the University of California, Santa Cruz, was honoured with a life-sciences prize for his research revealing the centrality of RNA to protein synthesis. Some argue that he missed out on winning the 2009 Nobel Prize in Chemistrybecause of the award’s limitation to three winners. And this year’s Nobel laureate for physiology or medicine, Yoshinori Ohsumi at the Tokyo Institute of Technology, in Japan, also picked up a Breakthrough gong for his work on autophagy, cells’ recycling system.

    The other life-sciences winners were: geneticist Stephen Elledge at Harvard Medical School in Boston, Massachusetts, for elucidating how cells sense and respond to DNA damage; developmental biologist Roeland Nusse at Stanford University in California for pioneering research into the Wnt signalling pathway, which transmits signals from outside to inside cells; and geneticist Huda Zoghbi at Baylor College of Medicine in Houston, Texas, for discovering the causes of the neurological disordersspinocerebellar ataxia and Rett syndrome.

    The Breakthrough prize in mathematics went to Jean Bourgain at the Institute for Advanced Study in Princeton, New Jersey, for work on the geometry of multidimensional spaces and techniques for solving partial differential equations, with applications to quantum physics, and other research. Bourgain also won the $1-million Shaw Prize in mathematics in 2010.

    The award ceremony, hosted by movie star Morgan Freeman, also honoured six early-career scientists, and the winner of a junior science video-making prize.

    See the full article here .

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  • richardmitnick 10:26 am on September 9, 2016 Permalink | Reply
    Tags: , , , , Scientific American   

    From SA: “Promising Links Found between Different Causes of Parkinson’s” 

    Scientific American

    Scientific American

    September 8, 2016
    Karen Weintraub

    Glitches in cells’ mitochondria power plants underlie various types of cases.

    Mitochondrion, coloured transmission electron micrograph (TEM). Credit: CNRI Getty Images

    Researchers have long believed that problems with mitochondria—the power plants of cells—underlie some cases of Parkinson’s disease. Now a new study details those problems, and suggests that they may form a common thread linking previously unexplained cases of the disease with those caused by different genetic anomalies or toxins.

    Finding a common mechanism behind different suspected causes of Parkinson’s suggests that there might also be a common means to measure, treat or cure it, says Marco Baptista, research director at the nonprofit Michael J. Fox Foundation, a leading center for study and advocacy in the fight against Parkinson’s.

    The study, published Thursday in Cell Stem Cell, did identify a possible way to reverse the damage of Parkinson’s—but only in individual cells and fruit flies. Finding a treatment that does the same thing in people will be challenging, Baptista says.

    Roughly one million Americans have Parkinson’s disease, which is characterized by motor problems and can cause other symptoms including cognitive and gastrointestinal difficulties. About 1 to 2 percent of cases are linked to mutations in the LRRK2 gene, with far fewer associated with genes known as PINK1 and Parkin. Exposure to environmental factors such as toxic chemicals can also lead to Parkinson’s, although most cases have no obvious cause.

    In the new paper Xinnan Wang, an assistant professor of neurosurgery at Stanford University, and her colleagues show that mitochondria are underpowered in several types of Parkinson’s and that these mitochondria also release toxic chemicals. Looking at fly models of the disease as well as cells taken from patients, the researchers found that they could correct these problems and reverse neurodegeneration if they reduced levels of a protein involved in mitochondrial activity. “I think it’s a really cool piece of work,” says Thomas Schwarz, a professor of neurology and neurobiology at Harvard University who was not involved in the research but was Wang’s postdoctoral adviser.

    It had been clear that Parkinson’s cases caused by toxins, or by Parkin or PINK1 mutations, involved mitochondria problems, Schwarz says. But the new paper shows that Parkinson’s driven by the LRRK2 gene is also subject to the same mechanism and hints that unexplained cases may also involve the same difficulties in clearing faulty mitochondria from cells. “Here’s the best evidence yet that even those forms are some sort of mitochondriopathy,” Schwarz says. “Seeing those completely disparate, unrelated spontaneous cases—linked up to this question of how are mitochondria cleared and how is their movement controlled—is absolutely fascinating.”

    One question that remains is why would a general problem of cellular physiology cause Parkinson’s? Both Schwarz and Wang have hypotheses: Wang says that the brain cells whose degeneration leads to Parkinson’s—the cells that control release of the neurotransmitter dopamine—are particularly energy-dependent and vulnerable to stress. Deprive a skin cell of energy and it won’t work as efficiently; deprive a dopaminergic neuron of energy and it may die, she adds.

    Schwarz says these neurons are also distinctive in their anatomy. They have so many branches linking them to other brain cells that they can extend up to 4.5 meters in length. Mitochondria are distributed along these branches and must continually be refreshed, with old ones cleared out on the order of some 33,000 mitochondria per cell each day. “That’s just a staggering burden for the cell to carry,” says Schwarz, who in his own research explores how mitochondria move along these axons. “That’s why even a minor slowing or defect in the way the mitochondria are cleared out, or damaged proteins are dealt with, winds up being a major crisis for a cell that has 4.5 meters of axon, compared to a liver cell or even your average neuron elsewhere in the brain.” Figuring out a way to measure this overload before it brings about symptoms of Parkinson’s might lead to earlier diagnoses, before irrevocable damage is done, he adds.

    The paper released Thursday addresses the mystery of how Parkinson’s caused by PINK1 and Parkin mutations, which are known to affect mitochondria, could share the same symptoms as those caused by mutations in the LRRK2 gene, which is involved in how cells take out their trash. Wang and her team found that problems turn up when spent mitochondria are not cleared properly from the cell, a situation that provides a link between the two problems. The different mutations may act on the mitochondria differently but both end up causing the same mitochondrial dysfunction, Wang says. These dysfunctional mitochondria also produce toxins, much like a power plant does, she says, further damaging the cells.

    Asa Abeliovich, a pathologist and neurologist at Columbia University who was not part of this study, says the paper effectively links these two genetic routes to Parkinson’s: the garbage disposal problem and the toxic accumulation that occurs when cellular energy plants go awry. Abeliovich, however, thinks it is still speculative to conclude these problems are also to blame for the noninherited cases of Parkinson’s.

    Wang agrees that she needs to test her theories in other models of Parkinson’s before declaring that a cure might lie in fixing mitochondrial problems. Just because the team found the mitochondrial problems in human cells and in a fly model of Parkinson’s “doesn’t necessarily mean that in humans it is the cause [of Parkinson’s],” Wang says, “but suggests it is a possibility—[and] suggests a future direction to look in human patients and see if lowering this protein has any therapeutic benefits.”

    See the full article here .

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  • richardmitnick 6:31 am on September 8, 2016 Permalink | Reply
    Tags: , Karl Deisseroth at Stanford University and Ed Boyden at the Massachusetts Institute of Technology, , , Scientific American, Zhuo-Hua Pan   

    From SA: “He May Have Invented One of Neuroscience’s Biggest Advances–but You’ve Never Heard of Him” 

    Scientific American

    Scientific American

    September 6, 2016
    Anna Vlasits

    Credit: KIYOSHI TAKAHASE SEGUNDO Getty Images, iStockphoto, Thinkstock

    The next revolution in medicine just might come from a new lab technique that makes neurons sensitive to light. The technique, called optogenetics, is one of the biggest breakthroughs in neuroscience in decades. It has the potential to cure blindness, treat Parkinson’s disease, and relieve chronic pain. Moreover, it’s become widely used to probe the workings of animals’ brains in the lab, leading to breakthroughs in scientists’ understanding of things like sleep, addiction, and sensation.

    So it’s not surprising that the two Americans hailed as inventors of optogenetics are rock stars in the science world. Karl Deisseroth at Stanford University and Ed Boyden at the Massachusetts Institute of Technology have collected tens of millions in grants and won millions in prize money in recent years. They’ve stocked their labs with the best equipment and the brightest minds. They’ve been lauded in the media and celebrated at conferences around the world. They’re considered all but certain to win a Nobel Prize.

    There’s only one problem with this story:

    It just may be that Zhuo-Hua Pan invented optogenetics first.

    Zhuo-Hua Pan

    Even many neuroscientists have never heard of Pan.

    Pan, 60, is a vision scientist at Wayne State University in Detroit who began his research career in his home country of China. He moved to the United States in the 1980s to pursue his PhD and never left. He wears wire-rimmed glasses over a broad nose framed by smile-lines in his cheeks. His colleagues describe him as a pure scientist: modest, dedicated, careful.

    Pan was driven by a desire to cure blindness. In the early 2000s, he imagined that putting a light-sensitive protein into the eye could restore vision in the blind—compensating for the death of rods and cones by making other cells light-sensitive.

    That was the germ of the idea of optogenetics—taking a protein that converts light into electrical activity and putting it into neurons. That way, scientists could shine light and stimulate the neurons remotely, allowing them to manipulate brain circuits. Others had experimented with trying to make neurons light-sensitive before, but those strategies hadn’t caught on because they lacked the right light-sensitive protein.

    That all changed with the first molecular description [PNAS] of channelrhodopsin, published in 2003.

    Channelrhodopsin, a protein made by green algae, responds to light by pumping ions into cells, which helps the algae search out sunlight.

    That “was one of the most exciting things in my life,” Pan said. “I thought, wow! This is the molecule we are looking for. This is the light sensor we are looking for.”

    By February 2004, he was trying channelrhodopsin out in ganglion cells—the neurons in our eyes that connect directly to the brain—that he had cultured in a dish. They became electrically active in response to light. Over the moon with excitement, Pan applied for a grant from the National Institutes of Health. The NIH awarded him $300,000, with the comment that his research was “quite an unprecedented, highly innovative proposal, bordering on the unknown.”

    Pan didn’t know it at the time but he was racing against research groups across the United States and around the world to put channelrhodopsin into neurons.

    Deisseroth and Boyden were working at Stanford, where Deisseroth was finishing a postdoc and Boyden was finishing graduate school. At least two other groups were in the game as well, led by Stefan Herlitze and Lynn Landmesser, who were at Case Western Reserve University at the time, and Hiromu Yawo at Tohoku University in Japan.

    And they were by no means the only scientists experimenting with ways to control neurons with light. By 2004, Gero Miesenbock and Richard Kramer had already published articles using other, more complicated molecules for that purpose. But channelrhodopsin was the tool that was about to revolutionize the field.

    The Stanford group had been toying with the idea of controlling neurons with light for quite some time. They had also noticed the paper about the discovery of channelrhodopsin. Deisseroth got in touch with the paper’s author, Georg Nagel, in March 2004 (a month after Pan’s first success getting channelrhodopsin into neurons) and asked if Nagel would collaborate, sharing the channelrhodopsin DNA so Boyden could try it out in neurons. Nagel shared the DNA, and in August 2004, Boyden shined light on a brain neuron in a dish and recorded electrical activity from the channelrhodopsin.

    Pan had done the same thing with retina neurons six months earlier. But then he got scooped.

    ‘We didn’t feel very lucky’

    Boyden, who is now a professor at MIT, was surprised when told by STAT that Pan ran the experiment first.

    “Wow. Interesting. I didn’t know that,” Boyden said.

    “It’s funny to think about how science regards when something is proven,” he added, noting that scientists build on each others’ work, sometimes working together while at other times working in parallel, scrambling onto one another’s shoulders. “There’s both intentional and unintentional teamwork,” he said.

    The Stanford press office said Deisseroth was unavailable. In response to questions provided by STAT, spokesman Bruce Goldman wrote that Pan’s study was “a far cry from the use of optogenetics … to open up a new world of precision neuroscience. That’s the potential revealed in Dr. Deisseroth’s widely cited 2005 publication.”

    Pan said he might have mentioned the timing of his experiment to Boyden once several years ago, but, Pan said, “I didn’t want to take too much time to talk about this because people feel uncomfortable.”

    That sentiment is in keeping with Pan’s wider approach—diligent, reserved, outside the limelight. Wayne State is a small university not known for its scientific research. Pan had gone to a state school for his PhD, then done mostly obscure research for decades. These things may have contributed to what happened next, when he tried to get his invention out into the world: It wasn’t seen as the big advance it was.

    Pan spent the summer of 2004 figuring out how to get the channelrhodopsin protein into a living eye. He settled on the idea of using a virus, which could infect cells in the eye and sneak the channelrhodopsin DNA inside. His colleague, Alexander Dizhoor, a professor at Salus University, engineered the channelrhodopsin DNA to add the gene for a protein that fluoresced green under blue light, so they could track where the channelrhodopsin ended up.

    In July 2004, Pan dosed his first rat with the virus. About five weeks later, he looked at the retinas to see if it had worked. What he saw was a sea of green—thousands of ganglion cells had the green protein coupled to channelrhodopsin in their membranes. And when he stuck an electrode in one of those cells and turned on a lamp, the cell responded with a flurry of electrical activity. The channelrhodopsin was working. It was just a first step, but it was a revolutionary step—indicating that Pan’s method may just be able to restore sight to the blind.

    “Everything turned out beautifully,” Pan said.

    So Pan and Dizhoor wrote a paper about their work and submitted it to Nature on November 25, 2004, according to the submission letter Pan shared with STAT. The editors at Nature suggested they send it on to a more specialized journal called Nature Neuroscience, which rejected it. Early the next year, Pan sent the paper to the Journal of Neuroscience, where it was reviewed but then again rejected.

    Disheartened, Pan set to work revising his paper, and in May 2005 traveled to Fort Lauderdale, Fla. for the Association for Research in Vision and Opthamology conference, where he described his work using channelrhodopsin in neurons. That single lecture, lasting just 15 minutes, would come to be his clearest stake along the timeline of invention.

    It was what came next that would make that stake matter. A few months later, in August of 2005, Nature Neuroscience published a paper about using channelrhodopsin to make neurons sensitive to light. The paper was by Edward Boyden and Karl Deisseroth.

    Pan heard the news from a colleague who emailed him the paper. “I felt terrible. I felt terrible,” Pan said, pausing. “We didn’t feel very lucky.”

    Met with a shrug

    Deisseroth and Boyden’s paper was slightly different than Pan’s. They simply demonstrated that they could use channelrhodopsin to control neurons’ activity in a dish; Pan had waited to publish until he could make it work in a live animal. And Deisseroth and Boyden had shown incredibly precise time control, by turning the light on for just a millisecond. But their technical feat was essentially the same: They had used channelrhodopsin to successfully make neurons in a dish respond to illumination.

    The Stanford paper took a little while to take off, but take off it did. The work jump-started both Deisseroth’s and Boyden’s careers, landing them big money grants and talented students for their labs—Deisseroth at Stanford and Boyden at MIT. The New York Times started writing about Deisseroth’s breakthroughs with optogenetics in 2007, and the citations of the research paper took off exponentially.

    By the time Pan finally managed to publish his paper, in Neuron in April 2006, it was mostly met with a shrug. Richard Kramer, a neuroscientist at UC Berkeley who was also studying vision, remembers, “It wasn’t that creative, it was just ‘Oh look, you can put channelrhodopsin in neurons from the brain, you can also put it in neurons from the retina.’ Was it impressive? No.”

    Those handful of months seem to have made all the difference.

    Why didn’t Pan’s paper get published first? He may never know the answer. After Boyden’s paper came out, Pan wrote to the editor at Nature Neuroscience asking how they could have rejected his paper but published Boyden’s.

    In her response, the editor replied that while the papers were similar, Boyden et al. presented theirs as a new technology rather than as a scientific finding. Pan’s paper, it seemed, was too narrow, only focusing on using channelrhodopsin to restore vision, while Boyden’s paper took the broad view of thinking of channelrhodopsin as a tool for neuroscience in general.

    The reviews that other researchers submitted to the Journal of Neuroscience shed some more light on what people thought of Pan’s paper. One reviewer liked it and had some minor suggestions for improvement. The other, in a single long paragraph, said the research was “ambitious” and “very preliminary” and concluded that “there is too little here to entice most neuroscientists.”

    In hindsight, Pan’s coauthor Dizhoor can’t help but laugh while reading that. Reviewers would ultimately greenlight an expanded version of Pan’s paper, in 2006, with minimal revisions.

    But that hasn’t elevated Pan to the optogenetics pantheon. In terms of publication, he was quite late to the party, with three different groups publishing papers about channelrhodopsin before he did. He didn’t share in two big prizes that recently went to Deisseroth and Boyden, the Brain Prize in 2013 (1 million euros split between six inventors of optogenetics) and the Breakthrough Prize in 2015 ($3 million each to Boyden and Deisseroth).

    Since 2005, Deisseroth has been awarded over $18 million in NIH grants for his work on optogenetics, and Boyden has received more than $10 million. Both have other major projects that bring in additional funding to their labs each year. Boyden is a prolific speaker who’s given multiple TED talks; Deisseroth was the subject of an in-depth profile in the New Yorker in 2015.

    Pan, on the other hand, has cumulatively received just over $3 million over the past 10 years and holds one NIH grant—the bare minimum to keep a research program going. Most of the accolades for his work have come from Wayne State University. According to his website, he’s been invited to give a couple of talks—most recently at a technology show in Russia.

    Rules of the invention game

    The whole saga raises the question of what it means to invent something in science. It’s a question that has plagued scientists in recent years—including the ongoing CRISPR patent fight—as research becomes ever more global and the spoils of biotechnology and medical discoveries become ever more valuable.

    The answer, it turns out, shifts depending on context.

    Fellow academics often consider the first scientists to publish a paper on a technique the discoverers or inventors of that technique.

    But that metric can be problematic, as Pan’s experience shows. In a recent essay in the journal eLife, Ronald Vale and Anthony Hyman, two biologists, laid out the problem. They point out that “the delay between the submission of a paper and its publication can range from a few weeks to more than two years,” adding that journals “slow down and create inequities in how knowledge is transferred from the scientist to the worldwide scientific community.”

    And reviewers can be biased toward familiar names or prestigious institutions. Blinded review, in which the author’s name is redacted, has been suggested as a way to minimize that effect, but many scientists are skeptical that it would work, since research is often discussed ahead of time at conferences.

    Vale and Hyman advocate, instead, for scientists to post drafts of their work on “preprint servers” such as bioRxiv before they submit it to journals. If such a server had been widely used by neuroscientists in 2004, Pan could have posted his rejected findings there, staking his claim.

    But whether that would mean he would be on the short list for the Nobel Prize is unclear. Kramer thinks that even if Pan had published on bioRxiv, he’d be shut out because he wasn’t the first to publish a peer-reviewed paper on the technique. That’s what will matter if and when the inventors of optogenetics win the Nobel.

    The legal system doesn’t play by quite the same rules. According to an American Bar Association representative specializing in patent law, to prove precedence for a patent in the early 2000s, most of the time you needed to show both “when someone had actually conceived of the invention—that’s sort of in your mind the lightbulb going off, ‘Aha! I have it!’—and when the invention was reduced to practice—that means you’ve actually done it and you’ve proven that your idea can work.”

    By those standards, a discovery happens at the time of its demonstration in the lab, even before it’s been posted on a preprint server.

    Then there’s the court of public opinion. Scientists are increasingly public personalities, running Twitter accounts and appearing on late-night talk shows.

    “The quality rising to the top is a little more influenced by non-scientific things than it used to be,” said Richard Masland, an emeritus professor at Harvard Medical School, who also holds patents on gene therapy for blindness.

    Being at Wayne State University might have meant that Pan didn’t have the resources to get a high-profile paper published. There’s the actual costs of doing high quality of research, but in addition, senior researchers at top universities usually mentor junior professors, reading their work and helping them take it to the next level.

    Pan agrees that fact may have put him at a disadvantage compared with scientists at prestigious institutions like MIT or Stanford. “Of course, I cannot prove that with evidence,” he said. And Pan’s modesty and non-native language abilities may have kept him from promoting himself as well as Boyden and Deisseroth did.

    “He’s just not as public a speaker and presenter as other people in the field. And this is an important part of the whole game of being able to get out there and sell yourself,” Kramer, the UC Berkeley vision researcher, said.

    That publicity can be self-reinforcing. Landmesser, the Case Western professor who worked on channelrhodopsin in the beginning, said, “I think there’s always a tendency [that] whoever gets there first gets more publicity, let’s put it that way.”

    A university PR video can spawn a national news article, which spurs someone to think of your name in nominations for a nice cash prize, which leads to some TV appearances. The word “inventor” gets used at some point and before you know it you’re Google’s automatic answer to the question “Who invented optogenetics?”

    Ultimately, both Pan and the team of Boyden and Deisseroth won patents for their discoveries.

    Pan’s May 2005 lecture threatened to derail the Boyden-Deisseroth patent for a while—the US patent office rejected it multiple times because Pan’s abstract was published more than a year before they got around to filing.

    Eventually, Deisseroth and Boyden signed a document stating that they had invented this method of using channelrhodopsin privately in the lab before Pan’s conference abstract was published. The relevant patent was issued in March 2016, almost 10 years after they filed.

    Now, Deisseroth is a cofounder and scientific advisor at Circuit Therapeutics, a company developing a wide range of therapies based on optogenetics, presumably using Deisseroth’s patented inventions. (Circuit Therapeutics declined to comment on specifics of their intellectual property licenses.)

    Pan won a patent as well, to use channelrhodopsin to restore vision in the eye. His patent was licensed by RetroSense, which won an award from the Angel Capital Association in 2015. Retrosense—whose CEO in passing told STAT about Pan’s role in the invention of optogenetics—began clinical trials this year to put the algae proteins in blind people using gene therapy. It’s the first application of optogenetics in humans and the first time a non-human gene is being used in a gene therapy trial.

    Right now, there are blind people in Texas walking around with algae DNA and proteins in their eyes. And that was what Pan was in it for all along. “One thing I still feel glad about is that even right now our clinical study is still ahead of anyone,” Pan said.

    But given that there are no gene therapies approved for clinical use in the United States, the road to successfully using optogenetics in humans will likely be a long one. Yang Dan, a professor of neuroscience at UC Berkeley who uses optogenetics to study sleep, isn’t betting on optogenetics cures being in the clinic any time soon. “I believe that these safety checks will take a long, long time,” she said.

    As for the invention itself, some scientists say Pan may not have had the big, award-worthy vision that Deisseroth and Boyden had. Stefan Herlitze, one of the others who was scooped for the first publication about channelrhodopsin in neurons, said, “Of course I have to say, Deisseroth and Boyden, they really developed the field further.”

    Boyden echoed this. “Karl and I were very interested in the general question of how to control cell types in the brain,” he said. “In recent years, we worked to push these molecules to their logical limits.”

    So maybe it doesn’t matter who invented optogenetics, just who has stretched science’s boundaries the furthest.

    Asked whether he deserves the recognition that Boyden and Deisseroth have enjoyed, Pan declined to answer. He later told STAT that Deisseroth “also did a very excellent job, no doubt. But he’s also very lucky because if our paper was ahead of him, the story would be different. We would have gotten more credit.”

    That is about as much as Pan is willing to say about the way his cards fell. Today he’s still in Detroit. He’s been working on new versions of channelrhodopsin that could be used to cure blindness. “My lab is a very small lab,” Pan said, “We’re mainly interested in trying to restore vision.”

    See the full article here .

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  • richardmitnick 10:26 am on August 12, 2016 Permalink | Reply
    Tags: , , New Imaging Technique Provides First Look at Gene Activity in the Living Human Brain, Scientific American   

    From SA: “New Imaging Technique Provides First Look at Gene Activity in the Living Human Brain” 

    Scientific American

    Scientific American

    August 11, 2016
    Sharon Begley

    Credit: CORBIS

    Don’t let the pretty tangerine and lemon-yellow glow in the brain pictures fool you. If its inventors are right, an elegant new neuroimaging tool provides more than fetching pictures: It shows for the first time where genes are being turned on or off in living brains, scientists reported on Wednesday.

    Until now, gene activation in human brains could be detected only in dead ones. By revealing DNA’s on-off choreography in brains that are still thinking, feeling, and remembering, the new technique promises to reveal genetic underpinnings of mental health and, perhaps one day, detect the earliest hints of a brain being gripped by Alzheimer’s, schizophrenia, or other diseases.

    “This is really exciting, pioneering work,” said John Satterlee of the National Institute on Drug Abuse, who coordinated the NIH’s program to study patterns of gene silencing and gene activation, and who was not involved in this study. “They took us to a place we didn’t know anything about”—patterns of gene expression in living human brains—“and showed us the lay of the land.”

    Brain epigenetics—which genes are turned on or off in different structures—has become a hot topic, as neuroscientists realized that the sequences of inherited DNA explain very little about psychiatric illnesses. In contrast, which genes are turned on and off might be important in a wide range of brain disorders, including addiction, Alzheimer’s disease, Rett syndrome, depression, and schizophrenia, as well as age-related changes. And because life events can alter genes’ on-off state, epigenetic changes might be how tragedy, trauma, and other experiences cause long-term changes in the brain.

    Gene activity “is so responsive to the environment, we simply can’t study it outside of its natural context,” said chemist Jacob Hooker of Massachusetts General Hospital, who led the research, published in Science Translational Medicine. “[Dead] brains and living brains will look very different.”

    The new technique is a cousin of PET. Traditional PET detects the emission of subatomic particles called positrons from radioactively tagged glucose, the brain’s energy source, and thus reveals which brain regions are active. This version of PET detects positrons coming from radioactively-tagged “Martinostat,” a small molecule Hooker and his colleagues created in 2012. (They patented and licensed Martinostat.) Given intravenously, the molecule slips through the blood-brain barrier (thanks to a clutch of atoms that “acts like a greaseball,” Hooker said). Once in the brain, it binds to enzymes called HDACs that turn off genes—including genes important in forming synapses and therefore learning and memory. PET detects the positrons, and presto: a brain map showing where genes are being turned off.

    That could be a first step at discovering where, in the brain, the genetic lights go out, triggering illness.

    Hooker’s team administered Martinostat (named for the Martinos Center for Biomedical Imaging at MGH) to eight healthy volunteers. The scientists were trying to show that the technique could work in living brains, but beyond that proof of principle, they also made some tentative discoveries.

    The molecules that silence genes were most abundant in the cerebellum, in the back of the brain, which regulates movements, and the putamen, which does that plus coordinate some forms of learning. The gene-silencing molecules were least abundant in the hippocampus (forming memories) and amygdala (processing and producing emotions such as anger). It’s not clear what might explain that pattern, but one possibility is that regions with the fewest of these molecules have the greatest potential for “neuroplasticity,” or altering their neuronal connections in response to the life the brain’s owner leads.

    More striking than the differences among brain regions was the unexpected similarity between people. Regions with lots of gene silencing in one person’s brain were also regions with lots of silencing in others’ brains, while regions without much gene silencing were also mostly the same.

    The uniformity suggests there might be a baseline pattern of gene activation in healthy, living brains. If so, then deviations from that pattern might be used to diagnose illnesses before symptoms appear. In the brains of deceased Alzheimer’s patients, for instance, the hippocampus is shot through with gene-silencing molecules.

    “I’m hoping these colorful maps let us compare healthy brains with the brains of people with schizophrenia, Alzheimer’s, and other diseases,” pinpointing regions with aberrant patterns of gene expression, Hooker said.

    The new PET technique cannot identify which specific genes are being turned off. But that can be done in dead brains, said Hooker, “and we’re trying to map out which genes are involved” in which conditions.

    His team has already used the new technique to image the gene-expression patterns in the brains of nine people with schizophrenia and a few with Huntington’s disease. They have funding to start doing so with Alzheimer’s patients. The results might show how gene-silencing gone wrong explains the conditions and, one day, point the way to treatments. “This is really the first step in being able to look” at how genetic on-off signals might cause, or at least be harbingers of, such brain diseases, said the NIH’s Satterlee.

    That possibility has already caught the attention of the biotech industry. Cambridge, Mass.-based start-up Rodin Therapeutics is working on developing drugs that, by inhibiting gene-silencing enzymes, might treat Alzheimer’s, Parkinson’s, and PTSD. The approach has enough promise that biotech giant Biogen is willing to pay $500 million for it.

    See the full article here .

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