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"content": "\u003cp>Scientists continue to speak out against the prospect of producing engineered embryos that could lead to “designer babies.”\u003c/p>\n\u003cp>[pullquote align='right']‘You could have done just as well by throwing a dart at the genome and saying, ‘OK, we’re going to look at this gene and see if it’s associated with depression.’[/pullquote]\u003c/p>\n\u003cp>Leaders of the American Society of Gene and Cell Therapy \u003ca href=\"https://www.asgct.org/research/news/april-2019/scientific-leaders-call-for-global-moratorium-on-g\">sent a letter\u003c/a> on April 24 to Alex Azar, the secretary of health and human services, adding their voices to the call for a moratorium on experiments that could alter the genes passed down to future generations.\u003c/p>\n\u003cp>This move follows a \u003ca href=\"https://www.npr.org/sections/health-shots/2019/03/13/701549223/call-for-global-moratorium-on-creating-gene-edited-babies\">widely criticized experiment \u003c/a>in China last year that apparently produced children with edited genomes.\u003c/p>\n\u003cp>The concern is largely ethical. The reality is that biologists probably couldn’t produce designer babies even if they wanted to.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>It turns out that the genetics underlying desirable traits such as athleticism, intelligence and beauty are so complicated it may not ever be possible to make targeted changes.\u003c/p>\n\u003cp>Back in the day of Gregor Mendel, the monk who modified the traits of the pea plants in his 19th century garden, it seemed that traits were based on simple elements (later dubbed “genes”). But by the 1920s, \u003ca href=\"https://www.ncbi.nlm.nih.gov/pubmed/28987627\">it was becoming clear\u003c/a> that human traits involved many genes acting in concert.\u003c/p>\n\u003cp>Still, during the heyday of the Human Genome Project at the end of the 20th century, hopes were high that common diseases might be explained through the interaction of just a handful of genes. You may recall all those stories about scientists hunting “the gene for” various diseases. Hundreds of scientific papers purported to show strong candidates for these critical genes.\u003c/p>\n\u003cp>British comedian John Cleese poked fun at this idea\u003ca href=\"https://www.youtube.com/watch?v=-M-vnmejwXo&feature=youtu.be\"> in a video skit\u003c/a>, where he pointed on a chart to “the gene which we scientists now know makes us eat coconut ice cream after a fish dinner.”\u003c/p>\n\u003cp>But the scientific effort to find genes for common conditions was largely a flop (with a few notable exceptions, such as Alzheimer’s and breast cancer). For example, hundreds of studies over the years have reportedly found genes associated with schizophrenia.\u003c/p>\n\u003cp>“When we look at the 20 most studied genes investigated for schizophrenia, \u003ca href=\"https://www.biologicalpsychiatryjournal.com/article/S0006-3223(17)31772-9/fulltext\">we find basically no evidence\u003c/a> that any of those are associated at levels greater than we’d expect due to chance,” says \u003ca href=\"https://www.colorado.edu/ibg/matthew-keller\">Matthew Keller\u003c/a> at the University of Colorado.\u003c/p>\n\u003cp>His lab also looked at the early claims for genes linked to depression. \u003ca href=\"https://www.ncbi.nlm.nih.gov/pubmed/30845820\">Those, too, went nowhere\u003c/a>.\u003c/p>\n\u003cp>“You could have done just as well by throwing a dart at the genome and saying, ‘OK, we’re going to look at this gene and see if it’s associated with depression,’ ” he says.\u003c/p>\n\u003cp>Instead, scientists found that thousands upon thousands of genes are associated with common diseases and common traits. And most of them have just a tiny influence on the risk of a disease, often just a small fraction of a percent.\u003c/p>\n\u003cp>Human traits, like height, follow the same story.\u003c/p>\n\u003cp>\u003ca href=\"https://profiles.stanford.edu/jonathan-pritchard\">Jonathan Pritchard\u003c/a>, a Howard Hughes investigator at Stanford University, has looked into the genetics of height, which is one of the most thoroughly studied traits. “It quickly became clear there’s huge numbers of variants that affect height,” he says. “We have estimated that it’s probably something like 100,000 variants across the genome, so most of the genome affects height by a small amount.”\u003c/p>\n\u003cp>A few years ago, he suggested that height and presumably other common traits are “omnigenetic,” meaning they involve all of our genes.\u003c/p>\n\u003cp>If that’s the case, each gene must influence many different traits. A gene linked to height might affect the basic mechanism inside many cells. So editing one gene would affect not only height but who knows what else.\u003c/p>\n\u003cp>Pritchard and his colleagues \u003ca href=\"https://www.cell.com/cell/fulltext/S0092-8674(19)30400-3\">published a paper\u003c/a> Thursday that reveals the nature of the variants related to complex traits like height. The genetic variation isn’t in the genes themselves (the DNA code that tells cells what proteins to produce) but in genetic elements that regulate those genes at the same time they influence other tasks.\u003c/p>\n\u003cp>His findings suggest our genes work as an interconnected network. It’s not a predictable machine as much as it is a flock of starlings, which wheels in the sky based on group dynamics.\u003c/p>\n\u003cp>That phenomenon makes our biology a challenge to understand, let alone engineer, Pritchard says. “We find nature as it is, not really as we wish it to be,” he says, a bit wistfully.\u003c/p>\n\u003cp>Pritchard’s concept of omnigenetics is not wholly accepted by his peers.\u003c/p>\n\u003cp>The logical conclusion is that genetics is “such a mush that we can’t understand it,” says \u003ca href=\"https://www.ebi.ac.uk/about/people/ewan-birney\">Ewan Birney\u003c/a> at the European Bioinformatics Institute. “I find that a bit depressing.”\u003c/p>\n\u003cp>Birney still holds out hope that, as we learn more about genetics, clearer mechanisms will emerge.\u003c/p>\n\u003cp>But in any event, there’s no question that complicated traits involve thousands of genes with multiple purposes.\u003c/p>\n\u003cp>“If anybody thinks we can understand how to change genomes to improve things, they don’t have an appreciation for the lack of knowledge that we have,” Birney says.\u003c/p>\n\u003cp>In the case of \u003ca href=\"https://www.npr.org/sections/health-shots/2018/11/28/671375070/facing-backlash-chinese-scientist-defends-gene-editing-research-on-babies\">the rogue Chinese experiment\u003c/a>, the scientist attempted to edit a gene to create a variant that apparently protects people from HIV infection, resulting in the birth of genetically engineered twins. But going back to the idea that genes all play multiple roles, it’s not clear what else this alteration has done to the children.\u003c/p>\n\u003cp>Birney also notes there’s a big difference between engineering a designer baby with desirable characteristics and fixing a genetic flaw. “We’re much better at understanding when things break, and we call those genetic diseases,” Birney says.\u003c/p>\n\u003cp>There, gene editing could be brought to bear. A broken gene could be edited. But there are other options that carry less risk.\u003c/p>\n\u003cp>There is already an effective technology, called preimplantation genetic diagnosis, which allows doctors to look for these single-gene flaws in fertilized eggs and select only those that are free of the genetic disease to be implanted in the mother’s womb.\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp>This approach is widely regarded as ethical. And the child isn’t a “designer baby,” but ends up with a natural set of genes.\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2019 NPR. To see more, visit https://www.npr.org.\u003cimg decoding=\"async\" src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Why+Making+A+%27Designer+Baby%27+Would+Be+Easier+Said+Than+Done&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>Scientists continue to speak out against the prospect of producing engineered embryos that could lead to “designer babies.”\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>Leaders of the American Society of Gene and Cell Therapy \u003ca href=\"https://www.asgct.org/research/news/april-2019/scientific-leaders-call-for-global-moratorium-on-g\">sent a letter\u003c/a> on April 24 to Alex Azar, the secretary of health and human services, adding their voices to the call for a moratorium on experiments that could alter the genes passed down to future generations.\u003c/p>\n\u003cp>This move follows a \u003ca href=\"https://www.npr.org/sections/health-shots/2019/03/13/701549223/call-for-global-moratorium-on-creating-gene-edited-babies\">widely criticized experiment \u003c/a>in China last year that apparently produced children with edited genomes.\u003c/p>\n\u003cp>The concern is largely ethical. The reality is that biologists probably couldn’t produce designer babies even if they wanted to.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>It turns out that the genetics underlying desirable traits such as athleticism, intelligence and beauty are so complicated it may not ever be possible to make targeted changes.\u003c/p>\n\u003cp>Back in the day of Gregor Mendel, the monk who modified the traits of the pea plants in his 19th century garden, it seemed that traits were based on simple elements (later dubbed “genes”). But by the 1920s, \u003ca href=\"https://www.ncbi.nlm.nih.gov/pubmed/28987627\">it was becoming clear\u003c/a> that human traits involved many genes acting in concert.\u003c/p>\n\u003cp>Still, during the heyday of the Human Genome Project at the end of the 20th century, hopes were high that common diseases might be explained through the interaction of just a handful of genes. You may recall all those stories about scientists hunting “the gene for” various diseases. Hundreds of scientific papers purported to show strong candidates for these critical genes.\u003c/p>\n\u003cp>British comedian John Cleese poked fun at this idea\u003ca href=\"https://www.youtube.com/watch?v=-M-vnmejwXo&feature=youtu.be\"> in a video skit\u003c/a>, where he pointed on a chart to “the gene which we scientists now know makes us eat coconut ice cream after a fish dinner.”\u003c/p>\n\u003cp>But the scientific effort to find genes for common conditions was largely a flop (with a few notable exceptions, such as Alzheimer’s and breast cancer). For example, hundreds of studies over the years have reportedly found genes associated with schizophrenia.\u003c/p>\n\u003cp>“When we look at the 20 most studied genes investigated for schizophrenia, \u003ca href=\"https://www.biologicalpsychiatryjournal.com/article/S0006-3223(17)31772-9/fulltext\">we find basically no evidence\u003c/a> that any of those are associated at levels greater than we’d expect due to chance,” says \u003ca href=\"https://www.colorado.edu/ibg/matthew-keller\">Matthew Keller\u003c/a> at the University of Colorado.\u003c/p>\n\u003cp>His lab also looked at the early claims for genes linked to depression. \u003ca href=\"https://www.ncbi.nlm.nih.gov/pubmed/30845820\">Those, too, went nowhere\u003c/a>.\u003c/p>\n\u003cp>“You could have done just as well by throwing a dart at the genome and saying, ‘OK, we’re going to look at this gene and see if it’s associated with depression,’ ” he says.\u003c/p>\n\u003cp>Instead, scientists found that thousands upon thousands of genes are associated with common diseases and common traits. And most of them have just a tiny influence on the risk of a disease, often just a small fraction of a percent.\u003c/p>\n\u003cp>Human traits, like height, follow the same story.\u003c/p>\n\u003cp>\u003ca href=\"https://profiles.stanford.edu/jonathan-pritchard\">Jonathan Pritchard\u003c/a>, a Howard Hughes investigator at Stanford University, has looked into the genetics of height, which is one of the most thoroughly studied traits. “It quickly became clear there’s huge numbers of variants that affect height,” he says. “We have estimated that it’s probably something like 100,000 variants across the genome, so most of the genome affects height by a small amount.”\u003c/p>\n\u003cp>A few years ago, he suggested that height and presumably other common traits are “omnigenetic,” meaning they involve all of our genes.\u003c/p>\n\u003cp>If that’s the case, each gene must influence many different traits. A gene linked to height might affect the basic mechanism inside many cells. So editing one gene would affect not only height but who knows what else.\u003c/p>\n\u003cp>Pritchard and his colleagues \u003ca href=\"https://www.cell.com/cell/fulltext/S0092-8674(19)30400-3\">published a paper\u003c/a> Thursday that reveals the nature of the variants related to complex traits like height. The genetic variation isn’t in the genes themselves (the DNA code that tells cells what proteins to produce) but in genetic elements that regulate those genes at the same time they influence other tasks.\u003c/p>\n\u003cp>His findings suggest our genes work as an interconnected network. It’s not a predictable machine as much as it is a flock of starlings, which wheels in the sky based on group dynamics.\u003c/p>\n\u003cp>That phenomenon makes our biology a challenge to understand, let alone engineer, Pritchard says. “We find nature as it is, not really as we wish it to be,” he says, a bit wistfully.\u003c/p>\n\u003cp>Pritchard’s concept of omnigenetics is not wholly accepted by his peers.\u003c/p>\n\u003cp>The logical conclusion is that genetics is “such a mush that we can’t understand it,” says \u003ca href=\"https://www.ebi.ac.uk/about/people/ewan-birney\">Ewan Birney\u003c/a> at the European Bioinformatics Institute. “I find that a bit depressing.”\u003c/p>\n\u003cp>Birney still holds out hope that, as we learn more about genetics, clearer mechanisms will emerge.\u003c/p>\n\u003cp>But in any event, there’s no question that complicated traits involve thousands of genes with multiple purposes.\u003c/p>\n\u003cp>“If anybody thinks we can understand how to change genomes to improve things, they don’t have an appreciation for the lack of knowledge that we have,” Birney says.\u003c/p>\n\u003cp>In the case of \u003ca href=\"https://www.npr.org/sections/health-shots/2018/11/28/671375070/facing-backlash-chinese-scientist-defends-gene-editing-research-on-babies\">the rogue Chinese experiment\u003c/a>, the scientist attempted to edit a gene to create a variant that apparently protects people from HIV infection, resulting in the birth of genetically engineered twins. But going back to the idea that genes all play multiple roles, it’s not clear what else this alteration has done to the children.\u003c/p>\n\u003cp>Birney also notes there’s a big difference between engineering a designer baby with desirable characteristics and fixing a genetic flaw. “We’re much better at understanding when things break, and we call those genetic diseases,” Birney says.\u003c/p>\n\u003cp>There, gene editing could be brought to bear. A broken gene could be edited. But there are other options that carry less risk.\u003c/p>\n\u003cp>There is already an effective technology, called preimplantation genetic diagnosis, which allows doctors to look for these single-gene flaws in fertilized eggs and select only those that are free of the genetic disease to be implanted in the mother’s womb.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>This approach is widely regarded as ethical. And the child isn’t a “designer baby,” but ends up with a natural set of genes.\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2019 NPR. To see more, visit https://www.npr.org.\u003cimg decoding=\"async\" src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Why+Making+A+%27Designer+Baby%27+Would+Be+Easier+Said+Than+Done&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n\u003c/div>\u003c/p>",
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"content": "\u003cp>\u003cem>Editor’s note: The following story was produced by Richmond High School students for \u003ca href=\"https://ww2.kqed.org/education/2018/04/18/youth-takeover-of-kqed-news-starts-april-23/\" target=\"_blank\" rel=\"noopener\">\u003cspan style=\"font-weight: 400\">Youth Takeover\u003c/span>\u003c/a> week at KQED.\u003c/em>\u003c/p>\n\u003cp>Imagine you’re asleep and you suddenly open your eyes. You try to reposition yourself, but something’s wrong. Your body won’t move, and it’s as if something is holding you down. You hear scratching in the corner of the room, then see a pitch-black figure. You think it’s just your mind playing tricks, until the figure starts moving, slowly. It’s getting closer. You shut your eyes, but you can hear it shuffling toward you.\u003c/p>\n\u003cp>This is what sleep paralysis is like.\u003c/p>\n\u003cp>\u003cspan style=\"font-weight: 400\">Sleep paralysis usually occurs when you’re, well, asleep, says Allen Jenkins, a psychology teacher at Richmond High School.\u003c/span>\u003c/p>\n\u003cp>\u003cspan style=\"font-weight: 400\">“Your brain is telling you to go to sleep and to not move, because when you walk around in your sleep, that’s not good,” he said. “But some people have a problem with that not turning off. So when they wake up, they still can’t move.” \u003c/span>\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>\u003cspan style=\"font-weight: 400\">People undergoing sleep paralysis might also feel pressure on their chest, a sense of dread and difficulty taking a breath. Some people also report experiencing hallucinations, like a shadowy figure in the darkness. \u003c/span>\u003c/p>\n\u003cp>\u003cspan style=\"font-weight: 400\">Even if a person experiences stimulation that doesn’t come from their environment, it can still happen within their brain. \u003c/span>\u003c/p>\n\u003cp>\u003cspan style=\"font-weight: 400\">“Everything you experience is perception. Your processing in your brain can be overactive,” Jenkins said. \u003c/span>\u003cspan style=\"font-weight: 400\">“You can think of it like dreaming when you’re wide awake. It seems real to you, but it just doesn’t happen to be occurring.” \u003c/span>\u003c/p>\n\u003cp>\u003cspan style=\"font-weight: 400\">Leslie Saechao, a student at Richmond High School, has experienced sleep paralysis. “I felt like I saw something in the dark. It was like a figure,” she said.\u003c/span>\u003c/p>\n\u003cfigure id=\"attachment_1940747\" class=\"wp-caption alignright\" style=\"max-width: 756px\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"wp-image-1940747 size-full\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2029/04/sleep-paralysis.jpeg\" alt=\"\" width=\"756\" height=\"933\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2029/04/sleep-paralysis.jpeg 1512w, https://cdn.kqed.org/wp-content/uploads/sites/35/2029/04/sleep-paralysis-160x197.jpeg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2029/04/sleep-paralysis-800x987.jpeg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2029/04/sleep-paralysis-768x948.jpeg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2029/04/sleep-paralysis-1020x1259.jpeg 1020w, https://cdn.kqed.org/wp-content/uploads/sites/35/2029/04/sleep-paralysis-972x1200.jpeg 972w\" sizes=\"(max-width: 756px) 100vw, 756px\">\u003cfigcaption class=\"wp-caption-text\">Nayeli Pena, Yvette Villicana and Evelyn Mendoza, Richmond High School students.\u003c/figcaption>\u003c/figure>\n\u003cp>Saechao recalls lying in bed awake past midnight, feeling “paralyzed,” and seeing a blurry figure.\u003c/p>\n\u003cp>The incident has made her “paranoid” about sleeping, so she covers her face at night.\u003c/p>\n\u003cp>“I sleep next to the wall so I won’t see anything,” she said.\u003c/p>\n\u003cp>Sleep paralysis can occur as you fall asleep or as you wake up. It goes away by itself after a few seconds or a few minutes. People who experience this are usually in their teens, 20s and 30s.\u003c/p>\n\u003cp>Researchers believe sleep paralysis happens when someone’s sleep cycle is disrupted, and especially when they’re in a dream state. This occurs in the rapid eye movement or REM stage of sleep, and can be caused by anxiety and stress.\u003c/p>\n\u003cp>Yvette Villicaña first experienced sleep paralysis when she was in middle school.\u003c/p>\n\u003cp>“It’s not as overwhelming for me as other people, because I don’t see shadowy figures,” she said. “I try to move, but sometimes I can’t. And after some time, it does go away. I used to think I was the only \u003cspan style=\"font-weight: 400\">one who experienced this.”\u003c/span>\u003c/p>\n\u003cp>\u003cspan style=\"font-weight: 400\"> After working on this story for KQED’s “\u003ca href=\"https://ww2.kqed.org/education/2018/04/18/youth-takeover-of-kqed-news-starts-april-23/\">Youth Takeover\u003c/a>,” Villicaña says it’s good to know she’s not alone, but it’s tough to realize other people have more traumatic experiences because of their hallucinations.\u003c/span>\u003c/p>\n\u003cp>Sleep paralysis is harmless by itself but can lead to insomnia or narcolepsy, a more serious condition that causes uncontrollable sleepiness during the day.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\u003cspan style=\"font-weight: 400\">You can try to stop sleep paralysis by avoiding naps and not sleeping on your back, because it makes you feel vulnerable. Consult a mental health professional for stress or anxiety. And if it doesn’t go away, seek help from a sleep specialist. \u003c/span>\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>\u003cspan style=\"font-weight: 400\">People undergoing sleep paralysis might also feel pressure on their chest, a sense of dread and difficulty taking a breath. Some people also report experiencing hallucinations, like a shadowy figure in the darkness. \u003c/span>\u003c/p>\n\u003cp>\u003cspan style=\"font-weight: 400\">Even if a person experiences stimulation that doesn’t come from their environment, it can still happen within their brain. \u003c/span>\u003c/p>\n\u003cp>\u003cspan style=\"font-weight: 400\">“Everything you experience is perception. Your processing in your brain can be overactive,” Jenkins said. \u003c/span>\u003cspan style=\"font-weight: 400\">“You can think of it like dreaming when you’re wide awake. It seems real to you, but it just doesn’t happen to be occurring.” \u003c/span>\u003c/p>\n\u003cp>\u003cspan style=\"font-weight: 400\">Leslie Saechao, a student at Richmond High School, has experienced sleep paralysis. “I felt like I saw something in the dark. It was like a figure,” she said.\u003c/span>\u003c/p>\n\u003cfigure id=\"attachment_1940747\" class=\"wp-caption alignright\" style=\"max-width: 756px\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"wp-image-1940747 size-full\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2029/04/sleep-paralysis.jpeg\" alt=\"\" width=\"756\" height=\"933\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2029/04/sleep-paralysis.jpeg 1512w, https://cdn.kqed.org/wp-content/uploads/sites/35/2029/04/sleep-paralysis-160x197.jpeg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2029/04/sleep-paralysis-800x987.jpeg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2029/04/sleep-paralysis-768x948.jpeg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2029/04/sleep-paralysis-1020x1259.jpeg 1020w, https://cdn.kqed.org/wp-content/uploads/sites/35/2029/04/sleep-paralysis-972x1200.jpeg 972w\" sizes=\"(max-width: 756px) 100vw, 756px\">\u003cfigcaption class=\"wp-caption-text\">Nayeli Pena, Yvette Villicana and Evelyn Mendoza, Richmond High School students.\u003c/figcaption>\u003c/figure>\n\u003cp>Saechao recalls lying in bed awake past midnight, feeling “paralyzed,” and seeing a blurry figure.\u003c/p>\n\u003cp>The incident has made her “paranoid” about sleeping, so she covers her face at night.\u003c/p>\n\u003cp>“I sleep next to the wall so I won’t see anything,” she said.\u003c/p>\n\u003cp>Sleep paralysis can occur as you fall asleep or as you wake up. It goes away by itself after a few seconds or a few minutes. People who experience this are usually in their teens, 20s and 30s.\u003c/p>\n\u003cp>Researchers believe sleep paralysis happens when someone’s sleep cycle is disrupted, and especially when they’re in a dream state. This occurs in the rapid eye movement or REM stage of sleep, and can be caused by anxiety and stress.\u003c/p>\n\u003cp>Yvette Villicaña first experienced sleep paralysis when she was in middle school.\u003c/p>\n\u003cp>“It’s not as overwhelming for me as other people, because I don’t see shadowy figures,” she said. “I try to move, but sometimes I can’t. And after some time, it does go away. I used to think I was the only \u003cspan style=\"font-weight: 400\">one who experienced this.”\u003c/span>\u003c/p>\n\u003cp>\u003cspan style=\"font-weight: 400\"> After working on this story for KQED’s “\u003ca href=\"https://ww2.kqed.org/education/2018/04/18/youth-takeover-of-kqed-news-starts-april-23/\">Youth Takeover\u003c/a>,” Villicaña says it’s good to know she’s not alone, but it’s tough to realize other people have more traumatic experiences because of their hallucinations.\u003c/span>\u003c/p>\n\u003cp>Sleep paralysis is harmless by itself but can lead to insomnia or narcolepsy, a more serious condition that causes uncontrollable sleepiness during the day.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\u003cspan style=\"font-weight: 400\">You can try to stop sleep paralysis by avoiding naps and not sleeping on your back, because it makes you feel vulnerable. Consult a mental health professional for stress or anxiety. And if it doesn’t go away, seek help from a sleep specialist. \u003c/span>\u003c/p>\n\n\u003c/div>\u003c/p>",
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"content": "\u003cp>A federal court on Monday heard arguments over when to start the trial of former Theranos CEO Elizabeth Holmes and her former No. 2 Sunny Balwani, who are accused of defrauding investors, patients, and doctors in a blood-testing scandal that has rocked the business world and captivated the public imagination.\u003c/p>\n\u003cp>A judge proposed a trial start date of July 8, multiple news organizations reported from a status conference in federal court in San Jose on Monday. But the trial will likely start later than that, perhaps even next year. The next status conference for the case is scheduled for July 1. Whenever it happens, the trial is certain to draw attention far beyond the world of health care.\u003c/p>\n\u003cp>Holmes and Balwani are charged with two counts of conspiracy to commit wire fraud and nine counts of wire fraud. They each face a maximum of 20 years in prison and up to $2.7 million in fines, a figure that doesn’t include any cash the government might demand as restitution for the alleged fraud. Holmes and Balwani have each pleaded not guilty.\u003c/p>\n\u003cp>According to prosecutors, the former couple presided over a yearslong fraudulent scheme, lying about the capabilities of their blood-testing technology while making grand projections about future profits.\u003c/p>\n\u003cp>Last year, Holmes and Theranos settled similar fraud charges brought by the Securities and Exchange Commission. Balwani has contested the SEC charges.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>Holmes stepped down from the company in June, and Theranos shut down in September.\u003c/p>\n\u003cp>The impending trial is the latest twist in a saga that began when Holmes dropped out of Stanford as a 19-year-old sophomore to found Theranos. Her company soared to a $9 billion valuation, the largest of any venture-backed health care firm, on the promise that it could diagnose scores of diseases with only the blood from a pin prick. But the story came unstuck in 2015 with a series of damning revelations in The Wall Street Journal, setting in motion a series of lawsuits, layoffs, and regulatory crackdowns that would eventually doom the company.\u003c/p>\n\u003cp>The saga has since become the subject of a book, a podcast, and competing documentaries.\u003c/p>\n\u003cp>It’s not clear yet what strategy Holmes’s lawyers will deploy to defend her in the upcoming trial. But a motion they filed last week suggests that it could involve jabbing at John Carreyrou, the Wall Street Journal reporter who broke the story of wrongdoing at Theranos and whose reporting spurred a series of regulatory investigations.\u003c/p>\n\u003cp>“The jury should be aware that an outside actor, eager to break a story (and portray the story as a work of investigative journalism), was exerting influence on the regulatory process in a way that appears to have warped the agencies’ focus on the company and possibly biased the agencies’ findings against it,” Holmes’s lawyers wrote in their motion. In an apparent effort to bolster that defense, Holmes’s lawyers are also seeking records documenting Carreyrou’s communications with the Food and Drug Administration and the Centers for Medicare and Medicaid Services.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\u003cem>\u003cspan style=\"font-weight: 400;\">This \u003ca href=\"https://www.statnews.com/2019/04/22/criminal-trial-for-ex-theranos-ceo-elizabeth-holmes-may-start-this-summer/\" target=\"_blank\" rel=\"noopener\">story\u003c/a> was originally published by \u003ca href=\"https://www.statnews.com/\" target=\"_blank\" rel=\"noopener\">STAT\u003c/a>, an online publication of Boston Globe Media that covers health, medicine, and scientific discovery. \u003c/span>\u003c/em>\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>A federal court on Monday heard arguments over when to start the trial of former Theranos CEO Elizabeth Holmes and her former No. 2 Sunny Balwani, who are accused of defrauding investors, patients, and doctors in a blood-testing scandal that has rocked the business world and captivated the public imagination.\u003c/p>\n\u003cp>A judge proposed a trial start date of July 8, multiple news organizations reported from a status conference in federal court in San Jose on Monday. But the trial will likely start later than that, perhaps even next year. The next status conference for the case is scheduled for July 1. Whenever it happens, the trial is certain to draw attention far beyond the world of health care.\u003c/p>\n\u003cp>Holmes and Balwani are charged with two counts of conspiracy to commit wire fraud and nine counts of wire fraud. They each face a maximum of 20 years in prison and up to $2.7 million in fines, a figure that doesn’t include any cash the government might demand as restitution for the alleged fraud. Holmes and Balwani have each pleaded not guilty.\u003c/p>\n\u003cp>According to prosecutors, the former couple presided over a yearslong fraudulent scheme, lying about the capabilities of their blood-testing technology while making grand projections about future profits.\u003c/p>\n\u003cp>Last year, Holmes and Theranos settled similar fraud charges brought by the Securities and Exchange Commission. Balwani has contested the SEC charges.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>Holmes stepped down from the company in June, and Theranos shut down in September.\u003c/p>\n\u003cp>The impending trial is the latest twist in a saga that began when Holmes dropped out of Stanford as a 19-year-old sophomore to found Theranos. Her company soared to a $9 billion valuation, the largest of any venture-backed health care firm, on the promise that it could diagnose scores of diseases with only the blood from a pin prick. But the story came unstuck in 2015 with a series of damning revelations in The Wall Street Journal, setting in motion a series of lawsuits, layoffs, and regulatory crackdowns that would eventually doom the company.\u003c/p>\n\u003cp>The saga has since become the subject of a book, a podcast, and competing documentaries.\u003c/p>\n\u003cp>It’s not clear yet what strategy Holmes’s lawyers will deploy to defend her in the upcoming trial. But a motion they filed last week suggests that it could involve jabbing at John Carreyrou, the Wall Street Journal reporter who broke the story of wrongdoing at Theranos and whose reporting spurred a series of regulatory investigations.\u003c/p>\n\u003cp>“The jury should be aware that an outside actor, eager to break a story (and portray the story as a work of investigative journalism), was exerting influence on the regulatory process in a way that appears to have warped the agencies’ focus on the company and possibly biased the agencies’ findings against it,” Holmes’s lawyers wrote in their motion. In an apparent effort to bolster that defense, Holmes’s lawyers are also seeking records documenting Carreyrou’s communications with the Food and Drug Administration and the Centers for Medicare and Medicaid Services.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\u003cem>\u003cspan style=\"font-weight: 400;\">This \u003ca href=\"https://www.statnews.com/2019/04/22/criminal-trial-for-ex-theranos-ceo-elizabeth-holmes-may-start-this-summer/\" target=\"_blank\" rel=\"noopener\">story\u003c/a> was originally published by \u003ca href=\"https://www.statnews.com/\" target=\"_blank\" rel=\"noopener\">STAT\u003c/a>, an online publication of Boston Globe Media that covers health, medicine, and scientific discovery. \u003c/span>\u003c/em>\u003c/p>\n\n\u003c/div>\u003c/p>",
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"title": "'Mind-Blowing' Ethical Issues Arise as Brains of Dead Pigs Are Partially Revived",
"headTitle": "‘Mind-Blowing’ Ethical Issues Arise as Brains of Dead Pigs Are Partially Revived | KQED",
"content": "\u003cp>The brains of dead pigs have been somewhat revived by scientists hours after the animals were killed in a slaughterhouse.\u003c/p>\n\u003cp>The Yale University research team is careful to say that none of the brains regained the kind of organized electrical activity associated with consciousness or awareness. Still, the experiment \u003ca href=\"https://www.nature.com/articles/s41586-019-1099-1\" target=\"_blank\" rel=\"noopener\">described\u003c/a> Wednesday in the journal \u003cem>Nature \u003c/em>showed that a surprising amount of cellular function was either preserved or restored.\u003c/p>\n\u003cp>[pullquote]Implications of the study have staggered ethicists contemplating how the research should move forward and how it fits into the understanding of what separates the living from the dead.[/pullquote]The implications of this study have staggered ethicists, as they contemplate how this research should move forward and how it fits into the current understanding of what separates the living from the dead.\u003c/p>\n\u003cp>“It was mind-blowing,” says \u003ca href=\"https://law.duke.edu/fac/farahany/\" target=\"_blank\" rel=\"noopener\">Nita Farahany\u003c/a>, who studies the ethics of emerging technologies at Duke Law School. “My initial reaction was pretty shocked. It’s a groundbreaking discovery, but it also really fundamentally changes a lot of what the existing beliefs are in neuroscience about the irreversible loss of brain function once there is deprivation of oxygen to the brain.”\u003c/p>\n\u003cp>The brain is extremely sensitive to a lack of oxygen and shuts down quickly. But researchers have long known that viable cells can be removed from post-mortem brains hours after death, says \u003ca href=\"https://medicine.yale.edu/lab/sestan/\" target=\"_blank\" rel=\"noopener\">Nenad Sestan\u003c/a>, a neuroscientist at the Yale School of Medicine in New Haven, Conn.\u003c/p>\n\u003cp>Such cells can be studied in a lab dish, Sestan says, “but the problem is, once you do that, you are losing the 3D organization of the brain.”\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>He and some colleagues wondered whether it might be possible to study brain cells while leaving them in an intact organ. Doing so meant somehow supplying them with oxygen, nutrients and various other cell-protective chemicals.\u003c/p>\n\u003cp>The scientists have spent the past six years developing a technique to do that, testing their methods on around 300 pig heads they obtained from a local pork processing center.\u003c/p>\n\u003cp>“This really was a shot-in-the-dark project,” says team member Stefano Daniele. “We had no preconceived notion of whether or not this could work.”\u003c/p>\n\u003cp>After deciding on the final version of their technology, which they call Brain\u003cem>Ex\u003c/em>, they did a detailed study using 32 pig heads. Daniele says that while at the slaughterhouse, he and fellow researcher \u003ca href=\"https://medicine.yale.edu/intranet/facultybydept/zvonimir_vrselja.profile\" target=\"_blank\" rel=\"noopener\">Zvonimir Vrselja\u003c/a> flushed the brains to clear out residual blood and to cool down the tissue.\u003c/p>\n\u003cp>Back at the lab, they removed the brains from the pigs’ heads and placed the isolated brains in an experimental chamber. The researchers hooked key blood vessels up to a device that pumped in a specially formulated chemical cocktail for six hours, starting about four hours after the pigs had been killed.\u003c/p>\n\u003cp>These brains ended up looking dramatically different from pig brains that were left alone to deteriorate. “We found that tissue and cellular structure is preserved and cell death is reduced. In addition, some molecular and cellular functions were restored,” Sestan says. “This is not a living brain, but it is a cellularly active brain.”\u003c/p>\n\u003cp>The researchers’ approach offers a new way to study brain diseases or injuries in the lab and to explore the basic biology of the brain. “We could actually answer questions that we can’t now,” Vrselja says.\u003c/p>\n\u003cp>“This is a real breakthrough for brain research. It’s a new tool that bridges the gap between basic neuroscience and clinical research,” agrees \u003ca href=\"https://www.braininitiative.nih.gov/about/contact-us\" target=\"_blank\" rel=\"noopener\">Andrea Beckel-Mitchener\u003c/a> of the National Institute of Mental Health who works with the BRAIN Initiative. The \u003ca href=\"https://www.braininitiative.nih.gov/\" target=\"_blank\" rel=\"noopener\">BRAIN Initiative\u003c/a>, which started in 2013 to accelerate neuroscience research, provided funding for the work.\u003c/p>\n\u003cp>The researchers emphasize that the goal was definitely not to restore consciousness in these pig brains. “It was something that the researchers were actively worried about,” says \u003ca href=\"https://bioethics.yale.edu/people/our-primary-team/stephen-latham\">Stephen Latham\u003c/a>, a Yale bioethicist who worked with the team.\u003c/p>\n\u003cp>The scientists constantly monitored the pig brains’ electrical activity, Latham says. If they had seen any evidence that signals associated with consciousness had emerged, they would have used anesthesia and cooling to shut that down immediately.\u003c/p>\n\u003cp>“And the reason is that they didn’t want to do an experiment that raises the ethical questions that would be raised if consciousness were being evoked in this brain,” Latham says, “without first getting some kind of serious ethical guidance.”\u003c/p>\n\u003cp>The special solution pumped into the brains included the anti-seizure drug lamotrigine, which is known to block or dampen neuronal activity. That’s because “the researchers thought that brain cells might be better preserved and their function might be better restored if they were not active,” Latham says.\u003c/p>\n\u003cp>But tests done on single cells taken from the pig brains, which involved washing off the solution, showed that individual cells were capable of electrochemical responses. So it’s unclear whether the team would have seen global electrical activity linked to consciousness in the pig brains if the neuronal-activity blocker had been left out of the treatment or if the blocker had been removed after cells had partly revived.\u003c/p>\n\u003cp>“That’s a very important question, and one that we have discussed at length,” Daniele says. “We cannot speak with any scientific certainty to that point since we did not run those experiments.”\u003c/p>\n\u003cp>The potential ethical questions raised by this research range from how to protect animal welfare to how it might affect organ donation from people declared brain-dead.\u003c/p>\n\u003cp>“The science is so new that we all need to work together to think proactively about its ethical implications so that we can responsibly shape how this science moves forward,” says \u003ca href=\"https://www.ninds.nih.gov/node/15093\" target=\"_blank\" rel=\"noopener\">Khara Ramos\u003c/a>, director of the neuroethics program at the National Institute of Neurological Disorders and Stroke.\u003c/p>\n\u003cp>A few years ago, the Yale researchers consulted with a neuroethics working group convened by the National Institutes of Health’s BRAIN Initiative. That’s how Farahany learned of the research. She says these results need to be replicated in other labs to see whether they hold up.\u003c/p>\n\u003cp>But if they do, the findings challenge a lot of assumptions that underlie legal and ethical controls on experiments.\u003c/p>\n\u003cp>“If it’s a dead animal, it’s not subject to any research protections because you wouldn’t expect that it would suffer from any pain or distress or need to be thought about in terms of humane care,” Farahany says. But if that animal’s brain can be even partially revived, she asks, then “what do we need to do immediately, today, in order to ensure that there’s adequate protections in place for animal research subjects?”\u003c/p>\n\u003cp>What’s more, she adds, “immediately people are going to recognize the potential of this research. If, in fact, it is possible to restore cellular activity to brain tissue that we thought was irreversibly lost in the past, of course people are going to want to apply this eventually in humans.”\u003c/p>\n\u003cp>While there are protections in place for human research subjects, that’s not so much the case for dead human tissue, says \u003ca href=\"https://clinicalcenter.nih.gov/meet-our-doctors/cgrady.html\" target=\"_blank\" rel=\"noopener\">Christine Grady\u003c/a>, chief of the department of bioethics at the NIH Clinical Center.\u003c/p>\n\u003cp>“Once a human dies and their tissue is in a laboratory, there are many fewer restrictions on what can be done,” Grady says. “It is interesting to think about this issue in light of this experiment.”\u003c/p>\n\u003cp>In a commentary that accompanied the research paper in \u003cem>Nature\u003c/em>, Farahany and her colleagues \u003ca href=\"https://law.stanford.edu/directory/henry-t-greely/\" target=\"_blank\" rel=\"noopener\">Henry Greely\u003c/a> and \u003ca href=\"https://psychandneuro.duke.edu/people/charlie-giattino\" target=\"_blank\" rel=\"noopener\">Charles Giattino\u003c/a> say the work reminds them of a line from the 1987 movie \u003cem>The Princess Bride\u003c/em>: “There’s a big difference between mostly dead and all dead. Mostly dead is slightly alive.”\u003c/p>\n\u003cp>Research like this could complicate the effort to secure organs for transplant from people who have been declared brain-dead, according to another commentary written by Case Western Reserve University bioethicists \u003ca href=\"https://case.edu/medicine/bioethics/about/faculty-staff/stuart-youngner\" target=\"_blank\" rel=\"noopener\">Stuart Youngner\u003c/a> and \u003ca href=\"https://case.edu/medicine/bioethics/about/faculty-staff/insoo-hyun\" target=\"_blank\" rel=\"noopener\">Insoo Hyun\u003c/a>.\u003c/p>\n\u003cp>If people who are declared brain-dead could become candidates for attempts at brain resuscitation, they write, “it could become harder for physicians or family members to be convinced that further medical intervention is futile.”\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2019 NPR. To see more, visit https://www.npr.org.\u003cimg decoding=\"async\" src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Scientists+Restore+Some+Function+In+The+Brains+Of+Dead+Pigs&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\u003cp>[ad floatright]\u003c/p>\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>He and some colleagues wondered whether it might be possible to study brain cells while leaving them in an intact organ. Doing so meant somehow supplying them with oxygen, nutrients and various other cell-protective chemicals.\u003c/p>\n\u003cp>The scientists have spent the past six years developing a technique to do that, testing their methods on around 300 pig heads they obtained from a local pork processing center.\u003c/p>\n\u003cp>“This really was a shot-in-the-dark project,” says team member Stefano Daniele. “We had no preconceived notion of whether or not this could work.”\u003c/p>\n\u003cp>After deciding on the final version of their technology, which they call Brain\u003cem>Ex\u003c/em>, they did a detailed study using 32 pig heads. Daniele says that while at the slaughterhouse, he and fellow researcher \u003ca href=\"https://medicine.yale.edu/intranet/facultybydept/zvonimir_vrselja.profile\" target=\"_blank\" rel=\"noopener\">Zvonimir Vrselja\u003c/a> flushed the brains to clear out residual blood and to cool down the tissue.\u003c/p>\n\u003cp>Back at the lab, they removed the brains from the pigs’ heads and placed the isolated brains in an experimental chamber. The researchers hooked key blood vessels up to a device that pumped in a specially formulated chemical cocktail for six hours, starting about four hours after the pigs had been killed.\u003c/p>\n\u003cp>These brains ended up looking dramatically different from pig brains that were left alone to deteriorate. “We found that tissue and cellular structure is preserved and cell death is reduced. In addition, some molecular and cellular functions were restored,” Sestan says. “This is not a living brain, but it is a cellularly active brain.”\u003c/p>\n\u003cp>The researchers’ approach offers a new way to study brain diseases or injuries in the lab and to explore the basic biology of the brain. “We could actually answer questions that we can’t now,” Vrselja says.\u003c/p>\n\u003cp>“This is a real breakthrough for brain research. It’s a new tool that bridges the gap between basic neuroscience and clinical research,” agrees \u003ca href=\"https://www.braininitiative.nih.gov/about/contact-us\" target=\"_blank\" rel=\"noopener\">Andrea Beckel-Mitchener\u003c/a> of the National Institute of Mental Health who works with the BRAIN Initiative. The \u003ca href=\"https://www.braininitiative.nih.gov/\" target=\"_blank\" rel=\"noopener\">BRAIN Initiative\u003c/a>, which started in 2013 to accelerate neuroscience research, provided funding for the work.\u003c/p>\n\u003cp>The researchers emphasize that the goal was definitely not to restore consciousness in these pig brains. “It was something that the researchers were actively worried about,” says \u003ca href=\"https://bioethics.yale.edu/people/our-primary-team/stephen-latham\">Stephen Latham\u003c/a>, a Yale bioethicist who worked with the team.\u003c/p>\n\u003cp>The scientists constantly monitored the pig brains’ electrical activity, Latham says. If they had seen any evidence that signals associated with consciousness had emerged, they would have used anesthesia and cooling to shut that down immediately.\u003c/p>\n\u003cp>“And the reason is that they didn’t want to do an experiment that raises the ethical questions that would be raised if consciousness were being evoked in this brain,” Latham says, “without first getting some kind of serious ethical guidance.”\u003c/p>\n\u003cp>The special solution pumped into the brains included the anti-seizure drug lamotrigine, which is known to block or dampen neuronal activity. That’s because “the researchers thought that brain cells might be better preserved and their function might be better restored if they were not active,” Latham says.\u003c/p>\n\u003cp>But tests done on single cells taken from the pig brains, which involved washing off the solution, showed that individual cells were capable of electrochemical responses. So it’s unclear whether the team would have seen global electrical activity linked to consciousness in the pig brains if the neuronal-activity blocker had been left out of the treatment or if the blocker had been removed after cells had partly revived.\u003c/p>\n\u003cp>“That’s a very important question, and one that we have discussed at length,” Daniele says. “We cannot speak with any scientific certainty to that point since we did not run those experiments.”\u003c/p>\n\u003cp>The potential ethical questions raised by this research range from how to protect animal welfare to how it might affect organ donation from people declared brain-dead.\u003c/p>\n\u003cp>“The science is so new that we all need to work together to think proactively about its ethical implications so that we can responsibly shape how this science moves forward,” says \u003ca href=\"https://www.ninds.nih.gov/node/15093\" target=\"_blank\" rel=\"noopener\">Khara Ramos\u003c/a>, director of the neuroethics program at the National Institute of Neurological Disorders and Stroke.\u003c/p>\n\u003cp>A few years ago, the Yale researchers consulted with a neuroethics working group convened by the National Institutes of Health’s BRAIN Initiative. That’s how Farahany learned of the research. She says these results need to be replicated in other labs to see whether they hold up.\u003c/p>\n\u003cp>But if they do, the findings challenge a lot of assumptions that underlie legal and ethical controls on experiments.\u003c/p>\n\u003cp>“If it’s a dead animal, it’s not subject to any research protections because you wouldn’t expect that it would suffer from any pain or distress or need to be thought about in terms of humane care,” Farahany says. But if that animal’s brain can be even partially revived, she asks, then “what do we need to do immediately, today, in order to ensure that there’s adequate protections in place for animal research subjects?”\u003c/p>\n\u003cp>What’s more, she adds, “immediately people are going to recognize the potential of this research. If, in fact, it is possible to restore cellular activity to brain tissue that we thought was irreversibly lost in the past, of course people are going to want to apply this eventually in humans.”\u003c/p>\n\u003cp>While there are protections in place for human research subjects, that’s not so much the case for dead human tissue, says \u003ca href=\"https://clinicalcenter.nih.gov/meet-our-doctors/cgrady.html\" target=\"_blank\" rel=\"noopener\">Christine Grady\u003c/a>, chief of the department of bioethics at the NIH Clinical Center.\u003c/p>\n\u003cp>“Once a human dies and their tissue is in a laboratory, there are many fewer restrictions on what can be done,” Grady says. “It is interesting to think about this issue in light of this experiment.”\u003c/p>\n\u003cp>In a commentary that accompanied the research paper in \u003cem>Nature\u003c/em>, Farahany and her colleagues \u003ca href=\"https://law.stanford.edu/directory/henry-t-greely/\" target=\"_blank\" rel=\"noopener\">Henry Greely\u003c/a> and \u003ca href=\"https://psychandneuro.duke.edu/people/charlie-giattino\" target=\"_blank\" rel=\"noopener\">Charles Giattino\u003c/a> say the work reminds them of a line from the 1987 movie \u003cem>The Princess Bride\u003c/em>: “There’s a big difference between mostly dead and all dead. Mostly dead is slightly alive.”\u003c/p>\n\u003cp>Research like this could complicate the effort to secure organs for transplant from people who have been declared brain-dead, according to another commentary written by Case Western Reserve University bioethicists \u003ca href=\"https://case.edu/medicine/bioethics/about/faculty-staff/stuart-youngner\" target=\"_blank\" rel=\"noopener\">Stuart Youngner\u003c/a> and \u003ca href=\"https://case.edu/medicine/bioethics/about/faculty-staff/insoo-hyun\" target=\"_blank\" rel=\"noopener\">Insoo Hyun\u003c/a>.\u003c/p>\n\u003cp>If people who are declared brain-dead could become candidates for attempts at brain resuscitation, they write, “it could become harder for physicians or family members to be convinced that further medical intervention is futile.”\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2019 NPR. To see more, visit https://www.npr.org.\u003cimg decoding=\"async\" src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Scientists+Restore+Some+Function+In+The+Brains+Of+Dead+Pigs&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cp>[dl_subscribe]At first, the idea of using porcupine quills to patch up wounds sounds torturous. But now researchers are taking inspiration from the spiky rodent to make a new type of surgical staple that may be less damaging — and painful — than current staples.\u003c/p>\n\u003cp>Worldwide, surgeons perform more than 4 million procedures annually, usually using sutures and staples to close wounds in patients. Yet, these traditional tools designed to aid healing can create their own problems.\u003c/p>\n\u003cp>Doctors often use surgical staples because they’re faster to insert than sutures, which require a needle and thread. But current surgical staples, which are made of metal, tear tissue on the way in and cause more damage when bent to stay in place, said Jeff Karp, a bioengineer at Brigham and Women’s Hospital in Boston and professor of medicine at Harvard Medical School.\u003c/p>\n\u003cp>“We’ve been using sutures and staples for decades, and they’ve been incredibly useful,” said Karp. “But there are challenges in terms of placing them for minimally invasive procedures.”\u003c/p>\n\u003cp>Staples that work like porcupine quills could solve those challenges, Karp said.\u003c/p>\n\u003cfigure id=\"attachment_1939841\" class=\"wp-caption aligncenter\" style=\"max-width: 640px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_quill_full_length.jpg\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"wp-image-1939841 size-large\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_quill_full_length-1020x574.jpg\" alt=\"\" width=\"640\" height=\"360\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_quill_full_length-1020x574.jpg 1020w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_quill_full_length-160x90.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_quill_full_length-800x450.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_quill_full_length-768x432.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_quill_full_length-1200x675.jpg 1200w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_quill_full_length-1920x1080.jpg 1920w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_quill_full_length.jpg 2048w\" sizes=\"auto, (max-width: 640px) 100vw, 640px\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Porcupines use the sharp dark tips of their modified hairs, called quills, for defense. \u003ccite>(Josh Cassidy/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Karp and his team have been searching for new ways doctors can hold tissue together. For inspiration, they turned to nature.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>In one brainstorming session, the researchers thought of the porcupine and its quill.\u003c/p>\n\u003cp>The North American porcupine appears cute, but it has upward of 30,000 menacing quills over most of its body. The slow-moving herbivore delivers them only as a last-resort defense against predators.\u003c/p>\n\u003cfigure id=\"attachment_1939843\" class=\"wp-caption aligncenter\" style=\"max-width: 500px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_eat_leaf.gif\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-full wp-image-1939843\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_eat_leaf.gif\" alt=\"\" width=\"500\" height=\"281\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">All porcupines, including this North American porcupine, eat only plant foods. \u003ccite>(Josh Cassidy/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Generally, the quills, which are specialized hairs, lie flat on the mammal’s body. Only when threatened will the porcupine erect them. And contrary to popular belief, they don’t shoot them out from their bodies.\u003c/p>\n\u003cp>“The wonderful thing about porcupines is that they seem to feel secure,” said \u003ca href=\"http://biology.qc.cuny.edu/people/faculty/dr-uldis-roze/\">Uldis Roze\u003c/a>, biology professor emeritus at Queens College, City University of New York. “They feel like they’re not in danger, and they’re sweet.”\u003c/p>\n\u003cfigure id=\"attachment_1939846\" class=\"wp-caption aligncenter\" style=\"max-width: 640px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_eats_acorn.jpg\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-large wp-image-1939846\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_eats_acorn-1020x574.jpg\" alt=\"\" width=\"640\" height=\"360\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_eats_acorn-1020x574.jpg 1020w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_eats_acorn-160x90.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_eats_acorn-800x450.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_eats_acorn-768x432.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_eats_acorn-1200x675.jpg 1200w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_eats_acorn-1920x1080.jpg 1920w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_eats_acorn.jpg 2048w\" sizes=\"auto, (max-width: 640px) 100vw, 640px\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">When the porcupine is relaxed, its other hairs and fur hide most of the quills. \u003ccite>(Josh Cassidy/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Any potential predator unfamiliar with a porcupine, such as a dog or mountain lion, would be wise to heed its warnings across three senses, according to Roze’s book, “\u003ca href=\"http://www.cornellpress.cornell.edu/book/?GCOI=80140100667570\">The North American Porcupine\u003c/a>.” The adult’s contrasting black-and-white pattern on the quills and other hairs — known as aposematic coloration — is a visual warning signal. A unique pungent odor and ominous teeth-clattering should alarm the nose and ears.\u003c/p>\n\u003cp>Should the predator ignore these signs and attack, the porcupine will use its powerful spiky tail to slap at the aggressor. Each quill is held in place by its own special structure in the porcupine’s skin. The contact from colliding with a predator causes the skin to release the quills from the porcupine’s body.\u003c/p>\n\u003cfigure id=\"attachment_1939848\" class=\"wp-caption aligncenter\" style=\"max-width: 500px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/04/DL607_Glove_quilled_by_porcupine.gif\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-full wp-image-1939848\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/04/DL607_Glove_quilled_by_porcupine.gif\" alt=\"\" width=\"500\" height=\"281\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">A quill detaches from the porcupine’s body only from physical impact with a predator. \u003ccite>(Josh Cassidy/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>North American porcupine quills pack a hidden punch: microscopic, backward-facing barbs.\u003c/p>\n\u003cp>Covering just the needlelike tip of the quills, the barbs make removing a quill difficult, because they flare out when pulled in the opposite direction.\u003c/p>\n\u003cp>That means that if a predator gets quilled, the quill might never come out. When scientists examine the skulls of deceased mountain lions, Roze said, they often find the tips of porcupine quills embedded in their jaws.\u003c/p>\n\u003cp>“The mountain lion just accepts it,” said Roze. “It’s part of the work of killing a porcupine.”\u003c/p>\n\u003cp>Of course, that mountain lion’s days of porcupine feasting may end forever if the quills keep it from eating or end up in the cat’s vulnerable internal organs.\u003c/p>\n\u003cfigure id=\"attachment_1939851\" class=\"wp-caption aligncenter\" style=\"max-width: 500px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/04/DL607_Removing_quill_from_finger.gif\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-full wp-image-1939851\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/04/DL607_Removing_quill_from_finger.gif\" alt=\"\" width=\"500\" height=\"281\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">The backward-facing barbs hook the quill into the predator’s body. \u003ccite>(Josh Cassidy/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Still, a quill passing through the body is far from painless — it’s excruciating — as Roze knows from personal experience. He was once quilled in his bicep when up in a tree trying to catch an agile porcupine. Despite his wife’s suggestion to seek medical care, he waited two harrowing days until the quill traveled in one direction and cleanly exited his lower arm. He kept the quill as a souvenir.\u003c/p>\n\u003cp>The quill’s barbs made penetration into his flesh easier. They also helped drive the quill through until it either exited or reached a stopping point, such as bone.\u003c/p>\n\u003cp>Those barbs are the main attraction to Karp. He and his team \u003ca href=\"https://doi.org/10.1073/pnas.1216441109\">ran experiments\u003c/a> comparing a barbed quill to a barbless quill. They measured the forces required to insert and remove the quills.\u003c/p>\n\u003cfigure id=\"attachment_1939854\" class=\"wp-caption aligncenter\" style=\"max-width: 640px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_Barbs_microscopic.jpg\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-large wp-image-1939854\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_Barbs_microscopic-1020x574.jpg\" alt=\"\" width=\"640\" height=\"360\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_Barbs_microscopic-1020x574.jpg 1020w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_Barbs_microscopic-160x90.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_Barbs_microscopic-800x450.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_Barbs_microscopic-768x432.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_Barbs_microscopic-1200x675.jpg 1200w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_Barbs_microscopic-1920x1080.jpg 1920w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_Barbs_microscopic.jpg 2048w\" sizes=\"auto, (max-width: 640px) 100vw, 640px\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">The overlapping microscopic barbs cover only the quill’s tip. \u003ccite>(Woo Kyung Cho/Chungnam National University)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>The results show that the barbs are dual-functional.\u003c/p>\n\u003cp>“They’re reducing the penetration force and increasing the pullout force,” said Karp. “It’s pretty neat.”\u003c/p>\n\u003cp>The team also discovered that the barbs do minimal damage by making a more perfect hole in the tissue on their way in. A barbless quill or surgical staple tears the tissue and creates gaps that are susceptible to infection.\u003c/p>\n\u003cp>A new medical staple designed with two barbed tips would require much less effort to place, and the barbs, with their gripping power, would hold it in position without needing to bend the staple.\u003c/p>\n\u003cfigure id=\"attachment_1939857\" class=\"wp-caption aligncenter\" style=\"max-width: 500px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/04/DL607_Barbed_staple_enters_skin.gif\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-full wp-image-1939857\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/04/DL607_Barbed_staple_enters_skin.gif\" alt=\"\" width=\"500\" height=\"281\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">A surgical staple with barbs like those on a porcupine quill could cause little tissue damage, similar to the way a serrated knife cuts a tomato. \u003ccite>(XVIVO Scientific Animation)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Karp said he anticipates making the new staples out of biodegradable material so they would fully dissolve over time without having to be pulled out. That could eliminate the need for a follow-up visit to remove them, he said.\u003c/p>\n\u003cp>The challenge now is recreating the full barb’s shape.\u003c/p>\n\u003cp>“Nature has designs that humans can’t achieve yet, at least at large scale,” Karp said. “Large-scale manufacturing is a human problem.”\u003c/p>\n\u003cp>But he estimated that if the right technologies become available, human testing of tools inspired by porcupine quills could begin in two to five years.\u003c/p>\n\u003cp>“This could be an enabler for smaller incisions to be made in a large number of surgeries,” Karp said. That would be good news for both surgeons and patients.\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp>Visit “Penelope” the porcupine at \u003ca href=\"https://lindsaywildlife.org/\">Lindsay Wildlife Experience\u003c/a> in Walnut Creek, California.\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>At first, the idea of using porcupine quills to patch up wounds sounds torturous. But now researchers are taking inspiration from the spiky rodent to make a new type of surgical staple that may be less damaging — and painful — than current staples.\u003c/p>\n\u003cp>Worldwide, surgeons perform more than 4 million procedures annually, usually using sutures and staples to close wounds in patients. Yet, these traditional tools designed to aid healing can create their own problems.\u003c/p>\n\u003cp>Doctors often use surgical staples because they’re faster to insert than sutures, which require a needle and thread. But current surgical staples, which are made of metal, tear tissue on the way in and cause more damage when bent to stay in place, said Jeff Karp, a bioengineer at Brigham and Women’s Hospital in Boston and professor of medicine at Harvard Medical School.\u003c/p>\n\u003cp>“We’ve been using sutures and staples for decades, and they’ve been incredibly useful,” said Karp. “But there are challenges in terms of placing them for minimally invasive procedures.”\u003c/p>\n\u003cp>Staples that work like porcupine quills could solve those challenges, Karp said.\u003c/p>\n\u003cfigure id=\"attachment_1939841\" class=\"wp-caption aligncenter\" style=\"max-width: 640px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_quill_full_length.jpg\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"wp-image-1939841 size-large\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_quill_full_length-1020x574.jpg\" alt=\"\" width=\"640\" height=\"360\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_quill_full_length-1020x574.jpg 1020w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_quill_full_length-160x90.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_quill_full_length-800x450.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_quill_full_length-768x432.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_quill_full_length-1200x675.jpg 1200w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_quill_full_length-1920x1080.jpg 1920w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_quill_full_length.jpg 2048w\" sizes=\"auto, (max-width: 640px) 100vw, 640px\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Porcupines use the sharp dark tips of their modified hairs, called quills, for defense. \u003ccite>(Josh Cassidy/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Karp and his team have been searching for new ways doctors can hold tissue together. For inspiration, they turned to nature.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>In one brainstorming session, the researchers thought of the porcupine and its quill.\u003c/p>\n\u003cp>The North American porcupine appears cute, but it has upward of 30,000 menacing quills over most of its body. The slow-moving herbivore delivers them only as a last-resort defense against predators.\u003c/p>\n\u003cfigure id=\"attachment_1939843\" class=\"wp-caption aligncenter\" style=\"max-width: 500px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_eat_leaf.gif\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-full wp-image-1939843\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_eat_leaf.gif\" alt=\"\" width=\"500\" height=\"281\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">All porcupines, including this North American porcupine, eat only plant foods. \u003ccite>(Josh Cassidy/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Generally, the quills, which are specialized hairs, lie flat on the mammal’s body. Only when threatened will the porcupine erect them. And contrary to popular belief, they don’t shoot them out from their bodies.\u003c/p>\n\u003cp>“The wonderful thing about porcupines is that they seem to feel secure,” said \u003ca href=\"http://biology.qc.cuny.edu/people/faculty/dr-uldis-roze/\">Uldis Roze\u003c/a>, biology professor emeritus at Queens College, City University of New York. “They feel like they’re not in danger, and they’re sweet.”\u003c/p>\n\u003cfigure id=\"attachment_1939846\" class=\"wp-caption aligncenter\" style=\"max-width: 640px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_eats_acorn.jpg\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-large wp-image-1939846\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_eats_acorn-1020x574.jpg\" alt=\"\" width=\"640\" height=\"360\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_eats_acorn-1020x574.jpg 1020w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_eats_acorn-160x90.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_eats_acorn-800x450.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_eats_acorn-768x432.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_eats_acorn-1200x675.jpg 1200w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_eats_acorn-1920x1080.jpg 1920w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_eats_acorn.jpg 2048w\" sizes=\"auto, (max-width: 640px) 100vw, 640px\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">When the porcupine is relaxed, its other hairs and fur hide most of the quills. \u003ccite>(Josh Cassidy/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Any potential predator unfamiliar with a porcupine, such as a dog or mountain lion, would be wise to heed its warnings across three senses, according to Roze’s book, “\u003ca href=\"http://www.cornellpress.cornell.edu/book/?GCOI=80140100667570\">The North American Porcupine\u003c/a>.” The adult’s contrasting black-and-white pattern on the quills and other hairs — known as aposematic coloration — is a visual warning signal. A unique pungent odor and ominous teeth-clattering should alarm the nose and ears.\u003c/p>\n\u003cp>Should the predator ignore these signs and attack, the porcupine will use its powerful spiky tail to slap at the aggressor. Each quill is held in place by its own special structure in the porcupine’s skin. The contact from colliding with a predator causes the skin to release the quills from the porcupine’s body.\u003c/p>\n\u003cfigure id=\"attachment_1939848\" class=\"wp-caption aligncenter\" style=\"max-width: 500px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/04/DL607_Glove_quilled_by_porcupine.gif\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-full wp-image-1939848\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/04/DL607_Glove_quilled_by_porcupine.gif\" alt=\"\" width=\"500\" height=\"281\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">A quill detaches from the porcupine’s body only from physical impact with a predator. \u003ccite>(Josh Cassidy/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>North American porcupine quills pack a hidden punch: microscopic, backward-facing barbs.\u003c/p>\n\u003cp>Covering just the needlelike tip of the quills, the barbs make removing a quill difficult, because they flare out when pulled in the opposite direction.\u003c/p>\n\u003cp>That means that if a predator gets quilled, the quill might never come out. When scientists examine the skulls of deceased mountain lions, Roze said, they often find the tips of porcupine quills embedded in their jaws.\u003c/p>\n\u003cp>“The mountain lion just accepts it,” said Roze. “It’s part of the work of killing a porcupine.”\u003c/p>\n\u003cp>Of course, that mountain lion’s days of porcupine feasting may end forever if the quills keep it from eating or end up in the cat’s vulnerable internal organs.\u003c/p>\n\u003cfigure id=\"attachment_1939851\" class=\"wp-caption aligncenter\" style=\"max-width: 500px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/04/DL607_Removing_quill_from_finger.gif\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-full wp-image-1939851\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/04/DL607_Removing_quill_from_finger.gif\" alt=\"\" width=\"500\" height=\"281\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">The backward-facing barbs hook the quill into the predator’s body. \u003ccite>(Josh Cassidy/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Still, a quill passing through the body is far from painless — it’s excruciating — as Roze knows from personal experience. He was once quilled in his bicep when up in a tree trying to catch an agile porcupine. Despite his wife’s suggestion to seek medical care, he waited two harrowing days until the quill traveled in one direction and cleanly exited his lower arm. He kept the quill as a souvenir.\u003c/p>\n\u003cp>The quill’s barbs made penetration into his flesh easier. They also helped drive the quill through until it either exited or reached a stopping point, such as bone.\u003c/p>\n\u003cp>Those barbs are the main attraction to Karp. He and his team \u003ca href=\"https://doi.org/10.1073/pnas.1216441109\">ran experiments\u003c/a> comparing a barbed quill to a barbless quill. They measured the forces required to insert and remove the quills.\u003c/p>\n\u003cfigure id=\"attachment_1939854\" class=\"wp-caption aligncenter\" style=\"max-width: 640px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_Barbs_microscopic.jpg\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-large wp-image-1939854\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_Barbs_microscopic-1020x574.jpg\" alt=\"\" width=\"640\" height=\"360\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_Barbs_microscopic-1020x574.jpg 1020w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_Barbs_microscopic-160x90.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_Barbs_microscopic-800x450.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_Barbs_microscopic-768x432.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_Barbs_microscopic-1200x675.jpg 1200w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_Barbs_microscopic-1920x1080.jpg 1920w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/04/DL607_Porcupines_Barbs_microscopic.jpg 2048w\" sizes=\"auto, (max-width: 640px) 100vw, 640px\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">The overlapping microscopic barbs cover only the quill’s tip. \u003ccite>(Woo Kyung Cho/Chungnam National University)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>The results show that the barbs are dual-functional.\u003c/p>\n\u003cp>“They’re reducing the penetration force and increasing the pullout force,” said Karp. “It’s pretty neat.”\u003c/p>\n\u003cp>The team also discovered that the barbs do minimal damage by making a more perfect hole in the tissue on their way in. A barbless quill or surgical staple tears the tissue and creates gaps that are susceptible to infection.\u003c/p>\n\u003cp>A new medical staple designed with two barbed tips would require much less effort to place, and the barbs, with their gripping power, would hold it in position without needing to bend the staple.\u003c/p>\n\u003cfigure id=\"attachment_1939857\" class=\"wp-caption aligncenter\" style=\"max-width: 500px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/04/DL607_Barbed_staple_enters_skin.gif\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-full wp-image-1939857\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/04/DL607_Barbed_staple_enters_skin.gif\" alt=\"\" width=\"500\" height=\"281\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">A surgical staple with barbs like those on a porcupine quill could cause little tissue damage, similar to the way a serrated knife cuts a tomato. \u003ccite>(XVIVO Scientific Animation)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Karp said he anticipates making the new staples out of biodegradable material so they would fully dissolve over time without having to be pulled out. That could eliminate the need for a follow-up visit to remove them, he said.\u003c/p>\n\u003cp>The challenge now is recreating the full barb’s shape.\u003c/p>\n\u003cp>“Nature has designs that humans can’t achieve yet, at least at large scale,” Karp said. “Large-scale manufacturing is a human problem.”\u003c/p>\n\u003cp>But he estimated that if the right technologies become available, human testing of tools inspired by porcupine quills could begin in two to five years.\u003c/p>\n\u003cp>“This could be an enabler for smaller incisions to be made in a large number of surgeries,” Karp said. That would be good news for both surgeons and patients.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>Visit “Penelope” the porcupine at \u003ca href=\"https://lindsaywildlife.org/\">Lindsay Wildlife Experience\u003c/a> in Walnut Creek, California.\u003c/p>\n\n\u003c/div>\u003c/p>",
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"title": "A Gulp of Genetically Modified Bacteria Might Someday Treat a Range of Illnesses",
"headTitle": "A Gulp of Genetically Modified Bacteria Might Someday Treat a Range of Illnesses | KQED",
"content": "\u003cp>Instead of eating a typical breakfast every day, Jonah Reeder gulps down a special protein shake.\u003c/p>\n\u003cp>“The nutrients in it like to sit at the bottom, so I usually have to shake it up and get all the nutrients from the protein and everything,” says Reeder, 21, of Farmington, Utah, as he shakes a big plastic bottle.\u003c/p>\n\u003caside class=\"pullquote alignright\">‘I think that’s very cool that they found a way to use a natural probiotic that’s found in the digestive tract to help the human body.’\u003ccite>Johah Reeder, Farmington, Utah\u003c/cite>\u003c/aside>\n\u003cp>Reeder was born with a \u003ca href=\"https://ghr.nlm.nih.gov/condition/phenylketonuria\">rare genetic disorder called phenylketonuria\u003c/a>, or PKU. If he eats meat, drinks milk or consumes other common sources of protein, toxic levels of the amino acid phenylalanine could build up in his body and damage his brain.\u003c/p>\n\u003cp>So Reeder gets his protein from the shake, which is rich in other amino acids, vitamins and proteins that don’t contain phenylalanine.\u003c/p>\n\u003cp>“It’s a really healthy drink,” Reeder says. “It’s basically protein, except without phenylalanine.”\u003c/p>\n\u003cp>But Reeder hopes a new approach for treating diseases could help people like him. The idea is to use bacteria that have been genetically modified to do what Reeder’s body can’t — get rid of phenylalanine.\u003c/p>\n\u003cp>“I’m really excited to help out and hopefully find a treatment for PKU,” Reeder said recently, as he prepared to volunteer for a study testing the modified bacteria.\u003c/p>\n\u003cp>The bacteria Reeder is helping test are part of a new field of medical research that has emerged from two realms of biomedical science. One is the study of the \u003ca href=\"https://www.npr.org/series/218987212/microbiome\">human microbiome\u003c/a>, the microbes that inhabit our bodies. The other is synthetic biology, a field that looks at genetically engineering living organisms, including bacteria in the human gut.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>“It’s a new world of being able to use synthetic biology to program microbes to treat diseases, which I believe is the future,” says \u003ca href=\"https://silver.med.harvard.edu/\">Pamela Silver\u003c/a>, a synthetic biologist at Harvard Medical School in Boston.\u003c/p>\n\u003cp>Scientists hope to genetically modify microbes from the human microbiome to treat a range of diseases, including digestive disorders like \u003ca href=\"https://www.niddk.nih.gov/health-information/digestive-diseases/ulcerative-colitis\">ulcerative colitis \u003c/a>and \u003ca href=\"https://www.cdc.gov/ibd/what-is-IBD.htm\">inflammatory bowel disease\u003c/a>.\u003c/p>\n\u003cp>“Microbes are something that we as synthetic biologists see as highly engineer-able. We understand how to engineer microbes so it seems like the perfect interface between synthetic biology and health,” Silver says.\u003c/p>\n\u003cp>One company, \u003ca href=\"https://www.actobio.com/\">ActoBio Therapeutics \u003c/a>of Ghent, Belgium, has just started using genetically engineered microbes to try to treat \u003ca href=\"https://medlineplus.gov/diabetestype1.html\">Type 1 diabetes\u003c/a>. Another one, \u003ca href=\"https://www.oragenics.com/\">Oragenics of Tampa, Fla.,\u003c/a> is testing a modified bacterium to treat mouth sores caused by cancer chemotherapy. And \u003ca href=\"http://oselinc.com/home/\">Osel\u003c/a> of Mountain View, Calif., hopes engineered microbes could prevent HIV infections.\u003c/p>\n\u003cp>Reeder is helping test modified \u003ca href=\"https://www.cdc.gov/ecoli/index.html\">E. coli\u003c/a> bacteria. While some types of \u003cem>E. coli\u003c/em> can cause serious illness, the \u003cem>E. coli\u003c/em> type being used in the study is found in the human gut.\u003c/p>\n\u003cp>“It is a naturally occurring probiotic bacteria,” says Caroline Kurtz, a scientist at \u003ca href=\"https://www.synlogictx.com/\">Synlogic\u003c/a>, a Cambridge, Mass., biotech company, which created the modified version of the organism.\u003c/p>\n\u003cp>“We can enhance its function by introducing genes [or] by changing genes that are there, and design the cells to either produce something or consume something that may be beneficial for a patient,” Kurtz says.\u003c/p>\n\u003cp>Synlogic has also engineered \u003cem>E. coli\u003c/em> to rid life-threatening levels of ammonia from the bodies of people with \u003ca href=\"https://www.mayoclinic.org/diseases-conditions/cirrhosis/symptoms-causes/syc-20351487\">cirrhosis of the liver\u003c/a>.\u003c/p>\n\u003cp>“This is a really exciting new modality that allows us to think about therapies in a new way and really look at diseases in a whole new way: a living medicine that can respond to its environment,” Kurtz says.\u003c/p>\n\u003cp>Preliminary research involving mice and healthy adults \u003ca href=\"http://stm.sciencemag.org/lookup/doi/10.1126/scitranslmed.aau7975\">published recently\u003c/a> in the journal \u003cem>Science Translational Medicine\u003c/em> indicates Synlogic’s \u003cem>E. coli \u003c/em>are safe and may work. So the company is now testing them in patients with cirrhosis and PKU.\u003c/p>\n\u003cp>Reeder admits he was a little nervous when he first heard about all this.\u003c/p>\n\u003cp>“When you hear about \u003cem>E. coli\u003c/em> you think: sickness, throwing up. So I was a little bit skeptical. I wasn’t sure what to think because I was going to be ingesting \u003cem>E. coli\u003c/em>,” Reeder says.\u003c/p>\n\u003cp>But the more he learned about it, the more excited Reeder got about trying the engineered microbes.\u003c/p>\n\u003cp>“I think that’s very cool that they found a way to use a natural probiotic that’s found in the digestive tract to help the human body,” Reeder says.\u003c/p>\n\u003cp>Reeder spent the weekend in the clinic so doctors could monitor him closely and run tests as he ingested what normally would be dangerous amounts of protein. He then swallowed either the engineered \u003cem>E. coli\u003c/em> or a placebo. He wasn’t told which.\u003c/p>\n\u003cp>“It was liquid solution. It tasted kind of like mint taffy. It was pretty sweet,” he says.\u003c/p>\n\u003cp>Reeder thinks he got the engineered microbes.\u003c/p>\n\u003cp>“I could immediately feel my cognitive abilities falling down after drinking the 20 grams of protein. And then I took the drug and I started feeling a lot better. I obtained more energy and my cognitive abilities got quicker,” he says.\u003c/p>\n\u003cp>“It was really cool to feel that. I could tell it was working. It was pretty cool,” Reeder says.\u003c/p>\n\u003cp>Much more research is needed to know whether genetically engineered microbes are safe and really work. But Synlogic hopes to report results from the cirrhosis and PKU studies later this year.\u003c/p>\n\u003cp>Before any of these experimental treatments could be used routinely, they would have to be reviewed and approved by the Food and Drug Administration. That’s a process that could take years.\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2019 NPR. To see more, visit https://www.npr.org.\u003cimg decoding=\"async\" src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=A+Gulp+Of+Genetically+Modified+Bacteria+Might+Someday+Treat+A+Range+Of+Illnesses&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\u003cp>\u003c/p>\n",
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"excerpt": "Researchers think genetically engineered versions of microbes that can live in humans could help treat some rare genetic disorders and perhaps help with Type 1 diabetes, cirrhosis and cancer.",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>Instead of eating a typical breakfast every day, Jonah Reeder gulps down a special protein shake.\u003c/p>\n\u003cp>“The nutrients in it like to sit at the bottom, so I usually have to shake it up and get all the nutrients from the protein and everything,” says Reeder, 21, of Farmington, Utah, as he shakes a big plastic bottle.\u003c/p>\n\u003caside class=\"pullquote alignright\">‘I think that’s very cool that they found a way to use a natural probiotic that’s found in the digestive tract to help the human body.’\u003ccite>Johah Reeder, Farmington, Utah\u003c/cite>\u003c/aside>\n\u003cp>Reeder was born with a \u003ca href=\"https://ghr.nlm.nih.gov/condition/phenylketonuria\">rare genetic disorder called phenylketonuria\u003c/a>, or PKU. If he eats meat, drinks milk or consumes other common sources of protein, toxic levels of the amino acid phenylalanine could build up in his body and damage his brain.\u003c/p>\n\u003cp>So Reeder gets his protein from the shake, which is rich in other amino acids, vitamins and proteins that don’t contain phenylalanine.\u003c/p>\n\u003cp>“It’s a really healthy drink,” Reeder says. “It’s basically protein, except without phenylalanine.”\u003c/p>\n\u003cp>But Reeder hopes a new approach for treating diseases could help people like him. The idea is to use bacteria that have been genetically modified to do what Reeder’s body can’t — get rid of phenylalanine.\u003c/p>\n\u003cp>“I’m really excited to help out and hopefully find a treatment for PKU,” Reeder said recently, as he prepared to volunteer for a study testing the modified bacteria.\u003c/p>\n\u003cp>The bacteria Reeder is helping test are part of a new field of medical research that has emerged from two realms of biomedical science. One is the study of the \u003ca href=\"https://www.npr.org/series/218987212/microbiome\">human microbiome\u003c/a>, the microbes that inhabit our bodies. The other is synthetic biology, a field that looks at genetically engineering living organisms, including bacteria in the human gut.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>“It’s a new world of being able to use synthetic biology to program microbes to treat diseases, which I believe is the future,” says \u003ca href=\"https://silver.med.harvard.edu/\">Pamela Silver\u003c/a>, a synthetic biologist at Harvard Medical School in Boston.\u003c/p>\n\u003cp>Scientists hope to genetically modify microbes from the human microbiome to treat a range of diseases, including digestive disorders like \u003ca href=\"https://www.niddk.nih.gov/health-information/digestive-diseases/ulcerative-colitis\">ulcerative colitis \u003c/a>and \u003ca href=\"https://www.cdc.gov/ibd/what-is-IBD.htm\">inflammatory bowel disease\u003c/a>.\u003c/p>\n\u003cp>“Microbes are something that we as synthetic biologists see as highly engineer-able. We understand how to engineer microbes so it seems like the perfect interface between synthetic biology and health,” Silver says.\u003c/p>\n\u003cp>One company, \u003ca href=\"https://www.actobio.com/\">ActoBio Therapeutics \u003c/a>of Ghent, Belgium, has just started using genetically engineered microbes to try to treat \u003ca href=\"https://medlineplus.gov/diabetestype1.html\">Type 1 diabetes\u003c/a>. Another one, \u003ca href=\"https://www.oragenics.com/\">Oragenics of Tampa, Fla.,\u003c/a> is testing a modified bacterium to treat mouth sores caused by cancer chemotherapy. And \u003ca href=\"http://oselinc.com/home/\">Osel\u003c/a> of Mountain View, Calif., hopes engineered microbes could prevent HIV infections.\u003c/p>\n\u003cp>Reeder is helping test modified \u003ca href=\"https://www.cdc.gov/ecoli/index.html\">E. coli\u003c/a> bacteria. While some types of \u003cem>E. coli\u003c/em> can cause serious illness, the \u003cem>E. coli\u003c/em> type being used in the study is found in the human gut.\u003c/p>\n\u003cp>“It is a naturally occurring probiotic bacteria,” says Caroline Kurtz, a scientist at \u003ca href=\"https://www.synlogictx.com/\">Synlogic\u003c/a>, a Cambridge, Mass., biotech company, which created the modified version of the organism.\u003c/p>\n\u003cp>“We can enhance its function by introducing genes [or] by changing genes that are there, and design the cells to either produce something or consume something that may be beneficial for a patient,” Kurtz says.\u003c/p>\n\u003cp>Synlogic has also engineered \u003cem>E. coli\u003c/em> to rid life-threatening levels of ammonia from the bodies of people with \u003ca href=\"https://www.mayoclinic.org/diseases-conditions/cirrhosis/symptoms-causes/syc-20351487\">cirrhosis of the liver\u003c/a>.\u003c/p>\n\u003cp>“This is a really exciting new modality that allows us to think about therapies in a new way and really look at diseases in a whole new way: a living medicine that can respond to its environment,” Kurtz says.\u003c/p>\n\u003cp>Preliminary research involving mice and healthy adults \u003ca href=\"http://stm.sciencemag.org/lookup/doi/10.1126/scitranslmed.aau7975\">published recently\u003c/a> in the journal \u003cem>Science Translational Medicine\u003c/em> indicates Synlogic’s \u003cem>E. coli \u003c/em>are safe and may work. So the company is now testing them in patients with cirrhosis and PKU.\u003c/p>\n\u003cp>Reeder admits he was a little nervous when he first heard about all this.\u003c/p>\n\u003cp>“When you hear about \u003cem>E. coli\u003c/em> you think: sickness, throwing up. So I was a little bit skeptical. I wasn’t sure what to think because I was going to be ingesting \u003cem>E. coli\u003c/em>,” Reeder says.\u003c/p>\n\u003cp>But the more he learned about it, the more excited Reeder got about trying the engineered microbes.\u003c/p>\n\u003cp>“I think that’s very cool that they found a way to use a natural probiotic that’s found in the digestive tract to help the human body,” Reeder says.\u003c/p>\n\u003cp>Reeder spent the weekend in the clinic so doctors could monitor him closely and run tests as he ingested what normally would be dangerous amounts of protein. He then swallowed either the engineered \u003cem>E. coli\u003c/em> or a placebo. He wasn’t told which.\u003c/p>\n\u003cp>“It was liquid solution. It tasted kind of like mint taffy. It was pretty sweet,” he says.\u003c/p>\n\u003cp>Reeder thinks he got the engineered microbes.\u003c/p>\n\u003cp>“I could immediately feel my cognitive abilities falling down after drinking the 20 grams of protein. And then I took the drug and I started feeling a lot better. I obtained more energy and my cognitive abilities got quicker,” he says.\u003c/p>\n\u003cp>“It was really cool to feel that. I could tell it was working. It was pretty cool,” Reeder says.\u003c/p>\n\u003cp>Much more research is needed to know whether genetically engineered microbes are safe and really work. But Synlogic hopes to report results from the cirrhosis and PKU studies later this year.\u003c/p>\n\u003cp>Before any of these experimental treatments could be used routinely, they would have to be reviewed and approved by the Food and Drug Administration. That’s a process that could take years.\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2019 NPR. To see more, visit https://www.npr.org.\u003cimg decoding=\"async\" src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=A+Gulp+Of+Genetically+Modified+Bacteria+Might+Someday+Treat+A+Range+Of+Illnesses&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\u003cp>\u003c/p>\n\u003c/div>\u003c/p>",
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"title": "The Case Against 'Statistical Significance' in Scientific Research",
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"content": "\u003cp>A recent study that questioned the healthfulness of eggs raised a perpetual question: Why do studies, as has been the case with health research involving eggs, so often flip-flop from one answer to another?\u003c/p>\n\u003cp>The truth isn’t changing all the time. But one reason for the fluctuations is that scientists have a hard time handling the uncertainty that’s inherent in all studies. There’s a new push to address this shortcoming in a widely used – and abused – scientific method.\u003c/p>\n\u003cp>Scientists and statisticians are putting forth a bold idea: Ban the very concept of “statistical significance.”\u003c/p>\n\u003caside class=\"pullquote alignright\">‘Failure to make these changes are really now starting to have a sustained negative impact on how science is conducted.’\u003ccite>Ron Wasserstein, American Statistical Association\u003c/cite>\u003c/aside>\n\u003cp>We hear that phrase all the time in relation to scientific studies. Critics, who are numerous, say that declaring a result to be statistically significant or not essentially forces complicated questions to be answered as true or false.\u003c/p>\n\u003cp>“The world is much more uncertain than that,” says Nicole Lazar, a professor of statistics at the University of Georgia. She is involved in the latest push to ban the use of the term “statistical significance.”\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>An entire issue of the journal \u003ca href=\"https://amstat.tandfonline.com/toc/utas20/current\" target=\"_blank\" rel=\"noopener\">\u003cem>The American Statistician\u003c/em>\u003c/a> is devoted to this question, with 43 articles and a 17,500-word editorial that Lazar co-authored.\u003c/p>\n\u003cp>Some of the scientists involved in that effort also wrote\u003ca href=\"https://www.nature.com/articles/d41586-019-00857-9\" target=\"_blank\" rel=\"noopener\"> a more digestible commentary\u003c/a> that appears in Thursday’s issue of \u003cem>Nature\u003c/em>. More than 850 scientists and statisticians told the \u003cem>Nature\u003c/em> commentary authors they want to endorse this idea.\u003c/p>\n\u003cp>In the early 20th century, the father of statistics, R.A. Fisher, developed a test of significance. It involves a variable called the p-value, that he intended to be a guide for judging results.\u003c/p>\n\u003cp>Over the years, scientists have warped that idea beyond all recognition. They’ve created an arbitrary threshold for the p-value, typically 0.05, and they use that to declare whether a scientific result is significant or not.\u003c/p>\n\u003cp>This shortcut often determines whether studies get published or not, whether scientists get promoted and who gets grant funding.\u003c/p>\n\u003cp>“It’s really gotten stretched all out of proportion,” says \u003ca href=\"https://www.amstat.org/ASA/About/Ronald-L-Wasserstein.aspx\" target=\"_blank\" rel=\"noopener\">Ron Wasserstein\u003c/a>, the executive director of the American Statistical Association. He’s been advocating this change for years and he’s not alone.\u003c/p>\n\u003cp>“Failure to make these changes are really now starting to have a sustained negative impact on how science is conducted,” he says. “It’s time to start making the changes. It’s time to move on.”\u003c/p>\n\u003cp>There are many downsides to this, he says. One is that scientists have been known to massage their data to make their results hit this magic threshold. Arguably worse, scientists often find that they can’t publish their interesting (if somewhat ambiguous) results if they aren’t statistically significant. But that information is actually still useful, and advocates say it’s wasteful simply to throw it away.\u003c/p>\n\u003cp>There are some prominent voices in the world of statistics who reject the call to abolish the term “statistical significance.”\u003c/p>\n\u003cp>“\u003cem>Nature\u003c/em> ought to invite somebody to bring out the weakness and dangers of some of these recommendations,” says Deborah Mayo, a philosopher of science at Virginia Tech.\u003c/p>\n\u003cp>“Banning the word ‘significance’ may well free researchers from being held accountable when they downplay negative results” and otherwise manipulate their findings, she notes.\u003c/p>\n\u003cp>“We should be very wary of giving up on something that allows us to hold researchers accountable.”\u003c/p>\n\u003cp>Her desire to keep “statistical significance” is deeply embedded.\u003c/p>\n\u003cp>Scientists – like the rest of us – are far more likely to believe that a result is true if it’s statistically significant. Still, \u003ca href=\"https://www.kellogg.northwestern.edu/faculty/directory/mcshane_blake.aspx\" target=\"_blank\" rel=\"noopener\">Blake McShane\u003c/a>, a statistician at the Kellogg School of Management at Northwestern University, says we put far too much faith in the concept.\u003c/p>\n\u003cp>“All statistics naturally bounce around quite a lot from study to study to study,” McShane says. That’s because there’s lots of variation from one group of people to another, and also because subtle differences in approach can lead to different conclusions.\u003c/p>\n\u003cp>So, he says, we shouldn’t be at all surprised if a result that’s statistically significant in one study doesn’t meet that threshold in the next.\u003c/p>\n\u003cp>McShane, who co-authored the \u003cem>Nature \u003c/em>commentary, says this phenomenon also partly explains why studies done in one lab are frequently not reproduced in other labs. This is sometimes referred to as the “reproducibility crisis,” when in fact, the apparent conflict between studies may be an artifact of relying on the concept of statistical significance.\u003c/p>\n\u003cp>But despite these flaws, science embraces statistical significance because it’s a shortcut that provides at least some insight into the strength of an observation.\u003c/p>\n\u003cp>Journals are reluctant to abandon the concept. “\u003cem>Nature\u003c/em> is not seeking to change how it considers statistical analysis in evaluation of papers at this time,” the journal noted in an editorial that accompanies the commentary.\u003c/p>\n\u003cp>\u003ca href=\"https://www.plos.org/people#loc-veronique-kiermer\" target=\"_blank\" rel=\"noopener\">Veronique Kiermer\u003c/a>, publisher and executive editor of the PLOS journals, bemoans the over-reliance on statistical significance, but says her journals don’t have the leverage to force a change.\u003c/p>\n\u003cp>“The problem is that the practice is so ingrained in the research community,” she writes in an email, “that change needs to start there, when hypotheses are formulated, experiments designed and analyzed, and when researchers decide whether to write up and publish their work.”\u003c/p>\n\u003cp>One problem is what would scientists use instead of statistical significance. The advocates for change say the community can still use the p-value test, but as part of a broader approach to measuring uncertainty.\u003c/p>\n\u003cp>A bit more humility would also be in order, these advocates for change say.\u003c/p>\n\u003cp>“Uncertainty is present always,” Wasserstein says. “That’s part of science. So rather than trying to dance around it, we [should] accept it.”\u003c/p>\n\u003cp>That goes a bit against human nature. After all, we want answers, not more questions.\u003c/p>\n\u003cp>But McShane says arriving at a yes/no answer about whether to eat eggs is too simplistic. If we step beyond that, we can ask more important questions. How big is the risk? How likely is it to be real? What are the costs and benefits to an individual?\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp>Lazar has an even more extreme view. She says when she hears about individual studies, like the egg one, her statistical intuition leads her to shrug: “I don’t even pay attention to it anymore.”\u003c/p>\n\u003cdiv class=\"fullattribution\">\u003cem>Copyright 2019 \u003ca href=\"https://www.npr.org\" target=\"_blank\" rel=\"noopener\">NPR\u003c/a>.\u003cimg decoding=\"async\" src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Statisticians%27+Call+To+Arms%3A+Reject+Significance+And+Embrace+Uncertainty%21+&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/em>\u003c/div>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>A recent study that questioned the healthfulness of eggs raised a perpetual question: Why do studies, as has been the case with health research involving eggs, so often flip-flop from one answer to another?\u003c/p>\n\u003cp>The truth isn’t changing all the time. But one reason for the fluctuations is that scientists have a hard time handling the uncertainty that’s inherent in all studies. There’s a new push to address this shortcoming in a widely used – and abused – scientific method.\u003c/p>\n\u003cp>Scientists and statisticians are putting forth a bold idea: Ban the very concept of “statistical significance.”\u003c/p>\n\u003caside class=\"pullquote alignright\">‘Failure to make these changes are really now starting to have a sustained negative impact on how science is conducted.’\u003ccite>Ron Wasserstein, American Statistical Association\u003c/cite>\u003c/aside>\n\u003cp>We hear that phrase all the time in relation to scientific studies. Critics, who are numerous, say that declaring a result to be statistically significant or not essentially forces complicated questions to be answered as true or false.\u003c/p>\n\u003cp>“The world is much more uncertain than that,” says Nicole Lazar, a professor of statistics at the University of Georgia. She is involved in the latest push to ban the use of the term “statistical significance.”\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>An entire issue of the journal \u003ca href=\"https://amstat.tandfonline.com/toc/utas20/current\" target=\"_blank\" rel=\"noopener\">\u003cem>The American Statistician\u003c/em>\u003c/a> is devoted to this question, with 43 articles and a 17,500-word editorial that Lazar co-authored.\u003c/p>\n\u003cp>Some of the scientists involved in that effort also wrote\u003ca href=\"https://www.nature.com/articles/d41586-019-00857-9\" target=\"_blank\" rel=\"noopener\"> a more digestible commentary\u003c/a> that appears in Thursday’s issue of \u003cem>Nature\u003c/em>. More than 850 scientists and statisticians told the \u003cem>Nature\u003c/em> commentary authors they want to endorse this idea.\u003c/p>\n\u003cp>In the early 20th century, the father of statistics, R.A. Fisher, developed a test of significance. It involves a variable called the p-value, that he intended to be a guide for judging results.\u003c/p>\n\u003cp>Over the years, scientists have warped that idea beyond all recognition. They’ve created an arbitrary threshold for the p-value, typically 0.05, and they use that to declare whether a scientific result is significant or not.\u003c/p>\n\u003cp>This shortcut often determines whether studies get published or not, whether scientists get promoted and who gets grant funding.\u003c/p>\n\u003cp>“It’s really gotten stretched all out of proportion,” says \u003ca href=\"https://www.amstat.org/ASA/About/Ronald-L-Wasserstein.aspx\" target=\"_blank\" rel=\"noopener\">Ron Wasserstein\u003c/a>, the executive director of the American Statistical Association. He’s been advocating this change for years and he’s not alone.\u003c/p>\n\u003cp>“Failure to make these changes are really now starting to have a sustained negative impact on how science is conducted,” he says. “It’s time to start making the changes. It’s time to move on.”\u003c/p>\n\u003cp>There are many downsides to this, he says. One is that scientists have been known to massage their data to make their results hit this magic threshold. Arguably worse, scientists often find that they can’t publish their interesting (if somewhat ambiguous) results if they aren’t statistically significant. But that information is actually still useful, and advocates say it’s wasteful simply to throw it away.\u003c/p>\n\u003cp>There are some prominent voices in the world of statistics who reject the call to abolish the term “statistical significance.”\u003c/p>\n\u003cp>“\u003cem>Nature\u003c/em> ought to invite somebody to bring out the weakness and dangers of some of these recommendations,” says Deborah Mayo, a philosopher of science at Virginia Tech.\u003c/p>\n\u003cp>“Banning the word ‘significance’ may well free researchers from being held accountable when they downplay negative results” and otherwise manipulate their findings, she notes.\u003c/p>\n\u003cp>“We should be very wary of giving up on something that allows us to hold researchers accountable.”\u003c/p>\n\u003cp>Her desire to keep “statistical significance” is deeply embedded.\u003c/p>\n\u003cp>Scientists – like the rest of us – are far more likely to believe that a result is true if it’s statistically significant. Still, \u003ca href=\"https://www.kellogg.northwestern.edu/faculty/directory/mcshane_blake.aspx\" target=\"_blank\" rel=\"noopener\">Blake McShane\u003c/a>, a statistician at the Kellogg School of Management at Northwestern University, says we put far too much faith in the concept.\u003c/p>\n\u003cp>“All statistics naturally bounce around quite a lot from study to study to study,” McShane says. That’s because there’s lots of variation from one group of people to another, and also because subtle differences in approach can lead to different conclusions.\u003c/p>\n\u003cp>So, he says, we shouldn’t be at all surprised if a result that’s statistically significant in one study doesn’t meet that threshold in the next.\u003c/p>\n\u003cp>McShane, who co-authored the \u003cem>Nature \u003c/em>commentary, says this phenomenon also partly explains why studies done in one lab are frequently not reproduced in other labs. This is sometimes referred to as the “reproducibility crisis,” when in fact, the apparent conflict between studies may be an artifact of relying on the concept of statistical significance.\u003c/p>\n\u003cp>But despite these flaws, science embraces statistical significance because it’s a shortcut that provides at least some insight into the strength of an observation.\u003c/p>\n\u003cp>Journals are reluctant to abandon the concept. “\u003cem>Nature\u003c/em> is not seeking to change how it considers statistical analysis in evaluation of papers at this time,” the journal noted in an editorial that accompanies the commentary.\u003c/p>\n\u003cp>\u003ca href=\"https://www.plos.org/people#loc-veronique-kiermer\" target=\"_blank\" rel=\"noopener\">Veronique Kiermer\u003c/a>, publisher and executive editor of the PLOS journals, bemoans the over-reliance on statistical significance, but says her journals don’t have the leverage to force a change.\u003c/p>\n\u003cp>“The problem is that the practice is so ingrained in the research community,” she writes in an email, “that change needs to start there, when hypotheses are formulated, experiments designed and analyzed, and when researchers decide whether to write up and publish their work.”\u003c/p>\n\u003cp>One problem is what would scientists use instead of statistical significance. The advocates for change say the community can still use the p-value test, but as part of a broader approach to measuring uncertainty.\u003c/p>\n\u003cp>A bit more humility would also be in order, these advocates for change say.\u003c/p>\n\u003cp>“Uncertainty is present always,” Wasserstein says. “That’s part of science. So rather than trying to dance around it, we [should] accept it.”\u003c/p>\n\u003cp>That goes a bit against human nature. After all, we want answers, not more questions.\u003c/p>\n\u003cp>But McShane says arriving at a yes/no answer about whether to eat eggs is too simplistic. If we step beyond that, we can ask more important questions. How big is the risk? How likely is it to be real? What are the costs and benefits to an individual?\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>Lazar has an even more extreme view. She says when she hears about individual studies, like the egg one, her statistical intuition leads her to shrug: “I don’t even pay attention to it anymore.”\u003c/p>\n\u003cdiv class=\"fullattribution\">\u003cem>Copyright 2019 \u003ca href=\"https://www.npr.org\" target=\"_blank\" rel=\"noopener\">NPR\u003c/a>.\u003cimg decoding=\"async\" src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Statisticians%27+Call+To+Arms%3A+Reject+Significance+And+Embrace+Uncertainty%21+&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/em>\u003c/div>\n\n\u003c/div>\u003c/p>",
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"content": "\u003cp>Dr. Thomas Boyce, an emeritus professor of pediatrics and psychiatry at the University of California, San Francisco, has treated children who seem to be completely unflappable and unfazed by their surroundings — as well as those who are extremely sensitive to their environments. Over the years, he began to liken these two types of children to two very different flowers: dandelions and orchids.\u003c/p>\n\u003cp>Broadly speaking, says \u003ca href=\"https://profiles.ucsf.edu/tom.boyce\" target=\"_blank\" rel=\"noopener\">Boyce\u003c/a> — who also has spent nearly 40 years studying the human stress response, especially in children — most kids tend to be like dandelions, fairly resilient and able to cope with stress and adversity in their lives. But a minority of kids, those he calls “orchid children,” are more sensitive and biologically reactive to their circumstances, which makes it harder for them to deal with stressful situations.[contextly_sidebar id=”IvCr36i4S1EYhLjR3xMTzjOHrdmBka5u”]\u003c/p>\n\u003cp>Like the flower, Boyce says, “the orchid child is the child who shows great sensitivity and susceptibility to both bad and good environments in which he or she finds herself or himself.”\u003c/p>\n\u003cp>Given supportive, nurturing conditions, orchid children can thrive — especially, Boyce says, if they have the comfort of a regular routine.\u003c/p>\n\u003cp>“Orchid children seem to thrive on having things like dinner every night in the same place at the same time with the same people, having certain kinds of rituals that the family goes through week to week, month to month,” he says. “This kind of routine and sameness of life from day to day, week to week, seems to be something that is helpful to kids with these great susceptibilities.”\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>Boyce’s new book is \u003cem>The Orchid and the Dandelion: Why Some Children Struggle and How All Can Thri\u003c/em>ve\u003cem>. \u003c/em>He appeared this week on \u003ca href=\"https://www.npr.org/programs/fresh-air/2019/03/04/699939149\" target=\"_blank\" rel=\"noopener\">Fresh Air\u003c/a> with host Dave Davies to discuss it.\u003cem>\u003cbr>\n\u003c/em>\u003c/p>\n\u003chr>\n\u003cp>\u003cstrong>Interview highlights:\u003c/strong>\u003c/p>\n\u003cp>\u003cstrong>On the lab test he did to determine if a child is an orchid or a dandelion\u003c/strong>\u003c/p>\n\u003cp>We made an effort to try to understand these individual differences between children in how they respond biologically to mild, common kinds of challenges and stressors, and the way we did that was we brought them into a laboratory setting. We sat them down in front of an examiner — a research assistant that they had not previously met — and we asked them to go through a series of mildly challenging tasks. These were things like recounting a series of digits that the examiner asked them to say and increasing that from first three to four to five digits; having them just engage in a conversation with this examiner, who might ask them about their birthday or presents or something about their family. That, in itself, is a challenge for a young child. Putting a drop of lemon juice on the tongue was another kind of challenge that was evocative of these changes in biological response. …\u003c/p>\n\u003cp>We measured their stress response using the two primary stress response systems in the human brain. [One was] the \u003ca href=\"http://www.yourhormones.info/hormones/cortisol/\" target=\"_blank\" rel=\"noopener\">cortisol system\u003c/a>, which is centered in the hypothalamus of the brain. This is the system that releases the stress hormone cortisol, which has profound effects on both immune function and cardiovascular functioning.\u003c/p>\n\u003cp>And then the second stress response system is the \u003ca href=\"https://faculty.washington.edu/chudler/auto.html\" target=\"_blank\" rel=\"noopener\">autonomic nervous system\u003c/a>, or the “fight-or-flight” system. This is the one that is responsible for the sweaty palms and a little bit of tremulousness, the dilation of the pupils, all of these things that we associate with the fight-or-flight response. So we were monitoring responsivity and both of those systems as the children went through these mildly challenging tasks. …\u003c/p>\n\u003cp>We found that there were huge differences [among] children. There were some children at the high end of the spectrum, who had dramatic reactivity in both the cortisol system and the fight-or-flight system, and there were other children who had almost no biological response to the challenges that we presented to them.\u003c/p>\n\u003cp>\u003cstrong>On how a child’s responsivity to stressors can be connected to physical and emotional behavioral outcomes\u003c/strong>\u003c/p>\n\u003cp>We find in our research that the same kinds of patterns of response are found for both physical illnesses, like severe respiratory disease, pneumonia, asthma and so on, as well as or more [in] emotional behavioral outcomes, like anxiety and depression and externalizing kinds of symptoms. So we believe that the same patterns of susceptibility that we find in the orchid child versus the dandelion child work themselves out not only for physical ailments but also for psychosocial and emotional problems. And we believe that the same kinds of underlying biological processes work for both. …\u003c/p>\n\u003cp>We do know, for example, that these two stress response systems … the cortisol system and the fight-or-flight system, the autonomic nervous system, both of those have powerful effects on the immune system, so they can alter the child’s ability to build an immune defense against viruses and bacteria that he or she may be exposed to. And they have also powerful effects on the cardiovascular system, so [they] could eventually, in adult life, predispose to developing hypertension, high blood pressure or other kinds of cardiovascular risk.\u003c/p>\n\u003cp>\u003cstrong>On how children’s experiences can vary, even within the same family\u003c/strong>\u003c/p>\n\u003cp>The experience of children within a given family, the siblings within a family — although they are being reared with the same parents in the same house in the same neighborhood — they actually have quite different kinds of experiences that depend upon the birth order of the child, the gender of the child, to some extent differences in genetic sequence. It is a way of talking about these dramatic differences that kids from different birth orders and different genders have within a given family.\u003c/p>\n\u003cp>\u003cstrong>On pushing orchid kids to stretch to do new or difficult things\u003c/strong>\u003c/p>\n\u003cp>I think that this is probably the most difficult parenting task in raising an orchid child. The parent of an orchid child needs to walk this very fine line between, on the one hand, not pushing them into circumstances that are really going to overwhelm them and make them greatly fearful, but, on the other hand, not protecting them so much that they don’t have experiences of mastery of these kinds of fearful situations.\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp>\u003cem>Sam Briger and Seth Kelley produced and edited the \u003ca href=\"https://www.npr.org/sections/health-shots/2019/03/04/699979387/is-your-child-an-orchid-or-a-dandelion-unlocking-the-science-of-sensitive-kids\" target=\"_blank\" rel=\"noopener\">audio version\u003c/a> of this interview, which aired on Fresh Air. Bridget Bentz and Molly Seavy-Nesper adapted it for the Web.\u003c/em>\u003c/p>\n\u003cdiv class=\"fullattribution\">\u003cem>Copyright 2019 \u003ca href=\"https://www.npr.org/programs/fresh-air/\" target=\"_blank\" rel=\"noopener\">Fresh Air\u003c/a>.\u003c/em>\u003c/div>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>Dr. Thomas Boyce, an emeritus professor of pediatrics and psychiatry at the University of California, San Francisco, has treated children who seem to be completely unflappable and unfazed by their surroundings — as well as those who are extremely sensitive to their environments. Over the years, he began to liken these two types of children to two very different flowers: dandelions and orchids.\u003c/p>\n\u003cp>Broadly speaking, says \u003ca href=\"https://profiles.ucsf.edu/tom.boyce\" target=\"_blank\" rel=\"noopener\">Boyce\u003c/a> — who also has spent nearly 40 years studying the human stress response, especially in children — most kids tend to be like dandelions, fairly resilient and able to cope with stress and adversity in their lives. But a minority of kids, those he calls “orchid children,” are more sensitive and biologically reactive to their circumstances, which makes it harder for them to deal with stressful situations.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>Like the flower, Boyce says, “the orchid child is the child who shows great sensitivity and susceptibility to both bad and good environments in which he or she finds herself or himself.”\u003c/p>\n\u003cp>Given supportive, nurturing conditions, orchid children can thrive — especially, Boyce says, if they have the comfort of a regular routine.\u003c/p>\n\u003cp>“Orchid children seem to thrive on having things like dinner every night in the same place at the same time with the same people, having certain kinds of rituals that the family goes through week to week, month to month,” he says. “This kind of routine and sameness of life from day to day, week to week, seems to be something that is helpful to kids with these great susceptibilities.”\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>Boyce’s new book is \u003cem>The Orchid and the Dandelion: Why Some Children Struggle and How All Can Thri\u003c/em>ve\u003cem>. \u003c/em>He appeared this week on \u003ca href=\"https://www.npr.org/programs/fresh-air/2019/03/04/699939149\" target=\"_blank\" rel=\"noopener\">Fresh Air\u003c/a> with host Dave Davies to discuss it.\u003cem>\u003cbr>\n\u003c/em>\u003c/p>\n\u003chr>\n\u003cp>\u003cstrong>Interview highlights:\u003c/strong>\u003c/p>\n\u003cp>\u003cstrong>On the lab test he did to determine if a child is an orchid or a dandelion\u003c/strong>\u003c/p>\n\u003cp>We made an effort to try to understand these individual differences between children in how they respond biologically to mild, common kinds of challenges and stressors, and the way we did that was we brought them into a laboratory setting. We sat them down in front of an examiner — a research assistant that they had not previously met — and we asked them to go through a series of mildly challenging tasks. These were things like recounting a series of digits that the examiner asked them to say and increasing that from first three to four to five digits; having them just engage in a conversation with this examiner, who might ask them about their birthday or presents or something about their family. That, in itself, is a challenge for a young child. Putting a drop of lemon juice on the tongue was another kind of challenge that was evocative of these changes in biological response. …\u003c/p>\n\u003cp>We measured their stress response using the two primary stress response systems in the human brain. [One was] the \u003ca href=\"http://www.yourhormones.info/hormones/cortisol/\" target=\"_blank\" rel=\"noopener\">cortisol system\u003c/a>, which is centered in the hypothalamus of the brain. This is the system that releases the stress hormone cortisol, which has profound effects on both immune function and cardiovascular functioning.\u003c/p>\n\u003cp>And then the second stress response system is the \u003ca href=\"https://faculty.washington.edu/chudler/auto.html\" target=\"_blank\" rel=\"noopener\">autonomic nervous system\u003c/a>, or the “fight-or-flight” system. This is the one that is responsible for the sweaty palms and a little bit of tremulousness, the dilation of the pupils, all of these things that we associate with the fight-or-flight response. So we were monitoring responsivity and both of those systems as the children went through these mildly challenging tasks. …\u003c/p>\n\u003cp>We found that there were huge differences [among] children. There were some children at the high end of the spectrum, who had dramatic reactivity in both the cortisol system and the fight-or-flight system, and there were other children who had almost no biological response to the challenges that we presented to them.\u003c/p>\n\u003cp>\u003cstrong>On how a child’s responsivity to stressors can be connected to physical and emotional behavioral outcomes\u003c/strong>\u003c/p>\n\u003cp>We find in our research that the same kinds of patterns of response are found for both physical illnesses, like severe respiratory disease, pneumonia, asthma and so on, as well as or more [in] emotional behavioral outcomes, like anxiety and depression and externalizing kinds of symptoms. So we believe that the same patterns of susceptibility that we find in the orchid child versus the dandelion child work themselves out not only for physical ailments but also for psychosocial and emotional problems. And we believe that the same kinds of underlying biological processes work for both. …\u003c/p>\n\u003cp>We do know, for example, that these two stress response systems … the cortisol system and the fight-or-flight system, the autonomic nervous system, both of those have powerful effects on the immune system, so they can alter the child’s ability to build an immune defense against viruses and bacteria that he or she may be exposed to. And they have also powerful effects on the cardiovascular system, so [they] could eventually, in adult life, predispose to developing hypertension, high blood pressure or other kinds of cardiovascular risk.\u003c/p>\n\u003cp>\u003cstrong>On how children’s experiences can vary, even within the same family\u003c/strong>\u003c/p>\n\u003cp>The experience of children within a given family, the siblings within a family — although they are being reared with the same parents in the same house in the same neighborhood — they actually have quite different kinds of experiences that depend upon the birth order of the child, the gender of the child, to some extent differences in genetic sequence. It is a way of talking about these dramatic differences that kids from different birth orders and different genders have within a given family.\u003c/p>\n\u003cp>\u003cstrong>On pushing orchid kids to stretch to do new or difficult things\u003c/strong>\u003c/p>\n\u003cp>I think that this is probably the most difficult parenting task in raising an orchid child. The parent of an orchid child needs to walk this very fine line between, on the one hand, not pushing them into circumstances that are really going to overwhelm them and make them greatly fearful, but, on the other hand, not protecting them so much that they don’t have experiences of mastery of these kinds of fearful situations.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>\u003cem>Sam Briger and Seth Kelley produced and edited the \u003ca href=\"https://www.npr.org/sections/health-shots/2019/03/04/699979387/is-your-child-an-orchid-or-a-dandelion-unlocking-the-science-of-sensitive-kids\" target=\"_blank\" rel=\"noopener\">audio version\u003c/a> of this interview, which aired on Fresh Air. Bridget Bentz and Molly Seavy-Nesper adapted it for the Web.\u003c/em>\u003c/p>\n\u003cdiv class=\"fullattribution\">\u003cem>Copyright 2019 \u003ca href=\"https://www.npr.org/programs/fresh-air/\" target=\"_blank\" rel=\"noopener\">Fresh Air\u003c/a>.\u003c/em>\u003c/div>\n\n\u003c/div>\u003c/p>",
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"title": "FDA Approves First Major Depression Treatment in Decades",
"headTitle": "FDA Approves First Major Depression Treatment in Decades | KQED",
"content": "\u003cp>The Food and Drug Administration on Tuesday approved esketamine, the first major depression treatment to hit the U.S. market in decades and a new option for patients who haven’t responded to existing therapies.\u003c/p>\n\u003cp>Esketamine — developed by Johnson & Johnson and delivered as a nasal spray — was tested in combination with oral antidepressants in patients with what’s known as treatment-resistant depression. The drug is related to ketamine, a common anesthetic that’s sometimes misused recreationally. Many experts have hailed esketamine as a critical option for patients in dire need of new treatments — particularly because it might \u003ca href=\"https://www.statnews.com/2018/07/03/fast-acting-antidepressants-clinical-trials/\" target=\"_blank\" rel=\"noopener\">work faster\u003c/a> than existing antidepressants.[contextly_sidebar id=”wpaMiTiEavHYfZeJHTCfjFSpMgrPcXap”]\u003c/p>\n\u003cp>“The unmet need is really huge,” said Dr. Husseini Manji, the global head of neuroscience therapeutics at Janssen, the subsidiary of Johnson & Johnson that developed the drug, which will be called Spravato.\u003c/p>\n\u003cp>Janssen said the cost of the treatment will depend on the dose used per session and how many sessions a person will need, both of which can vary. The wholesale acquisition cost: between $590 and $885 per treatment session. That means the wholesale acquisition cost for the first month of treatment — which includes two sessions a week — will range from $4,720 to $6,785.\u003c/p>\n\u003cp>But an approval — and subsequently, anticipated insurance coverage for esketamine — is welcome news for the growing number of patients who have \u003ca href=\"https://www.statnews.com/2018/09/24/ketamine-clinics-severe-depression-treatment/\" target=\"_blank\" rel=\"noopener\">paid thousands of dollars\u003c/a> out of pocket in recent years to receive off-label infusions of ketamine as a treatment for depression.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>The drug’s labeling will include a warning that patients who take esketamine are at risk for sedation and issues with attention, judgement, and thinking. It will also warn that there is a risk of misuse, abuse, and suicidal thoughts after taking esketamine. Patients who receive the drug will have to be monitored for at least two hours every time they get esketamine.\u003c/p>\n\u003cp>Johnson & Johnson submitted five Phase 3 studies on the drug: three-short term studies, one maintenance study, and a long-term safety study. Aside from the safety study, two of those turned up positive, clinically significant results. One was a randomized trial in adults under age 65 with treatment-resistant depression who were started on an oral antidepressant and esketamine. After a month, roughly 70 percent of patients who received the treatment responded, compared to just over half in a placebo group. An improvement of 50 percent or more on a common depression rating scale was seen as a successful response.\u003c/p>\n\u003cp>The other positive study was a maintenance-of-effect study, in which participants who responded to esketamine in one of the short-term studies were randomly assigned to either keep taking it or be switched to a placebo. The FDA generally wants to see two successful studies for approval — but historically, withdrawal studies haven’t counted toward that total.\u003c/p>\n\u003cp>But the FDA said the evidence — and input from external advisers — played a role in the decision to approve the drug.\u003c/p>\n\u003cp>“Controlled clinical trials that studied the safety and efficacy of this drug, along with careful review through the FDA’s drug approval process including a robust discussion with our external advisory committees, were important to our decision to approve this treatment,” Dr. Tiffany Farchione, acting director of the Division of Psychiatry Products in the FDA’s Center for Drug Evaluation and Research, said in a statement.\u003c/p>\n\u003cp>Not all experts are convinced there was enough data to approve esketamine yet.\u003c/p>\n\u003cp>“The threshold has been two adequate and well-controlled trials. In this case, they only got one,” Dr. Erick Turner, a psychiatrist at Oregon Health and Science University, told STAT in an interview last month. Turner serves on the FDA advisory committee that recommended last month that the FDA approve esketamine, but didn’t take part in that meeting.\u003c/p>\n\u003cp>The committee emphasized the need for a robust strategy to prevent diversion and misuse, given that ketamine is commonly abused. Ketamine is a combination of two enantiomers, or mirror image molecules. Esketamine is what’s known as the s-enantiomer. But the experts generally agreed that the risk of abuse with esketamine seems to be low.\u003c/p>\n\u003cp>“There will be all kinds of monitoring to make sure the drug doesn’t get diverted,” Manji said. That includes strict distribution requirements and a suspicious order monitoring program.\u003c/p>\n\u003cp>The FDA has also expressed concern that patients could be harmed if they experience dissociation, or an out-of-body experience that can leave people less aware of their surroundings. In briefing documents submitted before the advisory committee meeting, the agency also noted six deaths — including three suicides — among patients who were taking the drug. But FDA reviewers said that given that the patients had severe illnesses and there wasn’t a pattern seen in the deaths, it’s “difficult to consider these deaths as drug related.”\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>Johnson & Johnson is also testing esketamine as a treatment for people with depression who are at risk of suicide, and is expected to release results from a study on suicidal patients this year. Allergan is also in the late stages of testing an experimental, fast-acting antidepressant called rapastinel. An Allergan spokesperson said that the company anticipates that the need to monitor patients and restrict activities after rapastinel will be “minimal” compared to the requirements for esketamine. The company also said there seems to be a lower rate of dissociative effects with rapastinel. The drug is being tested alone, in combination with other treatments for major depression, and in patients with depression who are at risk of suicide.\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>The Food and Drug Administration on Tuesday approved esketamine, the first major depression treatment to hit the U.S. market in decades and a new option for patients who haven’t responded to existing therapies.\u003c/p>\n\u003cp>Esketamine — developed by Johnson & Johnson and delivered as a nasal spray — was tested in combination with oral antidepressants in patients with what’s known as treatment-resistant depression. The drug is related to ketamine, a common anesthetic that’s sometimes misused recreationally. Many experts have hailed esketamine as a critical option for patients in dire need of new treatments — particularly because it might \u003ca href=\"https://www.statnews.com/2018/07/03/fast-acting-antidepressants-clinical-trials/\" target=\"_blank\" rel=\"noopener\">work faster\u003c/a> than existing antidepressants.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>“The unmet need is really huge,” said Dr. Husseini Manji, the global head of neuroscience therapeutics at Janssen, the subsidiary of Johnson & Johnson that developed the drug, which will be called Spravato.\u003c/p>\n\u003cp>Janssen said the cost of the treatment will depend on the dose used per session and how many sessions a person will need, both of which can vary. The wholesale acquisition cost: between $590 and $885 per treatment session. That means the wholesale acquisition cost for the first month of treatment — which includes two sessions a week — will range from $4,720 to $6,785.\u003c/p>\n\u003cp>But an approval — and subsequently, anticipated insurance coverage for esketamine — is welcome news for the growing number of patients who have \u003ca href=\"https://www.statnews.com/2018/09/24/ketamine-clinics-severe-depression-treatment/\" target=\"_blank\" rel=\"noopener\">paid thousands of dollars\u003c/a> out of pocket in recent years to receive off-label infusions of ketamine as a treatment for depression.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>The drug’s labeling will include a warning that patients who take esketamine are at risk for sedation and issues with attention, judgement, and thinking. It will also warn that there is a risk of misuse, abuse, and suicidal thoughts after taking esketamine. Patients who receive the drug will have to be monitored for at least two hours every time they get esketamine.\u003c/p>\n\u003cp>Johnson & Johnson submitted five Phase 3 studies on the drug: three-short term studies, one maintenance study, and a long-term safety study. Aside from the safety study, two of those turned up positive, clinically significant results. One was a randomized trial in adults under age 65 with treatment-resistant depression who were started on an oral antidepressant and esketamine. After a month, roughly 70 percent of patients who received the treatment responded, compared to just over half in a placebo group. An improvement of 50 percent or more on a common depression rating scale was seen as a successful response.\u003c/p>\n\u003cp>The other positive study was a maintenance-of-effect study, in which participants who responded to esketamine in one of the short-term studies were randomly assigned to either keep taking it or be switched to a placebo. The FDA generally wants to see two successful studies for approval — but historically, withdrawal studies haven’t counted toward that total.\u003c/p>\n\u003cp>But the FDA said the evidence — and input from external advisers — played a role in the decision to approve the drug.\u003c/p>\n\u003cp>“Controlled clinical trials that studied the safety and efficacy of this drug, along with careful review through the FDA’s drug approval process including a robust discussion with our external advisory committees, were important to our decision to approve this treatment,” Dr. Tiffany Farchione, acting director of the Division of Psychiatry Products in the FDA’s Center for Drug Evaluation and Research, said in a statement.\u003c/p>\n\u003cp>Not all experts are convinced there was enough data to approve esketamine yet.\u003c/p>\n\u003cp>“The threshold has been two adequate and well-controlled trials. In this case, they only got one,” Dr. Erick Turner, a psychiatrist at Oregon Health and Science University, told STAT in an interview last month. Turner serves on the FDA advisory committee that recommended last month that the FDA approve esketamine, but didn’t take part in that meeting.\u003c/p>\n\u003cp>The committee emphasized the need for a robust strategy to prevent diversion and misuse, given that ketamine is commonly abused. Ketamine is a combination of two enantiomers, or mirror image molecules. Esketamine is what’s known as the s-enantiomer. But the experts generally agreed that the risk of abuse with esketamine seems to be low.\u003c/p>\n\u003cp>“There will be all kinds of monitoring to make sure the drug doesn’t get diverted,” Manji said. That includes strict distribution requirements and a suspicious order monitoring program.\u003c/p>\n\u003cp>The FDA has also expressed concern that patients could be harmed if they experience dissociation, or an out-of-body experience that can leave people less aware of their surroundings. In briefing documents submitted before the advisory committee meeting, the agency also noted six deaths — including three suicides — among patients who were taking the drug. But FDA reviewers said that given that the patients had severe illnesses and there wasn’t a pattern seen in the deaths, it’s “difficult to consider these deaths as drug related.”\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>Johnson & Johnson is also testing esketamine as a treatment for people with depression who are at risk of suicide, and is expected to release results from a study on suicidal patients this year. Allergan is also in the late stages of testing an experimental, fast-acting antidepressant called rapastinel. An Allergan spokesperson said that the company anticipates that the need to monitor patients and restrict activities after rapastinel will be “minimal” compared to the requirements for esketamine. The company also said there seems to be a lower rate of dissociative effects with rapastinel. The drug is being tested alone, in combination with other treatments for major depression, and in patients with depression who are at risk of suicide.\u003c/p>\n\n\u003c/div>\u003c/p>",
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"content": "\u003cp class=\"danger-zone\">For the second time, doctors appear to have put HIV into “sustained remission” with a stem cell transplant — effectively curing the recipient.\u003c/p>\n\u003cp class=\"danger-zone\">Their work, which was published in \u003cem>Nature\u003c/em> and will be presented at the annual Conference on Retroviruses and Opportunistic Infections in Seattle on Tuesday, may encourage scientists working on new gene therapies based on similar principles and give hope to those living with the infection.\u003c/p>\n\u003cp class=\"danger-zone\">The case comes nearly 10 years after Timothy Ray Brown announced he was the so-called “Berlin Patient” — the first person who was functionally cured of HIV and able to stop taking antiretroviral drugs after an intensive round of chemotherapy and radiation and two bone marrow transplants.\u003c/p>\n\u003cp class=\"danger-zone\">The person who received this latest transplant in London has not taken antiretroviral drugs since September 2017; he is not identified in the paper.\u003c/p>\n\u003cp class=\"danger-zone\">“Those of us in the field have been waiting for a second cure via this approach,” said Dr. Keith Jerome, one of the leaders of HIV cure research at the Fred Hutchinson Cancer Research Center. “As long as Timothy Brown was the only [one], we’d have always wondered if there something unique about it.”\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp class=\"danger-zone\">Jerome was not involved in the research published Tuesday.\u003c/p>\n\u003cp class=\"danger-zone\">The researchers behind the paper are from an array of British, Spanish, Dutch and Singaporean institutions; the lead author is \u003ca href=\"https://www.ucl.ac.uk/infection-immunity/people/professor-ravindra-gupta\" target=\"_blank\" rel=\"noopener\">Ravindra K. Gupta\u003c/a>, who is affiliated with the University of Cambridge, Imperial College London, and University College London.\u003c/p>\n\u003cp>Experts caution that this news should not be interpreted as having found a cure for everyone with HIV.\u003c/p>\n\u003cp>“It doesn’t change things for the average person with HIV right now,” said Dr. Bruce Walker, the director of the \u003ca href=\"http://www.ragoninstitute.org/\" target=\"_blank\" rel=\"noopener\">Ragon Institute\u003c/a>, a research institute affiliated with Massachusetts General Hospital, Harvard, and MIT that specializes in HIV/AIDS and infectious diseases. (Walker was also uninvolved with the Nature research.) “It does change things in terms of the research agenda, because it further indicates that this is a potentially viable pathway forward to achieve a cure.”\u003c/p>\n\u003cp>That potentially viable pathway runs through a receptor called CCR5. CCR5 is one of a handful of receptors that HIV can use to get into a particular kind of cell.\u003c/p>\n\u003cp>Those cells, called CD4-positive T-cells, are vital to a person’s immune system. “You can sort of think of [these] cells as the generals that are helping to orchestrate an effective defense,” Walker said. “If they’re not there, things tend to go haywire.”\u003c/p>\n\u003cp>Some people have a particular mutation in the genes that encode the CCR5 receptor that prevents the HIV virus from using it to get in to these T-cells — and no entry means no infection.\u003c/p>\n\u003cp>The person whose case is described in Tuesday’s paper got a transplant of the stem cells that produce blood and immune system cells — typically found in a person’s bone marrow — with this mutation from a donor; about \u003ca href=\"https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.0030339\" target=\"_blank\" rel=\"noopener\">10 percent of people\u003c/a> in some Northern European countries naturally carry the mutation.\u003c/p>\n\u003cp>Like Timothy Brown, this person’s transplant happened as part of his cancer treatment. After doctors diagnosed him with an advanced case of Hodgkin’s lymphoma, the person went through chemotherapy and a transplant from a donor picked in part for his or her CCR5 mutation.\u003c/p>\n\u003cp>Unlike Brown, though, this person’s cancer treatment didn’t involve full-body radiation, and his chemotherapy was also far gentler. That’s encouraging, but Walker, the Ragon researcher, noted the risks from even this regimen were still too great to offer these kind of stem cell transplants outside of cancer treatment. Given that the life expectancy for people with HIV on antiretroviral medications has increased dramatically — and, \u003ca href=\"https://www.statnews.com/2017/05/10/hiv-life-expectancy-study/\">one study found\u003c/a>, is now a nearly normal one, “there’s a very high bar for subjecting people to any additional risk,” he said. “This wasn’t without risk, but was much less [risky].”\u003c/p>\n\u003cp>The CCR5 mutation’s virus-blocking power can be simulated with a drug. Since 2007, Viiv Healthcare, a joint venture initially formed by Pfizer and GlaxoSmithKline, has marketed a drug, called Selzentry in the United States, that prevents HIV from using the CCR5 receptor by binding to the receptor itself.\u003c/p>\n\u003cp>But that drug has the same issues that most drugs have: it needs to be taken every day. “Just like any other suppressive therapy for HIV, as soon as a person stops taking the drug, the virus comes roaring back,” said Fred Hutchinson’s Jerome. In an ideal world, the treatment for HIV would look more like Luxturna, a recently approved gene therapy for a form of blindness \u003ca href=\"https://www.statnews.com/2018/03/21/gene-therapy-luxturna-launch/\">that’s injected just once\u003c/a> into a person’s eye, and less like Lipitor.\u003c/p>\n\u003cp>“The beauty of a transplantation or a gene therapy approach targeting CCR5 — that’s the kind of thing that looks like you can do it once, and then the person’s cured,” Jerome said. “They don’t need to worry about the virus any more, they don’t need to worry about their access to drugs or remembering to take it every day.”\u003c/p>\n\u003cp>The most infamous gene therapy experiment targeting CCR5 is undoubtedly He Jiankui’s, which \u003ca href=\"https://www.statnews.com/2018/11/26/claim-of-crispred-baby-girls-stuns-genome-editing-summit/\">created human embryos\u003c/a> — and, later, actual children — with a CRISPR-mutated CCR5 gene. His announcement triggered a massive backlash from \u003ca href=\"https://www.statnews.com/2019/01/24/crispr-babies-show-need-for-more-specific-rules/\">scientists, ethicists\u003c/a>, and \u003ca href=\"https://www.statnews.com/2019/02/25/crispr-babies-study-china-government-funding/\">the Chinese government\u003c/a>.\u003c/p>\n\u003cp>Less controversial gene editing work is ongoing, too. Sangamo Therapeutics, for example, is working on genetically editing \u003ca href=\"https://www.sangamo.com/pipeline\" target=\"_blank\" rel=\"noopener\">T-cells and stem cells\u003c/a> to carry the CCR5 mutation. According to the company’s pipeline chart, that treatment is in early-stage clinical trials.\u003c/p>\n\u003cp>Tuesday’s paper — and the concept of using CCR5 as the basis for future treatments — comes with caveats. For one thing, not all HIV viruses use CCR5 receptors to get into a cell; viruses that use other co-receptors exist, though they’re rarer. And even if a treatment can stop the virus from infecting new cells, it tends to linger in previously infected ones.\u003c/p>\n\u003cp>“The virus may still be hiding out someplace and it may come back 10 years from now,” Walker noted. “You can never be absolutely certain that a cure has been achieved.”\u003c/p>\n\u003cp>But to Jerome, the Fred Hutchinson Cancer Research Center researcher, a new report of even an uncertain cure is meaningful. “It’s a reminder about how difficult this challenge is and how difficult this virus is to deal with, but at the same time, it provides hope,” he said.\u003c/p>\n\u003cp>“Now there’s not one, but two people that others living with HIV can look toward for encouragement,” he added.\u003c/p>\n\u003cp>\u003cem>\u003cspan style=\"font-weight: 400\">This \u003ca href=\"https://www.statnews.com/2019/03/04/second-person-effectively-cured-of-hiv/?utm_source=STAT+Newsletters&utm_campaign=68de2d8f55-MR_COPY_08&utm_medium=email&utm_term=0_8cab1d7961-68de2d8f55-149648249\" target=\"_blank\" rel=\"noopener\">story\u003c/a> was originally published by\u003ca href=\"https://www.statnews.com/\" target=\"_blank\" rel=\"noopener\"> STAT\u003c/a>, an online publication of Boston Globe Media that covers health, medicine, and scientific discovery. \u003c/span>\u003c/em>\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp> \u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp class=\"danger-zone\">For the second time, doctors appear to have put HIV into “sustained remission” with a stem cell transplant — effectively curing the recipient.\u003c/p>\n\u003cp class=\"danger-zone\">Their work, which was published in \u003cem>Nature\u003c/em> and will be presented at the annual Conference on Retroviruses and Opportunistic Infections in Seattle on Tuesday, may encourage scientists working on new gene therapies based on similar principles and give hope to those living with the infection.\u003c/p>\n\u003cp class=\"danger-zone\">The case comes nearly 10 years after Timothy Ray Brown announced he was the so-called “Berlin Patient” — the first person who was functionally cured of HIV and able to stop taking antiretroviral drugs after an intensive round of chemotherapy and radiation and two bone marrow transplants.\u003c/p>\n\u003cp class=\"danger-zone\">The person who received this latest transplant in London has not taken antiretroviral drugs since September 2017; he is not identified in the paper.\u003c/p>\n\u003cp class=\"danger-zone\">“Those of us in the field have been waiting for a second cure via this approach,” said Dr. Keith Jerome, one of the leaders of HIV cure research at the Fred Hutchinson Cancer Research Center. “As long as Timothy Brown was the only [one], we’d have always wondered if there something unique about it.”\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp class=\"danger-zone\">Jerome was not involved in the research published Tuesday.\u003c/p>\n\u003cp class=\"danger-zone\">The researchers behind the paper are from an array of British, Spanish, Dutch and Singaporean institutions; the lead author is \u003ca href=\"https://www.ucl.ac.uk/infection-immunity/people/professor-ravindra-gupta\" target=\"_blank\" rel=\"noopener\">Ravindra K. Gupta\u003c/a>, who is affiliated with the University of Cambridge, Imperial College London, and University College London.\u003c/p>\n\u003cp>Experts caution that this news should not be interpreted as having found a cure for everyone with HIV.\u003c/p>\n\u003cp>“It doesn’t change things for the average person with HIV right now,” said Dr. Bruce Walker, the director of the \u003ca href=\"http://www.ragoninstitute.org/\" target=\"_blank\" rel=\"noopener\">Ragon Institute\u003c/a>, a research institute affiliated with Massachusetts General Hospital, Harvard, and MIT that specializes in HIV/AIDS and infectious diseases. (Walker was also uninvolved with the Nature research.) “It does change things in terms of the research agenda, because it further indicates that this is a potentially viable pathway forward to achieve a cure.”\u003c/p>\n\u003cp>That potentially viable pathway runs through a receptor called CCR5. CCR5 is one of a handful of receptors that HIV can use to get into a particular kind of cell.\u003c/p>\n\u003cp>Those cells, called CD4-positive T-cells, are vital to a person’s immune system. “You can sort of think of [these] cells as the generals that are helping to orchestrate an effective defense,” Walker said. “If they’re not there, things tend to go haywire.”\u003c/p>\n\u003cp>Some people have a particular mutation in the genes that encode the CCR5 receptor that prevents the HIV virus from using it to get in to these T-cells — and no entry means no infection.\u003c/p>\n\u003cp>The person whose case is described in Tuesday’s paper got a transplant of the stem cells that produce blood and immune system cells — typically found in a person’s bone marrow — with this mutation from a donor; about \u003ca href=\"https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.0030339\" target=\"_blank\" rel=\"noopener\">10 percent of people\u003c/a> in some Northern European countries naturally carry the mutation.\u003c/p>\n\u003cp>Like Timothy Brown, this person’s transplant happened as part of his cancer treatment. After doctors diagnosed him with an advanced case of Hodgkin’s lymphoma, the person went through chemotherapy and a transplant from a donor picked in part for his or her CCR5 mutation.\u003c/p>\n\u003cp>Unlike Brown, though, this person’s cancer treatment didn’t involve full-body radiation, and his chemotherapy was also far gentler. That’s encouraging, but Walker, the Ragon researcher, noted the risks from even this regimen were still too great to offer these kind of stem cell transplants outside of cancer treatment. Given that the life expectancy for people with HIV on antiretroviral medications has increased dramatically — and, \u003ca href=\"https://www.statnews.com/2017/05/10/hiv-life-expectancy-study/\">one study found\u003c/a>, is now a nearly normal one, “there’s a very high bar for subjecting people to any additional risk,” he said. “This wasn’t without risk, but was much less [risky].”\u003c/p>\n\u003cp>The CCR5 mutation’s virus-blocking power can be simulated with a drug. Since 2007, Viiv Healthcare, a joint venture initially formed by Pfizer and GlaxoSmithKline, has marketed a drug, called Selzentry in the United States, that prevents HIV from using the CCR5 receptor by binding to the receptor itself.\u003c/p>\n\u003cp>But that drug has the same issues that most drugs have: it needs to be taken every day. “Just like any other suppressive therapy for HIV, as soon as a person stops taking the drug, the virus comes roaring back,” said Fred Hutchinson’s Jerome. In an ideal world, the treatment for HIV would look more like Luxturna, a recently approved gene therapy for a form of blindness \u003ca href=\"https://www.statnews.com/2018/03/21/gene-therapy-luxturna-launch/\">that’s injected just once\u003c/a> into a person’s eye, and less like Lipitor.\u003c/p>\n\u003cp>“The beauty of a transplantation or a gene therapy approach targeting CCR5 — that’s the kind of thing that looks like you can do it once, and then the person’s cured,” Jerome said. “They don’t need to worry about the virus any more, they don’t need to worry about their access to drugs or remembering to take it every day.”\u003c/p>\n\u003cp>The most infamous gene therapy experiment targeting CCR5 is undoubtedly He Jiankui’s, which \u003ca href=\"https://www.statnews.com/2018/11/26/claim-of-crispred-baby-girls-stuns-genome-editing-summit/\">created human embryos\u003c/a> — and, later, actual children — with a CRISPR-mutated CCR5 gene. His announcement triggered a massive backlash from \u003ca href=\"https://www.statnews.com/2019/01/24/crispr-babies-show-need-for-more-specific-rules/\">scientists, ethicists\u003c/a>, and \u003ca href=\"https://www.statnews.com/2019/02/25/crispr-babies-study-china-government-funding/\">the Chinese government\u003c/a>.\u003c/p>\n\u003cp>Less controversial gene editing work is ongoing, too. Sangamo Therapeutics, for example, is working on genetically editing \u003ca href=\"https://www.sangamo.com/pipeline\" target=\"_blank\" rel=\"noopener\">T-cells and stem cells\u003c/a> to carry the CCR5 mutation. According to the company’s pipeline chart, that treatment is in early-stage clinical trials.\u003c/p>\n\u003cp>Tuesday’s paper — and the concept of using CCR5 as the basis for future treatments — comes with caveats. For one thing, not all HIV viruses use CCR5 receptors to get into a cell; viruses that use other co-receptors exist, though they’re rarer. And even if a treatment can stop the virus from infecting new cells, it tends to linger in previously infected ones.\u003c/p>\n\u003cp>“The virus may still be hiding out someplace and it may come back 10 years from now,” Walker noted. “You can never be absolutely certain that a cure has been achieved.”\u003c/p>\n\u003cp>But to Jerome, the Fred Hutchinson Cancer Research Center researcher, a new report of even an uncertain cure is meaningful. “It’s a reminder about how difficult this challenge is and how difficult this virus is to deal with, but at the same time, it provides hope,” he said.\u003c/p>\n\u003cp>“Now there’s not one, but two people that others living with HIV can look toward for encouragement,” he added.\u003c/p>\n\u003cp>\u003cem>\u003cspan style=\"font-weight: 400\">This \u003ca href=\"https://www.statnews.com/2019/03/04/second-person-effectively-cured-of-hiv/?utm_source=STAT+Newsletters&utm_campaign=68de2d8f55-MR_COPY_08&utm_medium=email&utm_term=0_8cab1d7961-68de2d8f55-149648249\" target=\"_blank\" rel=\"noopener\">story\u003c/a> was originally published by\u003ca href=\"https://www.statnews.com/\" target=\"_blank\" rel=\"noopener\"> STAT\u003c/a>, an online publication of Boston Globe Media that covers health, medicine, and scientific discovery. \u003c/span>\u003c/em>\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cp>Killer whales, Japanese aphids and \u003cem>Homo sapiens\u003c/em> \u003cem>—\u003c/em> they’re among the few organisms whose females live on long past the age of reproduction.\u003c/p>\n\u003cp>Since the name of the evolutionary game is survival and reproduction, the phenomenon begs explanation — why live longer than you can reproduce? In the 1960s, researchers came up with the “grandmother hypothesis” to explain the human side of things. The hypothesis is that the help of grandmothers enables mothers to have more children. So women who had the genetic makeup for longer living would ultimately have more grandchildren carrying their longevity genes. (Sorry, grandfathers, you’re not included in this picture.)\u003c/p>\n\u003cp>\u003ca href=\"https://www.cell.com/current-biology/fulltext/S0960-9822(19)30008-9\" target=\"_blank\" rel=\"noopener\">Two studies\u003c/a> published Thursday in \u003cem>Current Biology\u003c/em> take another look at this hypothesis and add new insights into the role grandmothers play.\u003c/p>\n\u003cp>The first hard evidence for the grandmother hypothesis was gathered by \u003ca href=\"https://faculty.utah.edu/u0030555-KRISTEN_HAWKES/research/index.hml\" target=\"_blank\" rel=\"noopener\">Kristen Hawkes\u003c/a>, an anthropologist at the University of Utah who was studying the Hadza people, a group of hunter-gatherers in northern Tanzania. Hawkes was struck by “how productive these old ladies were” at foraging for food, and she later documented how their help allowed mothers to have more children.\u003c/p>\n\u003cp>If our long post-reproductive lives evolved because of grandmothers, we should be able to find fingerprints of the benefits of grandmothering in many cultures. But the circumstances of modern life differ drastically from those we faced at the beginning of our evolutionary story.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>The studies in \u003cem>Current Biology\u003c/em> turned to the detailed records of two preindustrial populations, one in what is now Quebec and the other in Finland. The researchers mined these rich databases to quantify the reproductive boost that grandmothers provide and to help us better understand the limits of their help.\u003c/p>\n\u003cp>In 1608, French Catholic priests in what is present-day Quebec began recording every birth, death and marriage in their parish. As settlers continued to arrive, multiply and fill the St. Lawrence Valley, parish records ballooned. “We had the data set of the first French settlers coming off the first boat,” says \u003ca href=\"https://www.ubishops.ca/academic-programs/faculty-of-arts-and-science/natural-sciences-and-mathematics/biological-sciences/faculty/name/patrick-bergeron/\" target=\"_blank\" rel=\"noopener\">Patrick Bergeron\u003c/a>, an evolutionary biologist at Bishop’s University, who co-authored the study.\u003c/p>\n\u003cp>The population was mostly French and mostly farmers and was fairly mobile. That homogeneity helped the researchers isolate the effect of grandmothers and see if it mattered how close, geographically, a daughter was to her mother.\u003c/p>\n\u003cp>Hawkes explains that this approach adds nuance to previous studies of the grandmother hypothesis, which didn’t directly measure proximity. “After all, if you’re in Quebec but your grandma’s in Cleveland, she may not be much help,” she says.\u003c/p>\n\u003cp>\u003ca href=\"http://www.iee.unibe.ch/about_us/team/index_eng.html\" target=\"_blank\" rel=\"noopener\">Sacha Engelhardt\u003c/a>, a postdoctoral researcher at the University of Bern who conducted research for this study at Université de Sherbrooke, looked for groups of sisters in which some left home and others stayed put. If being close to grandma helps, the homebodies should have had more kids than their adventurous sisters.\u003c/p>\n\u003cp>It turned out that staying close to grandma paid off in family size. Women who lived 200 miles from mom had, on average, 1.75 fewer children than their sisters who lived in the same parish as their mother. “Women in those days had a lot of kids, on average almost eight,” says Engelhardt. But times were tough, and about half of a woman’s offspring died before age 15. Such harsh conditions led to a range of reproductive success; the number of grandkids per grandmother in this database ranged from one to 195.\u003c/p>\n\u003cp>Being geographically close to grandma curbed child mortality too and allowed mothers to start having kids at a younger age.\u003c/p>\n\u003cp>Altogether, these results are what you’d expect if the grandmother hypothesis is true. “These results are really interesting,” says Hawkes. “They took a much more fine-grained approach, and it gives us a clearer picture of the effect of grandmothers.”\u003c/p>\n\u003cp>But if grandmas are so beneficial, why don’t they live even longer — long enough to help their great-grandchildren grow up and have kids of their own?\u003c/p>\n\u003cp>To answer that question, you need to consider not only how much help a grandmother can give but also how the opportunity for a grandmother to help changes over time. If a grandmother’s abilities deteriorate with age or if there just aren’t as many grandkids around to help, the evolutionary benefits of living longer might disappear.\u003c/p>\n\u003cp>The second study, conducted by Simon Chapman, a Ph.D. student at the University of Turku in Finland, looked at a database of preindustrial Finns to answer this question. From 1731 to 1895, all births, deaths and marriages were recorded by the state. Finns moved around much less than the French settlers of the previous study, so most grandchildren lived close to their grandparents.\u003c/p>\n\u003cp>In Finland too, the presence of a grandmother boosted a daughter’s total number of offspring. But closer inspection revealed some caveats.\u003c/p>\n\u003cp>The study shows that the opportunity for grandmas to help was not constant over the years. On average, a woman became a grandmother in her 40s, and the number of grandkids she cared for steadily rose, peaking in her early 60s and then diminishing into her mid-70s.\u003c/p>\n\u003cp>Having a grandmother age 50 to 75 increased a toddler’s chance of surviving from age 2 to 5 by 30 percent. But the researchers found that the benefits of having a grandmother petered out after she passed age 75. In fact, the presence of an older paternal grandmother reduced a newborn’s probability of surviving to age 2 by 37 percent.\u003c/p>\n\u003cp>Why? Too many mouths to feed, according to Chapman. “At this time, paternal grandmothers often lived in the same home as their son and may have required extra care,” he says. That may have shifted resources away from younger grandchildren.\u003c/p>\n\u003cp>Chapman says that together, these results help explain why selection has extended human lives past our reproductive prime, but only up to a point. Grandma can help when her grandchildren are growing up and she is likely in her 50s, 60s and early 70s. As both these studies demonstrate, grandmas can make a big difference in these years, and that reproductive boost helps push human life past the normal finish line of old age.\u003c/p>\n\u003cp>But as grandkids grow older, grandma’s help doesn’t have the same impact, and the evolutionary value of living much longer decreases. Chapman found that grandmothers’ mortality rates shoot up just when this dip in opportunity for helping arrives.\u003c/p>\n\u003cp>\u003ca href=\"https://www.rosalynlapier.com/\" target=\"_blank\" rel=\"noopener\">Rosalyn LaPier\u003c/a> is intrigued by the results of these new studies. She examines the benefits of grandmothers on a societal and cultural level. Currently a professor at the University of Montana who studies how indigenous cultures transmit knowledge, LaPier grew up on the Blackfeet reservation in Montana and spent countless afternoons with her grandmother learning about the land and plants that sustain their culture.\u003c/p>\n\u003cp>For most of human history, this kind of knowledge was transmitted orally. “In North American indigenous communities, you see the transmission of agricultural knowledge across generations,” she says. “In many cases from grandmother to grandchild.”\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp>\u003cem>\u003cem>Jonathan Lambert is an intern on NPR’s Science Desk.\u003c/em> \u003cem>You can follow him on Twitter:\u003c/em> \u003ca href=\"https://twitter.com/evolambert\" target=\"_blank\" rel=\"noopener\">@evolambert\u003c/a>\u003c/em>\u003c/p>\n\u003cdiv class=\"fullattribution\">\u003cem>Copyright 2019 \u003ca href=\"https://www.npr.org\" target=\"_blank\" rel=\"noopener\">NPR\u003c/a>.\u003c/em>\u003c/div>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>Killer whales, Japanese aphids and \u003cem>Homo sapiens\u003c/em> \u003cem>—\u003c/em> they’re among the few organisms whose females live on long past the age of reproduction.\u003c/p>\n\u003cp>Since the name of the evolutionary game is survival and reproduction, the phenomenon begs explanation — why live longer than you can reproduce? In the 1960s, researchers came up with the “grandmother hypothesis” to explain the human side of things. The hypothesis is that the help of grandmothers enables mothers to have more children. So women who had the genetic makeup for longer living would ultimately have more grandchildren carrying their longevity genes. (Sorry, grandfathers, you’re not included in this picture.)\u003c/p>\n\u003cp>\u003ca href=\"https://www.cell.com/current-biology/fulltext/S0960-9822(19)30008-9\" target=\"_blank\" rel=\"noopener\">Two studies\u003c/a> published Thursday in \u003cem>Current Biology\u003c/em> take another look at this hypothesis and add new insights into the role grandmothers play.\u003c/p>\n\u003cp>The first hard evidence for the grandmother hypothesis was gathered by \u003ca href=\"https://faculty.utah.edu/u0030555-KRISTEN_HAWKES/research/index.hml\" target=\"_blank\" rel=\"noopener\">Kristen Hawkes\u003c/a>, an anthropologist at the University of Utah who was studying the Hadza people, a group of hunter-gatherers in northern Tanzania. Hawkes was struck by “how productive these old ladies were” at foraging for food, and she later documented how their help allowed mothers to have more children.\u003c/p>\n\u003cp>If our long post-reproductive lives evolved because of grandmothers, we should be able to find fingerprints of the benefits of grandmothering in many cultures. But the circumstances of modern life differ drastically from those we faced at the beginning of our evolutionary story.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>The studies in \u003cem>Current Biology\u003c/em> turned to the detailed records of two preindustrial populations, one in what is now Quebec and the other in Finland. The researchers mined these rich databases to quantify the reproductive boost that grandmothers provide and to help us better understand the limits of their help.\u003c/p>\n\u003cp>In 1608, French Catholic priests in what is present-day Quebec began recording every birth, death and marriage in their parish. As settlers continued to arrive, multiply and fill the St. Lawrence Valley, parish records ballooned. “We had the data set of the first French settlers coming off the first boat,” says \u003ca href=\"https://www.ubishops.ca/academic-programs/faculty-of-arts-and-science/natural-sciences-and-mathematics/biological-sciences/faculty/name/patrick-bergeron/\" target=\"_blank\" rel=\"noopener\">Patrick Bergeron\u003c/a>, an evolutionary biologist at Bishop’s University, who co-authored the study.\u003c/p>\n\u003cp>The population was mostly French and mostly farmers and was fairly mobile. That homogeneity helped the researchers isolate the effect of grandmothers and see if it mattered how close, geographically, a daughter was to her mother.\u003c/p>\n\u003cp>Hawkes explains that this approach adds nuance to previous studies of the grandmother hypothesis, which didn’t directly measure proximity. “After all, if you’re in Quebec but your grandma’s in Cleveland, she may not be much help,” she says.\u003c/p>\n\u003cp>\u003ca href=\"http://www.iee.unibe.ch/about_us/team/index_eng.html\" target=\"_blank\" rel=\"noopener\">Sacha Engelhardt\u003c/a>, a postdoctoral researcher at the University of Bern who conducted research for this study at Université de Sherbrooke, looked for groups of sisters in which some left home and others stayed put. If being close to grandma helps, the homebodies should have had more kids than their adventurous sisters.\u003c/p>\n\u003cp>It turned out that staying close to grandma paid off in family size. Women who lived 200 miles from mom had, on average, 1.75 fewer children than their sisters who lived in the same parish as their mother. “Women in those days had a lot of kids, on average almost eight,” says Engelhardt. But times were tough, and about half of a woman’s offspring died before age 15. Such harsh conditions led to a range of reproductive success; the number of grandkids per grandmother in this database ranged from one to 195.\u003c/p>\n\u003cp>Being geographically close to grandma curbed child mortality too and allowed mothers to start having kids at a younger age.\u003c/p>\n\u003cp>Altogether, these results are what you’d expect if the grandmother hypothesis is true. “These results are really interesting,” says Hawkes. “They took a much more fine-grained approach, and it gives us a clearer picture of the effect of grandmothers.”\u003c/p>\n\u003cp>But if grandmas are so beneficial, why don’t they live even longer — long enough to help their great-grandchildren grow up and have kids of their own?\u003c/p>\n\u003cp>To answer that question, you need to consider not only how much help a grandmother can give but also how the opportunity for a grandmother to help changes over time. If a grandmother’s abilities deteriorate with age or if there just aren’t as many grandkids around to help, the evolutionary benefits of living longer might disappear.\u003c/p>\n\u003cp>The second study, conducted by Simon Chapman, a Ph.D. student at the University of Turku in Finland, looked at a database of preindustrial Finns to answer this question. From 1731 to 1895, all births, deaths and marriages were recorded by the state. Finns moved around much less than the French settlers of the previous study, so most grandchildren lived close to their grandparents.\u003c/p>\n\u003cp>In Finland too, the presence of a grandmother boosted a daughter’s total number of offspring. But closer inspection revealed some caveats.\u003c/p>\n\u003cp>The study shows that the opportunity for grandmas to help was not constant over the years. On average, a woman became a grandmother in her 40s, and the number of grandkids she cared for steadily rose, peaking in her early 60s and then diminishing into her mid-70s.\u003c/p>\n\u003cp>Having a grandmother age 50 to 75 increased a toddler’s chance of surviving from age 2 to 5 by 30 percent. But the researchers found that the benefits of having a grandmother petered out after she passed age 75. In fact, the presence of an older paternal grandmother reduced a newborn’s probability of surviving to age 2 by 37 percent.\u003c/p>\n\u003cp>Why? Too many mouths to feed, according to Chapman. “At this time, paternal grandmothers often lived in the same home as their son and may have required extra care,” he says. That may have shifted resources away from younger grandchildren.\u003c/p>\n\u003cp>Chapman says that together, these results help explain why selection has extended human lives past our reproductive prime, but only up to a point. Grandma can help when her grandchildren are growing up and she is likely in her 50s, 60s and early 70s. As both these studies demonstrate, grandmas can make a big difference in these years, and that reproductive boost helps push human life past the normal finish line of old age.\u003c/p>\n\u003cp>But as grandkids grow older, grandma’s help doesn’t have the same impact, and the evolutionary value of living much longer decreases. Chapman found that grandmothers’ mortality rates shoot up just when this dip in opportunity for helping arrives.\u003c/p>\n\u003cp>\u003ca href=\"https://www.rosalynlapier.com/\" target=\"_blank\" rel=\"noopener\">Rosalyn LaPier\u003c/a> is intrigued by the results of these new studies. She examines the benefits of grandmothers on a societal and cultural level. Currently a professor at the University of Montana who studies how indigenous cultures transmit knowledge, LaPier grew up on the Blackfeet reservation in Montana and spent countless afternoons with her grandmother learning about the land and plants that sustain their culture.\u003c/p>\n\u003cp>For most of human history, this kind of knowledge was transmitted orally. “In North American indigenous communities, you see the transmission of agricultural knowledge across generations,” she says. “In many cases from grandmother to grandchild.”\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>\u003cem>\u003cem>Jonathan Lambert is an intern on NPR’s Science Desk.\u003c/em> \u003cem>You can follow him on Twitter:\u003c/em> \u003ca href=\"https://twitter.com/evolambert\" target=\"_blank\" rel=\"noopener\">@evolambert\u003c/a>\u003c/em>\u003c/p>\n\u003cdiv class=\"fullattribution\">\u003cem>Copyright 2019 \u003ca href=\"https://www.npr.org\" target=\"_blank\" rel=\"noopener\">NPR\u003c/a>.\u003c/em>\u003c/div>\n\n\u003c/div>\u003c/p>",
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"title": "Making Sense of the CRISPR Patent Dispute Between the University of California and Broad",
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"content": "\u003cp>Anyone fond of intricate intellectual property disputes (and really, who isn’t?) is going to have their cup runnething over when it comes to the long-running battle between the University of California and Harvard/MIT’s Broad Institute to determine who will get to cash in the most on their seminal CRISPR/Cas 9 discoveries.\u003c/p>\n\u003cp>CRISPR/Cas9 is a precise gene-editing technology. Scientists can use it to home in on specific locations within the human genetic code to swap out a problematic section of DNA with a corrected segment. The advance has created enormous excitement over its potential for curing or preventing genetic diseases, and galvanized an \u003ca href=\"https://www.kqed.org/futureofyou/435096/as-human-gene-editing-advances-doudna-says-ethical-discussions-cant-wait\" target=\"_blank\" rel=\"noopener\">ethical debate\u003c/a> over \u003ca href=\"https://www.kqed.org/science/1934926/trying-to-understand-the-crispr-baby-five-things-to-read\" target=\"_blank\" rel=\"noopener\">human genome editing\u003c/a>.\u003c/p>\n\u003cp>\u003ca href=\"https://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2017/11/DESKTOP_CRISPR_171115.jpg\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"aligncenter size-large wp-image-1938166\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2039/02/DESKTOP_CRISPR_171115-1-1020x677.jpg\" alt=\"\" width=\"640\" height=\"425\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2039/02/DESKTOP_CRISPR_171115-1-1020x677.jpg 1020w, https://cdn.kqed.org/wp-content/uploads/sites/35/2039/02/DESKTOP_CRISPR_171115-1-160x106.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2039/02/DESKTOP_CRISPR_171115-1-800x531.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2039/02/DESKTOP_CRISPR_171115-1-768x510.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2039/02/DESKTOP_CRISPR_171115-1-1200x797.jpg 1200w, https://cdn.kqed.org/wp-content/uploads/sites/35/2039/02/DESKTOP_CRISPR_171115-1.jpg 1280w\" sizes=\"(max-width: 640px) 100vw, 640px\">\u003c/a>\u003c/p>\n\u003cp>UC and Broad have been slugging it out in administrative hearings and the courts since 2014, when Broad, which had paid for an expedited review, received a key patent while UC still waited for approval on its own filing. UC eventually \u003ca href=\"https://www.kqed.org/futureofyou/444391/uc-loses-appeal-on-crispr-patent\" target=\"_blank\" rel=\"noopener\">lost\u003c/a> the legal fight, but on Feb. 8, \u003ca href=\"https://www.reuters.com/article/us-ucberkeley-ip-crispr/university-of-california-to-be-granted-pioneering-crispr-patent-idUSKCN1PX25K\" target=\"_blank\" rel=\"noopener\">news broke\u003c/a> that the U.S. Patent and Trademark Office will finally issue UC’s foundational CRISPR/Cas9 patent. Not everyone expected the decision, and it has created a potentially even bigger muddle over who will get paid for what should the considerable hopes for the technology come to fruition.\u003c/p>\n\u003cp>To sort out the complexities, KQED spoke with two people following the case, reporter \u003ca href=\"https://www.statnews.com/2019/02/08/the-university-of-california-gets-its-key-crispr-patent/\" target=\"_blank\" rel=\"noopener\">Sharon Begley\u003c/a> of the health news website \u003ca href=\"https://www.statnews.com/\" target=\"_blank\" rel=\"noopener\">STAT,\u003c/a> and \u003ca href=\"https://www.nyls.edu/faculty/faculty-profiles/faculty_profiles/jacob-s-sherkow/\" target=\"_blank\" rel=\"noopener\">Professor Jacob Sherkow\u003c/a>, of the Innovation Center for Law and Technology at New York Law School. Some key points …\u003c/p>\n\u003cp>\u003cstrong>What’s the history of the dispute between Broad and UC? \u003c/strong>\u003c/p>\n\u003cp>In 2012, University of California Berkeley biochemist \u003ca href=\"https://chemistry.berkeley.edu/faculty/chem/doudna\" target=\"_blank\" rel=\"noopener\">Jennifer Doudna\u003c/a> and colleagues made a seminal discovery about how to use CRISPR/Cas9 for gene editing, performing their experiments on DNA in a test tube. UC subsequently filed with the United States Patent and Trademark Office for a patent on the process.\u003c/p>\n\u003cp>In 2013, a group led by molecular biologist \u003ca href=\"https://www.broadinstitute.org/bios/feng-zhang\" target=\"_blank\" rel=\"noopener\">Feng Zhang\u003c/a> at the Broad Institute in Boston also edited genes using CRISPR. This team was able to edit the DNA inside of actual mouse and human cells. Broad filed for a patent on its process, and in 2014 the United States Patent and Trademark Office granted the patents.\u003c/p>\n\u003cp>At that point, UC claimed the Broad patents “interfered” with the patent for which UC had applied. “That’s called an interference proceeding,” Begley said of the legal maneuver. “Lawyers make gazillions of dollars on it.”\u003c/p>\n\u003cp>But the tactic didn’t work. In February 2017, the Patent office ruled that Broad’s patents were sufficiently different from the one UC claimed, so no interference had occurred. UC then took Broad to court, and in September 2018, the U.S. Court of Appeals for the Federal Circuit affirmed the patent office’s decision to award Broad its patents.\u003c/p>\n\u003cp>“So at this point, and again, we’re six years later, UC’s (2013) patent application is still sitting there at the Patent and Trademark Office,” said Begley. “And what happened on February 8 is that the patent office finally said, ‘UC, we are going to give you this patent that you applied for on the basic use of CRISPR in all kinds of cells.’ And that should be very good news for UC.”\u003c/p>\n\u003cp>Jacob Sherkow, a patent law expert who has been following the case closely, wrote in an email that he was surprised at the news that UC is going to be awarded the patent for which it filed in 2013. He thought UC would run into trouble given the filing of an earlier patent from a Lithuanian researcher named Virginijus Šikšnys, who won the prestigious Kavli Prize last year for “seminal” CRISPR advances. Science magazine \u003ca href=\"https://www.sciencemag.org/news/2018/06/prestigious-prize-overshadowed-crispr-researcher-wins-spotlight\" target=\"_blank\" rel=\"noopener\">called\u003c/a> Šikšnys an “overshadowed” researcher in the field.\u003c/p>\n\u003cp>“Surprisingly — and I wasn’t the only one surprised — the patent office assigned the patent to a new examiner, who simply allowed the patent with only minimal comment,” Sherkow said.\u003c/p>\n\u003cp>\u003cstrong>How much are these patents worth?\u003c/strong>\u003c/p>\n\u003cp>A lot of companies are trying to produce human therapies using CRISPR. If they succeed, “that market almost certainly will be worth tens of billions of dollars per year,” said Begley. But the holder of the patent that enables these advances won’t get a huge slice. Despite early reports that the patents might be worth billions of dollars, she said the figure will “almost certainly be in the millions of dollars.”\u003c/p>\n\u003cp>Sherkow’s back-of-the-envelope calculation puts that figure at “easily tens of millions” per year, or $100 million over the life of the patent. Developments over the last several years, he says, have diminished the stakes.\u003c/p>\n\u003cp>“When the case was first filed, it was unclear whether enzymes other than Cas9 would have the same efficacy. Now, \u003ca href=\"https://www.latimes.com/science/sciencenow/la-sci-sn-crisper-casx-cas12b-20190204-story.html\" target=\"_blank\" rel=\"noopener\">we’ve got a riot\u003c/a>: Cas12, CasX, CasY, etc. ”\u003c/p>\n\u003cp>Begley said the scientists she’s spoken to “have sort of been rooting for UC because it’s a public institution,” whereas Harvard and MIT are private universities. With the funding difficulties UC has had over the years, “if a significant revenue stream can come to UC as a result of [CRISPR patents], there’s just a lot of people who are hoping that happens,” Begley said.\u003c/p>\n\u003cp>\u003cstrong>Is the dispute over? \u003c/strong>\u003c/p>\n\u003cp>The Broad Institute could challenge UC’s patents in a procedure called a post-grant review, said Sherkow. He said Broad has nine months from the date the UC patent is issued to do that.\u003c/p>\n\u003cp>“Alternatively, there may be an opportunity to bring a lawsuit in federal court challenging the UC patent,” he said.\u003c/p>\n\u003cp>For now, it appears UC and Broad may both need to be compensated for any applications using CRISPR in humans. Begley said we’re “years away” from knowing the final outcome of the dispute. “Not until there’s an actual commercialized therapy.”\u003c/p>\n\u003cp>And there could be one more complication down the road: Another expert in intellectual property and innovation, Stanford Law Professor Lisa Larrimore Ouellette, \u003ca href=\"https://www.statnews.com/2019/02/08/the-university-of-california-gets-its-key-crispr-patent/\" target=\"_blank\" rel=\"noopener\">told Begley\u003c/a> that UC’s patent could be vulnerable to challenges based on something called the “enablement clause,” which requires that patents allow for anyone to follow a series of steps to carry out the invention. Sherkow agreed UC’s patent may fall short in this regard.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>\u003cem>Brian Watt and Danielle Venton contributed to this post.\u003c/em>\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n",
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"excerpt": "Recent news that the U.S. Patent and Trademark Office will award a key CRISPR/Cas9 patent to the University of California may create even more complications in its long-running dispute with the Broad Institute.",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>Anyone fond of intricate intellectual property disputes (and really, who isn’t?) is going to have their cup runnething over when it comes to the long-running battle between the University of California and Harvard/MIT’s Broad Institute to determine who will get to cash in the most on their seminal CRISPR/Cas 9 discoveries.\u003c/p>\n\u003cp>CRISPR/Cas9 is a precise gene-editing technology. Scientists can use it to home in on specific locations within the human genetic code to swap out a problematic section of DNA with a corrected segment. The advance has created enormous excitement over its potential for curing or preventing genetic diseases, and galvanized an \u003ca href=\"https://www.kqed.org/futureofyou/435096/as-human-gene-editing-advances-doudna-says-ethical-discussions-cant-wait\" target=\"_blank\" rel=\"noopener\">ethical debate\u003c/a> over \u003ca href=\"https://www.kqed.org/science/1934926/trying-to-understand-the-crispr-baby-five-things-to-read\" target=\"_blank\" rel=\"noopener\">human genome editing\u003c/a>.\u003c/p>\n\u003cp>\u003ca href=\"https://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2017/11/DESKTOP_CRISPR_171115.jpg\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"aligncenter size-large wp-image-1938166\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2039/02/DESKTOP_CRISPR_171115-1-1020x677.jpg\" alt=\"\" width=\"640\" height=\"425\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2039/02/DESKTOP_CRISPR_171115-1-1020x677.jpg 1020w, https://cdn.kqed.org/wp-content/uploads/sites/35/2039/02/DESKTOP_CRISPR_171115-1-160x106.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2039/02/DESKTOP_CRISPR_171115-1-800x531.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2039/02/DESKTOP_CRISPR_171115-1-768x510.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2039/02/DESKTOP_CRISPR_171115-1-1200x797.jpg 1200w, https://cdn.kqed.org/wp-content/uploads/sites/35/2039/02/DESKTOP_CRISPR_171115-1.jpg 1280w\" sizes=\"(max-width: 640px) 100vw, 640px\">\u003c/a>\u003c/p>\n\u003cp>UC and Broad have been slugging it out in administrative hearings and the courts since 2014, when Broad, which had paid for an expedited review, received a key patent while UC still waited for approval on its own filing. UC eventually \u003ca href=\"https://www.kqed.org/futureofyou/444391/uc-loses-appeal-on-crispr-patent\" target=\"_blank\" rel=\"noopener\">lost\u003c/a> the legal fight, but on Feb. 8, \u003ca href=\"https://www.reuters.com/article/us-ucberkeley-ip-crispr/university-of-california-to-be-granted-pioneering-crispr-patent-idUSKCN1PX25K\" target=\"_blank\" rel=\"noopener\">news broke\u003c/a> that the U.S. Patent and Trademark Office will finally issue UC’s foundational CRISPR/Cas9 patent. Not everyone expected the decision, and it has created a potentially even bigger muddle over who will get paid for what should the considerable hopes for the technology come to fruition.\u003c/p>\n\u003cp>To sort out the complexities, KQED spoke with two people following the case, reporter \u003ca href=\"https://www.statnews.com/2019/02/08/the-university-of-california-gets-its-key-crispr-patent/\" target=\"_blank\" rel=\"noopener\">Sharon Begley\u003c/a> of the health news website \u003ca href=\"https://www.statnews.com/\" target=\"_blank\" rel=\"noopener\">STAT,\u003c/a> and \u003ca href=\"https://www.nyls.edu/faculty/faculty-profiles/faculty_profiles/jacob-s-sherkow/\" target=\"_blank\" rel=\"noopener\">Professor Jacob Sherkow\u003c/a>, of the Innovation Center for Law and Technology at New York Law School. Some key points …\u003c/p>\n\u003cp>\u003cstrong>What’s the history of the dispute between Broad and UC? \u003c/strong>\u003c/p>\n\u003cp>In 2012, University of California Berkeley biochemist \u003ca href=\"https://chemistry.berkeley.edu/faculty/chem/doudna\" target=\"_blank\" rel=\"noopener\">Jennifer Doudna\u003c/a> and colleagues made a seminal discovery about how to use CRISPR/Cas9 for gene editing, performing their experiments on DNA in a test tube. UC subsequently filed with the United States Patent and Trademark Office for a patent on the process.\u003c/p>\n\u003cp>In 2013, a group led by molecular biologist \u003ca href=\"https://www.broadinstitute.org/bios/feng-zhang\" target=\"_blank\" rel=\"noopener\">Feng Zhang\u003c/a> at the Broad Institute in Boston also edited genes using CRISPR. This team was able to edit the DNA inside of actual mouse and human cells. Broad filed for a patent on its process, and in 2014 the United States Patent and Trademark Office granted the patents.\u003c/p>\n\u003cp>At that point, UC claimed the Broad patents “interfered” with the patent for which UC had applied. “That’s called an interference proceeding,” Begley said of the legal maneuver. “Lawyers make gazillions of dollars on it.”\u003c/p>\n\u003cp>But the tactic didn’t work. In February 2017, the Patent office ruled that Broad’s patents were sufficiently different from the one UC claimed, so no interference had occurred. UC then took Broad to court, and in September 2018, the U.S. Court of Appeals for the Federal Circuit affirmed the patent office’s decision to award Broad its patents.\u003c/p>\n\u003cp>“So at this point, and again, we’re six years later, UC’s (2013) patent application is still sitting there at the Patent and Trademark Office,” said Begley. “And what happened on February 8 is that the patent office finally said, ‘UC, we are going to give you this patent that you applied for on the basic use of CRISPR in all kinds of cells.’ And that should be very good news for UC.”\u003c/p>\n\u003cp>Jacob Sherkow, a patent law expert who has been following the case closely, wrote in an email that he was surprised at the news that UC is going to be awarded the patent for which it filed in 2013. He thought UC would run into trouble given the filing of an earlier patent from a Lithuanian researcher named Virginijus Šikšnys, who won the prestigious Kavli Prize last year for “seminal” CRISPR advances. Science magazine \u003ca href=\"https://www.sciencemag.org/news/2018/06/prestigious-prize-overshadowed-crispr-researcher-wins-spotlight\" target=\"_blank\" rel=\"noopener\">called\u003c/a> Šikšnys an “overshadowed” researcher in the field.\u003c/p>\n\u003cp>“Surprisingly — and I wasn’t the only one surprised — the patent office assigned the patent to a new examiner, who simply allowed the patent with only minimal comment,” Sherkow said.\u003c/p>\n\u003cp>\u003cstrong>How much are these patents worth?\u003c/strong>\u003c/p>\n\u003cp>A lot of companies are trying to produce human therapies using CRISPR. If they succeed, “that market almost certainly will be worth tens of billions of dollars per year,” said Begley. But the holder of the patent that enables these advances won’t get a huge slice. Despite early reports that the patents might be worth billions of dollars, she said the figure will “almost certainly be in the millions of dollars.”\u003c/p>\n\u003cp>Sherkow’s back-of-the-envelope calculation puts that figure at “easily tens of millions” per year, or $100 million over the life of the patent. Developments over the last several years, he says, have diminished the stakes.\u003c/p>\n\u003cp>“When the case was first filed, it was unclear whether enzymes other than Cas9 would have the same efficacy. Now, \u003ca href=\"https://www.latimes.com/science/sciencenow/la-sci-sn-crisper-casx-cas12b-20190204-story.html\" target=\"_blank\" rel=\"noopener\">we’ve got a riot\u003c/a>: Cas12, CasX, CasY, etc. ”\u003c/p>\n\u003cp>Begley said the scientists she’s spoken to “have sort of been rooting for UC because it’s a public institution,” whereas Harvard and MIT are private universities. With the funding difficulties UC has had over the years, “if a significant revenue stream can come to UC as a result of [CRISPR patents], there’s just a lot of people who are hoping that happens,” Begley said.\u003c/p>\n\u003cp>\u003cstrong>Is the dispute over? \u003c/strong>\u003c/p>\n\u003cp>The Broad Institute could challenge UC’s patents in a procedure called a post-grant review, said Sherkow. He said Broad has nine months from the date the UC patent is issued to do that.\u003c/p>\n\u003cp>“Alternatively, there may be an opportunity to bring a lawsuit in federal court challenging the UC patent,” he said.\u003c/p>\n\u003cp>For now, it appears UC and Broad may both need to be compensated for any applications using CRISPR in humans. Begley said we’re “years away” from knowing the final outcome of the dispute. “Not until there’s an actual commercialized therapy.”\u003c/p>\n\u003cp>And there could be one more complication down the road: Another expert in intellectual property and innovation, Stanford Law Professor Lisa Larrimore Ouellette, \u003ca href=\"https://www.statnews.com/2019/02/08/the-university-of-california-gets-its-key-crispr-patent/\" target=\"_blank\" rel=\"noopener\">told Begley\u003c/a> that UC’s patent could be vulnerable to challenges based on something called the “enablement clause,” which requires that patents allow for anyone to follow a series of steps to carry out the invention. Sherkow agreed UC’s patent may fall short in this regard.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"info": "KQED’s statewide radio news program providing daily coverage of issues, trends and public policy decisions.",
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"order": 8
},
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},
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"order": 1
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"info": "\u003cem>Code Switch\u003c/em>, which listeners will hear in the first part of the hour, has fearless and much-needed conversations about race. Hosted by journalists of color, the show tackles the subject of race head-on, exploring how it impacts every part of society — from politics and pop culture to history, sports and more.\u003cbr />\u003cbr />\u003cem>Life Kit\u003c/em>, which will be in the second part of the hour, guides you through spaces and feelings no one prepares you for — from finances to mental health, from workplace microaggressions to imposter syndrome, from relationships to parenting. The show features experts with real world experience and shares their knowledge. Because everyone needs a little help being human.\u003cbr />\u003cbr />\u003ca href=\"https://www.npr.org/podcasts/510312/codeswitch\">\u003cem>Code Switch\u003c/em> offical site and podcast\u003c/a>\u003cbr />\u003ca href=\"https://www.npr.org/lifekit\">\u003cem>Life Kit\u003c/em> offical site and podcast\u003c/a>\u003cbr />",
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"id": "commonwealth-club",
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"meta": {
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"source": "WNYC"
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"id": "fresh-air",
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"hidden-brain": {
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"hyphenacion": {
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"tagline": "Where conversation and cultura meet",
"info": "What kind of no sabo word is Hyphenación? For us, it’s about living within a hyphenation. Like being a third-gen Mexican-American from the Texas border now living that Bay Area Chicano life. Like Xorje! Each week we bring together a couple of hyphenated Latinos to talk all about personal life choices: family, careers, relationships, belonging … everything is on the table. ",
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"jerrybrown": {
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"title": "The Political Mind of Jerry Brown",
"tagline": "Lessons from a lifetime in politics",
"info": "The Political Mind of Jerry Brown brings listeners the wisdom of the former Governor, Mayor, and presidential candidate. Scott Shafer interviewed Brown for more than 40 hours, covering the former governor's life and half-century in the political game – and Brown has some lessons he'd like to share. ",
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"order": 18
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"title": "Latino USA",
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"info": "Latino USA, the radio journal of news and culture, is the only national, English-language radio program produced from a Latino perspective.",
"imageSrc": "https://ww2.kqed.org/radio/wp-content/uploads/sites/50/2018/04/latinoUsa.jpg",
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},
"marketplace": {
"id": "marketplace",
"title": "Marketplace",
"info": "Our flagship program, helmed by Kai Ryssdal, examines what the day in money delivered, through stories, conversations, newsworthy numbers and more. Updated Monday through Friday at about 3:30 p.m. PT.",
"airtime": "MON-FRI 4pm-4:30pm, MON-WED 6:30pm-7pm",
"imageSrc": "https://cdn.kqed.org/wp-content/uploads/2024/04/Marketplace-Podcast-Tile-360x360-1.jpg",
"officialWebsiteLink": "https://www.marketplace.org/",
"meta": {
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"source": "American Public Media"
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"masters-of-scale": {
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"title": "Masters of Scale",
"info": "Masters of Scale is an original podcast in which LinkedIn co-founder and Greylock Partner Reid Hoffman sets out to describe and prove theories that explain how great entrepreneurs take their companies from zero to a gazillion in ingenious fashion.",
"airtime": "Every other Wednesday June 12 through October 16 at 8pm (repeats Thursdays at 2am)",
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"source": "WaitWhat"
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"rss": "https://rss.art19.com/masters-of-scale"
}
},
"mindshift": {
"id": "mindshift",
"title": "MindShift",
"tagline": "A podcast about the future of learning and how we raise our kids",
"info": "The MindShift podcast explores the innovations in education that are shaping how kids learn. Hosts Ki Sung and Katrina Schwartz introduce listeners to educators, researchers, parents and students who are developing effective ways to improve how kids learn. We cover topics like how fed-up administrators are developing surprising tactics to deal with classroom disruptions; how listening to podcasts are helping kids develop reading skills; the consequences of overparenting; and why interdisciplinary learning can engage students on all ends of the traditional achievement spectrum. This podcast is part of the MindShift education site, a division of KQED News. KQED is an NPR/PBS member station based in San Francisco. You can also visit the MindShift website for episodes and supplemental blog posts or tweet us \u003ca href=\"https://twitter.com/MindShiftKQED\">@MindShiftKQED\u003c/a> or visit us at \u003ca href=\"/mindshift\">MindShift.KQED.org\u003c/a>",
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"imageAlt": "KQED MindShift: How We Will Learn",
"officialWebsiteLink": "/mindshift/",
"meta": {
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"source": "kqed",
"order": 12
},
"link": "/podcasts/mindshift",
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"google": "https://podcasts.google.com/feed/aHR0cHM6Ly9mZWVkcy5tZWdhcGhvbmUuZm0vS1FJTkM1NzY0NjAwNDI5",
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}
},
"morning-edition": {
"id": "morning-edition",
"title": "Morning Edition",
"info": "\u003cem>Morning Edition\u003c/em> takes listeners around the country and the world with multi-faceted stories and commentaries every weekday. Hosts Steve Inskeep, David Greene and Rachel Martin bring you the latest breaking news and features to prepare you for the day.",
"airtime": "MON-FRI 3am-9am",
"imageSrc": "https://cdn.kqed.org/wp-content/uploads/2024/04/Morning-Edition-Podcast-Tile-360x360-1.jpg",
"officialWebsiteLink": "https://www.npr.org/programs/morning-edition/",
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"onourwatch": {
"id": "onourwatch",
"title": "On Our Watch",
"tagline": "Deeply-reported investigative journalism",
"info": "For decades, the process for how police police themselves has been inconsistent – if not opaque. In some states, like California, these proceedings were completely hidden. After a new police transparency law unsealed scores of internal affairs files, our reporters set out to examine these cases and the shadow world of police discipline. On Our Watch brings listeners into the rooms where officers are questioned and witnesses are interrogated to find out who this system is really protecting. Is it the officers, or the public they've sworn to serve?",
"imageSrc": "https://cdn.kqed.org/wp-content/uploads/2024/04/On-Our-Watch-Podcast-Tile-703x703-1.jpg",
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