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"title": "Samurai Wasps Say 'Smell Ya Later, Stink Bugs'",
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"content": "\u003cp>[dl_subscribe]\u003c/p>\n\u003cfigure id=\"attachment_1937646\" class=\"wp-caption alignleft\" style=\"max-width: 640px\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-large wp-image-1937646\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/02/OSU-Stink-Bug-Colonies-e1549314495795-1020x1360.jpg\" alt=\"Colonies of brown marmorated stink bugs reared at Oregon State University.\" width=\"640\" height=\"853\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2019/02/OSU-Stink-Bug-Colonies-e1549314495795-1020x1360.jpg 1020w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/02/OSU-Stink-Bug-Colonies-e1549314495795-160x213.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/02/OSU-Stink-Bug-Colonies-e1549314495795-800x1067.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/02/OSU-Stink-Bug-Colonies-e1549314495795-768x1024.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/02/OSU-Stink-Bug-Colonies-e1549314495795-900x1200.jpg 900w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/02/OSU-Stink-Bug-Colonies-e1549314495795-1920x2560.jpg 1920w\" sizes=\"auto, (max-width: 640px) 100vw, 640px\">\u003cfigcaption class=\"wp-caption-text\">Colonies of brown marmorated stink bugs reared at Oregon State University. \u003ccite>(Jenny Oh/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>It looks rather harmless at first glance. With a speckled exterior and a shieldlike shape, the brown marmorated stink bug doesn’t appear to be different from any other six-legged insect that might pop up in your garden. But this particular bug, which arrived in the U.S. from Asia in the mid-1990s and smells like old socks when it is squashed, is a real nuisance. Not only can it \u003ca href=\"https://www.newyorker.com/magazine/2018/03/12/when-twenty-six-thousand-stinkbugs-invade-your-home\">invade homes by the thousands\u003c/a> in the wintertime, it’s one formidable agricultural pest, eating millions of dollars of peaches, apples and other crops since 2010.\u003c/p>\n\u003cp>Scientists are now investigating a new tactic in the war on the stink bugs: the possibility of relying on one of the bug’s natural enemies, the samurai wasp.\u003c/p>\n\u003cfigure id=\"attachment_1937648\" class=\"wp-caption alignright\" style=\"max-width: 640px\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-large wp-image-1937648\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/02/Samurai-wasp-and-stink-bug-eggs-1020x765.jpg\" alt=\"A samurai wasp sits on a mass of stink bug eggs at Oregon State University.\" width=\"640\" height=\"480\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2019/02/Samurai-wasp-and-stink-bug-eggs-1020x765.jpg 1020w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/02/Samurai-wasp-and-stink-bug-eggs-160x120.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/02/Samurai-wasp-and-stink-bug-eggs-800x600.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/02/Samurai-wasp-and-stink-bug-eggs-768x576.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/02/Samurai-wasp-and-stink-bug-eggs-1200x900.jpg 1200w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/02/Samurai-wasp-and-stink-bug-eggs-1920x1440.jpg 1920w\" sizes=\"auto, (max-width: 640px) 100vw, 640px\">\u003cfigcaption class=\"wp-caption-text\">A samurai wasp sits on a mass of stink bug eggs at Oregon State University. \u003ccite>(Jenny Oh/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Also native to Asia, this parasitic wasp keeps the stink bug population in check there. How? By colonizing its rivals’ eggs.\u003c/p>\n\u003cp>A female wasp will lay its own egg inside of a stink bug’s egg. About two weeks later, an adult samurai wasp will emerge. Between 60 to 90 percent of stink bug eggs in Asia are destroyed this way.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>But introducing a non-native biological control can pose risks, as previous scientists have discovered when trying to manage invasive species. In the late 1800s, mongooses released in Hawaii to manage rat populations wiped out native birds and turtles instead. In 1935, \u003ca href=\"https://australianmuseum.net.au/learn/animals/frogs/cane-toad/\">cane toads deployed in Australia\u003c/a> not only failed to reduce the beetles that were infesting sugar cane plantations, but they also created a host of other problems — including inadvertently killing animals that fed on the poisonous amphibians.\u003c/p>\n\u003cp>Scientists who were considering bringing samurai wasps into the U.S. discovered \u003ca href=\"https://www.sciencemag.org/news/2018/08/scientists-spent-years-plan-import-wasp-kill-stinkbugs-then-it-showed-its-own\">they’d already hitchhiked here on their own\u003c/a>. The wasps have settled down in Oregon, where stink bugs have been feasting on hazelnuts and berries. David Lowenstein, a postdoctoral research associate at \u003ca href=\"https://agsci.oregonstate.edu/bmsb/brown-marmorated-stink-bug\" target=\"_blank\" rel=\"noopener\">Oregon State University\u003c/a>, has been rearing both stink bug and samurai wasp colonies.\u003c/p>\n\u003cfigure id=\"attachment_1937649\" class=\"wp-caption alignleft\" style=\"max-width: 640px\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-large wp-image-1937649\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/02/David-Lowenstein-at-OSU-e1549314469808-1020x1360.jpg\" alt=\"David Lowenstein at Oregon State University.\" width=\"640\" height=\"853\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2019/02/David-Lowenstein-at-OSU-e1549314469808-1020x1360.jpg 1020w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/02/David-Lowenstein-at-OSU-e1549314469808-160x213.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/02/David-Lowenstein-at-OSU-e1549314469808-800x1067.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/02/David-Lowenstein-at-OSU-e1549314469808-768x1024.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/02/David-Lowenstein-at-OSU-e1549314469808-900x1200.jpg 900w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/02/David-Lowenstein-at-OSU-e1549314469808-1920x2560.jpg 1920w\" sizes=\"auto, (max-width: 640px) 100vw, 640px\">\u003cfigcaption class=\"wp-caption-text\">David Lowenstein at Oregon State University. \u003ccite>(Jenny Oh/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>“We hope that the wasp, which controls the stink bug well in its native range of China and South Korea, will do the same in the USA,” he said.\u003c/p>\n\u003cp>Lowenstein said he has spent the last two years distributing the wasp around parts of Oregon where stink bugs are a threat to agriculture.\u003c/p>\n\u003cp>“I’ve had some success getting the wasps to survive the winter and be detected a year later,” he said.\u003c/p>\n\u003cp>What’s the biggest challenge with using the samurai wasps on a wider scale? Rearing and releasing thousands of them at multiple locations.\u003c/p>\n\u003cp>“To get a high number of samurai wasps, I need to also obtain enough stink bug eggs,” Lowenstein said.\u003c/p>\n\u003cp>He and his team will release more wasps this summer, and he’s hoping they’ll find a partner to help them rear and release much larger numbers within two to three years.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>It could take much longer before the samurai wasp can be used for pest control around the country, as it has been found in only 12 states and Washington, D.C. But research is moving forward in other states, including New Jersey and California. While commercial crops grown in California haven’t felt the effects yet of the stink bug, \u003ca href=\"https://cisr.ucr.edu/brown_marmorated_stinkbug.html\" target=\"_blank\" rel=\"noopener\">researchers at UC Riverside\u003c/a> are still studying them — and samurai wasps — in the event that they pose a serious risk to the state’s multibillion-dollar agricultural industry. While there’s no sign of the wasps in California yet, chances are they’ll be following their foe from other states, too.\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>But introducing a non-native biological control can pose risks, as previous scientists have discovered when trying to manage invasive species. In the late 1800s, mongooses released in Hawaii to manage rat populations wiped out native birds and turtles instead. In 1935, \u003ca href=\"https://australianmuseum.net.au/learn/animals/frogs/cane-toad/\">cane toads deployed in Australia\u003c/a> not only failed to reduce the beetles that were infesting sugar cane plantations, but they also created a host of other problems — including inadvertently killing animals that fed on the poisonous amphibians.\u003c/p>\n\u003cp>Scientists who were considering bringing samurai wasps into the U.S. discovered \u003ca href=\"https://www.sciencemag.org/news/2018/08/scientists-spent-years-plan-import-wasp-kill-stinkbugs-then-it-showed-its-own\">they’d already hitchhiked here on their own\u003c/a>. The wasps have settled down in Oregon, where stink bugs have been feasting on hazelnuts and berries. David Lowenstein, a postdoctoral research associate at \u003ca href=\"https://agsci.oregonstate.edu/bmsb/brown-marmorated-stink-bug\" target=\"_blank\" rel=\"noopener\">Oregon State University\u003c/a>, has been rearing both stink bug and samurai wasp colonies.\u003c/p>\n\u003cfigure id=\"attachment_1937649\" class=\"wp-caption alignleft\" style=\"max-width: 640px\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-large wp-image-1937649\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/02/David-Lowenstein-at-OSU-e1549314469808-1020x1360.jpg\" alt=\"David Lowenstein at Oregon State University.\" width=\"640\" height=\"853\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2019/02/David-Lowenstein-at-OSU-e1549314469808-1020x1360.jpg 1020w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/02/David-Lowenstein-at-OSU-e1549314469808-160x213.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/02/David-Lowenstein-at-OSU-e1549314469808-800x1067.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/02/David-Lowenstein-at-OSU-e1549314469808-768x1024.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/02/David-Lowenstein-at-OSU-e1549314469808-900x1200.jpg 900w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/02/David-Lowenstein-at-OSU-e1549314469808-1920x2560.jpg 1920w\" sizes=\"auto, (max-width: 640px) 100vw, 640px\">\u003cfigcaption class=\"wp-caption-text\">David Lowenstein at Oregon State University. \u003ccite>(Jenny Oh/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>“We hope that the wasp, which controls the stink bug well in its native range of China and South Korea, will do the same in the USA,” he said.\u003c/p>\n\u003cp>Lowenstein said he has spent the last two years distributing the wasp around parts of Oregon where stink bugs are a threat to agriculture.\u003c/p>\n\u003cp>“I’ve had some success getting the wasps to survive the winter and be detected a year later,” he said.\u003c/p>\n\u003cp>What’s the biggest challenge with using the samurai wasps on a wider scale? Rearing and releasing thousands of them at multiple locations.\u003c/p>\n\u003cp>“To get a high number of samurai wasps, I need to also obtain enough stink bug eggs,” Lowenstein said.\u003c/p>\n\u003cp>He and his team will release more wasps this summer, and he’s hoping they’ll find a partner to help them rear and release much larger numbers within two to three years.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>It could take much longer before the samurai wasp can be used for pest control around the country, as it has been found in only 12 states and Washington, D.C. But research is moving forward in other states, including New Jersey and California. While commercial crops grown in California haven’t felt the effects yet of the stink bug, \u003ca href=\"https://cisr.ucr.edu/brown_marmorated_stinkbug.html\" target=\"_blank\" rel=\"noopener\">researchers at UC Riverside\u003c/a> are still studying them — and samurai wasps — in the event that they pose a serious risk to the state’s multibillion-dollar agricultural industry. While there’s no sign of the wasps in California yet, chances are they’ll be following their foe from other states, too.\u003c/p>\n\n\u003c/div>\u003c/p>",
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"content": "\u003cp>In the early morning hours of Sunday, March 10, clocks will spring forward, as the popular reminder goes, from 1:59 a.m. to 3:00 a.m. There will be no 2 a.m. It will be as if it has evaporated. This means that, if your day runs on a schedule, you’ll lose an hour of sleep.\u003c/p>\n\u003cp>Daylight saving time is here. \u003c/p>\n\u003cp>While many people enjoy the extra light in the evenings that comes with “springing forward,” the switch comes with some pretty clear side effects.\u003c/p>\n\u003cp>A number of medical studies indicate the collective loss of sleep leads to increased \u003ca href=\"http://www.cbsnews.com/news/study-ties-daylight-saving-time-change-to-rise-in-heart-attacks/\" target=\"_blank\" rel=\"noopener\">heart attacks\u003c/a> and \u003ca href=\"https://www.aan.com/PressRoom/Home/PressRelease/1440\" target=\"_blank\" rel=\"noopener\">stroke\u003c/a>. And one study estimated as many as \u003ca href=\"https://www.aeaweb.org/conference/2015/retrieve.php?pdfid=544\" target=\"_blank\" rel=\"noopener\">17 percent more accidents nationwide\u003c/a>.\u003c/p>\n\u003cp>How can one little lost hour cause so much havoc? The answer lies in our cells.\u003c/p>\n\u003caside class=\"alignright\">\n\u003cfigure>\u003ca href=\"https://www.kqed.org/science/1933282/spring-forward-fall-back-or-neither-why-changing-our-clocks-might-fade-into-history\">\u003cimg decoding=\"async\" src=\"https://ww2.kqed.org/wp-content/uploads/sites/35/2018/10/14065v.jpg\" alt=\"An image of Benjamin Franklin.\">\u003c/a>\u003c/figure>\n\u003cp>\u003cem>\u003ca href=\"https://www.kqed.org/science/1933282/spring-forward-fall-back-or-neither-why-changing-our-clocks-might-fade-into-history\" target=\"_blank\" rel=\"noopener\">Read about the pros and cons of Daylight Saving Time and it’s historical roots in the writings of Benjamin Franklin.\u003cbr>\n\u003c/a>\u003c/em>\u003c/p>\n\u003c/aside>\n\u003cp>Benjamin Smarr is a UC Berkeley researcher who studies the watime dictates changes in our brains and our behavior.\u003c/p>\n\u003cp>“We have circadian clocks in every cell in our body. Every organ in our body is made up of cells trying to keep time,” Smarr said.\u003c/p>\n\u003cp>When our timing is out of whack — from missed sleep, an altered schedule, or jet lag\u003cstrong> — \u003c/strong>it misaligns biologically coordinated processes like attention and perception, digestion, emotions and even blood pressure.\u003c/p>\n\u003cp>One system falling apart looks scary, says Smarr. But when multiple and contrary functions are competing with each other — “it’s time to sleep,” “no it’s time to digest,” “no it’s time to be active,” — it’s the recipe for a physiological nightmare.\u003c/p>\n\u003cp>To add insult to sometimes literal injury, there are scant, if any, energy savings now associated with daylight saving time. (Though there did used to be when DST was first popularized during World War I.)\u003c/p>\n\u003cp>For these and other reasons, many states, including California, Oregon and Washington, are considering doing away with twice-yearly time changes. Already Puerto Rico, Arizona and Hawaii keep their clocks steady.\u003c/p>\n\u003cp>Last November \u003ca href=\"https://www.kqed.org/science/1933945/proposition-7-california-favors-year-round-daylight-time\" target=\"_blank\" rel=\"noopener\">California voters chose to ask the Legislature\u003c/a> to consider enacting year-round DST, subject to federal approval. A bill, introduced by South and East Bay Democrat Kansen Chu, is now in committee in the assembly awaiting a hearing, possibly as soon as this month.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>\u003c/p>\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>In the early morning hours of Sunday, March 10, clocks will spring forward, as the popular reminder goes, from 1:59 a.m. to 3:00 a.m. There will be no 2 a.m. It will be as if it has evaporated. This means that, if your day runs on a schedule, you’ll lose an hour of sleep.\u003c/p>\n\u003cp>Daylight saving time is here. \u003c/p>\n\u003cp>While many people enjoy the extra light in the evenings that comes with “springing forward,” the switch comes with some pretty clear side effects.\u003c/p>\n\u003cp>A number of medical studies indicate the collective loss of sleep leads to increased \u003ca href=\"http://www.cbsnews.com/news/study-ties-daylight-saving-time-change-to-rise-in-heart-attacks/\" target=\"_blank\" rel=\"noopener\">heart attacks\u003c/a> and \u003ca href=\"https://www.aan.com/PressRoom/Home/PressRelease/1440\" target=\"_blank\" rel=\"noopener\">stroke\u003c/a>. And one study estimated as many as \u003ca href=\"https://www.aeaweb.org/conference/2015/retrieve.php?pdfid=544\" target=\"_blank\" rel=\"noopener\">17 percent more accidents nationwide\u003c/a>.\u003c/p>\n\u003cp>How can one little lost hour cause so much havoc? The answer lies in our cells.\u003c/p>\n\u003caside class=\"alignright\">\n\u003cfigure>\u003ca href=\"https://www.kqed.org/science/1933282/spring-forward-fall-back-or-neither-why-changing-our-clocks-might-fade-into-history\">\u003cimg decoding=\"async\" src=\"https://ww2.kqed.org/wp-content/uploads/sites/35/2018/10/14065v.jpg\" alt=\"An image of Benjamin Franklin.\">\u003c/a>\u003c/figure>\n\u003cp>\u003cem>\u003ca href=\"https://www.kqed.org/science/1933282/spring-forward-fall-back-or-neither-why-changing-our-clocks-might-fade-into-history\" target=\"_blank\" rel=\"noopener\">Read about the pros and cons of Daylight Saving Time and it’s historical roots in the writings of Benjamin Franklin.\u003cbr>\n\u003c/a>\u003c/em>\u003c/p>\n\u003c/aside>\n\u003cp>Benjamin Smarr is a UC Berkeley researcher who studies the watime dictates changes in our brains and our behavior.\u003c/p>\n\u003cp>“We have circadian clocks in every cell in our body. Every organ in our body is made up of cells trying to keep time,” Smarr said.\u003c/p>\n\u003cp>When our timing is out of whack — from missed sleep, an altered schedule, or jet lag\u003cstrong> — \u003c/strong>it misaligns biologically coordinated processes like attention and perception, digestion, emotions and even blood pressure.\u003c/p>\n\u003cp>One system falling apart looks scary, says Smarr. But when multiple and contrary functions are competing with each other — “it’s time to sleep,” “no it’s time to digest,” “no it’s time to be active,” — it’s the recipe for a physiological nightmare.\u003c/p>\n\u003cp>To add insult to sometimes literal injury, there are scant, if any, energy savings now associated with daylight saving time. (Though there did used to be when DST was first popularized during World War I.)\u003c/p>\n\u003cp>For these and other reasons, many states, including California, Oregon and Washington, are considering doing away with twice-yearly time changes. Already Puerto Rico, Arizona and Hawaii keep their clocks steady.\u003c/p>\n\u003cp>Last November \u003ca href=\"https://www.kqed.org/science/1933945/proposition-7-california-favors-year-round-daylight-time\" target=\"_blank\" rel=\"noopener\">California voters chose to ask the Legislature\u003c/a> to consider enacting year-round DST, subject to federal approval. A bill, introduced by South and East Bay Democrat Kansen Chu, is now in committee in the assembly awaiting a hearing, possibly as soon as this month.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"title": "Grandmothers May Be Key to Understanding Human Longevity",
"headTitle": "Grandmothers May Be Key to Understanding Human Longevity | KQED",
"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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"content": "\u003cp>[dl_subscribe]On a sunny day near Martinez, California, a friendly-looking German shepherd named Zinka rushes down the crisscrossing trails of Briones Regional Park wearing a vest covered in sensors, batteries and wires. She’s followed by her trainer, Shay Cook, who keeps up at the end of a long leash.\u003c/p>\n\u003cp>The duo trains to track people who have passed through an area — hours or even days later. Their search and rescue training allows them to find a single person across backcountry woods, neighborhoods or even a bustling university campus packed full of students. They also search for missing people lost in natural disasters like fires and earthquakes.\u003c/p>\n\u003cp>But today, they’re in pursuit of something different: clues in a scientific experiment about how odors disperse over time, and how the brain deciphers information about the invisible world of smells that surround us.\u003c/p>\n\u003cp>Every dog owner knows that dogs are able to pick up scents that don’t seem to catch the attention of people. One study estimated that dogs can pick up odors up to 100,000 times better than humans can.\u003c/p>\n\u003cp>“It’s a treat to go out and watch a search and rescue dog work a trail and see them find the person at the end,” said Judy Jinn, a graduate student in the \u003ca href=\"http://jacobs.berkeley.edu/\">lab of Dr. Lucia Jacobs\u003c/a> at UC Berkeley. “If you’ve never seen it before, it’s pretty amazing.”\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>Jinn is wrapping up a study that seeks to shed some light on the surprisingly complex question of how dogs can track a target using tiny amounts of odor that people don’t even notice.\u003c/p>\n\u003cp>“It actually hasn’t been studied very well in the past,” she said. “But it’s picking up now.”\u003c/p>\n\u003cfigure id=\"attachment_1938259\" class=\"wp-caption aligncenter\" style=\"max-width: 500px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/02/DL604_DogNoses_TrackingInGrass.gif\">\u003cimg loading=\"lazy\" decoding=\"async\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/02/DL604_DogNoses_TrackingInGrass.gif\" alt=\"\" width=\"500\" height=\"281\" class=\"size-full wp-image-1938259\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Search and rescue dog Zinka and her trainer Shay Cook are able to track target hikers off trail \u003ccite>(Josh Cassidy/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>The experiment is part of a collaboration between six universities across the country funded by the National Science Foundation’s Brain Initiative. It’s called the \u003ca href=\"https://odornavigation.org/\">Odor Navigation Project\u003c/a>. The collaborators come from disparate fields of study, including animal behavior, genetics, physiology and fluid mechanics, to study how animals use smell to understand their surroundings.\u003c/p>\n\u003cp>The national project has a far-reaching goal: to help develop more effective devices — perhaps even a new generation of robots that seek specific odors — to detect explosives, drugs and other dangerous chemicals in airports, subways, factories and other locations.\u003c/p>\n\u003cp>For Jinn’s contribution to the project, she set up an experiment in which a “target hiker” would walk a preset route along crisscrossing trails in the park. Then she used GPS and other sensors attached to the search dog’s harness to record how closely Zinka followed the hiker’s path.\u003c/p>\n\u003cp>In the experiment, the target hiker would get a one-hour head start — although Zinka can track people even days later. Even rain doesn’t stop her keen sense of smell.\u003c/p>\n\u003cp>By following the search team with a portable weather station, Jinn found that the dog was able to follow the target hiker’s trail more closely under humid conditions. She said she thinks the humidity might help trap scent particles on the ground and on vegetation instead of letting them be blown away by the wind. Jinn hopes to have her results published this year.\u003c/p>\n\u003cp>Researchers haven’t fully come to an agreement on exactly what it is that dogs are smelling. Jinn thinks that dogs detect traces of vapors emitted from tiny amounts of dead skin cells, hair and sweat that people shed as they walk.\u003c/p>\n\u003cp>\u003ca href=\"https://www.colorado.edu/lab/ecological-fluids/\">John Crimaldi\u003c/a>, who studies fluid mechanics at the University of Colorado Boulder, is looking at the structure of the odors themselves. He’s the lead principal investigator of the Odor Navigation Project. Crimaldi and his lab use special techniques to study the physics of how odors move around in air and water.\u003c/p>\n\u003cp>It turns out there are everyday examples of the way invisible odors disperse all around us.\u003c/p>\n\u003cp>“When you see a plume of smoke coming out of a smokestack or what milk looks like when you pour it into your coffee, it has that very complex structure to it,” Crimaldi said. “They’re actually all using the same physics.”\u003c/p>\n\u003cp>One of Crimaldi’s studies involves using lasers to measure how a fluorescent dye spreads out in a large tank of water. Researchers use the data of how the dye dissipates unevenly over time to create computer models that replicate the motion of the chemicals swirling around.\u003c/p>\n\u003cp>Then the researchers run different computer programs that inspect the model for the source of the plume. Crimaldi wants to know which algorithms do a better job of locating the source of the odor within the model.\u003c/p>\n\u003cp>“Ultimately, we want to build a mechanistic model so that we can actually understand how the brain functions when searching for an odor source,” he said. “We want to find the optimal strategies that you might use to program a robot to do similar tasks like search and rescue.”\u003c/p>\n\u003cp>While Crimaldi looks at the structure of smells, other labs participating in the Odor Navigation Project are focused on the tools animals use to detect odors by “reverse engineering a dog’s nose.”\u003c/p>\n\u003cfigure id=\"attachment_1938282\" class=\"wp-caption aligncenter\" style=\"max-width: 500px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/02/DL604_DogNoses_OlfactoryRecessProfileCompositeLabeled-1.gif\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-full wp-image-1938282\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/02/DL604_DogNoses_OlfactoryRecessProfileCompositeLabeled-1.gif\" alt=\"\" width=\"500\" height=\"281\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Profile shot of Zinka, a black German shepherd search dog, showing the location of the nasal passageway with the olfactory recess highlighted in yellow. \u003ccite>(Josh Cassidy/KQED and Brent Craven/Penn State University)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>While working at Penn State University, Brent Craven and his colleagues looked at the anatomy of a dog’s nose, and how air moves through it.\u003c/p>\n\u003cp>Craven and his colleagues use scanning technologies like MRI to peer inside the skulls of different mammals. They’ve found that many of the animals that are considered to have a strong sense of smell, like dogs, tend to have a similar structure in the back of their noses.\u003c/p>\n\u003cp>“It’s called an olfactory recess,” Craven said. “It’s in a dead-end region like a cul-de-sac at the back of the nose. That’s where the sensors are located.”\u003c/p>\n\u003cfigure id=\"attachment_1938284\" class=\"wp-caption aligncenter\" style=\"max-width: 500px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/02/DL604_DogNoses_OlfactoryRecessMRIScan.gif\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-full wp-image-1938284\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/02/DL604_DogNoses_OlfactoryRecessMRIScan.gif\" alt=\"\" width=\"500\" height=\"281\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">MRI scan of the inside of a Labrador’s skull showing the curved turbinates. \u003ccite>((Brent Craven/Penn State University)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>It’s full of delicate bones, known as turbinates, that are covered in mucus membranes. The bones twist and coil like a maze inside the dog’s skull. The turbinates are covered with sensory cells called olfactory neurons that feed information to the brain.\u003c/p>\n\u003cp>Dogs have about 600,00 olfactory neurons. That’s 15 times what humans have.\u003c/p>\n\u003cp>Humans have olfactory neurons in a little patch at the top of the inside of their noses. Since there’s no special structure to house them, the air that people smell mixes with the rest of the air we breathe. Since all of our sensors are in the same area, they can get bombarded by smells, making it harder to distinguish individual odors.\u003c/p>\n\u003cp>But according to Craven, dogs aren’t unique when it comes to their keen sense of smell.\u003c/p>\n\u003cp>Based on the structures the scientists found in the MRI scans, many animals have a sense of smell comparable to dogs.\u003c/p>\n\u003cp>“They all have this similar olfactory recess,” Craven said. “Humans, and some other primates basically, are the ones that aren’t as good.”\u003c/p>\n\u003cp>The Penn State University researchers used data from the scans to create a computer model that mimics the anatomy of the dog’s nose, inside and out.\u003c/p>\n\u003cp>They ran tests on the computer model to see how air moved through the delicate structures to find clues that could lead to new designs for trace chemical detectors.\u003c/p>\n\u003cp>One advantage that dogs have over people is the shape of their nostrils. It has to do with those slits running along the sides of their nostrils.\u003c/p>\n\u003cp>\u003ca href=\"https://www.nist.gov/people/matthew-e-staymates\">Matthew Staymates\u003c/a> is a mechanical engineer at the National Institute of Standards and Technology, a federal government lab in Gaithersburg, Maryland. He studies ways to improve detectors for explosives, drugs and toxic industrial chemicals. And to do that, Staymates is interested in how the shape of dog nostrils helps them detect smells so accurately.\u003c/p>\n\u003cp>Staymates, whose work is funded separately from the Odor Navigation Project, took the computer model of a dog’s nose developed at Penn State and printed it out using a 3-D printer to create an anatomically correct artificial dog nose, complete with the turbinates and olfactory recess.\u003c/p>\n\u003cp>He fit the model nose with an air hose that mimics a dog’s natural sniffing speed. Dogs sniff in and out about five times per second.\u003c/p>\n\u003cp>“It sniffs like a real dog,” Staymates said.\u003c/p>\n\u003cfigure id=\"attachment_1938287\" class=\"wp-caption aligncenter\" style=\"max-width: 500px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/02/DL604_DogNoses_ArtificialNose_StaymatesNIST.gif\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"wp-image-1938287 size-full\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/02/DL604_DogNoses_ArtificialNose_StaymatesNIST.gif\" alt=\"\" width=\"500\" height=\"280\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">An anatomically correct 3-D printed artificial dog nose made by Matthew Staymates at the National Institute of Standards and Technology. Made using data from MRI scans of a Labrador’s skull, the shape of dog nostrils creates a low-pressure zone sucking in air from the front and exhaling the air to the rear. \u003ccite>(Matthew Staymates/National Institute of Standards and Technology)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>By viewing the nose using a specialized filming technique called Schlieren imaging, Staymates was able to see how the shape of dog nostrils allows them to inhale from the front and then shunt the exhaled air out and back. That creates a momentary low-pressure area in front of the dog’s nose.\u003c/p>\n\u003cp>Even though the artificial nose is inhaling and exhaling the same volume, air rushes in from the front to fill that area of low pressure. That allows dogs to get a fresh sample from the area in front of them with each sniff.\u003c/p>\n\u003cfigure id=\"attachment_1938290\" class=\"wp-caption aligncenter\" style=\"max-width: 500px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/02/DL604_DogNoses_NostrilVentGraphics.gif\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"wp-image-1938290 size-full\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/02/DL604_DogNoses_NostrilVentGraphics.gif\" alt=\"\" width=\"500\" height=\"281\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">The slits on the side of a dog’s nostrils expand and contract to sniff in fresh air from the front and exhale air back and toward the rear, as shown with graphics representing odor. \u003ccite>(Josh Cassidy/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>By mimicking the shape of the nostrils, Staymates proposes that new detectors could not only sample the area directly adjacent to the devices, but could also pull in air from farther away, allowing them to extend their reach.\u003c/p>\n\u003cp>“Most of the current generation of detectors for drugs, or chemical and biological threats, basically just suck air through a hole and analyze it,” Staymates said. “But dogs have an active sampling system that interacts with its environment in a really unique way, a very sophisticated way.”\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp>Check out more in this \u003ca href=\"https://www.pbs.org/newshour/science/inside-nose-rescue-dog\">PBS NewsHour Video\u003c/a>\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>On a sunny day near Martinez, California, a friendly-looking German shepherd named Zinka rushes down the crisscrossing trails of Briones Regional Park wearing a vest covered in sensors, batteries and wires. She’s followed by her trainer, Shay Cook, who keeps up at the end of a long leash.\u003c/p>\n\u003cp>The duo trains to track people who have passed through an area — hours or even days later. Their search and rescue training allows them to find a single person across backcountry woods, neighborhoods or even a bustling university campus packed full of students. They also search for missing people lost in natural disasters like fires and earthquakes.\u003c/p>\n\u003cp>But today, they’re in pursuit of something different: clues in a scientific experiment about how odors disperse over time, and how the brain deciphers information about the invisible world of smells that surround us.\u003c/p>\n\u003cp>Every dog owner knows that dogs are able to pick up scents that don’t seem to catch the attention of people. One study estimated that dogs can pick up odors up to 100,000 times better than humans can.\u003c/p>\n\u003cp>“It’s a treat to go out and watch a search and rescue dog work a trail and see them find the person at the end,” said Judy Jinn, a graduate student in the \u003ca href=\"http://jacobs.berkeley.edu/\">lab of Dr. Lucia Jacobs\u003c/a> at UC Berkeley. “If you’ve never seen it before, it’s pretty amazing.”\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>Jinn is wrapping up a study that seeks to shed some light on the surprisingly complex question of how dogs can track a target using tiny amounts of odor that people don’t even notice.\u003c/p>\n\u003cp>“It actually hasn’t been studied very well in the past,” she said. “But it’s picking up now.”\u003c/p>\n\u003cfigure id=\"attachment_1938259\" class=\"wp-caption aligncenter\" style=\"max-width: 500px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/02/DL604_DogNoses_TrackingInGrass.gif\">\u003cimg loading=\"lazy\" decoding=\"async\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/02/DL604_DogNoses_TrackingInGrass.gif\" alt=\"\" width=\"500\" height=\"281\" class=\"size-full wp-image-1938259\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Search and rescue dog Zinka and her trainer Shay Cook are able to track target hikers off trail \u003ccite>(Josh Cassidy/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>The experiment is part of a collaboration between six universities across the country funded by the National Science Foundation’s Brain Initiative. It’s called the \u003ca href=\"https://odornavigation.org/\">Odor Navigation Project\u003c/a>. The collaborators come from disparate fields of study, including animal behavior, genetics, physiology and fluid mechanics, to study how animals use smell to understand their surroundings.\u003c/p>\n\u003cp>The national project has a far-reaching goal: to help develop more effective devices — perhaps even a new generation of robots that seek specific odors — to detect explosives, drugs and other dangerous chemicals in airports, subways, factories and other locations.\u003c/p>\n\u003cp>For Jinn’s contribution to the project, she set up an experiment in which a “target hiker” would walk a preset route along crisscrossing trails in the park. Then she used GPS and other sensors attached to the search dog’s harness to record how closely Zinka followed the hiker’s path.\u003c/p>\n\u003cp>In the experiment, the target hiker would get a one-hour head start — although Zinka can track people even days later. Even rain doesn’t stop her keen sense of smell.\u003c/p>\n\u003cp>By following the search team with a portable weather station, Jinn found that the dog was able to follow the target hiker’s trail more closely under humid conditions. She said she thinks the humidity might help trap scent particles on the ground and on vegetation instead of letting them be blown away by the wind. Jinn hopes to have her results published this year.\u003c/p>\n\u003cp>Researchers haven’t fully come to an agreement on exactly what it is that dogs are smelling. Jinn thinks that dogs detect traces of vapors emitted from tiny amounts of dead skin cells, hair and sweat that people shed as they walk.\u003c/p>\n\u003cp>\u003ca href=\"https://www.colorado.edu/lab/ecological-fluids/\">John Crimaldi\u003c/a>, who studies fluid mechanics at the University of Colorado Boulder, is looking at the structure of the odors themselves. He’s the lead principal investigator of the Odor Navigation Project. Crimaldi and his lab use special techniques to study the physics of how odors move around in air and water.\u003c/p>\n\u003cp>It turns out there are everyday examples of the way invisible odors disperse all around us.\u003c/p>\n\u003cp>“When you see a plume of smoke coming out of a smokestack or what milk looks like when you pour it into your coffee, it has that very complex structure to it,” Crimaldi said. “They’re actually all using the same physics.”\u003c/p>\n\u003cp>One of Crimaldi’s studies involves using lasers to measure how a fluorescent dye spreads out in a large tank of water. Researchers use the data of how the dye dissipates unevenly over time to create computer models that replicate the motion of the chemicals swirling around.\u003c/p>\n\u003cp>Then the researchers run different computer programs that inspect the model for the source of the plume. Crimaldi wants to know which algorithms do a better job of locating the source of the odor within the model.\u003c/p>\n\u003cp>“Ultimately, we want to build a mechanistic model so that we can actually understand how the brain functions when searching for an odor source,” he said. “We want to find the optimal strategies that you might use to program a robot to do similar tasks like search and rescue.”\u003c/p>\n\u003cp>While Crimaldi looks at the structure of smells, other labs participating in the Odor Navigation Project are focused on the tools animals use to detect odors by “reverse engineering a dog’s nose.”\u003c/p>\n\u003cfigure id=\"attachment_1938282\" class=\"wp-caption aligncenter\" style=\"max-width: 500px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/02/DL604_DogNoses_OlfactoryRecessProfileCompositeLabeled-1.gif\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-full wp-image-1938282\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/02/DL604_DogNoses_OlfactoryRecessProfileCompositeLabeled-1.gif\" alt=\"\" width=\"500\" height=\"281\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Profile shot of Zinka, a black German shepherd search dog, showing the location of the nasal passageway with the olfactory recess highlighted in yellow. \u003ccite>(Josh Cassidy/KQED and Brent Craven/Penn State University)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>While working at Penn State University, Brent Craven and his colleagues looked at the anatomy of a dog’s nose, and how air moves through it.\u003c/p>\n\u003cp>Craven and his colleagues use scanning technologies like MRI to peer inside the skulls of different mammals. They’ve found that many of the animals that are considered to have a strong sense of smell, like dogs, tend to have a similar structure in the back of their noses.\u003c/p>\n\u003cp>“It’s called an olfactory recess,” Craven said. “It’s in a dead-end region like a cul-de-sac at the back of the nose. That’s where the sensors are located.”\u003c/p>\n\u003cfigure id=\"attachment_1938284\" class=\"wp-caption aligncenter\" style=\"max-width: 500px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/02/DL604_DogNoses_OlfactoryRecessMRIScan.gif\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-full wp-image-1938284\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/02/DL604_DogNoses_OlfactoryRecessMRIScan.gif\" alt=\"\" width=\"500\" height=\"281\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">MRI scan of the inside of a Labrador’s skull showing the curved turbinates. \u003ccite>((Brent Craven/Penn State University)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>It’s full of delicate bones, known as turbinates, that are covered in mucus membranes. The bones twist and coil like a maze inside the dog’s skull. The turbinates are covered with sensory cells called olfactory neurons that feed information to the brain.\u003c/p>\n\u003cp>Dogs have about 600,00 olfactory neurons. That’s 15 times what humans have.\u003c/p>\n\u003cp>Humans have olfactory neurons in a little patch at the top of the inside of their noses. Since there’s no special structure to house them, the air that people smell mixes with the rest of the air we breathe. Since all of our sensors are in the same area, they can get bombarded by smells, making it harder to distinguish individual odors.\u003c/p>\n\u003cp>But according to Craven, dogs aren’t unique when it comes to their keen sense of smell.\u003c/p>\n\u003cp>Based on the structures the scientists found in the MRI scans, many animals have a sense of smell comparable to dogs.\u003c/p>\n\u003cp>“They all have this similar olfactory recess,” Craven said. “Humans, and some other primates basically, are the ones that aren’t as good.”\u003c/p>\n\u003cp>The Penn State University researchers used data from the scans to create a computer model that mimics the anatomy of the dog’s nose, inside and out.\u003c/p>\n\u003cp>They ran tests on the computer model to see how air moved through the delicate structures to find clues that could lead to new designs for trace chemical detectors.\u003c/p>\n\u003cp>One advantage that dogs have over people is the shape of their nostrils. It has to do with those slits running along the sides of their nostrils.\u003c/p>\n\u003cp>\u003ca href=\"https://www.nist.gov/people/matthew-e-staymates\">Matthew Staymates\u003c/a> is a mechanical engineer at the National Institute of Standards and Technology, a federal government lab in Gaithersburg, Maryland. He studies ways to improve detectors for explosives, drugs and toxic industrial chemicals. And to do that, Staymates is interested in how the shape of dog nostrils helps them detect smells so accurately.\u003c/p>\n\u003cp>Staymates, whose work is funded separately from the Odor Navigation Project, took the computer model of a dog’s nose developed at Penn State and printed it out using a 3-D printer to create an anatomically correct artificial dog nose, complete with the turbinates and olfactory recess.\u003c/p>\n\u003cp>He fit the model nose with an air hose that mimics a dog’s natural sniffing speed. Dogs sniff in and out about five times per second.\u003c/p>\n\u003cp>“It sniffs like a real dog,” Staymates said.\u003c/p>\n\u003cfigure id=\"attachment_1938287\" class=\"wp-caption aligncenter\" style=\"max-width: 500px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/02/DL604_DogNoses_ArtificialNose_StaymatesNIST.gif\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"wp-image-1938287 size-full\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/02/DL604_DogNoses_ArtificialNose_StaymatesNIST.gif\" alt=\"\" width=\"500\" height=\"280\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">An anatomically correct 3-D printed artificial dog nose made by Matthew Staymates at the National Institute of Standards and Technology. Made using data from MRI scans of a Labrador’s skull, the shape of dog nostrils creates a low-pressure zone sucking in air from the front and exhaling the air to the rear. \u003ccite>(Matthew Staymates/National Institute of Standards and Technology)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>By viewing the nose using a specialized filming technique called Schlieren imaging, Staymates was able to see how the shape of dog nostrils allows them to inhale from the front and then shunt the exhaled air out and back. That creates a momentary low-pressure area in front of the dog’s nose.\u003c/p>\n\u003cp>Even though the artificial nose is inhaling and exhaling the same volume, air rushes in from the front to fill that area of low pressure. That allows dogs to get a fresh sample from the area in front of them with each sniff.\u003c/p>\n\u003cfigure id=\"attachment_1938290\" class=\"wp-caption aligncenter\" style=\"max-width: 500px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/02/DL604_DogNoses_NostrilVentGraphics.gif\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"wp-image-1938290 size-full\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/02/DL604_DogNoses_NostrilVentGraphics.gif\" alt=\"\" width=\"500\" height=\"281\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">The slits on the side of a dog’s nostrils expand and contract to sniff in fresh air from the front and exhale air back and toward the rear, as shown with graphics representing odor. \u003ccite>(Josh Cassidy/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>By mimicking the shape of the nostrils, Staymates proposes that new detectors could not only sample the area directly adjacent to the devices, but could also pull in air from farther away, allowing them to extend their reach.\u003c/p>\n\u003cp>“Most of the current generation of detectors for drugs, or chemical and biological threats, basically just suck air through a hole and analyze it,” Staymates said. “But dogs have an active sampling system that interacts with its environment in a really unique way, a very sophisticated way.”\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>Check out more in this \u003ca href=\"https://www.pbs.org/newshour/science/inside-nose-rescue-dog\">PBS NewsHour Video\u003c/a>\u003c/p>\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",
"headTitle": "Making Sense of the CRISPR Patent Dispute Between the University of California and Broad | KQED",
"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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"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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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>\u003cem>Brian Watt and Danielle Venton contributed to this post.\u003c/em>\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"title": "Researchers Find a Web of Factors Behind MS",
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"content": "\u003cp>As the story goes, nearly 80 years ago on the Faroe Islands — a stark North Atlantic archipelago 200 miles off the coast of Scotland — a neurologic epidemic may have washed, or rather convoyed, ashore.\u003c/p>\n\u003cp>Before 1940 the incidence of multiple sclerosis on the Faroes was near, if not actually, zero, according to the \u003ca href=\"https://www.ncbi.nlm.nih.gov/pubmed/11165464\" target=\"_blank\" rel=\"noopener\">tantalizing lore\u003c/a> I recall from medical school. Yet in the years following British occupation of the islands during World War II, the rate of MS rose dramatically, leading many researchers to assume the outbreak was caused by some unknown germ transmitted by the foreign soldiers.\u003c/p>\n\u003cp>We now know that MS is not infectious in the true sense of the word. It is not contagious in the way, say, the flu is.\u003c/p>\n\u003cp>But infection does likely play a role in MS.\u003c/p>\n\u003cp>As may be the case in \u003ca href=\"https://www.npr.org/sections/health-shots/2018/09/09/645629133/infectious-theory-of-alzheimers-disease-draws-fresh-interest\" target=\"_blank\" rel=\"noopener\">Alzheimer’s disease\u003c/a>, it’s looking more and more as though MS strikes when infectious, genetic and immune factors gang up to eventually impair the function of neurons in the brain and spinal cord. Researchers are hoping to better understand this network of influences to develop more effective ways to treat MS and perhaps prevent it in the first place.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>In the MS-free brain, electrical impulses zip down \u003ca href=\"https://en.wikipedia.org/wiki/Axon\" target=\"_blank\" rel=\"noopener\">nerve fibers called axons\u003c/a> causing the release of neurotransmitters. The wiring allows neurons to communicate with each other and generate biologic wonders like thought, sensation and movement.\u003c/p>\n\u003cp>In many regions of the brain those axons are encased in an insulating jacket of protein and fat called myelin, which increases the speed that electrical nerve impulses travel.\u003c/p>\n\u003cp>In MS, myelin breaks down and scars – it becomes “sclerotic” and degrades nerve function. A pickle for researchers has been figuring out how this process starts.\u003c/p>\n\u003cp>There is certainly a genetic component at work: The risk of developing MS is 1 in 1,000 in the general population; it rises to about 1 in 4 in identical twins in which one twin is affected.\u003c/p>\n\u003cp>Even so, genes don’t explain it all. MS occurs more frequently at higher latitudes, suggesting that vitamin D deficiency might play a role in disease risk (the vitamin’s production in the body is dependent on sun exposure). Smoking also increases risk for the disease, as does obesity.\u003c/p>\n\u003cp>And while the tale of the Faroe Islands is disputed – large scale retroactive epidemiological studies are notoriously hard to pull off – it is for the most part accepted that microbes play some role in MS given that dozens of microbes, including the Epstein-Barr virus, have been tied to MS.\u003c/p>\n\u003cp>Yet more than 30 years of research suggests that risk factors in MS ultimately converge on the crux of its pathology: a misguided immune attack on myelin. Research in animals and humans supports the idea that MS develops when a type of white blood cell called a T-cell attacks specific proteins in myelin, making the axons less able to conduct electrical impulses efficiently.\u003c/p>\n\u003cp>The immune siege appears to be a result of something called “molecular mimicry.” Normally the body’s immune system attacks foreign invaders like viruses and bacteria. If a molecule that’s part of the body happens to closely resemble a portion of an intruding microbe, then both molecules can be targeted.\u003c/p>\n\u003cp>Put another way, say a particular protein on the surface of a virus is similar in structure to a protein found in myelin. The immune system ramps up to clear the virus but also attacks the myelin. It’s a case of mistaken identity, of collateral damage.\u003c/p>\n\u003cp>\u003ca href=\"http://www.en.neurologie.usz.ch/about-us/Pages/team.aspx\" target=\"_blank\" rel=\"noopener\">Dr. Roland Martin from the University Hospital of Zurich\u003c/a> in Switzerland is among the researchers who over the years helped identify which myelin proteins and peptides – biologic building blocks made of amino acids — come under attack in MS and which cells and immune molecules do the attacking.\u003c/p>\n\u003cp>“The idea of molecular mimicry is one of the most important ones in MS,” Martin says. “We and others have shown that mimicry between myelin peptides and viral and bacterial peptides indeed exists.”\u003c/p>\n\u003cp>And a number of proteins that make up myelin have been identified as helping spark the immune activity behind MS, possibly in response to similar microbial cousins.\u003c/p>\n\u003cp>Now, a \u003ca href=\"https://www.zora.uzh.ch/id/eprint/158835/1/2018_Planas_GDP_L-Fucose_Sci_Transl._Med._in_press.pdf\" target=\"_blank\" rel=\"noopener\">paper co-authored by Martin\u003c/a>, and published in October in \u003cem>Science and Translational Medicine\u003c/em>, reports on an additional nonmyelin-related protein that also may be involved.\u003c/p>\n\u003cp>Martin and his colleagues examined protein samples from the brains of 31 people who had died from suspected or confirmed MS. T-cells from 12 people reacted to the clunkily named enzyme, guanosine diphosphate-L-fucose synthase – or GDP-L-fucose synthase. The enzyme is normally involved in processing sugars essential to cellular function and communication, including that of neurons.\u003c/p>\n\u003cp>Paper co-author \u003ca href=\"https://www.multiplesclerosis.uzh.ch/en/coretopics/psospedra.html\" target=\"_blank\" rel=\"noopener\">Mireia Sospedra\u003c/a>, also of the University Hospital of Zurich, likens the enzyme to the iceberg’s ominous tip. “Yes, [myelin proteins] make sense but we think they might be not the only ones involved,” she speculates. “We think is that other auto-antigens might be involved in initiating the disease.”\u003c/p>\n\u003cp>She believes that the attack on this newly identified auto-antigen triggers tissue damage that exposes other proteins in myelin that are subsequently attacked themselves.\u003c/p>\n\u003cp>Sospedra also makes the point that culprit antigens might be different in everyone. The structure of our molecular machinery is genetically determined. Certain variants in, say, myelin protein structure might be more prone to immune attack; also genetic variation in immune cells themselves could influence how the body responds to a particular infection.\u003c/p>\n\u003cp>Northwestern University \u003ca href=\"https://www.feinberg.northwestern.edu/faculty-profiles/az/profile.html?xid=14949\" target=\"_blank\" rel=\"noopener\">immunology professor Stephen Miller\u003c/a> – who was not involved in the new research but who has collaborated with Martin in the past — sees the findings as revealing another piece in the MS puzzle.\u003c/p>\n\u003cp>“I don’t think there’s one particular virus or bacteria or environmental factor that triggers MS in every patient. There are probably many things that can trigger an autoimmune reaction against a particular infection,” he says. “But the more antigens we identify that can contribute to the disease the better.”\u003c/p>\n\u003cp>Regardless of the particular “cause” in a given patient, Martin, Miller and a number of other researchers are hard at work trying to thwart the MS immune attack in the first place using by coaxing the body into building up a familiarity and tolerance to suspected antigens, something called immunotolerance therapy. It’s a similar concept to how certain allergies can be thwarted by exposure to small amounts of a particular allergen.\u003c/p>\n\u003cp>“Think of it as a sort of negative vaccine,” says Miller. “We want less immune activity, not more.”\u003c/p>\n\u003cp>The sizable batch of approved MS medications for the most part work by broadly suppressing the immune system. They help control symptoms but also leave patients vulnerable to side effects like common infections.\u003c/p>\n\u003cp>Antigen-specific therapy only tames the immune response to specific antigens of interest. In theory it should come with fewer risks.\u003c/p>\n\u003cp>Miller recently co-founded a startup called \u003ca href=\"https://www.courpharma.com/about/\" target=\"_blank\" rel=\"noopener\">Cour Pharmaceuticals\u003c/a> through which he and his colleagues are studying the potential for immunotolerance therapy for MS and a number of other conditions, including celiac disease and Type I diabetes. The experimental therapy they plan to test involves attaching known MS-inducing antigens to biodegradable nanoparticles which they will then inject into trial patients. But for now they’ve just completed a phase I study testing their approach in celiac disease, with a phase II trial about to begin.\u003c/p>\n\u003cp>Martin’s group is pursuing a similar approach in which they chemically combine red or white blood cells with MS antigens and infuse them back into patients to induce tolerance.\u003c/p>\n\u003cp>This research is at a very early stage, but both groups are optimistic.\u003c/p>\n\u003cp>“Several of us in academia — and also the pharmaceutical industry — are pursing the long-standing dream of many immunologists: inducing tolerance against specific target antigens in autoimmune diseases like MS,” says Martin. “I am confident that sooner or later, we will be successful.”\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp>\u003cem>Bret Stetka is a writer based in New York and an editorial director at \u003c/em>\u003ca href=\"http://www.medscape.com/public/bios/bio-bretstetka\" target=\"_blank\" rel=\"noopener\">Medscape\u003c/a>.\u003cem> A graduate of the University of Virginia School of Medicine, Stetka has had his work published by \u003c/em>Wired, Scientific American\u003cem> and The Atlantic.com. He’s also on Twitter: \u003c/em>\u003ca href=\"https://twitter.com/BretStetka\" target=\"_blank\" rel=\"noopener\">@BretStetka\u003c/a>.\u003c/p>\n\u003cdiv class=\"fullattribution\">\u003cem>Copyright 2019 \u003ca href=\"http://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>As the story goes, nearly 80 years ago on the Faroe Islands — a stark North Atlantic archipelago 200 miles off the coast of Scotland — a neurologic epidemic may have washed, or rather convoyed, ashore.\u003c/p>\n\u003cp>Before 1940 the incidence of multiple sclerosis on the Faroes was near, if not actually, zero, according to the \u003ca href=\"https://www.ncbi.nlm.nih.gov/pubmed/11165464\" target=\"_blank\" rel=\"noopener\">tantalizing lore\u003c/a> I recall from medical school. Yet in the years following British occupation of the islands during World War II, the rate of MS rose dramatically, leading many researchers to assume the outbreak was caused by some unknown germ transmitted by the foreign soldiers.\u003c/p>\n\u003cp>We now know that MS is not infectious in the true sense of the word. It is not contagious in the way, say, the flu is.\u003c/p>\n\u003cp>But infection does likely play a role in MS.\u003c/p>\n\u003cp>As may be the case in \u003ca href=\"https://www.npr.org/sections/health-shots/2018/09/09/645629133/infectious-theory-of-alzheimers-disease-draws-fresh-interest\" target=\"_blank\" rel=\"noopener\">Alzheimer’s disease\u003c/a>, it’s looking more and more as though MS strikes when infectious, genetic and immune factors gang up to eventually impair the function of neurons in the brain and spinal cord. Researchers are hoping to better understand this network of influences to develop more effective ways to treat MS and perhaps prevent it in the first place.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>In the MS-free brain, electrical impulses zip down \u003ca href=\"https://en.wikipedia.org/wiki/Axon\" target=\"_blank\" rel=\"noopener\">nerve fibers called axons\u003c/a> causing the release of neurotransmitters. The wiring allows neurons to communicate with each other and generate biologic wonders like thought, sensation and movement.\u003c/p>\n\u003cp>In many regions of the brain those axons are encased in an insulating jacket of protein and fat called myelin, which increases the speed that electrical nerve impulses travel.\u003c/p>\n\u003cp>In MS, myelin breaks down and scars – it becomes “sclerotic” and degrades nerve function. A pickle for researchers has been figuring out how this process starts.\u003c/p>\n\u003cp>There is certainly a genetic component at work: The risk of developing MS is 1 in 1,000 in the general population; it rises to about 1 in 4 in identical twins in which one twin is affected.\u003c/p>\n\u003cp>Even so, genes don’t explain it all. MS occurs more frequently at higher latitudes, suggesting that vitamin D deficiency might play a role in disease risk (the vitamin’s production in the body is dependent on sun exposure). Smoking also increases risk for the disease, as does obesity.\u003c/p>\n\u003cp>And while the tale of the Faroe Islands is disputed – large scale retroactive epidemiological studies are notoriously hard to pull off – it is for the most part accepted that microbes play some role in MS given that dozens of microbes, including the Epstein-Barr virus, have been tied to MS.\u003c/p>\n\u003cp>Yet more than 30 years of research suggests that risk factors in MS ultimately converge on the crux of its pathology: a misguided immune attack on myelin. Research in animals and humans supports the idea that MS develops when a type of white blood cell called a T-cell attacks specific proteins in myelin, making the axons less able to conduct electrical impulses efficiently.\u003c/p>\n\u003cp>The immune siege appears to be a result of something called “molecular mimicry.” Normally the body’s immune system attacks foreign invaders like viruses and bacteria. If a molecule that’s part of the body happens to closely resemble a portion of an intruding microbe, then both molecules can be targeted.\u003c/p>\n\u003cp>Put another way, say a particular protein on the surface of a virus is similar in structure to a protein found in myelin. The immune system ramps up to clear the virus but also attacks the myelin. It’s a case of mistaken identity, of collateral damage.\u003c/p>\n\u003cp>\u003ca href=\"http://www.en.neurologie.usz.ch/about-us/Pages/team.aspx\" target=\"_blank\" rel=\"noopener\">Dr. Roland Martin from the University Hospital of Zurich\u003c/a> in Switzerland is among the researchers who over the years helped identify which myelin proteins and peptides – biologic building blocks made of amino acids — come under attack in MS and which cells and immune molecules do the attacking.\u003c/p>\n\u003cp>“The idea of molecular mimicry is one of the most important ones in MS,” Martin says. “We and others have shown that mimicry between myelin peptides and viral and bacterial peptides indeed exists.”\u003c/p>\n\u003cp>And a number of proteins that make up myelin have been identified as helping spark the immune activity behind MS, possibly in response to similar microbial cousins.\u003c/p>\n\u003cp>Now, a \u003ca href=\"https://www.zora.uzh.ch/id/eprint/158835/1/2018_Planas_GDP_L-Fucose_Sci_Transl._Med._in_press.pdf\" target=\"_blank\" rel=\"noopener\">paper co-authored by Martin\u003c/a>, and published in October in \u003cem>Science and Translational Medicine\u003c/em>, reports on an additional nonmyelin-related protein that also may be involved.\u003c/p>\n\u003cp>Martin and his colleagues examined protein samples from the brains of 31 people who had died from suspected or confirmed MS. T-cells from 12 people reacted to the clunkily named enzyme, guanosine diphosphate-L-fucose synthase – or GDP-L-fucose synthase. The enzyme is normally involved in processing sugars essential to cellular function and communication, including that of neurons.\u003c/p>\n\u003cp>Paper co-author \u003ca href=\"https://www.multiplesclerosis.uzh.ch/en/coretopics/psospedra.html\" target=\"_blank\" rel=\"noopener\">Mireia Sospedra\u003c/a>, also of the University Hospital of Zurich, likens the enzyme to the iceberg’s ominous tip. “Yes, [myelin proteins] make sense but we think they might be not the only ones involved,” she speculates. “We think is that other auto-antigens might be involved in initiating the disease.”\u003c/p>\n\u003cp>She believes that the attack on this newly identified auto-antigen triggers tissue damage that exposes other proteins in myelin that are subsequently attacked themselves.\u003c/p>\n\u003cp>Sospedra also makes the point that culprit antigens might be different in everyone. The structure of our molecular machinery is genetically determined. Certain variants in, say, myelin protein structure might be more prone to immune attack; also genetic variation in immune cells themselves could influence how the body responds to a particular infection.\u003c/p>\n\u003cp>Northwestern University \u003ca href=\"https://www.feinberg.northwestern.edu/faculty-profiles/az/profile.html?xid=14949\" target=\"_blank\" rel=\"noopener\">immunology professor Stephen Miller\u003c/a> – who was not involved in the new research but who has collaborated with Martin in the past — sees the findings as revealing another piece in the MS puzzle.\u003c/p>\n\u003cp>“I don’t think there’s one particular virus or bacteria or environmental factor that triggers MS in every patient. There are probably many things that can trigger an autoimmune reaction against a particular infection,” he says. “But the more antigens we identify that can contribute to the disease the better.”\u003c/p>\n\u003cp>Regardless of the particular “cause” in a given patient, Martin, Miller and a number of other researchers are hard at work trying to thwart the MS immune attack in the first place using by coaxing the body into building up a familiarity and tolerance to suspected antigens, something called immunotolerance therapy. It’s a similar concept to how certain allergies can be thwarted by exposure to small amounts of a particular allergen.\u003c/p>\n\u003cp>“Think of it as a sort of negative vaccine,” says Miller. “We want less immune activity, not more.”\u003c/p>\n\u003cp>The sizable batch of approved MS medications for the most part work by broadly suppressing the immune system. They help control symptoms but also leave patients vulnerable to side effects like common infections.\u003c/p>\n\u003cp>Antigen-specific therapy only tames the immune response to specific antigens of interest. In theory it should come with fewer risks.\u003c/p>\n\u003cp>Miller recently co-founded a startup called \u003ca href=\"https://www.courpharma.com/about/\" target=\"_blank\" rel=\"noopener\">Cour Pharmaceuticals\u003c/a> through which he and his colleagues are studying the potential for immunotolerance therapy for MS and a number of other conditions, including celiac disease and Type I diabetes. The experimental therapy they plan to test involves attaching known MS-inducing antigens to biodegradable nanoparticles which they will then inject into trial patients. But for now they’ve just completed a phase I study testing their approach in celiac disease, with a phase II trial about to begin.\u003c/p>\n\u003cp>Martin’s group is pursuing a similar approach in which they chemically combine red or white blood cells with MS antigens and infuse them back into patients to induce tolerance.\u003c/p>\n\u003cp>This research is at a very early stage, but both groups are optimistic.\u003c/p>\n\u003cp>“Several of us in academia — and also the pharmaceutical industry — are pursing the long-standing dream of many immunologists: inducing tolerance against specific target antigens in autoimmune diseases like MS,” says Martin. “I am confident that sooner or later, we will be successful.”\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>\u003cem>Bret Stetka is a writer based in New York and an editorial director at \u003c/em>\u003ca href=\"http://www.medscape.com/public/bios/bio-bretstetka\" target=\"_blank\" rel=\"noopener\">Medscape\u003c/a>.\u003cem> A graduate of the University of Virginia School of Medicine, Stetka has had his work published by \u003c/em>Wired, Scientific American\u003cem> and The Atlantic.com. He’s also on Twitter: \u003c/em>\u003ca href=\"https://twitter.com/BretStetka\" target=\"_blank\" rel=\"noopener\">@BretStetka\u003c/a>.\u003c/p>\n\u003cdiv class=\"fullattribution\">\u003cem>Copyright 2019 \u003ca href=\"http://www.npr.org\" target=\"_blank\" rel=\"noopener\">NPR\u003c/a>.\u003c/em>\u003c/div>\n\n\u003c/div>\u003c/p>",
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"content": "\u003cp>[dl_subscribe]Potato Bug. Child of the Earth. Old Bald-Headed Man. Skull Insects. Devil’s Baby. Spawn of Satan. There’s a fairly long list of imaginative nicknames that refer to Jerusalem crickets, those six-legged insects with eerily humanlike faces and prominent striped abdomens. And they can get quite large, too: Some measure over 3 inches long and weigh more than a mouse, so they can be quite unnerving if you see them crawling around in your backyard in summertime.\u003c/p>\n\u003cfigure id=\"attachment_1935419\" class=\"wp-caption aligncenter\" style=\"max-width: 640px\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"wp-image-1935419 size-large\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2018/12/DL_602JerusalemCricket_CLOSEUP_FACE-1020x574.jpg\" alt=\"Jerusalem cricket\" width=\"640\" height=\"360\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2018/12/DL_602JerusalemCricket_CLOSEUP_FACE-1020x574.jpg 1020w, https://cdn.kqed.org/wp-content/uploads/sites/35/2018/12/DL_602JerusalemCricket_CLOSEUP_FACE-160x90.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2018/12/DL_602JerusalemCricket_CLOSEUP_FACE-800x450.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2018/12/DL_602JerusalemCricket_CLOSEUP_FACE-768x432.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2018/12/DL_602JerusalemCricket_CLOSEUP_FACE-1200x675.jpg 1200w, https://cdn.kqed.org/wp-content/uploads/sites/35/2018/12/DL_602JerusalemCricket_CLOSEUP_FACE-1920x1080.jpg 1920w, https://cdn.kqed.org/wp-content/uploads/sites/35/2018/12/DL_602JerusalemCricket_CLOSEUP_FACE-1180x664.jpg 1180w, https://cdn.kqed.org/wp-content/uploads/sites/35/2018/12/DL_602JerusalemCricket_CLOSEUP_FACE-960x540.jpg 960w, https://cdn.kqed.org/wp-content/uploads/sites/35/2018/12/DL_602JerusalemCricket_CLOSEUP_FACE-240x135.jpg 240w, https://cdn.kqed.org/wp-content/uploads/sites/35/2018/12/DL_602JerusalemCricket_CLOSEUP_FACE-375x211.jpg 375w, https://cdn.kqed.org/wp-content/uploads/sites/35/2018/12/DL_602JerusalemCricket_CLOSEUP_FACE-520x293.jpg 520w\" sizes=\"auto, (max-width: 640px) 100vw, 640px\">\u003cfigcaption class=\"wp-caption-text\">The beady-eyed gaze of a male Jerusalem cricket. \u003ccite>(Josh Cassidy/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>One individual who finds them compelling, and not creepy, has been \u003ca href=\"https://books.google.com/books?id=CFItJVfOFDAC&pg=PR5&lpg=PR5&dq=North+and+Central+America+Jerusalem+crickets+(Orthoptera:+Stenopelmatidae):+taxonomy,+distribution,+life+cycle,+ecology+and+related+biology+of+the+American+species&source=bl&ots=z4nC#v=onepage&q=North%20and%20Central%20America%20Jerusalem%20crickets%20(Orthoptera%3A%20Stenopelmatidae)%3A%20taxonomy%2C%20distribution%2C%20life%20cycle%2C%20ecology%20and%20related%20biology%20of%20the%20American%20species&f=false\" target=\"_blank\" rel=\"noopener\">studying Jerusalem crickets for over 40 years\u003c/a>: David Weissman, a research associate in entomology affiliated with the \u003ca href=\"https://www.calacademy.org/\" target=\"_blank\" rel=\"noopener\">California Academy of Sciences\u003c/a> in San Francisco. He’s now considered the world’s foremost expert, since no one else has been as captivated or singlemindedly devoted to learning more about them.\u003c/p>\n\u003cfigure id=\"attachment_1935368\" class=\"wp-caption alignleft\" style=\"max-width: 300px\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"wp-image-1935368\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2018/12/David_Weissman-e1544121188909.jpg\" alt=\"David Weissmann\" width=\"300\" height=\"400\">\u003cfigcaption class=\"wp-caption-text\">David Weissman, research associate in entomology with the California Academy of Sciences \u003ccite>(Courtesy of David Weissman)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>“In the past, entomologists have focused on insects that are out in the daytime — beetles, butterflies — that are pretty and easier to collect,” Weissman says. “I think it’s great spending the night out collecting bugs, but most people don’t.”\u003c/p>\n\u003cp>Splitting his time between his career as an entomologist and anesthesiologist, which helped support his field work, he didn’t think it would be that difficult to catalog all the different species of Jerusalem crickets. But now he’s planning on publishing a paper in the next two years that will name and describe more than 60 species, which aren’t actually true crickets although they’re somewhat related. And they’re primarily found in the western United States, Mexico and Central America — not Jerusalem.\u003c/p>\n\u003cp>“People have asked me, ‘Why don’t you go to the tropics for field work?’ ” says Weissman. “And I’ve been there. It’s wonderful, but it’s overwhelming, too. There’s so much there. And why go to tropics when you have such neat problems in your own backyard?”\u003c/p>\n\u003cfigure id=\"attachment_1935627\" class=\"wp-caption alignright\" style=\"max-width: 500px\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-full wp-image-1935627\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2018/12/DL602_FEMALE_DRUM.gif\" alt=\"A female Jerusalem cricket drums to respond to a mate.\" width=\"500\" height=\"281\">\u003cfigcaption class=\"wp-caption-text\">A female Jerusalem cricket drums in response to a potential mate. \u003ccite>(Josh Cassidy/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>While much of their general behavior is still not widely understood, Jerusalem crickets typically live solitary lives underground. They’ll emerge at night to scavenge for roots, tubers and smaller insects for their meals. And it’s also when they come out to serenade potential partners with a musical ritual: To attract a mate, adult crickets use their abdomens to drum the ground and generate low-frequency sound waves.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>“Drumming makes sense in Jerusalem crickets,” says Weissman. “The adults are out at night wandering around. It’s dark. They don’t fly. They don’t have wings to sing with. How do they find each other?”\u003c/p>\n\u003cp>If a male begins drumming and a female senses the vibrations, she’ll respond with a longer drumming sequence so that he’ll have enough time to track her down. The drumming can vary between one beat every other second up to 40 beats per second.\u003c/p>\n\u003cp>[youtube https://www.youtube.com/watch?v=Nrx37y63ZCM&w=560&h=315]\u003c/p>\n\u003cp>This duet is actually quite rare among insects. With crickets and katydids, Weissman says, “the male sings and the female comes to the male.” But with Jerusalem crickets, both of them participate in this percussive courtship.\u003c/p>\n\u003cp>“They have very keen vibratory sensors to help locate each other because they don’t have ears, so they’re actually feeling the vibrations,” says Weissman. These are located in all six of their legs and might be the most vibration-sensitive organs in the animal kingdom.\u003c/p>\n\u003cp>Many Jerusalem cricket species have their own unique drum pattern; they only respond to the tune of their own kind. Some Jerusalem cricket species also produce “sex clarification drums,” a distinct drum rhythm where males indicate which sex they are.\u003c/p>\n\u003cp>[youtube https://www.youtube.com/watch?v=IJJi1W6SOsE&w=560&h=315]\u003c/p>\n\u003cp>When they finally mate, they maneuver themselves into a position that would test the prowess of skilled gymnasts. And occasionally, the female will eat the male afterward. Weissman and other researchers aren’t sure why this happens.\u003c/p>\n\u003cp>“Praying mantises and black widows are a little bit different than Jerusalem crickets. In those cases, the female eats the male either during mating or before they mate. In Jerusalem crickets, the female doesn’t eat the male until after they’re done mating. The question is: Why? The male just lies there. Why would he let himself get eaten after he’s already done his thing and could easily run away?”\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>Weissman theorizes that perhaps the female “only mates once. Therefore, by letting her eat him, he fertilizes all her eggs and gives her good nutrients for his offspring. But there’s a problem with that. She can mate repeatedly in the laboratory. And he can also mate repeatedly. I don’t know why he lets her do that. It doesn’t happen very often … around 5 percent of the time. We can come up with all kinds of theories, but these hypotheses could take a lifetime to prove.”\u003c/p>\n\n",
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"excerpt": "With their big heads and beady black eyes, Jerusalem crickets aren't winning any beauty contests. But that doesn't stop them from finding mates. They use their bulbous bellies to serenade each other with some furious drumming. \r\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>Potato Bug. Child of the Earth. Old Bald-Headed Man. Skull Insects. Devil’s Baby. Spawn of Satan. There’s a fairly long list of imaginative nicknames that refer to Jerusalem crickets, those six-legged insects with eerily humanlike faces and prominent striped abdomens. And they can get quite large, too: Some measure over 3 inches long and weigh more than a mouse, so they can be quite unnerving if you see them crawling around in your backyard in summertime.\u003c/p>\n\u003cfigure id=\"attachment_1935419\" class=\"wp-caption aligncenter\" style=\"max-width: 640px\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"wp-image-1935419 size-large\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2018/12/DL_602JerusalemCricket_CLOSEUP_FACE-1020x574.jpg\" alt=\"Jerusalem cricket\" width=\"640\" height=\"360\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2018/12/DL_602JerusalemCricket_CLOSEUP_FACE-1020x574.jpg 1020w, https://cdn.kqed.org/wp-content/uploads/sites/35/2018/12/DL_602JerusalemCricket_CLOSEUP_FACE-160x90.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2018/12/DL_602JerusalemCricket_CLOSEUP_FACE-800x450.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2018/12/DL_602JerusalemCricket_CLOSEUP_FACE-768x432.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2018/12/DL_602JerusalemCricket_CLOSEUP_FACE-1200x675.jpg 1200w, https://cdn.kqed.org/wp-content/uploads/sites/35/2018/12/DL_602JerusalemCricket_CLOSEUP_FACE-1920x1080.jpg 1920w, https://cdn.kqed.org/wp-content/uploads/sites/35/2018/12/DL_602JerusalemCricket_CLOSEUP_FACE-1180x664.jpg 1180w, https://cdn.kqed.org/wp-content/uploads/sites/35/2018/12/DL_602JerusalemCricket_CLOSEUP_FACE-960x540.jpg 960w, https://cdn.kqed.org/wp-content/uploads/sites/35/2018/12/DL_602JerusalemCricket_CLOSEUP_FACE-240x135.jpg 240w, https://cdn.kqed.org/wp-content/uploads/sites/35/2018/12/DL_602JerusalemCricket_CLOSEUP_FACE-375x211.jpg 375w, https://cdn.kqed.org/wp-content/uploads/sites/35/2018/12/DL_602JerusalemCricket_CLOSEUP_FACE-520x293.jpg 520w\" sizes=\"auto, (max-width: 640px) 100vw, 640px\">\u003cfigcaption class=\"wp-caption-text\">The beady-eyed gaze of a male Jerusalem cricket. \u003ccite>(Josh Cassidy/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>One individual who finds them compelling, and not creepy, has been \u003ca href=\"https://books.google.com/books?id=CFItJVfOFDAC&pg=PR5&lpg=PR5&dq=North+and+Central+America+Jerusalem+crickets+(Orthoptera:+Stenopelmatidae):+taxonomy,+distribution,+life+cycle,+ecology+and+related+biology+of+the+American+species&source=bl&ots=z4nC#v=onepage&q=North%20and%20Central%20America%20Jerusalem%20crickets%20(Orthoptera%3A%20Stenopelmatidae)%3A%20taxonomy%2C%20distribution%2C%20life%20cycle%2C%20ecology%20and%20related%20biology%20of%20the%20American%20species&f=false\" target=\"_blank\" rel=\"noopener\">studying Jerusalem crickets for over 40 years\u003c/a>: David Weissman, a research associate in entomology affiliated with the \u003ca href=\"https://www.calacademy.org/\" target=\"_blank\" rel=\"noopener\">California Academy of Sciences\u003c/a> in San Francisco. He’s now considered the world’s foremost expert, since no one else has been as captivated or singlemindedly devoted to learning more about them.\u003c/p>\n\u003cfigure id=\"attachment_1935368\" class=\"wp-caption alignleft\" style=\"max-width: 300px\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"wp-image-1935368\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2018/12/David_Weissman-e1544121188909.jpg\" alt=\"David Weissmann\" width=\"300\" height=\"400\">\u003cfigcaption class=\"wp-caption-text\">David Weissman, research associate in entomology with the California Academy of Sciences \u003ccite>(Courtesy of David Weissman)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>“In the past, entomologists have focused on insects that are out in the daytime — beetles, butterflies — that are pretty and easier to collect,” Weissman says. “I think it’s great spending the night out collecting bugs, but most people don’t.”\u003c/p>\n\u003cp>Splitting his time between his career as an entomologist and anesthesiologist, which helped support his field work, he didn’t think it would be that difficult to catalog all the different species of Jerusalem crickets. But now he’s planning on publishing a paper in the next two years that will name and describe more than 60 species, which aren’t actually true crickets although they’re somewhat related. And they’re primarily found in the western United States, Mexico and Central America — not Jerusalem.\u003c/p>\n\u003cp>“People have asked me, ‘Why don’t you go to the tropics for field work?’ ” says Weissman. “And I’ve been there. It’s wonderful, but it’s overwhelming, too. There’s so much there. And why go to tropics when you have such neat problems in your own backyard?”\u003c/p>\n\u003cfigure id=\"attachment_1935627\" class=\"wp-caption alignright\" style=\"max-width: 500px\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-full wp-image-1935627\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2018/12/DL602_FEMALE_DRUM.gif\" alt=\"A female Jerusalem cricket drums to respond to a mate.\" width=\"500\" height=\"281\">\u003cfigcaption class=\"wp-caption-text\">A female Jerusalem cricket drums in response to a potential mate. \u003ccite>(Josh Cassidy/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>While much of their general behavior is still not widely understood, Jerusalem crickets typically live solitary lives underground. They’ll emerge at night to scavenge for roots, tubers and smaller insects for their meals. And it’s also when they come out to serenade potential partners with a musical ritual: To attract a mate, adult crickets use their abdomens to drum the ground and generate low-frequency sound waves.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>“Drumming makes sense in Jerusalem crickets,” says Weissman. “The adults are out at night wandering around. It’s dark. They don’t fly. They don’t have wings to sing with. How do they find each other?”\u003c/p>\n\u003cp>If a male begins drumming and a female senses the vibrations, she’ll respond with a longer drumming sequence so that he’ll have enough time to track her down. The drumming can vary between one beat every other second up to 40 beats per second.\u003c/p>\n\u003cp>\u003c/p>\u003cp>\u003cspan class='utils-parseShortcode-shortcodes-__youtubeShortcode__embedYoutube'>\n \u003cspan class='utils-parseShortcode-shortcodes-__youtubeShortcode__embedYoutubeInside'>\n \u003ciframe\n loading='lazy'\n class='utils-parseShortcode-shortcodes-__youtubeShortcode__youtubePlayer'\n type='text/html'\n src='//www.youtube.com/embed/Nrx37y63ZCM'\n title='//www.youtube.com/embed/Nrx37y63ZCM'\n allowfullscreen='true'\n style='border:0;'>\u003c/iframe>\n \u003c/span>\n \u003c/span>\u003c/p>\u003cp>\u003c/p>\n\u003cp>This duet is actually quite rare among insects. With crickets and katydids, Weissman says, “the male sings and the female comes to the male.” But with Jerusalem crickets, both of them participate in this percussive courtship.\u003c/p>\n\u003cp>“They have very keen vibratory sensors to help locate each other because they don’t have ears, so they’re actually feeling the vibrations,” says Weissman. These are located in all six of their legs and might be the most vibration-sensitive organs in the animal kingdom.\u003c/p>\n\u003cp>Many Jerusalem cricket species have their own unique drum pattern; they only respond to the tune of their own kind. Some Jerusalem cricket species also produce “sex clarification drums,” a distinct drum rhythm where males indicate which sex they are.\u003c/p>\n\u003cp>\u003c/p>\u003cp>\u003cspan class='utils-parseShortcode-shortcodes-__youtubeShortcode__embedYoutube'>\n \u003cspan class='utils-parseShortcode-shortcodes-__youtubeShortcode__embedYoutubeInside'>\n \u003ciframe\n loading='lazy'\n class='utils-parseShortcode-shortcodes-__youtubeShortcode__youtubePlayer'\n type='text/html'\n src='//www.youtube.com/embed/IJJi1W6SOsE'\n title='//www.youtube.com/embed/IJJi1W6SOsE'\n allowfullscreen='true'\n style='border:0;'>\u003c/iframe>\n \u003c/span>\n \u003c/span>\u003c/p>\u003cp>\u003c/p>\n\u003cp>When they finally mate, they maneuver themselves into a position that would test the prowess of skilled gymnasts. And occasionally, the female will eat the male afterward. Weissman and other researchers aren’t sure why this happens.\u003c/p>\n\u003cp>“Praying mantises and black widows are a little bit different than Jerusalem crickets. In those cases, the female eats the male either during mating or before they mate. In Jerusalem crickets, the female doesn’t eat the male until after they’re done mating. The question is: Why? The male just lies there. Why would he let himself get eaten after he’s already done his thing and could easily run away?”\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>Weissman theorizes that perhaps the female “only mates once. Therefore, by letting her eat him, he fertilizes all her eggs and gives her good nutrients for his offspring. But there’s a problem with that. She can mate repeatedly in the laboratory. And he can also mate repeatedly. I don’t know why he lets her do that. It doesn’t happen very often … around 5 percent of the time. We can come up with all kinds of theories, but these hypotheses could take a lifetime to prove.”\u003c/p>\n\n\u003c/div>\u003c/p>",
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"content": "\u003cp>[dl_subscribe]Most Bay Area hikers pass right by without ever noticing, but a careful eye can spot tiny towers rising up from the forest floor. These mysterious little tubes, barely an inch high, are the homes of a particularly sneaky predator — the California turret spider.\u003c/p>\n\u003cp>“To me, the turrets look just like the rook in a chess set,” said Trent Pearce, a naturalist for the East Bay Regional Park District, as he scanned the terrain at Briones Regional Park in Martinez. “The spiders themselves are super-burly — like a tiny tarantula the size of your pinky nail.”\u003c/p>\n\u003cfigure id=\"attachment_1936601\" class=\"wp-caption aligncenter\" style=\"max-width: 640px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_hidden01b.jpg\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-large wp-image-1936601\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_hidden01b-1020x574.jpg\" alt=\"\" width=\"640\" height=\"360\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_hidden01b-1020x574.jpg 1020w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_hidden01b-160x90.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_hidden01b-800x450.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_hidden01b-768x432.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_hidden01b-1200x675.jpg 1200w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_hidden01b-1920x1080.jpg 1920w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_hidden01b-1180x664.jpg 1180w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_hidden01b-960x540.jpg 960w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_hidden01b-240x135.jpg 240w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_hidden01b-375x211.jpg 375w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_hidden01b-520x293.jpg 520w\" sizes=\"auto, (max-width: 640px) 100vw, 640px\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Turret spiders are ambush hunters, remaining motionless while they wait for unsuspecting prey to approach within striking distance. \u003ccite>(Josh Cassidy/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Turret spiders build their towers along creekbeds and under fallen trees in forested areas throughout Central and Northern California. They use whatever mud, moss, bark and leaves they can find nearby, making their turrets extremely well camouflaged.\u003c/p>\n\u003cp>They line the inside of their tiny castles with pearly white silk, which makes the structure supple and resilient.\u003c/p>\n\u003cp>Each turret leads down to a burrow that can extend 6 inches underground. The spiders spend their days down there in the dark, protected from the sun and predators.\u003c/p>\n\u003cfigure id=\"attachment_1936603\" class=\"wp-caption aligncenter\" style=\"max-width: 640px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_silk_turret.jpg\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"wp-image-1936603 size-large\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_silk_turret-1020x574.jpg\" alt=\"\" width=\"640\" height=\"360\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_silk_turret-1020x574.jpg 1020w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_silk_turret-160x90.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_silk_turret-800x450.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_silk_turret-768x432.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_silk_turret-1200x675.jpg 1200w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_silk_turret-1920x1080.jpg 1920w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_silk_turret-1180x664.jpg 1180w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_silk_turret-960x540.jpg 960w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_silk_turret-240x135.jpg 240w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_silk_turret-375x211.jpg 375w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_silk_turret-520x293.jpg 520w\" sizes=\"auto, (max-width: 640px) 100vw, 640px\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Turret spiders use their silk to line their turrets, giving the tower structure and flexibility. \u003ccite>(Josh Cassidy/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>As night falls, they climb up to the entrance of the turrets to wait for unsuspecting prey, like beetles, to happen by.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>Turret spiders are ambush hunters. While remaining hidden inside their turrets, they’re able to sense the vibrations created by their prey’s footsteps.\u003c/p>\n\u003cp>That’s when the turret spider strikes, busting out of the hollow tower like an eight-legged jack-in-the-box. With lightning speed the spider swings its fangs down like daggers, injecting venom into its prey before dragging it down into the burrow.\u003c/p>\n\u003cp>“It’s like the scene in a horror movie where the monster appears out of nowhere — you can’t not jump,” Pearce said.\u003c/p>\n\u003cp>But human footsteps and loud voices are enough to scare turret spiders into retreating down into their burrows. So it takes patience to get a glimpse of one in action.\u003c/p>\n\u003cfigure id=\"attachment_1936606\" class=\"wp-caption aligncenter\" style=\"max-width: 500px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/01/DL601_TurretSpiders_StrikeBeetle01.gif\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-full wp-image-1936606\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/01/DL601_TurretSpiders_StrikeBeetle01.gif\" alt=\"\" width=\"500\" height=\"281\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Turret spiders are ambush hunters, bursting out from their camouflaged turrets to capture their prey before dragging it down into their underground burrows. \u003ccite>(Josh Cassidy/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Turret spiders belong to a group called mygalomorphs, along with their more famous relatives, such as tarantulas. While most spiders build webs to ensnare their prey, mygalomorphs tend to live underground. They have large fangs that point down instead of pinching together from the sides, like most spiders.\u003c/p>\n\u003cp>Different mygalomorph spiders can be found all over the world, but it turns out California is a bit of a hot spot.\u003c/p>\n\u003cfigure id=\"attachment_1936611\" class=\"wp-caption aligncenter\" style=\"max-width: 640px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_tarantula.jpg\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-large wp-image-1936611\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_tarantula-1020x574.jpg\" alt=\"\" width=\"640\" height=\"360\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_tarantula-1020x574.jpg 1020w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_tarantula-160x90.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_tarantula-800x450.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_tarantula-768x432.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_tarantula-1200x675.jpg 1200w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_tarantula-1920x1080.jpg 1920w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_tarantula-1180x664.jpg 1180w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_tarantula-960x540.jpg 960w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_tarantula-240x135.jpg 240w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_tarantula-375x211.jpg 375w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_tarantula-520x293.jpg 520w\" sizes=\"auto, (max-width: 640px) 100vw, 640px\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Like turret spiders, tarantulas also live underground and ambush prey from their homes at night. \u003ccite>(Craig Rosa/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>While tarantulas and trapdoor spiders tend to get more attention, turret spiders have captured the interest of James Starrett, a researcher from UC Davis.\u003c/p>\n\u003cp>Starrett scours the state, comparing the genetics of different populations of turret spiders throughout their range. He works with his colleague, Marshal Hedin of San Diego State University, to better understand how the changing environment might have shaped how they evolved in California.\u003c/p>\n\u003cp>“Geologic activity shaped the mountain ranges, which in turn affected the path of rivers,” Starrett said, “and the movement of those ranges influenced how the spider populations got to be isolated or come back into contact over time.”\u003c/p>\n\u003cfigure id=\"attachment_1936615\" class=\"wp-caption aligncenter\" style=\"max-width: 500px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/01/DL601_TurretSpiders_LungeAtLeaf.gif\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-full wp-image-1936615\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/01/DL601_TurretSpiders_LungeAtLeaf.gif\" alt=\"\" width=\"500\" height=\"281\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Using a leaf or blade of grass to gently tickle a spider’s turret at night can sometimes provoke a strike. \u003ccite>(Josh Cassidy/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Starrett has become an expert in finding the well-hidden turrets. He explains that turret spiders are long-lived. Females may stay in the same burrow for up to 16 years.\u003c/p>\n\u003cp>In the fall, mature male spiders venture out from their burrows in search of mates. It’s a risky endeavor to approach an agreeable female spider without falling victim to an ambush. Males typically die after mating. The females eventually lay eggs inside their burrows.\u003c/p>\n\u003cp>In the next few months, as winter and spring rains saturate California forests, the turret spiderlings will hatch and venture out from their mother’s turret. They usually dig their own individual burrows close by, so it’s common to find a large turret surrounded by several smaller ones.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>“That turns that little area into a minefield for a moth or bug that lands on the ground,” Starrett said. “It never really gets old seeing them jump out and grab their prey. It always makes you jump back.”\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>Most Bay Area hikers pass right by without ever noticing, but a careful eye can spot tiny towers rising up from the forest floor. These mysterious little tubes, barely an inch high, are the homes of a particularly sneaky predator — the California turret spider.\u003c/p>\n\u003cp>“To me, the turrets look just like the rook in a chess set,” said Trent Pearce, a naturalist for the East Bay Regional Park District, as he scanned the terrain at Briones Regional Park in Martinez. “The spiders themselves are super-burly — like a tiny tarantula the size of your pinky nail.”\u003c/p>\n\u003cfigure id=\"attachment_1936601\" class=\"wp-caption aligncenter\" style=\"max-width: 640px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_hidden01b.jpg\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-large wp-image-1936601\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_hidden01b-1020x574.jpg\" alt=\"\" width=\"640\" height=\"360\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_hidden01b-1020x574.jpg 1020w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_hidden01b-160x90.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_hidden01b-800x450.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_hidden01b-768x432.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_hidden01b-1200x675.jpg 1200w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_hidden01b-1920x1080.jpg 1920w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_hidden01b-1180x664.jpg 1180w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_hidden01b-960x540.jpg 960w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_hidden01b-240x135.jpg 240w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_hidden01b-375x211.jpg 375w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_hidden01b-520x293.jpg 520w\" sizes=\"auto, (max-width: 640px) 100vw, 640px\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Turret spiders are ambush hunters, remaining motionless while they wait for unsuspecting prey to approach within striking distance. \u003ccite>(Josh Cassidy/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Turret spiders build their towers along creekbeds and under fallen trees in forested areas throughout Central and Northern California. They use whatever mud, moss, bark and leaves they can find nearby, making their turrets extremely well camouflaged.\u003c/p>\n\u003cp>They line the inside of their tiny castles with pearly white silk, which makes the structure supple and resilient.\u003c/p>\n\u003cp>Each turret leads down to a burrow that can extend 6 inches underground. The spiders spend their days down there in the dark, protected from the sun and predators.\u003c/p>\n\u003cfigure id=\"attachment_1936603\" class=\"wp-caption aligncenter\" style=\"max-width: 640px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_silk_turret.jpg\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"wp-image-1936603 size-large\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_silk_turret-1020x574.jpg\" alt=\"\" width=\"640\" height=\"360\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_silk_turret-1020x574.jpg 1020w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_silk_turret-160x90.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_silk_turret-800x450.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_silk_turret-768x432.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_silk_turret-1200x675.jpg 1200w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_silk_turret-1920x1080.jpg 1920w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_silk_turret-1180x664.jpg 1180w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_silk_turret-960x540.jpg 960w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_silk_turret-240x135.jpg 240w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_silk_turret-375x211.jpg 375w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_silk_turret-520x293.jpg 520w\" sizes=\"auto, (max-width: 640px) 100vw, 640px\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Turret spiders use their silk to line their turrets, giving the tower structure and flexibility. \u003ccite>(Josh Cassidy/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>As night falls, they climb up to the entrance of the turrets to wait for unsuspecting prey, like beetles, to happen by.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>Turret spiders are ambush hunters. While remaining hidden inside their turrets, they’re able to sense the vibrations created by their prey’s footsteps.\u003c/p>\n\u003cp>That’s when the turret spider strikes, busting out of the hollow tower like an eight-legged jack-in-the-box. With lightning speed the spider swings its fangs down like daggers, injecting venom into its prey before dragging it down into the burrow.\u003c/p>\n\u003cp>“It’s like the scene in a horror movie where the monster appears out of nowhere — you can’t not jump,” Pearce said.\u003c/p>\n\u003cp>But human footsteps and loud voices are enough to scare turret spiders into retreating down into their burrows. So it takes patience to get a glimpse of one in action.\u003c/p>\n\u003cfigure id=\"attachment_1936606\" class=\"wp-caption aligncenter\" style=\"max-width: 500px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/01/DL601_TurretSpiders_StrikeBeetle01.gif\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-full wp-image-1936606\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/01/DL601_TurretSpiders_StrikeBeetle01.gif\" alt=\"\" width=\"500\" height=\"281\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Turret spiders are ambush hunters, bursting out from their camouflaged turrets to capture their prey before dragging it down into their underground burrows. \u003ccite>(Josh Cassidy/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Turret spiders belong to a group called mygalomorphs, along with their more famous relatives, such as tarantulas. While most spiders build webs to ensnare their prey, mygalomorphs tend to live underground. They have large fangs that point down instead of pinching together from the sides, like most spiders.\u003c/p>\n\u003cp>Different mygalomorph spiders can be found all over the world, but it turns out California is a bit of a hot spot.\u003c/p>\n\u003cfigure id=\"attachment_1936611\" class=\"wp-caption aligncenter\" style=\"max-width: 640px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_tarantula.jpg\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-large wp-image-1936611\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_tarantula-1020x574.jpg\" alt=\"\" width=\"640\" height=\"360\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_tarantula-1020x574.jpg 1020w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_tarantula-160x90.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_tarantula-800x450.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_tarantula-768x432.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_tarantula-1200x675.jpg 1200w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_tarantula-1920x1080.jpg 1920w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_tarantula-1180x664.jpg 1180w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_tarantula-960x540.jpg 960w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_tarantula-240x135.jpg 240w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_tarantula-375x211.jpg 375w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/DL601_Turret_Spider_tarantula-520x293.jpg 520w\" sizes=\"auto, (max-width: 640px) 100vw, 640px\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Like turret spiders, tarantulas also live underground and ambush prey from their homes at night. \u003ccite>(Craig Rosa/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>While tarantulas and trapdoor spiders tend to get more attention, turret spiders have captured the interest of James Starrett, a researcher from UC Davis.\u003c/p>\n\u003cp>Starrett scours the state, comparing the genetics of different populations of turret spiders throughout their range. He works with his colleague, Marshal Hedin of San Diego State University, to better understand how the changing environment might have shaped how they evolved in California.\u003c/p>\n\u003cp>“Geologic activity shaped the mountain ranges, which in turn affected the path of rivers,” Starrett said, “and the movement of those ranges influenced how the spider populations got to be isolated or come back into contact over time.”\u003c/p>\n\u003cfigure id=\"attachment_1936615\" class=\"wp-caption aligncenter\" style=\"max-width: 500px\">\u003ca href=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/01/DL601_TurretSpiders_LungeAtLeaf.gif\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-full wp-image-1936615\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/01/DL601_TurretSpiders_LungeAtLeaf.gif\" alt=\"\" width=\"500\" height=\"281\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Using a leaf or blade of grass to gently tickle a spider’s turret at night can sometimes provoke a strike. \u003ccite>(Josh Cassidy/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Starrett has become an expert in finding the well-hidden turrets. He explains that turret spiders are long-lived. Females may stay in the same burrow for up to 16 years.\u003c/p>\n\u003cp>In the fall, mature male spiders venture out from their burrows in search of mates. It’s a risky endeavor to approach an agreeable female spider without falling victim to an ambush. Males typically die after mating. The females eventually lay eggs inside their burrows.\u003c/p>\n\u003cp>In the next few months, as winter and spring rains saturate California forests, the turret spiderlings will hatch and venture out from their mother’s turret. They usually dig their own individual burrows close by, so it’s common to find a large turret surrounded by several smaller ones.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>“That turns that little area into a minefield for a moth or bug that lands on the ground,” Starrett said. “It never really gets old seeing them jump out and grab their prey. It always makes you jump back.”\u003c/p>\n\n\u003c/div>\u003c/p>",
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"title": "Cancer Death Rate in the U.S. Has Been Falling for Last 25 Years",
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"content": "\u003cp>NEW YORK (AP) — The U.S. cancer death rate has hit a milestone: It’s been falling for at least 25 years, according to a new report.\u003c/p>\n\u003cp>Lower smoking rates are translating into fewer deaths. Advances in early detection and treatment also are having a positive impact, experts say.\u003c/p>\n\u003cp>But it’s not all good news. Obesity-related cancer deaths are rising, and prostate cancer deaths are no longer dropping, said Rebecca Siegel, lead author of the American Cancer Society report published Tuesday.\u003c/p>\n\u003cp>Cancer also remains the nation’s No. 2 killer. The society predicts there will be more than 1.7 million new cancer cases, and more than 600,000 cancer deaths, in the U.S. this year.\u003c/p>\n\u003cp>Here’s a breakdown of the report:\u003c/p>\n\u003ch2>\u003cstrong>Decline\u003c/strong>\u003c/h2>\n\u003cp>There’s been a lot of bad news recently regarding U.S. death rates. In 2017, increases were seen in fatalities from seven of the 10 leading causes of death, according to recently released government data. But cancer has been something of a bright spot.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>The nation’s cancer death rate was increasing until the early 1990s. It has been dropping since, falling 27 percent between 1991 and 2016, the Cancer Society reported.\u003c/p>\n\u003cp>Lung cancer is the main reason. Among cancers, it has long killed the most people, especially men. But the lung cancer death rate dropped by nearly 50 percent among men since 1991. It was a delayed effect from a decline in smoking that began in the 1960s, Siegel said.\u003c/p>\n\u003ch2>Prostate Cancer\u003c/h2>\n\u003cp>The report has some mixed news about prostate cancer, the second leading cause of cancer death in men.\u003c/p>\n\u003cp>The prostate cancer death rate fell by half over two decades, but experts have been wondering whether the trend changed after a 2011 decision by the U.S. Preventive Services Task Force to stop recommending routine testing of men using the PSA blood test. That decision was prompted by concerns the test was leading to over-diagnosis and over-treatment.\u003c/p>\n\u003cp>The prostate cancer death rate flattened from 2013 to 2016. So while the PSA testing may have surfaced cases that didn’t actually need treatment, it may also have prevented some cancer deaths, the report suggests.\u003c/p>\n\u003ch2>Obesity\u003c/h2>\n\u003cp>Of the most common types of cancer in the U.S., all the ones with increasing death rates are linked to obesity, including cancers of the pancreas and uterus.\u003c/p>\n\u003cp>Another is liver cancer. Liver cancer deaths have been increasing since the 1970s, and initially most of the increase was tied to hepatitis C infections spread among people who abuse drugs. But now obesity accounts for a third of liver cancer deaths, and is more of a factor than hepatitis, Siegel said.\u003c/p>\n\u003cp>The nation’s growing obesity epidemic was first identified as a problem in the 1990s. It can take decades to see how a risk factor influences cancer rates, “so we may just be seeing the tip of the iceberg in terms of the effect of the obesity epidemic on cancer,” Siegel said.\u003c/p>\n\u003ch2>Disparity\u003c/h2>\n\u003cp>There’s been a decline in the historic racial gap in cancer death rates, but an economic gap is growing — especially when it comes to deaths that could be prevented by early screening and treatment, better eating and less smoking.\u003c/p>\n\u003cp>In the early 1970s, colon cancer death rates in the poorest counties were 20 percent lower than those in affluent counties; now they’re 30 percent higher. Cervical cancer deaths are twice as high for women in poor counties now, compared with women in affluent counties. And lung and liver cancer death rates are 40 percent higher for men in poor counties.\u003c/p>\n\u003cp>Dr. Darrell Gray, deputy director of Ohio State University’s Center for Cancer Health Equity, called the findings “important but not surprising.”\u003c/p>\n\u003cp>“We’ve known for some time that race is a surrogate” for other factors, like poverty and difficulty getting to — or paying for — doctor’s appointments, he said.\u003c/p>\n\u003cp>\u003cem>The Associated Press Health & Science Department receives \u003ca href=\"https://www.ap.org/press-releases/2018/ap-hhmi-expand-collaboration-to-bolster-health-science-coverage\">support\u003c/a> from the Howard Hughes Medical Institute’s Department of Science Education. The AP is solely responsible for all content.\u003c/em>\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\u003cem>Copyright 2019 \u003ca href=\"https://www.apnews.com/b5589e095abb4a0e9022bcffe9ed38b3\">Associated Press\u003c/a>.\u003c/em>\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>NEW YORK (AP) — The U.S. cancer death rate has hit a milestone: It’s been falling for at least 25 years, according to a new report.\u003c/p>\n\u003cp>Lower smoking rates are translating into fewer deaths. Advances in early detection and treatment also are having a positive impact, experts say.\u003c/p>\n\u003cp>But it’s not all good news. Obesity-related cancer deaths are rising, and prostate cancer deaths are no longer dropping, said Rebecca Siegel, lead author of the American Cancer Society report published Tuesday.\u003c/p>\n\u003cp>Cancer also remains the nation’s No. 2 killer. The society predicts there will be more than 1.7 million new cancer cases, and more than 600,000 cancer deaths, in the U.S. this year.\u003c/p>\n\u003cp>Here’s a breakdown of the report:\u003c/p>\n\u003ch2>\u003cstrong>Decline\u003c/strong>\u003c/h2>\n\u003cp>There’s been a lot of bad news recently regarding U.S. death rates. In 2017, increases were seen in fatalities from seven of the 10 leading causes of death, according to recently released government data. But cancer has been something of a bright spot.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>The nation’s cancer death rate was increasing until the early 1990s. It has been dropping since, falling 27 percent between 1991 and 2016, the Cancer Society reported.\u003c/p>\n\u003cp>Lung cancer is the main reason. Among cancers, it has long killed the most people, especially men. But the lung cancer death rate dropped by nearly 50 percent among men since 1991. It was a delayed effect from a decline in smoking that began in the 1960s, Siegel said.\u003c/p>\n\u003ch2>Prostate Cancer\u003c/h2>\n\u003cp>The report has some mixed news about prostate cancer, the second leading cause of cancer death in men.\u003c/p>\n\u003cp>The prostate cancer death rate fell by half over two decades, but experts have been wondering whether the trend changed after a 2011 decision by the U.S. Preventive Services Task Force to stop recommending routine testing of men using the PSA blood test. That decision was prompted by concerns the test was leading to over-diagnosis and over-treatment.\u003c/p>\n\u003cp>The prostate cancer death rate flattened from 2013 to 2016. So while the PSA testing may have surfaced cases that didn’t actually need treatment, it may also have prevented some cancer deaths, the report suggests.\u003c/p>\n\u003ch2>Obesity\u003c/h2>\n\u003cp>Of the most common types of cancer in the U.S., all the ones with increasing death rates are linked to obesity, including cancers of the pancreas and uterus.\u003c/p>\n\u003cp>Another is liver cancer. Liver cancer deaths have been increasing since the 1970s, and initially most of the increase was tied to hepatitis C infections spread among people who abuse drugs. But now obesity accounts for a third of liver cancer deaths, and is more of a factor than hepatitis, Siegel said.\u003c/p>\n\u003cp>The nation’s growing obesity epidemic was first identified as a problem in the 1990s. It can take decades to see how a risk factor influences cancer rates, “so we may just be seeing the tip of the iceberg in terms of the effect of the obesity epidemic on cancer,” Siegel said.\u003c/p>\n\u003ch2>Disparity\u003c/h2>\n\u003cp>There’s been a decline in the historic racial gap in cancer death rates, but an economic gap is growing — especially when it comes to deaths that could be prevented by early screening and treatment, better eating and less smoking.\u003c/p>\n\u003cp>In the early 1970s, colon cancer death rates in the poorest counties were 20 percent lower than those in affluent counties; now they’re 30 percent higher. Cervical cancer deaths are twice as high for women in poor counties now, compared with women in affluent counties. And lung and liver cancer death rates are 40 percent higher for men in poor counties.\u003c/p>\n\u003cp>Dr. Darrell Gray, deputy director of Ohio State University’s Center for Cancer Health Equity, called the findings “important but not surprising.”\u003c/p>\n\u003cp>“We’ve known for some time that race is a surrogate” for other factors, like poverty and difficulty getting to — or paying for — doctor’s appointments, he said.\u003c/p>\n\u003cp>\u003cem>The Associated Press Health & Science Department receives \u003ca href=\"https://www.ap.org/press-releases/2018/ap-hhmi-expand-collaboration-to-bolster-health-science-coverage\">support\u003c/a> from the Howard Hughes Medical Institute’s Department of Science Education. The AP is solely responsible for all content.\u003c/em>\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\u003cem>Copyright 2019 \u003ca href=\"https://www.apnews.com/b5589e095abb4a0e9022bcffe9ed38b3\">Associated Press\u003c/a>.\u003c/em>\u003c/p>\n\n\u003c/div>\u003c/p>",
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"title": "For Peanut Allergy Sufferers, A Look at the Latest Treatment Research",
"headTitle": "For Peanut Allergy Sufferers, A Look at the Latest Treatment Research | KQED",
"content": "\u003cp>Whenever I see a report touting possible new peanut allergy treatments, I devour it. I can’t help it. It’s an occupational hazard for any health journalist whose reporting specialty and medical history intertwine.\u003c/p>\n\u003cp>I write about the business of health care, focusing on how consumers interact with the system — what we pay, what we get and why American care costs so much. But in this particular instance, I have another kind of authority: 26 years of life-threatening allergies to nuts and peanuts.\u003c/p>\n\u003cp>So last month, when California-based Aimmune Therapeutics sparked optimistic headlines after releasing clinical trial results that its allergy product, AR101, would reduce the risks linked to an accidental exposure to peanuts, I received the usual wave of questions from friends, co-workers and my parents: Would you try it? Could this help?\u003c/p>\n\u003cp>Aimmune is just one company eyeing the prize. Childhood peanut allergy diagnoses increased \u003ca href=\"https://www.sciencedaily.com/releases/2017/10/171027085541.htm\">more than 20 percent\u003c/a> in the United States from 2010 to 2017. The global market for relief is worth as much as $2 billion. The French drugmaker DBV Technologies is also working to commercialize a peanut allergy patch. \u003ca href=\"http://www.camallergy.com/about/\">Other companies\u003c/a>, including industry giant \u003ca href=\"https://clinicaltrials.gov/ct2/show/NCT03463135\">Sanofi\u003c/a>, are following their \u003ca href=\"http://www.intrommune.com/oral-mucosal-therapy-omit/\">lead\u003c/a>.\u003c/p>\n\u003cp>If any one of them succeeds, it could change my life.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>My friends call nuts “Shefali poison.” My allergies first surfaced when, as a 15-month-old, I picked Thai noodles off an aunt’s plate and developed hives on my face, and then a few months later when I tasted my mom’s kaju barfi – an Indian dessert with cashews – and ended up in the hospital. Nobody in my family had ever heard of peanut allergies.\u003c/p>\n\u003cp>I’ve carried epinephrine since I was 7 years old. My friends are trained to inject it in my leg, the standard procedure for an emergency allergen exposure. Though I luckily haven’t had to take a shot of it since I was 4. (Another child in my Montessori class had a peanut butter sandwich for lunch.)\u003c/p>\n\u003cp>My mom also recalls another incident when she had to pick me up early from day care because the class was making peanut butter bird feeders. And I spent too many years of pre-adolescence eating lunch at the designated “peanut-free table.” Now, I can only dream of flying to visit my parents for Christmas without worrying about whether my seatmate’s snacks might induce anaphylaxis. And yes, \u003ca href=\"https://www.teenvogue.com/story/deathly-peanut-butter-kiss\">kissing someone\u003c/a> who has just eaten peanut butter would put my life in danger.\u003c/p>\n\u003cp>But are these pills and patches a true breakthrough for people like me?\u003c/p>\n\u003cp>I approached the question as I would any other assignment. I read the research, called immunologists, and spoke with economists and drug pricing experts about whether these treatments offer meaningful benefit.\u003c/p>\n\u003cp>One of the first things I heard: “We are still in the infancy of these treatments,” said Dr. Corinne Keet, a pediatric allergist at Johns Hopkins University.\u003c/p>\n\u003cfigure id=\"attachment_1936503\" class=\"wp-caption alignnone\" style=\"max-width: 770px\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-full wp-image-1936503\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/01/Shefali.jpg\" alt=\"\" width=\"770\" height=\"513\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/Shefali.jpg 770w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/Shefali-160x107.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/Shefali-768x512.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/Shefali-240x160.jpg 240w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/Shefali-375x250.jpg 375w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/Shefali-520x346.jpg 520w\" sizes=\"(max-width: 770px) 100vw, 770px\">\u003cfigcaption class=\"wp-caption-text\">Shefali Luthra (second from right), pictured in the seventh grade with her school math team, carried epinephrine in a fanny pack as a child, in case she had an allergic reaction. \u003ccite>(Courtesy of the Luthra family)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Medically, there’s a lot we don’t know about the risks, how much these drugs could help and how long any effects would last.\u003c/p>\n\u003cp>“None of these treatments have been shown to prevent fatal reaction,” Keet emphasized.\u003c/p>\n\u003cp>The idea behind them is to desensitize people. Aimmune’s “peanut pill” is modeled on the oral therapies some specialists use to wean allergic kids back on to nuts. This approach has gained popularity in recent years, especially for children with multiple allergies, or when it’s a substance particularly hard to avoid.\u003c/p>\n\u003cp>A colleague’s young daughter, who was born with multiple allergies, used that very treatment, as did a younger cousin of mine who, for the first several years of her life, was allergic to — not joking — almost everything but fruits and vegetables. In my case, this therapy came into vogue after I was too old to have a good chance of it weakening my sensitivities.\u003c/p>\n\u003cp>How it works: Kids ingest tiny, escalating doses of peanut protein. They then stay on peanut protein — Aimmune recommends the pill, though other doctors I spoke to suggested a little bit of peanut — as a maintenance drug.\u003c/p>\n\u003cp>But it’s unclear how much the new therapies would improve upon that ad hoc oral immunotherapy allergists are already offering. Instead of drugs, they use store-bought peanut protein, usually de-fatted peanut flour available online for as little as $1 a pound. This method isn’t approved by the Food and Drug Administration, and often isn’t covered by insurance — though doctors’ visits can be billed as “food challenges” or other visits that are typically covered.\u003c/p>\n\u003cp>In contrast, Aimmune’s product \u003ca href=\"https://www.latimes.com/business/la-fi-peanut-allergy-treatment-20180220-story.html\">is expected\u003c/a> to cost between $5,000 and $10,000 for the first six months of use, and $300 to $400 per month after. \u003ca href=\"https://www.reuters.com/article/us-biotech-peanuts/biotech-companies-chase-elusive-peanut-allergy-treatment-idUSKCN0SL2LK20151027\">Analysts predict\u003c/a> DBV’s will cost more than $6,000 for a year’s supply, though the company says it has not yet determined a price. DBV, Aimmune’s chief rival, has come up with a wearable skin patch that would transmit tiny, desensitizing protein doses. It declined to estimate a price, but it does not view oral immunotherapy as a competitor, said Joseph Becker, a company spokesman.\u003c/p>\n\u003cp>“There’s excitement, there’s caution and a lot of unanswered questions,” warned Dr. Erwin Gelfand, a pediatrics and immunology professor at the University of Colorado.\u003c/p>\n\u003caside class=\"pullquote alignright\">For an allergic kid, even the possibility [of a reaction] is maybe one of the most terrifying things you can imagine.\u003c/aside>\n\u003cp>According to Aimmune’s results, published in the prestigious \u003ca href=\"https://www.nejm.org/doi/full/10.1056/NEJMoa1812856\">New England Journal of Medicine\u003c/a>, two-thirds of allergic children could ingest 600 milligrams of peanut without harm after going through treatment.\u003c/p>\n\u003cp>To be clear, even with Aimmune’s help, someone like me still couldn’t safely eat PB&J. But it would desensitize me enough that I could taste a friend’s wine even if he recently ate pad thai.\u003c/p>\n\u003cp>Still, the treatment comes with caveats.\u003c/p>\n\u003cp>While 496 children started the trial, only 372 completed it. Of the 20 percent who backed out, half did so because of adverse events. About 14 percent of kids getting treatment still had to take epinephrine, and one experienced anaphylaxis, a severe reaction that can involve rashes, vomiting, a tightening throat and difficulty breathing. (For an allergic kid, even the possibility is maybe one of the most terrifying things you can imagine.)\u003c/p>\n\u003cp>Children who completed the regimen still had to take small doses of peanut protein daily, either the Aimmune drug or a controlled peanut serving. Statistically significant benefits were clear only in patients through age 17, though Dr. Daniel Adelman, the company’s chief medical officer, said Aimmune plans to do a follow-up trial for adults.\u003c/p>\n\u003cp>And the results don’t indicate who is likely to benefit, or how long improvements would last. That’s impossible to know, Adelman said, though he suggested accidental peanut exposure is scary enough — and pure avoidance ineffective enough — that the treatment is still worth it.\u003c/p>\n\u003cp>But all this means that anyone who has gone through Aimmune’s regimen would still want to carry epinephrine, and try to avoid peanuts.\u003c/p>\n\u003cp>“Not everybody responds well,” Gelfand said. When you factor in those details, the results are “not all that impressive,” he argued.\u003c/p>\n\u003cp>Dr. Tina Sindher, a pediatric allergist at Stanford University, pointed out that the Aimmune pill is a repackaged, clinically tested version of that homegrown oral therapy many allergists have already been using. DBV’s peanut patch, Viaskin, to a lesser extent, is the same — more convenient, perhaps, and more regulated, but still a variation on the existing medical approach.\u003c/p>\n\u003cp>“This concept has been around for a long time,” she said.\u003c/p>\n\u003cp>What’s new is the addition of labor, standardization and federal oversight — which companies then say demonstrates increased value.\u003c/p>\n\u003cp>It highlights a pattern \u003ca href=\"https://khn.org/news/fish-oil-drug-looks-heart-healthy-just-dont-swallow-it-hook-line-and-sinker/\">I’ve noticed\u003c/a> from my reporting: Drugmakers develop medication that refines a low-tech remedy, run a clinical trial to secure FDA approval, and then sell it at a higher price. For pharma, it’s a logical way to profit. But it puts patients in a bind.\u003c/p>\n\u003cp>“The hard outcome is we have these new products and they’re just about as good or slightly better than what we have,” said Nicholson Price, an assistant professor at the University of Michigan Law School, who studies drug pricing. “And they’re a lot more expensive.” He noted: “That’s when the choices get hard, and we’re not good at making hard choices.”\u003c/p>\n\u003cp>Also skeptical? The closest authority I know: my mother, who raised me with peanut allergies when they were more or less unheard of, and is now doing it all over again for my 10-year-old brother. (My other brother, my twin, was allergy-free until about a year ago.)\u003c/p>\n\u003cp>“It’s not worth it,” my mom told me. Her concern? Getting any of us to maintain a peanut dose — without knowing how long that reduced sensitivity would last — could induce what she called “a false sense of security.”\u003c/p>\n\u003cp>This thinking isn’t out of line, Sindher suggested. The way these studies are touted, she said, often “gloss over the fact that there’s a lot we don’t know.”\u003c/p>\n\u003cp>So for now, I’ll have to maintain my distance from the newsroom stash of Reese’s Pieces. My epinephrine and I aren’t parting ways anytime soon.\u003c/p>\n\u003cp>\u003cem>KHN’s coverage of children’s health care issues is supported in part by the \u003ca href=\"https://www.hsfoundation.org/\">Heising-Simons Foundation\u003c/a>.\u003c/em>\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp>\u003cem>\u003ca href=\"https://khn.org/\">Kaiser Health News\u003c/a> (KHN) is a national health policy news service. It is an editorially independent program of the \u003ca href=\"https://www.kff.org/\">Henry J. Kaiser Family Foundation\u003c/a> which is not affiliated with Kaiser Permanente.\u003c/em>\u003c/p>\n\n",
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"excerpt": "Whenever I see a report touting possible new peanut allergy treatments, I devour it. I can’t help it. It’s an occupational hazard for any health journalist whose reporting specialty and medical history intertwine.\r\n ",
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"description": "Whenever I see a report touting possible new peanut allergy treatments, I devour it. I can’t help it. It’s an occupational hazard for any health journalist whose reporting specialty and medical history intertwine.\r\n ",
"title": "For Peanut Allergy Sufferers, A Look at the Latest Treatment Research | KQED",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>Whenever I see a report touting possible new peanut allergy treatments, I devour it. I can’t help it. It’s an occupational hazard for any health journalist whose reporting specialty and medical history intertwine.\u003c/p>\n\u003cp>I write about the business of health care, focusing on how consumers interact with the system — what we pay, what we get and why American care costs so much. But in this particular instance, I have another kind of authority: 26 years of life-threatening allergies to nuts and peanuts.\u003c/p>\n\u003cp>So last month, when California-based Aimmune Therapeutics sparked optimistic headlines after releasing clinical trial results that its allergy product, AR101, would reduce the risks linked to an accidental exposure to peanuts, I received the usual wave of questions from friends, co-workers and my parents: Would you try it? Could this help?\u003c/p>\n\u003cp>Aimmune is just one company eyeing the prize. Childhood peanut allergy diagnoses increased \u003ca href=\"https://www.sciencedaily.com/releases/2017/10/171027085541.htm\">more than 20 percent\u003c/a> in the United States from 2010 to 2017. The global market for relief is worth as much as $2 billion. The French drugmaker DBV Technologies is also working to commercialize a peanut allergy patch. \u003ca href=\"http://www.camallergy.com/about/\">Other companies\u003c/a>, including industry giant \u003ca href=\"https://clinicaltrials.gov/ct2/show/NCT03463135\">Sanofi\u003c/a>, are following their \u003ca href=\"http://www.intrommune.com/oral-mucosal-therapy-omit/\">lead\u003c/a>.\u003c/p>\n\u003cp>If any one of them succeeds, it could change my life.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>My friends call nuts “Shefali poison.” My allergies first surfaced when, as a 15-month-old, I picked Thai noodles off an aunt’s plate and developed hives on my face, and then a few months later when I tasted my mom’s kaju barfi – an Indian dessert with cashews – and ended up in the hospital. Nobody in my family had ever heard of peanut allergies.\u003c/p>\n\u003cp>I’ve carried epinephrine since I was 7 years old. My friends are trained to inject it in my leg, the standard procedure for an emergency allergen exposure. Though I luckily haven’t had to take a shot of it since I was 4. (Another child in my Montessori class had a peanut butter sandwich for lunch.)\u003c/p>\n\u003cp>My mom also recalls another incident when she had to pick me up early from day care because the class was making peanut butter bird feeders. And I spent too many years of pre-adolescence eating lunch at the designated “peanut-free table.” Now, I can only dream of flying to visit my parents for Christmas without worrying about whether my seatmate’s snacks might induce anaphylaxis. And yes, \u003ca href=\"https://www.teenvogue.com/story/deathly-peanut-butter-kiss\">kissing someone\u003c/a> who has just eaten peanut butter would put my life in danger.\u003c/p>\n\u003cp>But are these pills and patches a true breakthrough for people like me?\u003c/p>\n\u003cp>I approached the question as I would any other assignment. I read the research, called immunologists, and spoke with economists and drug pricing experts about whether these treatments offer meaningful benefit.\u003c/p>\n\u003cp>One of the first things I heard: “We are still in the infancy of these treatments,” said Dr. Corinne Keet, a pediatric allergist at Johns Hopkins University.\u003c/p>\n\u003cfigure id=\"attachment_1936503\" class=\"wp-caption alignnone\" style=\"max-width: 770px\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-full wp-image-1936503\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/01/Shefali.jpg\" alt=\"\" width=\"770\" height=\"513\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/Shefali.jpg 770w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/Shefali-160x107.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/Shefali-768x512.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/Shefali-240x160.jpg 240w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/Shefali-375x250.jpg 375w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/01/Shefali-520x346.jpg 520w\" sizes=\"(max-width: 770px) 100vw, 770px\">\u003cfigcaption class=\"wp-caption-text\">Shefali Luthra (second from right), pictured in the seventh grade with her school math team, carried epinephrine in a fanny pack as a child, in case she had an allergic reaction. \u003ccite>(Courtesy of the Luthra family)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Medically, there’s a lot we don’t know about the risks, how much these drugs could help and how long any effects would last.\u003c/p>\n\u003cp>“None of these treatments have been shown to prevent fatal reaction,” Keet emphasized.\u003c/p>\n\u003cp>The idea behind them is to desensitize people. Aimmune’s “peanut pill” is modeled on the oral therapies some specialists use to wean allergic kids back on to nuts. This approach has gained popularity in recent years, especially for children with multiple allergies, or when it’s a substance particularly hard to avoid.\u003c/p>\n\u003cp>A colleague’s young daughter, who was born with multiple allergies, used that very treatment, as did a younger cousin of mine who, for the first several years of her life, was allergic to — not joking — almost everything but fruits and vegetables. In my case, this therapy came into vogue after I was too old to have a good chance of it weakening my sensitivities.\u003c/p>\n\u003cp>How it works: Kids ingest tiny, escalating doses of peanut protein. They then stay on peanut protein — Aimmune recommends the pill, though other doctors I spoke to suggested a little bit of peanut — as a maintenance drug.\u003c/p>\n\u003cp>But it’s unclear how much the new therapies would improve upon that ad hoc oral immunotherapy allergists are already offering. Instead of drugs, they use store-bought peanut protein, usually de-fatted peanut flour available online for as little as $1 a pound. This method isn’t approved by the Food and Drug Administration, and often isn’t covered by insurance — though doctors’ visits can be billed as “food challenges” or other visits that are typically covered.\u003c/p>\n\u003cp>In contrast, Aimmune’s product \u003ca href=\"https://www.latimes.com/business/la-fi-peanut-allergy-treatment-20180220-story.html\">is expected\u003c/a> to cost between $5,000 and $10,000 for the first six months of use, and $300 to $400 per month after. \u003ca href=\"https://www.reuters.com/article/us-biotech-peanuts/biotech-companies-chase-elusive-peanut-allergy-treatment-idUSKCN0SL2LK20151027\">Analysts predict\u003c/a> DBV’s will cost more than $6,000 for a year’s supply, though the company says it has not yet determined a price. DBV, Aimmune’s chief rival, has come up with a wearable skin patch that would transmit tiny, desensitizing protein doses. It declined to estimate a price, but it does not view oral immunotherapy as a competitor, said Joseph Becker, a company spokesman.\u003c/p>\n\u003cp>“There’s excitement, there’s caution and a lot of unanswered questions,” warned Dr. Erwin Gelfand, a pediatrics and immunology professor at the University of Colorado.\u003c/p>\n\u003caside class=\"pullquote alignright\">For an allergic kid, even the possibility [of a reaction] is maybe one of the most terrifying things you can imagine.\u003c/aside>\n\u003cp>According to Aimmune’s results, published in the prestigious \u003ca href=\"https://www.nejm.org/doi/full/10.1056/NEJMoa1812856\">New England Journal of Medicine\u003c/a>, two-thirds of allergic children could ingest 600 milligrams of peanut without harm after going through treatment.\u003c/p>\n\u003cp>To be clear, even with Aimmune’s help, someone like me still couldn’t safely eat PB&J. But it would desensitize me enough that I could taste a friend’s wine even if he recently ate pad thai.\u003c/p>\n\u003cp>Still, the treatment comes with caveats.\u003c/p>\n\u003cp>While 496 children started the trial, only 372 completed it. Of the 20 percent who backed out, half did so because of adverse events. About 14 percent of kids getting treatment still had to take epinephrine, and one experienced anaphylaxis, a severe reaction that can involve rashes, vomiting, a tightening throat and difficulty breathing. (For an allergic kid, even the possibility is maybe one of the most terrifying things you can imagine.)\u003c/p>\n\u003cp>Children who completed the regimen still had to take small doses of peanut protein daily, either the Aimmune drug or a controlled peanut serving. Statistically significant benefits were clear only in patients through age 17, though Dr. Daniel Adelman, the company’s chief medical officer, said Aimmune plans to do a follow-up trial for adults.\u003c/p>\n\u003cp>And the results don’t indicate who is likely to benefit, or how long improvements would last. That’s impossible to know, Adelman said, though he suggested accidental peanut exposure is scary enough — and pure avoidance ineffective enough — that the treatment is still worth it.\u003c/p>\n\u003cp>But all this means that anyone who has gone through Aimmune’s regimen would still want to carry epinephrine, and try to avoid peanuts.\u003c/p>\n\u003cp>“Not everybody responds well,” Gelfand said. When you factor in those details, the results are “not all that impressive,” he argued.\u003c/p>\n\u003cp>Dr. Tina Sindher, a pediatric allergist at Stanford University, pointed out that the Aimmune pill is a repackaged, clinically tested version of that homegrown oral therapy many allergists have already been using. DBV’s peanut patch, Viaskin, to a lesser extent, is the same — more convenient, perhaps, and more regulated, but still a variation on the existing medical approach.\u003c/p>\n\u003cp>“This concept has been around for a long time,” she said.\u003c/p>\n\u003cp>What’s new is the addition of labor, standardization and federal oversight — which companies then say demonstrates increased value.\u003c/p>\n\u003cp>It highlights a pattern \u003ca href=\"https://khn.org/news/fish-oil-drug-looks-heart-healthy-just-dont-swallow-it-hook-line-and-sinker/\">I’ve noticed\u003c/a> from my reporting: Drugmakers develop medication that refines a low-tech remedy, run a clinical trial to secure FDA approval, and then sell it at a higher price. For pharma, it’s a logical way to profit. But it puts patients in a bind.\u003c/p>\n\u003cp>“The hard outcome is we have these new products and they’re just about as good or slightly better than what we have,” said Nicholson Price, an assistant professor at the University of Michigan Law School, who studies drug pricing. “And they’re a lot more expensive.” He noted: “That’s when the choices get hard, and we’re not good at making hard choices.”\u003c/p>\n\u003cp>Also skeptical? The closest authority I know: my mother, who raised me with peanut allergies when they were more or less unheard of, and is now doing it all over again for my 10-year-old brother. (My other brother, my twin, was allergy-free until about a year ago.)\u003c/p>\n\u003cp>“It’s not worth it,” my mom told me. Her concern? Getting any of us to maintain a peanut dose — without knowing how long that reduced sensitivity would last — could induce what she called “a false sense of security.”\u003c/p>\n\u003cp>This thinking isn’t out of line, Sindher suggested. The way these studies are touted, she said, often “gloss over the fact that there’s a lot we don’t know.”\u003c/p>\n\u003cp>So for now, I’ll have to maintain my distance from the newsroom stash of Reese’s Pieces. My epinephrine and I aren’t parting ways anytime soon.\u003c/p>\n\u003cp>\u003cem>KHN’s coverage of children’s health care issues is supported in part by the \u003ca href=\"https://www.hsfoundation.org/\">Heising-Simons Foundation\u003c/a>.\u003c/em>\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>\u003cem>\u003ca href=\"https://khn.org/\">Kaiser Health News\u003c/a> (KHN) is a national health policy news service. It is an editorially independent program of the \u003ca href=\"https://www.kff.org/\">Henry J. Kaiser Family Foundation\u003c/a> which is not affiliated with Kaiser Permanente.\u003c/em>\u003c/p>\n\n\u003c/div>\u003c/p>",
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"title": "New Software Can Spot Genetic Mutations Using Photos",
"headTitle": "New Software Can Spot Genetic Mutations Using Photos | KQED",
"content": "\u003cp>[dropcap]S[/dropcap]ome people’s faces — or even just a photo of them — hint at the genes they carry. And now, an algorithm can predict not only whether they carry a genetic mutation, but which genes were mutated.\u003c/p>\n\u003cp>The \u003ca href=\"https://www.nature.com/articles/s41591-018-0279-0\">study\u003c/a>, published Monday in Nature Medicine, is the latest from a Boston-based company called FDNA, one of a \u003ca href=\"https://www.statnews.com/2017/04/10/facial-recognition-genetic-disorders/\">few organizations creating software\u003c/a> that can help physicians diagnose genetic syndromes based just on a face — and may serve an important validation of the company’s technology, said Yaron Gurovich, the company’s chief technology officer.\u003c/p>\n\u003cp>“We went for this high-impact journal to prove beyond any doubt that this technology is good, it performs as we say, we can stand behind it, and now it opens a lot of doors to publish more,” he said.\u003c/p>\n\u003cp>The study itself is a collection of experiments testing how the results of algorithms — FDNA refers to them as DeepGestalt — stack up against clinicians’ diagnoses. In one of the experiments, DeepGestalt’s performance was better than random chance when picking which of five genetic mutations might be causing a condition called Noonan syndrome. It was correct 64 percent of the time, far more than the 20 percent success rate that would be expected from guesswork.\u003c/p>\n\u003cp>“This is new — we’ve never published something like this before,” Gurovich said.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>Gurovich is quick to say that the tool isn’t specifically or only for Noonan syndrome. His team chose the condition because there are already published studies about how well humans can distinguish between the various faces associated with it. FDNA is already working on another paper Gurovich said will show that the tool can be used more broadly. It’s going through the peer review process, he said, but a \u003ca href=\"https://www.biorxiv.org/content/early/2018/11/21/473306\">preprint version\u003c/a> is available.\u003c/p>\n\u003caside class=\"pullquote alignright\">‘This is new — we’ve never published something like this before.’\u003ccite>Yaron Gurovich, FDNA\u003c/cite>\u003c/aside>\n\u003cp>One expert on Noonan syndrome, Dr. Bruce Gelb, the director of the Mindich Child Health and Development Institute and a professor at the Icahn School of Medicine at Mount Sinai, cautioned that being able to pick apart a person’s genotype based on facial features is not generally going to be useful for people with the condition.\u003c/p>\n\u003cp>Noonan syndrome comes with a variety of symptoms, including difficulty learning, facial appearance, short stature, and heart issues — including issues with valves or the muscles of the heart itself. A few have a very high risk of leukemia.\u003c/p>\n\u003cp>Some children with Noonan syndrome attend special education classes; others develop typically and can attend mainstream classes. Many can live independently when they’re adults. “It varies a lot,” Gelb said.\u003c/p>\n\u003cp>The genetic cause of Noonan syndrome can vary, too. Mutations in a few different genes can lead to the condition; some mutations cause more serious problems than others. All of the genes, however, are linked to one vital biochemical pathway. Gelb and his research group \u003ca href=\"https://www.nature.com/articles/ng772.epdf?referrer_access_token=pyqbUoC1N6pu4ONrbf7p-dRgN0jAjWel9jnR3ZoTv0N_aEXfBZJ5UdikqtmfwCNXtbaW16rct1gXy0ybOILq30HDNTADZng2FuE6EIQ5rZUCeTxb0IcHHWK4FYeWQUzl1RC37x8AUQ5VhWgJ_gCtuexxd6Hbv9Jdi_kTnCSJ58A%3D&tracking_referrer=www.statnews.com\">have discovered\u003c/a> \u003ca href=\"https://www.nature.com/articles/ng1939.epdf?referrer_access_token=YGvl4Y4X_QshFYTfu2YjQ9RgN0jAjWel9jnR3ZoTv0Mrh-TZl36dLirUZe-74nzZOxlFsdIHF50ddu1dNrJfeaq9wkfjaVZoRTGs8sbI39nA6vpr1CpXKLQdwf7hvAQbSEiKx9tRYNbP-HvhG0GxWgTtRX2Ai6LzUREdlZecehg%3D&tracking_referrer=www.statnews.com\">some of them\u003c/a>.\u003c/p>\n\u003cp>For example, children whose RAS1 gene is mutated almost always get hypertrophic cardiomyopathy, a condition in which the muscles of the heart get thick, making it difficult for the heart to pump normally. Children with mutations in a gene called KRAS have some of the most severe forms of the syndrome and some of the worst neurological and heart outcomes.\u003c/p>\n\u003cp>There aren’t any drugs to treat Noonan syndrome, or many other developmental syndromes like it.\u003c/p>\n\u003cp>Understanding how a child with Noonan syndrome will develop can help health care providers figure out what medical problems they may face, Gelb said. But the algorithm isn’t likely to replace a genetic test, he said — which doctors can undertake easily if they notice something off in a particular region of a fetus’ neck.\u003c/p>\n\u003cp>“I don’t know why they undertook this, exactly,” he said of FDNA’s work. “It’s inconceivable to me that one wouldn’t send off the panel testing and figure out which one it actually is.” Even in low-resource countries — at least in those with a medical geneticist — such genetic testing is becoming more widely available, he said.\u003c/p>\n\u003cp>Gelb also pointed out that the paper only used a set of images of young children — a choice that may have set the algorithm up for success. “The facial features are most obvious in a toddler or young child, and it can kind of melt away in adolescence by the time they hit adulthood,” he said.\u003c/p>\n\u003cp>He acknowledged that the algorithm’s success rate, however, is “impressive” and could be especially useful for clinicians who don’t have hyper-specialized knowledge about a given genetic condition.\u003c/p>\n\u003cp>And using a tool like FDNA’s could show clinicians what genes they should ask labs to test, Gurovich suggested. “If you consider the phenotype properly, you are able to increase your odds of a diagnosis,” he said — something that he said humans can’t quite do.\u003c/p>\n\u003cp>“There are geneticists that have tried to do this. They couldn’t. We can.”\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\u003cem>This \u003ca href=\"https://www.statnews.com/2019/01/07/algorithm-spot-genetic-mutation-photo/\">story\u003c/a> was originally published by STAT, an online publication of Boston Globe Media that covers health, medicine, and scientific discovery.\u003c/em>\u003c/p>\n\n",
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"excerpt": "Some people’s faces, or even just a photo of them, hint at the genes they carry. According to a study out today, a new algorithm can predict not only whether they carry a genetic mutation, but which genes were mutated.\r\n\r\nThe study, published Monday in Nature Medicin",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>\u003c/p>\u003cp>\u003cspan class=\"utils-parseShortcode-shortcodes-__dropcapShortcode__dropcap\">S\u003c/span>\u003c/p>\u003cp>ome people’s faces — or even just a photo of them — hint at the genes they carry. And now, an algorithm can predict not only whether they carry a genetic mutation, but which genes were mutated.\u003c/p>\n\u003cp>The \u003ca href=\"https://www.nature.com/articles/s41591-018-0279-0\">study\u003c/a>, published Monday in Nature Medicine, is the latest from a Boston-based company called FDNA, one of a \u003ca href=\"https://www.statnews.com/2017/04/10/facial-recognition-genetic-disorders/\">few organizations creating software\u003c/a> that can help physicians diagnose genetic syndromes based just on a face — and may serve an important validation of the company’s technology, said Yaron Gurovich, the company’s chief technology officer.\u003c/p>\n\u003cp>“We went for this high-impact journal to prove beyond any doubt that this technology is good, it performs as we say, we can stand behind it, and now it opens a lot of doors to publish more,” he said.\u003c/p>\n\u003cp>The study itself is a collection of experiments testing how the results of algorithms — FDNA refers to them as DeepGestalt — stack up against clinicians’ diagnoses. In one of the experiments, DeepGestalt’s performance was better than random chance when picking which of five genetic mutations might be causing a condition called Noonan syndrome. It was correct 64 percent of the time, far more than the 20 percent success rate that would be expected from guesswork.\u003c/p>\n\u003cp>“This is new — we’ve never published something like this before,” Gurovich said.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>Gurovich is quick to say that the tool isn’t specifically or only for Noonan syndrome. His team chose the condition because there are already published studies about how well humans can distinguish between the various faces associated with it. FDNA is already working on another paper Gurovich said will show that the tool can be used more broadly. It’s going through the peer review process, he said, but a \u003ca href=\"https://www.biorxiv.org/content/early/2018/11/21/473306\">preprint version\u003c/a> is available.\u003c/p>\n\u003caside class=\"pullquote alignright\">‘This is new — we’ve never published something like this before.’\u003ccite>Yaron Gurovich, FDNA\u003c/cite>\u003c/aside>\n\u003cp>One expert on Noonan syndrome, Dr. Bruce Gelb, the director of the Mindich Child Health and Development Institute and a professor at the Icahn School of Medicine at Mount Sinai, cautioned that being able to pick apart a person’s genotype based on facial features is not generally going to be useful for people with the condition.\u003c/p>\n\u003cp>Noonan syndrome comes with a variety of symptoms, including difficulty learning, facial appearance, short stature, and heart issues — including issues with valves or the muscles of the heart itself. A few have a very high risk of leukemia.\u003c/p>\n\u003cp>Some children with Noonan syndrome attend special education classes; others develop typically and can attend mainstream classes. Many can live independently when they’re adults. “It varies a lot,” Gelb said.\u003c/p>\n\u003cp>The genetic cause of Noonan syndrome can vary, too. Mutations in a few different genes can lead to the condition; some mutations cause more serious problems than others. All of the genes, however, are linked to one vital biochemical pathway. Gelb and his research group \u003ca href=\"https://www.nature.com/articles/ng772.epdf?referrer_access_token=pyqbUoC1N6pu4ONrbf7p-dRgN0jAjWel9jnR3ZoTv0N_aEXfBZJ5UdikqtmfwCNXtbaW16rct1gXy0ybOILq30HDNTADZng2FuE6EIQ5rZUCeTxb0IcHHWK4FYeWQUzl1RC37x8AUQ5VhWgJ_gCtuexxd6Hbv9Jdi_kTnCSJ58A%3D&tracking_referrer=www.statnews.com\">have discovered\u003c/a> \u003ca href=\"https://www.nature.com/articles/ng1939.epdf?referrer_access_token=YGvl4Y4X_QshFYTfu2YjQ9RgN0jAjWel9jnR3ZoTv0Mrh-TZl36dLirUZe-74nzZOxlFsdIHF50ddu1dNrJfeaq9wkfjaVZoRTGs8sbI39nA6vpr1CpXKLQdwf7hvAQbSEiKx9tRYNbP-HvhG0GxWgTtRX2Ai6LzUREdlZecehg%3D&tracking_referrer=www.statnews.com\">some of them\u003c/a>.\u003c/p>\n\u003cp>For example, children whose RAS1 gene is mutated almost always get hypertrophic cardiomyopathy, a condition in which the muscles of the heart get thick, making it difficult for the heart to pump normally. Children with mutations in a gene called KRAS have some of the most severe forms of the syndrome and some of the worst neurological and heart outcomes.\u003c/p>\n\u003cp>There aren’t any drugs to treat Noonan syndrome, or many other developmental syndromes like it.\u003c/p>\n\u003cp>Understanding how a child with Noonan syndrome will develop can help health care providers figure out what medical problems they may face, Gelb said. But the algorithm isn’t likely to replace a genetic test, he said — which doctors can undertake easily if they notice something off in a particular region of a fetus’ neck.\u003c/p>\n\u003cp>“I don’t know why they undertook this, exactly,” he said of FDNA’s work. “It’s inconceivable to me that one wouldn’t send off the panel testing and figure out which one it actually is.” Even in low-resource countries — at least in those with a medical geneticist — such genetic testing is becoming more widely available, he said.\u003c/p>\n\u003cp>Gelb also pointed out that the paper only used a set of images of young children — a choice that may have set the algorithm up for success. “The facial features are most obvious in a toddler or young child, and it can kind of melt away in adolescence by the time they hit adulthood,” he said.\u003c/p>\n\u003cp>He acknowledged that the algorithm’s success rate, however, is “impressive” and could be especially useful for clinicians who don’t have hyper-specialized knowledge about a given genetic condition.\u003c/p>\n\u003cp>And using a tool like FDNA’s could show clinicians what genes they should ask labs to test, Gurovich suggested. “If you consider the phenotype properly, you are able to increase your odds of a diagnosis,” he said — something that he said humans can’t quite do.\u003c/p>\n\u003cp>“There are geneticists that have tried to do this. They couldn’t. We can.”\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\u003cem>This \u003ca href=\"https://www.statnews.com/2019/01/07/algorithm-spot-genetic-mutation-photo/\">story\u003c/a> was originally published by STAT, an online publication of Boston Globe Media that covers health, medicine, and scientific discovery.\u003c/em>\u003c/p>\n\n\u003c/div>\u003c/p>",
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"content": "\u003cp>\u003cem>\u003ca href=\"https://twitter.com/jetjocko\" target=\"_blank\" rel=\"noopener noreferrer\">Adam Rogers\u003c/a> is a Senior Correspondent for Wired and the author of “Proof: The Science of Booze.” He recently sat down with KQED’s Danielle Venton to talk about the science of hangovers. And yes, they were at a bar. These questions and answers have been edited for length and clarity.\u003c/em>\u003c/p>\n\u003cp>\u003cstrong>Let’s get right to it: Can you take anything \u003cem>before\u003c/em> you drink to prevent a hangover?\u003c/strong>\u003c/p>\n\u003cp>There’s nothing anyone has discovered that you can eat before you go out that you can drink as much as you want and not get a hangover. There’s one molecule derived from a plant called Hovenia, the oriental raisin, that \u003ca href=\"https://www.newscientist.com/article/dn21337-chinese-tree-extract-stops-rats-getting-drunk/\" target=\"_blank\" rel=\"noopener noreferrer\">seems to actually work\u003c/a> in people to lessen the effects of alcohol and to lessen the effects of a hangover. Nobody’s really done the kind of tests in people to figure out how best to administer it and how it works. There have been other compounds that have shown smaller effects; \u003ca href=\"https://www.kqed.org/science/25567/how-science-can-help-prevent-a-bad-hangover\" target=\"_blank\" rel=\"noopener noreferrer\">prickly pear is one\u003c/a>.\u003c/p>\n\u003cp>\u003cstrong>But still, if you have enough alcohol, you’re getting a hangover no matter what.\u003c/strong>\u003c/p>\n\u003cp>Yeah, that’s a true thing.\u003c/p>\n\u003cp>\u003cstrong>Can you prevent a hangover by drinking one type of alcohol over another? \u003c/strong>\u003c/p>\n\u003cp>Mostly it does not matter what you drink, because it really seems to be a matter of quantity. There is some research that says some alcohols like brown liquors will give you a worse hangover or at least a hangover of a different character than a clear alcohol like gin, or especially vodka, will.\u003c/p>\n\u003cp>Pure vodka is only ethanol and water, with none of the moleclues called congeners that give different liquors various colors, smells and tastes. Some research has shown congeners can make a hangover worse, but nobody knows which congeners or what the mechanism is.\u003c/p>\n\u003cp>https://www.youtube.com/watch?v=HKwNHpPSzP0\u003c/p>\n\u003cp>\u003cstrong>But wait. What is a hangover, anyway? Do we know what alcohol does to the body to make you feel like you have the flu?\u003c/strong>\u003c/p>\n\u003cp>The flu’s the right parallel to draw, because the best science that’s there now — and there’s not that much of it — says that a hangover is an inflammatory response. Why it does that, nobody is sure. One of the things people are reasonably sure of is that you start to show signs of a hangover when your blood alcohol level goes back down to zero.\u003c/p>\n\u003cp>It is true that the kind of damage that alcohol inflicts on the liver if you drink a lot over time is inflammatory damage — when you’re on the way to cirrhosis.\u003c/p>\n\u003cp>There’s a hypothesis, though it’s not well worked out, that a hangover is related to the toxicity of methanol. The alcohol we drink is ethanol, but in some alcoholic drinks there’s still a tiny bit of methanol. Methanol messes up the body’s ability to metabolize oxygen; when they talk about cheap alcohol making you go blind, they’re talking about methanol.\u003c/p>\n\u003cp>[ad fullwidth]\u003cbr>\nBut it’s a real bummer that there’s actually very little scientists understand confidently about what causes hangovers. Of all the psychoactive chemicals that people consume recreationally, alcohol is one of the least understood. People understand marijuana way better than they understand booze.\u003c/p>\n\u003cp>\u003cstrong>The effects of alcoholism are terrible on society. And it is no fun to have a hangover, but being out with friends, drinking — we have whiskey in front of us right now — it’s really fun. Why are humans so drawn to alcohol?\u003c/strong>\u003c/p>\n\u003cp>There aren’t a lot of ways that people have to chemically modulate their own feelings. When we find one, we tend to glom onto it. People have been consuming alcohol for at least 10,000 years. It might be the reason we started farming, is to have grains so we can make beer as well as bread.\u003c/p>\n\u003cp>\u003cstrong>So we’re talking about the founding of civilization.\u003c/strong>\u003c/p>\n\u003cp>We are talking about the founding of civilization. There’s a Faulkner quote, “Civilization is distillation.” And I think he meant it as a metaphor, but I actually like it as more literal-minded. Once you learn how to distill, that’s one of the first examples of scientists having a real impact on the universe around us, literally how we feel and how we see things.\u003c/p>\n\u003cp>\u003cstrong>Any last advice for drinkers on New Year’s Eve? \u003c/strong>\u003c/p>\n\u003cp>To the extent that I would give advice, here it is: Try to remember to drink a glass of water or seltzer in between each drink. You’re going to drink, okay, but you want that experience to slow down, because alcohol will screw with your sense of time. Also, the reason you’re out having those drinks is for the theater of it, to experience the feelings that the alcohol gives you, and to meet with your friends. You don’t want to rush that.\u003c/p>\n\u003cp>\u003c/p>\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>\u003cem>\u003ca href=\"https://twitter.com/jetjocko\" target=\"_blank\" rel=\"noopener noreferrer\">Adam Rogers\u003c/a> is a Senior Correspondent for Wired and the author of “Proof: The Science of Booze.” He recently sat down with KQED’s Danielle Venton to talk about the science of hangovers. And yes, they were at a bar. These questions and answers have been edited for length and clarity.\u003c/em>\u003c/p>\n\u003cp>\u003cstrong>Let’s get right to it: Can you take anything \u003cem>before\u003c/em> you drink to prevent a hangover?\u003c/strong>\u003c/p>\n\u003cp>There’s nothing anyone has discovered that you can eat before you go out that you can drink as much as you want and not get a hangover. There’s one molecule derived from a plant called Hovenia, the oriental raisin, that \u003ca href=\"https://www.newscientist.com/article/dn21337-chinese-tree-extract-stops-rats-getting-drunk/\" target=\"_blank\" rel=\"noopener noreferrer\">seems to actually work\u003c/a> in people to lessen the effects of alcohol and to lessen the effects of a hangover. Nobody’s really done the kind of tests in people to figure out how best to administer it and how it works. There have been other compounds that have shown smaller effects; \u003ca href=\"https://www.kqed.org/science/25567/how-science-can-help-prevent-a-bad-hangover\" target=\"_blank\" rel=\"noopener noreferrer\">prickly pear is one\u003c/a>.\u003c/p>\n\u003cp>\u003cstrong>But still, if you have enough alcohol, you’re getting a hangover no matter what.\u003c/strong>\u003c/p>\n\u003cp>Yeah, that’s a true thing.\u003c/p>\n\u003cp>\u003cstrong>Can you prevent a hangover by drinking one type of alcohol over another? \u003c/strong>\u003c/p>\n\u003cp>Mostly it does not matter what you drink, because it really seems to be a matter of quantity. There is some research that says some alcohols like brown liquors will give you a worse hangover or at least a hangover of a different character than a clear alcohol like gin, or especially vodka, will.\u003c/p>\n\u003cp>Pure vodka is only ethanol and water, with none of the moleclues called congeners that give different liquors various colors, smells and tastes. Some research has shown congeners can make a hangover worse, but nobody knows which congeners or what the mechanism is.\u003c/p>\u003c/p>\u003cp>\u003cspan class='utils-parseShortcode-shortcodes-__youtubeShortcode__embedYoutube'>\n \u003cspan class='utils-parseShortcode-shortcodes-__youtubeShortcode__embedYoutubeInside'>\n \u003ciframe\n loading='lazy'\n class='utils-parseShortcode-shortcodes-__youtubeShortcode__youtubePlayer'\n type='text/html'\n src='//www.youtube.com/embed/HKwNHpPSzP0'\n title='//www.youtube.com/embed/HKwNHpPSzP0'\n allowfullscreen='true'\n style='border:0;'>\u003c/iframe>\n \u003c/span>\n \u003c/span>\u003c/p>\u003cp>\u003cp>\u003cstrong>But wait. What is a hangover, anyway? Do we know what alcohol does to the body to make you feel like you have the flu?\u003c/strong>\u003c/p>\n\u003cp>The flu’s the right parallel to draw, because the best science that’s there now — and there’s not that much of it — says that a hangover is an inflammatory response. Why it does that, nobody is sure. One of the things people are reasonably sure of is that you start to show signs of a hangover when your blood alcohol level goes back down to zero.\u003c/p>\n\u003cp>It is true that the kind of damage that alcohol inflicts on the liver if you drink a lot over time is inflammatory damage — when you’re on the way to cirrhosis.\u003c/p>\n\u003cp>There’s a hypothesis, though it’s not well worked out, that a hangover is related to the toxicity of methanol. The alcohol we drink is ethanol, but in some alcoholic drinks there’s still a tiny bit of methanol. Methanol messes up the body’s ability to metabolize oxygen; when they talk about cheap alcohol making you go blind, they’re talking about methanol.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cbr>\nBut it’s a real bummer that there’s actually very little scientists understand confidently about what causes hangovers. Of all the psychoactive chemicals that people consume recreationally, alcohol is one of the least understood. People understand marijuana way better than they understand booze.\u003c/p>\n\u003cp>\u003cstrong>The effects of alcoholism are terrible on society. And it is no fun to have a hangover, but being out with friends, drinking — we have whiskey in front of us right now — it’s really fun. Why are humans so drawn to alcohol?\u003c/strong>\u003c/p>\n\u003cp>There aren’t a lot of ways that people have to chemically modulate their own feelings. When we find one, we tend to glom onto it. People have been consuming alcohol for at least 10,000 years. It might be the reason we started farming, is to have grains so we can make beer as well as bread.\u003c/p>\n\u003cp>\u003cstrong>So we’re talking about the founding of civilization.\u003c/strong>\u003c/p>\n\u003cp>We are talking about the founding of civilization. There’s a Faulkner quote, “Civilization is distillation.” And I think he meant it as a metaphor, but I actually like it as more literal-minded. Once you learn how to distill, that’s one of the first examples of scientists having a real impact on the universe around us, literally how we feel and how we see things.\u003c/p>\n\u003cp>\u003cstrong>Any last advice for drinkers on New Year’s Eve? \u003c/strong>\u003c/p>\n\u003cp>To the extent that I would give advice, here it is: Try to remember to drink a glass of water or seltzer in between each drink. You’re going to drink, okay, but you want that experience to slow down, because alcohol will screw with your sense of time. Also, the reason you’re out having those drinks is for the theater of it, to experience the feelings that the alcohol gives you, and to meet with your friends. You don’t want to rush that.\u003c/p>\n\u003cp>\u003c/p>\n\u003c/div>\u003c/p>",
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