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"content": "\u003cp>Kate Bowler's new memoir, \u003cem>Everything Happens for a Reason And Other Lies I've Loved\u003c/em>, is a funny, intimate portrait of living in that nether space between life and death. In it, she shares her experiences with incurable stage 4 cancer and gives advice on what not to say to those who are terminally ill.\u003c/p>\n\u003caside class=\"alignright\">\n\u003cul>3 things not say to someone terminally ill, from author Kate Bowler...\n\u003cli>'Everything happens for a reason.'\u003c/li>\u003cli>'How are the treatments going?'\n\u003c/li>\u003cli>How are you really?\u003c/li>\u003c/ul>\n\u003c/aside>\n\u003cp>Bowler is also the host of\u003ca href=\"https://www.npr.org/podcasts/583447646/everything-happens\" target=\"_blank\" rel=\"noopener\"> Everything Happens\u003c/a>, a new podcast.\u003c/p>\n\u003cp>She writes that sometimes silence is the best response: \"The truth is that no one knows what to say. It's awkward. Pain is awkward. Tragedy is awkward. People's weird, suffering bodies are awkward. But take the advice of one man, who wrote to me with his policy: Show up and shut up.\"\u003c/p>\n\u003cp>\u003cstrong>Interview Highlights\u003c/strong>\u003c/p>\n\u003cp>\u003cstrong>On why she wrote Everything Happens For A Reason\u003c/strong>\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>Suddenly at [age] 35, I get this stage 4 cancer diagnosis, and it's just like a bomb went off and everything around me is debris. And I'm thinking, \"Oh my gosh, did I actually maybe expect that everything was going to work out for me?\" And so I wrote the book more like a theological excavation project, like I was just trying to get down to the studs of what I really expected from my life. 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I was trying to learn how to give up really quickly, like looking at my beautiful husband and just immediately all the stuff you're supposed to say, which is just like, \"I have loved you forever,\" and \"All I want for you is love.\"\u003c/p>\n\u003cp>... You have these impossible thoughts like, \"You will live without me,\" and \"Please take care of our kid.\" And like you're trying to do all that hard work and then in the same moment, they're trying to rush in and say, \"We're going to fight this.\" There's all these plans they want to pour their certainty in, to remake the foundation. And there's this, kind of, almost terrible exchange, where you're trying to remake the world as it was. But it's all come apart.\u003c/p>\n\u003cp>\u003cstrong>On whether she has had conversations with her 4-year-old son about death\u003c/strong>\u003c/p>\n\u003cp>He is entirely impervious to all of this, in the best way. But I do think the thing that has radically changed is I really was, before, trying to create this little bubble around him and us, 'cause I thought, like, \"It's my job to protect you,\" and then I realized that I would be the worst thing that happened to him if this went badly.\u003c/p>\n\u003cp>So then I thought like, \"OK, parenting strategy change.\" And I thought, 'Well, if I can just teach you that there is still beauty in others in the midst of pain, then like, that's my job.\" So we work a lot on like, \"How are you feeling?\" like, \"I feel frustrated.\" And then getting him to notice the feelings of others.\u003c/p>\n\u003cp>\u003cstrong>On how she has learned to cope with negative news about her diagnosis\u003c/strong>\u003c/p>\n\u003cp>Well I have rules for when things are too sad, 'cause sometimes, just the reality of things really feels like an avalanche, and it's just going to sweep everything away. So I do make rules for the day, like don't talk about sad things after 9 p.m., so I try to make my day a little gentler. I try to make other people's day a little gentler. The other thing I do is I try really stupid stuff, like I got terrible news a couple months ago, which thankfully turned out to be a medical error.\u003c/p>\n\u003cp>It was a scan and it looked brutal, but I spent that week thinking like, \"This is my last year for sure.\" And it was weird because the next day, I turned to a friend and I said, \"Would you like to go visit the world's largest Ukrainian sausage?\" And he was like, \"Oh, I'm in.\"\u003c/p>\n\u003cp>\u003cstrong>On her list of things not to say to someone with terminal cancer, including \"How are the treatments going and how are you really?\" [book excerpt]\u003c/strong>\u003c/p>\n\u003cp>This is the toughest one of all. I can hear you trying to be in my world and be on my side. But picture the worst thing that's ever happened to you. Got it? Now try to put it in a sentence. Now say it aloud 50 times a day. Does your head hurt? Do you feel sad? Me too. So let's just see if I want to talk about it today, because sometimes I do and sometimes I want a hug and a recap of American Ninja Warrior.\u003c/p>\n\u003cp>\u003cem>Jeffrey Pierre and Miranda Kennedy produced and edited this interview for broadcast. Sydnee Monday and April Fulton adapted it for the Web.\u003c/em>\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>Copyright 2018 NPR. To see more, visit \u003ca href=\"http://www.npr.org/\" target=\"_blank\" rel=\"noopener\">http://www.npr.org/\u003c/a>.\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>Kate Bowler's new memoir, \u003cem>Everything Happens for a Reason And Other Lies I've Loved\u003c/em>, is a funny, intimate portrait of living in that nether space between life and death. In it, she shares her experiences with incurable stage 4 cancer and gives advice on what not to say to those who are terminally ill.\u003c/p>\n\u003caside class=\"alignright\">\n\u003cul>3 things not say to someone terminally ill, from author Kate Bowler...\n\u003cli>'Everything happens for a reason.'\u003c/li>\u003cli>'How are the treatments going?'\n\u003c/li>\u003cli>How are you really?\u003c/li>\u003c/ul>\n\u003c/aside>\n\u003cp>Bowler is also the host of\u003ca href=\"https://www.npr.org/podcasts/583447646/everything-happens\" target=\"_blank\" rel=\"noopener\"> Everything Happens\u003c/a>, a new podcast.\u003c/p>\n\u003cp>She writes that sometimes silence is the best response: \"The truth is that no one knows what to say. It's awkward. Pain is awkward. Tragedy is awkward. People's weird, suffering bodies are awkward. But take the advice of one man, who wrote to me with his policy: Show up and shut up.\"\u003c/p>\n\u003cp>\u003cstrong>Interview Highlights\u003c/strong>\u003c/p>\n\u003cp>\u003cstrong>On why she wrote Everything Happens For A Reason\u003c/strong>\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>Suddenly at [age] 35, I get this stage 4 cancer diagnosis, and it's just like a bomb went off and everything around me is debris. And I'm thinking, \"Oh my gosh, did I actually maybe expect that everything was going to work out for me?\" And so I wrote the book more like a theological excavation project, like I was just trying to get down to the studs of what I really expected from my life. And I think I was a lot more sure than I realized ... maybe that I was the architect of my own life, that I could overcome anything with a little pluck and determination.\u003c/p>\n\u003cp>\u003cstrong>On how a cancer diagnosis changed her outlook on life\u003c/strong>\u003c/p>\n\u003cp>I kind of pictured my life like it was this life enhancement project, and like my life is like a bucket and I'm supposed to put all the things in the bucket. And the whole purpose is to figure out how to have as many good things coexisting at the same time.And then when everything falls apart, you totally have to switch imagination, like maybe instead, life is just vine to vine. And you're like grabbing onto something, and you're just hoping for dear life it doesn't break.\u003c/p>\n\u003cp>\u003cstrong>On how that diagnosis affected her relationship to friends and family\u003c/strong>\u003c/p>\n\u003cp>I went from feeling like a normal person to all of a sudden, like this spaghetti bowl of cancer. I was trying to learn how to give up really quickly, like looking at my beautiful husband and just immediately all the stuff you're supposed to say, which is just like, \"I have loved you forever,\" and \"All I want for you is love.\"\u003c/p>\n\u003cp>... You have these impossible thoughts like, \"You will live without me,\" and \"Please take care of our kid.\" And like you're trying to do all that hard work and then in the same moment, they're trying to rush in and say, \"We're going to fight this.\" There's all these plans they want to pour their certainty in, to remake the foundation. And there's this, kind of, almost terrible exchange, where you're trying to remake the world as it was. But it's all come apart.\u003c/p>\n\u003cp>\u003cstrong>On whether she has had conversations with her 4-year-old son about death\u003c/strong>\u003c/p>\n\u003cp>He is entirely impervious to all of this, in the best way. But I do think the thing that has radically changed is I really was, before, trying to create this little bubble around him and us, 'cause I thought, like, \"It's my job to protect you,\" and then I realized that I would be the worst thing that happened to him if this went badly.\u003c/p>\n\u003cp>So then I thought like, \"OK, parenting strategy change.\" And I thought, 'Well, if I can just teach you that there is still beauty in others in the midst of pain, then like, that's my job.\" So we work a lot on like, \"How are you feeling?\" like, \"I feel frustrated.\" And then getting him to notice the feelings of others.\u003c/p>\n\u003cp>\u003cstrong>On how she has learned to cope with negative news about her diagnosis\u003c/strong>\u003c/p>\n\u003cp>Well I have rules for when things are too sad, 'cause sometimes, just the reality of things really feels like an avalanche, and it's just going to sweep everything away. So I do make rules for the day, like don't talk about sad things after 9 p.m., so I try to make my day a little gentler. I try to make other people's day a little gentler. The other thing I do is I try really stupid stuff, like I got terrible news a couple months ago, which thankfully turned out to be a medical error.\u003c/p>\n\u003cp>It was a scan and it looked brutal, but I spent that week thinking like, \"This is my last year for sure.\" And it was weird because the next day, I turned to a friend and I said, \"Would you like to go visit the world's largest Ukrainian sausage?\" And he was like, \"Oh, I'm in.\"\u003c/p>\n\u003cp>\u003cstrong>On her list of things not to say to someone with terminal cancer, including \"How are the treatments going and how are you really?\" [book excerpt]\u003c/strong>\u003c/p>\n\u003cp>This is the toughest one of all. I can hear you trying to be in my world and be on my side. But picture the worst thing that's ever happened to you. Got it? Now try to put it in a sentence. Now say it aloud 50 times a day. Does your head hurt? Do you feel sad? Me too. So let's just see if I want to talk about it today, because sometimes I do and sometimes I want a hug and a recap of American Ninja Warrior.\u003c/p>\n\u003cp>\u003cem>Jeffrey Pierre and Miranda Kennedy produced and edited this interview for broadcast. Sydnee Monday and April Fulton adapted it for the Web.\u003c/em>\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>Copyright 2018 NPR. To see more, visit \u003ca href=\"http://www.npr.org/\" target=\"_blank\" rel=\"noopener\">http://www.npr.org/\u003c/a>.\u003c/p>\n\n\u003c/div>\u003c/p>",
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"content": "\u003cp>Getting a \u003ca href=\"http://www.sfgate.com/health/article/Helen-Sanford-Diller-fund-UCSF-cancer-center-3296458.php\" target=\"_blank\" rel=\"noopener\">$500 million donation\u003c/a> is the stuff of dreams for a university head. In January 2017, when UCSF announced that the Helen Diller Foundation was contributing a half-billion dollars, school Chancellor Sam Hawgood said, “I have to pinch myself every time I think about it.”\u003c/p>\n\u003cp>Hawgood’s going to have to keep pinching. The Helen Diller Foundation has now doubled down on its gift to the university with another $500 million donation. The funds will be used to build a new, state of the art hospital at UCSF's Parnassus Heights campus by 2030. The new hospital will be built on the site currently occupied by the Langley Porter Psychiatric Hospital, which will be torn down. Langley outpatient services will be relocated to a new building in San Francisco's Dogpatch neighborhood; inpatient services will remain somewhere on the Parnassus campus.\u003c/p>\n\u003cp>Hawgood called the donation \"transformative\" and \"beyond my wildest expectations,\" not to mention \"an exhilarating experience.\"\u003c/p>\n\u003cp>\"I couldn’t be more delighted for what it means for the patients we will care for for generations to come,\" he said.\u003c/p>\n\u003cp>The new funds will bring the foundation’s total donations to the university to roughly $1.15 billion, putting the school right at the top of of the \u003ca href=\"https://www.chronicle.com/article/Major-Private-Gifts-to-Higher/128264\" target=\"_blank\" rel=\"noopener\">list\u003c/a> of academic institutions that have received massive funds from a single organization.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>UCSF, part of the University of California system, includes schools of medicine, dentistry, nursing and pharmacy. The entire institution is dedicated to health sciences and biomedicine. Tracing its \u003ca href=\"https://www.ucsf.edu/about/history-1\" target=\"_blank\" rel=\"noopener\">roots\u003c/a> back to 1864, the university has five Nobel Prize winners on staff, and an impressive portfolio of \u003ca href=\"https://www.ucsf.edu/about/achievements\" target=\"_blank\" rel=\"noopener\">scientific achievements\u003c/a>, including the discovery of vitamin E back in 1923 and the co-discovery of HIV in 1983.\u003c/p>\n\u003cp>The new hospital at Parnassus Heights will take over inpatient care now administered in UCSF's Moffitt building, part of the Moffitt-Long Hospital at \u003ca href=\"https://www.google.com/maps/place/505+Parnassus+Ave,+San+Francisco,+CA+94143/@37.7630895,-122.4600031,17z/data=!3m1!4b1!4m5!3m4!1s0x8085875762cbdad5:0x30442fa9192ab3e1!8m2!3d37.7630895!4d-122.4578144\" target=\"_blank\" rel=\"noopener\">505 Parnassus Avenue\u003c/a>. Without retrofitting, Moffitt would no longer be able to house patients after 2030, according to state law. The new hospital will also be part of UCSF Health, the health care network \u003ca href=\"https://www.ucsf.edu/news/2015/10/136716/ucsf-health-system-expand-care-throughout-bay-area-and-beyond\" target=\"_blank\" rel=\"noopener\">launched\u003c/a> by the university in 2015.\u003c/p>\n\u003cp>In 2003, the university opened a more modern campus in San Francisco's Mission Bay neighborhood. The school is just now beginning a year-long planning process to upgrade the Parnassus Heights site. Renovations are part of a $5 billion fundraising campaign, which includes the Diller donation for the hospital.\u003c/p>\n\u003cp>\"The majority of the campus was built between 1950 and the mid-1970s. So the facilities are showing their age,\" Hawgood said. \"We’ll be looking to refurbish many of the research buildings ... Science has moved on; the need for different kinds of facilities are also required.\"\u003c/p>\n\u003cp>\u003cstrong>Diller Largesse\u003c/strong>\u003c/p>\n\u003cp>UCSF pushed back the announcement about the donation a couple of days out of respect for the Diller family, who saw its partriarch, Sanford Diller, \u003ca href=\"https://www.sfchronicle.com/business/article/Real-estate-developer-philanthropist-Sanford-12553646.php\" target=\"_blank\" rel=\"noopener\">die\u003c/a> last Friday at the age of 89. Diller was a billionaire who made his money as founder of the Prometheus Real Estate Group, one of the largest owners of apartment buildings in the Bay Area.\u003c/p>\n\u003cp>He and his wife, Helen, who died in 2015, established the Helen Diller Family Foundation in 1999. In 2003, the foundation donated $35 million to create the Helen Diller Family Comprehensive Care Center, at UCSF's Mission Bay Campus. Back then, $35 million was the largest gift by a single donor in UCSF history. But that amount was dwarfed by the family's whopping $500 million donation in late 2015. At the time, it was matched only by \u003ca href=\"https://www.philanthropy.com/factfile/gifts_detail?GiftDonorJoin_a_DonorID=PGDON1706\" target=\"_blank\" rel=\"noopener\">$500 million gifts\u003c/a> to each of two Oregon universities from Nike co-founder \u003ca href=\"https://www.philanthropy.com/factfile/gifts_detail?GiftDonorJoin_a_DonorID=PGDON1706\" target=\"_blank\" rel=\"noopener\">Phil Knight\u003c/a>. (Knight also gave $400 million to Stanford in 2016.)\u003c/p>\n\u003cp>A billion-dollars-plus to a single educational institution, albeit a public one, did get us thinking about the issue of\u003ca href=\"https://www.google.com/search?q=effective+philanthrop\" target=\"_blank\" rel=\"noopener\"> effective philanthropy\u003c/a>. So we reached out for comment to \u003ca href=\"https://www.princeton.edu/news/2017/02/16/qa-singer-philosopher-his-craft-and-practicing-it-princeton\" target=\"_blank\" rel=\"noopener\">Peter Singer\u003c/a>, a philosopher, author and professor of bioethics at Princeton University, who has taken a utilitarian approach to charitable giving.\u003c/p>\n\u003cp>\"No, it's clearly not the best use of the money,\" he wrote in an email. \"Health is a vital area for philanthropy, but not in an area that is already, by world standards, extraordinarily well-served ... .\"\u003c/p>\n\u003cp>Why \u003cem>have\u003c/em> the Dillers showered so much largesse on UCSF?\u003c/p>\n\u003cp>\"We are native San Franciscans, and are proud to give back to our community,” \u003ca href=\"https://www.ucsf.edu/news/2003/10/4698/35-million-gift-supports-construction-helen-diller-family-cancer-researc\" target=\"_blank\" rel=\"noopener\">said\u003c/a> Helen Diller, in 2003. “Our family is extremely enthused about cancer research at UCSF. ... (W)e have been presented with the joy of participating in the development of an entirely new section of this very beautiful city.”\u003c/p>\n\u003cp>She repeated her feelings of attachment to the city, and to UCSF, in a 2009 interview with the \u003ca href=\"http://www.sfgate.com/health/article/Helen-Sanford-Diller-fund-UCSF-cancer-center-3296458.php\" target=\"_blank\" rel=\"noopener\">San Francisco Chronicle\u003c/a>, which provides a good window into some of her motivations. \"I was born in San Francisco at Mount Zion hospital. UCSF is known to have the finest scientists and doctors,\" she said.\u003c/p>\n\u003cp>She continued: \"There is a Hebrew expression, '\u003cem>Tikkun olam\u003c/em>,' which means to repair the world. My parents did things in a small way because that is what they could do. Now we are doing what we are able to do.\"\u003c/p>\n\u003cp>The bulk of the initial $500 million Diller donation went toward retaining and recruiting faculty and supporting students at UCSF’s four professional schools, some of it in the form of scholarships. UCSF also created a discretionary $100 million \"innovation fund.\"\u003c/p>\n\u003cp>The family is also known for contributing to Jewish causes, funding UC Berkeley and UC Santa Cruz Jewish studies programs, renovating the \u003ca href=\"https://en.wikipedia.org/wiki/Julius_Kahn_(congressman)\" target=\"_blank\" rel=\"noopener\">Julius Kahn\u003c/a> in the Presidio, and a leadership \u003ca href=\"http://dillerteenfellows.org/en/\" target=\"_blank\" rel=\"noopener\">program\u003c/a> for Jewish teenagers.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>In recognition of the latest donation, UCSF has renamed its complex of medical buildings on campus as the UCSF Helen Diller Medical Center at Parnassus Heights.\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>Getting a \u003ca href=\"http://www.sfgate.com/health/article/Helen-Sanford-Diller-fund-UCSF-cancer-center-3296458.php\" target=\"_blank\" rel=\"noopener\">$500 million donation\u003c/a> is the stuff of dreams for a university head. In January 2017, when UCSF announced that the Helen Diller Foundation was contributing a half-billion dollars, school Chancellor Sam Hawgood said, “I have to pinch myself every time I think about it.”\u003c/p>\n\u003cp>Hawgood’s going to have to keep pinching. The Helen Diller Foundation has now doubled down on its gift to the university with another $500 million donation. The funds will be used to build a new, state of the art hospital at UCSF's Parnassus Heights campus by 2030. The new hospital will be built on the site currently occupied by the Langley Porter Psychiatric Hospital, which will be torn down. Langley outpatient services will be relocated to a new building in San Francisco's Dogpatch neighborhood; inpatient services will remain somewhere on the Parnassus campus.\u003c/p>\n\u003cp>Hawgood called the donation \"transformative\" and \"beyond my wildest expectations,\" not to mention \"an exhilarating experience.\"\u003c/p>\n\u003cp>\"I couldn’t be more delighted for what it means for the patients we will care for for generations to come,\" he said.\u003c/p>\n\u003cp>The new funds will bring the foundation’s total donations to the university to roughly $1.15 billion, putting the school right at the top of of the \u003ca href=\"https://www.chronicle.com/article/Major-Private-Gifts-to-Higher/128264\" target=\"_blank\" rel=\"noopener\">list\u003c/a> of academic institutions that have received massive funds from a single organization.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>UCSF, part of the University of California system, includes schools of medicine, dentistry, nursing and pharmacy. The entire institution is dedicated to health sciences and biomedicine. Tracing its \u003ca href=\"https://www.ucsf.edu/about/history-1\" target=\"_blank\" rel=\"noopener\">roots\u003c/a> back to 1864, the university has five Nobel Prize winners on staff, and an impressive portfolio of \u003ca href=\"https://www.ucsf.edu/about/achievements\" target=\"_blank\" rel=\"noopener\">scientific achievements\u003c/a>, including the discovery of vitamin E back in 1923 and the co-discovery of HIV in 1983.\u003c/p>\n\u003cp>The new hospital at Parnassus Heights will take over inpatient care now administered in UCSF's Moffitt building, part of the Moffitt-Long Hospital at \u003ca href=\"https://www.google.com/maps/place/505+Parnassus+Ave,+San+Francisco,+CA+94143/@37.7630895,-122.4600031,17z/data=!3m1!4b1!4m5!3m4!1s0x8085875762cbdad5:0x30442fa9192ab3e1!8m2!3d37.7630895!4d-122.4578144\" target=\"_blank\" rel=\"noopener\">505 Parnassus Avenue\u003c/a>. Without retrofitting, Moffitt would no longer be able to house patients after 2030, according to state law. The new hospital will also be part of UCSF Health, the health care network \u003ca href=\"https://www.ucsf.edu/news/2015/10/136716/ucsf-health-system-expand-care-throughout-bay-area-and-beyond\" target=\"_blank\" rel=\"noopener\">launched\u003c/a> by the university in 2015.\u003c/p>\n\u003cp>In 2003, the university opened a more modern campus in San Francisco's Mission Bay neighborhood. The school is just now beginning a year-long planning process to upgrade the Parnassus Heights site. Renovations are part of a $5 billion fundraising campaign, which includes the Diller donation for the hospital.\u003c/p>\n\u003cp>\"The majority of the campus was built between 1950 and the mid-1970s. So the facilities are showing their age,\" Hawgood said. \"We’ll be looking to refurbish many of the research buildings ... Science has moved on; the need for different kinds of facilities are also required.\"\u003c/p>\n\u003cp>\u003cstrong>Diller Largesse\u003c/strong>\u003c/p>\n\u003cp>UCSF pushed back the announcement about the donation a couple of days out of respect for the Diller family, who saw its partriarch, Sanford Diller, \u003ca href=\"https://www.sfchronicle.com/business/article/Real-estate-developer-philanthropist-Sanford-12553646.php\" target=\"_blank\" rel=\"noopener\">die\u003c/a> last Friday at the age of 89. Diller was a billionaire who made his money as founder of the Prometheus Real Estate Group, one of the largest owners of apartment buildings in the Bay Area.\u003c/p>\n\u003cp>He and his wife, Helen, who died in 2015, established the Helen Diller Family Foundation in 1999. In 2003, the foundation donated $35 million to create the Helen Diller Family Comprehensive Care Center, at UCSF's Mission Bay Campus. Back then, $35 million was the largest gift by a single donor in UCSF history. But that amount was dwarfed by the family's whopping $500 million donation in late 2015. At the time, it was matched only by \u003ca href=\"https://www.philanthropy.com/factfile/gifts_detail?GiftDonorJoin_a_DonorID=PGDON1706\" target=\"_blank\" rel=\"noopener\">$500 million gifts\u003c/a> to each of two Oregon universities from Nike co-founder \u003ca href=\"https://www.philanthropy.com/factfile/gifts_detail?GiftDonorJoin_a_DonorID=PGDON1706\" target=\"_blank\" rel=\"noopener\">Phil Knight\u003c/a>. (Knight also gave $400 million to Stanford in 2016.)\u003c/p>\n\u003cp>A billion-dollars-plus to a single educational institution, albeit a public one, did get us thinking about the issue of\u003ca href=\"https://www.google.com/search?q=effective+philanthrop\" target=\"_blank\" rel=\"noopener\"> effective philanthropy\u003c/a>. So we reached out for comment to \u003ca href=\"https://www.princeton.edu/news/2017/02/16/qa-singer-philosopher-his-craft-and-practicing-it-princeton\" target=\"_blank\" rel=\"noopener\">Peter Singer\u003c/a>, a philosopher, author and professor of bioethics at Princeton University, who has taken a utilitarian approach to charitable giving.\u003c/p>\n\u003cp>\"No, it's clearly not the best use of the money,\" he wrote in an email. \"Health is a vital area for philanthropy, but not in an area that is already, by world standards, extraordinarily well-served ... .\"\u003c/p>\n\u003cp>Why \u003cem>have\u003c/em> the Dillers showered so much largesse on UCSF?\u003c/p>\n\u003cp>\"We are native San Franciscans, and are proud to give back to our community,” \u003ca href=\"https://www.ucsf.edu/news/2003/10/4698/35-million-gift-supports-construction-helen-diller-family-cancer-researc\" target=\"_blank\" rel=\"noopener\">said\u003c/a> Helen Diller, in 2003. “Our family is extremely enthused about cancer research at UCSF. ... (W)e have been presented with the joy of participating in the development of an entirely new section of this very beautiful city.”\u003c/p>\n\u003cp>She repeated her feelings of attachment to the city, and to UCSF, in a 2009 interview with the \u003ca href=\"http://www.sfgate.com/health/article/Helen-Sanford-Diller-fund-UCSF-cancer-center-3296458.php\" target=\"_blank\" rel=\"noopener\">San Francisco Chronicle\u003c/a>, which provides a good window into some of her motivations. \"I was born in San Francisco at Mount Zion hospital. UCSF is known to have the finest scientists and doctors,\" she said.\u003c/p>\n\u003cp>She continued: \"There is a Hebrew expression, '\u003cem>Tikkun olam\u003c/em>,' which means to repair the world. My parents did things in a small way because that is what they could do. Now we are doing what we are able to do.\"\u003c/p>\n\u003cp>The bulk of the initial $500 million Diller donation went toward retaining and recruiting faculty and supporting students at UCSF’s four professional schools, some of it in the form of scholarships. UCSF also created a discretionary $100 million \"innovation fund.\"\u003c/p>\n\u003cp>The family is also known for contributing to Jewish causes, funding UC Berkeley and UC Santa Cruz Jewish studies programs, renovating the \u003ca href=\"https://en.wikipedia.org/wiki/Julius_Kahn_(congressman)\" target=\"_blank\" rel=\"noopener\">Julius Kahn\u003c/a> in the Presidio, and a leadership \u003ca href=\"http://dillerteenfellows.org/en/\" target=\"_blank\" rel=\"noopener\">program\u003c/a> for Jewish teenagers.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>In recognition of the latest donation, UCSF has renamed its complex of medical buildings on campus as the UCSF Helen Diller Medical Center at Parnassus Heights.\u003c/p>\n\n\u003c/div>\u003c/p>",
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"disqusTitle": "A Tiny Pulse of Electricity to the Brain Can Boost Memory",
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"content": "\u003cp>A little electrical brain stimulation can go a long way in boosting memory.\u003c/p>\n\u003cp>The key is to deliver a tiny pulse of electricity to exactly the right place at exactly the right moment, a team \u003ca href=\"http://nature.com/articles/doi:10.1038/s41467-017-02753-0\" target=\"_blank\" rel=\"noopener\">reports\u003c/a> in Tuesday's \u003cem>Nature Communications\u003c/em>.\u003c/p>\n\u003cp>\"We saw a 15 percent improvement in memory,\" says \u003ca href=\"https://psychology.sas.upenn.edu/people/michael-kahana\" target=\"_blank\" rel=\"noopener\">Michael Kahana\u003c/a>, a professor of psychology at the University of Pennsylvania and an author of the study.\u003c/p>\n\u003cp>The approach hints at a new way of treating people with memory problems caused by a brain injury or Alzheimer's disease, Kahana says. But the technology is still far from widespread use.\u003c/p>\n\u003cp>Kahana has spent years trying to understand why the brain often fails to store information we want it to keep.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>\"When we're trying to study a list of items, sometimes the items stick and sometimes we have momentary lapses where we don't seem to remember anything,\" he says.\u003c/p>\n\u003cp>[contextly_sidebar id=\"w3ybK8P4RrrgdzChQHgt9AKIj7mlCTPN\"]\u003c/p>\n\u003cp>Kahana and a team of researchers thought there must be a way to help the brain do better. So they had a computer learn to recognize patterns of electrical activity indicating that the brain was about to have a memory lapse.\u003c/p>\n\u003cp>Then the team had the computer intervene by delivering a pulse of electricity to different areas of the brain just before the lapse was going to occur. And in the area involved in recalling words, the approach worked.\u003c/p>\n\u003cp>\"When we stimulated the left temporal cortex, we found that memory was improved significantly,\" Kahana says. \"When we stimulated other parts of the brain, memory was, by and large, impaired.\"\u003c/p>\n\u003cp>The experiment was done with 25 patients with epilepsy who were in the hospital awaiting surgery to treat their seizures. That meant doctors had already inserted wires into their brains to monitor electrical activity.\u003c/p>\n\u003caside class=\"pullquote aligncenter\">\"We didn't just do this for the sake of science.\"\u003ccite>Michael Sperling, neurologist\u003c/cite>\u003c/aside>\n\u003cp>But epilepsy patients tend to have memory problems and other brain anomalies, says \u003ca href=\"http://hospitals.jefferson.edu/find-a-doctor/s/sperling-michael-r.html\" target=\"_blank\" rel=\"noopener\">Michael Sperling\u003c/a>, an author of the study and director of the Comprehensive Epilepsy Center at Thomas Jefferson University in Philadelphia.\u003c/p>\n\u003cp>\"We still really lack any experiments in people with other conditions to know for certain whether [the treatment] would prove effective or not,\" Sperling says.\u003c/p>\n\u003cp>Even so, Sperling is optimistic that the research will lead to an implantable device that can improve memory in at least some patients. \"There's a good chance that something like this will come available,\" he says, \"I would hope within the next half dozen years, or so.\"\u003c/p>\n\u003cp>The memory research is being funded by the military's Defense Advanced Research Projects Agency. It's part of an effort by the agency to develop technologies to help military personnel and veterans with memory problems caused by brain injuries.\u003c/p>\n\u003cp>\"We didn't just do this for the sake of science,\" says \u003ca href=\"https://www.darpa.mil/staff/dr-justin-sanchez\" target=\"_blank\" rel=\"noopener\">Justin Sanchez\u003c/a>, who directs DARPA's biological technologies office. \"We wanted a real technology that could ultimately make its way out into the world.\"\u003c/p>\n\u003cp>DARPA-funded scientists are already working on a version of the brain stimulation system that could be implanted in a person, Sanchez says. And this sort of technology could eventually extend beyond people who have memory impairments, he says.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\"If any of us could get a 15 percent boost in our memory, that would be transformative,\" Sanchez says.\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2018 NPR. To see more, visit \u003ca href=\"http://www.npr.org/\">http://www.npr.org/\u003c/a>.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=A+Tiny+Pulse+Of+Electricity+Can+Help+The+Brain+Form+Lasting+Memories&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>A little electrical brain stimulation can go a long way in boosting memory.\u003c/p>\n\u003cp>The key is to deliver a tiny pulse of electricity to exactly the right place at exactly the right moment, a team \u003ca href=\"http://nature.com/articles/doi:10.1038/s41467-017-02753-0\" target=\"_blank\" rel=\"noopener\">reports\u003c/a> in Tuesday's \u003cem>Nature Communications\u003c/em>.\u003c/p>\n\u003cp>\"We saw a 15 percent improvement in memory,\" says \u003ca href=\"https://psychology.sas.upenn.edu/people/michael-kahana\" target=\"_blank\" rel=\"noopener\">Michael Kahana\u003c/a>, a professor of psychology at the University of Pennsylvania and an author of the study.\u003c/p>\n\u003cp>The approach hints at a new way of treating people with memory problems caused by a brain injury or Alzheimer's disease, Kahana says. But the technology is still far from widespread use.\u003c/p>\n\u003cp>Kahana has spent years trying to understand why the brain often fails to store information we want it to keep.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>\"When we're trying to study a list of items, sometimes the items stick and sometimes we have momentary lapses where we don't seem to remember anything,\" he says.\u003c/p>\n\u003cp>\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>Kahana and a team of researchers thought there must be a way to help the brain do better. So they had a computer learn to recognize patterns of electrical activity indicating that the brain was about to have a memory lapse.\u003c/p>\n\u003cp>Then the team had the computer intervene by delivering a pulse of electricity to different areas of the brain just before the lapse was going to occur. And in the area involved in recalling words, the approach worked.\u003c/p>\n\u003cp>\"When we stimulated the left temporal cortex, we found that memory was improved significantly,\" Kahana says. \"When we stimulated other parts of the brain, memory was, by and large, impaired.\"\u003c/p>\n\u003cp>The experiment was done with 25 patients with epilepsy who were in the hospital awaiting surgery to treat their seizures. That meant doctors had already inserted wires into their brains to monitor electrical activity.\u003c/p>\n\u003caside class=\"pullquote aligncenter\">\"We didn't just do this for the sake of science.\"\u003ccite>Michael Sperling, neurologist\u003c/cite>\u003c/aside>\n\u003cp>But epilepsy patients tend to have memory problems and other brain anomalies, says \u003ca href=\"http://hospitals.jefferson.edu/find-a-doctor/s/sperling-michael-r.html\" target=\"_blank\" rel=\"noopener\">Michael Sperling\u003c/a>, an author of the study and director of the Comprehensive Epilepsy Center at Thomas Jefferson University in Philadelphia.\u003c/p>\n\u003cp>\"We still really lack any experiments in people with other conditions to know for certain whether [the treatment] would prove effective or not,\" Sperling says.\u003c/p>\n\u003cp>Even so, Sperling is optimistic that the research will lead to an implantable device that can improve memory in at least some patients. \"There's a good chance that something like this will come available,\" he says, \"I would hope within the next half dozen years, or so.\"\u003c/p>\n\u003cp>The memory research is being funded by the military's Defense Advanced Research Projects Agency. It's part of an effort by the agency to develop technologies to help military personnel and veterans with memory problems caused by brain injuries.\u003c/p>\n\u003cp>\"We didn't just do this for the sake of science,\" says \u003ca href=\"https://www.darpa.mil/staff/dr-justin-sanchez\" target=\"_blank\" rel=\"noopener\">Justin Sanchez\u003c/a>, who directs DARPA's biological technologies office. \"We wanted a real technology that could ultimately make its way out into the world.\"\u003c/p>\n\u003cp>DARPA-funded scientists are already working on a version of the brain stimulation system that could be implanted in a person, Sanchez says. And this sort of technology could eventually extend beyond people who have memory impairments, he says.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\"If any of us could get a 15 percent boost in our memory, that would be transformative,\" Sanchez says.\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2018 NPR. To see more, visit \u003ca href=\"http://www.npr.org/\">http://www.npr.org/\u003c/a>.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=A+Tiny+Pulse+Of+Electricity+Can+Help+The+Brain+Form+Lasting+Memories&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n\u003c/div>\u003c/p>",
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"disqusTitle": "Migraine Injections May Finally Offer Relief For Sufferers",
"title": "Migraine Injections May Finally Offer Relief For Sufferers",
"headTitle": "KQED Future of You | KQED Science",
"content": "\u003cp>Humans have suffered from migraines for millennia. Yet, despite decades of research, there isn't a drug on the market today that prevents them by targeting the underlying cause. All of that could change in a few months when the FDA is expected to announce its decision about new therapies that have the potential to turn migraine treatment on its head.\u003c/p>\n\u003cp>The new therapies are based on research begun in the 1980s showing that people in the throes of a migraine attack have high levels of a protein called calcitonin gene–related peptide (CGRP) in their blood.\u003c/p>\n\u003cp>[contextly_sidebar id=\"ECfTe7PnuepSCIujv8538j2RQRMlQ2J6\"]Step by step, researchers tracked and studied this neurochemical's effects. They found that \u003ca href=\"https://www.ncbi.nlm.nih.gov/pubmed/11993614\" target=\"_blank\" rel=\"noopener\">injecting\u003c/a> the peptide into the blood of people prone to migraines triggers migraine-like headaches, whereas people not prone to migraines experienced, at most, mild pain. Blocking transmission of\u003ca href=\"http://onlinelibrary.wiley.com/doi/10.1111/bcp.12686/pdf\" target=\"_blank\" rel=\"noopener\"> CGRP in mice\u003c/a> appeared to prevent migraine-like symptoms. And so a few companies started developing a pill that might do the same in humans.\u003c/p>\n\u003cp>Clinical trials of the first pills were effective against migraine but halted in 2011 over concerns about potential liver damage. So, four pharmaceutical companies rejiggered their approach. To bypass the liver, all four instead looked to an injectable therapy called monoclonal antibodies — tiny immune molecules most commonly used to treat cancer. Not only do these bypass the liver to block CGRP, but one injection appears to be effective for up to three months with almost no noticeable side effects.\u003c/p>\n\u003cp>Two manufacturers, Amgen (in collaboration with Novartis) and Teva Pharmaceuticals, have completed clinical trials and expect to hear from the FDA by June whether the therapies have been approved. Two more companies, Eli Lilly and Alder Biopharmaceuticals, plan to file for FDA approval later this year.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>\u003cstrong>Current treatments don't always work\u003c/strong>\u003c/p>\n\u003cp>It's been a long time coming. Right now, the only available preventive treatments are accidental discoveries: A number of people prescribed medications for depression, high blood pressure and epilepsy discovered migraine relief, too. Now, many of those drugs, including propranolol and topiramate, have been tested and approved for migraine. But no one drug works for everyone, and side effects can prove intolerable or downright unpleasant.\u003c/p>\n\u003cp>Migraines are throbbing, one-sided headaches that can be accompanied by nausea as well as sensitivity to light, sound, smell, and movement. At their best, the headaches are an annoyance. At their worst, they can be completely debilitating. So for those of us who get numerous migraines each month, the prospect of a new approach feels almost life-changing.\u003c/p>\n\u003caside class=\"pullquote aligncenter\">“By age 25, I started to wonder if there was something seriously wrong with my head.”\u003ccite>Lauren Gravitz\u003c/cite>\u003c/aside>\n\u003cp>According to \u003ca href=\"https://www.cdc.gov/mmwr/volumes/66/wr/mm6624a8.htm\" target=\"_blank\" rel=\"noopener\">one recent survey\u003c/a> by the Centers for Disease Control and Prevention, about 10 percent of men and 20 percent of women in the U.S. reported having had a migraine in the last three months. And \u003ca href=\"https://www.ncbi.nlm.nih.gov/pubmed/21063918?dopt=Abstract\" target=\"_blank\" rel=\"noopener\">up to two percent\u003c/a> of all Americans has at least 15 migraine days every single month. The toll such pain can take on health, morale, and productivity is substantial.\u003c/p>\n\u003cp>My own migraines started when I was 13. They struck a few times a week and I thought \u003ca href=\"https://americanmigrainefoundation.org/understanding-migraine/identifying-treating-migraine/\" target=\"_blank\" rel=\"noopener\">they were normal headaches\u003c/a>. For a while, I tried the usual over the counter pain relievers but, one by one, they stopped working. By age 25, I started to wonder if there was something seriously wrong with my head. My general practitioner diagnosed me with migraines, gave me my first preventive medication — an antidepressant — then sent me to see a specialist.\u003c/p>\n\u003cp>Since that day more than 17 years ago, I have tried six preventive prescription medications. Not one helped. I alternated among four different, neurologist-recommended supplements, all to no avail. I received bi-monthly injections of magnesium and participated in one of the first clinical trials of Botox. And while Botox seemed to decrease my migraines by one or two per month, it wasn't enough to bother fighting about it with a new insurance company. I exercised regularly. I experimented with an elimination diet that left me eating nothing but broccoli and white rice, but still the migraines came. I averaged about 15 to 20 each month.\u003c/p>\n\u003cp>Still, I considered myself lucky. The headaches almost never came with nausea, and I had medications that typically ousted them within an hour or two. All told, I usually lost only a few hours of productivity a week.\u003c/p>\n\u003cp>When I grew older and had two children, my body changed and my migraines changed, too. I get them less frequently now, but when they come, they can stick around for a few days or even a week. Abortive medications still work, except when they don't. So when I heard about a new approach that was making its way through a number of pharmaceutical company pipelines, I began combing through the \u003ca href=\"http://www.clinicaltrials.gov\" target=\"_blank\" rel=\"noopener\">national clinical trials database\u003c/a> to find a trial near me. I found one about 80 miles away, which didn't seem too far a trek considering the tantalizing reward of a migraine-free life. I made an appointment.\u003c/p>\n\u003cp>\u003cstrong>Clinical trials seem promising\u003c/strong>\u003c/p>\n\u003cp>\u003ca href=\"https://www.mayoclinic.org/biographies/dodick-david-w-m-d/bio-20053142\" target=\"_blank\" rel=\"noopener\">David Dodick\u003c/a>, a neurologist at the Mayo Clinic in Phoenix, Ariz., has been involved in multiple clinical trials with each of the four anti-CGRP antibody treatments in development. And, he admits, he's optimistic. He has good reason to be: Each of the therapies decreases migraine frequency by at least one to two days per month. \"In a field where, over time, the progress and pace of research in understanding the underlying biology and mechanism of disease has been slow, this was very exciting,\" he says.\u003c/p>\n\u003cp>Because migraines are not life-threatening, most drugs have to pass a pretty high bar to be approved. And so far, patients on the experimental treatments report limited side effects that consist mostly of \u003ca href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5383797/\" target=\"_blank\" rel=\"noopener\">pain at the injection site\u003c/a>. Unlike the current preventive medications, there is no nausea, no fuzzy thinking, no nerve pain, no weight loss or gain. And instead of remembering to take a daily pill, there is just a once-monthly injection.\u003c/p>\n\u003cp>Neurologists already have patients eager to test these therapies, especially when everything else they've tried hasn't worked. \"There's a big hole to fill, both in prevention and acute therapies,\" says \u003ca href=\"https://nyheadache.com/staff/alexander-mauskop/\" target=\"_blank\" rel=\"noopener\">Alexander Mauskop\u003c/a>, director of the New York Headache Center in New York City. (Full disclosure: He's my former neurologist.) \"If I have someone who's really suffering and can't find a solution, I tell them that in June I might have something new for them to try.\" Right now, he says, he has a list of about two dozen such patients.\u003c/p>\n\u003cp>\u003cstrong>High price tag\u003c/strong>\u003c/p>\n\u003cp>Even if the new therapies are approved, however, patients may still have to jump through a number of hoops to get them. Biologic therapies like these are expensive, and treatment could \u003ca href=\"https://www.theverge.com/2016/5/24/11712554/migraine-drug-treatment-headache-cost-pharmaceutical-health-insurance\" target=\"_blank\" rel=\"noopener\">reportedly range\u003c/a> anywhere from $8,000 to $18,000 a year. At that price, Mauskop and other neurologists expect insurance companies to require patients to have tried just about everything else first.\u003c/p>\n\u003cp>The other hitch at this stage is a lack of long-term safety data. \"If someone is well-controlled with Botox or another drug, I'd not suggest they switch,\" Mauskop says. \"With Vioxx, it took 10 years before they discovered that it increased the risk of heart problems.\"\u003c/p>\n\u003cp>Side effects are a potential concern. \u003ca href=\"https://physiciandirectory.brighamandwomens.org/Details/124\" target=\"_blank\" rel=\"noopener\">Elizabeth Loder\u003c/a>, chief of headache at Brigham and Women's Hospital in Boston, points out that because CGRP constricts blood vessels, there may be potential long-term effects on blood pressure or other cardiovascular function. In women of childbearing age, who are the ones most prone to frequent migraines, \"you can imagine that might have effects on fertility or placental function.\"\u003c/p>\n\u003cp>Right now, the longest patients have been on one of these new therapies is one to two years.\u003c/p>\n\u003cp>I ask Mauskop whether he'd recommend I enroll in a clinical trial, given my failure to respond to most everything else. He pauses, noting that he's no longer my neurologist and that he can't really give me any suggestions. But then he says that, since I'd previously shown some response to Botox, perhaps I might want to give it another try. I think about my two young children and my risk tolerance. Perhaps in ten years I'll feel differently. For now, however, I pick up the phone and cancel my clinical trial appointment.\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp>\u003cem>Lauren Gravitz is a science writer and editor in Hershey, Penn. Her work has appeared in \u003c/em>Nature\u003cem>, \u003c/em>The Economist\u003cem>, \u003c/em>Aeon\u003cem>, \u003c/em>Discover\u003cem>, \u003c/em>The Oprah Magazine\u003cem>, and more. Find her at \u003ca href=\"http://www.laurengravitz.com\" target=\"_blank\" rel=\"noopener\">www.laurengravitz.com\u003c/a> and \u003ca href=\"https://twitter.com/lyrebard\">@lyrebard\u003c/a>.\u003c/em>\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2018 NPR. To see more, visit \u003ca href=\"http://www.npr.org/\" target=\"_blank\" rel=\"noopener\">http://www.npr.org/\u003c/a>.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Gone+With+A+Shot%3F+Hopeful+New+Signs+Of+Relief+For+Migraine+Sufferers&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>Humans have suffered from migraines for millennia. Yet, despite decades of research, there isn't a drug on the market today that prevents them by targeting the underlying cause. All of that could change in a few months when the FDA is expected to announce its decision about new therapies that have the potential to turn migraine treatment on its head.\u003c/p>\n\u003cp>The new therapies are based on research begun in the 1980s showing that people in the throes of a migraine attack have high levels of a protein called calcitonin gene–related peptide (CGRP) in their blood.\u003c/p>\n\u003cp>\u003c/p>\u003cp>\u003c/p>\u003cp>Step by step, researchers tracked and studied this neurochemical's effects. They found that \u003ca href=\"https://www.ncbi.nlm.nih.gov/pubmed/11993614\" target=\"_blank\" rel=\"noopener\">injecting\u003c/a> the peptide into the blood of people prone to migraines triggers migraine-like headaches, whereas people not prone to migraines experienced, at most, mild pain. Blocking transmission of\u003ca href=\"http://onlinelibrary.wiley.com/doi/10.1111/bcp.12686/pdf\" target=\"_blank\" rel=\"noopener\"> CGRP in mice\u003c/a> appeared to prevent migraine-like symptoms. And so a few companies started developing a pill that might do the same in humans.\u003c/p>\n\u003cp>Clinical trials of the first pills were effective against migraine but halted in 2011 over concerns about potential liver damage. So, four pharmaceutical companies rejiggered their approach. To bypass the liver, all four instead looked to an injectable therapy called monoclonal antibodies — tiny immune molecules most commonly used to treat cancer. Not only do these bypass the liver to block CGRP, but one injection appears to be effective for up to three months with almost no noticeable side effects.\u003c/p>\n\u003cp>Two manufacturers, Amgen (in collaboration with Novartis) and Teva Pharmaceuticals, have completed clinical trials and expect to hear from the FDA by June whether the therapies have been approved. Two more companies, Eli Lilly and Alder Biopharmaceuticals, plan to file for FDA approval later this year.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>\u003cstrong>Current treatments don't always work\u003c/strong>\u003c/p>\n\u003cp>It's been a long time coming. Right now, the only available preventive treatments are accidental discoveries: A number of people prescribed medications for depression, high blood pressure and epilepsy discovered migraine relief, too. Now, many of those drugs, including propranolol and topiramate, have been tested and approved for migraine. But no one drug works for everyone, and side effects can prove intolerable or downright unpleasant.\u003c/p>\n\u003cp>Migraines are throbbing, one-sided headaches that can be accompanied by nausea as well as sensitivity to light, sound, smell, and movement. At their best, the headaches are an annoyance. At their worst, they can be completely debilitating. So for those of us who get numerous migraines each month, the prospect of a new approach feels almost life-changing.\u003c/p>\n\u003caside class=\"pullquote aligncenter\">“By age 25, I started to wonder if there was something seriously wrong with my head.”\u003ccite>Lauren Gravitz\u003c/cite>\u003c/aside>\n\u003cp>According to \u003ca href=\"https://www.cdc.gov/mmwr/volumes/66/wr/mm6624a8.htm\" target=\"_blank\" rel=\"noopener\">one recent survey\u003c/a> by the Centers for Disease Control and Prevention, about 10 percent of men and 20 percent of women in the U.S. reported having had a migraine in the last three months. And \u003ca href=\"https://www.ncbi.nlm.nih.gov/pubmed/21063918?dopt=Abstract\" target=\"_blank\" rel=\"noopener\">up to two percent\u003c/a> of all Americans has at least 15 migraine days every single month. The toll such pain can take on health, morale, and productivity is substantial.\u003c/p>\n\u003cp>My own migraines started when I was 13. They struck a few times a week and I thought \u003ca href=\"https://americanmigrainefoundation.org/understanding-migraine/identifying-treating-migraine/\" target=\"_blank\" rel=\"noopener\">they were normal headaches\u003c/a>. For a while, I tried the usual over the counter pain relievers but, one by one, they stopped working. By age 25, I started to wonder if there was something seriously wrong with my head. My general practitioner diagnosed me with migraines, gave me my first preventive medication — an antidepressant — then sent me to see a specialist.\u003c/p>\n\u003cp>Since that day more than 17 years ago, I have tried six preventive prescription medications. Not one helped. I alternated among four different, neurologist-recommended supplements, all to no avail. I received bi-monthly injections of magnesium and participated in one of the first clinical trials of Botox. And while Botox seemed to decrease my migraines by one or two per month, it wasn't enough to bother fighting about it with a new insurance company. I exercised regularly. I experimented with an elimination diet that left me eating nothing but broccoli and white rice, but still the migraines came. I averaged about 15 to 20 each month.\u003c/p>\n\u003cp>Still, I considered myself lucky. The headaches almost never came with nausea, and I had medications that typically ousted them within an hour or two. All told, I usually lost only a few hours of productivity a week.\u003c/p>\n\u003cp>When I grew older and had two children, my body changed and my migraines changed, too. I get them less frequently now, but when they come, they can stick around for a few days or even a week. Abortive medications still work, except when they don't. So when I heard about a new approach that was making its way through a number of pharmaceutical company pipelines, I began combing through the \u003ca href=\"http://www.clinicaltrials.gov\" target=\"_blank\" rel=\"noopener\">national clinical trials database\u003c/a> to find a trial near me. I found one about 80 miles away, which didn't seem too far a trek considering the tantalizing reward of a migraine-free life. I made an appointment.\u003c/p>\n\u003cp>\u003cstrong>Clinical trials seem promising\u003c/strong>\u003c/p>\n\u003cp>\u003ca href=\"https://www.mayoclinic.org/biographies/dodick-david-w-m-d/bio-20053142\" target=\"_blank\" rel=\"noopener\">David Dodick\u003c/a>, a neurologist at the Mayo Clinic in Phoenix, Ariz., has been involved in multiple clinical trials with each of the four anti-CGRP antibody treatments in development. And, he admits, he's optimistic. He has good reason to be: Each of the therapies decreases migraine frequency by at least one to two days per month. \"In a field where, over time, the progress and pace of research in understanding the underlying biology and mechanism of disease has been slow, this was very exciting,\" he says.\u003c/p>\n\u003cp>Because migraines are not life-threatening, most drugs have to pass a pretty high bar to be approved. And so far, patients on the experimental treatments report limited side effects that consist mostly of \u003ca href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5383797/\" target=\"_blank\" rel=\"noopener\">pain at the injection site\u003c/a>. Unlike the current preventive medications, there is no nausea, no fuzzy thinking, no nerve pain, no weight loss or gain. And instead of remembering to take a daily pill, there is just a once-monthly injection.\u003c/p>\n\u003cp>Neurologists already have patients eager to test these therapies, especially when everything else they've tried hasn't worked. \"There's a big hole to fill, both in prevention and acute therapies,\" says \u003ca href=\"https://nyheadache.com/staff/alexander-mauskop/\" target=\"_blank\" rel=\"noopener\">Alexander Mauskop\u003c/a>, director of the New York Headache Center in New York City. (Full disclosure: He's my former neurologist.) \"If I have someone who's really suffering and can't find a solution, I tell them that in June I might have something new for them to try.\" Right now, he says, he has a list of about two dozen such patients.\u003c/p>\n\u003cp>\u003cstrong>High price tag\u003c/strong>\u003c/p>\n\u003cp>Even if the new therapies are approved, however, patients may still have to jump through a number of hoops to get them. Biologic therapies like these are expensive, and treatment could \u003ca href=\"https://www.theverge.com/2016/5/24/11712554/migraine-drug-treatment-headache-cost-pharmaceutical-health-insurance\" target=\"_blank\" rel=\"noopener\">reportedly range\u003c/a> anywhere from $8,000 to $18,000 a year. At that price, Mauskop and other neurologists expect insurance companies to require patients to have tried just about everything else first.\u003c/p>\n\u003cp>The other hitch at this stage is a lack of long-term safety data. \"If someone is well-controlled with Botox or another drug, I'd not suggest they switch,\" Mauskop says. \"With Vioxx, it took 10 years before they discovered that it increased the risk of heart problems.\"\u003c/p>\n\u003cp>Side effects are a potential concern. \u003ca href=\"https://physiciandirectory.brighamandwomens.org/Details/124\" target=\"_blank\" rel=\"noopener\">Elizabeth Loder\u003c/a>, chief of headache at Brigham and Women's Hospital in Boston, points out that because CGRP constricts blood vessels, there may be potential long-term effects on blood pressure or other cardiovascular function. In women of childbearing age, who are the ones most prone to frequent migraines, \"you can imagine that might have effects on fertility or placental function.\"\u003c/p>\n\u003cp>Right now, the longest patients have been on one of these new therapies is one to two years.\u003c/p>\n\u003cp>I ask Mauskop whether he'd recommend I enroll in a clinical trial, given my failure to respond to most everything else. He pauses, noting that he's no longer my neurologist and that he can't really give me any suggestions. But then he says that, since I'd previously shown some response to Botox, perhaps I might want to give it another try. I think about my two young children and my risk tolerance. Perhaps in ten years I'll feel differently. For now, however, I pick up the phone and cancel my clinical trial appointment.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>\u003cem>Lauren Gravitz is a science writer and editor in Hershey, Penn. Her work has appeared in \u003c/em>Nature\u003cem>, \u003c/em>The Economist\u003cem>, \u003c/em>Aeon\u003cem>, \u003c/em>Discover\u003cem>, \u003c/em>The Oprah Magazine\u003cem>, and more. Find her at \u003ca href=\"http://www.laurengravitz.com\" target=\"_blank\" rel=\"noopener\">www.laurengravitz.com\u003c/a> and \u003ca href=\"https://twitter.com/lyrebard\">@lyrebard\u003c/a>.\u003c/em>\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2018 NPR. To see more, visit \u003ca href=\"http://www.npr.org/\" target=\"_blank\" rel=\"noopener\">http://www.npr.org/\u003c/a>.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Gone+With+A+Shot%3F+Hopeful+New+Signs+Of+Relief+For+Migraine+Sufferers&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n\u003c/div>\u003c/p>",
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"content": "\u003cp> \u003c/p>\n\u003cp>https://www.youtube.com/watch?v=6buimTAuKKs&feature=youtu.be&ab_channel=STAT\u003c/p>\n\u003cp>TOKYO — The world is getting older. Fast. By 2050, the global population of those age 65 and older is projected to nearly double to 1.6 billion.\u003c/p>\n\u003cp>This global graying has given birth to a new phrase: “super-aging.” A nation is said to be super-aged when more than 1 in 5 of its people are 65 and older.\u003c/p>\n\u003cp>The United States isn’t there yet, but the trend line points that way in decades to come. The number of Americans age 65 and older is expected to more than double from 46 million in 2016 to over 98 million by 2060. (The country will be just one percentage point short of official “super-aged” status.)\u003c/p>\n\u003caside class=\"alignleft\">\n\u003ch3>About This Project\u003c/h3>\n\u003cp>In two intimate video shorts, the journalist Shiho Fukada documents how the Japanese are experimenting with technology to help citizens live longer and healthier. Fukada spent nearly a year conducting interviews in Tokyo to pursue this assignment for STAT, which was produced with the help of a grant from the \u003ca href=\"https://pulitzercenter.org/\" target=\"_blank\" rel=\"noopener\">Pulitzer Center\u003c/a>.\u003c/p>\n\u003c/aside>\n\u003cp>Many of us have aging parents now, or will be getting up there ourselves by 2060. Will the U.S. health care system be able to cope with the gray tide? Where do we look for a glimpse or our aged future?\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>Japan, it turns out, might just be us, as we will be in 40 years.\u003c/p>\n\u003cp>The country has the largest percentage of older people in the world, with 27.3 percent of its citizens 65 years and older. There, necessity might be just the be mother of invention when it comes to approaches to elder care. In this special report, we take a look at how Japan is marrying its demographic shifts with its love of technology to find a way forward.\u003c/p>\n\u003cp>\u003c!-- iframe plugin v.4.3 wordpress.org/plugins/iframe/ -->\u003cbr>\n\u003ciframe width=\"640\" height=\"360\" src=\"//content.jwplatform.com/players/yWvbwAC1-jEuQjxp9.html\" frameborder=\"0\" marginwidth=\"0\" marginheight=\"0\" scrolling=\"auto\" class=\"iframe-class\">\u003c/iframe>\u003c/p>\n\u003cp>\u003cstrong>A Bot to Watch Over Me\u003c/strong>\u003c/p>\n\u003cp>Palro works for free every day and he knows no fatigue. Always cheerful, he wears many hats: dancer, exercise instructor, comedian, and fortune teller. But best of all, his patience never runs thin, no matter how many times seniors request the same things. It helps that he is a robot.\u003c/p>\n\u003cp>At the Flos Higashi-kojiya Senior Care Facility in Tokyo, seniors can keep themselves entertained with various recreational programs, such as crafts, karaoke, and bingo. But one program — called “Let’s play with Palro!” — has been gaining popularity lately.\u003c/p>\n\u003cp>Robots are still expensive. To help bring more robots to the elder care system, the Japanese government budgeted a 5.2 billion yen subsidy ($47.3 million) in 2015. And some Japanese are realizing that a robot is just about the best purchase they can make.\u003c/p>\n\u003cp>\u003cstrong>Virtually able\u003c/strong>\u003c/p>\n\u003cp>Its average life expectancy was the highest in the world, at 83.7 years (86.8 for women and 80.5 for men) in 2015, according to the WHO.\u003c/p>\n\u003cp>But what’s the point of living longer if you are not happy?\u003c/p>\n\u003cp>Kenta Toshima has an idea about that. Happiness can be found on a virtual journey.\u003c/p>\n\u003cp>Toshima is a therapist in Tokyo, and he’s spent most of his savings to travel the world, so that he can bring far-off lands back to his elderly patients.\u003cbr>\n\u003c!-- iframe plugin v.4.3 wordpress.org/plugins/iframe/ -->\u003cbr>\n\u003ciframe width=\"640\" height=\"360\" src=\"//content.jwplatform.com/players/LFAnUODv-jEuQjxp9.html\" frameborder=\"0\" marginwidth=\"0\" marginheight=\"0\" scrolling=\"auto\" class=\"iframe-class\">\u003c/iframe>\u003c/p>\n\u003cp>Will these two technologies make a dent in Japan’s aging problem? It’s hard to say at the moment. What is clear is that super-aging will continue to rise as a major social issue without solution in Japan. And if it doesn’t come up with novel solutions, how will the rest of the aging world?\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\u003cem>This \u003ca href=\"https://www.statnews.com/2018/02/05/aging-japan-robots-virtual-reality/\" target=\"_blank\" rel=\"noopener\">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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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp> \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/6buimTAuKKs'\n title='//www.youtube.com/embed/6buimTAuKKs'\n allowfullscreen='true'\n style='border:0;'>\u003c/iframe>\n \u003c/span>\n \u003c/span>\u003c/p>\u003cp>\u003cp>TOKYO — The world is getting older. Fast. By 2050, the global population of those age 65 and older is projected to nearly double to 1.6 billion.\u003c/p>\n\u003cp>This global graying has given birth to a new phrase: “super-aging.” A nation is said to be super-aged when more than 1 in 5 of its people are 65 and older.\u003c/p>\n\u003cp>The United States isn’t there yet, but the trend line points that way in decades to come. The number of Americans age 65 and older is expected to more than double from 46 million in 2016 to over 98 million by 2060. (The country will be just one percentage point short of official “super-aged” status.)\u003c/p>\n\u003caside class=\"alignleft\">\n\u003ch3>About This Project\u003c/h3>\n\u003cp>In two intimate video shorts, the journalist Shiho Fukada documents how the Japanese are experimenting with technology to help citizens live longer and healthier. Fukada spent nearly a year conducting interviews in Tokyo to pursue this assignment for STAT, which was produced with the help of a grant from the \u003ca href=\"https://pulitzercenter.org/\" target=\"_blank\" rel=\"noopener\">Pulitzer Center\u003c/a>.\u003c/p>\n\u003c/aside>\n\u003cp>Many of us have aging parents now, or will be getting up there ourselves by 2060. Will the U.S. health care system be able to cope with the gray tide? Where do we look for a glimpse or our aged future?\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>Japan, it turns out, might just be us, as we will be in 40 years.\u003c/p>\n\u003cp>The country has the largest percentage of older people in the world, with 27.3 percent of its citizens 65 years and older. There, necessity might be just the be mother of invention when it comes to approaches to elder care. In this special report, we take a look at how Japan is marrying its demographic shifts with its love of technology to find a way forward.\u003c/p>\n\u003cp>\u003c!-- iframe plugin v.4.3 wordpress.org/plugins/iframe/ -->\u003cbr>\n\u003ciframe width=\"640\" height=\"360\" src=\"//content.jwplatform.com/players/yWvbwAC1-jEuQjxp9.html\" frameborder=\"0\" marginwidth=\"0\" marginheight=\"0\" scrolling=\"auto\" class=\"iframe-class\">\u003c/iframe>\u003c/p>\n\u003cp>\u003cstrong>A Bot to Watch Over Me\u003c/strong>\u003c/p>\n\u003cp>Palro works for free every day and he knows no fatigue. Always cheerful, he wears many hats: dancer, exercise instructor, comedian, and fortune teller. But best of all, his patience never runs thin, no matter how many times seniors request the same things. It helps that he is a robot.\u003c/p>\n\u003cp>At the Flos Higashi-kojiya Senior Care Facility in Tokyo, seniors can keep themselves entertained with various recreational programs, such as crafts, karaoke, and bingo. But one program — called “Let’s play with Palro!” — has been gaining popularity lately.\u003c/p>\n\u003cp>Robots are still expensive. To help bring more robots to the elder care system, the Japanese government budgeted a 5.2 billion yen subsidy ($47.3 million) in 2015. And some Japanese are realizing that a robot is just about the best purchase they can make.\u003c/p>\n\u003cp>\u003cstrong>Virtually able\u003c/strong>\u003c/p>\n\u003cp>Its average life expectancy was the highest in the world, at 83.7 years (86.8 for women and 80.5 for men) in 2015, according to the WHO.\u003c/p>\n\u003cp>But what’s the point of living longer if you are not happy?\u003c/p>\n\u003cp>Kenta Toshima has an idea about that. Happiness can be found on a virtual journey.\u003c/p>\n\u003cp>Toshima is a therapist in Tokyo, and he’s spent most of his savings to travel the world, so that he can bring far-off lands back to his elderly patients.\u003cbr>\n\u003c!-- iframe plugin v.4.3 wordpress.org/plugins/iframe/ -->\u003cbr>\n\u003ciframe width=\"640\" height=\"360\" src=\"//content.jwplatform.com/players/LFAnUODv-jEuQjxp9.html\" frameborder=\"0\" marginwidth=\"0\" marginheight=\"0\" scrolling=\"auto\" class=\"iframe-class\">\u003c/iframe>\u003c/p>\n\u003cp>Will these two technologies make a dent in Japan’s aging problem? It’s hard to say at the moment. What is clear is that super-aging will continue to rise as a major social issue without solution in Japan. And if it doesn’t come up with novel solutions, how will the rest of the aging world?\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\u003cem>This \u003ca href=\"https://www.statnews.com/2018/02/05/aging-japan-robots-virtual-reality/\" target=\"_blank\" rel=\"noopener\">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>A \u003ca href=\"https://www.hrw.org/report/2018/02/05/they-want-docile/how-nursing-homes-united-states-overmedicate-people-dementia\" target=\"_blank\" rel=\"noopener\">study\u003c/a> published Monday by \u003ca href=\"https://www.hrw.org/report/2018/02/05/they-want-docile/how-nursing-homes-united-states-overmedicate-people-dementia\" target=\"_blank\" rel=\"noopener\">Human Rights Watch\u003c/a> finds that about 179,000 nursing home residents are being given antipsychotic drugs, even though they don't have schizophrenia or other serious mental illnesses that those drugs are designed to treat.\u003c/p>\n\u003cp>Most of these residents have Alzheimer's disease or another form of dementia and \u003ca href=\"https://www.nimh.nih.gov/health/topics/mental-health-medications/index.shtml#part_149866\" target=\"_blank\" rel=\"noopener\">antipsychotics\u003c/a> aren't approved for that. What's more, antipsychotic drugs come with a \"\u003ca href=\"https://www.accessdata.fda.gov/drugsatfda_docs/label/2009/020272s056,020588s044,021346s033,021444s03lbl.pdf\" target=\"_blank\" rel=\"noopener\">black box warning\u003c/a>\" from the FDA, stating that they increase the risk of death in older people with dementia.\u003c/p>\n\u003cp>The study concluded that antipsychotic drugs were often administered without informed consent and for the purpose of making dementia patients easier to handle in understaffed facilities.\u003c/p>\n\u003cp>Researchers focused on six states, including California and Texas, which have the most skilled nursing facilities. They used publicly available data, along with hundreds of interviews with residents, families and state ombudsmen, the officials who deal with complaints about long term care facilities.\u003c/p>\n\u003cp>In 2012, the federal government \u003ca href=\"https://www.cms.gov/Medicare/Provider-Enrollment-and-Certification/SurveyCertificationGenInfo/National-Partnership-to-Improve-Dementia-Care-in-Nursing-Homes.html\" target=\"_blank\" rel=\"noopener\">began a \u003c/a>program to reduce the use of antipsychotic drugs in nursing homes, in partnership with the nursing home industry, and advocacy organizations. \u003ca href=\"https://www.cms.gov/Newsroom/MediaReleaseDatabase/Fact-sheets/2017-Fact-Sheet-items/2017-10-02.html\" target=\"_blank\" rel=\"noopener\">Since then\u003c/a>, the use of the drugs has dropped by about a third nationwide, from 23.9 percent of residents in 2012 to 15.7 percent at the beginning of 2017. The Centers for Medicare and Medicaid Services have called for an additional 15 percent reduction by 2019 for those nursing homes that have lagged in curtailing their use of antipsychotics.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>But the Human Rights Watch study contends that the federal government hasn't done nearly enough. It faults the government for failing to enforce \u003ca href=\"https://www.medicare.gov/what-medicare-covers/part-a/rights-in-snf.html\" target=\"_blank\" rel=\"noopener\">laws that exist to protect nursing home residents\u003c/a> from what are sometimes called \"chemical restraints.\"\u003c/p>\n\u003cp>An NPR investigation into the first few years of the government's program to reduce the use of antipsychotic drugs found that \u003ca href=\"https://www.npr.org/sections/health-shots/2014/12/09/368538773/nursing-homes-rarely-penalized-for-oversedating-patients\" target=\"_blank\" rel=\"noopener\">only 2 percent\u003c/a> of cases were deemed serious enough to trigger a fine.\u003c/p>\n\u003cp>The study also calls for the government to strengthen informed consent procedures and to establish minimum staffing levels, something that has long been opposed by the nursing home industry.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\u003ca href=\"https://www.ahcancal.org/Pages/Default.aspx\" target=\"_blank\" rel=\"noopener\">The American Health Care Association\u003c/a>, which represents most nursing homes, said in a \u003ca href=\"https://www.ahcancal.org/News/news_releases/Pages/AHCA-Responds-to-Human-Rights-Watch-Report.aspx\" target=\"_blank\" rel=\"noopener\">statement\u003c/a> that the report \"does little to highlight the effort launched by our profession in 2012 that has resulted in a dramatic decline in the use of these medications.\"\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2018 NPR. To see more, visit \u003ca href=\"http://www.npr.org/\" target=\"_blank\" rel=\"noopener\">http://www.npr.org/\u003c/a>.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Risky+Antipsychotic+Drugs+Still+Overprescribed+In+Nursing+Homes&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>A \u003ca href=\"https://www.hrw.org/report/2018/02/05/they-want-docile/how-nursing-homes-united-states-overmedicate-people-dementia\" target=\"_blank\" rel=\"noopener\">study\u003c/a> published Monday by \u003ca href=\"https://www.hrw.org/report/2018/02/05/they-want-docile/how-nursing-homes-united-states-overmedicate-people-dementia\" target=\"_blank\" rel=\"noopener\">Human Rights Watch\u003c/a> finds that about 179,000 nursing home residents are being given antipsychotic drugs, even though they don't have schizophrenia or other serious mental illnesses that those drugs are designed to treat.\u003c/p>\n\u003cp>Most of these residents have Alzheimer's disease or another form of dementia and \u003ca href=\"https://www.nimh.nih.gov/health/topics/mental-health-medications/index.shtml#part_149866\" target=\"_blank\" rel=\"noopener\">antipsychotics\u003c/a> aren't approved for that. What's more, antipsychotic drugs come with a \"\u003ca href=\"https://www.accessdata.fda.gov/drugsatfda_docs/label/2009/020272s056,020588s044,021346s033,021444s03lbl.pdf\" target=\"_blank\" rel=\"noopener\">black box warning\u003c/a>\" from the FDA, stating that they increase the risk of death in older people with dementia.\u003c/p>\n\u003cp>The study concluded that antipsychotic drugs were often administered without informed consent and for the purpose of making dementia patients easier to handle in understaffed facilities.\u003c/p>\n\u003cp>Researchers focused on six states, including California and Texas, which have the most skilled nursing facilities. They used publicly available data, along with hundreds of interviews with residents, families and state ombudsmen, the officials who deal with complaints about long term care facilities.\u003c/p>\n\u003cp>In 2012, the federal government \u003ca href=\"https://www.cms.gov/Medicare/Provider-Enrollment-and-Certification/SurveyCertificationGenInfo/National-Partnership-to-Improve-Dementia-Care-in-Nursing-Homes.html\" target=\"_blank\" rel=\"noopener\">began a \u003c/a>program to reduce the use of antipsychotic drugs in nursing homes, in partnership with the nursing home industry, and advocacy organizations. \u003ca href=\"https://www.cms.gov/Newsroom/MediaReleaseDatabase/Fact-sheets/2017-Fact-Sheet-items/2017-10-02.html\" target=\"_blank\" rel=\"noopener\">Since then\u003c/a>, the use of the drugs has dropped by about a third nationwide, from 23.9 percent of residents in 2012 to 15.7 percent at the beginning of 2017. The Centers for Medicare and Medicaid Services have called for an additional 15 percent reduction by 2019 for those nursing homes that have lagged in curtailing their use of antipsychotics.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cp>We’d all like to be a little happier.\u003c/p>\n\u003cp>The problem is that \u003ca href=\"http://sonjalyubomirsky.com/wp-content/themes/sonjalyubomirsky/papers/LSS2005.pdf\">much of what determines happiness is outside of our control\u003c/a>. Some of us are genetically predisposed to see the world through rose-colored glasses, while others have a generally negative outlook. Bad things happen, to us and in the world. People can be unkind, and jobs can be tedious.\u003c/p>\n\u003caside class=\"pullquote alignright\">An analysis of 1 million teens showed those who spent more time on the internet, playing computer games, on social media, texting, using video chat or watching TV were less happy.\u003c/aside>\n\u003cp> But we do have some control over how we spend our leisure time. That’s one reason why it’s worth asking which leisure time activities are linked to happiness, and which aren’t.\u003c/p>\n\u003cp>In \u003ca href=\"http://psycnet.apa.org/doiLanding?doi=10.1037%2Femo0000403\">a new analysis of 1 million U.S. teens\u003c/a>, my co-authors and I looked at how teens were spending their free time and which activities correlated with happiness, and which didn’t.\u003c/p>\n\u003cp>We wanted to see if changes in the way teens spend their free time might partially explain a startling drop in teens’ happiness after 2012 – and perhaps the decline in adults’ happiness since 2000 as well.\u003c/p>\n\u003ch2>A possible culprit emerges\u003c/h2>\n\u003cp>In our study, \u003ca href=\"http://www.monitoringthefuture.org/\">we analyzed data\u003c/a> from a nationally representative survey of eighth-, 10th- and 12th-graders that’s been conducted annually since 1991.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>Every year, teens are asked about their general happiness, in addition to how they spend their time. We found that teens who spent more time seeing their friends in person, exercising, playing sports, attending religious services, reading or even doing homework were happier. However, teens who spent more time on the internet, playing computer games, on social media, texting, using video chat or watching TV were less happy.\u003c/p>\n\u003cp>In other words, every activity that didn’t involve a screen was linked to more happiness, and every activity that involved a screen was linked to less happiness. The differences were considerable: Teens who spent more than five hours a day online were twice as likely to be unhappy as those who spent less than an hour a day.\u003c/p>\n\u003cp>Of course, it might be that unhappy people seek out screen activities. However, a growing number of studies show that most of the causation goes from screen use to unhappiness, not the other way around.\u003c/p>\n\u003cp>In \u003ca href=\"http://online.liebertpub.com/doi/abs/10.1089/cyber.2016.0259?journalCode=cyber\">one experiment\u003c/a>, people who were randomly assigned to give up Facebook for a week ended that time happier, less lonely and less depressed than those who continued to use Facebook. In another study, young adults required to give up Facebook for their jobs \u003ca href=\"https://papers.ssrn.com/sol3/papers.cfm?abstract_id=2916158\">were happier than those who kept their accounts\u003c/a>. In addition, \u003ca href=\"https://www.sciencedirect.com/science/article/pii/S1755296616300862\">several\u003c/a> \u003ca href=\"http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0069841\">longitudinal\u003c/a> \u003ca href=\"https://link.springer.com/article/10.1007/s11482-016-9458-7\">studies\u003c/a> show that screen time leads to unhappiness but \u003ca href=\"https://www.ncbi.nlm.nih.gov/pubmed/28093386\">unhappiness doesn’t lead to more screen time\u003c/a>.\u003c/p>\n\u003cp>If you wanted to give advice based on this research, it would be very simple: Put down your phone or tablet and go do something – just about anything – else.\u003c/p>\n\u003ch2>It’s not just teens\u003c/h2>\n\u003cp>These links between happiness and time use are worrying news, as the current generation of teens (whom I call “iGen” \u003ca href=\"http://www.simonandschuster.com/books/iGen/Jean-M-Twenge/9781501151989\">in my book of the same name\u003c/a>) spends more time with screens than any previous generation. Time spent online doubled between 2006 and 2016, and 82 percent of 12th-graders now use social\u003cbr>\nmedia every day (up from 51 percent in 2008).\u003c/p>\n\u003cp>Sure enough, teens’ happiness suddenly plummeted after 2012 (the year when the majority of Americans owned smartphones). So did teens’ self-esteem and their satisfaction with their lives, especially their satisfaction with their friends, the amount of fun they were having, and their lives as a whole. These declines in well-being mirror other studies finding sharp increases in mental health issues among iGen, including in \u003ca href=\"http://journals.sagepub.com/doi/abs/10.1177/2167702617723376\">depressive symptoms\u003c/a>, \u003ca href=\"http://pediatrics.aappublications.org/content/early/2016/11/10/peds.2016-1878\">major depression\u003c/a>, \u003ca href=\"https://jamanetwork.com/journals/jama/article-abstract/2664031/\">self-harm\u003c/a> and \u003ca href=\"https://www.cdc.gov/mmwr/volumes/66/wr/mm6630a6.htm\">suicide\u003c/a>. Especially compared to the \u003ca href=\"http://journals.sagepub.com/doi/abs/10.1111/j.1467-9280.2008.02204.x\">optimistic and almost relentlessly positive millennials\u003c/a>, iGen is markedly less self-assured, and more are depressed.\u003c/p>\n\u003cp>A similar trend might be occurring for adults: My co-authors and I previously found that \u003ca href=\"http://journals.sagepub.com/doi/abs/10.1177/1948550615602933?journalCode=sppa\">adults over age 30 were less happy than they were 15 years ago\u003c/a>, and that \u003ca href=\"https://www.ncbi.nlm.nih.gov/pubmed/28265779\">adults were having sex less frequently\u003c/a>. There may be many reasons for these trends, but \u003ca href=\"http://www.cnn.com/2016/06/30/health/americans-screen-time-nielsen/index.html\">adults are also spending more time with screens\u003c/a> than they used to. That might mean less face-to-face time with other people, including with their sexual partners. The result: \u003ca href=\"http://journals.sagepub.com/doi/full/10.1177/1948550615616462\">less sex and less happiness\u003c/a>.\u003c/p>\n\u003cp>Although both teen and adult happiness dropped during the years of high unemployment amid the Great Recession (2008-2010), happiness didn’t rebound in the years after 2012 \u003ca href=\"https://www.economicgreenfield.com/2016/01/08/u-3-and-u-6-unemployment-rate-long-term-reference-charts-as-of-january-8-2016/\">when the economy was doing progressively better\u003c/a>. Instead, happiness continued to decline as the economy improved, making it unlikely that economic cycles were to blame for lower happiness after 2012.\u003c/p>\n\u003cp>Growing income inequality could play a role, especially for adults. But if so, one would expect that happiness would have been dropping continuously since the 1980s, \u003ca href=\"https://www.cbsnews.com/news/dreaming-of-a-better-gini/\">when income inequality began to grow\u003c/a>. Instead, happiness began to decline around 2000 for adults and around 2012 for teens. Nevertheless, it’s possible that concerns about the job market and income inequality reached a tipping point in the early 2000s.\u003c/p>\n\u003cp>Somewhat surprisingly, we found that teens who didn’t use digital media at all were actually a little less happy than those who used digital media a little bit (less than an hour a day). Happiness was then steadily lower with more hours of use. Thus, the happiest teens were those who used digital media, \u003ca href=\"https://theconversation.com/does-apple-have-an-obligation-to-make-the-iphone-safer-for-kids-89822\">but for a limited amount of time\u003c/a>.\u003c/p>\n\u003cp>The answer, then, is not to give up technology entirely. Instead, the solution is a familiar adage: everything in moderation. Use your phone for all the cool things it’s good for. And then set it down and go do something else.\u003c/p>\n\u003cp>You might be happier for it.\u003c/p>\n\u003cp>\u003cem>\u003ca href=\"https://theconversation.com/profiles/jean-twenge-315939\">Jean Twenge \u003c/a>is a professor of psychology,\u003c/em> at \u003cem>\u003ca href=\"http://theconversation.com/institutions/san-diego-state-university-1241\">San Diego State University\u003c/a>\u003c/em>\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\u003cem>This article was originally published on \u003ca href=\"http://theconversation.com\">The Conversation\u003c/a>.\u003c/em>\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>We’d all like to be a little happier.\u003c/p>\n\u003cp>The problem is that \u003ca href=\"http://sonjalyubomirsky.com/wp-content/themes/sonjalyubomirsky/papers/LSS2005.pdf\">much of what determines happiness is outside of our control\u003c/a>. Some of us are genetically predisposed to see the world through rose-colored glasses, while others have a generally negative outlook. Bad things happen, to us and in the world. People can be unkind, and jobs can be tedious.\u003c/p>\n\u003caside class=\"pullquote alignright\">An analysis of 1 million teens showed those who spent more time on the internet, playing computer games, on social media, texting, using video chat or watching TV were less happy.\u003c/aside>\n\u003cp> But we do have some control over how we spend our leisure time. That’s one reason why it’s worth asking which leisure time activities are linked to happiness, and which aren’t.\u003c/p>\n\u003cp>In \u003ca href=\"http://psycnet.apa.org/doiLanding?doi=10.1037%2Femo0000403\">a new analysis of 1 million U.S. teens\u003c/a>, my co-authors and I looked at how teens were spending their free time and which activities correlated with happiness, and which didn’t.\u003c/p>\n\u003cp>We wanted to see if changes in the way teens spend their free time might partially explain a startling drop in teens’ happiness after 2012 – and perhaps the decline in adults’ happiness since 2000 as well.\u003c/p>\n\u003ch2>A possible culprit emerges\u003c/h2>\n\u003cp>In our study, \u003ca href=\"http://www.monitoringthefuture.org/\">we analyzed data\u003c/a> from a nationally representative survey of eighth-, 10th- and 12th-graders that’s been conducted annually since 1991.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>Every year, teens are asked about their general happiness, in addition to how they spend their time. We found that teens who spent more time seeing their friends in person, exercising, playing sports, attending religious services, reading or even doing homework were happier. However, teens who spent more time on the internet, playing computer games, on social media, texting, using video chat or watching TV were less happy.\u003c/p>\n\u003cp>In other words, every activity that didn’t involve a screen was linked to more happiness, and every activity that involved a screen was linked to less happiness. The differences were considerable: Teens who spent more than five hours a day online were twice as likely to be unhappy as those who spent less than an hour a day.\u003c/p>\n\u003cp>Of course, it might be that unhappy people seek out screen activities. However, a growing number of studies show that most of the causation goes from screen use to unhappiness, not the other way around.\u003c/p>\n\u003cp>In \u003ca href=\"http://online.liebertpub.com/doi/abs/10.1089/cyber.2016.0259?journalCode=cyber\">one experiment\u003c/a>, people who were randomly assigned to give up Facebook for a week ended that time happier, less lonely and less depressed than those who continued to use Facebook. In another study, young adults required to give up Facebook for their jobs \u003ca href=\"https://papers.ssrn.com/sol3/papers.cfm?abstract_id=2916158\">were happier than those who kept their accounts\u003c/a>. In addition, \u003ca href=\"https://www.sciencedirect.com/science/article/pii/S1755296616300862\">several\u003c/a> \u003ca href=\"http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0069841\">longitudinal\u003c/a> \u003ca href=\"https://link.springer.com/article/10.1007/s11482-016-9458-7\">studies\u003c/a> show that screen time leads to unhappiness but \u003ca href=\"https://www.ncbi.nlm.nih.gov/pubmed/28093386\">unhappiness doesn’t lead to more screen time\u003c/a>.\u003c/p>\n\u003cp>If you wanted to give advice based on this research, it would be very simple: Put down your phone or tablet and go do something – just about anything – else.\u003c/p>\n\u003ch2>It’s not just teens\u003c/h2>\n\u003cp>These links between happiness and time use are worrying news, as the current generation of teens (whom I call “iGen” \u003ca href=\"http://www.simonandschuster.com/books/iGen/Jean-M-Twenge/9781501151989\">in my book of the same name\u003c/a>) spends more time with screens than any previous generation. Time spent online doubled between 2006 and 2016, and 82 percent of 12th-graders now use social\u003cbr>\nmedia every day (up from 51 percent in 2008).\u003c/p>\n\u003cp>Sure enough, teens’ happiness suddenly plummeted after 2012 (the year when the majority of Americans owned smartphones). So did teens’ self-esteem and their satisfaction with their lives, especially their satisfaction with their friends, the amount of fun they were having, and their lives as a whole. These declines in well-being mirror other studies finding sharp increases in mental health issues among iGen, including in \u003ca href=\"http://journals.sagepub.com/doi/abs/10.1177/2167702617723376\">depressive symptoms\u003c/a>, \u003ca href=\"http://pediatrics.aappublications.org/content/early/2016/11/10/peds.2016-1878\">major depression\u003c/a>, \u003ca href=\"https://jamanetwork.com/journals/jama/article-abstract/2664031/\">self-harm\u003c/a> and \u003ca href=\"https://www.cdc.gov/mmwr/volumes/66/wr/mm6630a6.htm\">suicide\u003c/a>. Especially compared to the \u003ca href=\"http://journals.sagepub.com/doi/abs/10.1111/j.1467-9280.2008.02204.x\">optimistic and almost relentlessly positive millennials\u003c/a>, iGen is markedly less self-assured, and more are depressed.\u003c/p>\n\u003cp>A similar trend might be occurring for adults: My co-authors and I previously found that \u003ca href=\"http://journals.sagepub.com/doi/abs/10.1177/1948550615602933?journalCode=sppa\">adults over age 30 were less happy than they were 15 years ago\u003c/a>, and that \u003ca href=\"https://www.ncbi.nlm.nih.gov/pubmed/28265779\">adults were having sex less frequently\u003c/a>. There may be many reasons for these trends, but \u003ca href=\"http://www.cnn.com/2016/06/30/health/americans-screen-time-nielsen/index.html\">adults are also spending more time with screens\u003c/a> than they used to. That might mean less face-to-face time with other people, including with their sexual partners. The result: \u003ca href=\"http://journals.sagepub.com/doi/full/10.1177/1948550615616462\">less sex and less happiness\u003c/a>.\u003c/p>\n\u003cp>Although both teen and adult happiness dropped during the years of high unemployment amid the Great Recession (2008-2010), happiness didn’t rebound in the years after 2012 \u003ca href=\"https://www.economicgreenfield.com/2016/01/08/u-3-and-u-6-unemployment-rate-long-term-reference-charts-as-of-january-8-2016/\">when the economy was doing progressively better\u003c/a>. Instead, happiness continued to decline as the economy improved, making it unlikely that economic cycles were to blame for lower happiness after 2012.\u003c/p>\n\u003cp>Growing income inequality could play a role, especially for adults. But if so, one would expect that happiness would have been dropping continuously since the 1980s, \u003ca href=\"https://www.cbsnews.com/news/dreaming-of-a-better-gini/\">when income inequality began to grow\u003c/a>. Instead, happiness began to decline around 2000 for adults and around 2012 for teens. Nevertheless, it’s possible that concerns about the job market and income inequality reached a tipping point in the early 2000s.\u003c/p>\n\u003cp>Somewhat surprisingly, we found that teens who didn’t use digital media at all were actually a little less happy than those who used digital media a little bit (less than an hour a day). Happiness was then steadily lower with more hours of use. Thus, the happiest teens were those who used digital media, \u003ca href=\"https://theconversation.com/does-apple-have-an-obligation-to-make-the-iphone-safer-for-kids-89822\">but for a limited amount of time\u003c/a>.\u003c/p>\n\u003cp>The answer, then, is not to give up technology entirely. Instead, the solution is a familiar adage: everything in moderation. Use your phone for all the cool things it’s good for. And then set it down and go do something else.\u003c/p>\n\u003cp>You might be happier for it.\u003c/p>\n\u003cp>\u003cem>\u003ca href=\"https://theconversation.com/profiles/jean-twenge-315939\">Jean Twenge \u003c/a>is a professor of psychology,\u003c/em> at \u003cem>\u003ca href=\"http://theconversation.com/institutions/san-diego-state-university-1241\">San Diego State University\u003c/a>\u003c/em>\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\u003cem>This article was originally published on \u003ca href=\"http://theconversation.com\">The Conversation\u003c/a>.\u003c/em>\u003c/p>\n\n\u003c/div>\u003c/p>",
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"title": "New CRISPR Method Targeting Blindness In Mice Could Treat Hundreds Of Inherited Diseases",
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"content": "\u003cp>It might seem that scientists have never met a chunk of DNA they couldn’t edit in mice or isolated cells using\u003c/p>\n\u003cp>CRISPR\u003cstrong> —\u003c/strong> from mutations causing \u003ca href=\"https://www.nature.com/articles/nature25164\" target=\"_blank\" rel=\"noopener\">deafness\u003c/a> to those for \u003ca href=\"http://advances.sciencemag.org/content/4/1/eaap9004\" target=\"_blank\" rel=\"noopener\">Duchenne muscular dystrophy.\u003c/a> In fact, they are learning what every pencil- or Word-wielding editor knows: It’s much easier to improve something that’s in terrible shape than writing that’s near perfect.\u003c/p>\n\u003cp>In genome-editing, the challenge for CRISPR-wielding scientists is to edit only one of the two copies, or alleles, of every gene that people have, repairing the ever-so-slightly broken one and leaving the healthy one alone.\u003c/p>\n\u003cp>Now, in one of the first research papers scheduled for publication in the first journal dedicated to research on CRISPR, scientists in Boston \u003ca href=\"https://www.biorxiv.org/content/early/2018/01/29/197962\" target=\"_blank\" rel=\"noopener\">report\u003c/a> “allele specific” editing of a gene that, when mutated, destroys the eye’s photoreceptors and causes the form of blindness called retinitis pigmentosa.\u003c/p>\n\u003cp>[contextly_sidebar id=\"4VdUEhIyuniYpIiGF8VW99wqTQ1JaiBO\"]The achievement might one day help people with retinitis pigmentosa, which affects about 100,000 people in the U.S. But its greater significance is as a proof-of-concept. The hope is that the same trick might work in the hundreds of diseases, including Huntington’s disease and Marfan syndrome, where inheriting a single mutated gene (from mom \u003cem>or\u003c/em> dad) is enough to cause problems despite the presence of a healthy copy, too.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>“You want to target only the mutant allele without messing up the healthy one,” said Linzhao Cheng, of Johns Hopkins University School of Medicine, who is \u003ca href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4351458/\" target=\"_blank\" rel=\"noopener\">developing\u003c/a> allele-specific techniques for blood disorders. “But the alleles might differ in only one nucleotide,” one of the molecular “letters” that spell out the genetic code. “That makes allele-specific editing probably the most challenging situation for CRISPR.”\u003c/p>\n\u003cp>The Boston scientists, led by Dr. Qin Liu of the Ocular Genomics Institute at Massachusetts Eye & Ear Infirmary, aimed to remove the misspelled copy of the gene for rhodopsin, which makes up the rods (of rods and cones fame) in the eye. The misspelling consisted of a single wrong nucleotide. That seemingly minor glitch, called P23H, is enough to produce a rogue rhodopsin that is toxic to the healthy rhodopsins produced by the healthy copy.\u003c/p>\n\u003cp>“It just kills the photoreceptors,” said Dr. Stephen Rose, chief research officer at the Foundation Fighting Blindness, which helped fund Liu’s research. “But what if you could repair that one mutation and turn it back to the normal form? That’s the holy grail, to wave a magic wand and change a single wrong nucleotide to the right one.”\u003c/p>\n\u003caside class=\"pullquote alignright\">“You want to target only the mutant allele without messing up the healthy one.”\u003ccite>Linzhao Cheng, Johns Hopkins University.\u003c/cite>\u003c/aside>\n\u003cp>That’s what Liu and her colleagues report doing in the paper to be published in\u003cstrong> \u003c/strong>\u003ca href=\"http://online.liebertpub.com/toc/crispr/0/0\" target=\"_blank\" rel=\"noopener\">The CRISPR Journal\u003c/a>, whose first issue is due this month. They built standard CRISPR molecules: a target-finding molecule called a guide RNA and a snip-the-nucleotide enzyme, in this case a version of Cas9. They injected their CRISPR molecules under the retinas of days-old mice bred to have one good rhodopsin gene and one mutated copy.\u003c/p>\n\u003cp>The editing flopped. The target-finding molecule couldn’t tell the healthy gene from the one-letter-off copy.\u003c/p>\n\u003cp>Back at the drawing board, the scientists, who included Editas Medicine co-founder J. Keith Joung of Massachusetts General Hospital, created target-finding molecules that looked for shorter regions of DNA, hoping to avoid editing the healthy gene. That produced better results: Cas9 edited only the mutant allele. But it did so in very few of the cells. As long as there is a lot of mutant rhodopsin compared to healthy rhodopsin, the mutant proteins will kill the eyes’ rods.\u003c/p>\n\u003cp>The third time was the charm.\u003c/p>\n\u003cp>In addition to using the short target-finding molecules, the scientists also tweaked Cas9 so it made a beeline for tiny DNA mile markers (called PAMs). The mile markers nearest the disease-causing allele are, luckily, different from those near the healthy one. Including the go-to-PAM instruction in their CRISPR produced accurate editing and a lot of it: There were nearly three times as many healthy rhodopsin molecules as mutant ones, compared to similar numbers of healthy and mutant rhodopsin in cells that had not been CRISPR’d. That translated into healthier eyes, with treated mice having five or six rows of photoreceptors compared with three or four in untreated mice. (The mice were not tested for eyesight, however.)\u003c/p>\n\u003cp>[contextly_sidebar id=\"sdpN9QvSR4CNAVKzz3djOr9Ogv4R5axT\"]As always with CRISPR, there is a danger of editing unintended regions of DNA. The scientists checked potential “off target” sites; nine were fine, and one was inadvertently edited in 3 percent of treated cells, though with no apparent ill effects.\u003c/p>\n\u003cp>“It’s nice work,” said biologist Tara Moore of Ulster University, who is \u003ca href=\"https://www.nature.com/articles/s41598-017-16279-4\" target=\"_blank\" rel=\"noopener\">developing\u003c/a> allele-specific CRISPR editing for eye diseases. Exploiting DNA’s tiny mile markers, the PAMs, offers the best shot at allele-specific editing, she said: “Otherwise it’s “a challenge,” and the chance of hitting the disease-causing DNA but sparing the healthy copy “is low.”\u003c/p>\n\u003cp>The mouse study raises hopes that allele-specific editing might work not only for the mutation in retinitis pigmentosa but also “for most, if not all, human dominant alleles,” the scientists wrote.\u003c/p>\n\u003cp>Liu said she was not permitted to speak to reporters about the paper until The CRISPR Journal published it. The study was also funded by the National Institutes of Health and Mass. General.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\u003cem>This \u003ca href=\"https://www.statnews.com/2018/02/02/crispr-blindness-retinitis-pigmentosa/\" target=\"_blank\" rel=\"noopener\">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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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>It might seem that scientists have never met a chunk of DNA they couldn’t edit in mice or isolated cells using\u003c/p>\n\u003cp>CRISPR\u003cstrong> —\u003c/strong> from mutations causing \u003ca href=\"https://www.nature.com/articles/nature25164\" target=\"_blank\" rel=\"noopener\">deafness\u003c/a> to those for \u003ca href=\"http://advances.sciencemag.org/content/4/1/eaap9004\" target=\"_blank\" rel=\"noopener\">Duchenne muscular dystrophy.\u003c/a> In fact, they are learning what every pencil- or Word-wielding editor knows: It’s much easier to improve something that’s in terrible shape than writing that’s near perfect.\u003c/p>\n\u003cp>In genome-editing, the challenge for CRISPR-wielding scientists is to edit only one of the two copies, or alleles, of every gene that people have, repairing the ever-so-slightly broken one and leaving the healthy one alone.\u003c/p>\n\u003cp>Now, in one of the first research papers scheduled for publication in the first journal dedicated to research on CRISPR, scientists in Boston \u003ca href=\"https://www.biorxiv.org/content/early/2018/01/29/197962\" target=\"_blank\" rel=\"noopener\">report\u003c/a> “allele specific” editing of a gene that, when mutated, destroys the eye’s photoreceptors and causes the form of blindness called retinitis pigmentosa.\u003c/p>\n\u003cp>\u003c/p>\u003cp>\u003c/p>\u003cp>The achievement might one day help people with retinitis pigmentosa, which affects about 100,000 people in the U.S. But its greater significance is as a proof-of-concept. The hope is that the same trick might work in the hundreds of diseases, including Huntington’s disease and Marfan syndrome, where inheriting a single mutated gene (from mom \u003cem>or\u003c/em> dad) is enough to cause problems despite the presence of a healthy copy, too.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>“You want to target only the mutant allele without messing up the healthy one,” said Linzhao Cheng, of Johns Hopkins University School of Medicine, who is \u003ca href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4351458/\" target=\"_blank\" rel=\"noopener\">developing\u003c/a> allele-specific techniques for blood disorders. “But the alleles might differ in only one nucleotide,” one of the molecular “letters” that spell out the genetic code. “That makes allele-specific editing probably the most challenging situation for CRISPR.”\u003c/p>\n\u003cp>The Boston scientists, led by Dr. Qin Liu of the Ocular Genomics Institute at Massachusetts Eye & Ear Infirmary, aimed to remove the misspelled copy of the gene for rhodopsin, which makes up the rods (of rods and cones fame) in the eye. The misspelling consisted of a single wrong nucleotide. That seemingly minor glitch, called P23H, is enough to produce a rogue rhodopsin that is toxic to the healthy rhodopsins produced by the healthy copy.\u003c/p>\n\u003cp>“It just kills the photoreceptors,” said Dr. Stephen Rose, chief research officer at the Foundation Fighting Blindness, which helped fund Liu’s research. “But what if you could repair that one mutation and turn it back to the normal form? That’s the holy grail, to wave a magic wand and change a single wrong nucleotide to the right one.”\u003c/p>\n\u003caside class=\"pullquote alignright\">“You want to target only the mutant allele without messing up the healthy one.”\u003ccite>Linzhao Cheng, Johns Hopkins University.\u003c/cite>\u003c/aside>\n\u003cp>That’s what Liu and her colleagues report doing in the paper to be published in\u003cstrong> \u003c/strong>\u003ca href=\"http://online.liebertpub.com/toc/crispr/0/0\" target=\"_blank\" rel=\"noopener\">The CRISPR Journal\u003c/a>, whose first issue is due this month. They built standard CRISPR molecules: a target-finding molecule called a guide RNA and a snip-the-nucleotide enzyme, in this case a version of Cas9. They injected their CRISPR molecules under the retinas of days-old mice bred to have one good rhodopsin gene and one mutated copy.\u003c/p>\n\u003cp>The editing flopped. The target-finding molecule couldn’t tell the healthy gene from the one-letter-off copy.\u003c/p>\n\u003cp>Back at the drawing board, the scientists, who included Editas Medicine co-founder J. Keith Joung of Massachusetts General Hospital, created target-finding molecules that looked for shorter regions of DNA, hoping to avoid editing the healthy gene. That produced better results: Cas9 edited only the mutant allele. But it did so in very few of the cells. As long as there is a lot of mutant rhodopsin compared to healthy rhodopsin, the mutant proteins will kill the eyes’ rods.\u003c/p>\n\u003cp>The third time was the charm.\u003c/p>\n\u003cp>In addition to using the short target-finding molecules, the scientists also tweaked Cas9 so it made a beeline for tiny DNA mile markers (called PAMs). The mile markers nearest the disease-causing allele are, luckily, different from those near the healthy one. Including the go-to-PAM instruction in their CRISPR produced accurate editing and a lot of it: There were nearly three times as many healthy rhodopsin molecules as mutant ones, compared to similar numbers of healthy and mutant rhodopsin in cells that had not been CRISPR’d. That translated into healthier eyes, with treated mice having five or six rows of photoreceptors compared with three or four in untreated mice. (The mice were not tested for eyesight, however.)\u003c/p>\n\u003cp>\u003c/p>\u003cp>\u003c/p>\u003cp>As always with CRISPR, there is a danger of editing unintended regions of DNA. The scientists checked potential “off target” sites; nine were fine, and one was inadvertently edited in 3 percent of treated cells, though with no apparent ill effects.\u003c/p>\n\u003cp>“It’s nice work,” said biologist Tara Moore of Ulster University, who is \u003ca href=\"https://www.nature.com/articles/s41598-017-16279-4\" target=\"_blank\" rel=\"noopener\">developing\u003c/a> allele-specific CRISPR editing for eye diseases. Exploiting DNA’s tiny mile markers, the PAMs, offers the best shot at allele-specific editing, she said: “Otherwise it’s “a challenge,” and the chance of hitting the disease-causing DNA but sparing the healthy copy “is low.”\u003c/p>\n\u003cp>The mouse study raises hopes that allele-specific editing might work not only for the mutation in retinitis pigmentosa but also “for most, if not all, human dominant alleles,” the scientists wrote.\u003c/p>\n\u003cp>Liu said she was not permitted to speak to reporters about the paper until The CRISPR Journal published it. The study was also funded by the National Institutes of Health and Mass. General.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\u003cem>This \u003ca href=\"https://www.statnews.com/2018/02/02/crispr-blindness-retinitis-pigmentosa/\" target=\"_blank\" rel=\"noopener\">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>The number of transgender people in America has \u003ca href=\"http://williamsinstitute.law.ucla.edu/wp-content/uploads/How-Many-Adults-Identify-as-Transgender-in-the-United-States.pdf\" target=\"_blank\" rel=\"noopener\">doubled\u003c/a> in the last decade, but that doesn't mean the medical profession has caught up. Transgender patients are often unable to find quality health care. \u003ca href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4802845/\" target=\"_blank\" rel=\"noopener\">Research\u003c/a> shows they may face stigma and discrimination, and that they can't find medical interventions like hormone therapy and/or sex reassignment surgery.\u003c/p>\n\u003caside class=\"alignright\">\n\u003ch3>Tell Us Your Story\u003c/h3>\n\u003cp>Are you a transgender person who has struggled to find appropriate care, or a doctor who has struggled to learn to provide care? \u003ca href=\"#health\">Tell us your story\u003c/a> in the question box at the bottom of this post. Your responses will be kept confidential and will not be shared without your permission.\u003c/p>\n\u003c/aside>\n\u003cp>Ximena Lopez is a pediatric endocrinologist at Children’s Health in Dallas, Texas, one of the few in the country who specialize in care for transgender youth. Recently she shared the story of her steep learning curve at the \u003ca href=\"http://www.tedmed.com/\">TEDMED\u003c/a> conference in Palm Springs.\u003c/p>\n\u003cp>I caught up with her afterward. The following interview, in Lopez's words, has been edited for length and clarity:\u003c/p>\n\u003cp>\u003cstrong>Parents Desperate for Help\u003cbr>\n\u003c/strong>\u003c/p>\n\u003cp>I was not prepared when my first transgender child walked into my clinic. I didn’t get any training in medical school, my residency or my sub-specialty training to care for transgender children. And there were people in my clinic who questioned whether I should take the appointment. I decided to see whether I could help, but I didn't think I'd actually provide care.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>During the first appointment, the most striking thing was how desperate the parents were for help. They told me they had called 100 doctors and nobody wanted to provide treatment to stop Tyler's puberty. Then they said, 'We don't care if you experiment with our child. We will do anything for his mental health.'\u003c/p>\n\u003cp>They used a phrase that really stayed with me, 'We prefer to have a living son than a dead daughter.'\u003c/p>\n\u003cp>I knew I had to help.\u003c/p>\n\u003cp>\u003cstrong>[contextly_sidebar id=\"ypQ0S1VFkkumYcqXsE0vYCCbmOzMzDkc\"]Very Little Expertise Available\u003c/strong>\u003c/p>\n\u003cp>I went to the mental health team in my hospital for their expertise and they said, 'We have no experience whatsoever. The only time we've seen transgender patients is when they're trying to commit suicide and admitted to the psychiatric unit.'\u003c/p>\n\u003cp>Fortunately, I eventually found a specialist in Boston and a local psychiatrist to help me navigate suppressing Tyler's puberty.\u003c/p>\n\u003cp>Puberty suppression is a reversible step. It buys time to explore gender identity. So even if the child changed his or her mind later on, we could stop the puberty suppression and puberty will just restart.\u003c/p>\n\u003cp>\u003cb>It's Not a Choice\u003c/b>\u003c/p>\n\u003cp>Gender dysphoria is the conflict that exists when a person's physical or assigned gender is different than how they feel or identify. It's very clear that it's not a choice. That's what I've learned from my patients. Parents have been dealing with this for a long time. They've had years of denial -- mourning the child that they're losing, and then accepting the child they have.\u003c/p>\n\u003cp>When parents are not supportive the risk of suicide attempt can be as high as 60 percent. And when parents are very supportive it can be as low as 4 percent. The difference is just incredible, so parental support is more than critical.\u003c/p>\n\u003cp>Society should see transgender people as just normal people. I think we as humans tend to be afraid of what's different and what's new.\u003c/p>\n\u003cp>\u003cstrong>[contextly_sidebar id=\"3gWXSODBjp95u08FGWK1bohVUcxSPy5g\"]Biological Basis for Transgender Identity\u003c/strong>\u003c/p>\n\u003cp>There's very little known. There's no genetic explanation. We do know that 40 to 60 percent of identical twins are transgender. For example, if one identical twin is transgender, the odds of the other twin being transgender is 40 to 60 percent. That means there probably is a genetic link because that's a high prevalence. But it's not 100 percent. We don't know anything about the specific gene or genes.\u003c/p>\n\u003cp>The other thing is there is a new brain imaging study that is called a functional MRI (fMRI) that show subtle differences in movement in the brain between regular males and females. \u003ca href=\"http://scholar.google.com/scholar_url?url=https://www.researchgate.net/profile/Alicia_Garcia-Falgueras/publication/24377907_Sexual_differentiation_of_the_human_brain_in_relation_to_gender_identity_and_sexual_orientation/links/0046353982a9ca6d8e000000.pdf&hl=en&sa=X&scisig=AAGBfm19NmQGvQy8twJNvMaPYGD17MaCvg&nossl=1&oi=scholarr\" target=\"_blank\" rel=\"noopener\">Researchers\u003c/a> looked at transgender people before they received any hormone therapy or any treatment that could affect brain function or morphology, and transgender people have differences that put them more aligned with the gender they identify with. In other words, their brains are actually acting more like the brain that they identify with rather than their biological gender.\u003cbr>\n\u003ca name=\"health\">\u003c/a>\u003c/p>\n\u003ch2>Have you been able to find appropriate health care for your needs as a transgender person? Why or why not? Tell us your story; your responses will be kept confidential and will never be shared without your permission.\u003c/h2>\n\u003cp>[transgenderhealthcare]\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\u003cem>Editor's Note: We will post Ximena Lopez's TEDMED talk here as soon as it is available.\u003c/em>\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>The number of transgender people in America has \u003ca href=\"http://williamsinstitute.law.ucla.edu/wp-content/uploads/How-Many-Adults-Identify-as-Transgender-in-the-United-States.pdf\" target=\"_blank\" rel=\"noopener\">doubled\u003c/a> in the last decade, but that doesn't mean the medical profession has caught up. Transgender patients are often unable to find quality health care. \u003ca href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4802845/\" target=\"_blank\" rel=\"noopener\">Research\u003c/a> shows they may face stigma and discrimination, and that they can't find medical interventions like hormone therapy and/or sex reassignment surgery.\u003c/p>\n\u003caside class=\"alignright\">\n\u003ch3>Tell Us Your Story\u003c/h3>\n\u003cp>Are you a transgender person who has struggled to find appropriate care, or a doctor who has struggled to learn to provide care? \u003ca href=\"#health\">Tell us your story\u003c/a> in the question box at the bottom of this post. Your responses will be kept confidential and will not be shared without your permission.\u003c/p>\n\u003c/aside>\n\u003cp>Ximena Lopez is a pediatric endocrinologist at Children’s Health in Dallas, Texas, one of the few in the country who specialize in care for transgender youth. Recently she shared the story of her steep learning curve at the \u003ca href=\"http://www.tedmed.com/\">TEDMED\u003c/a> conference in Palm Springs.\u003c/p>\n\u003cp>I caught up with her afterward. The following interview, in Lopez's words, has been edited for length and clarity:\u003c/p>\n\u003cp>\u003cstrong>Parents Desperate for Help\u003cbr>\n\u003c/strong>\u003c/p>\n\u003cp>I was not prepared when my first transgender child walked into my clinic. I didn’t get any training in medical school, my residency or my sub-specialty training to care for transgender children. And there were people in my clinic who questioned whether I should take the appointment. I decided to see whether I could help, but I didn't think I'd actually provide care.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>During the first appointment, the most striking thing was how desperate the parents were for help. They told me they had called 100 doctors and nobody wanted to provide treatment to stop Tyler's puberty. Then they said, 'We don't care if you experiment with our child. We will do anything for his mental health.'\u003c/p>\n\u003cp>They used a phrase that really stayed with me, 'We prefer to have a living son than a dead daughter.'\u003c/p>\n\u003cp>I knew I had to help.\u003c/p>\n\u003cp>\u003cstrong>\u003c/p>\u003cp>\u003c/p>\u003cp>Very Little Expertise Available\u003c/strong>\u003c/p>\n\u003cp>I went to the mental health team in my hospital for their expertise and they said, 'We have no experience whatsoever. The only time we've seen transgender patients is when they're trying to commit suicide and admitted to the psychiatric unit.'\u003c/p>\n\u003cp>Fortunately, I eventually found a specialist in Boston and a local psychiatrist to help me navigate suppressing Tyler's puberty.\u003c/p>\n\u003cp>Puberty suppression is a reversible step. It buys time to explore gender identity. So even if the child changed his or her mind later on, we could stop the puberty suppression and puberty will just restart.\u003c/p>\n\u003cp>\u003cb>It's Not a Choice\u003c/b>\u003c/p>\n\u003cp>Gender dysphoria is the conflict that exists when a person's physical or assigned gender is different than how they feel or identify. It's very clear that it's not a choice. That's what I've learned from my patients. Parents have been dealing with this for a long time. They've had years of denial -- mourning the child that they're losing, and then accepting the child they have.\u003c/p>\n\u003cp>When parents are not supportive the risk of suicide attempt can be as high as 60 percent. And when parents are very supportive it can be as low as 4 percent. The difference is just incredible, so parental support is more than critical.\u003c/p>\n\u003cp>Society should see transgender people as just normal people. I think we as humans tend to be afraid of what's different and what's new.\u003c/p>\n\u003cp>\u003cstrong>\u003c/p>\u003cp>\u003c/p>\u003cp>Biological Basis for Transgender Identity\u003c/strong>\u003c/p>\n\u003cp>There's very little known. There's no genetic explanation. We do know that 40 to 60 percent of identical twins are transgender. For example, if one identical twin is transgender, the odds of the other twin being transgender is 40 to 60 percent. That means there probably is a genetic link because that's a high prevalence. But it's not 100 percent. We don't know anything about the specific gene or genes.\u003c/p>\n\u003cp>The other thing is there is a new brain imaging study that is called a functional MRI (fMRI) that show subtle differences in movement in the brain between regular males and females. \u003ca href=\"http://scholar.google.com/scholar_url?url=https://www.researchgate.net/profile/Alicia_Garcia-Falgueras/publication/24377907_Sexual_differentiation_of_the_human_brain_in_relation_to_gender_identity_and_sexual_orientation/links/0046353982a9ca6d8e000000.pdf&hl=en&sa=X&scisig=AAGBfm19NmQGvQy8twJNvMaPYGD17MaCvg&nossl=1&oi=scholarr\" target=\"_blank\" rel=\"noopener\">Researchers\u003c/a> looked at transgender people before they received any hormone therapy or any treatment that could affect brain function or morphology, and transgender people have differences that put them more aligned with the gender they identify with. In other words, their brains are actually acting more like the brain that they identify with rather than their biological gender.\u003cbr>\n\u003ca name=\"health\">\u003c/a>\u003c/p>\n\u003ch2>Have you been able to find appropriate health care for your needs as a transgender person? Why or why not? Tell us your story; your responses will be kept confidential and will never be shared without your permission.\u003c/h2>\n\u003cp>[transgenderhealthcare]\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\u003cem>Editor's Note: We will post Ximena Lopez's TEDMED talk here as soon as it is available.\u003c/em>\u003c/p>\n\n\u003c/div>\u003c/p>",
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"disqusTitle": "Flu Vaccine This Year Was a Dud According to Early Data",
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"content": "\u003cp>As the country battles an especially fierce flu season, experts have struggled to explain why one family of virus — the influenza A virus H3N2 — that has infected a lot of people in recent years is causing so much damage again this winter.\u003c/p>\n\u003cp>[contextly_sidebar id=\"pMmCXaibLUwxTcHOuOXFWa0DdskcP6kV\"]Now, new data from north of the border sheds some light on the question.\u003c/p>\n\u003cp>Canadian influenza researchers reported Thursday in the online journal \u003cem>Eurosurveillance\u003c/em> that the first reckoning of how well the flu vaccine is protecting against H3N2 viruses this year in North America has a dismal answer: not very.\u003c/p>\n\u003cp>Their midseason estimate, based on data from the four provinces where roughly 80 percent of Canadians live, suggested that the H3N2 component of the vaccine is 17 percent effective at preventing infection. Last year it was estimated at 37 percent in Canada and 34 percent in the U.S.\u003c/p>\n\u003cp>Public health authorities have come to expect protection against H3N2 — the weak link of the vaccine — to be in the low-to-mid 30 percent range at best. But this estimate is half that. And the fact that it was so much lower came as a surprise to the Centers for Disease Control and Prevention’s flu experts, who have yet to analyze their midseason flu vaccine effectiveness data.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>“It was lower than what the Canadians or we experienced last year,” said Alicia Fry, head of epidemiology for the CDC’s influenza division. Given that there haven’t been major changes in the viruses, “it is a surprising result.”\u003c/p>\n\u003cp>Fry said the CDC surveillance network will stop collecting data for their interim analysis next week, and the agency will publish their findings mid-month. Both teams will also reanalyze their surveillance data at the end of the season, when more data typically brings a sharper focus to the findings.\u003c/p>\n\u003cp>The new research also reported that — at least in Canada — a new subgroup of the H3N2 clan has become the dominant H3N2 viruses causing illness this season. It may be that the vaccine isn’t targeting that group of viruses effectively. The U.S. is seeing a similar pattern, said Jacqueline Katz, deputy director of the CDC’s influenza division.\u003c/p>\n\u003cp>Whatever the reason, the findings confirm the fact that people who’ve been vaccinated are among those contracting flu this season.\u003c/p>\n\u003cp>“This is low protection. And the overall message is: People who have been vaccinated should not consider themselves invincible against this H3N2 virus that’s circulating,” said Dr. Danuta Skowronski, lead author of the report and an influenza epidemiologist at the British Columbia Center for Disease Control.\u003c/p>\n\u003cp>“That means getting early medical care, antiviral treatment for those at high risk of influenza complications. That’s the main value of reporting these midseason estimates.”\u003c/p>\n\u003cp>In working-age adults, the estimated protection is lower still: 10 percent. That is in line with the protection level Australia saw in its harsh winter 2017 flu season.\u003c/p>\n\u003cp>Because of the small number of people studied — 689 — the confidence intervals around the estimates are wide. You can think of them as the margins of error around a polling number that is said to be accurate within, for example, 3 percentage points up or down.\u003c/p>\n\u003cp>And in the case of the assessment of the H3N2 component, the confidence intervals cross zero, which means the researchers cannot rule out the possibility there was no benefit from that part of the vaccine. But based on statistical calculations, the 17 percent overall and 10 percent among working-age adults is more likely to be correct, Skowronski said.\u003c/p>\n\u003cp>That low protection level among working-age adults could explain why the CDC has reported unusually high flu hospitalization rates among people aged 50 to 64 this year.\u003c/p>\n\u003cp>The Canadian data may provide clues into what is happening in the United States. But flu season activity varies across geographic regions, and it will be important to see U.S. data to see if the Canadian patterns are reflective of what is happening here.\u003c/p>\n\u003cp>It’s already clear they are not a perfect match. There is considerably more influenza B illness in Canada this year than there has been in the U.S. In fact, where flu B infections make up less than 20 percent of lab-confirmed flu cases here so far this year, the corresponding figure in Canada is about 40 percent. And in this study, flu B infections made up 51 percent of the confirmed flu cases.\u003c/p>\n\u003cp>The vaccine’s performance against influenza B viruses was substantially better than it was against H3N2. The study estimated the flu shot protected about 55 percent of people who received it against influenza B viruses.\u003c/p>\n\u003cp>That’s especially interesting given that most of the flu shots given in Canada targeted the wrong flu B viruses.\u003c/p>\n\u003cp>There are two lineages of influenza B viruses. Some flu shots target both, but older products contain protection against just one. More than two-thirds of the vaccines used in Canada protect against only one B virus, and this year the virus included in those products is not the one causing the most illness.\u003c/p>\n\u003cp>Even though the two B viruses are quite different genetically, the vaccine appears to be offering cross-protection, Skowronski said.\u003c/p>\n\u003cp>More than three-quarters of flu vaccines used in the U.S. target both flu B viruses.\u003c/p>\n\u003cp>The report does not estimate how well this year’s vaccine protects against H1N1 viruses. Skowronski said there has simply been too little H1N1 disease in Canada so far this winter to make that calculation. Fry said the CDC hopes to be able to give an estimate of how well the H1N1 component of the vaccine is working.\u003c/p>\n\u003cp>Likewise, the Canadian team could not estimate how protective the vaccine has been against H3N2 in children. The end-of-season analysis should be able to answer that question, she said.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\u003cem>\u003cspan style=\"font-weight: 400\"> This \u003ca href=\"https://www.statnews.com/2018/02/01/flu-vaccine-protection-h3n2/\" target=\"_blank\" rel=\"noopener\">story\u003c/a> was originally published by STAT, an online publication of Boston Globe Media that covers health, medicine, and scientific discovery. \u003c/span>\u003c/em>\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>As the country battles an especially fierce flu season, experts have struggled to explain why one family of virus — the influenza A virus H3N2 — that has infected a lot of people in recent years is causing so much damage again this winter.\u003c/p>\n\u003cp>\u003c/p>\u003cp>\u003c/p>\u003cp>Now, new data from north of the border sheds some light on the question.\u003c/p>\n\u003cp>Canadian influenza researchers reported Thursday in the online journal \u003cem>Eurosurveillance\u003c/em> that the first reckoning of how well the flu vaccine is protecting against H3N2 viruses this year in North America has a dismal answer: not very.\u003c/p>\n\u003cp>Their midseason estimate, based on data from the four provinces where roughly 80 percent of Canadians live, suggested that the H3N2 component of the vaccine is 17 percent effective at preventing infection. Last year it was estimated at 37 percent in Canada and 34 percent in the U.S.\u003c/p>\n\u003cp>Public health authorities have come to expect protection against H3N2 — the weak link of the vaccine — to be in the low-to-mid 30 percent range at best. But this estimate is half that. And the fact that it was so much lower came as a surprise to the Centers for Disease Control and Prevention’s flu experts, who have yet to analyze their midseason flu vaccine effectiveness data.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>“It was lower than what the Canadians or we experienced last year,” said Alicia Fry, head of epidemiology for the CDC’s influenza division. Given that there haven’t been major changes in the viruses, “it is a surprising result.”\u003c/p>\n\u003cp>Fry said the CDC surveillance network will stop collecting data for their interim analysis next week, and the agency will publish their findings mid-month. Both teams will also reanalyze their surveillance data at the end of the season, when more data typically brings a sharper focus to the findings.\u003c/p>\n\u003cp>The new research also reported that — at least in Canada — a new subgroup of the H3N2 clan has become the dominant H3N2 viruses causing illness this season. It may be that the vaccine isn’t targeting that group of viruses effectively. The U.S. is seeing a similar pattern, said Jacqueline Katz, deputy director of the CDC’s influenza division.\u003c/p>\n\u003cp>Whatever the reason, the findings confirm the fact that people who’ve been vaccinated are among those contracting flu this season.\u003c/p>\n\u003cp>“This is low protection. And the overall message is: People who have been vaccinated should not consider themselves invincible against this H3N2 virus that’s circulating,” said Dr. Danuta Skowronski, lead author of the report and an influenza epidemiologist at the British Columbia Center for Disease Control.\u003c/p>\n\u003cp>“That means getting early medical care, antiviral treatment for those at high risk of influenza complications. That’s the main value of reporting these midseason estimates.”\u003c/p>\n\u003cp>In working-age adults, the estimated protection is lower still: 10 percent. That is in line with the protection level Australia saw in its harsh winter 2017 flu season.\u003c/p>\n\u003cp>Because of the small number of people studied — 689 — the confidence intervals around the estimates are wide. You can think of them as the margins of error around a polling number that is said to be accurate within, for example, 3 percentage points up or down.\u003c/p>\n\u003cp>And in the case of the assessment of the H3N2 component, the confidence intervals cross zero, which means the researchers cannot rule out the possibility there was no benefit from that part of the vaccine. But based on statistical calculations, the 17 percent overall and 10 percent among working-age adults is more likely to be correct, Skowronski said.\u003c/p>\n\u003cp>That low protection level among working-age adults could explain why the CDC has reported unusually high flu hospitalization rates among people aged 50 to 64 this year.\u003c/p>\n\u003cp>The Canadian data may provide clues into what is happening in the United States. But flu season activity varies across geographic regions, and it will be important to see U.S. data to see if the Canadian patterns are reflective of what is happening here.\u003c/p>\n\u003cp>It’s already clear they are not a perfect match. There is considerably more influenza B illness in Canada this year than there has been in the U.S. In fact, where flu B infections make up less than 20 percent of lab-confirmed flu cases here so far this year, the corresponding figure in Canada is about 40 percent. And in this study, flu B infections made up 51 percent of the confirmed flu cases.\u003c/p>\n\u003cp>The vaccine’s performance against influenza B viruses was substantially better than it was against H3N2. The study estimated the flu shot protected about 55 percent of people who received it against influenza B viruses.\u003c/p>\n\u003cp>That’s especially interesting given that most of the flu shots given in Canada targeted the wrong flu B viruses.\u003c/p>\n\u003cp>There are two lineages of influenza B viruses. Some flu shots target both, but older products contain protection against just one. More than two-thirds of the vaccines used in Canada protect against only one B virus, and this year the virus included in those products is not the one causing the most illness.\u003c/p>\n\u003cp>Even though the two B viruses are quite different genetically, the vaccine appears to be offering cross-protection, Skowronski said.\u003c/p>\n\u003cp>More than three-quarters of flu vaccines used in the U.S. target both flu B viruses.\u003c/p>\n\u003cp>The report does not estimate how well this year’s vaccine protects against H1N1 viruses. Skowronski said there has simply been too little H1N1 disease in Canada so far this winter to make that calculation. Fry said the CDC hopes to be able to give an estimate of how well the H1N1 component of the vaccine is working.\u003c/p>\n\u003cp>Likewise, the Canadian team could not estimate how protective the vaccine has been against H3N2 in children. The end-of-season analysis should be able to answer that question, she said.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\u003cem>\u003cspan style=\"font-weight: 400\"> This \u003ca href=\"https://www.statnews.com/2018/02/01/flu-vaccine-protection-h3n2/\" target=\"_blank\" rel=\"noopener\">story\u003c/a> was originally published by STAT, an online publication of Boston Globe Media that covers health, medicine, and scientific discovery. \u003c/span>\u003c/em>\u003c/p>\n\n\u003c/div>\u003c/p>",
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"disqusTitle": "Why Family Members Can Get Different Ancestry Results From DNA Tests",
"title": "Why Family Members Can Get Different Ancestry Results From DNA Tests",
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"content": "\u003cp>Maybe you got one of those find-your-ancestry kits over the holidays. You've sent off your awkwardly-collected saliva sample, and you're awaiting your results. If your experience is anything like that of me and my mom, you may find surprises — not the dramatic \"switched at birth\" kind, but results that are really different from what you expected.\u003c/p>\n\u003caside class=\"pullquote alignright\">While we get half our genes from each parent, a process called recombination means that each egg and each sperm carries a different mix of the genes from each.\u003c/aside>\n\u003cp>My mom, Carmen Grayson, taught history for 45 years, high school and college, retiring from Hampton University in the late 1990s. But retired history professors never really retire, so she has been researching her family's migrations, through both paper records and now a DNA test. Her father was French Canadian, and her mother (my namesake, Gisella D'Appollonia) was born of Italian parents. They moved to Canada about a decade before my grandmother was born in 1909.\u003c/p>\n\u003cp>Last fall, we sent away to get our DNA tested by \u003ca href=\"https://www.helix.com/\">Helix\u003c/a>, the company that works with National Geographic. Mom's results: 31 percent from Italy and Southern Europe. That made sense because of her Italian mother. But \u003cem>my\u003c/em> Helix results didn't even have an \"Italy and Southern European\" category. How could I have 50 percent of Mom's DNA and not have any Italian? We do look alike, and she says there is little chance we were switched at birth.\u003c/p>\n\u003cp>[contextly_sidebar id=\"BCKB7ylkmMa5eccVlIQnzjjA2KxxcRsY\"]We decided to get a second opinion and sent away to another company, \u003ca href=\"https://www.23andme.com/\">23andMe.\u003c/a> We opened our results together and were just as surprised. This time, I at least had a category for southern Europe. But Mom came back as 25 percent southern European, me only 6 percent. And the Italian? Mom had 11.3 percent to my 1.6. So maybe the first test wasn't wrong. But how could I have an Italian grandmother and almost no Italian genes?\u003c/p>\n\u003cp>To answer this question, Mom and I drove up to Baltimore to visit \u003ca href=\"https://www.hopkinsmedicine.org/profiles/results/directory/profile/3205347/aravinda-chakravarti\">Dr. Aravinda Chakravarti\u003c/a> of the Johns Hopkins University School of Medicine and the Bloomberg School of Public Health, who has spent his career studying genetics and human health.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>\"That's surprising,\" he told us when we showed him the results. \"But it may still be in the limits of error that these methods have.\"\u003c/p>\n\u003cp>The science for analyzing one's genome is good, Chakravarti says. But the ways the companies analyze the genes leave lots of room for interpretation. So, he says, these tests \"would be most accurate at the level of continental origins, and as you go to higher and higher resolution, they would become less and less accurate.\"\u003c/p>\n\u003cp>As in my case — the results got me to Europe, just not Italy.\u003c/p>\n\u003cp>My 23andMe test also showed less than 1 percent of South Asian, Sub-Saharan African, and East Asian & Native American. This, Chakravarti says, is likely true because the genetics of people on a continental level are so different, and it's not likely South Asian is going to look like European. \"Resolving a difference between, say, an African genome and an East Asian genome would be easy,\" he says. \"But resolving that same difference between one part of East Asia and another part of East Asia is much more difficult.\"\u003c/p>\n\u003cp>I also learned that even though I got half my genes from Mom, they may not mirror hers.\u003c/p>\n\u003cp>We do have the genes we inherit — 50 percent from each parent. But \u003ca href=\"https://www.helix.com/blog/author/elissa-levin/\">Elissa Levin\u003c/a>, a genetic counselor and the director of policy and clinical affairs of Helix, says a process called recombination means that each egg and each sperm carries a different mix of a parent's genes.\u003c/p>\n\u003cp>\"When we talk about the 50 percent that gets inherited from Mom, there's a chance that you have a recombination that just gave you more of the northwest European part than the Italian part of your Mom's ancestry DNA,\" she says. That is also why siblings can have different ancestry results.\u003c/p>\n\u003cp>The companies compare customers' DNA samples to samples they have from people around the world who have lived in a certain area for generations. The samples come from some databases to which all scientists have access, and the companies may also collect their own.\u003c/p>\n\u003cp>\"We're able to look at, what are the specific markers, what are the specific segments of DNA that we're looking at that help us to identify, 'Those people are from this part of northern Europe or southern Europe or Southeast Asia,' \" Levin says.\u003c/p>\n\u003cp>As the companies collect more samples, their understanding of markers of people of a particular heritage should become more precise. But for now, the smaller the percentage of a population within a continent that is in the database, the less certain they are. Levin says Helix chooses to not report some of those smaller percentages.\u003c/p>\n\u003cp>The 23andMe reports results with a 50 percent confidence interval — they're 50 percent sure their geographic placement is correct. Move the setting up to 90 percent confidence, meaning your placement in a region is 90 percent certain, and that small 1.6 percent of my ancestry that is Italian disappears.\u003c/p>\n\u003cp>The ancestry tests also have to take into account the fact that humans have been migrating for millennia, mixing DNA along the way. To contend with that, the companies' analyses involve some \"random chance,\" as Levin puts it. A computer has to make a decision.\u003c/p>\n\u003cp>And the ancestry companies have to make judgment calls. \u003ca href=\"https://blog.23andme.com/health-traits/a-conversation-health-content-scientist-robin-smith/\">Robin Smith\u003c/a>, a senior product manager with 23andMe, says their computers compare the DNA with 31 groups. \"Let's say a piece of your DNA looks most like British and Irish but it also looks a little bit like French-German,\" he says. \"Based on some statistical measures, we'd decide whether to call that as British-Irish or French-German, or maybe we go up one level and call it northwestern European.\"\u003c/p>\n\u003cp>What does he think explains my case?\u003c/p>\n\u003cp>\"It was a bit surprising,\" he says. \"But in looking at the fact that you have some southern European and some French-German, the picture became a little clearer to me.\"\u003c/p>\n\u003cp>So, for now, my Italian grandmother doesn't show up in these tests. No matter — Chakravarti, Levin and Smith all say let the results \u003cem>add\u003c/em> to your life story. The DNA is just a piece of what makes you you.\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp>\u003cem>Gisele Grayson is a senior producer on NPR's Science Desk who runs the health reporting collaboration with member stations and \u003ca href=\"http://www.kaiserhealthnews.org\">Kaiser Health News\u003c/a>. \u003c/em>\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2018 NPR. To see more, visit http://www.npr.org/.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=My+Grandmother+Was+Italian.+Why+Aren%27t+My+Genes+Italian%3F&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n",
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"excerpt": "Popular DNA ancestry tests don't always find what people expect. That is because of how DNA rearranges itself when egg meets sperm — and the quirks of genetic databases.",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>Maybe you got one of those find-your-ancestry kits over the holidays. You've sent off your awkwardly-collected saliva sample, and you're awaiting your results. If your experience is anything like that of me and my mom, you may find surprises — not the dramatic \"switched at birth\" kind, but results that are really different from what you expected.\u003c/p>\n\u003caside class=\"pullquote alignright\">While we get half our genes from each parent, a process called recombination means that each egg and each sperm carries a different mix of the genes from each.\u003c/aside>\n\u003cp>My mom, Carmen Grayson, taught history for 45 years, high school and college, retiring from Hampton University in the late 1990s. But retired history professors never really retire, so she has been researching her family's migrations, through both paper records and now a DNA test. Her father was French Canadian, and her mother (my namesake, Gisella D'Appollonia) was born of Italian parents. They moved to Canada about a decade before my grandmother was born in 1909.\u003c/p>\n\u003cp>Last fall, we sent away to get our DNA tested by \u003ca href=\"https://www.helix.com/\">Helix\u003c/a>, the company that works with National Geographic. Mom's results: 31 percent from Italy and Southern Europe. That made sense because of her Italian mother. But \u003cem>my\u003c/em> Helix results didn't even have an \"Italy and Southern European\" category. How could I have 50 percent of Mom's DNA and not have any Italian? We do look alike, and she says there is little chance we were switched at birth.\u003c/p>\n\u003cp>\u003c/p>\u003cp>\u003c/p>\u003cp>We decided to get a second opinion and sent away to another company, \u003ca href=\"https://www.23andme.com/\">23andMe.\u003c/a> We opened our results together and were just as surprised. This time, I at least had a category for southern Europe. But Mom came back as 25 percent southern European, me only 6 percent. And the Italian? Mom had 11.3 percent to my 1.6. So maybe the first test wasn't wrong. But how could I have an Italian grandmother and almost no Italian genes?\u003c/p>\n\u003cp>To answer this question, Mom and I drove up to Baltimore to visit \u003ca href=\"https://www.hopkinsmedicine.org/profiles/results/directory/profile/3205347/aravinda-chakravarti\">Dr. Aravinda Chakravarti\u003c/a> of the Johns Hopkins University School of Medicine and the Bloomberg School of Public Health, who has spent his career studying genetics and human health.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>\"That's surprising,\" he told us when we showed him the results. \"But it may still be in the limits of error that these methods have.\"\u003c/p>\n\u003cp>The science for analyzing one's genome is good, Chakravarti says. But the ways the companies analyze the genes leave lots of room for interpretation. So, he says, these tests \"would be most accurate at the level of continental origins, and as you go to higher and higher resolution, they would become less and less accurate.\"\u003c/p>\n\u003cp>As in my case — the results got me to Europe, just not Italy.\u003c/p>\n\u003cp>My 23andMe test also showed less than 1 percent of South Asian, Sub-Saharan African, and East Asian & Native American. This, Chakravarti says, is likely true because the genetics of people on a continental level are so different, and it's not likely South Asian is going to look like European. \"Resolving a difference between, say, an African genome and an East Asian genome would be easy,\" he says. \"But resolving that same difference between one part of East Asia and another part of East Asia is much more difficult.\"\u003c/p>\n\u003cp>I also learned that even though I got half my genes from Mom, they may not mirror hers.\u003c/p>\n\u003cp>We do have the genes we inherit — 50 percent from each parent. But \u003ca href=\"https://www.helix.com/blog/author/elissa-levin/\">Elissa Levin\u003c/a>, a genetic counselor and the director of policy and clinical affairs of Helix, says a process called recombination means that each egg and each sperm carries a different mix of a parent's genes.\u003c/p>\n\u003cp>\"When we talk about the 50 percent that gets inherited from Mom, there's a chance that you have a recombination that just gave you more of the northwest European part than the Italian part of your Mom's ancestry DNA,\" she says. That is also why siblings can have different ancestry results.\u003c/p>\n\u003cp>The companies compare customers' DNA samples to samples they have from people around the world who have lived in a certain area for generations. The samples come from some databases to which all scientists have access, and the companies may also collect their own.\u003c/p>\n\u003cp>\"We're able to look at, what are the specific markers, what are the specific segments of DNA that we're looking at that help us to identify, 'Those people are from this part of northern Europe or southern Europe or Southeast Asia,' \" Levin says.\u003c/p>\n\u003cp>As the companies collect more samples, their understanding of markers of people of a particular heritage should become more precise. But for now, the smaller the percentage of a population within a continent that is in the database, the less certain they are. Levin says Helix chooses to not report some of those smaller percentages.\u003c/p>\n\u003cp>The 23andMe reports results with a 50 percent confidence interval — they're 50 percent sure their geographic placement is correct. Move the setting up to 90 percent confidence, meaning your placement in a region is 90 percent certain, and that small 1.6 percent of my ancestry that is Italian disappears.\u003c/p>\n\u003cp>The ancestry tests also have to take into account the fact that humans have been migrating for millennia, mixing DNA along the way. To contend with that, the companies' analyses involve some \"random chance,\" as Levin puts it. A computer has to make a decision.\u003c/p>\n\u003cp>And the ancestry companies have to make judgment calls. \u003ca href=\"https://blog.23andme.com/health-traits/a-conversation-health-content-scientist-robin-smith/\">Robin Smith\u003c/a>, a senior product manager with 23andMe, says their computers compare the DNA with 31 groups. \"Let's say a piece of your DNA looks most like British and Irish but it also looks a little bit like French-German,\" he says. \"Based on some statistical measures, we'd decide whether to call that as British-Irish or French-German, or maybe we go up one level and call it northwestern European.\"\u003c/p>\n\u003cp>What does he think explains my case?\u003c/p>\n\u003cp>\"It was a bit surprising,\" he says. \"But in looking at the fact that you have some southern European and some French-German, the picture became a little clearer to me.\"\u003c/p>\n\u003cp>So, for now, my Italian grandmother doesn't show up in these tests. No matter — Chakravarti, Levin and Smith all say let the results \u003cem>add\u003c/em> to your life story. The DNA is just a piece of what makes you you.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"info": "The Commonwealth Club of California is the nation's oldest and largest public affairs forum. As a non-partisan forum, The Club brings to the public airwaves diverse viewpoints on important topics. The Club's weekly radio broadcast - the oldest in the U.S., dating back to 1924 - is carried across the nation on public radio stations and is now podcasting. Our website archive features audio of our recent programs, as well as selected speeches from our long and distinguished history. This podcast feed is usually updated twice a week and is always un-edited.",
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"order": 9
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"id": "fresh-air",
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"airtime": "SUN 7:30pm-8pm",
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"tagline": "Where conversation and cultura meet",
"info": "What kind of no sabo word is Hyphenación? For us, it’s about living within a hyphenation. Like being a third-gen Mexican-American from the Texas border now living that Bay Area Chicano life. Like Xorje! Each week we bring together a couple of hyphenated Latinos to talk all about personal life choices: family, careers, relationships, belonging … everything is on the table. ",
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"order": 15
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"title": "The Political Mind of Jerry Brown",
"tagline": "Lessons from a lifetime in politics",
"info": "The Political Mind of Jerry Brown brings listeners the wisdom of the former Governor, Mayor, and presidential candidate. Scott Shafer interviewed Brown for more than 40 hours, covering the former governor's life and half-century in the political game – and Brown has some lessons he'd like to share. ",
"imageSrc": "https://cdn.kqed.org/wp-content/uploads/2024/04/The-Political-Mind-of-Jerry-Brown-Podcast-Tile-703x703-1.jpg",
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"order": 18
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"info": "Latino USA, the radio journal of news and culture, is the only national, English-language radio program produced from a Latino perspective.",
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"marketplace": {
"id": "marketplace",
"title": "Marketplace",
"info": "Our flagship program, helmed by Kai Ryssdal, examines what the day in money delivered, through stories, conversations, newsworthy numbers and more. Updated Monday through Friday at about 3:30 p.m. PT.",
"airtime": "MON-FRI 4pm-4:30pm, MON-WED 6:30pm-7pm",
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"source": "American Public Media"
},
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"masters-of-scale": {
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"title": "Masters of Scale",
"info": "Masters of Scale is an original podcast in which LinkedIn co-founder and Greylock Partner Reid Hoffman sets out to describe and prove theories that explain how great entrepreneurs take their companies from zero to a gazillion in ingenious fashion.",
"airtime": "Every other Wednesday June 12 through October 16 at 8pm (repeats Thursdays at 2am)",
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},
"mindshift": {
"id": "mindshift",
"title": "MindShift",
"tagline": "A podcast about the future of learning and how we raise our kids",
"info": "The MindShift podcast explores the innovations in education that are shaping how kids learn. Hosts Ki Sung and Katrina Schwartz introduce listeners to educators, researchers, parents and students who are developing effective ways to improve how kids learn. We cover topics like how fed-up administrators are developing surprising tactics to deal with classroom disruptions; how listening to podcasts are helping kids develop reading skills; the consequences of overparenting; and why interdisciplinary learning can engage students on all ends of the traditional achievement spectrum. This podcast is part of the MindShift education site, a division of KQED News. KQED is an NPR/PBS member station based in San Francisco. You can also visit the MindShift website for episodes and supplemental blog posts or tweet us \u003ca href=\"https://twitter.com/MindShiftKQED\">@MindShiftKQED\u003c/a> or visit us at \u003ca href=\"/mindshift\">MindShift.KQED.org\u003c/a>",
"imageSrc": "https://cdn.kqed.org/wp-content/uploads/2024/04/Mindshift-Podcast-Tile-703x703-1.jpg",
"imageAlt": "KQED MindShift: How We Will Learn",
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"meta": {
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"order": 12
},
"link": "/podcasts/mindshift",
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"google": "https://podcasts.google.com/feed/aHR0cHM6Ly9mZWVkcy5tZWdhcGhvbmUuZm0vS1FJTkM1NzY0NjAwNDI5",
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"morning-edition": {
"id": "morning-edition",
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"info": "\u003cem>Morning Edition\u003c/em> takes listeners around the country and the world with multi-faceted stories and commentaries every weekday. Hosts Steve Inskeep, David Greene and Rachel Martin bring you the latest breaking news and features to prepare you for the day.",
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"onourwatch": {
"id": "onourwatch",
"title": "On Our Watch",
"tagline": "Deeply-reported investigative journalism",
"info": "For decades, the process for how police police themselves has been inconsistent – if not opaque. In some states, like California, these proceedings were completely hidden. After a new police transparency law unsealed scores of internal affairs files, our reporters set out to examine these cases and the shadow world of police discipline. On Our Watch brings listeners into the rooms where officers are questioned and witnesses are interrogated to find out who this system is really protecting. Is it the officers, or the public they've sworn to serve?",
"imageSrc": "https://cdn.kqed.org/wp-content/uploads/2024/04/On-Our-Watch-Podcast-Tile-703x703-1.jpg",
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"order": 11
},
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"on-the-media": {
"id": "on-the-media",
"title": "On The Media",
"info": "Our weekly podcast explores how the media 'sausage' is made, casts an incisive eye on fluctuations in the marketplace of ideas, and examines threats to the freedom of information and expression in America and abroad. For one hour a week, the show tries to lift the veil from the process of \"making media,\" especially news media, because it's through that lens that we see the world and the world sees us",
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},
"link": "/radio/program/on-the-media",
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},
"pbs-newshour": {
"id": "pbs-newshour",
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"info": "Analysis, background reports and updates from the PBS NewsHour putting today's news in context.",
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"imageSrc": "https://cdn.kqed.org/wp-content/uploads/2024/04/PBS-News-Hour-Podcast-Tile-360x360-1.jpg",
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"apple": "https://itunes.apple.com/us/podcast/pbs-newshour-full-show/id394432287?mt=2",
"tuneIn": "https://tunein.com/radio/PBS-NewsHour---Full-Show-p425698/",
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},
"perspectives": {
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"order": 14
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"planet-money": {
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"info": "The economy explained. Imagine you could call up a friend and say, Meet me at the bar and tell me what's going on with the economy. Now imagine that's actually a fun evening.",
"airtime": "SUN 3pm-4pm",
"imageSrc": "https://ww2.kqed.org/radio/wp-content/uploads/sites/50/2018/04/planetmoney.jpg",
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},
"link": "/radio/program/planet-money",
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"apple": "https://itunes.apple.com/us/podcast/planet-money/id290783428?mt=2",
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},
"politicalbreakdown": {
"id": "politicalbreakdown",
"title": "Political Breakdown",
"tagline": "Politics from a personal perspective",
"info": "Political Breakdown is a new series that explores the political intersection of California and the nation. Each week hosts Scott Shafer and Marisa Lagos are joined with a new special guest to unpack politics -- with personality — and offer an insider’s glimpse at how politics happens.",
"airtime": "THU 6:30pm-7pm",
"imageSrc": "https://cdn.kqed.org/wp-content/uploads/2024/04/Political-Breakdown-2024-Podcast-Tile-703x703-1.jpg",
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"order": 5
},
"link": "/podcasts/politicalbreakdown",
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"possible": {
"id": "possible",
"title": "Possible",
"info": "Possible is hosted by entrepreneur Reid Hoffman and writer Aria Finger. Together in Possible, Hoffman and Finger lead enlightening discussions about building a brighter collective future. The show features interviews with visionary guests like Trevor Noah, Sam Altman and Janette Sadik-Khan. Possible paints an optimistic portrait of the world we can create through science, policy, business, art and our shared humanity. It asks: What if everything goes right for once? How can we get there? Each episode also includes a short fiction story generated by advanced AI GPT-4, serving as a thought-provoking springboard to speculate how humanity could leverage technology for good.",
"airtime": "SUN 2pm",
"imageSrc": "https://cdn.kqed.org/wp-content/uploads/2024/04/Possible-Podcast-Tile-360x360-1.jpg",
"officialWebsiteLink": "https://www.possible.fm/",
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"source": "Possible"
},
"link": "/radio/program/possible",
"subscribe": {
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"spotify": "https://open.spotify.com/show/730YpdUSNlMyPQwNnyjp4k"
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},
"pri-the-world": {
"id": "pri-the-world",
"title": "PRI's The World: Latest Edition",
"info": "Each weekday, host Marco Werman and his team of producers bring you the world's most interesting stories in an hour of radio that reminds us just how small our planet really is.",
"airtime": "MON-FRI 2pm-3pm",
"imageSrc": "https://cdn.kqed.org/wp-content/uploads/2024/04/The-World-Podcast-Tile-360x360-1.jpg",
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},
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