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"content": "\u003cp>\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2011/01/Horse1.jpg\">\u003cbr>\n\u003cem>Compared to lean beef, horse meat appears to have some nutritional advantages. Image courtesy of \u003ca href=\"http://www.flickr.com/photos/tambako/3897225180/\">Tambako the Jaguar/Flickr\u003c/a>.\u003c/em>\u003c/p>\n\u003cp>There's been much \u003ca href=\"http://eatocracy.cnn.com/2011/01/05/lunchtime-poll-making-a-meal-of-mustang/\">hoopla this week\u003c/a> over the ethical and cultural implications of eating, you guessed it, horse meat. The discussion was sparked by the \u003ca href=\"http://www.united-horsemen.org/summit-of-the-horse/\">Summit of the Horse\u003c/a>, a conference that convened the past 4 days in Las Vegas. The agenda of the conference was to “Restore humane and regulated horse processing,” that is, horse slaughter for human consumption.\u003c/p>\n\u003cp>Though the topic is controversial, what's one man's pet is another man's dinner. Horse meat consumption has been growing rapidly for the last several years \u003ca href=\"http://www.nytimes.com/2008/06/19/opinion/19iht-edjohnson.1.13829773.html?_r=1\">in France\u003c/a>, and is common in several other cultures including Belgium, Germany and Switzerland. In Japan, you can even get horse sushi.\u003c/p>\n\u003cp>But once we get past the sentiment and politics of eating Sea Biscuit, how healthy is horse meat?\u003c/p>\n\u003cp>Horse is generally leaner than cow. (Errr, beef—for starters, why doesn't horse meat get a cuter, less offensive name like beef or venison? Just saying.) And those who have tasted it describe it as having a “sweeter” flavor. For this article I chose a fairly lean, grass-fed strip steak for comparison.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>\u003cstrong>\u003ca href=\"http://nutritiondata.self.com/facts/lamb-veal-and-game-products/4639/2\">Horse meat\u003c/a> vs. \u003ca href=\"http://nutritiondata.self.com/facts/beef-products/10525/2\">Strip steak\u003c/a>\u003c/strong>\u003c/p>\n\u003cp>According to NutritionData, the strip steak has slightly fewer calories than horse (117 vs 133 calories per 100 grams), though this is obviously not be true for all cuts of beef. \u003ca href=\"http://nutritiondata.self.com/facts/beef-products/7491/2\">Sirloin\u003c/a>, for example, contains 142 calories. The meats also have very similar amounts of fat, cholesterol and protein when lean cuts are compared.\u003c/p>\n\u003cp>Where the meats really differ is iron concentration, with horse meat having double the iron (21% vs 10% DV) that beef contains. It is not surprising that a more athletic animal has more iron, but the magnitude of the difference is striking. Horse meat also contains substantially more vitamin B12 (50% vs 21% DV), but less B6, niacin and folate.\u003c/p>\n\u003cp>But what's truly impressive is the omega-3 fatty acid concentration in horse meat, which contains 360 mg (per 100 grams) compared to just 21 mg in strip steak. Omega-3s are essential fatty acids that need to be obtained from your diet. They are thought to be helpful in fighting against heart disease, stroke and neurodegeneration.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>Compared to lean beef, horse meat appears to have some nutritional advantages. If we do ever manage to get past the taboo, at least we know there's good nutrition on the other side.\u003c/p>\n\n",
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"content": "\u003cp>\u003cspan class=\"left\">\u003ca href=\"http://ww2.kqed.org/quest/audio/visiting-the-dentist-chair-of-the-future\">\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2010/12/dentist3001.jpg\" alt=\"\">\u003c/a>\u003cem>\u003c/em>\u003c/span>\u003c/p>\n\u003cp>It probably goes without saying -- the dentist’s chair isn’t the most popular place to visit. But going to the dentist may one day be a very different experience. Researchers at the University of California San Francisco are developing new technology that may make a dentist’s drill less common. \u003c/p>\n\u003cp>Inside one of the treatment rooms at the \u003ca href=\"http://dentistry.ucsf.edu\">UCSF School of Dentistry\u003c/a>, Dr. Peter Rechmann is holding a small tool that could be a very big leap forward in dentistry -- a laser. Unlike that familiar drill we love to hate, a laser drills into a tooth without making contact.\u003c/p>\n\u003cp>\u003c!--more-->\u003c/p>\n\u003cdiv style=\"border-bottom:1px dotted #cecece;height:20px;margin-bottom:10px\"> \u003c/div>\n\u003cp>[jwplayer config=\"QUEST Audio Player\" skin=\"http://ww2.kqed.org/quest/wp-content/themes/quest/glow.zip\" file=\"http://www.kqed.org/.stream/anon/radio/quest/2011/01/2011-01-03-quest.mp3\" ]\u003cbr>\n\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>\u003cem>Listen to the QUEST radio story \u003cstrong>\u003ca href=\"http://ww2.kqed.org/quest/audio/visiting-the-dentist-chair-of-the-future\">Visiting the Dentist Chair of the Future\u003c/a>\u003c/strong>.\u003c/em>\u003c/p>\n\u003cdiv style=\"border-bottom:1px dotted #cecece;height:20px;margin-bottom:10px\"> \u003c/div>\n\u003cp>“So you don’t feel vibration. Yes, you hear the sound, you hear the tck tck tck, but that’s it,” says Rechmann. That makes a big difference, especially when Rechmann is working with younger patients. “Kids typically fear things more than adults. And they don’t care, they like it. Sometimes they say, ‘Oh, that was interesting’.”\u003c/p>\n\u003cp>Lasers have been used in dentistry for about a decade, but mostly on soft tissues like gums. Rechmann says laser drills are becoming more common now that the cost is coming down. And he expects lasers to soon play an even bigger role by actually helping to prevent cavities.\u003c/p>\n\u003cp>Rechmann holds a pulled tooth and fires short laser pulses at a small area on the outside. “The temperature on the enameled surface gets heated up to between 400 and 1000 degrees Celsius. It sounds terrible but it’s not. It’s really just the outer surface,” he says.\u003c/p>\n\u003cp>The extreme temperature slightly alters the make up of the outer tooth enamel which, Rechmann says, makes it more resistant to tooth decay. They’re now testing the treatment in clinical trials and it could be available in one to three years.\u003c/p>\n\u003cp>“If you treat this once, OK, you should still keep on brushing your teeth, but it’s really strongly protecting your teeth,” says Rechmann.\u003c/p>\n\u003cp>Of course, what our teeth really need protection from are our own bacteria. They’re specially adapted to live in our mouth, which, with all the food we chew, is a pretty nice place to call home.\u003c/p>\n\u003cp>“It’s a very nice place. It’s nice and warm and comfortable,” says John Featherstone, Dean of the UCSF School of Dentistry.\u003c/p>\n\u003cp>“Bacteria produce acid – that’s their major waste product. And that acid dissolves the enamel in the teeth.” Featherstone says in the past, dentistry has been focused on cleaning up the damage done by these bacteria. Now, he also sees the field moving towards prevention.\u003c/p>\n\u003cp>“If we can diagnose as we can now early on, what it tells us is that there’s disease process going on and we have to halt the disease process,” says Featherstone.\u003c/p>\n\u003cp>But given our teeth brushing habits - or lack thereof - Featherstone says there will probably always be a need to fill cavities. But what if cavities could fill themselves?\u003c/p>\n\u003cp>Self-Filling Cavities\u003c/p>\n\u003cp>Stefan Habelitz is standing in front of a refrigerator that holds 20,000 pulled teeth, collected from local dental clinics. Habelitz is a material scientist. He studies the structure of teeth. \u003c/p>\n\u003cp>“It’s amazing, a really amazing structure. For an engineer, it’s a real feast,” says Habelitz.\u003c/p>\n\u003cp>Tooth enamel is the hardest substance in our body. It’s designed to break apart foods like seeds or hard candy. “But if it can’t, it will release stress by forming fractures, by forming cracks,” Habelitz says.\u003c/p>\n\u003cp>Those tiny cracks are actually good -- they’re part of the tooth’s design. They prevent it from being broken by one big crack. The problem with our teeth, Habelitz says, is that unlike our bones or skin, we can’t regrow tooth enamel. At least, not by ourselves.\u003c/p>\n\u003cp>“So let’s just drop these teeth in here.” Habelitz takes a few teeth with very large cavities and drops them into a beaker filled with a special solution. Tooth enamel is made of a mineral - so Habelitz says it’s not too difficult to remineralize or rebuild the enamel. That’s something the fluoride in toothpaste helps do. \u003c/p>\n\u003cp>“But once the bacteria makes it through the enamel, then it has been so far impossible to remineralize these legions,” says Habelitz.\u003c/p>\n\u003cp>That’s because deeper in the tooth in the material called dentin, minerals are mixed with organic structures, which are much harder to regrow. What Habelitz has in this beaker is a special compound that regrows the minerals and bonds them to the organic structures. \u003c/p>\n\u003cp>“So only when that link is established, the tissue that you build up again actually will be strong enough and stiff enough to support the pressure that you apply when you chew on your teeth,” he says.\u003c/p>\n\u003cp>One day, Habelitz says this process could be done right inside a patient’s mouth. The problem now is the process takes a long time -- several weeks to fill a small cavity. “It should be an approach that needs to be done at least within a day, ideally within a few minutes.”\u003c/p>\n\u003cp>Habelitz is working to speed up the process, though it will be years before it’s available. But even if he and his colleagues can only regrow a small amount of a tooth, that’s part of a tooth that doesn’t have to be filled.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp> 37.7634259 -122.4586312\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>\u003cem>Listen to the QUEST radio story \u003cstrong>\u003ca href=\"http://ww2.kqed.org/quest/audio/visiting-the-dentist-chair-of-the-future\">Visiting the Dentist Chair of the Future\u003c/a>\u003c/strong>.\u003c/em>\u003c/p>\n\u003cdiv style=\"border-bottom:1px dotted #cecece;height:20px;margin-bottom:10px\"> \u003c/div>\n\u003cp>“So you don’t feel vibration. Yes, you hear the sound, you hear the tck tck tck, but that’s it,” says Rechmann. That makes a big difference, especially when Rechmann is working with younger patients. “Kids typically fear things more than adults. And they don’t care, they like it. Sometimes they say, ‘Oh, that was interesting’.”\u003c/p>\n\u003cp>Lasers have been used in dentistry for about a decade, but mostly on soft tissues like gums. Rechmann says laser drills are becoming more common now that the cost is coming down. 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"content": "\u003cp>\u003cspan class=\"left\">\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2010/12/mistletoe1.jpg\" alt=\"\">\u003cem>Mistletoe grows on the branch of an oak tree in Briones Regional Park. Photo: \u003ca href=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2010/12/mistletoe1.jpg\">kqedquest\u003c/a>.\u003c/em>\u003c/span>\u003c/p>\n\u003cp>Have you been hanging out under the mistletoe at holiday parties, hoping for a kiss? Well, that mistletoe is more than a Christmas kissing custom. It’s a parasite that can harm trees—and a potential treatment for cancer.\u003c/p>\n\u003cp>\u003ca href=\"http://www.hastingsreserve.org/OakStory/Mistletoe2.html\">Mistletoe\u003c/a> lives on the branches of trees, and is a hemi-parasite; it produces some of its own food (it has green, photosynthetic leaves), but it gets nutrients and water from its host plant (its roots tap into the host plant, rather than the soil). If the mistletoe grows big enough, they can do some damage. Large mistletoe plants can weigh down tree branches and make them more likely to break off during a storm. If there are many mistletoe plants in a single tree, they can stunt the tree’s growth, make it more susceptible to disease, and even kill it. \u003c/p>\n\u003cp>\u003c!--more--> \u003c/p>\n\u003cp>There are several species of mistletoe living in California. Pacific mistletoe, \u003cem>Phoradendron villosum\u003c/em>, lives in the western US, and is a parasite on oak trees. European mistletoe, \u003cem>Viscum album\u003c/em>, parasitizes a wide range of species, including apple trees and maples. \u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>Mistletoe is spread from tree to tree by birds. They eat the white berries and spread the sticky seeds with their beaks or in their excrement.\u003c/p>\n\u003cp>Despite its parasitic tendencies, mistletoe has long been thought to have healing powers. In Greek legends and druid folklore, mistletoe was used to treat disease. And since the 1920s, scientists have been investigating mistletoe extract as potential cancer drug.\u003c/p>\n\u003cp>Several laboratory studies have shown that mistletoe extract can kill cancer cells—though other studies have shown that the extract has no effect. It seems that mistletoe growing on different types of trees (like apple, pine, oak, or elm) may have different medicinal properties. \u003c/p>\n\u003cp>Mistletoe extract seems to boost the immune system, by increasing the production and activity of white blood cells. (Don’t try this at home—mistletoe can be poisonous.) Several clinical trials, mostly in Europe, have tested mistletoe extract as a form of adjuvant therapy—a treatment that is given to cancer patients after their primary treatment, to decrease the risk that cancer will return. Patients were treated with mistletoe extract (injected under the skin), along with radiation and chemotherapy. Patience who received the mistletoe extract fared better than their counterparts who did not receive it. Additional studies are underway: check out the National Cancer Institute’s \u003ca href=\"http://www.cancer.gov/cancertopics/pdq/cam/mistletoe/patient/28.cdr#top\">Questions and Answers About Mistletoe\u003c/a>.\u003c/p>\n\u003cp>While you’re standing awkwardly under the mistletoe at your next cocktail party, you can wait quietly for that special someone, or you can strike up a conversation about mistletoe’s medicinal properties.\u003c/p>\n\u003cp>\u003cstrong>Related posts:\u003c/strong>\u003cbr>\n\u003ca href=\"http://www.kqed.org/quest/exploration/briones-regional-park-exploration\">Briones Regional Park Exploration\u003c/a>\u003c/p>\n\u003cp>\u003c/p>\n\u003cp> 37.879329 -122.2463347\u003c/p>\n\n",
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"content": "\u003cp>\u003cspan class=\"left\">\u003ca href=\"http://www.kqed.org/quest\">\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2010/12/Gilad-Warner211.jpg\" alt=\"\">\u003c/a>\u003cem>HIV researcher Gilad Doitsh talks with Dr. Warner Greene (seated) at the Gladstone Institute of Virology and Immunology in San Francisco. (Credit: Chris Goodfellow, Gladstone Institutes) \u003c/em>\u003c/span>\u003c/p>\n\u003cp>\u003cem>Reported for \u003ca href=\"http://www.kqed.org/news/\">KQEDnews.org\u003c/a>.\u003c/em>\u003c/p>\n\u003cp>For nearly 30 years scientists have known that a cell vital to the immune system dies off in patients with HIV, leading eventually to the onset of AIDS. But exactly when and how has remained a mystery - until now. \u003c/p>\n\u003cp>Researchers at the \u003ca href=\"http://www.gladstone.ucsf.edu/gladstone/site/givi/\">Gladstone Institute of Virology and Immunology\u003c/a> in San Francisco showed that the overwhelming majority of the cells die not from HIV, the virus that causes AIDS, but rather from the cell’s own defensive response to HIV even before the virus can make copies of itself. \u003c/p>\n\u003cp>The new insights may one day lead to new, more effective drugs to treat HIV. \u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>\u003c!--more-->\u003c/p>\n\u003cp>“The cells understand they've been attacked and they commit suicide,” said Gilad Doitsh, a research scientist and the lead author of the study, which was published last Wednesday in the scientific journal \u003cem>\u003ca href=\"http://www.cell.com/fulltext/S0092-8674%2810%2901245-6\">Cell\u003c/a>\u003c/em>.\u003c/p>\n\u003cp>“It’s as though the virus needs to go through several rooms of the cell without activating the alarm,” he said, “and if it stalls in one of those rooms, the alarm sounds and the cell kills itself.” \u003c/p>\n\u003cp>\u003cspan class=\"right\">\u003ca href=\"http://www.kqed.org/quest\">\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2010/11/GladstoneInstituteVirologyImmunology_Doitsh-21.jpg\" alt=\"\">\u003c/a>\u003cem>Gilad Doitsh, a molecular biologist at the Gladstone Institute of Virology and Immunology in San Francisco, studies the HIV virus. (Credit: Chris Goodfellow, Gladstone Institutes)\u003c/em>\u003c/span>\u003c/p>\n\u003cp>Doitsh and his colleagues, working at the University of California-San Francisco’s Mission Bay campus, focused their research on a type of white blood cells called 'CD4 T cells'. The cells play a critical role in fighting infection from bacteria and viruses. \u003c/p>\n\u003cp>CD4 T cells are also known as ‘helper cells’ because they help the production of a specific immune response – antibodies – to a specific bacteria or virus. After a bacteria or virus enters the body, communication occurs between different immune cells in the lymph tissues to develop an antibody which the immune system will then remember and reproduce if it encounters the same type of bacteria or virus weeks, months or even years later. \u003c/p>\n\u003cp>Though the human body has 10 types of immune cells, the main target of HIV is CD4 T cells. But despite this limited target, the immune system still can’t produce an antibody to marshal an effective, one-size-fits-all attack against the virus. \u003c/p>\n\u003cp>\"The major challenge of HIV is its ability to mutate or change. So we're constantly chasing the virus,” said Dr. Warner Greene, director of the Gladstone Institute of Virology and Immunology and a senior author of the study. \"It requires combination antiretroviral therapy to attack it. Single drugs will not work,” he added. \u003c/p>\n\u003cp>At least 26 drugs have been approved by the FDA to treat HIV, which infects roughly 60,000 people in the U.S. each year. Worldwide, more than 33 million people are living with HIV, with 10 million of them awaiting drug treatment, according to the \u003ca href=\"http://www.unaids.org/GlobalReport/default.htm\">United Nations\u003c/a>. \u003c/p>\n\u003cp>Doitsh’s team takes an unusually thorough approach when investigating the spread of HIV in the human body. \u003c/p>\n\u003cp>“Our lab is very, very unique. We process human tissues from the tonsils, spleen, cervix, skin, colon, blood, semen - any tissue where HIV multiplies or that serves as a vehicle to transmit HIV from person to person,” he said. “You see the virus behave differently depending on the tissue it has infected.” \u003c/p>\n\u003cp>According to Doitsh, most other labs researching HIV and AIDS study the virus in blood because of the ease of finding copies of the virus there, even though it’s not the site where the virus actually replicates, or makes copies, of itself. So Doitsh used tonsil and spleen tissues because they’re the principal places where the virus replicates. Being lymph organs, the tonsil and spleen also contain large amounts of CD4 T cells.\u003c/p>\n\u003cp>The researchers exposed the tonsil and spleen tissues to HIV. Then, to tell when the virus was actively replicating in the CD4 T cells, the scientists used a marker which turned green when the virus had fully hijacked the genetic machinery of the cell, tricking the cell into making thousands of new copies of the virus. \u003c/p>\n\u003cp>After binding to the CD4 T cell, the virus can’t directly enter the cell’s nucleus to take over its DNA, the genetic program which runs the cell. And since the virus doesn’t have DNA of its own, it has to convert its RNA, the genetic program on which it runs, to DNA in a process called ‘reverse transcription’. \u003c/p>\n\u003cp>When it has converted its RNA to DNA, HIV can then speak the genetic language of the CD4 T cell. It enters the infected cell’s nucleus and boots up its genetic program, which instructs the cell to make new copies of the virus, thereby amplifying HIV in the body. \u003c/p>\n\u003cp>And although all the CD4 T cells eventually died from infection by the virus, how they died was a bit of a surprise.\u003c/p>\n\u003cp>Only about 5 percent of the cells that died were \"productively\", or fully, infected with HIV. The other 95 percent “bystander” cells died not from the virus itself but from an alarm signal inside the cell which triggered it to commit suicide after it was exposed to the virus but before the virus could replicate inside it. \u003c/p>\n\u003cp>“These CD4 T cells commit suicide to protect the body, but you can't have all the soldiers commit suicide because then the country has no more army,” said Doitsh. \u003c/p>\n\u003cp>\u003cspan class=\"left\">\u003ca href=\"http://www.gladstone.ucsf.edu/gladstone/files/publicaffairs/DoitshCellCycle112410.jpg\">\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2010/11/GladstoneInstituteVirologyImmunology_DoitshCellCycle112410-22.jpg\" alt=\"\">\u003c/a>\u003cem>Graphic showing to the left, a CD4 T cell that commits suicide after infection by HIV, whereas the illustration on the right depicts a cell that allows HIV to replicate in it. (Click on image for a larger version) (Credit: Gilad Doitsh, Gladstone Institute of Virology and Immunology)\u003c/em>\u003c/span>\u003c/p>\n\u003cp>To figure out exactly when these CD4 T cell ‘soldiers’ committed suicide, Doitsh exposed the CD4 T cells to different antiretroviral drugs like AZT, AMD3100 and T20, which attack the virus at various stages of its life cycle. \u003c/p>\n\u003cp>While AZT failed to rescue the infected CD4 T cells from dying, the other drugs were able to save the CD4 T cells because they attacked the virus before it entered the nucleus of the cell. But Doitsh and his colleagues didn’t know if the cells were committing suicide early on, when the virus merely touched the cell to enter it, or later, when the virus had already entered the cell. \u003c/p>\n\u003cp>So they used another drug, Efavirenz, which attacks HIV after it has entered the cell but before it starts making copies of itself from within the cell’s nucleus. When the CD4 T cells were exposed to Efavirenz, they survived. \u003c/p>\n\u003cp>“People thought that the virus could be on the outside of the cell, that it’s enough to put the key into the lock to signal the destruction of the room,” said Doitsh. “We showed that it’s not the key in the lock but that the virus has to actually go inside the room - or the cell - for the cell to die.” \u003c/p>\n\u003cp>“It hasn't been very clear why these so-called ‘bystander cells’ also die,” said Tae-Wook Chun, a staff scientist who has been studying HIV for 12 years at the \u003ca href=\"http://www.niaid.nih.gov/topics/hivaids/Pages/Default.aspx\">National Institute of Allergy and Infectious Diseases\u003c/a> in Bethesda, Maryland. “The researchers found that these cells also get infected, although HIV doesn’t complete its life cycle in these cells. So they solved one of the mysteries in HIV research,” he added. \u003c/p>\n\u003cp>But that’s not all they found.\u003c/p>\n\u003cp>“The second huge surprise we found was that the mechanism of cell death was not a silent one. These cells do not go silently into the night,” said Greene.\u003c/p>\n\u003cp>Instead, Greene said they died a “fiery death,” causing “significant inflammation” as they erupted their cellular contents and released a chemical signal which recruited healthy CD4 T cells to the site of infection. \u003c/p>\n\u003cp>“It’s like a 911 call, with the dying cell saying, ‘we need more white blood cells to fight whatever infection is going on’” said Doitsh. “The new CD4 T cells want to help but HIV is there,” he added. \u003c/p>\n\u003cp>“It’s a vicious cycle, whereby the dying CD4 T cells release inflammatory signals that attract more cells to die,” said Greene. \u003c/p>\n\u003cp>This inflammatory response the researchers observed offers an interesting avenue to explore for the possible development of more effective HIV drugs.\u003c/p>\n\u003cp>“I think there are possibilities that we could block the inflammation component and therefore greatly modify the progression of disease,” said Greene. He also pointed out that primates like chimpanzees who are infected with a strain of HIV experience a drop in CD4 T cells but they don’t show signs of inflammation, nor crucially, do they develop AIDS. \u003c/p>\n\u003cp>Tae-Wook Chun at NIAID, however, cautioned that additional studies need to be done, perhaps with tissue from already infected HIV patients, to determine the clinical relevance of the findings. \u003c/p>\n\u003cp>The scientists will next try to track down the cellular sensor which detects HIV in the cell body and triggers the cellular suicide. They also want to study the virus to see if it has genes which allow it to turn off the cellular sensor in that small percentage of cells which become a host for making additional copies of the virus.\u003c/p>\n\u003cp>\u003cspan class=\"right\">\u003ca href=\"http://www.kqed.org/quest\">\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2010/11/GladstoneInstituteVirologyImmunology_scientist-21.jpg\" alt=\"\">\u003c/a>\u003cem>HIV researcher Mauricio Montano at work at the Gladstone Institute of Virology and Immunology. (Credit: Chris Goodfellow, Gladstone Institutes) \u003c/em>\u003c/span>\u003c/p>\n\u003cp>Gilad Doitsh spent seven years doing the research in Greene’s lab and confirming his results before he was confident enough to present his findings for publication. Today, he advises three doctoral students who are beginning to investigate the behavior of HIV, much like he did nearly a decade ago. \u003c/p>\n\u003cp>“I tell them we are like detectives,” said Doitsh. “We have a suspect – HIV. We’re sure he committed murder but we have to collect the best evidence to convince the jury so that this guy can go to jail.” \u003c/p>\n\u003cp>“You have to know every aspect of HIV. You take baby steps but if every step is solid, then you have enough proof to convict the suspect,” he added. \u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp> 37.767050 -122.391139\u003c/p>\n\n",
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"excerpt": "For nearly 30 years scientists have known that a cell vital to the immune system dies off in patients with HIV, leading eventually to the onset of AIDS. But exactly when and how has remained a mystery - until now.",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>\u003cspan class=\"left\">\u003ca href=\"http://www.kqed.org/quest\">\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2010/12/Gilad-Warner211.jpg\" alt=\"\">\u003c/a>\u003cem>HIV researcher Gilad Doitsh talks with Dr. Warner Greene (seated) at the Gladstone Institute of Virology and Immunology in San Francisco. (Credit: Chris Goodfellow, Gladstone Institutes) \u003c/em>\u003c/span>\u003c/p>\n\u003cp>\u003cem>Reported for \u003ca href=\"http://www.kqed.org/news/\">KQEDnews.org\u003c/a>.\u003c/em>\u003c/p>\n\u003cp>For nearly 30 years scientists have known that a cell vital to the immune system dies off in patients with HIV, leading eventually to the onset of AIDS. But exactly when and how has remained a mystery - until now. \u003c/p>\n\u003cp>Researchers at the \u003ca href=\"http://www.gladstone.ucsf.edu/gladstone/site/givi/\">Gladstone Institute of Virology and Immunology\u003c/a> in San Francisco showed that the overwhelming majority of the cells die not from HIV, the virus that causes AIDS, but rather from the cell’s own defensive response to HIV even before the virus can make copies of itself. \u003c/p>\n\u003cp>The new insights may one day lead to new, more effective drugs to treat HIV. \u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>\u003c!--more-->\u003c/p>\n\u003cp>“The cells understand they've been attacked and they commit suicide,” said Gilad Doitsh, a research scientist and the lead author of the study, which was published last Wednesday in the scientific journal \u003cem>\u003ca href=\"http://www.cell.com/fulltext/S0092-8674%2810%2901245-6\">Cell\u003c/a>\u003c/em>.\u003c/p>\n\u003cp>“It’s as though the virus needs to go through several rooms of the cell without activating the alarm,” he said, “and if it stalls in one of those rooms, the alarm sounds and the cell kills itself.” \u003c/p>\n\u003cp>\u003cspan class=\"right\">\u003ca href=\"http://www.kqed.org/quest\">\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2010/11/GladstoneInstituteVirologyImmunology_Doitsh-21.jpg\" alt=\"\">\u003c/a>\u003cem>Gilad Doitsh, a molecular biologist at the Gladstone Institute of Virology and Immunology in San Francisco, studies the HIV virus. (Credit: Chris Goodfellow, Gladstone Institutes)\u003c/em>\u003c/span>\u003c/p>\n\u003cp>Doitsh and his colleagues, working at the University of California-San Francisco’s Mission Bay campus, focused their research on a type of white blood cells called 'CD4 T cells'. The cells play a critical role in fighting infection from bacteria and viruses. \u003c/p>\n\u003cp>CD4 T cells are also known as ‘helper cells’ because they help the production of a specific immune response – antibodies – to a specific bacteria or virus. After a bacteria or virus enters the body, communication occurs between different immune cells in the lymph tissues to develop an antibody which the immune system will then remember and reproduce if it encounters the same type of bacteria or virus weeks, months or even years later. \u003c/p>\n\u003cp>Though the human body has 10 types of immune cells, the main target of HIV is CD4 T cells. But despite this limited target, the immune system still can’t produce an antibody to marshal an effective, one-size-fits-all attack against the virus. \u003c/p>\n\u003cp>\"The major challenge of HIV is its ability to mutate or change. So we're constantly chasing the virus,” said Dr. Warner Greene, director of the Gladstone Institute of Virology and Immunology and a senior author of the study. \"It requires combination antiretroviral therapy to attack it. Single drugs will not work,” he added. \u003c/p>\n\u003cp>At least 26 drugs have been approved by the FDA to treat HIV, which infects roughly 60,000 people in the U.S. each year. Worldwide, more than 33 million people are living with HIV, with 10 million of them awaiting drug treatment, according to the \u003ca href=\"http://www.unaids.org/GlobalReport/default.htm\">United Nations\u003c/a>. \u003c/p>\n\u003cp>Doitsh’s team takes an unusually thorough approach when investigating the spread of HIV in the human body. \u003c/p>\n\u003cp>“Our lab is very, very unique. We process human tissues from the tonsils, spleen, cervix, skin, colon, blood, semen - any tissue where HIV multiplies or that serves as a vehicle to transmit HIV from person to person,” he said. “You see the virus behave differently depending on the tissue it has infected.” \u003c/p>\n\u003cp>According to Doitsh, most other labs researching HIV and AIDS study the virus in blood because of the ease of finding copies of the virus there, even though it’s not the site where the virus actually replicates, or makes copies, of itself. So Doitsh used tonsil and spleen tissues because they’re the principal places where the virus replicates. Being lymph organs, the tonsil and spleen also contain large amounts of CD4 T cells.\u003c/p>\n\u003cp>The researchers exposed the tonsil and spleen tissues to HIV. Then, to tell when the virus was actively replicating in the CD4 T cells, the scientists used a marker which turned green when the virus had fully hijacked the genetic machinery of the cell, tricking the cell into making thousands of new copies of the virus. \u003c/p>\n\u003cp>After binding to the CD4 T cell, the virus can’t directly enter the cell’s nucleus to take over its DNA, the genetic program which runs the cell. And since the virus doesn’t have DNA of its own, it has to convert its RNA, the genetic program on which it runs, to DNA in a process called ‘reverse transcription’. \u003c/p>\n\u003cp>When it has converted its RNA to DNA, HIV can then speak the genetic language of the CD4 T cell. It enters the infected cell’s nucleus and boots up its genetic program, which instructs the cell to make new copies of the virus, thereby amplifying HIV in the body. \u003c/p>\n\u003cp>And although all the CD4 T cells eventually died from infection by the virus, how they died was a bit of a surprise.\u003c/p>\n\u003cp>Only about 5 percent of the cells that died were \"productively\", or fully, infected with HIV. The other 95 percent “bystander” cells died not from the virus itself but from an alarm signal inside the cell which triggered it to commit suicide after it was exposed to the virus but before the virus could replicate inside it. \u003c/p>\n\u003cp>“These CD4 T cells commit suicide to protect the body, but you can't have all the soldiers commit suicide because then the country has no more army,” said Doitsh. \u003c/p>\n\u003cp>\u003cspan class=\"left\">\u003ca href=\"http://www.gladstone.ucsf.edu/gladstone/files/publicaffairs/DoitshCellCycle112410.jpg\">\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2010/11/GladstoneInstituteVirologyImmunology_DoitshCellCycle112410-22.jpg\" alt=\"\">\u003c/a>\u003cem>Graphic showing to the left, a CD4 T cell that commits suicide after infection by HIV, whereas the illustration on the right depicts a cell that allows HIV to replicate in it. (Click on image for a larger version) (Credit: Gilad Doitsh, Gladstone Institute of Virology and Immunology)\u003c/em>\u003c/span>\u003c/p>\n\u003cp>To figure out exactly when these CD4 T cell ‘soldiers’ committed suicide, Doitsh exposed the CD4 T cells to different antiretroviral drugs like AZT, AMD3100 and T20, which attack the virus at various stages of its life cycle. \u003c/p>\n\u003cp>While AZT failed to rescue the infected CD4 T cells from dying, the other drugs were able to save the CD4 T cells because they attacked the virus before it entered the nucleus of the cell. But Doitsh and his colleagues didn’t know if the cells were committing suicide early on, when the virus merely touched the cell to enter it, or later, when the virus had already entered the cell. \u003c/p>\n\u003cp>So they used another drug, Efavirenz, which attacks HIV after it has entered the cell but before it starts making copies of itself from within the cell’s nucleus. When the CD4 T cells were exposed to Efavirenz, they survived. \u003c/p>\n\u003cp>“People thought that the virus could be on the outside of the cell, that it’s enough to put the key into the lock to signal the destruction of the room,” said Doitsh. “We showed that it’s not the key in the lock but that the virus has to actually go inside the room - or the cell - for the cell to die.” \u003c/p>\n\u003cp>“It hasn't been very clear why these so-called ‘bystander cells’ also die,” said Tae-Wook Chun, a staff scientist who has been studying HIV for 12 years at the \u003ca href=\"http://www.niaid.nih.gov/topics/hivaids/Pages/Default.aspx\">National Institute of Allergy and Infectious Diseases\u003c/a> in Bethesda, Maryland. “The researchers found that these cells also get infected, although HIV doesn’t complete its life cycle in these cells. So they solved one of the mysteries in HIV research,” he added. \u003c/p>\n\u003cp>But that’s not all they found.\u003c/p>\n\u003cp>“The second huge surprise we found was that the mechanism of cell death was not a silent one. These cells do not go silently into the night,” said Greene.\u003c/p>\n\u003cp>Instead, Greene said they died a “fiery death,” causing “significant inflammation” as they erupted their cellular contents and released a chemical signal which recruited healthy CD4 T cells to the site of infection. \u003c/p>\n\u003cp>“It’s like a 911 call, with the dying cell saying, ‘we need more white blood cells to fight whatever infection is going on’” said Doitsh. “The new CD4 T cells want to help but HIV is there,” he added. \u003c/p>\n\u003cp>“It’s a vicious cycle, whereby the dying CD4 T cells release inflammatory signals that attract more cells to die,” said Greene. \u003c/p>\n\u003cp>This inflammatory response the researchers observed offers an interesting avenue to explore for the possible development of more effective HIV drugs.\u003c/p>\n\u003cp>“I think there are possibilities that we could block the inflammation component and therefore greatly modify the progression of disease,” said Greene. He also pointed out that primates like chimpanzees who are infected with a strain of HIV experience a drop in CD4 T cells but they don’t show signs of inflammation, nor crucially, do they develop AIDS. \u003c/p>\n\u003cp>Tae-Wook Chun at NIAID, however, cautioned that additional studies need to be done, perhaps with tissue from already infected HIV patients, to determine the clinical relevance of the findings. \u003c/p>\n\u003cp>The scientists will next try to track down the cellular sensor which detects HIV in the cell body and triggers the cellular suicide. They also want to study the virus to see if it has genes which allow it to turn off the cellular sensor in that small percentage of cells which become a host for making additional copies of the virus.\u003c/p>\n\u003cp>\u003cspan class=\"right\">\u003ca href=\"http://www.kqed.org/quest\">\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2010/11/GladstoneInstituteVirologyImmunology_scientist-21.jpg\" alt=\"\">\u003c/a>\u003cem>HIV researcher Mauricio Montano at work at the Gladstone Institute of Virology and Immunology. (Credit: Chris Goodfellow, Gladstone Institutes) \u003c/em>\u003c/span>\u003c/p>\n\u003cp>Gilad Doitsh spent seven years doing the research in Greene’s lab and confirming his results before he was confident enough to present his findings for publication. Today, he advises three doctoral students who are beginning to investigate the behavior of HIV, much like he did nearly a decade ago. \u003c/p>\n\u003cp>“I tell them we are like detectives,” said Doitsh. “We have a suspect – HIV. We’re sure he committed murder but we have to collect the best evidence to convince the jury so that this guy can go to jail.” \u003c/p>\n\u003cp>“You have to know every aspect of HIV. You take baby steps but if every step is solid, then you have enough proof to convict the suspect,” he added. \u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>\u003cspan class=\"left\"><a title='By User:Nino Barbieri [CC-BY-SA-2.5 (www.creativecommons.org/licenses/by-sa/2.5)], from Wikimedia Commons' href='http://commons.wikimedia.org/wiki/File:-_Pumpkins_-.jpg\u003ca href=\"http://commons.wikimedia.org/wiki/File:-_Pumpkins_-.jpg\">\u003cimg alt=\"By User:Nino Barbieri [<a href="www.creativecommons.org/licenses/by-sa/2.5">CC-BY-SA-2.5</a>], <a href='http://commons.wikimedia.org/wiki/File:-_Pumpkins_-.jpg'>from Wikimedia Commons</a>\" src=\"http://upload.wikimedia.org/wikipedia/commons/thumb/0/0c/-_Pumpkins_-.jpg/256px--_Pumpkins_-.jpg\" title=\"Pumpkins\" class=\"alignnone\" width=\"256\" height=\"171\">\u003c/a>\u003cimg alt=\"\" src=\"http://upload.wikimedia.org/wikipedia/commons/thumb/0/0c/-_Pumpkins_-.jpg/256px--_Pumpkins_-.jpg\" title=\"Pumpkins\" class=\"alignnone\" width=\"256\" height=\"171\">'>\u003cimg width=\"300\" alt=\"- Pumpkins -\" src=\"http://upload.wikimedia.org/wikipedia/commons/thumb/0/0c/-_Pumpkins_-.jpg/256px--_Pumpkins_-.jpg\">\u003cem>By User: Nino Barbieri [\u003ca href=\"http://www.creativecommons.org/licenses/by-sa/2.5\">CC-BY-SA-2.5\u003c/a>], \u003ca href=\"http://commons.wikimedia.org/wiki/File:-_Pumpkins_-.jpg\">from Wikimedia Commons\u003c/a>\u003c/em>\u003c/span>\u003c/p>\n\u003cp>I come from a family of chefs; I love to cook and during Thanksgiving I am happiest in the kitchen. I can be in a kitchen for hours on end amongst knifes, produce, herbs and sauces in the midst of creation. It usually takes me the whole day to create a meal my family can consume in fifteen minutes flat. But since I cook, they end up doing the dishes so it works out!\u003c/p>\n\u003cp>For the past several years, I’ve focused on really healthy meals and have become much more interested in the nutritional impact of food. The average Thanksgiving dinner has a whopping 3500 calories; it would take about 7 hours of moderate biking to burn off the whole meal. I skip the sweeter version of sweet potatoes. I serve baked rosemary sweet potato fries; I’ve also tried ginger and lime infused butternut squash soup, cabbage steamed with apples and tomatoes, polenta with herbs and a trio of mushrooms instead of stuffing and pumpkin pudding instead of the pie. For the past several years, I have also brined my turkey and then used the leftovers to make turkey stock and turkey soup.\u003c/p>\n\u003cp>\u003c!--more-->\u003c/p>\n\u003cp>Most of my favorite recipes have come from a medical focused cookbook called SuperFoods RX by Dr. Stephen J. Pratt & Kathy Matthews. This book outlines the health benefits of fourteen powerhouse foods that aid in health and longevity in life. Four prominent Thanksgiving food items make the list:\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>\u003cstrong>Turkey\u003c/strong> – Turkey is in itself is a lean source of protein, but it also packs nutrients like Riboflavin, Niacin, Iron, Selenium, Zinc, Vitamin B6 and Vitamin B12. Eating turkey is good for your heart and also lowers the risk for cancer.\u003c/p>\n\u003cp>\u003cstrong>Pumpkin\u003c/strong> – This fruit is part of the gourd family (the same family that incorporates melons) and is very high in fiber and low in calories. It has a great deal of nutrients like potassium, pantothenic acid, magnesium, and vitamins C and E. It also has high concentrations of digestable carotenoids specifically alpha-carotene and beta-carotene. Carotenoids are linked to decreasing the risk of many cancers and women who have the highest dietary concentrations of cartenoids also have the lowest risk of breast cancer. These nutrients also lower the risk of heart disease as well as the risk for cataracts. \u003c/p>\n\u003cp>\u003cstrong>Sweet Potatoes\u003c/strong> - The sweet potato is a sidekick to pumpkin and has many of the same nutrients and health benefits.\u003cbr>\n\u003cstrong>\u003cbr>\nCranberries\u003c/strong> - Cranberries are a sidekick and cousins to Blueberries; both Cranberries and Blueberries are native to North America. These small berries have very high levels of antioxidant phytonutrients. Phytonutrients have been shown to aid in body cells communicating efficiently even aiding aging brain cells from further degeneration, preventing cellular level mutations, and fighting the onslaught of cancer cells. \u003c/p>\n\u003cp>Many of my recipes and health insights have come from this book. I have a very dog-eared and tattered copy of it on my kitchen shelf. To find more about these superfoods and the rest of the list go to the \u003ca href=\"http://www.superfoodsrx.com\">Superfoods RX website\u003c/a>.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp> 37.7699 -122.467174\u003c/p>\n\n\u003c/div>\u003c/p>",
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"content": "\u003cp>\u003cspan class=\"left\">\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2010/11/salt1.jpg\" alt=\"\">\u003cem>US dietary guidelines for sodium intake are not practical for the general population. Image courtesy of \u003ca href=\"http://www.flickr.com/photos/tudor/163906410/\">TheGiantVermin\u003c/a>.\u003c/em>\u003c/span>\u003c/p>\n\u003cp>Salt has had its share of bad press this year. In January, the Bloomberg administration in New York City proposed new legislation that would require restaurants and food manufacturers to cut salt content by 25% over five years. In June, the U.S dietary guidelines recommended the upper limit of sodium intake be reduced to 1,600 mg/day, a 40% decrease from the current average.\u003c/p>\n\u003cp>According to recent data published in the \u003cem>\u003ca href=\"http://www.ncbi.nlm.nih.gov/pubmed/20826631\">American Journal of Clinical Nutrition\u003c/a>\u003c/em> the recommendations may be misguided. The review examined data from 38 studies dating from 1957 to 2003. The studies measured the amount of sodium excreted in urine, a value that very accurately reflects total sodium intake. Importantly, there was no significant change in sodium levels over nearly five decades, despite vigorous public health initiatives to reduce salt intake.\u003c/p>\n\u003cp>\u003c!--more-->\u003c/p>\n\u003cp>The new data reinforces findings published in 2009 that examined sodium levels in populations across 33 different countries that showed a very narrow window of human sodium intake regardless of culture, lifestyle or eating patterns.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>In an editorial published in the same issue of \u003cem>AJCN\u003c/em>, UC Davis adjunct professor David McCarron explains that the available data makes it clear that sodium intake is not a variable that is easy to modify in the population.\u003c/p>\n\u003cp>According to McCarron, “These data should close the debate on whether there should be a recommended level of salt intake for the general population.”\u003c/p>\n\u003cp>\u003c/p>\n\u003cp> 38.539895 -121.751958\u003c/p>\n\n",
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"info": "A one-hour radio program to hear celebrated writers, artists and thinkers address contemporary ideas and values, often discussing the creative process. Please note: tapes or transcripts are not available",
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"airtime": "SUN 1pm-2pm, TUE 10pm, WED 1am",
"meta": {
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"source": "City Arts & Lectures"
},
"link": "https://www.cityarts.net",
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"rss": "https://www.cityarts.net/feed/"
}
},
"closealltabs": {
"id": "closealltabs",
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"officialWebsiteLink": "/podcasts/closealltabs",
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"order": 1
},
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"id": "code-switch-life-kit",
"title": "Code Switch / Life Kit",
"info": "\u003cem>Code Switch\u003c/em>, which listeners will hear in the first part of the hour, has fearless and much-needed conversations about race. Hosted by journalists of color, the show tackles the subject of race head-on, exploring how it impacts every part of society — from politics and pop culture to history, sports and more.\u003cbr />\u003cbr />\u003cem>Life Kit\u003c/em>, which will be in the second part of the hour, guides you through spaces and feelings no one prepares you for — from finances to mental health, from workplace microaggressions to imposter syndrome, from relationships to parenting. The show features experts with real world experience and shares their knowledge. Because everyone needs a little help being human.\u003cbr />\u003cbr />\u003ca href=\"https://www.npr.org/podcasts/510312/codeswitch\">\u003cem>Code Switch\u003c/em> offical site and podcast\u003c/a>\u003cbr />\u003ca href=\"https://www.npr.org/lifekit\">\u003cem>Life Kit\u003c/em> offical site and podcast\u003c/a>\u003cbr />",
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"id": "commonwealth-club",
"title": "Commonwealth Club of California Podcast",
"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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"source": "Commonwealth Club of California"
},
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"google": "https://podcasts.google.com/feed/aHR0cDovL3d3dy5jb21tb253ZWFsdGhjbHViLm9yZy9hdWRpby9wb2RjYXN0L3dlZWtseS54bWw",
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"title": "Forum",
"tagline": "The conversation starts here",
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"imageSrc": "https://cdn.kqed.org/wp-content/uploads/2024/04/Forum-Podcast-Tile-703x703-1.jpg",
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"order": 9
},
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"google": "https://podcasts.google.com/feed/aHR0cHM6Ly9mZWVkcy5tZWdhcGhvbmUuZm0vS1FJTkM5NTU3MzgxNjMz",
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"meta": {
"site": "radio",
"source": "WNYC"
},
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"apple": "https://itunes.apple.com/us/podcast/freakonomics-radio/id354668519",
"tuneIn": "https://tunein.com/podcasts/WNYC-Podcasts/Freakonomics-Radio-p272293/",
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},
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"id": "fresh-air",
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"apple": "https://itunes.apple.com/WebObjects/MZStore.woa/wa/viewPodcast?s=143441&mt=2&id=214089682&at=11l79Y&ct=nprdirectory",
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"info": "A live production of NPR and WBUR Boston, in collaboration with stations across the country, Here & Now reflects the fluid world of news as it's happening in the middle of the day, with timely, in-depth news, interviews and conversation. Hosted by Robin Young, Jeremy Hobson and Tonya Mosley.",
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"hidden-brain": {
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"info": "Shankar Vedantam uses science and storytelling to reveal the unconscious patterns that drive human behavior, shape our choices and direct our relationships.",
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"airtime": "SUN 7pm-8pm",
"meta": {
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"source": "NPR"
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"link": "/radio/program/hidden-brain",
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"how-i-built-this": {
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"title": "How I Built This with Guy Raz",
"info": "Guy Raz dives into the stories behind some of the world's best known companies. How I Built This weaves a narrative journey about innovators, entrepreneurs and idealists—and the movements they built.",
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"airtime": "SUN 7:30pm-8pm",
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"link": "/radio/program/how-i-built-this",
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"apple": "https://itunes.apple.com/us/podcast/how-i-built-this-with-guy-raz/id1150510297?mt=2",
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"hyphenacion": {
"id": "hyphenacion",
"title": "Hyphenación",
"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. ",
"imageSrc": "https://cdn.kqed.org/wp-content/uploads/2025/03/Hyphenacion_FinalAssets_PodcastTile.png",
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"officialWebsiteLink": "/podcasts/hyphenacion",
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"order": 15
},
"link": "/podcasts/hyphenacion",
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"spotify": "https://open.spotify.com/show/2p3Fifq96nw9BPcmFdIq0o?si=39209f7b25774f38",
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},
"jerrybrown": {
"id": "jerrybrown",
"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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"officialWebsiteLink": "/podcasts/jerrybrown",
"meta": {
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"order": 18
},
"link": "/podcasts/jerrybrown",
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},
"latino-usa": {
"id": "latino-usa",
"title": "Latino USA",
"airtime": "MON 1am-2am, SUN 6pm-7pm",
"info": "Latino USA, the radio journal of news and culture, is the only national, English-language radio program produced from a Latino perspective.",
"imageSrc": "https://ww2.kqed.org/radio/wp-content/uploads/sites/50/2018/04/latinoUsa.jpg",
"officialWebsiteLink": "http://latinousa.org/",
"meta": {
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},
"link": "/radio/program/latino-usa",
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"apple": "https://itunes.apple.com/WebObjects/MZStore.woa/wa/viewPodcast?s=143441&mt=2&id=79681317&at=11l79Y&ct=nprdirectory",
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"rss": "https://feeds.npr.org/510016/podcast.xml"
}
},
"marketplace": {
"id": "marketplace",
"title": "Marketplace",
"info": "Our flagship program, helmed by Kai Ryssdal, examines what the day in money delivered, through stories, conversations, newsworthy numbers and more. Updated Monday through Friday at about 3:30 p.m. PT.",
"airtime": "MON-FRI 4pm-4:30pm, MON-WED 6:30pm-7pm",
"imageSrc": "https://cdn.kqed.org/wp-content/uploads/2024/04/Marketplace-Podcast-Tile-360x360-1.jpg",
"officialWebsiteLink": "https://www.marketplace.org/",
"meta": {
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"source": "American Public Media"
},
"link": "/radio/program/marketplace",
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},
"masters-of-scale": {
"id": "masters-of-scale",
"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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"officialWebsiteLink": "https://mastersofscale.com/",
"meta": {
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"source": "WaitWhat"
},
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"rss": "https://rss.art19.com/masters-of-scale"
}
},
"mindshift": {
"id": "mindshift",
"title": "MindShift",
"tagline": "A podcast about the future of learning and how we raise our kids",
"info": "The MindShift podcast explores the innovations in education that are shaping how kids learn. Hosts Ki Sung and Katrina Schwartz introduce listeners to educators, researchers, parents and students who are developing effective ways to improve how kids learn. We cover topics like how fed-up administrators are developing surprising tactics to deal with classroom disruptions; how listening to podcasts are helping kids develop reading skills; the consequences of overparenting; and why interdisciplinary learning can engage students on all ends of the traditional achievement spectrum. This podcast is part of the MindShift education site, a division of KQED News. KQED is an NPR/PBS member station based in San Francisco. You can also visit the MindShift website for episodes and supplemental blog posts or tweet us \u003ca href=\"https://twitter.com/MindShiftKQED\">@MindShiftKQED\u003c/a> or visit us at \u003ca href=\"/mindshift\">MindShift.KQED.org\u003c/a>",
"imageSrc": "https://cdn.kqed.org/wp-content/uploads/2024/04/Mindshift-Podcast-Tile-703x703-1.jpg",
"imageAlt": "KQED MindShift: How We Will Learn",
"officialWebsiteLink": "/mindshift/",
"meta": {
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"source": "kqed",
"order": 12
},
"link": "/podcasts/mindshift",
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"google": "https://podcasts.google.com/feed/aHR0cHM6Ly9mZWVkcy5tZWdhcGhvbmUuZm0vS1FJTkM1NzY0NjAwNDI5",
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}
},
"morning-edition": {
"id": "morning-edition",
"title": "Morning Edition",
"info": "\u003cem>Morning Edition\u003c/em> takes listeners around the country and the world with multi-faceted stories and commentaries every weekday. Hosts Steve Inskeep, David Greene and Rachel Martin bring you the latest breaking news and features to prepare you for the day.",
"airtime": "MON-FRI 3am-9am",
"imageSrc": "https://cdn.kqed.org/wp-content/uploads/2024/04/Morning-Edition-Podcast-Tile-360x360-1.jpg",
"officialWebsiteLink": "https://www.npr.org/programs/morning-edition/",
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"link": "/radio/program/morning-edition"
},
"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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"officialWebsiteLink": "/podcasts/onourwatch",
"meta": {
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"source": "kqed",
"order": 11
},
"link": "/podcasts/onourwatch",
"subscribe": {
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"google": "https://podcasts.google.com/feed/aHR0cHM6Ly9mZWVkcy5ucHIub3JnLzUxMDM2MC9wb2RjYXN0LnhtbD9zYz1nb29nbGVwb2RjYXN0cw",
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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",
"airtime": "SUN 2pm-3pm, MON 12am-1am",
"imageSrc": "https://ww2.kqed.org/radio/wp-content/uploads/sites/50/2018/04/onTheMedia.png",
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"meta": {
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"source": "wnyc"
},
"link": "/radio/program/on-the-media",
"subscribe": {
"apple": "https://itunes.apple.com/us/podcast/on-the-media/id73330715?mt=2",
"tuneIn": "https://tunein.com/radio/On-the-Media-p69/",
"rss": "http://feeds.wnyc.org/onthemedia"
}
},
"pbs-newshour": {
"id": "pbs-newshour",
"title": "PBS NewsHour",
"info": "Analysis, background reports and updates from the PBS NewsHour putting today's news in context.",
"airtime": "MON-FRI 3pm-4pm",
"imageSrc": "https://cdn.kqed.org/wp-content/uploads/2024/04/PBS-News-Hour-Podcast-Tile-360x360-1.jpg",
"officialWebsiteLink": "https://www.pbs.org/newshour/",
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"source": "pbs"
},
"link": "/radio/program/pbs-newshour",
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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/",
"rss": "https://www.pbs.org/newshour/feeds/rss/podcasts/show"
}
},
"perspectives": {
"id": "perspectives",
"title": "Perspectives",
"tagline": "KQED's series of daily listener commentaries since 1991",
"info": "KQED's series of daily listener commentaries since 1991.",
"imageSrc": "https://cdn.kqed.org/wp-content/uploads/2025/01/Perspectives_Tile_Final.jpg",
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"officialWebsiteLink": "/perspectives/",
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"source": "kqed",
"order": 14
},
"link": "/perspectives",
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