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Warner,2","publishDate":1292287381,"status":"inherit","parent":10853,"modified":1292287381,"caption":null,"credit":null,"description":"\u003cp class=\"attachment\">\u003ca href='http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2010/12/Gilad-Warner22.jpg' title='Gilad - Warner,2'>\u003cimg width=\"300\" height=\"200\" src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2010/12/Gilad-Warner22.jpg\" class=\"attachment-medium\" alt=\"Gilad - Warner,2\" title=\"Gilad - Warner,2\" />\u003c/a>\u003c/p>","imgSizes":{"guest-author-32":{"file":"https://ww2.kqed.org/app/uploads/sites/39/2010/12/Gilad-Warner22-32x32.jpg","width":32,"height":32,"mimeType":"image/jpeg"},"guest-author-64":{"file":"https://ww2.kqed.org/app/uploads/sites/39/2010/12/Gilad-Warner22-64x64.jpg","width":64,"height":64,"mimeType":"image/jpeg"},"guest-author-96":{"file":"https://ww2.kqed.org/app/uploads/sites/39/2010/12/Gilad-Warner22-96x96.jpg","width":96,"height":96,"mimeType":"image/jpeg"},"guest-author-128":{"file":"https://ww2.kqed.org/app/uploads/sites/39/2010/12/Gilad-Warner22-128x128.jpg","width":128,"height":128,"mimeType":"image/jpeg"},"detail":{"file":"https://ww2.kqed.org/app/uploads/sites/39/2010/12/Gilad-Warner22-75x75.jpg","width":75,"height":75,"mimeType":"image/jpeg"},"kqedFullSize":{"file":"https://ww2.kqed.org/app/uploads/sites/39/2010/12/Gilad-Warner22.jpg","width":300,"height":200}},"fetchFailed":false,"isLoading":false}},"audioPlayerReducer":{"postId":"stream_live"},"authorsReducer":{"sheraz-sadiq":{"type":"authors","id":"6176","meta":{"index":"authors_1591205172","id":"6176","found":true},"name":"Sheraz Sadiq","firstName":"Sheraz","lastName":"Sadiq","slug":"sheraz-sadiq","email":"ssadiq@kqed.org","display_author_email":false,"staff_mastheads":[],"title":null,"bio":"Sheraz Sadiq is an Emmy Award-winning producer at San Francisco PBS affiliate KQED. In 2012, he received the AAAS Kavli Science Journalism award for a story he produced about the seismic retrofit of the Hetch Hetchy water delivery system which serves the San Francisco Bay Area. In addition to producing television content for KQED Science, he has also created online features and written news articles on scientific subjects ranging from astronomy to synthetic biology.","avatar":"https://secure.gravatar.com/avatar/9731b29e144af1965b0b7eaa56555561?s=600&d=blank&r=g","twitter":null,"facebook":null,"instagram":null,"linkedin":null,"sites":[{"site":"arts","roles":["editor"]},{"site":"quest","roles":["leadcoordinator","editor"]}],"headData":{"title":"Sheraz Sadiq | KQED","description":null,"ogImgSrc":"https://secure.gravatar.com/avatar/9731b29e144af1965b0b7eaa56555561?s=600&d=blank&r=g","twImgSrc":"https://secure.gravatar.com/avatar/9731b29e144af1965b0b7eaa56555561?s=600&d=blank&r=g"},"isLoading":false,"link":"/author/sheraz-sadiq"}},"breakingNewsReducer":{},"campaignFinanceReducer":{},"firebase":{"requesting":{},"requested":{},"timestamps":{},"data":{},"ordered":{},"auth":{"isLoaded":false,"isEmpty":true},"authError":null,"profile":{"isLoaded":false,"isEmpty":true},"listeners":{"byId":{},"allIds":[]},"isInitializing":false,"errors":[]},"navBarReducer":{"navBarId":"home","fullView":true,"showPlayer":false},"navMenuReducer":{"menus":[{"key":"menu1","items":[{"name":"News","link":"/","type":"title"},{"name":"Politics","link":"/politics"},{"name":"Science","link":"/science"},{"name":"Education","link":"/educationnews"},{"name":"Housing","link":"/housing"},{"name":"Immigration","link":"/immigration"},{"name":"Criminal Justice","link":"/criminaljustice"},{"name":"Silicon Valley","link":"/siliconvalley"},{"name":"Forum","link":"/forum"},{"name":"The California Report","link":"/californiareport"}]},{"key":"menu2","items":[{"name":"Arts & Culture","link":"/arts","type":"title"},{"name":"Critics’ Picks","link":"/thedolist"},{"name":"Cultural Commentary","link":"/artscommentary"},{"name":"Food & Drink","link":"/food"},{"name":"Bay Area Hip-Hop","link":"/bayareahiphop"},{"name":"Rebel Girls","link":"/rebelgirls"},{"name":"Arts Video","link":"/artsvideos"}]},{"key":"menu3","items":[{"name":"Podcasts","link":"/podcasts","type":"title"},{"name":"Bay Curious","link":"/podcasts/baycurious"},{"name":"Rightnowish","link":"/podcasts/rightnowish"},{"name":"The Bay","link":"/podcasts/thebay"},{"name":"On Our Watch","link":"/podcasts/onourwatch"},{"name":"Mindshift","link":"/podcasts/mindshift"},{"name":"Consider This","link":"/podcasts/considerthis"},{"name":"Political Breakdown","link":"/podcasts/politicalbreakdown"}]},{"key":"menu4","items":[{"name":"Live Radio","link":"/radio","type":"title"},{"name":"TV","link":"/tv","type":"title"},{"name":"Events","link":"/events","type":"title"},{"name":"For Educators","link":"/education","type":"title"},{"name":"Support KQED","link":"/support","type":"title"},{"name":"About","link":"/about","type":"title"},{"name":"Help Center","link":"https://kqed-helpcenter.kqed.org/s","type":"title"}]}]},"pagesReducer":{},"postsReducer":{"stream_live":{"type":"live","id":"stream_live","audioUrl":"https://streams.kqed.org/kqedradio","title":"Live Stream","excerpt":"Live Stream information currently unavailable.","link":"/radio","featImg":"","label":{"name":"KQED Live","link":"/"}},"stream_kqedNewscast":{"type":"posts","id":"stream_kqedNewscast","audioUrl":"https://www.kqed.org/.stream/anon/radio/RDnews/newscast.mp3?_=1","title":"KQED Newscast","featImg":"","label":{"name":"88.5 FM","link":"/"}},"quest_10853":{"type":"posts","id":"quest_10853","meta":{"index":"posts_1591205157","site":"quest","id":"10853","score":null,"sort":[1291224354000]},"guestAuthors":[],"slug":"aids-researchers-unlock-cell-death-mystery","title":"AIDS Researchers Unlock Cell Death Mystery","publishDate":1291224354,"format":"standard","headTitle":"QUEST | KQED Science","labelTerm":{"site":"quest"},"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","blocks":[],"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.","status":"publish","parent":0,"modified":1316922397,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":45,"wordCount":1777},"headData":{"title":"AIDS Researchers Unlock Cell Death Mystery | KQED","description":"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.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":""},"disqusIdentifier":"10853 http://www.kqed.org/quest/blog/2010/12/01/tiny-satellites-give-nasa-big-returns-2/","disqusUrl":"https://ww2.kqed.org/quest/2010/12/01/aids-researchers-unlock-cell-death-mystery/","disqusTitle":"AIDS Researchers Unlock Cell Death Mystery","path":"/quest/10853/aids-researchers-unlock-cell-death-mystery","audioTrackLength":null,"parsedContent":[{"type":"contentString","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>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"ad","attributes":{"named":{"label":"fullwidth"},"numeric":["fullwidth"]}},{"type":"contentString","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>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"ad","attributes":{"named":{"label":"floatright"},"numeric":["floatright"]}},{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp> 37.767050 -122.391139\u003c/p>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/quest/10853/aids-researchers-unlock-cell-death-mystery","authors":["6176"],"categories":["quest_4","quest_12"],"tags":["quest_89","quest_520","quest_1212","quest_1217","quest_1218","quest_1375","quest_1927","quest_13203","quest_3026","quest_3102"],"featImg":"quest_11177","label":"quest"},"quest_8411":{"type":"posts","id":"quest_8411","meta":{"index":"posts_1591205157","site":"quest","id":"8411","score":null,"sort":[1285099246000]},"guestAuthors":[],"slug":"scientists-work-to-develop-artificial-kidney","title":"Scientists Work on New Artificial Kidney","publishDate":1285099246,"format":"standard","headTitle":"QUEST | KQED Science","labelTerm":{"site":"quest"},"content":"\u003cp>\u003cspan class=\"left\">\u003ca href=\"http://www.kqed.org/quest\">\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2010/09/UCSF_2_991170061_shuvo-roy-phd-1952.jpg\" alt=\"\">\u003c/a>\u003cem>UCSF Bioengineer Shuvo Roy works on a model of an artificial, implantable kidney. (Credit: UCSF)\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>From his lab at the Mission Bay campus of the University of California-San Francisco, Shuvo Roy is leading a project with nearly 40 scientists from across the nation to develop the world’s first artificial, implantable kidney. \u003c/p>\n\u003cp>\"When you have kidney failure, the sickest of the sick tend to get on the transplant waiting list,” said Roy, an associate professor of bioengineering and therapeutic sciences at UCSF. \u003c/p>\n\u003cp>\u003c!--more-->\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>Roy is collaborating with scientists and biotech experts at ten other institutions, including the University of Michigan, the Cleveland Clinic and Case Western Reserve University. Drawing inspiration from Silicon Valley, the researchers have figured out how to take a room-sized dialysis machine and shrink it down to a cartridge the size of a coffee cup. \u003c/p>\n\u003cp>\"What we are motivated to do,” said Roy, “is come up with a solution that will provide the benefits of a healthy kidney to the vast majority of patients that are on dialysis and who have a very low chance of ever getting a transplant kidney.\"\u003c/p>\n\u003cp>The researchers have built the prototype of a device that can be implanted in patients and run without batteries or pumps. Their goal: have it in clinical trials in five to seven years.\u003c/p>\n\u003cp>Healthy kidneys filter toxins from blood. Dialysis machines do the same thing, but require patients to sit, often for three hours or more, several times a week. \u003c/p>\n\u003cp>The team’s artificial kidney filters blood using strips of silicon, etched with tiny pores. “We're applying state-of-the-art fabrication technologies used in making computer chips to achieve very precise features and dimensions at the nano-scale,\" said Roy. \u003c/p>\n\u003cp>By engineering super-thin silicon membranes at the microscopic scale, the scientists have done away with the need for pumps and large amounts of electricity used in traditional dialysis machines. Instead, the patient’s blood pressure is sufficient to pump the blood for filtration through the artificial kidney device. \u003c/p>\n\u003cp>\u003cspan class=\"left\">\u003ca href=\"http://www.kqed.org/quest\">\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2010/09/UCSF_2_kidney_991182869_QKPUF-L.jpg\" alt=\"\">\u003c/a>\u003cem>Scientist manipulates pieces of silicon membrane in a petri dish. (Credit: UCSF)\u003c/em>\u003c/span>\u003c/p>\n\u003cp>“This is really our contribution,” he said. “Because our silicon membranes don't require a lot of pressure for filtration, we can make them small enough and compact enough to fit inside the little cartridge.\"\u003c/p>\n\u003cp>Roy and his team have tested the filtration component of their artificial kidney device on animal models, including rats and pigs. Right now, they’re working to scale it up for use on humans.\u003c/p>\n\u003cp>According to the National Kidney Foundation, roughly 11 percent of adults in the U.S. suffer from stage one or higher chronic kidney disease, including nearly a million adults in the Bay Area. But most people don’t even know they have kidney disease, which is diagnosed with a simple blood test, until it’s too late. \u003c/p>\n\u003cp>“Until kidney disease gets to stages four or five, it's a silent disease,” said Patty McCormac, a registered nurse and a program director for the San Francisco office of the National Kidney Foundation.\u003c/p>\n\u003cp>Patients with End Stage Renal Disease, the last of five stages in chronic kidney disease, when the kidneys have ceased to work, must undergo dialysis. The only alternative is a kidney transplant. \u003c/p>\n\u003cp>Roughly every five minutes, all of the blood pumped from the heart is sent through the kidneys, which sit below the rib cage on either side of the spine. The five-inch organs filter the blood to remove toxins from drugs, for example, that are ingested and that build up from the daily metabolic activity of the liver and the muscles in the body. \u003c/p>\n\u003cp>They also perform the crucial job of balancing water, salts, minerals and acid in the blood through hormones and other chemical messages which are relayed from other parts of the body to let the kidneys know whether to increase or decrease the amount of water, mineral salts or acid in the blood. Kidneys also help regulate blood pressure and spur the production of red blood cells.\u003c/p>\n\u003cp>Some Bay Area kidney patients already are watching Roy’s research with the hope that one day it could change their lives.\u003c/p>\n\u003cp>David Anderson is a 60 year-old San Francisco resident who first started dialysis 11 years ago. After a four year wait, he received a kidney transplant in 2003, but the kidney failed in 2007. So he had to resume visits to the dialysis outpatient clinic at UCSF Mount Zion. \u003c/p>\n\u003cp>Anderson found out about Roy’s research in August while talking with a friend of his who had read about it on the internet. \u003c/p>\n\u003cp>“The potential that this artificial kidney might be available in five years has changed my outlook,” he said. “It has given me a more disciplined participation in my own treatment -- a discipline with my diet, which is more likely to keep me around for those five years.” \u003c/p>\n\u003cp>Although Anderson tolerates dialysis fairly well, many patients can experience fatigue, nausea and low blood pressure after the treatment. When Anderson started dialysis, he also suffered from hypertension, which along with diabetes, causes two-thirds of all cases of chronic kidney disease. \u003c/p>\n\u003cp>According to the U.S. Renal Data System, roughly 350,000 adults in the U.S. were on dialysis in 2007, including nearly 50,000 adults in California alone. \u003c/p>\n\u003cp>Dialysis is also expensive. In 2007, Medicare spent on average more than $72,000 per patient on dialysis treatments. The cost of the artificial kidney, Roy said, would be comparable to two years of dialysis treatments and cheaper in the long run as expensive immunosuppressant drugs would not be needed to maintain it. \u003c/p>\n\u003cp>If the researchers are successful, dialysis patients would experience a greatly enhanced level of mobility and independence. \u003c/p>\n\u003cp>“It would potentially be like having your own little artificial kidney, so you'd be able to get up and walk around. It would revolutionize treatment. The dialysis machines we use today, you're basically sitting in a chair for four hours at a time,” said Dr. Lynda Frassetto, a kidney doctor and professor of medicine at UCSF. “We don't let you get up.” \u003c/p>\n\u003cp>By using the tools of nanotechnology, some of which were developed at UC Berkeley, Roy and his team are able to cut shapes and precise patterns into silicon, much like electrical engineers do in designing a computer chip to carry out complex calculations and tasks. \u003c/p>\n\u003cp>But here the silicon is tailored to be the right size and shape for blood filtration, so tiny pores - a few billionths of a meter in size - are cut into silicon wafers, the same material from which computer chips are made. The silicon wafers are then cut into strips and assembled into rows which act as filters, the first stage of Roy’s artificial kidney.\u003c/p>\n\u003cp>Much like a real human kidney, the silicon filters take a portion of the patient’s blood and remove toxins from it, along with sugars, water and salts. The portion of the blood that is unfiltered returns to the body, eventually cycling back for filtration. \u003c/p>\n\u003cp>The filtered blood, or “filtrate”, then passes to a second compartment, the bioreactor, for additional processing. In the bioreactor, the filtrate passes over a bed of kidney cells, which could be cultured from the patient’s own kidneys or they could come from a donor. \u003c/p>\n\u003cp>“As the filtrate flows over this bed of cells, the bed of cells senses how much salts and sugars the body needs and they reabsorb the salts, sugars and much of the water back into the body”, said Roy. \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/39/2010/09/UCSF_Kidney_Model-pix.jpg\" alt=\"\">\u003c/a>\u003cem>Schematic image of the artificial implantable kidney device being developed at UCSF. Click \u003ca href=\"http://ww2.kqed.org/quest/wp-content/uploads/2010/09/UCSF_kidney_large.jpg\">here\u003c/a> for a larger image. (Credit: Dr. Shuvo Roy, UCSF)\u003c/em>\u003c/span>\u003c/p>\n\u003cp>So the bed of kidney cells would help perform a job that the most advanced dialysis machine currently can’t do: maintain the critical balance between water, salts and other constituents of blood, which healthy kidneys do automatically. \u003c/p>\n\u003cp>And even though the kidney cells may not come from the patient, they wouldn’t be rejected by the patient’s immune system - a problem that until now, has inhibited the development of an artificial, implantable kidney. This is because the silicon membrane on which they sit contains pores that are big enough to allow the filtered blood through where it mingles with the live kidney cells, but they’re too small for the body’s immune cells to pass through and attack them. \u003c/p>\n\u003cp>“So if they can use this artificial kidney filter and they don’t need to give people anti-rejection medication, that's huge,” said Frassetto. \u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp> 37.767050 -122.391139\u003c/p>\n\n","blocks":[],"excerpt":"A UCSF scientists is leading a team of nearly forty scientists across the nation to develop the world’s first artificial implantable kidney.","status":"publish","parent":0,"modified":1285099246,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":40,"wordCount":1480},"headData":{"title":"Scientists Work on New Artificial Kidney | KQED","description":"A UCSF scientists is leading a team of nearly forty scientists across the nation to develop the world’s first artificial implantable kidney.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":""},"disqusIdentifier":"8411 http://science.kqed.org/quest/2010/09/21/scientists-work-to-develop-artificial-kidney/","disqusUrl":"https://ww2.kqed.org/quest/2010/09/21/scientists-work-to-develop-artificial-kidney/","disqusTitle":"Scientists Work on New Artificial Kidney","path":"/quest/8411/scientists-work-to-develop-artificial-kidney","audioTrackLength":null,"parsedContent":[{"type":"contentString","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/39/2010/09/UCSF_2_991170061_shuvo-roy-phd-1952.jpg\" alt=\"\">\u003c/a>\u003cem>UCSF Bioengineer Shuvo Roy works on a model of an artificial, implantable kidney. (Credit: UCSF)\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>From his lab at the Mission Bay campus of the University of California-San Francisco, Shuvo Roy is leading a project with nearly 40 scientists from across the nation to develop the world’s first artificial, implantable kidney. \u003c/p>\n\u003cp>\"When you have kidney failure, the sickest of the sick tend to get on the transplant waiting list,” said Roy, an associate professor of bioengineering and therapeutic sciences at UCSF. \u003c/p>\n\u003cp>\u003c!--more-->\u003c/p>\n\u003cp>\u003c/p>\u003c/div>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"ad","attributes":{"named":{"label":"fullwidth"},"numeric":["fullwidth"]}},{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>Roy is collaborating with scientists and biotech experts at ten other institutions, including the University of Michigan, the Cleveland Clinic and Case Western Reserve University. Drawing inspiration from Silicon Valley, the researchers have figured out how to take a room-sized dialysis machine and shrink it down to a cartridge the size of a coffee cup. \u003c/p>\n\u003cp>\"What we are motivated to do,” said Roy, “is come up with a solution that will provide the benefits of a healthy kidney to the vast majority of patients that are on dialysis and who have a very low chance of ever getting a transplant kidney.\"\u003c/p>\n\u003cp>The researchers have built the prototype of a device that can be implanted in patients and run without batteries or pumps. Their goal: have it in clinical trials in five to seven years.\u003c/p>\n\u003cp>Healthy kidneys filter toxins from blood. Dialysis machines do the same thing, but require patients to sit, often for three hours or more, several times a week. \u003c/p>\n\u003cp>The team’s artificial kidney filters blood using strips of silicon, etched with tiny pores. “We're applying state-of-the-art fabrication technologies used in making computer chips to achieve very precise features and dimensions at the nano-scale,\" said Roy. \u003c/p>\n\u003cp>By engineering super-thin silicon membranes at the microscopic scale, the scientists have done away with the need for pumps and large amounts of electricity used in traditional dialysis machines. Instead, the patient’s blood pressure is sufficient to pump the blood for filtration through the artificial kidney device. \u003c/p>\n\u003cp>\u003cspan class=\"left\">\u003ca href=\"http://www.kqed.org/quest\">\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2010/09/UCSF_2_kidney_991182869_QKPUF-L.jpg\" alt=\"\">\u003c/a>\u003cem>Scientist manipulates pieces of silicon membrane in a petri dish. (Credit: UCSF)\u003c/em>\u003c/span>\u003c/p>\n\u003cp>“This is really our contribution,” he said. “Because our silicon membranes don't require a lot of pressure for filtration, we can make them small enough and compact enough to fit inside the little cartridge.\"\u003c/p>\n\u003cp>Roy and his team have tested the filtration component of their artificial kidney device on animal models, including rats and pigs. Right now, they’re working to scale it up for use on humans.\u003c/p>\n\u003cp>According to the National Kidney Foundation, roughly 11 percent of adults in the U.S. suffer from stage one or higher chronic kidney disease, including nearly a million adults in the Bay Area. But most people don’t even know they have kidney disease, which is diagnosed with a simple blood test, until it’s too late. \u003c/p>\n\u003cp>“Until kidney disease gets to stages four or five, it's a silent disease,” said Patty McCormac, a registered nurse and a program director for the San Francisco office of the National Kidney Foundation.\u003c/p>\n\u003cp>Patients with End Stage Renal Disease, the last of five stages in chronic kidney disease, when the kidneys have ceased to work, must undergo dialysis. The only alternative is a kidney transplant. \u003c/p>\n\u003cp>Roughly every five minutes, all of the blood pumped from the heart is sent through the kidneys, which sit below the rib cage on either side of the spine. The five-inch organs filter the blood to remove toxins from drugs, for example, that are ingested and that build up from the daily metabolic activity of the liver and the muscles in the body. \u003c/p>\n\u003cp>They also perform the crucial job of balancing water, salts, minerals and acid in the blood through hormones and other chemical messages which are relayed from other parts of the body to let the kidneys know whether to increase or decrease the amount of water, mineral salts or acid in the blood. Kidneys also help regulate blood pressure and spur the production of red blood cells.\u003c/p>\n\u003cp>Some Bay Area kidney patients already are watching Roy’s research with the hope that one day it could change their lives.\u003c/p>\n\u003cp>David Anderson is a 60 year-old San Francisco resident who first started dialysis 11 years ago. After a four year wait, he received a kidney transplant in 2003, but the kidney failed in 2007. So he had to resume visits to the dialysis outpatient clinic at UCSF Mount Zion. \u003c/p>\n\u003cp>Anderson found out about Roy’s research in August while talking with a friend of his who had read about it on the internet. \u003c/p>\n\u003cp>“The potential that this artificial kidney might be available in five years has changed my outlook,” he said. “It has given me a more disciplined participation in my own treatment -- a discipline with my diet, which is more likely to keep me around for those five years.” \u003c/p>\n\u003cp>Although Anderson tolerates dialysis fairly well, many patients can experience fatigue, nausea and low blood pressure after the treatment. When Anderson started dialysis, he also suffered from hypertension, which along with diabetes, causes two-thirds of all cases of chronic kidney disease. \u003c/p>\n\u003cp>According to the U.S. Renal Data System, roughly 350,000 adults in the U.S. were on dialysis in 2007, including nearly 50,000 adults in California alone. \u003c/p>\n\u003cp>Dialysis is also expensive. In 2007, Medicare spent on average more than $72,000 per patient on dialysis treatments. The cost of the artificial kidney, Roy said, would be comparable to two years of dialysis treatments and cheaper in the long run as expensive immunosuppressant drugs would not be needed to maintain it. \u003c/p>\n\u003cp>If the researchers are successful, dialysis patients would experience a greatly enhanced level of mobility and independence. \u003c/p>\n\u003cp>“It would potentially be like having your own little artificial kidney, so you'd be able to get up and walk around. It would revolutionize treatment. The dialysis machines we use today, you're basically sitting in a chair for four hours at a time,” said Dr. Lynda Frassetto, a kidney doctor and professor of medicine at UCSF. “We don't let you get up.” \u003c/p>\n\u003cp>By using the tools of nanotechnology, some of which were developed at UC Berkeley, Roy and his team are able to cut shapes and precise patterns into silicon, much like electrical engineers do in designing a computer chip to carry out complex calculations and tasks. \u003c/p>\n\u003cp>But here the silicon is tailored to be the right size and shape for blood filtration, so tiny pores - a few billionths of a meter in size - are cut into silicon wafers, the same material from which computer chips are made. The silicon wafers are then cut into strips and assembled into rows which act as filters, the first stage of Roy’s artificial kidney.\u003c/p>\n\u003cp>Much like a real human kidney, the silicon filters take a portion of the patient’s blood and remove toxins from it, along with sugars, water and salts. The portion of the blood that is unfiltered returns to the body, eventually cycling back for filtration. \u003c/p>\n\u003cp>The filtered blood, or “filtrate”, then passes to a second compartment, the bioreactor, for additional processing. In the bioreactor, the filtrate passes over a bed of kidney cells, which could be cultured from the patient’s own kidneys or they could come from a donor. \u003c/p>\n\u003cp>“As the filtrate flows over this bed of cells, the bed of cells senses how much salts and sugars the body needs and they reabsorb the salts, sugars and much of the water back into the body”, said Roy. \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/39/2010/09/UCSF_Kidney_Model-pix.jpg\" alt=\"\">\u003c/a>\u003cem>Schematic image of the artificial implantable kidney device being developed at UCSF. Click \u003ca href=\"http://ww2.kqed.org/quest/wp-content/uploads/2010/09/UCSF_kidney_large.jpg\">here\u003c/a> for a larger image. (Credit: Dr. Shuvo Roy, UCSF)\u003c/em>\u003c/span>\u003c/p>\n\u003cp>So the bed of kidney cells would help perform a job that the most advanced dialysis machine currently can’t do: maintain the critical balance between water, salts and other constituents of blood, which healthy kidneys do automatically. \u003c/p>\n\u003cp>And even though the kidney cells may not come from the patient, they wouldn’t be rejected by the patient’s immune system - a problem that until now, has inhibited the development of an artificial, implantable kidney. This is because the silicon membrane on which they sit contains pores that are big enough to allow the filtered blood through where it mingles with the live kidney cells, but they’re too small for the body’s immune cells to pass through and attack them. \u003c/p>\n\u003cp>“So if they can use this artificial kidney filter and they don’t need to give people anti-rejection medication, that's huge,” said Frassetto. \u003c/p>\n\u003cp>\u003c/p>\u003c/div>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"ad","attributes":{"named":{"label":"floatright"},"numeric":["floatright"]}},{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp> 37.767050 -122.391139\u003c/p>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/quest/8411/scientists-work-to-develop-artificial-kidney","authors":["6176"],"categories":["quest_4","quest_5","quest_8","quest_12"],"tags":["quest_221","quest_823","quest_13203","quest_2626","quest_3026"],"label":"quest"}},"programsReducer":{"possible":{"id":"possible","title":"Possible","info":"Possible is hosted by entrepreneur Reid Hoffman and writer Aria Finger. 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You ask the questions. You decide what Bay Curious investigates. 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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 />","airtime":"SUN 9pm-10pm","imageSrc":"https://cdn.kqed.org/wp-content/uploads/2024/04/Code-Switch-Life-Kit-Podcast-Tile-360x360-1.jpg","meta":{"site":"radio","source":"npr"},"link":"/radio/program/code-switch-life-kit","subscribe":{"apple":"https://podcasts.apple.com/podcast/1112190608?mt=2&at=11l79Y&ct=nprdirectory","google":"https://podcasts.google.com/feed/aHR0cHM6Ly93d3cubnByLm9yZy9yc3MvcG9kY2FzdC5waHA_aWQ9NTEwMzEy","spotify":"https://open.spotify.com/show/3bExJ9JQpkwNhoHvaIIuyV","rss":"https://feeds.npr.org/510312/podcast.xml"}},"commonwealth-club":{"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. 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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":{"site":"news","source":"kqed","order":"2"},"link":"/podcasts/mindshift","subscribe":{"apple":"https://podcasts.apple.com/us/podcast/mindshift-podcast/id1078765985","google":"https://podcasts.google.com/feed/aHR0cHM6Ly9mZWVkcy5tZWdhcGhvbmUuZm0vS1FJTkM1NzY0NjAwNDI5","npr":"https://www.npr.org/podcasts/464615685/mind-shift-podcast","stitcher":"https://www.stitcher.com/podcast/kqed/stories-teachers-share","spotify":"https://open.spotify.com/show/0MxSpNYZKNprFLCl7eEtyx"}},"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. 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