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"content": "\u003cp>\u003cspan class=\"left\">\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2010/12/AsianGlow1.jpg\" alt=\"\">\u003cem>If he drinks a lot, he can be up to 56 times more likely to\u003cbr>end up with esophageal cancer compared to a nondrinker.\u003c/em>\u003c/span>\u003c/p>\n\u003cp>Many people of East Asian descent react to alcohol with a red face, a racing heartbeat and a slight sick feeling in their stomach. This “Asian glow” is more than just annoying though. If they keep drinking anyway, it can be downright dangerous.\u003c/p>\n\u003cp>In addition to its obvious charms, drinking alcohol definitely has some drawbacks (besides beer goggles and nasty hangovers). One of these is an increased risk for getting cancer of the esophagus. One study I saw claimed that heavy drinkers are 18 times more likely to end up with esophageal cancer compared to teetotalers. \u003c/p>\n\u003cp>\u003c!--more-->\u003c/p>\n\u003cp>The risk is even higher for blushers. They are 56 times more likely to end up with this particular cancer if they are heavy drinkers. And even if they just have a couple of drinks a day, they are still at a 5 times higher risk. \u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>Unfortunately, the alcohol flushing response is pretty common. Scientists estimate that 36% of people of East Asian descent respond to alcohol this way. That’s over 500 million people worldwide. \u003c/p>\n\u003cp>All of these statistics are especially scary because esophageal cancer is so common. For example, it is the 7th leading cause of cancer death worldwide and the 7th most common cancer in men in the U.S. In some parts of Russia and China, the rates of this cancer range from 30-800 cases per 100,000 people. The rate in the U.S is 3-6 per 100,000.\u003c/p>\n\u003cp>Many if not most of these cancers happen because the patients drank too much alcohol and smoked too many cigarettes. One review article estimated that if heavy drinking blushers from Japan switched to just two drinks per day, the number of cases of esophageal cancer there would be cut in half. Undoubtedly the same thing is true elsewhere.\u003c/p>\n\u003cp>Everyone is at a higher risk for esophageal cancer when they drink because of how alcohol is broken down in the body. On the way to converting alcohol to the safer acetic acid, our bodies first turn it into acetaldehyde. And that is some nasty stuff!\u003c/p>\n\u003cp>Acetaldehyde likes to stick to and damage our DNA. Not only that, it also keeps our cells from repairing the damage. Since cancer happens because of DNA damage, it isn’t surprising that alcohol causes an increased risk for cancer.\u003c/p>\n\u003cp>People who blush from alcohol have a certain version of the ALDH2 gene that has \u003ca href=\"http://www.thetech.org/exhibits/online/ugenetics/BDETechDec/Screen3b.html\">trouble converting\u003c/a> alcohol into acetaldehyde. The end result is a build up of acetaldehyde that can damage DNA and so cause esophageal cancer.\u003c/p>\n\u003cp>Again, there is no increased risk if they don’t drink. In the absence of alcohol, they are just like anyone else. They just need to lay off the liquor.\u003c/p>\n\u003cp>Maybe these people need to find a new social lubricant. I guess it's too bad Prop 19 didn’t pass…\u003c/p>\n\u003cp>\u003ca href=\"http://www.thetech.org/exhibits/online/ugenetics/BDETechDec/\">A fun activity to learn more about the genetics and biology of the alcohol flushing response.\u003c/a>\u003c/p>\n\u003cp>\u003ca href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2659709/pdf/pmed.1000050.pdf\">A review article that raises an alarm about the risks of drinking alcohol as a blusher.\u003c/a>\u003c/p>\n\u003cp>\u003c/p>\n\u003cp> 37.7749295 -122.4194155\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>\u003cspan class=\"left\">\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2010/12/AsianGlow1.jpg\" alt=\"\">\u003cem>If he drinks a lot, he can be up to 56 times more likely to\u003cbr>end up with esophageal cancer compared to a nondrinker.\u003c/em>\u003c/span>\u003c/p>\n\u003cp>Many people of East Asian descent react to alcohol with a red face, a racing heartbeat and a slight sick feeling in their stomach. This “Asian glow” is more than just annoying though. If they keep drinking anyway, it can be downright dangerous.\u003c/p>\n\u003cp>In addition to its obvious charms, drinking alcohol definitely has some drawbacks (besides beer goggles and nasty hangovers). One of these is an increased risk for getting cancer of the esophagus. One study I saw claimed that heavy drinkers are 18 times more likely to end up with esophageal cancer compared to teetotalers. \u003c/p>\n\u003cp>\u003c!--more-->\u003c/p>\n\u003cp>The risk is even higher for blushers. They are 56 times more likely to end up with this particular cancer if they are heavy drinkers. And even if they just have a couple of drinks a day, they are still at a 5 times higher risk. \u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>Unfortunately, the alcohol flushing response is pretty common. Scientists estimate that 36% of people of East Asian descent respond to alcohol this way. That’s over 500 million people worldwide. \u003c/p>\n\u003cp>All of these statistics are especially scary because esophageal cancer is so common. For example, it is the 7th leading cause of cancer death worldwide and the 7th most common cancer in men in the U.S. In some parts of Russia and China, the rates of this cancer range from 30-800 cases per 100,000 people. The rate in the U.S is 3-6 per 100,000.\u003c/p>\n\u003cp>Many if not most of these cancers happen because the patients drank too much alcohol and smoked too many cigarettes. One review article estimated that if heavy drinking blushers from Japan switched to just two drinks per day, the number of cases of esophageal cancer there would be cut in half. Undoubtedly the same thing is true elsewhere.\u003c/p>\n\u003cp>Everyone is at a higher risk for esophageal cancer when they drink because of how alcohol is broken down in the body. On the way to converting alcohol to the safer acetic acid, our bodies first turn it into acetaldehyde. And that is some nasty stuff!\u003c/p>\n\u003cp>Acetaldehyde likes to stick to and damage our DNA. Not only that, it also keeps our cells from repairing the damage. Since cancer happens because of DNA damage, it isn’t surprising that alcohol causes an increased risk for cancer.\u003c/p>\n\u003cp>People who blush from alcohol have a certain version of the ALDH2 gene that has \u003ca href=\"http://www.thetech.org/exhibits/online/ugenetics/BDETechDec/Screen3b.html\">trouble converting\u003c/a> alcohol into acetaldehyde. The end result is a build up of acetaldehyde that can damage DNA and so cause esophageal cancer.\u003c/p>\n\u003cp>Again, there is no increased risk if they don’t drink. In the absence of alcohol, they are just like anyone else. They just need to lay off the liquor.\u003c/p>\n\u003cp>Maybe these people need to find a new social lubricant. I guess it's too bad Prop 19 didn’t pass…\u003c/p>\n\u003cp>\u003ca href=\"http://www.thetech.org/exhibits/online/ugenetics/BDETechDec/\">A fun activity to learn more about the genetics and biology of the alcohol flushing response.\u003c/a>\u003c/p>\n\u003cp>\u003ca href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2659709/pdf/pmed.1000050.pdf\">A review article that raises an alarm about the risks of drinking alcohol as a blusher.\u003c/a>\u003c/p>\n\u003cp>\u003c/p>\n\u003cp> 37.7749295 -122.4194155\u003c/p>\n\n\u003c/div>\u003c/p>",
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"content": "\u003cp>After more than a century of logging, California's old-growth redwood forests are only a fraction of what they once were. Today, they \u003ca href=\"http://www.parks.ca.gov/?page_id=24723\">remain in a narrow coastal band\u003c/a> that extends from Monterey Bay to the Oregon border. Most ancient redwoods are protected in parks. But now they are facing a new threat -- climate change.\u003c/p>\n\u003cp>Coast redwoods are among the largest living organisms on the planet. Their trunks can grow to 25 feet in diameter. Much of the tree is hidden from our view.\u003c/p>\n\u003cp>\"From down here, you can tell that they're tall but you can't tell too much about each tree,\" says Steve Sillett, a botany professor at Humboldt State University who has researched these trees for two decades.\u003c/p>\n\u003cp>To really study them, Sillett says, you have to go up.\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>[audio:http://www.kqed.org/.stream/anon/radio/quest/2010/12/2010-12-20-quest.mp3|titles=California's Redwoods Face Climate Change]\u003cem>Listen to the QUEST radio story \u003cstrong>\u003ca href=\"http://www.kqed.org/quest/radio/californias-redwoods-face-climate-change\">California's Redwoods Face Climate Change\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>Climbing a 360-foot redwood isn't for the faint of heart. Today, Sillett and his team are climbing one of the tallest trees in \u003ca href=\"http://www.parks.ca.gov/?page_id=434\">Montgomery Woods State Reserve\u003c/a> in Mendocino County. It's taller than a 35-story building.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>\"We don't use spikes or spurs. We don't injure the tree in any way when we're climbing it.\" Sillett and his research partner, Marie Antoine, clip their climbing harnesses onto long ropes that are fixed high in the tree. They pull themselves up with an ascender -- a metal clamp that slides up the rope and provides traction.\u003c/p>\n\u003cp>Sillett was one of the first scientists to explore the old-growth redwood canopy. Their treetops are home to an entire ecosystem of animals, fern thickets as big as a bus and even other trees that grow among the redwood branches.\u003c/p>\n\u003cp>\"The most freaked out I have ever been was when we found the first salamander up there. And I am 3-hundred feet up in a tree and there is a salamander cruising around,\" says Sillett.\u003c/p>\n\u003cp>\u003cstrong>Climbing Giants\u003c/strong>\u003c/p>\n\u003cp>Today, Sillett and Antoine are measuring the tree in an unprecedented way by doing complete structural inventory.\u003c/p>\n\u003cp>They start by measuring the trunk. Dangling gracefully from ropes, they stretch a tape measure around the tree. \"Let's do our first wrap at 40, so I'll go to 40,\" Sillett yells.\u003c/p>\n\u003cp>They continue down, measuring at different intervals. \"Three twenty-one point seven. So that's over 10 feet diameter,\" says Sillett.\u003c/p>\n\u003cp>They'll also measure every branch. \"We did have one tree that had 472 branches and 206 segments in it, which took about four days.\"\u003c/p>\n\u003cp>Sillett and his team are measuring hundreds of redwoods like this as \u003ca href=\"http://rcci.savetheredwoods.org/science/index.shtml\">part of a $2.5 million dollar study\u003c/a> funded by the \u003ca href=\"http://www.savetheredwoods.org/\">Save the Redwoods League\u003c/a>. With the data, he generates a 3D model of each tree. Once they measure the trees again in three years, the models will tell him how much the redwoods are growing.\u003c/p>\n\u003cp>\"Some years, there's a lot of growth, and some years there's almost no growth. And sometimes there's dieback and recovery,\" says Sillett. \"We suspect that the really tall trees, the tallest trees in the world, are among the most sensitive things to climate change.\"\u003c/p>\n\u003cp>Tall trees, Sillett says, are already under a great deal of stress. Simply lifting water hundreds of feet from the roots to the tree tops is difficult. And with the temperature and precipitation changes predicted by climate change models, these tall trees may show climate impacts first.\u003c/p>\n\u003cp>But scientists aren't just looking into future. They're also looking at the past.\u003c/p>\n\u003cp>\u003cstrong> \u003c/strong>\u003c/p>\n\u003cp>\u003cstrong>Fog Key to Redwoods\u003c/strong>\u003c/p>\n\u003cp>Todd Dawson, a scientist at UC Berkeley, holds a skinny tool that drills into a redwood tree and pulls out a thin core sample. The core shows the tree's growth rings.\u003c/p>\n\u003cp>\"You can see there's some very large rings here, so it was clear that when this tree was young, it was putting on a lot of growth every single year,\" says Dawson.\u003c/p>\n\u003cp>The rings further from the tree's center - the newer rings - look much smaller, though Dawson isn't sure why. \"They respond to changes in rainfall in a wetter year or a dryer year in how much wood they put on. But not only the rainfall or the temperature is important. For the coastal redwoods, it's also the fog.\"\u003c/p>\n\u003cp>Redwoods get their water from two places: rain and California's notorious coastal fog. Dawson says the trees are giant fog collectors. 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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>After more than a century of logging, California's old-growth redwood forests are only a fraction of what they once were. Today, they \u003ca href=\"http://www.parks.ca.gov/?page_id=24723\">remain in a narrow coastal band\u003c/a> that extends from Monterey Bay to the Oregon border. Most ancient redwoods are protected in parks. But now they are facing a new threat -- climate change.\u003c/p>\n\u003cp>Coast redwoods are among the largest living organisms on the planet. Their trunks can grow to 25 feet in diameter. Much of the tree is hidden from our view.\u003c/p>\n\u003cp>\"From down here, you can tell that they're tall but you can't tell too much about each tree,\" says Steve Sillett, a botany professor at Humboldt State University who has researched these trees for two decades.\u003c/p>\n\u003cp>To really study them, Sillett says, you have to go up.\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>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cem>Listen to the QUEST radio story \u003cstrong>\u003ca href=\"http://www.kqed.org/quest/radio/californias-redwoods-face-climate-change\">California's Redwoods Face Climate Change\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>Climbing a 360-foot redwood isn't for the faint of heart. Today, Sillett and his team are climbing one of the tallest trees in \u003ca href=\"http://www.parks.ca.gov/?page_id=434\">Montgomery Woods State Reserve\u003c/a> in Mendocino County. It's taller than a 35-story building.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>\"We don't use spikes or spurs. We don't injure the tree in any way when we're climbing it.\" Sillett and his research partner, Marie Antoine, clip their climbing harnesses onto long ropes that are fixed high in the tree. They pull themselves up with an ascender -- a metal clamp that slides up the rope and provides traction.\u003c/p>\n\u003cp>Sillett was one of the first scientists to explore the old-growth redwood canopy. Their treetops are home to an entire ecosystem of animals, fern thickets as big as a bus and even other trees that grow among the redwood branches.\u003c/p>\n\u003cp>\"The most freaked out I have ever been was when we found the first salamander up there. And I am 3-hundred feet up in a tree and there is a salamander cruising around,\" says Sillett.\u003c/p>\n\u003cp>\u003cstrong>Climbing Giants\u003c/strong>\u003c/p>\n\u003cp>Today, Sillett and Antoine are measuring the tree in an unprecedented way by doing complete structural inventory.\u003c/p>\n\u003cp>They start by measuring the trunk. Dangling gracefully from ropes, they stretch a tape measure around the tree. \"Let's do our first wrap at 40, so I'll go to 40,\" Sillett yells.\u003c/p>\n\u003cp>They continue down, measuring at different intervals. \"Three twenty-one point seven. So that's over 10 feet diameter,\" says Sillett.\u003c/p>\n\u003cp>They'll also measure every branch. \"We did have one tree that had 472 branches and 206 segments in it, which took about four days.\"\u003c/p>\n\u003cp>Sillett and his team are measuring hundreds of redwoods like this as \u003ca href=\"http://rcci.savetheredwoods.org/science/index.shtml\">part of a $2.5 million dollar study\u003c/a> funded by the \u003ca href=\"http://www.savetheredwoods.org/\">Save the Redwoods League\u003c/a>. With the data, he generates a 3D model of each tree. Once they measure the trees again in three years, the models will tell him how much the redwoods are growing.\u003c/p>\n\u003cp>\"Some years, there's a lot of growth, and some years there's almost no growth. And sometimes there's dieback and recovery,\" says Sillett. \"We suspect that the really tall trees, the tallest trees in the world, are among the most sensitive things to climate change.\"\u003c/p>\n\u003cp>Tall trees, Sillett says, are already under a great deal of stress. Simply lifting water hundreds of feet from the roots to the tree tops is difficult. And with the temperature and precipitation changes predicted by climate change models, these tall trees may show climate impacts first.\u003c/p>\n\u003cp>But scientists aren't just looking into future. They're also looking at the past.\u003c/p>\n\u003cp>\u003cstrong> \u003c/strong>\u003c/p>\n\u003cp>\u003cstrong>Fog Key to Redwoods\u003c/strong>\u003c/p>\n\u003cp>Todd Dawson, a scientist at UC Berkeley, holds a skinny tool that drills into a redwood tree and pulls out a thin core sample. The core shows the tree's growth rings.\u003c/p>\n\u003cp>\"You can see there's some very large rings here, so it was clear that when this tree was young, it was putting on a lot of growth every single year,\" says Dawson.\u003c/p>\n\u003cp>The rings further from the tree's center - the newer rings - look much smaller, though Dawson isn't sure why. \"They respond to changes in rainfall in a wetter year or a dryer year in how much wood they put on. But not only the rainfall or the temperature is important. For the coastal redwoods, it's also the fog.\"\u003c/p>\n\u003cp>Redwoods get their water from two places: rain and California's notorious coastal fog. Dawson says the trees are giant fog collectors. They actually absorb it through their leaves.\u003c/p>\n\u003cp>\"The fog is a very important water subsidy for these trees, and it's been declining over the last 50, 60, 100 years,\" says Dawson.\u003c/p>\n\u003cp>Dawson and others are looking into whether there's a link between a warming climate and \u003ca href=\"http://www.eurekalert.org/pub_releases/2010-02/uoc--fhd021110.php\">the decline in fog\u003c/a>. \"We're quite concerned about what those declines in fog actually mean for the future growth of the redwoods that grow along the coast.\"\u003c/p>\n\u003cp>Here's where the tree rings come in. By analyzing oxygen isotopes in the wood, Dawson can tell how much of the tree's water came from fog vs. rain in any given year. That gives him a forensic record of how the climate has affected the tree's growth. Given that some of these trees are thousands of years old, it's a long record.\u003c/p>\n\u003cp>\"We can then put that into models and predict: what are these trees going to respond to in the future? We may lose redwoods permanently at the drier, warmer ends of their range.\"\u003c/p>\n\u003cp>Dawson says if that happens, what they're learning in this soggy forest will help them protect redwoods. That could mean preserving more forests or even planting trees in new locations that one day may become a better environment for redwood trees.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\u003ciframe width=\"560\" height=\"315\" src=\"https://www.youtube.com/embed/O6KVJCAQOwk\" frameborder=\"0\" allowfullscreen>\u003c/iframe>\u003c/p>\n\n\u003c/div>\u003c/p>",
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"disqusTitle": "UCSF Scientists Bio-Hack Bacteria",
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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/UCSF_SynBio_Merrell_42_22.jpg\" alt=\"\">\u003c/a>\u003cem>UCSF bioengineering graduate student Alvin Tamsir places E.coli bacteria onto a petri dish in the lab. (Credit: Susan Merrell, 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>Researchers at the University of California-San Francisco have hacked into the genetic wiring of billions of individual bacteria and outfitted them with the kind of on/off switches normally found in computer chips, not living organisms.\u003c/p>\n\u003cp>The switches, which are built out of genes, allow the bacteria to listen for chemical signals and respond, much like computer chips that can perform powerful tasks.\u003c/p>\n\u003cp>The switches may one day help the development of biofuels that are cheaper and more powerful than gasoline, or a new suite of pharmaceuticals that could more effectively target and kill tumor cells with fewer side effects.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>\u003c!--more-->\u003c/p>\n\u003cp>“Scientists have been trying to engineer bacteria to be more programmable, to do various things, but biology is hard to program” said Alvin Tamsir a doctoral student at UCSF. “I want to generate the technology so that bacteria can be more programmable in a more predictable way.”\u003c/p>\n\u003cp>Tasmir was the lead author of a study on the subject that was published last week in the journal, \u003cem>\u003ca href=\"http://www.nature.com/nature/journal/vaop/ncurrent/full/nature09565.html\">Nature\u003c/a>\u003c/em>.\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/39/2010/12/UCSF_SynBio_Merrell_12_21.jpg\" alt=\"\">\u003c/a>\u003cem>UCSF bioengineering graduate student Alvin Tamsir. (Credit: Susan Merrell, UCSF)\u003c/em>\u003c/span>\u003c/p>\n\u003cp>By building new molecular circuits into bacteria, Tamsir and his team can now make the bacteria perform specific tasks, much like the millions of wires which comprise the electrical circuitry of a modern computer chip enable the dizzying array of complex calculations and tasks a computer can do in micro-seconds.\u003c/p>\n\u003cp>It’s all part of the new field of synthetic biology, where principles from computer science, electrical engineering and genetics, along with other sciences, mix together to reveal the tools and strategies for reprogramming the cellular machinery of living organisms like bacteria and yeast. Scientists and companies in the Bay Area and elsewhere, working on other synthetic biology project, already are developing a new generation of drugs and biofuels with bionic bacteria and yeast.\u003c/p>\n\u003cp>“Some of these drugs that we are working on right now require 40 genes. And you have to control when those genes turn on and for how long and in what order, and for all that, you need a circuit,” said \u003ca href=\"http://www.voigtlab.ucsf.edu/\">Christopher Voigt\u003c/a>, an associate professor at UCSF’s Department of Pharmaceutical Chemistry and the senior author of the study.\u003c/p>\n\u003cp>Tamsir and Voigt looked to the world of electrical engineering, where circuits bring the necessary level of control to millions of precisely timed calculations that a computer chip must complete to execute any task, like spellchecking a document or surfing the web.\u003c/p>\n\u003cp>To do these tasks, microscopic switches called “logic gates” are etched into the silicon of computer chips. The logic gates function according to a set of rules and are connected with wires that make up a circuit on the chip. Each of these logic gates receives an input, such as an electrical current, from the wires, and responds based on the kind of gate it is. For example, if it’s an “AND” gate, it will turn on and send its output of an electrical signal to the gate next to it, but only if it is getting inputs from the two wires that feed into it. If it’s an “OR” gate, it will turn on even if it is getting a signal from just one of the wires connected to it.\u003c/p>\n\u003cp>“In computers, complex tasks like opening a document or performing a calculation can be boiled down to simpler calculations performed by these logic gates,” said Tamsir. A modern Pentium chip can have more than a million logic gates, each one performing a tiny piece of the calculation or task at hand.\u003c/p>\n\u003cp>“But you don't have an engineer at Intel that is choosing exactly where each wire goes,” said Voigt. Instead, programming languages have automated the process, quickly and reliably reproducing on the computer chip the precise circuits of logic gates needed to carry out functions specified by a computer engineer.\u003c/p>\n\u003cp>“We are trying to create a programming language for cells,” Voigt added, “and ultimately have it so you can take any function you can imagine and convert that into a DNA sequence that carries out that function.”\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/39/2010/12/UCSF_SynBio_Merrell_84_21.jpg\" alt=\"\">\u003c/a>\u003cem>Four colonies of E. coli bacteria cells plated onto a petri dish. Each colony contains a billion cells. (Credit: Susan Merrell, UCSF)\u003c/em>\u003c/span>\u003c/p>\n\u003cp>But scientists can’t exactly take the hardware of tiny gates and wires on computer chips and insert them into living bacteria like E. coli. So Tamsir and his team had to engineer genes that would reprogram the DNA of E. coli, instructing it to make logic gates out of proteins that would help the bacteria perform more like a computer to carry out a specific task – in this case, to make a fluorescent yellow protein.\u003c/p>\n\u003cp>In computer chips, the metal wires that feed into a logic gate are physically separated so that the inputs going into one logic gate don’t cross with the wires of a nearby logic gate. But this isn’t the case with living bacteria. “Every gate is a molecule and they're all being run based on molecules and they're all crammed together in the bag that is the cell,” Voigt said.\u003c/p>\n\u003cp>Although the scientists created eight different colonies of bacteria, each with their own discrete logic gate, only four colonies were used at a time to see if they could link up to form a circuit that would yield the fluorescent protein.\u003c/p>\n\u003cp>One logic gate in one of the bacteria colonies may need two inputs, like a sugar and an antibiotic, to release its molecular output, such as an enzyme, that would then act as an input for a second set of logic gates. But this next set of logic gates may have been designed so that it produces its own molecular output only if it doesn’t receive the sugar and antibiotic inputs that triggered the activity of the first logic gate.\u003c/p>\n\u003cp>“It’s by combining multiple gates together that you get different behavior. And that's how electrical circuits behave - they use a lot of logic gates and combine them in various ways to get various functions,” said Tamsir. Similarly, the scientists were able to modify the behavior of their bacterial circuits by simply moving the location of the bacteria colonies in the petri dish, since each colony operated with its own set of logical rules for responding to the chemical inputs feeding into it.\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/39/2010/12/UCSF_SynBio_Tamsir_3a_21.jpg\" alt=\"\">\u003c/a>\u003cem> An illustrated wiring diagram showing two different kinds of logic gates (NOR and Buffer) operating in four bacteria colonies on a petri dish. The last bacteria colony, indicated in brown, completes the circuit to make fluorescent yellow protein. (Credit: Alvin Tamsir, UCSF)\u003c/em>\u003c/span>\u003c/p>\n\u003cp>Tamsir built 16 different kinds of genetic logic gates to program the bacterial 'computers'. Each one successfully suppressed or promoted the production of the fluorescent yellow protein depending on how it was linked together in the bacteria.\u003c/p>\n\u003cp>“The hard part,” said Tamsir, who has worked for more than two years on this research, “was combining different genetic parts so that when they are put together, they function as you want them to.”\u003c/p>\n\u003cp>Other researchers are taking note.\u003c/p>\n\u003cp>“They have begun the process of creating a characterized library of elements which can be used by other labs to build more complex systems,” said \u003ca href=\"http://www.bu.edu/ece/people/faculty/a-g/douglas-densmore/\">Douglas Densmore\u003c/a>, an assistant professor of computer and electrical engineering at Boston University who read the \u003cem>Nature \u003c/em>paper describing the UCSF team’s research.\u003c/p>\n\u003cp>Tamsir and his team now want to increase the complexity of their bacterial circuits by building even more sophisticated logic gates.\u003c/p>\n\u003cp>Voigt added that there are roughly 200 to 300 circuits that regulate different biological activities in E. coli bacteria.\u003c/p>\n\u003cp>“And that’s the good news – that it’s not millions,” he said. Unlike a computer chip, “the bacteria don’t require a lot of gates and if we had 100 gates, we could do some pretty amazing things,” Voigt said.\u003c/p>\n\u003cp>By designing more complex gates and more of them, he said a scientist could be “in full control of programming bacteria.” This arsenal of expanded logic gates could then coax the bacteria to produce more than just a biofuel or a low-cost malaria drug, like the one developed using synthetic biology by \u003ca href=\"http://www.amyrisbiotech.com/\">Amyris Biotechnologies\u003c/a> in Emeryville.\u003c/p>\n\u003cp>“Everything you see in biology -- such as a corn plant growing -- those complex processes are being implemented by natural circuitry,” said Voigt. “And one of the reasons that we can't access those functions is because we don't have that refined level of control.”\u003c/p>\n\u003cp>With the new system of logic gates snapping together to form synthetic circuits, the UCSF scientists have expanded that level of control and consequently, what bacteria or yeast could be programmed to do, like some day make synthetic wood, silk or antibiotics.\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/39/2010/12/UCSF_SynBio_Merrell_55_21.jpg\" alt=\"\">\u003c/a>\u003cem>UCSF bioengineering graduate student Alvin Tamsir handles test tubes containing E. coli bacteria. (Credit: Susan Merrell, UCSF)\u003c/em>\u003c/span>\u003c/p>\n\u003cp>\u003ca href=\"http://www.lifetechnologies.com/home.html\">Life Technologies\u003c/a>, a biotech firm based in Carlsbad, has partnered with Voigt’s lab to generate a software package that would allow other scientists to specify the kind of logic gates they want to run in the bacteria being used in their experiments. After a few keystrokes and some processing by the computer, the scientists would receive a recipe for making those logic gates, which could then be sequenced from the sugars and phosphates which make up genes, and inserted into their bacteria.\u003c/p>\n\u003cp>For Tamsir, the research is incredibly challenging but also extremely rewarding, a vital part of his doctorate degree in bioengineering which he hopes to complete in May. The 26 year-old scientist grew up tinkering with circuit boards and even derived programming inspiration from Lego Mindstorms, a line of robotic toys.\u003c/p>\n\u003cp>“I found out about the field of synthetic biology through Chris Voigt's lab. Right then, I knew that this was the right field of study for me,” he said. “It combines my love for computer programming with my love for biology.”\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp>37.767050 -122.391139\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>\u003c!--more-->\u003c/p>\n\u003cp>“Scientists have been trying to engineer bacteria to be more programmable, to do various things, but biology is hard to program” said Alvin Tamsir a doctoral student at UCSF. “I want to generate the technology so that bacteria can be more programmable in a more predictable way.”\u003c/p>\n\u003cp>Tasmir was the lead author of a study on the subject that was published last week in the journal, \u003cem>\u003ca href=\"http://www.nature.com/nature/journal/vaop/ncurrent/full/nature09565.html\">Nature\u003c/a>\u003c/em>.\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/39/2010/12/UCSF_SynBio_Merrell_12_21.jpg\" alt=\"\">\u003c/a>\u003cem>UCSF bioengineering graduate student Alvin Tamsir. (Credit: Susan Merrell, UCSF)\u003c/em>\u003c/span>\u003c/p>\n\u003cp>By building new molecular circuits into bacteria, Tamsir and his team can now make the bacteria perform specific tasks, much like the millions of wires which comprise the electrical circuitry of a modern computer chip enable the dizzying array of complex calculations and tasks a computer can do in micro-seconds.\u003c/p>\n\u003cp>It’s all part of the new field of synthetic biology, where principles from computer science, electrical engineering and genetics, along with other sciences, mix together to reveal the tools and strategies for reprogramming the cellular machinery of living organisms like bacteria and yeast. Scientists and companies in the Bay Area and elsewhere, working on other synthetic biology project, already are developing a new generation of drugs and biofuels with bionic bacteria and yeast.\u003c/p>\n\u003cp>“Some of these drugs that we are working on right now require 40 genes. And you have to control when those genes turn on and for how long and in what order, and for all that, you need a circuit,” said \u003ca href=\"http://www.voigtlab.ucsf.edu/\">Christopher Voigt\u003c/a>, an associate professor at UCSF’s Department of Pharmaceutical Chemistry and the senior author of the study.\u003c/p>\n\u003cp>Tamsir and Voigt looked to the world of electrical engineering, where circuits bring the necessary level of control to millions of precisely timed calculations that a computer chip must complete to execute any task, like spellchecking a document or surfing the web.\u003c/p>\n\u003cp>To do these tasks, microscopic switches called “logic gates” are etched into the silicon of computer chips. The logic gates function according to a set of rules and are connected with wires that make up a circuit on the chip. Each of these logic gates receives an input, such as an electrical current, from the wires, and responds based on the kind of gate it is. For example, if it’s an “AND” gate, it will turn on and send its output of an electrical signal to the gate next to it, but only if it is getting inputs from the two wires that feed into it. If it’s an “OR” gate, it will turn on even if it is getting a signal from just one of the wires connected to it.\u003c/p>\n\u003cp>“In computers, complex tasks like opening a document or performing a calculation can be boiled down to simpler calculations performed by these logic gates,” said Tamsir. A modern Pentium chip can have more than a million logic gates, each one performing a tiny piece of the calculation or task at hand.\u003c/p>\n\u003cp>“But you don't have an engineer at Intel that is choosing exactly where each wire goes,” said Voigt. Instead, programming languages have automated the process, quickly and reliably reproducing on the computer chip the precise circuits of logic gates needed to carry out functions specified by a computer engineer.\u003c/p>\n\u003cp>“We are trying to create a programming language for cells,” Voigt added, “and ultimately have it so you can take any function you can imagine and convert that into a DNA sequence that carries out that function.”\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/39/2010/12/UCSF_SynBio_Merrell_84_21.jpg\" alt=\"\">\u003c/a>\u003cem>Four colonies of E. coli bacteria cells plated onto a petri dish. Each colony contains a billion cells. (Credit: Susan Merrell, UCSF)\u003c/em>\u003c/span>\u003c/p>\n\u003cp>But scientists can’t exactly take the hardware of tiny gates and wires on computer chips and insert them into living bacteria like E. coli. So Tamsir and his team had to engineer genes that would reprogram the DNA of E. coli, instructing it to make logic gates out of proteins that would help the bacteria perform more like a computer to carry out a specific task – in this case, to make a fluorescent yellow protein.\u003c/p>\n\u003cp>In computer chips, the metal wires that feed into a logic gate are physically separated so that the inputs going into one logic gate don’t cross with the wires of a nearby logic gate. But this isn’t the case with living bacteria. “Every gate is a molecule and they're all being run based on molecules and they're all crammed together in the bag that is the cell,” Voigt said.\u003c/p>\n\u003cp>Although the scientists created eight different colonies of bacteria, each with their own discrete logic gate, only four colonies were used at a time to see if they could link up to form a circuit that would yield the fluorescent protein.\u003c/p>\n\u003cp>One logic gate in one of the bacteria colonies may need two inputs, like a sugar and an antibiotic, to release its molecular output, such as an enzyme, that would then act as an input for a second set of logic gates. But this next set of logic gates may have been designed so that it produces its own molecular output only if it doesn’t receive the sugar and antibiotic inputs that triggered the activity of the first logic gate.\u003c/p>\n\u003cp>“It’s by combining multiple gates together that you get different behavior. And that's how electrical circuits behave - they use a lot of logic gates and combine them in various ways to get various functions,” said Tamsir. Similarly, the scientists were able to modify the behavior of their bacterial circuits by simply moving the location of the bacteria colonies in the petri dish, since each colony operated with its own set of logical rules for responding to the chemical inputs feeding into it.\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/39/2010/12/UCSF_SynBio_Tamsir_3a_21.jpg\" alt=\"\">\u003c/a>\u003cem> An illustrated wiring diagram showing two different kinds of logic gates (NOR and Buffer) operating in four bacteria colonies on a petri dish. The last bacteria colony, indicated in brown, completes the circuit to make fluorescent yellow protein. (Credit: Alvin Tamsir, UCSF)\u003c/em>\u003c/span>\u003c/p>\n\u003cp>Tamsir built 16 different kinds of genetic logic gates to program the bacterial 'computers'. Each one successfully suppressed or promoted the production of the fluorescent yellow protein depending on how it was linked together in the bacteria.\u003c/p>\n\u003cp>“The hard part,” said Tamsir, who has worked for more than two years on this research, “was combining different genetic parts so that when they are put together, they function as you want them to.”\u003c/p>\n\u003cp>Other researchers are taking note.\u003c/p>\n\u003cp>“They have begun the process of creating a characterized library of elements which can be used by other labs to build more complex systems,” said \u003ca href=\"http://www.bu.edu/ece/people/faculty/a-g/douglas-densmore/\">Douglas Densmore\u003c/a>, an assistant professor of computer and electrical engineering at Boston University who read the \u003cem>Nature \u003c/em>paper describing the UCSF team’s research.\u003c/p>\n\u003cp>Tamsir and his team now want to increase the complexity of their bacterial circuits by building even more sophisticated logic gates.\u003c/p>\n\u003cp>Voigt added that there are roughly 200 to 300 circuits that regulate different biological activities in E. coli bacteria.\u003c/p>\n\u003cp>“And that’s the good news – that it’s not millions,” he said. Unlike a computer chip, “the bacteria don’t require a lot of gates and if we had 100 gates, we could do some pretty amazing things,” Voigt said.\u003c/p>\n\u003cp>By designing more complex gates and more of them, he said a scientist could be “in full control of programming bacteria.” This arsenal of expanded logic gates could then coax the bacteria to produce more than just a biofuel or a low-cost malaria drug, like the one developed using synthetic biology by \u003ca href=\"http://www.amyrisbiotech.com/\">Amyris Biotechnologies\u003c/a> in Emeryville.\u003c/p>\n\u003cp>“Everything you see in biology -- such as a corn plant growing -- those complex processes are being implemented by natural circuitry,” said Voigt. “And one of the reasons that we can't access those functions is because we don't have that refined level of control.”\u003c/p>\n\u003cp>With the new system of logic gates snapping together to form synthetic circuits, the UCSF scientists have expanded that level of control and consequently, what bacteria or yeast could be programmed to do, like some day make synthetic wood, silk or antibiotics.\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/39/2010/12/UCSF_SynBio_Merrell_55_21.jpg\" alt=\"\">\u003c/a>\u003cem>UCSF bioengineering graduate student Alvin Tamsir handles test tubes containing E. coli bacteria. (Credit: Susan Merrell, UCSF)\u003c/em>\u003c/span>\u003c/p>\n\u003cp>\u003ca href=\"http://www.lifetechnologies.com/home.html\">Life Technologies\u003c/a>, a biotech firm based in Carlsbad, has partnered with Voigt’s lab to generate a software package that would allow other scientists to specify the kind of logic gates they want to run in the bacteria being used in their experiments. After a few keystrokes and some processing by the computer, the scientists would receive a recipe for making those logic gates, which could then be sequenced from the sugars and phosphates which make up genes, and inserted into their bacteria.\u003c/p>\n\u003cp>For Tamsir, the research is incredibly challenging but also extremely rewarding, a vital part of his doctorate degree in bioengineering which he hopes to complete in May. The 26 year-old scientist grew up tinkering with circuit boards and even derived programming inspiration from Lego Mindstorms, a line of robotic toys.\u003c/p>\n\u003cp>“I found out about the field of synthetic biology through Chris Voigt's lab. Right then, I knew that this was the right field of study for me,” he said. “It combines my love for computer programming with my love for biology.”\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cp>\u003cspan class=\"left\">\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2010/12/512px-Teepause1.jpg\">\u003cem>The Water Processing Method.\u003c/em>\u003c/span>\u003c/p>\n\u003cp>There are some traditions I have around writing. First off, in my apartment I have my write or do nothing chair. The only two things I am allowed to do in it are write or do nothing. It is where I am sitting right now as I am type this. The second tradition is classical musical in the background; this is especially helpful for long bouts of writing requiring more focus. The third is a pot of tea. The third tradition is problematic late at night, as then I don’t sleep due to the caffeine. Which made me ponder an alternative and how it is derived – how is tea decaffeinated?\u003c/p>\n\u003cp>\u003c!--more-->\u003c/p>\n\u003cp>Real tea comes from the leaves from the \u003ca href=\"http://www.learn-about-tea.com/camellia-sinensis.html\">Camellia sinesis or Camellia assamica plant \u003c/a>. These leaves naturally contain caffeine in varying amounts. Black teas are the most strongly caffeinated while white teas contain the least amount of caffeine. At night, one could drink herbal tea but these are not actually genuine teas. They are just herbal tinctures derived from other plants. \u003c/p>\n\u003cp>One could enjoy an actual cup of decaffeinated tea by pouring out the first cup and re-steeping. This works best with loose-leaf tea; about 80% of the caffeine in tea is released in the first thirty seconds of steeping. Pouring out the first batch steeped and then adding more hot water will get rid of the majority of caffeine while maintaining the flavor of the tea. \u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>This is the water method of decaffeination. There are \u003ca href=\"http://recipes.howstuffworks.com/question480.htm\">three other methods\u003c/a> used for decaffeination:\u003c/p>\n\u003cp>Methylene chloride processing – in this process Methylene chloride is used as a solvent. Molecules of caffeine bond to the molecules of Methylene chloride. This processing can be done directly in a bath of Methylene chloride or indirectly by extracting the caffeine in a water bath. \u003c/p>\n\u003cp>Ethyl acetate processing – Ethyl acetate is a naturally occurring chemical in most fruits. Caffeine molecules bond to Ethyl acetate and caffeine can be removed either directly or indirectly using Ethyl acetate as the solvent. Products coined as “Naturally decaffeinated” are usually decaffeinated using this method. \u003c/p>\n\u003cp>Carbon dioxide processing – In this process, water softened materials are “pressure cooked” with the gas. At high pressures, CO2 sublimates and acts as both a gas and a liquid. As a solvent, the non-polar molecules will attract the smaller caffeine molecules. Since the flavor molecules are larger they remain intact. This process retains the flavor of the tea better than the other two solvent methods. \u003c/p>\n\u003cp>In all these methods some caffeine will remain but it drastically reduced. Federal regulations in the US mandate that labeled decaffeinated products must not contain more the 2.5% caffeine. So what happens to all the caffeine that is taken out in processing? It is put into other products. Soft drinks are primarily caffeinated from the caffeine taken out from decaffeination. So that soft drink might include the caffeine from tea leaves or coffee beans. So by choosing decaffeinated tea tonight, that caffeine was repurposed in another caffeine beverage! \u003c/p>\n\u003cp>\u003c/p>\n\u003cp> 37.7699 -122.467174\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>This is the water method of decaffeination. There are \u003ca href=\"http://recipes.howstuffworks.com/question480.htm\">three other methods\u003c/a> used for decaffeination:\u003c/p>\n\u003cp>Methylene chloride processing – in this process Methylene chloride is used as a solvent. Molecules of caffeine bond to the molecules of Methylene chloride. This processing can be done directly in a bath of Methylene chloride or indirectly by extracting the caffeine in a water bath. \u003c/p>\n\u003cp>Ethyl acetate processing – Ethyl acetate is a naturally occurring chemical in most fruits. Caffeine molecules bond to Ethyl acetate and caffeine can be removed either directly or indirectly using Ethyl acetate as the solvent. Products coined as “Naturally decaffeinated” are usually decaffeinated using this method. \u003c/p>\n\u003cp>Carbon dioxide processing – In this process, water softened materials are “pressure cooked” with the gas. At high pressures, CO2 sublimates and acts as both a gas and a liquid. As a solvent, the non-polar molecules will attract the smaller caffeine molecules. Since the flavor molecules are larger they remain intact. This process retains the flavor of the tea better than the other two solvent methods. \u003c/p>\n\u003cp>In all these methods some caffeine will remain but it drastically reduced. Federal regulations in the US mandate that labeled decaffeinated products must not contain more the 2.5% caffeine. So what happens to all the caffeine that is taken out in processing? It is put into other products. Soft drinks are primarily caffeinated from the caffeine taken out from decaffeination. So that soft drink might include the caffeine from tea leaves or coffee beans. So by choosing decaffeinated tea tonight, that caffeine was repurposed in another caffeine beverage! \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/39/2010/12/MonoLake2.21.jpg\" alt=\"\">\u003cem>Mono Lake, the source of the bacteria that can incorporate arsenic, rather than the usual phosphorus, into its DNA.\u003c/em>\u003c/span>The world is buzzing about the bacteria from \u003ca href=\"http://www.monolake.org/about/\">Mono Lake\u003c/a>. Astrobiologists from NASA discovered in the lab that this strain of bacteria, called GFAJ-1, can incorporate the element arsenic, instead of phosphorus, into the backbone of its DNA. Before \u003ca href=\"http://ww2.kqed.org/quest/2010/12/02/arsenic-bacteria/\">this discovery\u003c/a>, we thought all organisms needed phosphorus to live. Now, as QUEST blogger Ben Burress points out, \u003ca href=\"http://ww2.kqed.org/quest/2010/12/03/arsenic-and-old-lakes-nasa-finds-life-not-as-we-know-it/#respond\">life is no longer quite as we know it\u003c/a>—and this changes the way we think about the search for life on other planets. But before we go to Mars, let’s explore a very otherworldly place on earth—the place where the bacteria GFAJ-1 and its arsenic came from, Mono Lake.\u003c!--more-->\u003c/p>\n\u003cp>Mono Lake is on the east side of the Sierra Nevada Mountains, about 300 miles by car from San Francisco. It is an amazing landscape; the lake is set against the backdrop of the snow-capped mountains. There are crispy shrubs nearby, but no trees. Crusty white towers, called tufas, rise up from the water.\u003c/p>\n\u003cp>The water in the lake is snowmelt and rainwater runoff from the mountains. It enters the lake via streams. But the lake is a closed basin and has no drainage—water can only leave by evaporation. The water evaporates, but the salts and minerals, like arsenic, are left behind. As a result, the lake is very salty—twice as salty as the ocean—and is very alkaline, or basic.\u003c/p>\n\u003cp>That super-salty water may not seem very hospitable, but in fact the lake is full of life. In addition to the now-famous bacteria, the lake is home to \u003ca href=\"http://en.wikipedia.org/wiki/Brine_shrimp\">brine shrimp\u003c/a> and the larvae of alkaline flies. During the summer, the brine shrimp number in the trillions. They feed on algae that grow green at the lake’s surface. The brine shrimp are food for the two million migratory birds that stop at Mono Lake to feed each year, and the nesting populations of California Gulls and Snowy Plovers.\u003c/p>\n\u003cp>In addition to its cool geology and important role in North American bird ecology, Mono Lake is at the center of a water supply saga. Water levels in the lake were historically much higher. To get an idea of previous water levels, take a look at the tufas. They were formed while underwater. They’re made of calcium carbonate, which precipitated as fresh water bubbled up from the bottom of the lake. Thousands of years ago, the lake was as much as 900 feet deep, perhaps covering parts of Utah and Nevada. In recent history, the lake was about 170 feet deep.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>Beginning in the late 1800s, the freshwater streams that fed the lake were diverted by settlers so they could irrigate their farms. The water level started dropping. In 1941, four of the five streams that flowed into Mono Lake were diverted to the Los Angeles Aqueduct. Supplying the growing city of Los Angeles with water involved intrigue and duplicity and scandal, which were well documented in the book \u003ca href=\"http://www.amazon.com/Cadillac-Desert-American-Disappearing-Revised/dp/0140178244\">Cadillac Desert\u003c/a>. Between 1941 and 1982, because of the reduced freshwater input, the water level in Mono Lake dropped by 45 feet.\u003c/p>\n\u003cp>The drop in water level was bad for the migratory and resident birds, particularly the California Gulls, which nested on islands in the lake. As water evaporated, some islands become connected to the shore. The birds were no longer protected from roaming coyotes. And, more exposed shoreline meant that the wind kicked up alkaline dust storms. In addition the lake got saltier—at one point it was nearly three times as salty as the ocean.\u003c/p>\n\u003cp>In response to these changes, the \u003ca href=\"http://www.monolake.org/mlc/\">Mono Lake Committee\u003c/a>, the National Audubon Society, and other conservation groups have begun to \u003ca href=\"http://www.monolake.org/mlc/restoration\">restore\u003c/a> Mono Lake. It is now mandated that more water flow into the lake, and the water level has started to rise. The habitats and ecological processes of the lake are recovering. Additional discoveries, like the bacteria that can use arsenic to make its DNA, will hopefully rise out of Mono Lake in the future.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>37.977925 -119.131172\u003c/p>\n\n",
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"content": "\u003cp>\u003cspan class=\"left\">\u003ca href=\"http://www.kqed.org/quest\">\u003c/a>\u003cem>Collecting normal and albino redwood samples to compare.\u003c/em>\u003c/span>\u003c/p>\n\u003cp>In my last \u003ca href=\"http://www.kqed.org/quest/blog/2010/11/22/ghostbusters/\">blog \u003c/a>I talked about a new project just beginning at Stanford to figure out why some redwoods have white leaves instead of green. Stanford scientists are going to find the mutation that causes the albinism by comparing the DNA of albino and normal redwood clones. Not quite a needle in a haystack since most of the DNA between the two clones will be the same, but no walk in the park either. \u003c/p>\n\u003cp>\u003c!--more-->\u003c/p>\n\u003cp>Up until now I have been talking about a single mutation. This probably isn’t right. Most likely there will be more than one way to make an albino redwood. Just as there is \u003ca href=\"http://www.albinism.org/publications/what_is_albinism.html\">more than one way\u003c/a> to make a person with albinism. \u003c/p>\n\u003cp>There are lots of ways to make an albino because there are lots of genes involved in making a plant green. Knocking out any one of many of these genes will turn a plant white.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>These genes have the instructions for making the green pigment chlorophyll, for making all the parts needed to turn sunlight into sugar (aka photosynthesis), and for making chloroplasts. Chloroplasts are the part of a plant cell where chlorophyll lives and where photosynthesis happens. And they may actually make solving this little puzzle a little simpler.\u003c/p>\n\u003cp>Chloroplasts, like \u003ca href=\"http://www.kqed.org/quest/blog/2008/12/22/those-marvelous-mitochondria/\">mitochondria\u003c/a>, have their own DNA. Not a lot, but they do have something like \u003ca href=\"http://chloroplast.cbio.psu.edu/\">100 or so genes\u003c/a> (the exact number depends on the plant). This DNA is a remnant of plants’ evolutionary past. \u003c/p>\n\u003cp>A billion or two years ago, some ancestor to the modern plant engulfed a cyanobacterium. After many years, this cyanobacterium became a chloroplast.\u003c/p>\n\u003cp>In this process, most of the cyanobacterium’s genes migrated to the nucleus. But a few stayed behind. If the albino redwood has chloroplasts (even just sad little precursors called proplastids) and the reason for the albinism is a mutation in one of the chloroplast genes, then we might find our answer sooner rather than later.\u003c/p>\n\u003cp>This is true for a couple of reasons. First, there can be up to fifty copies of chloroplast genes in a plant cell. And second, the chloroplast genome is tiny. Both of these reasons mean scientists will need to do a lot less sequencing to read the chloroplast genome.\u003c/p>\n\u003cp>Of course, the mutation may not be in the chloroplast. But if not, then hopefully it will be in one of the known genes involved in making chlorophyll and/or chloroplasts. If so, then we still may get our answer sooner since we’ll be able to scan the DNA for these genes and look for differences.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>I’ll keep you updated as progress gets made. It is so cool to have the tools needed to solve a mystery like this. This is why I love science and why you should too. The chance to figure something out that no one else has.\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>\u003cspan class=\"left\">\u003ca href=\"http://www.kqed.org/quest\">\u003c/a>\u003cem>Collecting normal and albino redwood samples to compare.\u003c/em>\u003c/span>\u003c/p>\n\u003cp>In my last \u003ca href=\"http://www.kqed.org/quest/blog/2010/11/22/ghostbusters/\">blog \u003c/a>I talked about a new project just beginning at Stanford to figure out why some redwoods have white leaves instead of green. Stanford scientists are going to find the mutation that causes the albinism by comparing the DNA of albino and normal redwood clones. Not quite a needle in a haystack since most of the DNA between the two clones will be the same, but no walk in the park either. \u003c/p>\n\u003cp>\u003c!--more-->\u003c/p>\n\u003cp>Up until now I have been talking about a single mutation. This probably isn’t right. Most likely there will be more than one way to make an albino redwood. Just as there is \u003ca href=\"http://www.albinism.org/publications/what_is_albinism.html\">more than one way\u003c/a> to make a person with albinism. \u003c/p>\n\u003cp>There are lots of ways to make an albino because there are lots of genes involved in making a plant green. Knocking out any one of many of these genes will turn a plant white.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>These genes have the instructions for making the green pigment chlorophyll, for making all the parts needed to turn sunlight into sugar (aka photosynthesis), and for making chloroplasts. Chloroplasts are the part of a plant cell where chlorophyll lives and where photosynthesis happens. And they may actually make solving this little puzzle a little simpler.\u003c/p>\n\u003cp>Chloroplasts, like \u003ca href=\"http://www.kqed.org/quest/blog/2008/12/22/those-marvelous-mitochondria/\">mitochondria\u003c/a>, have their own DNA. Not a lot, but they do have something like \u003ca href=\"http://chloroplast.cbio.psu.edu/\">100 or so genes\u003c/a> (the exact number depends on the plant). This DNA is a remnant of plants’ evolutionary past. \u003c/p>\n\u003cp>A billion or two years ago, some ancestor to the modern plant engulfed a cyanobacterium. After many years, this cyanobacterium became a chloroplast.\u003c/p>\n\u003cp>In this process, most of the cyanobacterium’s genes migrated to the nucleus. But a few stayed behind. If the albino redwood has chloroplasts (even just sad little precursors called proplastids) and the reason for the albinism is a mutation in one of the chloroplast genes, then we might find our answer sooner rather than later.\u003c/p>\n\u003cp>This is true for a couple of reasons. First, there can be up to fifty copies of chloroplast genes in a plant cell. And second, the chloroplast genome is tiny. Both of these reasons mean scientists will need to do a lot less sequencing to read the chloroplast genome.\u003c/p>\n\u003cp>Of course, the mutation may not be in the chloroplast. But if not, then hopefully it will be in one of the known genes involved in making chlorophyll and/or chloroplasts. If so, then we still may get our answer sooner since we’ll be able to scan the DNA for these genes and look for differences.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>I’ll keep you updated as progress gets made. It is so cool to have the tools needed to solve a mystery like this. This is why I love science and why you should too. The chance to figure something out that no one else has.\u003c/p>\n\n\u003c/div>\u003c/p>",
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"disqusTitle": "Arsenic-Eating Bacteria Expands Definition of Life",
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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/AAAS-Science_wolfesimon1HR-22.jpg\" alt=\"\">\u003c/a>\u003cem> Scanning electron microscope image of the arsenic-loving bacteria GFAJ-1. (Credit: AAAS/Science) \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>A Bay Area biochemist has found a new strain of bacteria living in the briny shores of Mono Lake that can eat and thrive on arsenic, a substance highly toxic to most organisms. The discovery may lead to a significant shift in how scientists search for extraterrestrial life. \u003c/p>\n\u003cp>“All life that we know of requires carbon, hydrogen, oxygen, nitrogen, sulfur and phosphorus,” said Felisa Wolfe-Simon, the lead author of the study and a NASA Astrobiology Research Fellow in residence at the U.S. Geological Survey in Menlo Park. “We discovered an organism that can substitute one element for another,” she added. \u003c/p>\n\u003cp>Those six major elements comprise the building blocks of key components of living cells, such as DNA, RNA and proteins – the molecular switches which power the cells and instruct them to perform tasks critical for cellular growth and survival. Researchers know of no other microbe that can consume arsenic let alone substitute it for phosphorus, thereby expanding the definition of what constitutes life on Earth and elsewhere in the universe. \u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>\u003c!--more-->\u003c/p>\n\u003cp>“As someone who regularly gives lectures in which I state, ‘every living thing uses phosphorus to build its DNA’, the idea that I’m sitting here today discussing the possibility that that’s not true is quite shocking,” said James Elser, a professor at Arizona State University who participated in a NASA teleconference convened today to discuss the findings. \u003c/p>\n\u003cp>The discovery of the arsenic-loving microbe also “opens new doors” to explore what life may look like in other reaches of the solar system, on environments such as Mars or the moons of Jupiter and Saturn that have previously been thought to be too cold and harsh to support life. \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/39/2010/12/AAAS-Science_wolfesimon4HR-21.jpg\" alt=\"\">\u003c/a>\u003cem>Felicia Wolfe-Simon of the NASA Ames Research Center and USGS collects samples from a sediment core extracted from the shores of Mono Lake in eastern California. (Credit: Henry Bortman)\u003c/em>\u003c/span>\u003c/p>\n\u003cp>“We still don’t know everything there is to know about what might make a habitable environment on another planet or a satellite of another planet,” said Pamela Conrad, an astrobiologist at NASA’s Goddard Space Flight Center in Greenbelt, Maryland. “Perhaps arsenic is not an essential component for habitability or life but it may be one that can be tolerated and it opens our perspective to try and understand what other potential components may be tolerated or perhaps even essential that we presently haven’t thought of,” she added. \u003c/p>\n\u003cp>A paper describing the finding appears in this week’s edition of the journal \u003cem>\u003ca href=\"http://www.sciencemag.org/content/early/2010/12/01/science.1197258\">Science Express\u003c/a>\u003c/em>. \u003c/p>\n\u003cp>But before the embargo on the paper was lifted on Thursday, a flurry of speculation was set off earlier in the week that NASA had discovered proof of alien life, fueled by an ambiguous press release issued by NASA on Monday which trumpeted “an astrobiology finding that will impact the search for evidence of extraterrestrial life.” In fact, the embargo was lifted roughly two hours earlier than planned because reports of the finding, some of them erroneous, were already beginning to appear online in publications like \u003cem>The Huffington Post\u003c/em> and the \u003cem>Guardian\u003c/em>. \u003c/p>\n\u003cp>At the end of NASA’s Thursday teleconference, Mary Voytek, director of the Astrobiology Program at NASA headquarters in Washington, D.C. responded to a question from a \u003cem>USA Today\u003c/em> journalist about the disappointment felt by its readers that in fact, NASA would not be pulling E.T out of a hat. \u003c/p>\n\u003cp>“I guess what I would say is that while being able to announce the discovery of an extra-terrestrial would be an incredible announcement, from our perspective, this is a phenomenal finding. It will require some paragraphs in textbooks to be rewritten,” said Voytek. “It will fundamentally change how we define life and how we look for it, maybe we’ll be able to find E.T. now because we’ve got more information about what we might be looking for,” she added.\u003c/p>\n\u003cp>The research team, led by Wolfe-Simon, discovered the new strain of bacteria, GFAJ-1, in muddy sediment cores extracted from the shores of Mono Lake, located in eastern California, near the Sierra Nevada mountains. The 70 square-mile inland lake is highly salty and alkaline with high concentrations of naturally-occurring arsenic. It has been separated from freshwater for 50 years and teems with brine shrimp and algae. It also serves as a major stop-over point for migratory birds. \u003c/p>\n\u003cp>Wolfe-Simon chose to investigate how GFAJ-1 responded to arsenic because of the toxic compound’s chemical similarity to phosphorus. She pointed out that arsenic lies just below phosphorus on the periodic table and that their atoms are roughly the same in size. But arsenic is highly toxic to most living organisms because it disrupts metabolic pathways in the cells which take up arsenic readily, given its chemical similarity to phosphorus. \u003c/p>\n\u003cp>So Wolfe-Simon took the muddy samples containing the bacteria and grew them in petri dishes in a watery solution containing sugar and high levels of arsenic, while reducing the amount of phosphate salt the bacteria were fed. Eventually, the bacteria were fed only a diet of arsenic. \u003c/p>\n\u003cp>“It grew and it thrived, and this was amazing. Nothing should have grown,” said Simon. \u003c/p>\n\u003cp>In just six days, the bacteria multiplied twenty-fold as it wolfed down the arsenic. \u003c/p>\n\u003cp>Simon and her colleagues used radiolabeled arsenate, a form of arsenic, to track the movement of arsenic inside the bacteria. With the aid of additional laboratory techniques, they found that the bacteria’s cellular machinery of lipids, proteins, even its DNA, were now made up of arsenic. So the bacteria were able to fully substitute phosphorus, which provides the chemical backbone of DNA, for arsenic and still function and grow just fine. \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/39/2010/12/AAAS-Science_wolfesimon7HR-21.jpg\" alt=\"\">\u003c/a>\u003cem>Mono Lake, located in eastern California, next to the Sierra Nevada mountains, is highly saline and has high concentrations of arsenic. (Credit: Henry Bortman)\u003c/em>\u003c/span>\u003c/p>\n\u003cp>\"We know that some microbes can breathe arsenic, but what we've found is a microbe doing something new -- building parts of itself out of arsenic,\" said Wolfe-Simon.\u003c/p>\n\u003cp>And according to Professor Elser at Arizona State University, the discovery of a microbe that thrives on arsenic may have value beyond the lab and academic papers. Elser mused on the possibility of using GFAJ-1 to clean up naturally-occurring arsenic, which can pollute groundwater and lead to failure of organs such as the kidneys and liver if ingested. \u003c/p>\n\u003cp>Then there’s the burgeoning field of biofuels, the next generation of which include algae. But algae and other plants being cultivated for renewable fuels require phosphorus to grow. \u003c/p>\n\u003cp>“So what if someone was clever enough to be able to develop a bioenergy creature, a microorganism, based on this metabolism that doesn’t need phosphorus, so you don’t need to drain the fertilizer supply in order to solve the bioenergy problem,” said Elser. “It’s pretty exciting to think about the possibility of organisms that may be able to live without phosphorous,” he added. \u003c/p>\n\u003cp>For Felisa Wolfe-Simon, the discovery of the arsenic-loving bacteria is an important milestone in astrobiology, a discipline which combines chemistry, astronomy, biology and other sciences to understand the evolution of life and the future of life – on Earth and beyond. \u003c/p>\n\u003cp>“We’ve cracked open the door to what’s possible for life elsewhere in the universe and that’s profound and to understand how life has formed and where life is going,” she said. “And what else might we find, what else might we want to look for?”\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp> 37.52119957659491 -122.0086669921875\u003c/p>\n\n",
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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/AAAS-Science_wolfesimon1HR-22.jpg\" alt=\"\">\u003c/a>\u003cem> Scanning electron microscope image of the arsenic-loving bacteria GFAJ-1. (Credit: AAAS/Science) \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>A Bay Area biochemist has found a new strain of bacteria living in the briny shores of Mono Lake that can eat and thrive on arsenic, a substance highly toxic to most organisms. The discovery may lead to a significant shift in how scientists search for extraterrestrial life. \u003c/p>\n\u003cp>“All life that we know of requires carbon, hydrogen, oxygen, nitrogen, sulfur and phosphorus,” said Felisa Wolfe-Simon, the lead author of the study and a NASA Astrobiology Research Fellow in residence at the U.S. Geological Survey in Menlo Park. “We discovered an organism that can substitute one element for another,” she added. \u003c/p>\n\u003cp>Those six major elements comprise the building blocks of key components of living cells, such as DNA, RNA and proteins – the molecular switches which power the cells and instruct them to perform tasks critical for cellular growth and survival. Researchers know of no other microbe that can consume arsenic let alone substitute it for phosphorus, thereby expanding the definition of what constitutes life on Earth and elsewhere in the universe. \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>“As someone who regularly gives lectures in which I state, ‘every living thing uses phosphorus to build its DNA’, the idea that I’m sitting here today discussing the possibility that that’s not true is quite shocking,” said James Elser, a professor at Arizona State University who participated in a NASA teleconference convened today to discuss the findings. \u003c/p>\n\u003cp>The discovery of the arsenic-loving microbe also “opens new doors” to explore what life may look like in other reaches of the solar system, on environments such as Mars or the moons of Jupiter and Saturn that have previously been thought to be too cold and harsh to support life. \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/39/2010/12/AAAS-Science_wolfesimon4HR-21.jpg\" alt=\"\">\u003c/a>\u003cem>Felicia Wolfe-Simon of the NASA Ames Research Center and USGS collects samples from a sediment core extracted from the shores of Mono Lake in eastern California. (Credit: Henry Bortman)\u003c/em>\u003c/span>\u003c/p>\n\u003cp>“We still don’t know everything there is to know about what might make a habitable environment on another planet or a satellite of another planet,” said Pamela Conrad, an astrobiologist at NASA’s Goddard Space Flight Center in Greenbelt, Maryland. “Perhaps arsenic is not an essential component for habitability or life but it may be one that can be tolerated and it opens our perspective to try and understand what other potential components may be tolerated or perhaps even essential that we presently haven’t thought of,” she added. \u003c/p>\n\u003cp>A paper describing the finding appears in this week’s edition of the journal \u003cem>\u003ca href=\"http://www.sciencemag.org/content/early/2010/12/01/science.1197258\">Science Express\u003c/a>\u003c/em>. \u003c/p>\n\u003cp>But before the embargo on the paper was lifted on Thursday, a flurry of speculation was set off earlier in the week that NASA had discovered proof of alien life, fueled by an ambiguous press release issued by NASA on Monday which trumpeted “an astrobiology finding that will impact the search for evidence of extraterrestrial life.” In fact, the embargo was lifted roughly two hours earlier than planned because reports of the finding, some of them erroneous, were already beginning to appear online in publications like \u003cem>The Huffington Post\u003c/em> and the \u003cem>Guardian\u003c/em>. \u003c/p>\n\u003cp>At the end of NASA’s Thursday teleconference, Mary Voytek, director of the Astrobiology Program at NASA headquarters in Washington, D.C. responded to a question from a \u003cem>USA Today\u003c/em> journalist about the disappointment felt by its readers that in fact, NASA would not be pulling E.T out of a hat. \u003c/p>\n\u003cp>“I guess what I would say is that while being able to announce the discovery of an extra-terrestrial would be an incredible announcement, from our perspective, this is a phenomenal finding. It will require some paragraphs in textbooks to be rewritten,” said Voytek. “It will fundamentally change how we define life and how we look for it, maybe we’ll be able to find E.T. now because we’ve got more information about what we might be looking for,” she added.\u003c/p>\n\u003cp>The research team, led by Wolfe-Simon, discovered the new strain of bacteria, GFAJ-1, in muddy sediment cores extracted from the shores of Mono Lake, located in eastern California, near the Sierra Nevada mountains. The 70 square-mile inland lake is highly salty and alkaline with high concentrations of naturally-occurring arsenic. It has been separated from freshwater for 50 years and teems with brine shrimp and algae. It also serves as a major stop-over point for migratory birds. \u003c/p>\n\u003cp>Wolfe-Simon chose to investigate how GFAJ-1 responded to arsenic because of the toxic compound’s chemical similarity to phosphorus. She pointed out that arsenic lies just below phosphorus on the periodic table and that their atoms are roughly the same in size. But arsenic is highly toxic to most living organisms because it disrupts metabolic pathways in the cells which take up arsenic readily, given its chemical similarity to phosphorus. \u003c/p>\n\u003cp>So Wolfe-Simon took the muddy samples containing the bacteria and grew them in petri dishes in a watery solution containing sugar and high levels of arsenic, while reducing the amount of phosphate salt the bacteria were fed. Eventually, the bacteria were fed only a diet of arsenic. \u003c/p>\n\u003cp>“It grew and it thrived, and this was amazing. Nothing should have grown,” said Simon. \u003c/p>\n\u003cp>In just six days, the bacteria multiplied twenty-fold as it wolfed down the arsenic. \u003c/p>\n\u003cp>Simon and her colleagues used radiolabeled arsenate, a form of arsenic, to track the movement of arsenic inside the bacteria. With the aid of additional laboratory techniques, they found that the bacteria’s cellular machinery of lipids, proteins, even its DNA, were now made up of arsenic. So the bacteria were able to fully substitute phosphorus, which provides the chemical backbone of DNA, for arsenic and still function and grow just fine. \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/39/2010/12/AAAS-Science_wolfesimon7HR-21.jpg\" alt=\"\">\u003c/a>\u003cem>Mono Lake, located in eastern California, next to the Sierra Nevada mountains, is highly saline and has high concentrations of arsenic. (Credit: Henry Bortman)\u003c/em>\u003c/span>\u003c/p>\n\u003cp>\"We know that some microbes can breathe arsenic, but what we've found is a microbe doing something new -- building parts of itself out of arsenic,\" said Wolfe-Simon.\u003c/p>\n\u003cp>And according to Professor Elser at Arizona State University, the discovery of a microbe that thrives on arsenic may have value beyond the lab and academic papers. Elser mused on the possibility of using GFAJ-1 to clean up naturally-occurring arsenic, which can pollute groundwater and lead to failure of organs such as the kidneys and liver if ingested. \u003c/p>\n\u003cp>Then there’s the burgeoning field of biofuels, the next generation of which include algae. But algae and other plants being cultivated for renewable fuels require phosphorus to grow. \u003c/p>\n\u003cp>“So what if someone was clever enough to be able to develop a bioenergy creature, a microorganism, based on this metabolism that doesn’t need phosphorus, so you don’t need to drain the fertilizer supply in order to solve the bioenergy problem,” said Elser. “It’s pretty exciting to think about the possibility of organisms that may be able to live without phosphorous,” he added. \u003c/p>\n\u003cp>For Felisa Wolfe-Simon, the discovery of the arsenic-loving bacteria is an important milestone in astrobiology, a discipline which combines chemistry, astronomy, biology and other sciences to understand the evolution of life and the future of life – on Earth and beyond. \u003c/p>\n\u003cp>“We’ve cracked open the door to what’s possible for life elsewhere in the universe and that’s profound and to understand how life has formed and where life is going,” she said. “And what else might we find, what else might we want to look for?”\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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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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"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. 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"content": "\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>[ad fullwidth]\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",
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"link": "/radio/program/bbc-world-service",
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"apple": "https://itunes.apple.com/us/podcast/global-news-podcast/id135067274?mt=2",
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"rss": "https://podcasts.files.bbci.co.uk/p02nq0gn.rss"
}
},
"californiareport": {
"id": "californiareport",
"title": "The California Report",
"tagline": "California, day by day",
"info": "KQED’s statewide radio news program providing daily coverage of issues, trends and public policy decisions.",
"imageSrc": "https://cdn.kqed.org/wp-content/uploads/2024/04/The-California-Report-Podcast-Tile-703x703-1.jpg",
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"officialWebsiteLink": "/californiareport",
"meta": {
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"source": "kqed",
"order": 8
},
"link": "/californiareport",
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"amazon": "https://music.amazon.com/podcasts/26099305-72af-4542-9dde-ac1807fe36d5/kqed-s-the-california-report",
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}
},
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"id": "californiareportmagazine",
"title": "The California Report Magazine",
"tagline": "Your state, your stories",
"info": "Every week, The California Report Magazine takes you on a road trip for the ears: to visit the places and meet the people who make California unique. The in-depth storytelling podcast from the California Report.",
"airtime": "FRI 4:30pm-5pm, 6:30pm-7pm, 11pm-11:30pm",
"imageSrc": "https://cdn.kqed.org/wp-content/uploads/2024/04/The-California-Report-Magazine-Podcast-Tile-703x703-1.jpg",
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"officialWebsiteLink": "/californiareportmagazine",
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"order": 10
},
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"google": "https://podcasts.google.com/feed/aHR0cHM6Ly9mZWVkcy5tZWdhcGhvbmUuZm0vS1FJTkM3NjkwNjk1OTAz",
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},
"city-arts": {
"id": "city-arts",
"title": "City Arts & Lectures",
"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",
"imageSrc": "https://ww2.kqed.org/radio/wp-content/uploads/sites/50/2018/05/cityartsandlecture-300x300.jpg",
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"airtime": "SUN 1pm-2pm, TUE 10pm, WED 1am",
"meta": {
"site": "news",
"source": "City Arts & Lectures"
},
"link": "https://www.cityarts.net",
"subscribe": {
"tuneIn": "https://tunein.com/radio/City-Arts-and-Lectures-p692/",
"rss": "https://www.cityarts.net/feed/"
}
},
"closealltabs": {
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"officialWebsiteLink": "/podcasts/closealltabs",
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"order": 1
},
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"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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"meta": {
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"google": "https://podcasts.google.com/feed/aHR0cHM6Ly93d3cubnByLm9yZy9yc3MvcG9kY2FzdC5waHA_aWQ9NTEwMzEy",
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},
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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.",
"airtime": "THU 10pm, FRI 1am",
"imageSrc": "https://cdn.kqed.org/wp-content/uploads/2024/04/Commonwealth-Club-Podcast-Tile-360x360-1.jpg",
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"meta": {
"site": "news",
"source": "Commonwealth Club of California"
},
"link": "/radio/program/commonwealth-club",
"subscribe": {
"apple": "https://itunes.apple.com/us/podcast/commonwealth-club-of-california-podcast/id976334034?mt=2",
"google": "https://podcasts.google.com/feed/aHR0cDovL3d3dy5jb21tb253ZWFsdGhjbHViLm9yZy9hdWRpby9wb2RjYXN0L3dlZWtseS54bWw",
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},
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"id": "forum",
"title": "Forum",
"tagline": "The conversation starts here",
"info": "KQED’s live call-in program discussing local, state, national and international issues, as well as in-depth interviews.",
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"imageSrc": "https://cdn.kqed.org/wp-content/uploads/2024/04/Forum-Podcast-Tile-703x703-1.jpg",
"imageAlt": "KQED Forum with Mina Kim and Alexis Madrigal",
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"source": "kqed",
"order": 9
},
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"google": "https://podcasts.google.com/feed/aHR0cHM6Ly9mZWVkcy5tZWdhcGhvbmUuZm0vS1FJTkM5NTU3MzgxNjMz",
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},
"freakonomics-radio": {
"id": "freakonomics-radio",
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"imageSrc": "https://ww2.kqed.org/news/wp-content/uploads/sites/10/2018/05/freakonomicsRadio.png",
"officialWebsiteLink": "http://freakonomics.com/",
"airtime": "SUN 1am-2am, SAT 3pm-4pm",
"meta": {
"site": "radio",
"source": "WNYC"
},
"link": "/radio/program/freakonomics-radio",
"subscribe": {
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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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},
"fresh-air": {
"id": "fresh-air",
"title": "Fresh Air",
"info": "Hosted by Terry Gross, \u003cem>Fresh Air from WHYY\u003c/em> is the Peabody Award-winning weekday magazine of contemporary arts and issues. One of public radio's most popular programs, Fresh Air features intimate conversations with today's biggest luminaries.",
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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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"rss": "https://feeds.npr.org/381444908/podcast.xml"
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"here-and-now": {
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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": {
"id": "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"
},
"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.",
"imageSrc": "https://ww2.kqed.org/news/wp-content/uploads/sites/10/2018/05/howIBuiltThis.png",
"officialWebsiteLink": "https://www.npr.org/podcasts/510313/how-i-built-this",
"airtime": "SUN 7:30pm-8pm",
"meta": {
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"source": "npr"
},
"link": "/radio/program/how-i-built-this",
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"npr": "https://rpb3r.app.goo.gl/3zxy",
"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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},
"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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"apple": "https://itunes.apple.com/us/podcast/id1492194549",
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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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"source": "npr"
},
"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": {
"site": "news",
"source": "American Public Media"
},
"link": "/radio/program/marketplace",
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"rss": "https://feeds.publicradio.org/public_feeds/marketplace-pm/rss/rss"
}
},
"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"
},
"link": "/radio/program/masters-of-scale",
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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",
"imageAlt": "On Our Watch from NPR and KQED",
"officialWebsiteLink": "/podcasts/onourwatch",
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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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"rss": "https://feeds.npr.org/510360/podcast.xml"
}
},
"on-the-media": {
"id": "on-the-media",
"title": "On The Media",
"info": "Our weekly podcast explores how the media 'sausage' is made, casts an incisive eye on fluctuations in the marketplace of ideas, and examines threats to the freedom of information and expression in America and abroad. For one hour a week, the show tries to lift the veil from the process of \"making media,\" especially news media, because it's through that lens that we see the world and the world sees us",
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"info": "One of public radio's most dynamic voices, Sam Sanders helped launch The NPR Politics Podcast and hosted NPR's hit show It's Been A Minute. Now, the award-winning host returns with something brand new, The Sam Sanders Show. Every week, Sam Sanders and friends dig into the culture that shapes our lives: what's driving the biggest trends, how artists really think, and even the memes you can't stop scrolling past. Sam is beloved for his way of unpacking the world and bringing you up close to fresh currents and engaging conversations. The Sam Sanders Show is smart, funny and always a good time.",
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