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Lysergic acid diethylamide (LSD) has been credited, in part, for the creation of the iPhone, the polymerase chain reaction, as well as some pretty abstract artwork. Since the drug is classified as a Schedule 1 substance in the U.S., it's been more difficult for scientists to legally study the drug and learn about how it affects the brain. Therefore, when a study (or two) is published it makes the findings all the more fascinating. Two studies were published last week (one in Current Biology, the other in Cell) that examine how LSD produces such diverse effects and why the drug takes so long to wear off. The Scientist reports the findings from for the first study: For the Current Biology study, 21 volunteers were given a placebo, a small dose of LSD alone, or the same dose of LSD but with kentaserin, a serotonin 2A antagonist. Study participants who took the kentaserin reported virtually the same experiences as those who took the placebo, and fMRI brain scans confirmed similar brain activities across participants in both groups. The serotonin 2A antagonist "blocked all the effects of LSD, so it was like if people didn't take any drugs," coauthor Katrin Preller, neuroscientist at the Zurich University Hospital in Switzerland told The Verge. "All the typical symptoms -- hallucinations, everything -- were gone." As for why an LSD high lasts for so long, Angus Chen has written an in-depth report on PBS Newshour about the findings from the study published in Cell: LSD and other psychoactive drugs work by binding to specialized proteins called receptors on the surfaces of neural cells. On the receptor protein is a sculpted "pocket," into which molecules with the right shape can fit and thus stick to the cell, where they initiate changes in the brain. But different substances can often fit into the same receptor. Many receptors that bind LSD and DMT, for example, also fit the natural chemical messenger serotonin -- which is produced in the body and helps regulate mood. Figuring out how each drug interacts with the same receptor in a different way is key to understanding why an LSD trip lasts all day whereas an experience with extracted DMT is often over in 15 minutes or less. By freezing an LSD molecule bound to a single brain cell receptor as a crystal in a lab, researchers were able to get a 3-D x-ray image of the drug and the protein locked together. The image showed Bryan Rother, a pharmacologist at the University of North Carolina at Chapel Hill and senior author on the paper, and his co-authors something strange about the way LSD fit inside this receptor. Drugs typically come and go from receptor proteins like ships pulling in and out of a port. But when an LSD molecule lands on the receptor, the molecule snags onto a portion of the protein and folds it over itself as the molecule binds to the receptor. LSD seems to stimulate the receptor for the entire time it is trapped underneath the protein "lid," Roth says. Proteins are in constant motion, so he thinks the lid eventually flops open, allowing the drug to fly out and the effects to wear off. But the team ran computer models that suggest it could take hours for that to happen. Until then, the trip goes on.

BenBoy writes: A couple of years ago, a story surfaced about smarter mice: Scientists Create Super-intelligent Mice, Discover They're Also Very Laid Back. Well, implicit challenge accepted! 2017 brings us a report from Cell, via The Scientist: "Neural circuits in the amygdala are responsible for predatory behavior in mice, according to a study published January 12 in Cell. Using optogenetics, a technique that uses light to turn neural circuits on and off, a group of researchers led by neuroscientist Ivan de Araujo of Yale University was able to turn docile mice into ruthless hunters. Earlier research revealed that the amygdala, an almond-shaped brain structure most commonly linked to fear, was active when rats were hunting and feeding. To see whether this brain region was actually controlling predatory behavior, Araujo and colleagues decided to use optogenetics to selectively activate specific neurons in mice, with light. When the researchers activated the amygdala, docile mice attacked everything from bottle caps to live insects. Even when there was no prey in sight, the mice displayed feeding behavior -- moving their jaws and lifted their paws as if holding a piece of food. Once the light was switched off, the animals went back to peacefully strolling around their cages." Nuclear death-mice are, we assume, right around the corner.

New submitter rex.clts writes "In the IT security world, it is common practice to withhold specifics when announcing a newly discovered software vulnerability. The exact details regarding a buffer overflow or race condition are typically kept secret until a patch is available, to slow the proliferation of exploits against the hole. For the first time, this practice has been extended to medical publishing. A new form of Botulism has been identified, but its DNA sequence (the genetic code that makes up the toxin) has been withheld, until an antidote has been found. It seems that censorship in the name of "security" is spreading (with DHS involved this comes as no surprise.) Is this the right move?"

Dr. Tom writes "Scientists at MIT and other labs have created transgenic neurons that fire when exposed to light. The technique targets specific cell types in live primates. They are already talking about the possibilities for therapy and behavior modification by optically stimulating specific brain circuits."

An anonymous reader writes "British biologists have received government approval to create the world's first human stem cells from hybrid embryos, part pig, part human. The Warwick Medical School team, led by Justin St. John of the Clinical Sciences Research Institute, was granted the country's third animal-human embryo license from the Human Fertilisation and Embryology Authority, which goes into effect today (July 1)." The above link requires (free) registration; the Telegraph's coverage does not.

Ant sends in a disturbing report in The Scientist on an imminent threat to worldwide banana production. "The banana we eat today is not the one your grandparents ate. That one — known as the Gros Michel — was, by all accounts, bigger, tastier, and hardier than the variety we know and love, which is called the Cavendish. The unavailability of the Gros Michel is easily explained: it is virtually extinct. Introduced to our hemisphere in the late 19th century, the Gros Michel was almost immediately hit by a blight that wiped it out by 1960. The Cavendish was adopted at the last minute by the big banana companies — Chiquita and Dole — because it was resistant to that blight, a fungus known as Panama disease... [Now] Panama disease — or Fusarium wilt of banana — is back, and the Cavendish does not appear to be safe from this new strain, which appeared two decades ago in Malaysia, spread slowly at first, but is now moving at a geometrically quicker pace. There is no cure, and nearly every banana scientist says that though Panama disease has yet to hit the banana crops of Latin America, which feed our hemisphere, the question is not if this will happen, but when. Even worse, the malady has the potential to spread to dozens of other banana varieties, including African bananas, the primary source of nutrition for millions..."

GeneRegulator writes "The NY Times is running a story on communities that are forming around kids with rare genetic mutations. New technology that can scan chromosomes for small errors is being applied first to children with autism and other 'unexplained developmental delays.' It turns out that many of them have small deletions or duplications of DNA. Meanwhile, hundreds of little groups are forming around the banner of their children's shared mutations. As new research shows that many of us have small deletions and duplications of DNA that separate us from our parents, and that many of these "copy number variants" contribute to skills and senses, the families described in the story may presage the formation of all sorts of 'communities of the genetically rare' in the general population, not just amongst the developmentally delayed."

eldavojohn writes "A non-profit alumni group from the University of Wisconsin (WARF) has suffered a preliminary ruling against three of their recent patents regarding stem cells. Given that these patents have been upheld in prior rulings, there is a lot of speculation that they will be upheld in a future court case. From the PhysOrg article: 'The patents, which cover virtually all stem cell research in the country, have brought in at least $3.2 million and could net much more money before they expire in 2015, the newspaper said. Companies wanting to study the cells must buy licenses costing $75,000 to $400,000. The newspaper said WARF recently started waiving the fees if the research is conducted at universities or by non-profit groups.' Should universities (or groups within universities) be allowed to hold patents and intellectual property while at the same time gaining donations and grants as an educational institution — or for that matter government funds?"

Roland Piquepaille writes "The Wellcome Trust Sanger Institute is one of the largest genomics data centers in the world. In "The Hum and the Genome," the Scientist writes about the IT infrastructure needed to handle the avalanche of data that researchers have to analyze. With its 2,000 processors and its 300 terabytes of storage, the data center uses today about 0.75 megawatts (MW) of power at a cost of 140,000 per year (about $170K). But the data center will need more than a petabyte of storage within three years, and its yearly electricity bill will reach 500,000 (more than $600K) for about 1.4 MW, enough to power more than a thousand homes. The original article gets all the facts, but this summary contains all the essential numbers."

nucal writes "The 2003 Nobel Prize in Chemistry was awarded to Rod MacKinnon and Peter Agree for their work on proteins that form ion and water channels in cell membranes. In particular, solving the structure of potassium channels was a major achievement, since this was the first multispan transmembrane protein structure to be solved by X-ray crystallography. There is also structural information on aquaporins (water channels) as well."