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Researchers from the University of Basel in Switzerland have discovered that they can prevent the formation of metastases by fooling breast cancer cells into fat cells. The proof-of-concept study was published in the journal Cancer Cell. Technology Networks reports: Malignant cells can rapidly respond and adapt to changing microenvironmental conditions, by reactivating a cellular process called epithelial-mesenchymal transition (EMT), enabling them to alter their molecular properties and transdifferentiate into a different type of cell (cellular plasticity). Cancer cells can exploit EMT -- a process that is usually associated with the development of organs during embryogenesis -- in order to migrate away from the primary tumor and form secondary metastases. Cellular plasticity is linked to cancer survival, invasion, tumor heterogeneity and resistance to both chemo and targeted therapies. In addition, EMT and the inverse process termed mesenchymal-epithelial transition (MET) both play a role in a cancer cell's ability to metastasize.

Using mouse models of both murine and human breast cancer the team investigated whether they could therapeutically target cancer cells during the process of EMT -- whilst the cells are in a highly plastic state. When the mice were administered Rosiglitazone in combination with MEK inhibitors it provoked the transformation of the cancer cells into post-mitotic and functional adipocytes (fat cells). In addition, primary tumor growth was suppressed and metastasis was prevented. Since both drugs used in the preclinical study were FDA-approved the team are hopeful that it may be possible to translate this therapeutic approach to the clinic.

Long-time Slashdot reader Futurepower(R) shares this article about a newly-published study which counters previous theories that neurons stop developing after adolescence: Healthy men and women continue to produce new neurons throughout life, suggesting older people remain more cognitively and emotionally intact than previously believed, researchers found. For decades it was thought that adult brains were hard-wired and unable to form new cells. But a Columbia University study found older people continued to produce neurons in the hippocampus -- a part of the brain important for memory, emotion and cognition -- at a similar rate to young people....

However, the researchers also noted fewer blood vessels and connections between cells in the older brains, which Ms Boldrini said "may be linked to compromised cognitive-emotional resilience" in the elderly.
The article suggests these newest findings may be hotly debated.

"They come just a month after a University of California study suggested adults do not develop new neurons."

Rick Schumann writes about the findings of a new study published in the journal Neuron: A team of neuroscientists from Washington University in St. Louis, performing fMRI tests on 10 people to quantify the various connections between the cerebellum and the rest of the brain, are now being led to believe that the cerebellum actually plays a role in conscious thought, whereas previously it was believed it was only involved in sensory-motor function. What they found is that it appears that only 20 percent of the cerebellum was dedicated to physical motion, while the other 80 percent serves as an "editor" of the conscious thought process, refining and filtering thoughts in a sort of background process. This discovery may lead to changes in the way psychiatric patients are treated for disorders like schizophrenia, depression, and obsessive-compulsive behaviors.

Researchers at the Chinese Academy of Sciences were able to make baby mice with two moms and no dad. "The aim of the Chinese researchers was to work out which rules of reproduction they needed to break to make baby mice from same-sex parents," reports the BBC. "That in turn helps understand why the rules are so important." From the report: It was easier with double mums. The researchers took an egg from one mouse and a special type of cell -- a haploid embryonic stem cell -- from another. Both contained only half the required genetic instructions or DNA, but just bringing them together wasn't enough. The researchers had to use a technology called gene editing to delete three sets of genetic instructions to make them compatible (more on that later). The double-dad approach was slightly more complicated. It took a sperm, a male haploid embryonic stem cell, an egg that had all of its own genetic information removed and the deletion of seven genes to make it all work.

The reason we need to have sex is because our DNA -- our genetic code -- behaves differently depending on whether it comes from mum or dad, the study in Cell Stem Cell suggests. And without a female copy and a male copy our whole development gets thrown out of whack. It's called genomic imprinting with parts of the DNA in sperm and parts of the DNA in eggs getting different "stamps" that alter how they work. The bits of DNA carrying these stamps were the ones the researchers had to delete in order to make the baby mice viable.

An anonymous reader quotes a report from ScienceAlert: A new study argues that we have Neanderthals to thank for helping us cope with the viral tides we encountered as we marched around the globe. Stanford University researchers have identified DNA sequences that evolved in our ancient cousins can produce antivirus proteins, which more than likely gave some human populations the edge they needed to survive. Roughly 1 percent of our genome's coding was written in Neanderthal populations. But this is a broad average -- many families with African ancestry have zero, for instance, while other populations boast as much as 2 percent or more. So the question is how much of this difference comes down to the random drift of DNA being passed on around the globe, and how much is due to natural selection giving those with Neanderthal genes an advantage?

To build a case one way or another, the Stanford researchers put together a list of just over 4,500 virus-interacting proteins (VIP) made by our genome. These were all matched against a database of Neanderthal DNA that could be found in modern East Asian and European human populations, providing 152 VIP genes shared by both groups of human. Interestingly, all of these VIP genes were of a variety that interacted with RNA viruses -- pathogens that include influenza A, hepatitis C, and HIV. This isn't to say these viruses were problems for ancient humans, but rather that similar RNA viruses were more than likely prevalent enough to shape our evolution. The discovery supports a view of genetic exchange described as the 'poison-antidote' model.

XxtraLarGe shares a report: Wind power is booming in the United States. It's expanded 35-fold since 2000 and now provides 8% of the nation's electricity. The US Department of Energy expects wind turbine capacity to more than quadruple again by 2050. But a new study by a pair of Harvard researchers finds that a high amount of wind power could mean more climate warming, at least regionally and in the immediate decades ahead. The paper raises serious questions about just how much the United States or other nations should look to wind power to clean up electricity systems. The study, published in the journal Joule, found that if wind power supplied all US electricity demands, it would warm the surface of the continental United States by 0.24 C. That could significantly exceed the reduction in US warming achieved by decarbonizing the nation's electricity sector this century, which would be around 0.1 C. "If your perspective is the next 10 years, wind power actually has -- in some respects -- more climate impact than coal or gas," coauthor David Keith, a professor of applied physics and public policy at Harvard, said in a statement. "If your perspective is the next thousand years, then wind power is enormously cleaner than coal or gas."

An anonymous reader shares a report: The problem of energy storage has led to many creative solutions, like giant batteries. For a paper published today in the journal Chem, scientists trying to improve the solar cells themselves developed an integrated battery that works in three different ways. It can work like a normal solar cell by converting sunlight to electricity immediately, explains study author Song Jin, a chemist at the University of Wisconsin at Madison. It can store the solar energy, or it can simply be charged like a normal battery. It's a combination of two existing technologies: solar cells that harvest light, and a so-called flow battery. The most commonly used batteries, lithium-ion, store energy in solid materials, like various metals. Flow batteries, on the other hand, store energy in external liquid tanks. This means they are very easy to scale for large projects. Scaling up all the components of a lithium-ion battery might throw off the engineering, but for flow batteries, "you just make the tank bigger," says Timothy Cook, a University at Buffalo chemist and flow battery expert not involved in the study. "You really simplify how to make the battery grow in capacity," he adds. "We're not making flow batteries to power a cell phone, we're thinking about buildings or industrial sites.

MIT has developed a new type of battery that could be made partly from carbon dioxide captured from power plants. "Rather than attempting to convert carbon dioxide to specialized chemicals using metal catalysts, which is currently highly challenging, this battery could continuously convert carbon dioxide into a solid mineral carbonate as it discharges," reports SciTechDaily. From the report: While still based on early-stage research and far from commercial deployment, the new battery formulation could open up new avenues for tailoring electrochemical carbon dioxide conversion reactions, which may ultimately help reduce the emission of the greenhouse gas to the atmosphere. The battery is made from lithium metal, carbon, and an electrolyte that the researchers designed. The findings are described today in the journal Joule, in a paper by assistant professor of mechanical engineering Betar Gallant, doctoral student Aliza Khurram, and postdoc Mingfu He. [...] Gallant and her co-workers, whose expertise has to do with nonaqueous (not water-based) electrochemical reactions such as those that underlie lithium-based batteries, looked into whether carbon-dioxide-capture chemistry could be put to use to make carbon-dioxide-loaded electrolytes -- one of the three essential parts of a battery -- where the captured gas could then be used during the discharge of the battery to provide a power output.

This approach is different from releasing the carbon dioxide back to the gas phase for long-term storage, as is now used in carbon capture and sequestration, or CCS. That field generally looks at ways of capturing carbon dioxide from a power plant through a chemical absorption process and then either storing it in underground formations or chemically altering it into a fuel or a chemical feedstock. Instead, this team developed a new approach that could potentially be used right in the power plant waste stream to make material for one of the main components of a battery. While interest has grown recently in the development of lithium-carbon-dioxide batteries, which use the gas as a reactant during discharge, the low reactivity of carbon dioxide has typically required the use of metal catalysts. Not only are these expensive, but their function remains poorly understood, and reactions are difficult to control. By incorporating the gas in a liquid state, however, Gallant and her co-workers found a way to achieve electrochemical carbon dioxide conversion using only a carbon electrode. The key is to preactivate the carbon dioxide by incorporating it into an amine solution. "What we've shown for the first time is that this technique activates the carbon dioxide for more facile electrochemistry," Gallant says. "These two chemistries -- aqueous amines and nonaqueous battery electrolytes -- are not normally used together, but we found that their combination imparts new and interesting behaviors that can increase the discharge voltage and allow for sustained conversion of carbon dioxide."

The approach reportedly works, producing a lithium-carbon dioxide battery with voltage and capacity that are competitive with that of state-of-the-art lithium-gas batteries," reports SciTechDaily. "Moreover, the amine acts as a molecular promoter that is not consumed in the reaction."

Gul Dolen, a neuroscientist at the Johns Hopkins School of Medicine who studies how the cells and chemicals in animal brains influence animals' social lives, gave ecstasy to octopuses and recorded her observations. The study, published in the journal Current Biology, suggests that the psychoactive drug that can make people feel extra loving toward others also has the same effect on octopuses. An anonymous reader shares the report from The Atlantic: [Dolen] and her colleague Eric Edsinger put five Californian two-spot octopuses individually into the middle of three connected chambers and gave them free rein to explore. One of the adjacent chambers housed a second octopus, confined inside an overturned plastic basket. The other contained an unfamiliar object, such as a plastic flower or a Chewbacca figurine. Dolen and Edsinger measured how long the main animal spent in the company of its peer, and how long with the random toy. The free-moving individuals thoroughly explored the chambers, and from their movements, Dolen realized that individuals of any sex gravitate toward females, but avoid males. Next, she dosed the animals with ecstasy. Again, there's no precedent for this, but researchers often anesthetize octopuses by dunking them in ethanol -- a humane procedure with no lasting side effects. So Dolen and Edsinger submerged their octopuses in an MDMA solution, allowing them to absorb the drug through their gills. At first they used too high a dose, and the animals "freaked out and did all these color changes," Dolen says. But once the team found a more suitable dose, the animals behaved more calmly -- and more sociably. "With ecstasy in their system, the five octopuses spent far more time in the company of the same trapped male they once shunned," the report continues. "Even without a stopwatch, the change was obvious. Before the drug, they explored the chamber with the other octopus very tentatively."

"They mashed themselves against one wall, very slowly extended one arm, touched the [other animal], and went back to the other side," Dolen says. "But when they had MDMA, they had this very relaxed posture. They floated around, they wrapped their arms around the chamber, and they interacted with the other octopus in a much more fluid and generous way. They even exposed their [underside], where their mouth is, which is not something octopuses usually do."

An anonymous reader quotes a report from Gizmodo: Plastic products that boast of being "BPA-free" aren't necessarily any safer for us, suggests a new mouse study published Thursday in Current Biology. The chemicals used to replace BPA in these plastics can still leak out and affect the sperm and eggs of both male and female mice, it found. And these same effects could be happening in people. Bisphenol A, or BPA, is a chemical commonly used to create polycarbonate plastics and epoxy resins. These clear white plastics are themselves used in food and drink packaging, as well as consumer products and medical devices, while resins are used to coat metal products like canned foods. When these products degrade or are otherwise damaged (from being repeatedly heated in a microwave, for example), they can leach out BPA, exposing us to it. As a result, it's estimated that 93 percent of Americans have some level of BPA in their system.

While working on another project, the authors began seeing some but not all of their control mice, both male and female, develop reproductive problems. Though the mice had kept in cages made of polysulfone, not polycarbonate, the researchers noticed a whitish residue in some of the cages, indicating they had been damaged and were leaching chemicals. When Patricia Hunt, a researcher at the Center for Reproductive Biology at Washington State University, and her team analyzed the chemical signature of the damaged cages, they found both BPA and BPS, a bisphenol that is widely replacing BPA. The cases were polysulfone plastic, which is partly made from BPA, but it's advertised to be more heat and chemical resistant than polycarbonate and thus less likely to break down. Polysulfone isn't thought to degrade into BPS, but Hunt's team found that if certain chemical bonds in the plastic were broken in the right way, BPS could form. Following in the vein of their original experiments with BPA, Hunt's team exposed more mice to low doses of BPS, and compared their reproductive health to mice exposed to BPA and mice raised in fresh new cages, presumably free of any BPA/BPS contamination. The BPS mice had more defects in their egg and sperm cells than did the control mice, but the level of damage was similar to that seen in mice they exposed to the same dose of BPA alone. "Though manufacturers have shied away from making explicit claims about BPA replacements being safer, Hunt noted, customers have certainly assumed that they are safer," the report notes.

An anonymous reader quotes a report from The Guardian: The gut microbiome is the sum total of all the micro-organisms living in a person's gut, and has been shown to play a huge role in human health. New research has found probiotics -- usually taken as supplements or in foods such as yoghurt, kimchi or kefir -- can hinder a patient's gut microbiome from returning to normal after a course of antibiotics, and that different people respond to probiotics in dramatically different ways. In the first of two papers published in the journal Cell, researchers performed endoscopies and colonoscopies to sample and study the gut microbiomes of people who took antibiotics before and after probiotic consumption. Another group were given samples of their own gut microbiomes collected before consuming antibiotics. The researchers found the microbiomes of those who had taken the probiotics had suffered a "very severe disturbance." "Once the probiotics had colonized the gut, they completely inhibited the return of the indigenous microbiome which was disrupted during antibiotic treatment," said Eran Elinav, an immunologist at the Weizmann Institute of Science in Israel and lead author on the studies.

The scientists also compared the gut microbiomes of the gut intestinal tract of 25 volunteers with that of their stools. They found that stool bacteria only partially correlated with the microbiomes functioning inside their bodies. "So the fact that we all almost exclusively rely on stool in our microbiome research may not be a reliable way of studying gut microbiome health," said Elinav. In the second paper, the researchers examined the colonization and impact of probiotics on 15 people by sampling within their gastrointestinal tract. They divided the individuals into two groups: one were given a preparation made of 11 strains of very commonly used probiotics and the other were given a placebo. Of those who were given probiotics, he said, "We could group the individuals into two distinct groups: one which resisted the colonisation of the probiotics, and one in which the probiotics colonized the gut and modified the composition of the gut microbiome and the genes of the host individual."

An anonymous reader quotes a report from The Guardian: The gut microbiome is the sum total of all the micro-organisms living in a person's gut, and has been shown to play a huge role in human health. New research has found probiotics -- usually taken as supplements or in foods such as yoghurt, kimchi or kefir -- can hinder a patient's gut microbiome from returning to normal after a course of antibiotics, and that different people respond to probiotics in dramatically different ways. In the first of two papers published in the journal Cell, researchers performed endoscopies and colonoscopies to sample and study the gut microbiomes of people who took antibiotics before and after probiotic consumption. Another group were given samples of their own gut microbiomes collected before consuming antibiotics. The researchers found the microbiomes of those who had taken the probiotics had suffered a "very severe disturbance." "Once the probiotics had colonized the gut, they completely inhibited the return of the indigenous microbiome which was disrupted during antibiotic treatment," said Eran Elinav, an immunologist at the Weizmann Institute of Science in Israel and lead author on the studies.

The scientists also compared the gut microbiomes of the gut intestinal tract of 25 volunteers with that of their stools. They found that stool bacteria only partially correlated with the microbiomes functioning inside their bodies. "So the fact that we all almost exclusively rely on stool in our microbiome research may not be a reliable way of studying gut microbiome health," said Elinav. In the second paper, the researchers examined the colonization and impact of probiotics on 15 people by sampling within their gastrointestinal tract. They divided the individuals into two groups: one were given a preparation made of 11 strains of very commonly used probiotics and the other were given a placebo. Of those who were given probiotics, he said, "We could group the individuals into two distinct groups: one which resisted the colonisation of the probiotics, and one in which the probiotics colonized the gut and modified the composition of the gut microbiome and the genes of the host individual."

According to two complementary studies, sperm change their cargo as they travel the reproductive tract, which can have consequences on the viability of future offspring. Smithsonian reports: The legacy of a dad's behavior can even live on in his child if his epigenetic elements enter an embryo. For instance, mice born to fathers that experience stress can inherit the behavioral consequences of traumatic memories. Additionally, mouse dads with less-than-desirable diets can pass a wonky metabolism onto their kids. Upasna Sharma and Colin Conine, both working under Oliver Rando, a professor of biochemistry at the University of Massachusetts Medical School, were some of the researchers to report such findings in 2016. In their work, Sharma and Conine noted that, in mice, while immature testicular sperm contain DNA identical to that of mature sperm, immature sperm relay different epigenetic information. It turns out that sperm small RNAs undergo post-testes turnover, picking up intel on the father's physical health (or lack thereof) after they're manufactured, but before they exit the body. However, the exact pit stop at which these additional small RNAs hitch a ride remained unknown.

To solve the mystery, Sharma, who led the first of the two new studies, decided to track the composition of small RNAs within mouse sperm as they fled the testes and cruised through the epididymis. She and her colleagues isolated sperm of several different ages from mice, including those about to emerge from the testes, those entering the early part of the epididymis and those in the late part of the epididymis. Sharma was surprised to find that many small RNAs seemed to be discarded or destroyed upon entering the early epididymis; then, the newly vacated sperm reacquired epigenetic intel that reflected the father's state of being, boasting a full set by the time they left the late epididymis. There was only one possible source for the small RNA reacquisition: the cells of the epididymis -- which meant that cells outside of the sperm were transmitting information into future generations. [...] Colin Conine, who led the second of the two new studies, next tested if using immature sperm would have noticeable effects on the offspring of mice. He and his colleagues extracted sperm from the testes, early epididymis and late epididymis and injected them into eggs. All three types of sperm were able to fertilize eggs. However, when Conine transferred the resulting embryos into mouse surrogates, none derived from early epididymal sperm -- the intermediate stage devoid of most small RNAs -- implanted in the uterus. The least and most mature sperm of the bunch were winners -- but somehow, those in the middle were burning out, even though all their genes were intact. The only other explanation was that the defect was temporary. If this was the case, then perhaps, if fed the right small RNAs, the early epididymal sperm could be rescued.

According to two complementary studies, sperm change their cargo as they travel the reproductive tract, which can have consequences on the viability of future offspring. Smithsonian reports: The legacy of a dad's behavior can even live on in his child if his epigenetic elements enter an embryo. For instance, mice born to fathers that experience stress can inherit the behavioral consequences of traumatic memories. Additionally, mouse dads with less-than-desirable diets can pass a wonky metabolism onto their kids. Upasna Sharma and Colin Conine, both working under Oliver Rando, a professor of biochemistry at the University of Massachusetts Medical School, were some of the researchers to report such findings in 2016. In their work, Sharma and Conine noted that, in mice, while immature testicular sperm contain DNA identical to that of mature sperm, immature sperm relay different epigenetic information. It turns out that sperm small RNAs undergo post-testes turnover, picking up intel on the father's physical health (or lack thereof) after they're manufactured, but before they exit the body. However, the exact pit stop at which these additional small RNAs hitch a ride remained unknown.

To solve the mystery, Sharma, who led the first of the two new studies, decided to track the composition of small RNAs within mouse sperm as they fled the testes and cruised through the epididymis. She and her colleagues isolated sperm of several different ages from mice, including those about to emerge from the testes, those entering the early part of the epididymis and those in the late part of the epididymis. Sharma was surprised to find that many small RNAs seemed to be discarded or destroyed upon entering the early epididymis; then, the newly vacated sperm reacquired epigenetic intel that reflected the father's state of being, boasting a full set by the time they left the late epididymis. There was only one possible source for the small RNA reacquisition: the cells of the epididymis -- which meant that cells outside of the sperm were transmitting information into future generations. [...] Colin Conine, who led the second of the two new studies, next tested if using immature sperm would have noticeable effects on the offspring of mice. He and his colleagues extracted sperm from the testes, early epididymis and late epididymis and injected them into eggs. All three types of sperm were able to fertilize eggs. However, when Conine transferred the resulting embryos into mouse surrogates, none derived from early epididymal sperm -- the intermediate stage devoid of most small RNAs -- implanted in the uterus. The least and most mature sperm of the bunch were winners -- but somehow, those in the middle were burning out, even though all their genes were intact. The only other explanation was that the defect was temporary. If this was the case, then perhaps, if fed the right small RNAs, the early epididymal sperm could be rescued.

An anonymous reader quotes a report from Controlled Environments Magazine: Two high-speed electron microscopes. 7,062 brain slices. 21 million images. For a team of scientists at the Howard Hughes Medical Institute's Janelia Research Campus in Ashburn, Virginia, these numbers add up to a technical first: a high-resolution digital snapshot of the adult fruit fly brain. Researchers can now trace the path of any one neuron to any other neuron throughout the whole brain, says neuroscientist Davi Bock, a group leader at Janelia who reported the work along with his colleagues on July 19 in the journal Cell.

The fruit fly brain, roughly the size of a poppy seed, contains about 100,000 neurons (humans have 100 billion). Each neuron branches into a starburst of fine wires that touch the wires of other neurons. Neurons talk to one another through these touchpoints, or synapses, forming a dense mesh of communication circuits. Scientists can view these wires and synapses with an imaging technique called serial section transmission electron microscopy. First, they infuse the fly's brain with a cocktail of heavy metals. These metals pack into cell membranes and synapses, ultimately marking the outlines of each neuron and its connections. Then the researchers hit slices of the brain with a beam of electrons, which passes through everything except the metal-loaded parts. "It's the same way that x-rays go through your body except where they hit bone," Bock explains. The resulting images expose the brain's once-hidden nooks and crannies.

An anonymous reader shares a report: On Halloween in 1832, the naturalist Charles Darwin was onboard the HMS Beagle. He marveled at spiders that had landed on the ship after floating across huge ocean distances. "I caught some of the Aeronaut spiders which must have come at least 60 miles," he noted in his diary. "How inexplicable is the cause which induces these small insects, as it now appears in both hemispheres, to undertake their aerial excursions." Small spiders achieve flight by aiming their butts at the sky and releasing tendrils of silk to generate lift.

Darwin thought that electricity might be involved when he noticed that spider silk stands seemed to repel each other with electrostatic force, but many scientists assumed that the arachnids, known as "ballooning" spiders, were simply sailing on the wind like a paraglider. The wind power explanation has thus far been unable to account for observations of spiders rapidly launching into the air, even when winds are low, however. Now, these aerial excursions have been empirically determined to be largely powered by electricity, according to new research published Thursday in Current Biology. Led by Erica Morley, a sensory biophysicist at the University of Bristol, the study settles a longstanding debate about whether wind energy or electrostatic forces are responsible for spider ballooning locomotion.

Tests of brain tissue from nearly 1,000 people found that two strains of herpes virus were far more abundant in the brains of those with early-stage Alzheimer's than in healthy controls. "[S]cientists are divided on whether viruses are likely to be an active trigger, or whether the brains of people already on the path towards Alzheimer's are simply more vulnerable to infection," reports The Guardian. From the report: "The viral genomes were detectable in about 30% of Alzheimer's brains and virtually undetectable in the control group," said Sam Gandy, professor of neurology at the Icahn School of Medicine at Mount Sinai, New York and a co-author of the study. The study also suggested that the presence of the herpes viruses in the brain could influence or control the activity of various genes linked to an increased risk of Alzheimer's.

The scientists did not set out to look for a link between viruses and dementia. Instead they were hoping to pinpoint genes that were unusually active in the brains of people with the earliest stage of Alzheimer's. But when they studied brain tissue, comparing people with early-stage Alzheimer's and healthy controls, the most striking differences in gene activity were not found in human genes, but in genes belonging to two herpes virus strains, HHV6A and HHV7. And the abundance of the viruses correlated with clinical dementia scores of the donors.

An anonymous reader quotes a report from MIT Technology Review: While avoiding the worst dangers of climate change will likely require sucking carbon dioxide out of the sky, prominent scientists have long dismissed such technologies as far too expensive. But a detailed new analysis published today in the journal Joule finds that direct air capture may be practical after all. The study concludes it would cost between $94 and $232 per ton of captured carbon dioxide, if existing technologies were implemented on a commercial scale. One earlier estimate, published in Proceedings of the National Academies, put that figure at more than $1,000 (though the calculations were made on what's known as an avoided-cost basis, which would add about 10 percent to the new study's figures). Crucially, the lowest-cost design, optimized to produce and sell alternative fuels made from the captured carbon dioxide, could already be profitable with existing public policies in certain markets. The higher cost estimates are for plants that would deliver compressed carbon dioxide for permanent underground storage. David Keith, a Harvard physics professor and lead author of the paper, is also the founder of Carbon Engineering, "a Calgary-based startup that has spent the last nine years designing, refining, and testing a direct air capture pilot plant in Squamish, B.C.," reports MIT. "Carbon Engineering plans to combine the carbon captured at its plants with hydrogen to produce carbon-neutral synthetic fuels, a process the pilot facility has already been performing." The company has secured $30 million, but is seeking additional funds to build a larger facility that will begin selling fuels. CNBC notes that Carbon Engineering is owned by several private investors, including Bill Gates.

An anonymous reader quotes a report from The Guardian: Birds had to rediscover flight after the meteor strike that killed off the dinosaurs, scientists say. The cataclysm 66 million years ago not only wiped out Tyrannosaurus rex and ground-dwelling dinosaur species, but also flying birds, a detailed survey of the fossil record suggests. As forests burned around the world, the only birds to survive were flightless emu-like species that lived on the ground. The six to nine-mile-wide meteor struck the Earth off the coast of Mexico, releasing a million times more energy than the largest atomic bomb. Hot debris raining from the sky is thought to have triggered global wildfires immediately after the impact. It took hundreds or even thousands of years for the world's forests of palms and pines to recover. Fossil records from New Zealand, Japan, Europe and North America, all show evidence of mass deforestation. They also reveal that birds surviving the end of the Cretaceous period had long sturdy legs made for living on the ground. They resembled emus and kiwis, said the researchers whose findings are reported in the journal Current Biology.

An anonymous reader quotes a report from The Verge: Americans are saving energy because they don't go outside as much anymore, researchers say. It's a plus for the environment, though in another light (no pun intended), it's just sad. In 2012, Americans spent an extra eight days at home compared to 2003, according to the American Time Use Surveys. Being at home means using more energy by keeping the lights on and watching TV. But it also means less travel, and it means that fewer people are outside operating offices and stores. So overall in 2012, we saved 1,700 trillion British thermal units (BTU) of heat, or 1.8 percent of the national total, according to an analysis published today in the journal Joule. That's about how much energy Kentucky produced in all of 2015. Specifically in 2012, Americans spent one day less traveling and one week less in buildings other than their homes when compared to a decade earlier. The trend of staying indoors is especially strong for those ages 18 to 24: the youths spent 70 percent more time at home than the general population. At the other end of the age spectrum, those 65 and older were the only group that spent more time outside the home compared to 2003. Next, the researchers want to look at energy consumption changes in other countries as a result of lifestyle changes.

An anonymous reader quotes a report from Ars Technica: The twin long-tailed macaque monkeys are the first primates cloned using the same method that created the world's most famous sheep in 1996 -- a method called somatic cell nuclear transfer, or SCNT. The twins' genetic blueprints were swiped from fetal cells of another monkey. Researchers then popped the DNA into egg cells that they had also cleared of their DNA-containing nuclei. With a dash of compounds that spur embryo development, the reprogrammed cells developed into healthy baby monkeys in surrogate mother monkeys. The two were born about seven weeks ago in China and are developing normally so far, researchers reported Wednesday in the journal Cell. Though the overall SCNT method is the same as what was used for Dolly, researchers struggled for years to tweak it to work in primates. The procedure is delicate and required a lot of optimization -- not to mention DNA-swaps.

The researchers behind the cute clones, led by Zhen Liu of the Chinese Academy of Sciences, first tried using DNA from adult monkey cells. They created 192 embryos this way, implanting 181 of them into 42 surrogates, leading to 22 pregnant monkeys. But this resulted in the live birth of only two monkeys, both of which died within hours. Next, the researchers tried using DNA from fetal tissue. They created 109 embryos, implanted 79 of them into 21 surrogates, leading to pregnancy in six of them. Two female monkeys, Zhong Zhong and Hua Hua, resulted. The researchers attribute their success to new cell-imaging methods, tweaking the right mix of reprogramming compounds, and lots of practice.

A new study published in the journal Current Biology found that as much as 99 percent of baby green sea turtles in warm equatorial regions are being born female. "The study took a look at turtle populations at nesting sites at Raine Island and Moulter Cay in the northern Great Barrier Reef, an area plagued with unprecedented levels of coral bleaching from high temperatures," reports Futurism. "The researchers compared these populations with sea turtles living at sites in the cooler south." From the report: Using a new, non-invasive hormone test, the researchers from the U.S. National Oceanic and Atmospheric Administration (NOAA) Fisheries Department and the Queensland Department of Environment and Heritage Protection found that while 65 -69 percent of the turtles from the southern region were female, between 86.8 and 99.8 of turtles tested in the northern region were female, depending on age. The sex of green sea turtles, along with some other species of turtles, crocodiles, and alligators, is not regulated by the introduction of sex chromosomes at key points during early development, as seen in humans and other mammals. Their sex is actually influenced by the temperature at which the eggs are incubated, with warmer temperatures more likely to lead to females. The difference between predominately male and predominately female hatchlings is only a few degrees, such as that formerly found between the cool, damp bottom of a sandy sea turtle nest and the sun-warmed top. The ages of the female turtles in the north suggest that this population has experienced temperatures that cause this imbalance since at least the 1990s. Given that the warmer temperatures seen in northern Australia have been distributed around the globe, experts predict that other sea turtle populations in warm regions are also following the same trend.

schwit1 shares a report from ScienceAlert: It's crazy to think that we still don't quite understand the mechanism behind one of the most common medical interventions -- general anaesthetic. But researchers in Australia just got a step closer by discovering that one of the most commonly used anesthetic drugs doesn't just put us to sleep; it also disrupts communication between brain cells. The team investigated the drug propofol, a super-popular option for surgeries worldwide. A potent sedative, the drug is thought to put us to sleep through its effect on the GABA neurotransmitter system, the main regulator of our sleep-and-wake cycles in the brain. But anyone who's been "put under" will know that waking up from a general anesthetic feels rather different from your usual morning grogginess. On top of that, some people can experience serious side-effects, so scientists have been trying to figure out what else the drugs might be doing in the brain.

Using live neuron cell samples from rats and fruit flies, the researchers were able to track neurotransmitter activity thanks to a super-resolution microscope, and discovered that propofol messes with a key protein that nerve cells use to communicate with each other. This protein, called syntaxin1A, isn't just found in animal models - people have it, too. And it looks like the anesthetic drug puts the brakes on this protein, making otherwise normal brain cell connections sluggish, at least for a while. The researchers think this disruption could be key to how propofol allows for pain-free surgery to take place - first it knocks us out as a normal sleeping pill would, and then takes things up a notch by disrupting brain connectivity. The research has been published in Cell Reports.

An anonymous reader quotes a report from NPR: Older brains may forget more because they lose their rhythm at night. During deep sleep, older people have less coordination between two brain waves that are important to saving new memories, a team reports in the journal Neuron. The finding appears to answer a long-standing question about how aging can affect memory even in people who do not have Alzheimer's or some other brain disease. The study was the result of an effort to understand how the sleeping brain turns short-term memories into memories that can last a lifetime, says Matt Walker, the author of the book Why We Sleep. "What is it about sleep that seems to perform this elegant trick of cementing new facts into the neural architecture of the brain?" To find out, Walker and a team of scientists had 20 young adults learn 120 pairs of words. "Then we put electrodes on their head and we had them sleep," he says. The electrodes let researchers monitor the electrical waves produced by the brain during deep sleep. They focused on the interaction between slow waves, which occur every second or so, and faster waves called sleep spindles, which occur more than 12 times a second. The next morning the volunteers took a test to see how many word pairs they could still remember. And it turned out their performance was determined by how well their slow waves and spindles had synchronized during deep sleep.

Next, the team repeated the experiment with 32 people in their 60s and 70s. Their brain waves were less synchronized during deep sleep. They also remembered fewer word pairs the next morning. And, just like with young people, performance on the memory test was determined by how well their brain waves kept the beat, says Randolph Helfrich, an author of the new study and a postdoctoral fellow at UC Berkeley. The team also found a likely reason for the lack of coordination associated with aging: atrophy of an area of the brain involved in producing deep sleep. People with more atrophy had less rhythm in the brain, Walker says.

An anonymous reader shares a post from Scientific American, written by Bernardo Kastrup: An article on the neuroscience of infant consciousness, which attracted some interest a few years ago, asked: "When does your baby become conscious?" The premise, of course, was that babies aren't born conscious but, instead, develop consciousness at some point. Yet, it is hard to think that there is nothing it feels like to be a newborn. Newborns clearly seem to experience their own bodies, environment, the presence of their parents, etcetera -- albeit in an unreflective, present-oriented manner. And if it always feels like something to be a baby, then babies don't become conscious. Instead, they are conscious from the get-go. The problem is that, somewhat alarmingly, the word "consciousness" is often used in the literature as if it entailed or implied more than just the qualities of experience. Dijksterhuis and Nordgren, for instance, insisted that "it is very important to realize that attention is the key to distinguish between unconscious thought and conscious thought. Conscious thought is thought with attention." This implies that if a thought escapes attention, then it is unconscious.

Indeed, Jonathan Schooler has established a clear distinction between conscious and meta-conscious processes. Whereas both types entail the qualities of experience, meta-conscious processes also entail what he called re-representation. "Periodically attention is directed towards explicitly assessing the contents of experience. The resulting meta-consciousness involves an explicit re-representation of consciousness in which one interprets, describes or otherwise characterizes the state of one's mind.

Lithium-ion batteries that are resistant to exploding or catching fire have been developed by scientists. From a report: The devices produced sufficient energy for use in household electronics, but did not ignite -- even when punctured repeatedly with a nail. The batteries use a water-salt solution as their electrolyte, removing the risks carried by some non-aqueous commercial models. The research is published in the journal Joule. "In the past, if you wanted high energy, you would choose a non-aqueous lithium-ion battery, but you would have to compromise on safety. If you preferred safety, you could use an aqueous battery such as nickel/metal hydride, but you would have to settle for lower energy," said co-author Kang Xu, from the US Army Research Laboratory (ARL). "Now, we are showing that you can simultaneously have access to both high energy and high safety."

A new study unpicks why certain sounds can stir alarming memories, and reveals a new approach to wiping such memories from the brain. The Guardian reports: Published in the journal Neuron by Cho and his colleague Woong Bin Kim, the research reveals how the team used genetically modified mice to examine the pathways between the area of the brain involved in processing a particular sound and the area involved in emotional memories, known as the amygdala. In the first part of the experiment the team played both a high pitched and low-pitched tone to mice. But, when the high-pitched sound was played, the researchers also gave the mice a small electric shock to their feet. When the high-pitched tone was subsequently played on its own, the mice froze in fear; no such response was seen when the alternative, low-pitched, tone was played. The team then looked to see if there were differences between the high-pitch and low-pitch tone pathways in the brains of the mice, revealing that, among the mice exposed electric shocks, the connections within the "high-pitched" pathway had become stronger, while the other pathway remained unchanged. The team found that when mice were subsequently repeatedly exposed to high-pitched sounds without the shocks they lost their fear -- a process known as fear extinction.

But the team discovered that using a technique called optogenetics, it was possible to truly erase the unpleasant memories. This technique involved the researchers using a virus to introduce genes into particular neurons in the brains of the mice that were involved in the "high-pitch" pathways. Once inside the cells, the genes result in the production of proteins which respond to light, allowing researchers to control the activity of the neurons. Taking mice with the fearful memories, the team exposed the neurons involved in the "high-pitch" pathway to low-frequency light -- an approach which weakens the connections between the neurons. The upshot was that the mice no longer appeared fearful when they heard the high-pitched tone.

An anonymous reader shares an article: Geneticists are now using technology to isolate the precise genes responsible for excessive branching and flowering, characteristics which lead to less fruit and thus less yield for farmers. In a study published in the journal Cell last week, geneticist Zachary Lippman of Cold Spring Harbor Laboratory explains his research team's efforts to fix mutated tomatoes using CRISPR gene editing technology. By identifying the genes associated with undesired mutations, Lippman was able to edit them and suppress their effects. After playing with the plant architecture, Lippman's team was ultimately able to engineer highly productive plants that yielded more of the desired fruit and less of the unwanted flowers and branches. Original research paper; further reading on Nature magazine.

An anonymous reader quotes a report from Science Daily: Salk Institute scientists, building on earlier work that identified a gene pathway triggered by running, have discovered how to fully activate that pathway in sedentary mice with a chemical compound, mimicking the beneficial effects of exercise, including increased fat burning and stamina. The study, which appears in Cell Metabolism on May 2, 2017, not only deepens our understanding of aerobic endurance, but also offers people with heart conditions, pulmonary disease, type 2 diabetes or other health limitations the hope of achieving those benefits pharmacologically. Previous work by the Evans lab into a gene called PPAR delta (PPARD) offered intriguing clues: mice genetically engineered to have permanently activated PPARD became long-distance runners who were resistant to weight gain and highly responsive to insulin -- all qualities associated with physical fitness. The team found that a chemical compound called GW1516 (GW) similarly activated PPARD, replicating the weight control and insulin responsiveness in normal mice that had been seen in the engineered ones. However, GW did not affect endurance (how long the mice could run) unless coupled with daily exercise, which defeated the purpose of using it to replace exercise. In the current study, the Salk team gave normal mice a higher dose of GW, for a longer period of time (8 weeks instead of 4). Both the mice that received the compound and mice that did not were typically sedentary, but all were subjected to treadmill tests to see how long they could run until exhausted. Mice in the control group could run about 160 minutes before exhaustion. Mice on the drug, however, could run about 270 minutes -- about 70 percent longer. For both groups, exhaustion set in when blood sugar (glucose) dropped to around 70 mg/dl, suggesting that low glucose levels (hypoglycemia) are responsible for fatigue.

An anonymous reader shares an excerpt from a Science Magazine report: Even if you aren't elderly, your body is home to agents of senility -- frail and damaged cells that age us and promote disease. Now, researchers have developed a molecule that selectively destroys these so-called senescent cells. The compound makes old mice act and appear more youthful, providing hope that it may do the same for us. As we get older, senescent cells build up in our tissues, where researchers think they contribute to illnesses such as heart disease, arthritis, and diabetes. In the past, scientists have genetically modified mice to dispatch their senescent cells, allowing the rodents to live longer and reducing plaque buildup in their arteries. Such genetic alterations aren't practical for people, but researchers have reported at least seven compounds, known as senolytics, that kill senescent cells. A clinical trial is testing two of the drugs in patients with kidney disease, and other trials are in the works. However, current senolytic compounds, many of which are cancer drugs, come with downsides. They can kill healthy cells or trigger side effects such as a drop in the number of platelets, the cellular chunks that help our blood clot. Cell biologist Peter de Keizer of Erasmus University Medical Center in Rotterdam, the Netherlands, and colleagues were investigating how senescent cells stay alive when they uncovered a different strategy for attacking them. Senescent cells carry the type of DNA damage that should spur a protective protein, called p53, to put them down. Instead, the researchers found that a different protein, FOXO4, latches onto p53 and prevents it from doing its duty. To counteract this effect, De Keizer and colleagues designed a molecule, known as a peptide, that carries a shortened version of the segment of FOXO4 that attaches to p53. In a petri dish, this peptide prevented FOXO4 and p53 from hooking up, prompting senescent cells to commit suicide. But it spared healthy cells. The researchers then injected the molecule into mutant mice that age rapidly. These rodents live about half as long as normal mice, and when they are only a few months old, their fur starts to fall out, their kidneys begin to falter, and they become sluggish. However, the peptide boosted the density of their fur, reversed the kidney damage, and increased the amount of time they could scurry in a running wheel, the scientists report online today in Cell. When the researchers tested the molecule in normal, elderly mice, they saw a similar picture: In addition to helping their kidneys and fur, the molecule also increased their willingness to explore their surroundings.

An anonymous reader quotes a report from The Guardian: After spending six weeks cultivating an internal "memory palace," people more than doubled the number of words they could retain in a short time period and their performance remained impressive four months later. The technique, which involves conjuring up vivid images of objects in a familiar setting, is credited to the Greek poet Simonides of Ceos, and is a favored method among so-called memory athletes. The study also revealed that after just 40 days of training, people's brain activity shifted to more closely resemble that seen in some of the world's highest ranked memory champions, suggesting that memory training can alter the brain's wiring in subtle but powerful ways. The study, published in the journal Neuron, recruited 23 of the 50 top-scoring memory athletes in an annual contest called the World Memory Championships. The athletes were given 20 minutes to recall a list of 72 random nouns and they scored, on average, nearly 71 of the 72 words. By contrast, an untrained control group recalled an average of 26 words. This group then followed a daily 30-minute training regime where they practiced walking through a chosen familiar environment, such as their own home, and placing objects in specific locations. After 40 days of 30-minute training sessions, the participants who had average memory skills at the start more than doubled their memory capacity, recalling 62 words on average -- and four months later, without continued training, they could remember 48 words from a list of 72.

According to a new study published in the journal Cell, a certain type of fasting diet can trigger the pancreas to regenerate itself. Of course, the researchers advise people not to try this without medical advice. BBC reports: In the experiments, mice were put on a modified form of the "fasting-mimicking diet." It is like the human form of the diet when people spend five days on a low calorie, low protein, low carbohydrate but high unsaturated-fat diet. It resembles a vegan diet with nuts and soups, but with around 800 to 1,100 calories a day. Then they have 25 days eating what they want -- so overall it mimics periods of feast and famine. Previous research has suggested it can slow the pace of aging. But animal experiments showed the diet regenerated a special type of cell in the pancreas called a beta cell. These are the cells that detect sugar in the blood and release the hormone insulin if it gets too high. There were benefits in both type 1 and type 2 diabetes in the mouse experiments. Type 1 is caused by the immune system destroying beta cells and type 2 is largely caused by lifestyle and the body no longer responding to insulin. Further tests on tissue samples from people with type 1 diabetes produced similar effects.

An anonymous reader writes: An engineer in Japan has built a 1.6-inch "pollinator-bot" and successfully tested it in his lab. The drone's creator "has armed it with paintbrush hairs that are covered in a special gel sticky enough to pick pollen up, but not so sticky that it holds on to that pollen when it brushes up against something else," reports The Economist. They write that his experiments with the tiny drone "show that the drone can indeed carry pollen from flower to flower in the way an insect would -- though he has yet to confirm that seeds result from this pollination." While flown by a human pilot, next he hopes to equip the drones with their own flower-recognizing technology.

The Christian Science Monitor followed up with four experts, asking "Could a fleet of robo-pollinators replace, or at least supplement, the bees?" One said "There is no substitute for bees." Another pointed out that even if robo-bees are developed, some flowers will prove harder to pollinate than others. A third expert thought the technology could scale, though it would need to be mass-produced, and the engineers would need to develop a reusable pollen-collecting gel. But a fourth expert remained worried that it just couldn't scale without becoming too expensive. "I'm not sure that's going to be cheap enough to not make blueberries hundreds of dollars a pint."
Three of those experts also agreed that the best solution is just wild bees, because domesticated or not, "All they have to do is make sure to set aside enough land conducive to the bees' habitat."

An anonymous reader quotes a report from BBC: Why some people become enraged by sounds such as eating or breathing has been explained by brain scan studies. The condition, misophonia, is far more than simply disliking noises such as nails being scraped down a blackboard. UK scientists have shown some people's brains become hardwired to produce an "excessive" emotional response. Olana developed the condition when she was eight years old. Her trigger sounds include breathing, eating and rustling noises. Scientists, including Olana, at multiple centers in the UK scanned the brains of 20 misophonic people and 22 people without the condition. They were played a range of noises while they were in the MRI machine, including: neutral sounds such as rain; generally unpleasant sounds such as screaming; people's trigger sounds. The results, published in the journal Current Biology, revealed the part of the brain that joins our senses with our emotions -- the anterior insular cortex -- was overly active in misophonia. And it was wired up and connected to other parts of the brain differently in those with misophonia. Dr Sukhbinder Kumar, from Newcastle University, told BBC News: "They are going into overdrive when they hear these sounds, but the activity was specific to the trigger sounds not the other two sounds. The reaction is anger mostly, it's not disgust, the dominating emotion is the anger -- it looks like a normal response, but then it is going into overdrive." There are no treatments, but Olana has developed coping mechanisms such as using ear plugs. It is still not clear how common the disorder is, as there is no clear way of diagnosing it and it was only recently discovered. Ultimately, the researchers hope, understanding the difference in the misophonic brain will lead to new treatments. One idea is that low levels of targeted electricity passed through the skull, which is known to adjust brain function, could help.

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.

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.

New submitter baalcat writes: A new study reported by Neuroscience News sheds light on how we learn to pay attention in order to make the most of our life experiences. From the report: "The Wizard of Oz told Dorothy to 'pay no attention to that man behind the curtain' in an effort to distract her, but a new Princeton University study sheds light on how people learn and make decisions in real-world situations. The findings could eventually contribute to improved teaching and learning and the treatment of mental and addiction disorders in which people's perspectives are dysfunctional or fractured. Participants in the study performed a multidimensional trial-and-error learning task, while researchers scanned their brains using functional magnetic resonance imaging (fMRI). The researchers found that selective attention is used to determine the value of different options. The results also showed that selective attention shapes what we learn when something unexpected happens. For example, if your pizza is better or worse than expected, you attribute the learning to whatever your attention was focused on and not to features you decided to ignore. Finally, the researchers found that what we learn through this process teaches us what to pay attention to, creating a feedback cycle -- we learn about what we attend to, and we attend to what we learned high values for. 'If we want to understand learning, we can't ignore the fact that learning is almost always done in a multidimensional 'cluttered' environment,' says senior author Yael Niv, an associate professor in psychology and the Princeton Neuroscience Institute. 'We want kids to listen to the teacher, but a lot is going on in the classroom -- there is so much to look at inside it and out the window. So, it's important to understand how exactly attention and learning interact and how they shape each other.'" The study has been published in the journal Neuron.

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.

"The human brain reaches its adult volume by age 10, but the neurons that make it up continue to change for years after that," reports the New York Times, citing a new paper by neuroscience researchers that questions when "adulthood" really begins. An anonymous reader writes: One of the paper's authors -- an associate psychology professor at Harvard -- tells CNN that "There is no agreed-on benchmark that, when reached, would allow a neuroscientist to say 'Aha! This brain is fully developed'. However, it is safe to say that by almost any metric, the brain is continuing to develop actively well past the age of 18..."

"Some children, researchers have found, have neural networks that look as if they belong to an adult..." adds the Times, noting that adolescents also "do about as well as adults on cognition tests, for instance. But if they're feeling strong emotions, those scores can plummet. The problem seems to be that teenagers have not yet developed a strong brain system that keeps emotions under control."
And this cuts both ways, according to a psychologist at Temple University who wants the voting age lowered to 16. ("Sixteen-year-olds are just as good at logical reasoning as older people are," he tells the Times) But he also believes judges should consider the lack of emotional control when sentencing defendants -- even if they're in their early 20s. "Most crime situations that young people are involved in are emotionally arousing situations -- they're scared, or they're angry, intoxicated or whatever."

New submitter TheNinjaCoder writes: A new type of gene therapy is showing promise in reversing the aging process. The scientists are not claiming that aging can be eliminated, but say that in the foreseeable future treatments designed to slow the process could increase life expectancy. The Guardian explains the scientists' experiment in its report: "The rejuvenating treatment given to the mice was based on a technique that has previously been used to 'rewind' adult cells, such as skin cells, back into powerful stem cells, very similar to those seen in embryos. These so-called induced pluripotent stem (iPS) cells have the ability to multiply and turn into any cell type in the body and are already being tested in trials designed to provide 'spare parts' for patients. The treatment involved intermittently switching on the same four genes that are used to turn skin cells into iPS cells. The mice were genetically engineered in such a way that the four genes could be artificially switched on when the mice were exposed to a chemical in their drinking water. The scientists tested the treatment in mice with a genetic disorder, called progeria, which is linked to accelerated aging, DNA damage, organ dysfunction and dramatically shortened lifespan. After six weeks of treatment, the mice looked visibly younger, skin and muscle tone improved and they lived 30% longer. When the same genes were targeted in cells, DNA damage was reduced and the function of the cellular batteries, called the mitochondria, improved. Crucially, the mice did not have an increased cancer risk, suggesting that the treatment had successfully rewound cells without turning them all the way back into stem cells, which can proliferate uncontrollably in the body." The study has been published in the journal Cell.

Slashdot reader sciencehabit quotes Science magazine: Imagine spending your whole life seeing the world in black and white, and then seeing a vase of roses in full color for the first time. That's kind of what it was like for the scientists who have taken the first multicolor images of cells using an electron microscope. Electron microscopes can magnify an object up to 10 million times, allowing researchers to peer into the inner workings of, say, a cell or a fly's eye, but until now they've only been able to see in black and white. The new advance -- 15 years in the making -- uses three different kinds of rare earth metals called lanthanides...layered one-by-one over cells on a microscope slide. The microscope detects when each metal loses electrons and records each unique loss as an artificial color.

An anonymous reader quotes a report from NPR: The teenage brain has been characterized as a risk-taking machine, looking for quick rewards and thrills instead of acting responsibly. But these behaviors could actually make teens better than adults at certain kinds of learning. "In neuroscience, we tend to think that if healthy brains act in a certain way, there should be a reason for it," says Juliet Davidow, a postdoctoral researcher at Harvard University in the Affective Neuroscience and Development Lab and the lead author of the study, which was published Wednesday in the journal Neuron. But scientists and the public often focus on the negatives of teen behavior, so she and her colleagues set out to test the hypothesis that teenagers' drive for rewards, and the risk-taking that comes from it, exist for a reason. When it comes to what drives reward-seeking in teens, fingers have always been pointed at the striatum, a lobster-claw-shape structure in the brain. When something surprising and good happens -- say, you find $20 on the street -- your body produces the pleasure-related hormone dopamine, and the striatum responds. But the striatum isn't just involved in reward-seeking. It's also involved in learning from rewards, explains Daphna Shohamy, a cognitive neuroscientist at the Zuckerman Mind Brain Behavior Institute at Columbia University who worked on the study. She wanted to see if teenagers would be better at this type of learning than adults would. To test this, Shohamy and her colleagues used an fMRI scanner to watch brain activity in a group of adults and teenagers. They were looking at the striatum, but also in a different part of the brain called the hippocampus. The hippocampus (which looks like, and is named after, a seahorse) helps people remember things like dates and times: the who, what, when and where. As the adults and teens had their brains scanned, they played a game that rewarded players for guessing correctly. Between questions, participants saw random pictures of neutral objects. As expected, the reward-hungry teenagers figured out the game faster than the adults did. Surprisingly, the striatum was equally active in both teenagers and adults. But in teens, it also worked closely with their hippocampus.

An anonymous reader quotes a report from Live Science: Wilderness areas around the world have experienced catastrophic declines over the last two decades, with one-tenth of global wilderness lost since the 1990s, according to a new study. Since 1993, researchers found that a cumulative wilderness area twice the size of Alaska and half the size of the Amazon has been stripped and destroyed. The shrinking wilderness is due, in part, to human activity such as mining, logging, agriculture, and oil and gas exploration. The researchers said their findings underscore the need for international policies to recognize the value of wilderness and to protect wilderness areas from the threats they face. Central Africa and the Amazon saw the most wilderness decline, the researchers found. Of the roughly 1.27 million square miles (3.3 million square kilometers) of global wilderness lost, the Amazon accounted for nearly one-third, and 14 percent of the world's wilderness was lost from Central Africa, according to the study. The researchers determined that only 11.6 million square miles (30.1 million square km) of wilderness is left, which equates to just 20 percent of the Earth's total land mass. The study was published online in the journal Current Biology.

An anonymous reader writes: Scientists have found a eukaryote microbe that completely lacks mitochondria, which are the powerhouses inside eukaryotic cells, the type of cells that make up humans, animals, plants and fungi. All eukaryotic cells contain a nucleus, organelles and mitochondrion. Scientists believe they were once free-living bacteria that got engulfed by primitive, ancient cells that were evolving to become what they are today. Anna Karnkowska, a researcher in evolutionary biology at the University of British Columbia in Vancouver, found a gut microbe that contains no trace that it made any mitochondrial proteins at all. "That should theoretically kill the cell -- it shouldn't exist," she said. The researchers learned that these cells use a kind of machinery that is different than relying on mitochondria to assemble iron-sulfur clusters, which is thought to be a mitochondrial function. Michael Gray, biochemist at Dalhousie University in Halifax, Nova Scotia, calls the discovery of a eukaryote without any vestige of mitochondrion, "unprecedented." He adds, the results do not negate the idea that the acquisition of a mitochondrion was an important and perhaps defining event in the evolution of eukaryotic cells, because this organism's ancestors had mitochondria that were then lost after the cells acquired their non-mitochondrial system for making iron-sulfur clusters.

HughPickens.com writes: A common urban myth is that many fathers are cuckolded into raising children that genetically are not their own -- a fear fueled by the paternity tests that have become a standard staple of gossip magazines, talk shows, and TV series. Now, Carl Zimmer reports at the New York Times that our obsession with cuckolded fathers is seriously overblown as a number of recent genetic studies have challenged the notion that mistaken paternity is commonplace. It wasn't until DNA sequencing emerged in the 1990s that paternity tests earned the legal system's confidence. Labs were able to compare DNA markers in children to those of their purported fathers to see if they matched. As the lab tests piled up, researchers collated the results and came to a startling conclusion: 10 percent to 30 percent of the tested men were not the biological fathers of their children. There's only one problem with these previous studies: the results didn't come from a random sample of people. The people who ordered the tests already had reason to doubt paternity.

In a 2013 study, Dr. Maarten H.D. Larmuseau used Belgium's detailed birth records to reconstruct large family genealogies reaching back four centuries. Then the scientists tracked down living male descendants and asked to sequence their Y chromosomes. Y chromosomes are passed down in almost identical form from fathers to sons. Men who are related to the same male ancestor should also share his Y chromosome, providing that some unknown father didn't introduce his own Y [chromosome] somewhere along the way. Comparing the chromosomes of living related men, Larmuseau came up with a cuckoldry rate of less than 1 percent. Similar studies have generally produced the same low results in such countries as Spain, Italy and Germany, as well as agricultural villages in Mali. "The observed low EPP rates challenge the idea that women routinely 'shop around' for good genes by engaging in extra-pair copulations," concludes Larmuseau . "The (potential) genetic benefits of extra-pair children are unlikely to be offset by the (potential) costs of being caught, particularly in such a long-lived species as humans with heavy offspring dependence and massive parental investment."

schwit1 writes: A newly published study from Harvard biologists [here's a link to the paywalled paper's summary] shows how neurons can be dramatically changed from one type into another from within the brain and how neighboring neurons recognize the reprogrammed cells as different and adapt by changing how they communicate with them. Building on earlier work in which they disproved neurobiology dogma by "reprogramming" neurons — turning one form of neuron into another — in the brains of living animals, Harvard Stem Cell Institute researchers have now shown that the networks of communication among reprogrammed neurons and their neighbors can also be changed, or "rewired."

New submitter physick writes: The Blue Brain project at EPFL, Switzerland today published the results of more than 10 years work in reconstructing a cellular model of a piece of the somatosensory cortex of a juvenile rat. The paper in Cell describes the process of painstakingly assembling tens of thousands of digital neurons, establishing the location of their synapses, and simulating the resulting neocortical microcircuit on an IBM Blue Gene supercomputer. “This is a first draft reconstruction of a piece of neocortex and it’s beautiful,” said Henry Markram, director of the Blue Brain Project at the Swiss Federal Institute of Technology in Lausanne. “It’s like a fundamental building block of the brain.”

sciencehabit sends news that two commonly-prescribed drugs have been shown to influence how the human brain makes moral decisions. Citalopram is an SSRI used to treat depression, and levodopa is often used to combat Parkinson's disease. A new study (abstract) asked subjects to set a monetary value on receiving painful electric shocks — for themselves and for others (e.g. "Would you rather endure seven shocks to earn $10 or 10 shocks to earn $15?"). The study found that subjects on citalopram (which affects serotonin levels) were willing to give up more money to reduce shocks, both for themselves and others. Those on levodopa (which affects dopamine levels) made people just as willing to shock others as they were to shock themselves, when those on a placebo tended to be more reluctant to shock others. [Neuroscientist Molly] Crockett says those effects could suggests multiple underlying mechanisms. For example, excess dopamine might make our brain's reward system more responsive to the prospect of avoiding personal harm. Or it could tamp down our sense of uncertainty about what another person is experiencing, making us less hesitant to dole out pain. Serotonin, meanwhile, appeared to have a more general effect on aversion to harm, not just a heightened concern for another person. Such knowledge could eventually develop drugs that address disorders of social behavior, she says.

An anonymous reader writes: The first known virgin births in smalltooth sawfish have been documented in the wild. Researchers from the Florida Fish and Wildlife Conservation Commission used DNA to show that three percent of a Florida sawfish population was created by female-only reproduction. Dr Warren Booth, an evolutionary biologist at the University of Tulsa, who previously discovered an instance of parthenogenesis in snakes, said: "This is basically a very extreme form of inbreeding. Most people think of inbreeding as bad, but it could be helpful in purging deleterious mutations from a population." The findings were published in the journal Current Biology.

BarbaraHudson writes: CBC reports that Canadian scientists are turning blood into nerve cells. They do so by manipulating stem cells that have been taken from a patient's blood, eventually switching them into neural stem cells (abstract). These can then give rise to multiple different nerve cells suitable for use in the rest of the body. Team leader Mick Bhatia said, "We can actually take a patient's blood sample, as routinely performed in a doctor's office, and with it we can produce one million sensory neurons. We can also make central nervous system cells." They're working on turning the neural stem cells into motor neurons for treatment of diseases like Parkinson's and Alzheimer's.