100 Evolution News Articles
for September 2017
Click on the links below to get the full story from its source
9-23-17 Growing up
Growing up, after a study revealed that today’s teens are taking longer to embrace traditional symbols of adulthood, including getting a driver’s license, drinking, and dating. “The whole developmental pathway has slowed down,” said study author Jean Twenge.
9-23-17 4 crucial facts that prove biology doesn't cause inequality
4 crucial facts that prove biology doesn't cause inequality
In America, we've had a long history of people in positions of privilege and power who argue that innate biological differences between races or sexes explain why our society is unequal. Such people couch these arguments in the language of unflinching rationalism — they are merely acknowledging facts about human nature, facts they say may be uncomfortable, but which are firmly grounded in scientific evidence. Until our society is willing to accept the evidence, the argument goes, we won't effectively address the problem of inequality. "Once we acknowledge that not all differences are socially constructed or due to discrimination, we open our eyes to a more accurate view of the human condition which is necessary if we actually want to solve problems," wrote James Damore in his now-infamous Google memo, in which he argued that women are biologically less suitable for certain jobs in technology. Those who make these arguments are trying to claim scientific high ground, but their assertions are the product of speculation and confusion about core biological concepts. Since at least the early 20th century, scientists have tried to knock down these flawed arguments, but clearly many people still believe in the inherent biological superiority of whites or men or both. In our current political moment, these beliefs have come to the foreground, as white supremacists openly talk about their genetic superiority with reporters from national magazines, and march through the streets of American cities carrying the symbols of racist regimes, chanting that "Jews will not replace us." It is thus important to review why claims that biology contributes to racial and gender inequality are so often wrong. Here are four key facts about biology, sex, and race to keep in mind when you hear someone argue that biology explains why women or racial minorities don't enjoy the same pay, careers, or education as white men:
- Most genetic differences among humans don't break along racial or sex lines.
- Human populations have always been fluid.
- Showing that genetics affects a trait doesn't prove that racial differences are genetic.
- Culture has enormous effects on social outcomes.
(Webmaster's comment: All human beings must be treated equality and have the same rights simply because they are all human beings. No Exceptions Regardless of Genetics or Biology!)
9-22-17 Telling children they’re smart could tempt them to cheat
Telling children they’re smart could tempt them to cheat
Praising preschoolers for their smarts can backfire. Two studies show these children were more likely to cheat than kids who didn’t have a reputation to uphold. It’s hard not to compliment kids on certain things. When my little girls fancy themselves up in tutus, which is every single time we leave the house, people tell them how pretty they are. I know these folks’ intentions are good, but an abundance of compliments on clothes and looks sends messages I’d rather my girls didn’t absorb at ages 2 and 4. Or ever, for that matter. Our words, often spoken casually and without much thought, can have a big influence on little kids’ views of themselves and their behaviors. That’s very clear from two new studies on children who were praised for being smart. The studies, conducted in China on children ages 3 and 5, suggest that directly telling kids they’re smart, or that other people think they’re intelligent, makes them more likely to cheat to win a game.
9-22-17 New Zealand’s iconic kiwi birds may be losing their sight
New Zealand’s iconic kiwi birds may be losing their sight
Three Okarito brown kiwis living wild in New Zealand are completely blind but in good physical condition, suggesting the species is evolving to lose its sight. Not all birds need to see. Blind but perfectly healthy kiwis have been found living in New Zealand. The flightless nocturnal birds may be evolving to lose their eyesight altogether, suggest the researchers. The blind kiwis seem able to survive just as well using other senses such as touch, smell and hearing, so maintaining good eyesight might be a waste of energy. The blind birds were discovered during a study of 160 Okarito brown kiwis (Apteryx rowi) found in the Okarito forest on New Zealand’s South Island. “We found a very high prevalence of birds with eye lesions,” says Alan Tennyson at the Museum of New Zealand Te Papa Tongarewa in Wellington. “A third of them had eye problems.” But the biggest surprise was chancing upon three sightless birds. “The finding of completely blind birds in good physical condition was absolutely stunning,” says team member Christopher Murphy at the University of California, Davis. “No other birds are known to have a free-living population of blind [individuals],” says Tennyson. But plenty of other animals, such as moles and cave-dwelling fish, have evolved blindness. “Vision is not essential for survival in all animals.” The discovery could help explain how species lose their sense of sight, a process called regressive evolution.
9-22-17 The way poison frogs keep from poisoning themselves is complicated
The way poison frogs keep from poisoning themselves is complicated
Genetic change that protects from a toxin can cause ripple effects. The potent toxin epibatidine was first discovered in 1974, when it was isolated from the skin of the phantasmal poison frog, Epipedobates anthonyi. For some poison dart frogs, gaining resistance to one of their own toxins came with a price. The genetic change that gives one group of frogs immunity to a particularly lethal toxin also disrupts a key chemical messenger in the brain. But the frogs have managed to sidestep the potentially damaging side effect through other genetic tweaks, researchers report in the Sept. 22 Science. While other studies have identified genetic changes that give frogs resistance to particular toxins, this study “lets you look under the hood” to see the full effects of those changes and how the frogs are compensating, says Butch Brodie, an evolutionary biologist at the University of Virginia in Charlottesville who wasn’t involved in the research. Many poison dart frogs carry cocktails of toxic alkaloid molecules in their skin as a defense against predators (SN Online: 3/24/14). These toxins, picked up through the frogs’ diets, vary by species. Here, researchers studied frogs that carry epibatidine, a substance so poisonous that just a few millionths of a gram can kill a mouse.
9-22-17 New antibody attacks 99% of HIV strains
New antibody attacks 99% of HIV strains
Scientists have engineered an antibody that attacks 99% of HIV strains and can prevent infection in primates. It is built to attack three critical parts of the virus - making it harder for HIV to resist its effects. The work is a collaboration between the US National Institutes of Health and the pharmaceutical company Sanofi. The International Aids Society said it was an "exciting breakthrough". Human trials will start in 2018 to see if it can prevent or treat infection. Our bodies struggle to fight HIV because of the virus' incredible ability to mutate and change its appearance. These varieties of HIV - or strains - in a single patient are comparable to those of influenza during a worldwide flu season. So the immune system finds itself in a fight against an insurmountable number of strains of HIV.
9-22-17 Yoga’s brain boost
Yoga’s brain boost
Yoga and meditation are becoming increasingly mainstream activities in the U.S., and new research helps explain why. Daily sessions of either practice can have dramatic effects on brain function. Scientists asked 31 healthy people to engage in 25 minutes of hatha yoga, mindfulness meditation, and quiet reading in random order. Mental tasks completed before and after each session found that yoga and meditation led to greater improvements in the participants’ energy level, mood, executive function, and ability to control thoughts and emotions. “Hatha yoga and mindfulness meditation both focus the brain’s conscious processing power on a limited number of targets, like breathing and posing, and also reduce processing of nonessential information,” the study’s co-author, Peter Hall, tells ScienceDaily.com. That mental training, he said, apparently enables people “to focus more easily on what they choose to attend to in everyday life.”
9-22-17 Gene variant linked to Alzheimer’s disease is a triple threat
Gene variant linked to Alzheimer’s disease is a triple threat
APOE4 spurs brain plaques, tau tangles and inflammation. A genetic risk factor for Alzheimer’s disease is a double, make that triple, whammy. In addition to speeding up the development of brain plaques associated with Alzheimer’s, a gene variant known as APOE4 also makes tau tangles — another signature of the disease — worse, researchers report online September 20 in Nature. APOE4 protein also ramps up brain inflammation that kills brain cells, neuroscientist David Holtzman of Washington University School of Medicine in St. Louis and colleagues have discovered. “This paper is a tour de force,” says Robert Vassar, a neuroscientist at Northwestern University Feinberg School of Medicine in Chicago. “It’s a seminal study that’s going to be a landmark in the field” of Alzheimer’s research, Vassar predicts. For more than 20 years, researchers have known that people who carry the E4 version of the APOE gene are at increased risk of developing Alzheimer’s. A version of the gene called APOE3 has no effect on Alzheimer’s risk, whereas the APOE2 version protects against the disease. Molecular details for how APOE protein, which helps clear cholesterol from the body, affects brain cells are not understood. But Holtzman and other researchers previously demonstrated that plaques of amyloid-beta protein build up faster in the brains of APOE4 carriers (SN: 7/30/11, p. 9). Having A-beta plaques isn’t enough to cause the disease, Holtzman says. Tangles of another protein called tau are also required. Once tau tangles accumulate, brain cells begin to die and people develop dementia. In a series of new experiments, Holtzman and colleagues now show, for the first time, that there’s also a link between APOE4 and tau tangles.
9-22-17 Alarm as 'super malaria' spreads in South East Asia
Alarm as 'super malaria' spreads in South East Asia
The rapid spread of "super malaria" in South East Asia is an alarming global threat, scientists are warning. This dangerous form of the malaria parasite cannot be killed with the main anti-malaria drugs. It emerged in Cambodia but has since spread through parts of Thailand, Laos and has arrived in southern Vietnam. The team at the Oxford Tropical Medicine Research Unit in Bangkok said there was a real danger of malaria becoming untreatable. Prof Arjen Dondorp, the head of the unit, told the BBC News website: "We think it is a serious threat. "It is alarming that this strain is spreading so quickly through the whole region and we fear it can spread further [and eventually] jump to Africa."
9-22-17 Growing up
Growing up, after a study revealed that today’s teens are taking longer to embrace traditional symbols of adulthood, including getting a driver’s license, drinking, and dating. “The whole developmental pathway has slowed down,” said study author Jean Twenge.
9-22-17 A Viking Wonder Woman
A Viking Wonder Woman
Historical accounts of female Viking warriors are often discounted as myths. But new DNA tests of a warrior buried in Sweden more than 1,000 years ago provide the first genetic evidence that some women held powerful, high-status positions in Viking culture. The 10th-century grave site, which was uncovered in the 1880s, contained a sword, arrows, a battle knife, a spear, shields, and two horses. The Viking, who stood 5-foot-6, was also buried with a set of game pieces—an indication of the deceased’s expertise in battle tactics. The archaeologists who uncovered the grave 130 years ago assumed it belonged to a high-ranking male warrior. “I think that’s a mistake that archaeologists make quite often,” archaeologist Becky Gowland tells The Guardian. “When we do that, we’re just reproducing the past in our image.” A recent DNA analysis revealed that the Viking leader lacked a Y chromosome—confirming that “he” was actually a “she.”
9-22-17 Neanderthal brains 'grew more slowly'
Neanderthal brains 'grew more slowly'
A new study shows that Neanderthal brains developed more slowly than ours. An analysis of a Neanderthal child's skeleton suggests that its brain was still developing at a time when the brains of modern human children are fully formed. This is further evidence that this now extinct human was not more brutish and primitive than our species. The research has been published in the journal Science. Until now it had been thought that we were the only species whose brains developed relatively slowly. Unlike other apes and more primitive humans, Homo sapiens has an extended period of childhood lasting several years. This is because it takes time and energy to develop our large brain. Previous studies of Neanderthal remains indicated that they developed more quickly than modern humans - suggesting that their brains might be less sophisticated. But a team led by Prof Antonio Rosas of the Museum of Natural Sciences in Madrid found that if anything, Neanderthal brains may have developed more slowly than ours. "It was a surprise," he told BBC News. "When we started the study we were expecting something similar to the previous studies."
9-21-17 Walking to work or doing the vacuuming can extend your life
Walking to work or doing the vacuuming can extend your life
Just 30 minutes of easy exercise five days a week reduces your risk of premature death by 28 per cent, suggests the world’s largest study of physical activity. One in 12 deaths could be prevented with 30 minutes of physical activity five days a week. That’s the conclusion from the world’s largest study of physical activity, which analysed data from more than 130,000 people across 17 countries. At the start of the study, participants provided information on their socioeconomic status, lifestyle behaviours and medical history. They also answered a questionnaire about the physical activity they complete over a typical week. Participants were followed-up at least every three years to record information about cardiovascular disease and death for almost seven years. Over the period studied, Scott Lear, from McMaster University in Canada and his colleagues found that 150 minutes of activity per week reduced the risk of death from any cause by 28 per cent and rates of heart disease by a fifth. Being highly active was associated with even greater benefits: people who spent more than 750 minutes walking briskly each week reduced their risk of premature death by 36 per cent. Results showed that it was not necessary to run, swim or work out at the gym. Household chores such as vacuuming or scrubbing the floor, or merely walking to work provided enough exercise to protect the heart and extend life. “Going to the gym is great, but we only have so much time we can spend there. If we can walk to work, or at lunch time, that will help too,” says Lear. The World Health Organisation recommend that adults aged 18 to 64 do at least 150 minutes of moderate physical activity throughout the week, as well as muscle strengthening exercises at least two days a week.
9-21-17 Using new study to back high-fat, low-carb diets is flawed logic
Using new study to back high-fat, low-carb diets is flawed logic
Fans of high-fat, low-carb diets grasped at a recent study to declare their fringe view proven. They were wrong, say Anthony Warner and Katie Heath. “Low-fat diet could kill you,” reported The Telegraph. The origin of this surprising message was the publication of the innocuous-sounding Prospective Urban Rural Epidemiology (PURE) study. Its results “challenge decades of dietary advice“, said the Daily Mail. Many low-carb, high-fat campaigners likewise saw it as public vindication of their non-mainstream mantra. Aseem Malhotra, author of a recent book on low-carb diets, said that it was time for “a complete U-turn” in the UK’s approach to official advice on what to eat. Big claims, but did the results justify them? PURE looked at the diets of more than 135,000 people in 18 countries. Individuals were surveyed using questionnaires, and usually followed up for around seven years, with associations looked for between what they ate and cardiovascular disease and death. It is an important study, constituting a huge international undertaking and the first time these associations have been investigated at the same time across high, middle and low-income countries. But in a desire for headline-grabbing novelty, important points were lost. Did PURE show that a low-fat, high-carb diet is deadly? It did show a significant increase in mortality among those on diets very high in carbohydrates, although interestingly, no associated increase in heart disease. But PURE comes with all the limitations of observational studies, in which cause and effect are often impossible to establish. With the inclusion of such a diversity of countries, there may also be a few new limitations.
9-21-17 Ancient DNA sheds light on African history
Ancient DNA sheds light on African history
DNA from ancient remains has been used to reconstruct thousands of years of population history in Africa. Researchers sequenced the genomes of 16 individuals who lived between 8,000 and 1,000 years ago. The data shows how the invention and spread of farming had a major impact on the genes of people in Africa - just as it did in Europe and Asia. The findings are published in the journal Cell. The results suggest that populations related to the indigenous people of southern Africa had a wider distribution in the past. This southern African-like genetic background is found in hunter-gatherers from Malawi and Tanzania in the east of the continent. These hunters lived between 8,100 and 1,400 years ago. But the later spread of farmers from western Africa had a major impact on the genetic make-up of people in surrounding regions. Further DNA analysis revealed the hunter-gatherers in eastern Africa had mixed extensively with the incoming farmers. The researchers estimate that the mixing occurred between 8,000 and 4,000 years ago. The study also found possible evidence of migration into Africa from the Middle East. About 38% of the ancestry of a 3,100-year-old livestock herder from Tanzania was related to ancient farmers from the Levant region. "These results document a prehistoric population landscape that we didn't know about," said co-author Pontus Skoglund, from Harvard Medical School, US. "They document how farmer and herder migrations swept through eastern and southern Africa." The researchers also found tentative evidence of adaptive evolution - changes driven by environmental pressure - for genes involved in taste in the ancient individuals. These taste receptors are known to be important for detecting and learning to avoid poisonous plants.
9-21-17 Plate tectonics started at least 3.5 billion years ago
Plate tectonics started at least 3.5 billion years ago
Plate tectonics may have started as early as 3.5 billion years ago on Earth. That recycling of Earth’s surface leads to the separation of light-colored continental crust from darker, denser oceanic crust. Plate tectonics may have gotten a pretty early start in Earth’s history. Most estimates put the onset of when the large plates that make up the planet’s outer crust began shifting at around 3 billion years ago. But a new study in the Sept. 22 Science that analyzes titanium in continental rocks asserts that plate tectonics began 500 million years earlier. Nicolas Greber, now at the University of Geneva, and colleagues suggest that previous studies got it wrong because researchers relied on chemical analyses of silicon dioxide in shales, sedimentary rocks that bear the detritus of a variety of continental rocks. These rocks’ silicon dioxide composition can give researchers an idea of when continental rocks began to diverge in makeup from oceanic rocks as a result of plate tectonics. But weathering can wreak havoc on the chemical makeup of shales. To get around that problem, Greber’s team turned to a new tool: the ratios of two titanium isotopes, forms of the same element that have different masses. The proportion of titanium isotopes in the rocks is a useful stand-in for the difference in silicon dioxide concentration between continental and oceanic rocks, and isn’t so easily altered by weathering. Those data helped the team estimate that continental rocks — and therefore plate tectonics — were already going strong by 3.5 billion years ago.
9-21-17 The lecture that changed biology
The lecture that changed biology
Sixty years ago this week, one of the greatest British scientists, Francis Crick, gave a lecture in London in which he accurately predicted how genes work, setting the course for the genetic revolution we are now living through. Here, evolutionary biologist Professor Matthew Cobb from Manchester University unpicks the predictions that set a new course for how we understand the very stuff we are made from. In one lecture, it has been said that Francis Crick "permanently altered the logic of biology". Only four years earlier, he and the young American Jim Watson had solved the double helix structure of DNA, using data gathered by Rosalind Franklin. Aged 41, Crick was still five years away from winning the Nobel Prize for this work, but he had a reputation as a powerful and profound thinker. He gave his lecture - "On protein synthesis" - at University College London for the Society for Experimental Biology. In it, Crick spoke about how genes do what they do. At the time, this subject was still very murky - some scientists were not even convinced that genes were made of DNA. But Crick delivered four predictions about genes - and their link to the proteins that build our bodies. In each of these ideas, he was right. Crick started with the main thing that genes do: they control the production of proteins. The problem Crick explored was that the DNA in a gene is simply a chemical code - a string of something called bases - A, C, T, G. Crick had to explain how the cell could get from this one-dimensional sequence of bases in DNA to the complex three-dimensional structures of proteins. Even more puzzling was the fact that proteins can fold themselves into nearly any shape. Crick's answer was simple: the order of bases in the gene - what he called "genetic information" - corresponded to the order of the amino acids that make up each protein, and nothing more. There was no structural information about the protein that was encoded in the gene, he claimed. He called this the sequence hypothesis. (Webmaster's comment: American science builds on the work of scientists from other counties. But only when our Relgious Ignorance allows us.)
9-21-17 This ancient mind trick can vastly improve your memory
This ancient mind trick can vastly improve your memory
Arthur Conan Doyle's detective novel A Study in Scarlet (1887) we learn that Sherlock Holmes used the most effective memory system known: a memory palace. Although imagined memory palaces are still used by memory champions and the few who practice the memory arts, they are best known from Greco-Roman times when great orators, including Cicero, used them to ensure their rhetoric was smooth, detailed, and flawless. The physical memory palace, usually a streetscape or building interior, would become so familiar to the orator that it was always available to them in their imagination. By "placing" one piece of information in each site, they could mentally stroll through their memory palace, location by location, drawing out each portion of the speech in the required order without missing any element. Received opinion is that this method of loci, as the technique is also known, dates to before Simonides of Ceos (c. 556-468 BCE), who is often credited as the inventor. However there is ample circumstantial evidence that indigenous cultures the world over have been using it for far longer than that. There is a continuous record dating back at least 40,000 years for Australian Aboriginal cultures. Their songlines, along with Native American pilgrimage trails, Pacific Islanders' ceremonial roads, and the ceque system of the Inca at Cusco all exhibit exactly the same pattern as the memory palaces described by Cicero. At each sacred location along these paths, elders would sing, dance, or tell a story, all making the information associated with the location more memorable. The memory skills of indigenous elders exceed anything reported for the ancient Greeks. Research with the Native American Navajo people, for example, shows that they memorize a classification of more than 700 insects along with identification, habitats, and behavior. And that's just insects. A fully initiated indigenous elder would be able to relate stories equivalent to a field guide for all the birds, mammals, reptiles, fish, and hundreds of insects within their environment. Another study shows that the Hanunoo people of the Philippines were able to identify 1,625 plants, many of which were unknown to Western science at the time. Add to that knowledge of astronomy, timekeeping, navigation, legal and ethical guidelines, weather and seasons, complex genealogies and belief systems, and you have a vast encyclopedia stored in an interwoven memorized web: a web that is tied to a real or imagined memory palace.
9-21-17 Shhhh! Some plant-eating dinos snacked on crunchy critters
Shhhh! Some plant-eating dinos snacked on crunchy critters
Crustacean shells discovered in fossilized poop reveal diet secrets of ancient herbivores. Hadrosaurs like Gryposaurus monumentensis may have supplemented their veggie diets with meaty treats, roughly 75-million-year-old fossilized poop reveals. Some dinosaurs liked to cheat on their vegetarian diet. Based on the shape of their teeth and jaws, large plant-eating dinosaurs are generally thought to have been exclusively herbivorous. But for one group of dinosaurs, roughly 75-million-year-old poop tells another story. Their fossilized droppings, or coprolites, contained tiny fragments of mollusk and other crustacean shells along with an abundance of rotten wood, researchers report September 21 in Scientific Reports. Eating the crustaceans as well as the wood might have given the dinosaurs an extra dose of nutrients during breeding season to help form eggs and nourish the embryos. “Living herd animals do occasionally turn carnivore to fulfill a particular nutritional need,” says vertebrate paleontologist Paul Barrett of the Natural History Museum in London. “Sheep and cows are known to eat carcasses or bone when they have a deficiency in a mineral such as phosphorus or calcium, or if they’re pregnant or ill.” But the discovery that some plant-eating dinos also ate crustaceans is the first example of this behavior in an extinct herbivore, says Barrett, who was not involved in the new study.
9-21-17 Plant-eating dinosaurs strayed from veggie diet
Plant-eating dinosaurs strayed from veggie diet
The idea of plant-eating dinosaurs having a strict vegetarian diet has been called into question. New evidence suggests that some dinosaurs snacked on shellfish and insects as well as plant food. A study of fossilised droppings indicates duck-billed dinosaurs dined on crabs at certain times of the year. Fossil remains of dinosaur dinners is rare, so this pescatarian diet may have been overlooked in the past. The popular perception of what dinosaurs ate was simplistic, said Dr Karen Chin of the University of Colorado, Boulder, US, who led the research. "Plant-eating dinosaurs had more complex diets than we assumed that they had, and these diets included feeding on some animals, including at least crustaceans, and this was more like diets of modern plant-eating birds," she told BBC News. When the first dinosaur discoveries were made in the 1850s, some species were labelled plant-eaters because their teeth resembled those of living plant-eating mammals such as rhinos. The new evidence comes from an area of southern Utah that is regarded as a treasure trove of fossils from the Late Cretaceous Period, when dinosaurs were coming to the end of their reign. (Webmaster's comment: You'll evolve to use food energy where you find it.)
9-20-17 Brain farts: 9 ways your brain can make you feel stupid
Brain farts: 9 ways your brain can make you feel stupid
Ever walked into a room only to forget why you entered, accidentally called your boss “mum” or burst out laughing at bad news? Here’s what’s really going on. This brain fart is so common it even has its own name: the “doorway effect”. Intrigued by this frustrating experience, Gabriel Radvansky at the University of Notre Dame, Indiana, and his colleagues asked people to navigate a virtual environment. Occasionally the participants would pick up an object, causing it to disappear from view. Now and again they would be asked what they were carrying. If they had moved into a different room, they were slower and less accurate at remembering what the object was. Radvansky repeated the experiment in genuine rooms and found the same thing: people’s powers of recall are worse after they pass through a doorway than when they walk the same distance within a room. What’s going on? As we move around the world, our brain is thought to construct what Radvansky calls a temporary “event model” of our environment and our thoughts and actions in it. But storing several event models at once is inefficient. “New environments may require new sets of skills, and so it is best to focus our memory on what is currently at hand,” says Radvansky. Doorways seem to trigger the replacement of one event model with another. This swap makes us more likely to forget what happened in the first room. It’s not just doorways that trigger this shift – passing from rural fields into a town can do it too, or from highways to backstreets, upstairs to down.
- WHY DO I FORGET THE REASON I WALKED INTO THE ROOM?
- WHY DO RANDOM NOISES TURN INTO WORDS?
- WHY DOES STARING AT A WORD TURN IT TO NONSENSE?
- HOW CAN YOU SUDDENLY FORGET YOUR PIN?
- WHY IS THE DOOR HANDLE SMILING AT YOU?
- WHAT CAUSES FREUDIAN SLIPS?
- WHY DOES A RECORDING OF YOUR VOICE MAKE YOU CRINGE?
- WHY DOES BAD NEWS MAKE ME BURST OUT LAUGHING?
- HOW CAN SPEECH ON A LOOP TURN INTO SONG?
9-20-17 Why has a UK team genetically edited human embryos?
Why has a UK team genetically edited human embryos?
The aim of the work is to better understand embryonic development, rather than to see if genome editing could prevent diseases in children. Human embryos have been genetically edited in the UK for the first time, using a technique called CRISPR. But why do researchers think this is so important?
- What gene editing was carried out?
- Why was this work done?
- Is that all the team found?
- How could such work improve IVF?
- How does this new study compare with what’s been done before?
- Will the UK work help us to edit children’s genomes?
- What rules govern this kind of research?
(Webmaster's comment: In the United States this research is banned by Religious Ignorance!)
9-20-17 In a first, human embryos edited to explore gene function
In a first, human embryos edited to explore gene function
CRISPR/Cas9 is used to ‘knock out’ a gene needed to develop properly. A 5-day-old human embryo is usually composed of about 200 cells in a hollow ball configuration called a blastocyst. Embryos edited to remove the OCT4 gene fail to make normal blastocysts. For the first time, researchers have disabled a gene in human embryos to learn about its function. Using molecular scissors called CRISPR/Cas9, researchers made crippling cuts in the OCT4 gene, Kathy Niakan and colleagues report September 20 in Nature. The edits revealed a surprising role for the gene in the development of the placenta. Researchers commonly delete and disable genes in mice, fruit flies, yeast and other laboratory critters to investigate the genes’ normal roles, but have never done this before in human embryos. Last year, government regulators in the United Kingdom gave permission for Niakan, a developmental biologist at the Francis Crick Institute in London, and colleagues to perform gene editing on human embryos left over from in vitro fertilization treatments (SN Online: 2/1/16). The researchers spent nearly a year optimizing techniques in mouse embryos and human stem cells before conducting human embryo experiments, Niakan says. This groundbreaking research allows researchers to directly study human development genes, says developmental biologist Dieter Egli of Columbia University. “This is unheard of. It’s not something that has been possible,” he says. “What we know about human development is largely inferred from studies of mice, frogs and other model organisms.”
9-20-17 UK scientists edit DNA of human embryos
UK scientists edit DNA of human embryos
The blueprint for life - DNA - has been altered in human embryos for the first time in the UK. The team at the Francis Crick Institute are unravelling the mysteries of the earliest moments of life. Understanding what happens after a sperm fertilises an egg could lead to ways of improving IVF or explain why some women miscarry. The embryos were modified shortly after fertilisation and allowed to develop for seven days. The researchers are exploring one of the most astounding of transformations. We have all journeyed from a single fertilised egg to a human being - built from myriad different tissues ranging from bone to those needed to read this page. The first few steps on that journey are as critical as they are poorly understood. Breakthroughs in manipulating DNA have allowed the team at the Crick to turn off a gene - a genetic instruction - suspected to be of vital importance. The easiest way of working out how something works is to remove it and see what happens. So the researchers used the gene-editing tool Crispr-Cas9 to scour the billions of letters of genetic code, find their genetic target and break the DNA to effectively disable it. They were targeting a gene. You are unlikely to have heard of it, but OCT4 is a superstar in early embryo development. Its complete role is not understood but it acts like an army general issuing commands to keep development on track. The researchers used 41 embryos that had been donated by couples who no longer needed them for IVF. After performing the genetic modification, the team could watch how the embryos developed without OCT4. (Webmaster's comment: Of course all the Religious Ignorant in America are against this research. They are still trying to live by ignorance from 2000 years ago.)
9-20-17 By ganging up, HIV antibodies may defeat the virus
By ganging up, HIV antibodies may defeat the virus
Two new approaches — a one-two punch and a triple blow — stopped infection in monkeys. A combination of powerful antibodies might be able to stop HIV before it infects, as is happening to a T cell in this colorized micrograph. For certain HIV antibodies, having a buddy or two makes a big difference in the fight against the virus. Combining the antibodies, called broadly neutralizing antibodies, may stop more strains of HIV than any single one can do alone, two new studies suggest. A “triple-threat” antibody molecule can bind to three different spots on the virus, researchers report online September 20 in Science. In Science Translational Medicine, a second team describes a cocktail of two single antibodies that each target a different region of the virus. Both methods prevented infection from multiple strains of an HIV-like virus in monkeys. “We have known for many years that broadly neutralizing antibodies are extremely powerful antibodies,” says molecular biologist Nancy Haigwood of the Oregon Health & Science University in Portland, who was not involved in either study. Using more than one of these antibodies “is the most promising approach” to block HIV infection in humans because it offers more coverage, she says. This extra coverage is needed because HIV is a master of mutation. “It’s really adopted every bit of what I would call molecular trickery to outwit our immune system, and it’s a constant battle,” says Gary Nabel, coauthor of the study in Science and chief scientific officer of Sanofi in Cambridge, Mass. The immune system keeps trying to recognize parts of the virus, but mutations in the virus can alter those sites. “You really want to have this broadside attack against the virus that hits multiple targets,” he says.
9-20-17 Old fathers pass on more mutations to kids than old mothers
Old fathers pass on more mutations to kids than old mothers
A huge study of Icelanders suggests that older men pass on four times as many new mutations to their kids than women. Older fathers pass on more genetic mutations to their children than older mothers do, according to study that investigated the genomes of thousands of Icelandic parents and children. The researchers behind the work hope to understand how such mutations put children at risk of rare diseases. New mutations are genetic alterations that appear for the first time in eggs rather than being carried for generations. They are key drivers of evolution but some can be harmful. “An extraordinarily large percentage of rare diseases in children are rooted in mutations that are not found in their parents,” says Kári Stefánsson of deCODE genetics, a genetics company based in Iceland. “It’s important to figure out where these mutations are coming from.” To find out, Stefánsson and his colleagues sequenced the genomes of 14,688 Icelanders. The team used two different approaches that involved comparing the genome sequences of individuals with those of their parents, children and siblings. “If a sequence is not present in the parents but is present in the child, then it’s new,” says Stefánsson. They discovered that 80 per cent of new mutations come from the father, and that the number of mutations increases in line with the age of the parents. It makes sense that age affects the sex cells of men more than women. Women are thought to be born with all the eggs they will ever have. Although these cells age, they are not thought to divide. Men, on the other hand, are continually making sperm – and every cell division carries the risk of creating a new genetic mutation.
9-19-17 Size matters when it comes to extinction risk
Size matters when it comes to extinction risk
The biggest and the smallest of the world's animals are most at risk of dying out, according to a new analysis. Size matters when it comes to extinction risk, with vertebrates in the so-called "Goldilocks zone" - not too big and not too small - winning out, say scientists. Action is needed to protect animals at both ends of the scale, they say. Heavyweights are threatened mainly by hunting, while featherweights are losing out to pollution and logging. "The largest vertebrates are mostly threatened by direct killing by humans," said a team led by Prof Bill Ripple of Oregon State University in Corvallis, US. "Whereas the smallest species are more likely to have restricted geographic ranges - an important predictor of extinction risk - and be threatened by habitat degradation." The research adds to evidence that animals are dying out on such a scale that a sixth extinction is considered under way. This has prompted efforts to determine the key drivers of extinction risk. One clue is body size. Research on birds and mammals has shown that those with larger bodies are more likely to go extinct. Yet, when the researchers made a data base of thousands of birds, mammals, fish, amphibians and reptiles at risk of extinction, they found disproportionate losses at the large and small ends of the scale. "Surprisingly, we found that not only the largest of all vertebrate animal species are most threatened, but the very tiniest ones are also highly threatened with extinction," Prof Ripple told BBC News. (Webmaster's comment: And guess what creature is the cause of it. Human Beings!)
9-18-17 Sex and aggression linked in male mouse brains but not in female
Sex and aggression linked in male mouse brains but not in female
In male mice, the same brain cells influence both aggressive and sexual behaviours, but for the first time we now know that's not the case for females. Aggression and sexual behaviour are controlled by the same brain cells in male mice – but not in females. The finding suggests that males are more likely to become aggressive when they see a potential mate than females. The brain regions that contain these cells look similar in mice and humans, say the researchers behind the study, but they don’t yet know if their finding has relevance to human behaviour. Similar to humans, male mice are, on the whole, more aggressive than females. Because of this, most research into aggression has overlooked females, says Dayu Lin at New York University. “I would say 90 per cent of aggression studies have been done in males,” she says. “We know very little about aggression in females.” But females can be aggressive too. For instance, female mice can be aggressive when protecting their newborn pups. In 2011, Lin and her colleagues studied a region of the brain called the hypothalamus, responsible for regulating many different behaviours. They discovered a set of cells within this region in male mice that controlled both aggressive and sexual behaviours. When the cells were shut off, the mice didn’t mate or show aggression, but both behaviours could be triggered when the cells were stimulated. Now, they have shown that the cells controlling these behaviours are separate in female mice, in both those that haven’t mated and new mothers. The cells for aggression are close to the centre of the hypothalamus, while cells for sexual behaviour are at the edge, says Lin. “But in the male, the cells are totally mixed up and overlap.” This might be because some aspects of mating resemble aggression for male mice, says Lin. A male mouse will have to approach a female and mount her, for instance. Female mice stay still for mating, which looks nothing like aggression.
9-18-17 Blind people repurpose the brain’s visual areas for language
Blind people repurpose the brain’s visual areas for language
For the first time, language processing has been detected in areas of the brain that usually process vision, highlighting the organ’s extraordinary flexibility. People who are blind use parts of their brain that normally handle for vision to process language, as well as sounds – highlighting the brain’s extraordinary ability to requisition unused real estate for new functions. Neurons in the part of the brain normally responsible for vision synchronise their activity to the sounds of speech in blind people, says Olivier Collignon at the Catholic University of Louvain (UCL) in Belgium. “It’s a strong argument that the organisation of the language system… is not constrained by our genetic blueprint alone,” he says. The finding builds on previous research showing that the parts of the brain responsible for vision can learn to process other kinds of information, including touch and sound, in people who are blind. Collignon and his colleagues made the discovery using magnetoencephalography (MEG), which measures electrical activity in the brain. While they were being scanned, groups of sighted and blind volunteers were played three clips from an audio book. One recording was clear and easy to understand; another was distorted but still intelligible; and the third was modified so as to be completely incomprehensible. Both groups showed activity in the brain’s auditory cortex, a region that processes sounds, while listening to the clips. But the volunteers who were blind showed activity in the visual cortex, too. The blind volunteers also appeared to have neurons in their visual cortex that fired in sync with speech in the recording – but only when the clip was intelligible. This suggests that these cells are vital for understanding language, says Collignon.
9-18-17 Secrets of butterfly wing patterns revealed by gene hacking
Secrets of butterfly wing patterns revealed by gene hacking
Butterflies' wings have extraordinary patterns and colours, and it turns out they are controlled by a single "master gene" that performs many roles. Butterfly wings have been given make-overs by scientists who tweaked a “painting gene” to change their patterns and colours. The research has major implications for understanding how the so-called “rules of life” – genetics and evolution – shape biodiversity. The team used the powerful new gene-editing technique CRISPR/Cas9 to study the role of the WntA gene in creating one of nature’s greatest artworks, the butterfly wing. By removing the gene from seven butterfly species, they were able to radically alter the insect’s appearance. Wing patterns and colours changed in ways that were unexpected. The research showed how WntA acted as a master gene responsible for the trademark look of different butterflies. Lead scientist Arnaud Martin, from George Washington University in the US, said: “We know why butterflies have beautiful coloured patterns. It’s usually for sexual selection, for finding a mate, or it’s some kind of adaptation to protect themselves from predators. “What is more mysterious is how do they do it. How do you make stripes and dots, how do you make complexity, how do you fine-tune a given feature during long evolutionary time scales? “CRISPR allowed us to not only describe that this gene has evolved multiple roles within a single species, it also enabled a massive comparison between species and showed that pattern evolution has consisted of variations on a common theme.”
9-18-17 3-D scans of fossils suggest new fish family tree
3-D scans of fossils suggest new fish family tree
Analysis of specimens from China implies ray-finned fishes are younger than previously thought. Polypterus is a living member of a large group of vertebrates called ray-finned fishes. New evidence suggests that ray-finned fishes arose about 360 million years ago, after a major extinction event, then their diversity exploded. When it comes to some oddball fish, looks can be deceiving. Polypterus, today found only in Africa, and its close kin have generally been considered some of the most primitive ray-finned fishes alive, thanks in part to skeletal features that resemble those on some ancient fish. Now a new analysis of fish fossils of an early polypterid relative called Fukangichthys unearthed in China suggests that those features aren’t so old. The finding shakes up the evolutionary tree of ray-finned fishes, making the group as a whole about 20 million to 40 million years younger than thought, researchers propose online August 30 in Nature. Ray-finned fishes named for the spines, or rays, that support their fins — are the largest group of vertebrates, making up about half of all backboned animals. They include 30,000 living species, such as gars, bowfins and salmon. The group was thought to originate about 385 million years ago, in the Devonian Period. But the new research, using 3-D CT scans of the previously discovered fossils, shifts the fishes’ apparent origin to the start of the Carboniferous Period some 360 million years ago, says study coauthor Matt Friedman, a paleontologist at the University of Michigan in Ann Arbor.
9-18-17 Turkey's new school year: Jihad in, EVOLUTION out
Turkey's new school year: Jihad in, EVOLUTION out
Turkey's schools have begun the new academic year with a controversial curriculum that leaves out the theory of evolution and brings in the concept of jihad. For Turkey's Islamist-rooted government, the idea is for a new "education of values". Critics have denounced new textbooks as "sexist" and "anti-scientific", and complain of a major blow to secular education. "By embedding a jihadist education of values, they try to plague the brains of our little children, with the same understanding that transforms the Middle East into a bloodbath," said Bulent Tezcan of the secular, opposition CHP party. But the government has accused the opposition of creating black propaganda and trying to polarise Turkey ahead of elections in 2019. "When we say values, they understand something else. We are proud of our conservative-democrat stand, but we don't want everyone to be like us," says Education Minister Ismet Yilmaz. Textbooks explaining the idea of jihad are being rolled out in Turkey's religious vocational schools, known widely as Imam-Hatip high schools. They will then be offered to children in secondary schools as optional courses in a year's time.
9-18-17 What if dinosaurs hadn't died out?
What if dinosaurs hadn't died out?
It was the kind of cataclysm that we can scarcely imagine. When an asteroid 15km-wide (nine miles) slammed into planet Earth 66 million years ago, it struck with a force equivalent to about 10 billion Hiroshima bombs. A radioactive fireball seared everything for hundreds of miles in every direction and created tsunamis that sped halfway around the globe. Even the atmosphere may have started to burn, and no land animal more than 25kg (55lb) would survive; in fact, around 75% of all species became extinct. The so-called ‘non-avian’ dinosaurs didn’t have a hope, and only the small, feathered flying dinosaurs we know today as birds would make it through. But what if history had taken a different course? What if the asteroid had missed or arrived a few minutes earlier? That is the scenario suggested by researchers featured in The Day the Dinosaurs Died, a recent BBC documentary. These scientists – including geologist Sean Gulick of the University of Texas – argue that if the asteroid had arrived mere moments earlier or later, rather than hitting the shallow waters of Mexico’s Yucatan Peninsula, it would have plunged into the deep sea of the Pacific or Atlantic oceans, absorbing some of the force and limiting the expulsion of sulphur-rich sediments that choked the atmosphere for the months or years ahead. Had that been the case, there would still have been a catastrophe and extinctions, but some larger dinosaurs may have survived. Pondering the course of this alternative timeline is an intriguing thought experiment that dinosaur scientists are only too enthusiastic to speculate about. Would dinosaurs be here today? What new dinosaurs might have appeared? Would dinosaurs have developed human-like intelligence? Would mammals have remained in the shadows?
9-17-17 Why trained musicians are better at making decisions
Why trained musicians are better at making decisions
rents aware of how music training can boost their children's cognitive development may be eager to get them into a practice room as early as possible. But recent research suggests there may be an advantage to holding off for a few years. It reports that, faced with a complex decision-making task, participants who began musical training after age eight made better choices than those who started earlier, or never took lessons at all. "In addition to the rich sensori-motor benefits early music playing may have on the developing brain, music training may also confer long-lasting benefits in complex cognitive functions," writes a team led by Kirsten Smayda of the University of Texas–Austin. "The music classes offered during many children's elementary and high-school education in America may result in improved decision-making ability as an adult." In the journal Psychology of Music, Smayda and colleagues Bharath Chandrasekaran of UT–Austin and Darrell Worthy of Texas A&M, note that various regions of the brain develop at different rates. Specifically, they write that the prefrontal cortex — which is "a critical brain region for successful decision-making" — doesn't mature until relatively late in childhood.
9-17-17 Why is it so hard to swat a fly?
Why is it so hard to swat a fly?
Try to swat a fly and it will soon become clear that they're faster than you. Much faster. But how on Earth do these tiny creatures - with their minuscule brains - outwit us so easily? You've probably pondered it after chasing a fly around your house and flailing your shoe with repeated, unsuccessful swats. How does it move so fast? Can it read my mind? It was the question put to the BBC World Service CrowdScience team for our most recent episode addressing the apparent super powers of tiny animals. The answer is that, compared with you and me, flies essentially see the world in slow motion. To illustrate this, have a look at a clock with a ticking hand. As a human, you see the clock ticking at a particular speed. But for a turtle it would appear to be ticking at twice that speed. For most fly species, each tick would drag by about four times more slowly. In effect, the speed of time differs depending on your species. This happens because animals see the world around them like a continuous video. But in reality, they piece together images sent from the eyes to the brain in distinct flashes a set number of times per second. Humans average 60 flashes per second, turtles 15, and flies 250. The speed at which those images are processed by the brain is called the "flicker fusion rate". In general, the smaller the species, the faster its critical flicker fusion rate - and flies, in particular, put us to shame. Professor Roger Hardie, from the University of Cambridge, investigates how flies' eyes work, and he has an experiment to determine their flicker fusion rate. "The flicker fusion rate is simply how fast a light has to be turning on and off before it's perceived or seen as just a continuous light" says Prof Hardie. (Webmaster's comment: It's just evolution at work. Their survival depends on seeing movements faster than animals that might harm them so after millions of years of evolution they have evolved a very fast flicker fusion rate.)
9-16-17 Why do teenagers engage in risky behavior?
Why do teenagers engage in risky behavior?
According to current research, teenagers make bad decisions and take too many risks because the prefrontal cortex, the decision-making center, is still developing until around age 25. Now, new research suggests this may not be the case. Dr. Dan Romer and his colleagues at the University of Pennsylvania took a look at the research and didn't see sufficient evidence for the "structural deficit" theory in the literature. Yes, the brain's not fully developed in teens, they say, but that's not the problem behind bad decision making. Dr. Romer says most teens actually aren't impulsive. In fact, they're sort of hyper-rational. Their risky behavior is a choice teens make that is driven by a desire to explore the risk in favor of gaining experience. So, it's not a structural deficit that's causing this. Instead, it's a desire to gain experience. The conventional wisdom seemed to make a great deal of sense: The underdeveloped pre-frontal cortex creates an imbalance between the decision-making center and the regions in charge of motivation and reward, which have already matured. Researchers used this to explain why teens have poor impulse control or why they take risks that adults probably wouldn't, the theory being that the reward center is motivating the teen and the prefrontal cortex just isn't prepared to put the brakes, so to speak. But Dr. Romer points out that if risky behavior in teens was simply a function of biology, then more teens would probably have this problem. But, in reality, only a handful of teens are making the impulsive decision to drink and drive, for example, or to have unprotected sex. If this behavior were solely based in biology, there really should be a higher prevalence of it.
9-15-17 Out-Of-Body Experiences May Be Explained By Inner Ear Damage
Out-Of-Body Experiences May Be Explained By Inner Ear Damage
An out-of-body experience (OBE) can be described as the sensation of floating above your own body and getting a bird's eye view of your surroundings. This makes for great movie sequences, but a 2017 study published in Cortex suggests the spiritually transcendent awakening thing doesn't hold much weight. It's not your third-eye opening, but rather it may be your inner ear kind of buggin' out. More specifically, it's the vestibular system, which is made up of canals in the inner ear that track your balance and location in space; it's the same system that makes you dizzy and gets you carsick. The study, conducted by researchers from Aix-Marseille Université and the Centre des Vertiges, looked at 210 patients who have reported dizziness. Of that group, 14 percent said they've had OBEs. By contrast, only five percent of the control group of 210 healthy people said they've had an OBE. Add this significant difference to the previous anecdotal notion that the vestibular system plays a role in OBEs. ere's an easy way to think about how the vestibular system may cause this effect, according to Jason Braithwaite, a psychologist at Lancaster University: Your inner ear works to give your brain an idea of where you're existing in a space. Are you in a small room? Huge room? Are you moving? Your brain always has a bird's eye understanding of your space, but you experience the world through your eyes' perspective. But them something glitches in how your brain is receiving sensory information, so your bird's eye view takes over as a default. How's that for spiritual enlightenment?
9-15-17 Animal goo inspires better glue
Animal goo inspires better glue
Bio-inspired adhesives could make surgery smoother and safer. When startled, the dusky slug (Arion subfuscus) produces a goopy defense slime that slows down predators. Scientists are studying the chemical structure of this goo to make better surgical adhesives. Finding a great glue is a sticky task — especially if you want it to attach to something as slick as the inside of the human body. Even the strongest human-made adhesives don’t work well on wet surfaces like tissues and organs. For surgeons closing internal incisions, that’s more than an annoyance. The right glue could hold wounds together as effectively as stitches and staples with less damage to the surrounding soft tissue, enabling safer surgical procedures. A solution might be found under wet leaves on a forest floor, recent research suggests. Jianyu Li of McGill University in Montreal and colleagues have created a surgical glue that mimics the chemical recipe of goopy slime that slugs exude when they’re startled. The adhesive stuck to a pig heart even when the surface was coated in blood, the team reported in the July 28 Science. Using the glue to plug a hole in the pig heart worked so well that the heart still held in liquid after being inflated and deflated tens of thousands of times. Li, who did the research while at Harvard University, and colleagues also tested the glue in live rats with liver lacerations. It stopped the rats’ bleeding, and the animals didn’t appear to suffer any bad reaction from the adhesive. The glue has “excellent, excellent properties,” says Andrew Smith, a biologist at Ithaca College in New York.
9-15-17 How humans are still evolving
How humans are still evolving
Human evolution is often thought of as a process that ended millennia ago, when our ape-like ancestors morphed into Homo sapiens. But a new study has found that the process of natural selection continues, gradually weeding out life-shortening traits in modern humans, including genes that predispose people to heart disease, Alzheimer’s, and heavy smoking. Geneticists examined the genomes of 210,000 people of European descent in search of mutations associated with greater or lesser longevity. Natural selection—a basic mechanism of Darwin’s theory of evolution—is based on the principle that organisms best suited to their environments tend to survive longer, making it more likely that they’ll pass their genes on to future generations. The researchers found that the ApoE4 gene linked to Alzheimer’s is becoming less common, particularly among women. A gene mutation associated with a strong addiction to cigarette smoking in men is also on the decline, ScienceDaily?.com reports. “It may be that men who don’t carry these harmful mutations can have more children, or that men and women who live longer can help with their grandchildren, improving their chance of survival,” says the study’s co-author, Molly Przeworski. The analysis also reveals that genetic variants linked to heart disease, asthma, obesity, and high cholesterol all appear less frequently in people who live longer—an indication that humans may continue to adapt to a constantly changing environment.
9-15-17 A much older human ancestor
A much older human ancestor
A set of human-like footprints dating to 5.7 million years ago, discovered on the Greek island of Crete, challenge existing theories of how and when our species evolved. Prior to this discovery, the oldest confirmed hominin footprints were found in Tanzania and dated at a maximum of 3.65 million years. Anthropologists believed these ancient human relatives were isolated in Africa for several million years before spreading out to Europe and Asia. A new analysis of the prints found in Crete could complicate this evolutionary tale. “What makes this controversial is the age and location of the prints,” researcher Per Ahlberg tells ScienceDaily.com. At the time the prints were made, nearly 6 million years ago, Crete was still part of the Greek mainland and early human ancestors were theoretically still living in Africa and had ape-like feet. The fossils in Crete, however, have distinctly hominin-like features, including a predominant “big toe.” The animal didn’t have claws and walked upright on the soles of its feet—not its toes. “This discovery challenges the established narrative of early human evolution head-on and is likely to generate a lot of debate,” Ahlberg says.
9-15-17 Using Zika to attack brain tumors
Using Zika to attack brain tumors
The properties that make Zika devastating for unborn babies could make it an effective weapon against a common and deadly form of brain cancer. Zika targets neural stem cells—the precursors of neurons and other brain cells. For babies, this can result in severe birth defects. The virus isn’t as harmful for adult brains, which have fewer stem cells. With this in mind, scientists investigated whether Zika could be used to destroy stem cells that drive the growth of aggressive brain tumors, known as glioblastomas. The researchers found that Zika targeted and killed human glioblastoma stem cells in a lab without harming normal brain cells. Experiments on mice with glioblastomas also showed that Zika therapy slowed tumor growth and extended the rodents’ lives, reports BBC.com. “It looks like there’s a silver lining to Zika,” says researcher Michael Diamond. He says further testing is needed to make sure weakened forms of the virus are safe for humans.
9-15-17 Third-hand smoke in furniture and clothes damages mouse organs
Third-hand smoke in furniture and clothes damages mouse organs
Exposure to smoke residue increases rodents’ stress hormones and puts them at higher risk of diabetes, as well as harming their livers and brains. Exposure to “third-hand smoke” – residue left behind on carpets, clothing and furniture – appears to increase the risk of liver damage and diabetes in mice. Residues of cigarette smoke cause a cocktail of toxins to accumulate on surfaces and clothes. Such toxins are thought to resist removal by industrial cleaners. To investigate the potential health risks of third-hand smoke, Manuela Martins-Green at the University of California, Riverside, and her team exposed curtains, upholstery and carpets to levels of smoke similar to those found by the US Environmental Protection Agency in smokers’ homes. They then exposed caged mice to segments of these fabrics for up to six months, taking brain, liver and blood samples at various intervals. After one month, these mice experienced around a 50 per cent increase in inflammatory molecules in their blood and liver compared with control mice who weren’t exposed to the fabrics. Two months in, the team saw increased cell damage in the rodents’ liver and brain. At four months, cortisol levels had increased by 45 per cent compared with the controls. High cortisol levels have been linked to weight gain and a weakened immune system. At four months, mice exposed to the smoky fabrics saw a 30 per cent rise in the levels of fasting blood glucose and insulin – both measures put the mice at increased risk of diabetes. These levels were even higher at the six-month mark.
9-14-17 Robot made from a DNA strand could deliver cargo in your blood
Robot made from a DNA strand could deliver cargo in your blood
Micromachine with two feet and two arms could pick up and deliver drugs in the bloodstream or build chemical compounds, one tiny step at a time. You won’t read about a smaller robot than this one any time soon. It consists of just a single strand of DNA, and moves by taking tiny 6-nanometre steps – around a hundred-millionth the size of a human step. The robot can pick up and deliver microscopic cargo, so its creators hope it will one day be used to transport medicines to individual diseased cells or help assemble hard-to-make chemical compounds. Just as robots have been sent to places too distant for humans to visit, such as other planets, mastering molecular robotics would allow us to “send them to places that are perhaps too small for humans to go to, for example inside the bloodstream”, says Lulu Qian at the California Institute of Technology in Pasadena. But while plenty of tiny robots exist, and some have even been used in the bloodstream, they had to be much bigger than a DNA strand to be useful. “It is one of the first steps towards developing general-purpose DNA robots,” says Qian. The robot consists of a leg with two feet attached to two arms for carrying cargo. To test it, Qian created a flat 58-by-58-nanometre surface with little DNA stepping stones for it to hop between. As one foot lands, the other lifts up, causing it to randomly move from stone to stone until it eventually comes into contact with the desired cargo. It then picks up the load and continues to hop around until it finds the drop-off point. The objects collected and the drop-off point are pre-programmed by the robot’s chemical composition, which causes it to bind to particular substances. So although the path taken is random, the final destination is predictable.
9-14-17 Tumour bacteria sabotage chemotherapy by destroying cancer drugs
Tumour bacteria sabotage chemotherapy by destroying cancer drugs
Giving antibiotics to people with cancer could improve treatment by stopping bacteria from degrading anticancer drugs. Thanks to a chance discovery, researchers have uncovered one reason why chemotherapy drugs sometimes fail. It turns out that bacteria inside cancer cells can destroy some drugs, rendering them useless. The finding may explain why so few people with pancreatic cancer are successfully treated with the drug gemcitabine; bacteria that can destroy gemcitabine were discovered in three-quarters of biopsies from 113 people with pancreatic cancer. The drug is also used to treat colon and bladder cancer, and so the same effect may play a role in people with those cancers too, says the team behind the findings. Ravid Straussman at the Weizmann Institute of Science in Israel and his team made the discovery after getting puzzling results while they were investigating why healthy cells become “accomplices” to cancer cells, somehow helping them to resist drugs. They couldn’t explain why one particular group of skin cells prevented gemcitabine from killing neighbouring cancer cells. Straussman and his colleague Leore Geller noticed that the skin cells were infected with Mycoplasma bacteria, but initially dismissed it as contamination. “I almost gave up on the project,” says Straussman. In fact, it turns out that the bacteria destroy gemcitabine. “We found that the bacteria internalise then degrade the drug, deactivating it,” says Straussman. It does this by producing a “long form” of an enzyme called cytidine deaminase.
9-14-17 Vaccine and booster shot delivered together in degradable cubes
Vaccine and booster shot delivered together in degradable cubes
Microscopic degradable polymer cubes stuffed with vaccines could spell the end of booster jabs, and lead to a single vaccine that protects against all diseases. It might be small, but it packs a mighty punch. By cramming vaccines into microscopic containers that release their loads after a preset amount of time, we may have found a way to deliver a vaccine and a booster shot all in one injection. Kevin McHugh at the Massachusetts Institute of Technology and his colleagues have come up with a way of making drug-carrying particles that allow multiple doses of a vaccine to be delivered over weeks or even months. Until now, this has been out of reach. “Vaccines are notoriously unstable,” says McHugh, and they often don’t last long at body temperature. To make the microparticles, McHugh filled silicon cube moulds with a polymer that’s already used in implants and other medical devices. These cubes – which measure just a few hundred micrometres on each side – are then filled with tiny amounts of vaccine before a lid is fitted and the whole thing is heated slightly to seal it. The polymer breaks down when in contact with water, but you can extend the time it takes to degrade by altering the structure of the particles in the polymer.
9-14-17 Microbes hobble a widely used chemo drug
Microbes hobble a widely used chemo drug
In mice, antibiotics helped the cancer treatment regain its power. Tumor cells grown with bacteria could stave off a common chemotherapy drug because some bacteria can inactivate the drug. Some bacteria may shield tumor cells against a common chemotherapy drug. Certain types of bacteria make an enzyme that inactivates the drug gemcitabine, researchers report in the Sept. 15 Science. Gemcitabine is used to treat patients with pancreatic, lung, breast and bladder cancers. Bacteria that produce the enzyme cytidine deaminase converted the drug to an inactive form. That allowed tumor cells to survive gemcitabine treatment in lab dishes and mouse studies, Leore Geller of the Weizmann Institute of Science in Rehovot, Israel, and colleagues discovered. More than 98 percent of the enzyme-producing microbes belong to the Gammaproteobacteria class, which includes E. coli and about 250 bacterial genera. Pancreatic tumors taken from human patients also carried the enzyme-producing bacteria. Of 113 pancreatic ductal adenocarcinoma samples studied, 86 contained gemcitabine-inactivating bacteria. Antibiotics may correct the problem. In the study, Geller and colleagues infected mice that had colon cancer with the enzyme-producing bacteria. Tumors grew rapidly in infected mice treated with gemcitabine alone. Giving the mice antibiotics helped gemcitabine kill tumor cells, increasing the number of tumor cells going through a type of cell death called apoptosis from about 15 percent to 60 percent or more. That result may indicate that combinations of gemcitabine and antibiotics could make chemotherapy more effective for some cancer patients.
9-14-17 Two artificial sweeteners together take the bitter out of bittersweet
Two artificial sweeteners together take the bitter out of bittersweet
Saccharin and cyclamate can have a bitter aftertaste, but not when combined. Here’s why. Many people avoid artificial sweeteners because of a bitter aftertaste. But a combination of two of them, saccharin and cyclamate, blocks the bitter effects. Artificial sweeteners can have a not-so-sweet side — a bitter aftertaste. The flavor can be such a turnoff that some people avoid the additives entirely. Decades ago, people noticed that for two artificial sweeteners — saccharin and cyclamate, which can taste bitter on their own — the bitterness disappears when they’re combined. But no one really knew why. It turns out that saccharin doesn’t just activate sweet taste receptors, it also blocks bitter ones — the same bitter taste receptors that cyclamate activates. And the reverse is true, too. The result could make your bitter batter better. And it could help scientists find the next super sweetener. Saccharin is 300 times as sweet as sugar, and cyclamate is 30 to 40 times as sweet as the real deal. Saccharin has been in use since its discovery in 1879 and is best known as Sweet’N Low in the United States. Cyclamate was initially approved in the United States in 1951, but banned as a food additive in 1969 over concerns that it caused cancer in rats. It remains popular elsewhere, and is the sweetener behind Sweet’N Low in Canada. In the 1950s, scientists realized that the combination of the two (sold in Europe under brand names such as Assugrin), wasn’t nearly as bitter as either sweetener alone.
9-14-17 AI spots Alzheimer’s brain changes years before symptoms emerge
AI spots Alzheimer’s brain changes years before symptoms emerge
A machine-learning algorithm that examines MRI scans can identify alterations in how different regions of the brain are connected that indicate future disease. Artificial intelligence can identify changes in the brains of people likely to get Alzheimer’s disease almost a decade before doctors can diagnose the disease from symptoms alone. The technique uses non-invasive MRI scans to identify alterations in how regions of the brain are connected. Alzheimer’s is a neurodegenerative disease that is the leading cause of dementia for the elderly, eventually leading to loss of memory and cognitive functions. The race is on to diagnose the disease as early as possible. Although there is no cure, drugs in development are likely to work better the earlier they are given. An early diagnosis can also allow people to start making lifestyle changes to help slow the progression of the disease. In an effort to enable earlier diagnosis, Nicola Amoroso and Marianna La Rocca at the University of Bari in Italy and their colleagues developed a machine-learning algorithm to discern structural changes in the brain caused by Alzheimer’s disease. First, they trained the algorithm using 67 MRI scans, 38 of which were from people who had Alzheimer’s and 29 from healthy controls. The scans came from the Alzheimer’s Disease Neuroimaging Initiative database at the University of Southern California in Los Angeles. The idea was to teach the algorithm to correctly classify and discriminate between diseased and healthy brains. The researchers divided each brain scan into small regions and analysed the neuronal connectivity between them, without making any assumptions about the ideal size of these regions for diagnosis.
9-14-17 History of zero pushed back 500 years by ancient Indian text
History of zero pushed back 500 years by ancient Indian text
Carbon dating has revealed that the Bakshali manuscript housed in Oxford contains the earliest known version of our modern zero symbol -- and it is nearly 2000 years old. The symbol “0” is a familiar sight, but its origins are far from certain. A recent batch of carbon dating is causing the history of mathematics to be rewritten, as it has discovered zeros dating back to a period 500 years before previously seen. The numbers appear in an ancient Indian text called the Bakhshali manuscript, which consists of 70 leaves of birch bark, filled with mathematics and text in the form of Sanskrit. “It seems to be a training manual for Buddhist monks,” says Marcus du Sautoy at the University of Oxford. The manuscript was first discovered by a local farmer in 1881, and was named after the village it was found in, in what is now Pakistan. It’s been housed by the University of Oxford’s Bodleian library since 1902. Now, for the first time, the manuscript has been carbon dated – and this has immediately upturned some commonly held beliefs. It was originally thought that manuscript was from the 9th century, but the dating methods revealed that the oldest pages are from somewhere between 224 AD and 383 AD. This means that the manuscript predates a 9th century inscription of zero on the wall of a temple in Gwalior, India, which was previously considered to be the oldest recorded example of a zero.
9-14-17 Carbon dating reveals earliest origins of zero symbol
Carbon dating reveals earliest origins of zero symbol
Carbon dating shows an ancient Indian manuscript has the earliest recorded origin of the zero symbol. The Bakhshali manuscript is now believed to date from the 3rd or 4th Century, making it hundreds of years older than previously thought. It means the document, held in Oxford, has an earlier zero symbol than a temple in Gwailor, India. The finding is of "vital importance" to the history of mathematics, Richard Ovenden from Bodleian Libraries said. The zero symbol evolved from a dot used in ancient India and can be seen throughout the Bakhshali manuscript. The dot originally indicated orders of magnitude in a number system and eventually evolved to have a hollow centre, the Bodleian Libraries said. Earlier research had dated the Bakhshali manuscript to the 8th and 12th Century, but now carbon dating has shown it to be centuries older. Bodleian Libraries said scholars had previously struggled to date it because it is made of 70 leaves of birch bark and composed of material from three different periods. The manuscript was found by a farmer in a village called Bakhshali, in what is now Pakistan, in 1881 before being acquired by the indologist Rudolf Hoernle, who presented it to the Bodleian Libraries in 1902. The creation of zero was one of the "greatest breakthroughs" in mathematics, Prof Marcus Du Sautoy of the University of Oxford said.
9-13-17 Thousands of new lifeforms discovered that redraw tree of life
Thousands of new lifeforms discovered that redraw tree of life
THEY were right under our noses – thousands of novel microscopic life forms, now unmasked by genetic analysis. Many belong to entirely new groups, as different from other microbes as an insect is from a chimpanzee. Earth’s microorganisms are split into bacteria and archaea. They make up the vast majority of species, but until recently we could only study a tiny fraction. This is because less than 10 per cent can be grown in the lab. The rest only survive in their native environment – be it a cow’s guts or a deep-sea vent. Researchers call them microbial dark matter. However, a technique called metagenomics is bringing them to light. It involves sequencing all the DNA in an environmental sample – its metagenome – then piecing together the genomes of each microbe present. “It’s like getting a mix-up of lots of different jigsaw puzzles, and then trying to put together the pieces of each individual puzzle,” says Donovan Parks at the University of Queensland in Australia. Parks’ team analysed more than 1500 metagenomes uploaded to a public database. Each contained jumbles of DNA from places like soil, the ocean, industrial effluent and baboon faeces. Using heavy-duty computers to sift through this mess, the team reconstructed 7280 bacterial and 623 archaeal genomes. About a third were new to science (Nature Microbiology, doi.org/cczd). The new microbes add 20 major branches, or phyla, to the tree of life. “To give this context, every single insect on Earth belongs to just one phylum, and every single animal with a backbone belongs to one phylum, so this is crazy new levels of stuff,” says Nicholas Coleman at the University of Sydney.
9-13-17 Help for postpartum mood disorders can be hard to come by
Help for postpartum mood disorders can be hard to come by
Time and stigma keep too many women with postpartum mood disorders from asking for help. About half of the mothers in a small study reported that they were currently experiencing symptoms of a mood disorder. Words can’t describe the pandemonium that follows a child’s birth, but I’ll try anyway. After my first daughter was born, I felt like a giant had picked up my life, shaken it hard, martini-style, and returned it to the ground. The familiar objects in my life were all still there, but nothing seemed to be the same. The day we came home from the hospital as a family of three, my husband and I plunged headfirst into profound elation and profound exhaustion, often changing by the minute. We worried. We snipped at each other. We marveled at this new, beautiful person. The experience, as new parents the world over know, was intense. The first week home, my body took a bruising. I was recovering from the wildness that is childbirth. I was insanely thirsty and hungry. I was struggling to both breastfeed and pump every two hours, in an effort to boost my milk supply. And against this backdrop, my levels of estrogen and progesterone, after climbing to great heights during pregnancy, had fallen off a cliff. Massive reconfigurations were taking place, both in life and in my body. And at times, I felt like the whole thing could go south at any point. After talking to other new mothers, I now realize that almost everyone has a version of this same story. Childbirth and caring for a newborn is really, really hard, in many different ways.
9-13-17 Orchid gives up the secrets of its success
Orchid gives up the secrets of its success
The orchid is known for its beauty and once changed hands for vast sums. Now, scientists are gaining an insight into how the plant prized for its beauty colonised almost every habitat on Earth. A team in China has unpicked the genetic blueprint of an orchid that grows wild in the mountains of southeast China. The orchid in question, from the subfamily, Apostasiodea, split off from modern species millions of years ago. Researchers led by the Orchid Conservation and Research Centre of Shenzhen sequenced the genome of the orchid and compared it with more modern species. The data, published in the journal, Nature, "provides a reference for studying orchid evolution" and suggests distinctive features found only in orchids played a key role "in the tremendous radiation of the group", they say. The orchid is one of the biggest families of flowering plants. Many are grown for their beautiful flowers, while others are of economic importance, such as the source of the food flavouring, vanilla. Commenting on the study, Dr Trevor Dines, of the wild plant conservation charity, Plantlife, said orchids have a host of unique features that make them special and instantly recognisable. Bog orchid on a remote Snowdonia hillside, the flowers have the same underlying blueprint," he said. "This research reveals that elements of this blueprint appeared right at the very start of the evolution of the orchid family, and may well have helped in their spectacular subsequent evolution into the 26,500-28,000 species we know of today."
9-13-17 Skeleton ignites debate over whether women were Viking warriors
Skeleton ignites debate over whether women were Viking warriors
DNA analysis of bones buried with full battle gear identified as female. A woman from the Viking Age in Sweden, when raids such as this were launched, may have shattered gender barriers by becoming a warrior who was buried with weapons and horses, researchers report. Their controversial conclusion has stimulated debate over the roles of Viking women. Viking warriors have a historical reputation as tough guys, with an emphasis on testosterone. But scientists now say that DNA has unveiled a Viking warrior woman who was previously found in a roughly 1,000-year-old grave in Sweden. Until now, many researchers assumed that “she” was a “he” buried with a set of weapons and related paraphernalia worthy of a high-ranking military officer. If the woman was in fact a warrior, a team led by archaeologist Charlotte Hedenstierna-Jonson of Uppsala University in Sweden has identified the first female Viking to have participated in what was long considered a male pursuit. But the new report, published online September 8 in the American Journal of Physical Anthropology, has drawn criticism from some researchers. All that’s known for sure, they say, is that the skeleton assessed in the new report belonged to a woman who moved to the town where she was interred after spending her youth elsewhere. “Have we found the Mulan of Sweden, or a woman buried with the rank-symbols of a husband who died abroad?” asks archaeologist Søren Sindbæk of Aarhus University in Denmark. There’s no way to know what meanings Vikings attached to weapons placed in the Swedish grave, Sindbæk says. (Webmaster's comment: One skeleton of a woman warrior does not a race of women warriors make.)
9-12-17 Like sea stars, ancient echinoderms nibbled with tiny tube feet
Like sea stars, ancient echinoderms nibbled with tiny tube feet
Rare 430-million-year-old fossils preserve signs of these tentacle-like limbs. Tiny tube feet extend from this sea star’s arm. Uncommonly well-preserved fossils of an ancient relative of this echinoderm show it also had an array of these tentacle-like appendages. Sea stars and their relatives eat, breathe and scuttle around the seafloor with tiny tube feet. Now researchers have gotten their first-ever look at similar tentacle-like structures in an extinct group of these echinoderms. It was suspected that the ancient marine invertebrates, called edrioasteroids, had tube feet. But a set of unusually well-preserved fossils from around 430 million years ago, described September 13 in Proceedings of the Royal Society B, provides proof. Usually, when an echinoderm dies, “the tube feet are the first things that go,” says Colin Sumrall, a paleobiologist at the University of Tennessee, Knoxville who wasn’t part of the study. “The thing that’s so stunning is that they didn’t rot away.” An abundance of soft-bodied creatures from the Silurian Period, which lasted from 443 to 416 million years ago, are preserved in a fossil bed in Herefordshire, England. The edrioasteroids found in this bed were probably buried alive by volcanic ash, entrapped before their soft tissues could break down, says study coauthor Derek Briggs, a paleontologist at Yale University. Decaying tissue then left a void that was filled in by minerals, which preserved the shape of the appendages.
9-12-17 Neuroscience reveals 3 secrets that will make you emotionally intelligent
Neuroscience reveals 3 secrets that will make you emotionally intelligent
otional Intelligence. It's everywhere. They won't shut up about it. And yet nobody seems to be able to explain what it really means or how you develop it. Face it: You don't even know what an emotion is. Most people would say an emotion is a feeling. And what's a feeling? Umm… an emotion? Yeah, nice work there, Captain Circular. And it turns out the latest research shows that the little we know about emotions is actually all wrong. And I mean really wrong. Lisa Feldman Barrett is a professor of psychology at Northeastern University, with appointments at Massachusetts General Hospital and Harvard Medical School. Her new book How Emotions Are Made: The Secret Life of the Brain turns everything you know about the feels upside down. Buckle in. We're gonna learn the real story behind how emotions work, why they're so difficult to deal with, and why the secret to emotional intelligence might just be the Merriam-Webster dictionary. Time to fire up Occam's chainsaw. Let's get to work…
- Why we're wrong about emotions
- But if you only have concepts for "anger," "happiness," and "sadness" then that's all you're ever going to see.
- Emotions are concepts: They're not hardwired or universal. They're learned.
- Emotional intelligence starts with emotional granularity: If your doctor came back with a diagnosis of "you're sick," you'd sue the quack for malpractice. Doctors need to be able to distinguish between "chancre" and "cancer." And you need to know the difference between "sad" and "lonely."
- Emotional intelligence is in the dictionary: You can't feel Fremdschämen if you don't know what it is. So learn new emotion words so you can feel new emotions and increase your emotional granularity.
- Create new emotions: We could all use a little more "passion-o-rama" in our lives. Name those unnamed feelings you have and share them with others to make them real.
9-11-17 Eating more salt might save your life? Not so much
Eating more salt might save your life? Not so much
The Salt Fix is the latest book attempting to overturn well-established dietary advice, but it leaves a bad taste, says Anthony Warner. Newspaper headlines might lead you to wrongly believe that paradigm shifts in the world of nutrition occur regularly. Barely a week goes by without someone proclaiming that everything we know about diet needs turning on its head. Despite this, one truth has remained pretty much accepted. Keeping our intake of salt down to around 6 grams per day is generally accepted as good for health, and features in dietary advice worldwide. Clearly this has left a gap in the market, because nothing attracts attention more than questioning the nutritional orthodoxy. Enter James DiNicolantonio, a US-based researcher who has made other controversial claims. His book The Salt Fix attempts to upend the orthodoxy, as its subtitle makes clear: Why the experts got it all wrong – and how eating more [salt] might save your life. He asserts that despite what public health organisations have been telling us for decades, eating more salt than recommended is not, in most cases, linked to high blood pressure and to risk of heart disease and stroke. On the contrary, he says, it can help protect against heart disease, as well as insulin resistance, diabetes and kidney disease. The book’s references include dated research, bizarre opinion pieces and occasional anecdotes, to back up the central argument that we’ve been getting bad advice on salt for decades. This runs counter to overwhelming evidence to the contrary. Key studies that support the book’s premise are criticised by leading medical bodies.
9-11-17 Rat brains seen replaying scary memories as they sleep
Rat brains seen replaying scary memories as they sleep
Could this be where nightmares come from? When rats are given a fright while awake, their brains go on to replay their fear when they next fall sleep. Have we had our first peek at the source of nightmares? When rats are given a fright while they are awake, the fear centre of their brains gets reactivated when they next go to sleep. This could explain why people who go through frightening experiences often have nightmares afterwards, says György Buzsáki of New York University. Rats store mental maps of the world they experience in their hippocampi – two curved structures in the brain. Different places are processed by distinct groups of neurons in the hippocampi that fire together in sequence as rats run around a maze, for example. Later, after exploring an environment like this, these firing sequences have been seen replaying as the animals sleep, as if dreaming of the routes they’d taken. This process is thought to allow memories to become consolidated for longer term storage, and has recently been detected in people for the first time. Buzsáki’s team wondered if such memory replay might include not just spatial information but also how the animal was feeling at the time. They tested this by giving a rat an unpleasant but harmless experience – a puff of air in the face from a computer keyboard cleaner – at a particular spot along a route. As expected, the rats learned to fear that particular place. “They slow down before the location of the air puff, then run superfast away from it,” says Buzsáki’s colleague, Gabrielle Girardeau. “If you do it in the face of a human, they don’t like it either.”
9-11-17 ‘Dark matter’ microbes add 20 new branches to the tree of life
‘Dark matter’ microbes add 20 new branches to the tree of life
Over 90 per cent of microorganisms are unknown to science, but DNA analysis has unmasked thousands of them and made life's story far more complex. They were right under our noses all along – thousands of novel microscopic life forms, now unmasked by genetic analysis. Many belong to entirely new groups, as different from other microbes as an insect is from a chimpanzee. Earth’s microorganisms are split into groups called bacteria and archaea. Together, they make up the vast majority of species on the planet, but until recently we were only able to study a tiny fraction of them. This is because less than 10 per cent can be isolated and grown in the lab. The rest can only survive in the conditions of their native environment – be it a hydrothermal vent or the guts of a cow. Researchers call them microbial dark matter. However, a technique called metagenomics is bringing them to light. It involves taking an environmental sample, sequencing all the DNA in it – its metagenome – then piecing together the genomes of each of the microbes present. “It’s like getting a mix-up of lots of different jigsaw puzzles, and then trying to put together the pieces of each individual puzzle,” says Donovan Parks at the University of Queensland in Australia. Parks and his colleagues analysed more than 1500 metagenomes that researchers worldwide had uploaded to a public database. Each contained jumbles of DNA sequences collected from environments such as soil, the ocean, hydrothermal vents, industrial effluent, and cow and baboon faeces. Using heavy-duty computers to sift through this mess, the team ultimately reconstructed 7280 bacterial and 623 archaeal genomes – about a third of which were new to science.
9-11-17 Tiny worm burrows may reveal when first complex animals evolved
Tiny worm burrows may reveal when first complex animals evolved
Microscopic fossil burrows found in ancient rocks reveal that small worm-like animals existed more than half a billion years ago. A set of tiny burrows could resolve a big puzzle: how complex animals evolved and spread around the world without revealing their presence. The Cambrian explosion, roughly 541 million years ago, marks when recognisable animals burst onto the scene and began leaving obvious fossil evidence of their presence. But there’s a problem: molecular evidence suggests that the first simple animals, including sponges, evolved at least 635 million years ago. “Bilaterians” – complex animals with a head and a left and right side to their bodies – seem to have evolved later, but still tens of millions of years before the Cambrian explosion. There is some older fossil evidence suggesting the presence of simple animals, but the bilaterians have left mere shadows of their earliest history – even though they were rising to global dominance. The burrows that Luke Parry at the Royal Ontario Museum in Toronto, Canada, and his colleagues have found might help explain how they remained hidden. They come from a Brazilian site where the rocks were formed at the sea bottom between 555 and 541 million years ago – just before the Cambrian explosion. The burrows are microscopic. The largest are 0.6 millimetres in diameter, and the smallest are 50 micrometres wide. But they are filled with minerals, so the researchers could use CT scanning to produce detailed 3D images.
9-11-17 Science can’t forecast love
Science can’t forecast love
No magic mix of personality traits on paper can discern how romantic matches will turn out in real life. Extensive personality and partner preference questionnaires don’t predict who will strike romantic sparks upon meeting in person, a new study finds. Here’s some heartbreaking news for people pinning their hopes on online matchmaking sites: It’s virtually impossible to forecast a love connection. Maybe that’s not so shocking to survivors of the dating wars. But now science is weighing in. Extensive background data on two individuals — comparable to that collected by digital dating services — can’t predict whether that pair will romantically click during a four-minute, face-to-face speed date, say psychologist Samantha Joel of the University of Utah in Salt Lake City and colleagues. People know when an in-person meeting on a speed date has gone smoothly or felt right — and that bodes well for mutual attraction, the investigators report online August 30 in Psychological Science. But on paper, no blend of personal qualities and partner preferences thought to influence mate choices pegged which opposite-sex duos would hit it off, Joel’s group concludes. Joel expected that, say, a person who reported being attracted to extroverted people would generate the most chemistry with speed daters who reported being extroverted. Or, two people who reported being good-looking and having particularly warm personalities would feel especially attracted to one another after brief dates. But that’s not what Joel and coauthors Paul Eastwick of the University of California, Davis and Eli Finkel of Northwestern University in Evanston, Ill., found.
9-10-17 Which foods really belong in your fridge?
Which foods really belong in your fridge?
From butter to apples to stone fruit, what really needs to stay cool? ere has been many a heated debate over how to store delicate items like eggs and butter. Some swear that butter is fine when left covered on the counter — and there's nothing worse than hard butter come baking — or toast — time. And it's a shame to think that fruit, which looks so lovely piled into a stone bowl on the counter, needs to be hidden in the icebox. While it would be nice if really fresh, high-quality foods from your local farmer didn't need to be refrigerated, the truth is that refrigeration helps many items — though not all — remain at their peak longer. We wanted the answers to some of the oft-debated refrigeration mysteries. We went digging, and here's what we found:
- Eggs: Should be refrigerated in the United States
- Apples: Refrigerate
- Stone fruit: Refrigerate after ripening
- Nuts: Refrigerate
- Butter: Refrigerate, or keep just a few days' worth on the counter
- Soy sauce, fish sauce, and hot sauce: Refrigerate for longer life, but they won't spoil on the counter
- Flour: You can refrigerate, but why bother?
- Fresh herbs: Refrigerate, except for basil
9-10-17 Meet the vampire ant from hell with huge jaws and a metal horn
Meet the vampire ant from hell with huge jaws and a metal horn
Linguamyrmex vladi had ferocious snapping jaws and a horn reinforced with metal, which it may have used to puncture prey and drain their blood. A newly discovered species of prehistoric “hell ant” had anatomy that lived up to its demonic name, including a lethal feeding apparatus reinforced with metal. Hell ants are an extinct lineage from the Cretaceous Period. Instead of regular mouthparts, they had upward-facing blades. No living species have such facial anatomy. However, the hairs around hell ants’ mouths are reminiscent of hairs on modern trap-jaw ants that cause their mouths to snap shut when triggered. This has led to speculation that the hell ants’ mouthparts worked in a similar way. Some also had a horn-like appendage that jutted out over their tusk-like mandibles. This includes the new species, Linguamyrmex vladi, which Phillip Barden at the New Jersey Institute of Technology in Newark and his colleagues found preserved in 98-million-year-old amber. It may be that when another insect brushed the trigger hairs, the blade-like mandibles flipped up and impaled the prey against the horn, punching through its outer layer. “You have this sort of stopping plate, made to accommodate the mandibles closing and capturing prey,” says Barden. That’s not all. CT scans revealed that L. vladi’s horn was reinforced with metal.
9-8-17 Sugars in breast milk may fight harmful bacteria directly
Sugars in breast milk may fight harmful bacteria directly
Scientists may have found a sweet new way to fight Group B Strep: Sugars in some women’s breast milk busted up colonies of the potentially harmful bacteria in a small lab study. The results, published online June 1 in ACS Infectious Diseases and presented August 20 in Washington, D.C., at the American Chemical Society’s annual meeting, raise all sorts of possibilities. Perhaps these sugars keep Group B Strep in check and so babies don’t readily acquire infections while nursing. If so, and if researchers can identify the exact sugars responsible, those molecules might be converted into desperately needed new antibiotic drugs that could sidestep some of the problems, such as bacterial resistance, with existing antibiotics. For me, though, one of the most interesting findings was the variability among different women’s breast milk. Chemist Steven Townsend of Vanderbilt University in Nashville and his colleagues began with milk samples from five women. After isolating the collection of sugars in each, the researchers suspended the mix in water to reach the same concentration as in whole breast milk. Then the sugary slurry was applied to lab plates, along with Streptococcus agalactiae — Group B Strep. Of the five samples, one woman’s breast milk sugars were especially potent at preventing the bacteria from getting a foothold and multiplying, the researchers found. Another sample, from a different woman, showed middling effects against the bacteria. The three remaining samples weren’t effective. The researchers have since tested breast milk samples from another 20 or so women and are working on figuring out the exact identities of the bacteria-busting sugars.
9-9-17 Want to be more creative? Try listening to baroque music.
Want to be more creative? Try listening to baroque music.
The fear that Americans, in general, are becoming less creative has inspired stacks of studies, which identify a variety of techniques that may stimulate innovative thought. These range from mild inebriation to electrical stimulation of the brain. New research points to a simpler method: Crank up the music. Not just any music — something upbeat and stimulating, such as the opening movement of Antonio Vivaldi's The Four Seasons. In a study published in the online journal PLoS One, participants proved more skillful at generating creative ideas if that cheerful, chirpy concerto was playing in the background. "Creativity is one of the most important cognitive skills in our complex, fast-changing world," write Simone Ritter of Radboud University Nijmegen in the Netherlands, and Sam Ferguson of Australia's University of Technology Sydney. "Music listening can be easily integrated into daily life, and may provide an innovative means to facilitate creative cognition in an efficient ways in various scientific, educational, and organizational settings." Their study featured 155 people recruited online, the majority of whom were college students. All performed a series of creativity-related tests, including the well-known Alternative Uses Task, in which they were given three minutes to list as many "different and creative uses" they could come up with for a common object — in this case, a brick. Performance on that task is used to measure "divergent thinking," the ability to use one's imagination to come up with new concepts, or combine old ones in unexpected, fruitful ways.
9-9-17 Ankle fossil suggests our ancient ancestors leapt like acrobats
Ankle fossil suggests our ancient ancestors leapt like acrobats
A 52-million-year-old ankle bone hints at first primates jumping rather than clambering from tree to tree – but what drove them to evolve this way is a mystery. The first primate may have been a leaper, not a clamberer. For years, many biologists have argued that the common ancestor of all primates was a small animal that scampered along thin tree branches. Now a fossil discovered in France suggests the first primate might actually have been a bizarre monkey-like animal capable of acrobatic leaping. That makes it harder to work out what drove primate evolution. Primates first appear in the fossil record about 57 million years ago. They quickly divided into two groups – the “wet-nosed” primates that now include lemurs and the “dry-nosed” primates represented by tarsiers, monkeys, apes and humans. Primates on both sides of the divide have features in common, including grasping hands and feet, and nails rather than claws. This implies that these features evolved in the primate common ancestor. The proto-primate is often reconstructed as a small animal that used its hands and feet to grasp and run along thin branches, says Doug Boyer at Duke University in Durham, North Carolina. “It’s thought of as looking a little like a mouse lemur today – very much specialised for navigating the ends of branches where it could reach flowers, fruits and insects.” But a 52-million-year-old fossil ankle bone found near Marseilles, France, calls this idea into question. Boyer and his colleagues, who analysed the fossil, say it belonged to an early primate called Donrussellia provincialis, which was previously known only from fossil teeth.
9-8-17 We seem to be getting stupider and population ageing may be why
We seem to be getting stupider and population ageing may be why
Average IQ may be falling, a trend some think is due to smarter people having fewer children. Now evidence suggests longer lifespans may be to blame instead. We’re getting stupider – and our ageing population may be to blame. Since around 1975, average IQ scores seem to have been falling. Some have attributed this to the evolutionary effect of smarter women tending to have fewer children. But new evidence suggests population-wide intelligence could in fact be sinking because people now live longer, and certain types of intelligence falter with advanced age. For about a century, average IQ scores in wealthy nations rose in a steady and predictable way – by about three points a decade. This is thought to be thanks to improvements in social conditions like public health, nutrition and education. Since this trend – called the Flynn effect – was first noticed in the 1940s, it has been seen in many countries, from the Netherlands to Japan. But by 2004, researchers had begun to notice what appears to be a reversal in this trend, with average IQ scores going into decline. “The drop is around 7 to 10 IQ points per century,” says Michael Woodley of the Free University of Brussels in Belgium. The Flynn effect is supported by much evidence, and its reversal is still controversial. Even more controversial are some of the theories put forward to explain it. Woodley and some others subscribe to the fertility hypothesis. This posits that the most educated people in Western countries have been having fewer children than the rest of the population, which is bringing intelligence down, generation by generation.
9-8-17 Landmark gene therapy approved
Landmark gene therapy approved
In a major milestone in the fight against cancer, the Food and Drug Administration (FDA) last week approved a new treatment that genetically alters patients’ immune cells to make them seek out and destroy childhood leukemia. The landmark decision marks the first time gene therapy involving “living drugs” has been cleared for use in the U.S., reports The New York Times. It came after a study in which 83 percent of critically ill patients went into remission within three months of having the treatment. Marketed as Kymriah, the gene therapy was approved for children and adults up to age 25 with B-cell acute lymphoblastic leukemia, the most common childhood cancer in the U.S. It will be available to the 20 percent of patients who either don’t respond to standard treatment or relapse after initial therapy. Only about 600 people across the country will currently be eligible, but the one-time treatment is already being tested for a range of other diseases, including non-Hodgkin’s lymphoma and multiple myeloma. “We’re entering a new frontier in medical innovation,” says FDA Commissioner Scott Gottlieb. “New technologies such as gene and cell therapies hold out the potential to transform medicine.” Kymriah will cost $475,000—less than a bone marrow transplant, which can also cure some forms of leukemia.
9-8-17 New heart-attack drug
New heart-attack drug
Anti-inflammatory drugs could be just as effective as cholesterol-lowering statins in cutting the risk of heart attacks and strokes, new research shows. Only about half of people who have a heart attack have unhealthy cholesterol levels; in many cases, the main culprit is chronic inflammation that leads to clogged arteries. Statins can help, but a lot of heart-attack sufferers who are taking these drugs still have signs of inflammation. Researchers at Brigham and Women’s Hospital in Boston enlisted 10,000 of these patients and randomly assigned them to receive statins with either a placebo or one of three doses of canakinumab, an anti-inflammatory drug used to treat rare autoimmune disorders. After receiving injections every three months for about four years, those on the medium dose of the drug had a 15 percent lower risk for another heart attack, reports BBC?.com. “For the first time,” says lead author Paul Ridker, “we’ve been able to definitively show that lowering inflammation independent of cholesterol reduces cardiovascular risk.” Critics argue the drug’s modest benefits are offset by users’ increased risk for life-threatening infections, and by its hefty annual price tag: about $200,000.
9-8-17 More fat, fewer carbs
More fat, fewer carbs
One of the largest studies into how diet affects health and mortality has found that eating high quantities of carbohydrates increases risk of premature death more than excessive fat intake. Researchers led by a team at McMaster University in Canada studied health data from 135,000 people in 18 different countries across five continents. They also analyzed the participants’ diet, socioeconomic status, lifestyle, weight, and other variables. Over the seven-year study period, the people who ate the most carbohydrates—deriving 77 percent of their total daily calories from foods like bread and rice—had a nearly 30 percent higher risk of early death than those who ate less. People who took about 35 percent of their daily calories from fat, meanwhile, had a 23 percent lower risk of dying early. “We are hoping that dietary guidelines are reconsidered in light of the new findings,” study author Mahshid Dehghan tells Reuters.com. “What we are suggesting is moderation, as opposed to very low and very high intakes of fats and carbohydrates.”
9-8-17 Preservatives linked to obesity
Preservatives linked to obesity
Chemicals commonly added to processed foods and some everyday products could disrupt human hormones and lead to weight gain. Scientists at Cedars-Sinai Medical Center in Los Angeles used human stem cells to grow hormone-producing brain tissues involved in appetite and metabolism, and cells that form the lining of the gut. They then exposed these cells to three widely used chemicals, known as endocrine disruptors: the food preservative butylhydroxytoluene; perfluorooctanoic acid, a polymer in household products, including cookware and carpets; and the paint compound tributyltin. They found that each of these chemicals damaged the hormones that send signals between the gut and the brain to help people realize when they are full. If this communication system fails, people can overeat and gain weight, reports ScienceDaily?.com. Clive Svendsen of Cedars-Sinai says the findings “substantially improve our understanding of how endocrine disruptors may damage human hormonal systems and contribute to the obesity epidemic in the U.S.”
9-7-17 Do the colours you wear at work matter?
Do the colours you wear at work matter?
Does the colour of the clothes you wear at work matter? Could wearing a red tie or dress be the key to getting promoted? Pennsylvania bank boss John Spier was fed up with looking like a "stuffy banker". So after decades of wearing loose-fitting pinstripe suits and anonymous ties, he decided he wanted a fashion makeover. Taking a leap of faith, Mr Spier enlisted the help of a corporate stylist Toi Sweeney. Overnight his old wardrobe was binned, to be replaced with "warmer ties and a more fitted suit", says Mr Spier. "She was able to preserve the professional look I wanted without making me seem like a stuffy banker." Mr Spier says he went from an executive who rarely thought about what he was going to wear, to someone who likes wearing colourful ties. More importantly, he says the makeover has put a spring in his step, and made him more confident. The saying, "you never get a second chance to make a first impression" perhaps resonates most in the workplace, where bosses must exude authority but also friendliness, and the rest of us want to look professional, but stand out. Ms Sweeney believes "we are all products and your personal brand steps through the door before you do". (Webmaster's comment: What we wear influences how others preceive us. It's in our genetics!)
9-7-17 When a fungus invades the lungs, immune cells can tell it to self-destruct
When a fungus invades the lungs, immune cells can tell it to self-destruct
Mouse study points to why breathing in spores from one mold species doesn’t usually cause health problems. Aspergillus fumigatus is a common fungus found in soil. New immunology research is helping explain why the organism can make immunocompromised people so sick, while going undetected by healthy people. Immune cells can turn certain invaders on themselves, forcing them to prematurely self-destruct, researchers have discovered. In mice, when white blood cells in the lungs engulf spores of a common airborne fungus, these immune cells release an enzyme that sends the fungal cells into programmed cell death. That prevents the spores from setting up shop in the lungs and sparking a potentially deadly lung infection, the researchers report in the Sept. 8 Science. Found naturally in soil and decaying organic matter, the fungus, Aspergillus fumigatus, releases airborne spores that are found in small doses in the air people breathe every day. The finding may help explain why most people can regularly inhale the spores and not get sick. In people with weakened immune systems, though, this natural defense system doesn’t work. This research could eventually lead to better treatments for these patients.
9-7-17 Brain chemical lost in Parkinson’s may contribute to its own demise
Brain chemical lost in Parkinson’s may contribute to its own demise
In a hopeful note, treating dopamine-producing nerve cells with antioxidants lessened damage. In Parkinson's disease, a dangerous form of the chemical messenger dopamine may help destroy the nerve cells that produce it, a new study suggests. The brain chemical missing in Parkinson’s disease may have a hand in its own death. Dopamine, the neurotransmitter that helps keep body movements fluid, can kick off a toxic chain reaction that ultimately kills the nerve cells that make it, a new study suggests. By studying lab dishes of human nerve cells, or neurons, derived from Parkinson’s patients, researchers found that a harmful form of dopamine can inflict damage on cells in multiple ways. The result, published online September 7 in Science, “brings multiple pieces of the puzzle together,” says neuroscientist Teresa Hastings of the University of Pittsburgh School of Medicine. The finding also hints at a potential treatment for the estimated 10 million people worldwide with Parkinson’s: Less cellular damage occurred when some of the neurons were treated early on with antioxidants, molecules that can scoop up harmful chemicals inside cells. Study coauthor Dimitri Krainc, a neurologist and neuroscientist at Northwestern University Feinberg School of Medicine in Chicago, and colleagues took skin biopsies from healthy people and people with one of two types of Parkinson’s disease, inherited or spontaneously arising. The researchers then coaxed these skin cells into becoming dopamine-producing neurons. These cells were similar to those found in the substantia nigra, the movement-related region of the brain that degenerates in Parkinson’s.
9-7-17 Worrying we are ill when we aren’t is not as bad as it seems
Worrying we are ill when we aren’t is not as bad as it seems
Extreme health anxiety can be crippling but a lot of today's internet-fuelled "cyberchondria" doesn't need formal psychological treatment, says Zara Aziz. We are told there is a lot of health anxiety around, with reports that one in five outpatient appointments in the UK are taken up by “needlessly worried” people. Much of the blame is heaped on Doctor Google, alongside talk of wasted money. So what’s going on? How concerned should we be about the apparent wave of the worried? The one-in-five figure comes from researchers behind a new study for the UK’s National Institute for Health Research that looks at how health anxiety can be treated with talking therapies. Health anxiety – also known as illness anxiety disorder or hypochondriasis (a more stigmatising name) – is a medical diagnosis in its own right. Although it has long been recognised in various guises, it remains understudied. Earlier research puts the prevalence of health anxiety at between 3 and 13 per cent. But 10 to 20 per cent of “well” individuals can also have unfounded health worries at some point in their lives, even though this may not amount to a medically recognised problem. Health anxiety can also have upsides. A small amount can actually be a force for good, if it signals impending danger and leads us to seek appropriate medical help rather than ignoring symptoms until they are too advanced. Some studies have shown this effect in men, among whom increased health anxiety has aided earlier cancer detection. Such concern can help men overcome reluctance to go to the doctor, often cited as an obstacle to improving health outcomes. A similar association has not been seen in women.
9-7-17 Woolly rhinos may have grown strange extra ribs before going extinct
Woolly rhinos may have grown strange extra ribs before going extinct
Odd bones attached to neck could have signaled genetic trouble. s woolly rhinos dwindled to extinction, their odds of having odd ribs attached to their neck bones may have risen. Creatures are shown in a wall painting at Chauvet-Pont d’Arc Cave in southern France. As time ran out for the woolly rhino, strange things happened. Before going extinct, some of the beasts faced an unusually high risk of growing bizarre ribs in their neck, a new study suggests. Those misplaced ribs might have signaled the animals’ impending demise. Scientists examined neck bones from 32 woolly rhinos and found indented spots on five of them where ribs had once attached to the seventh cervical vertebra, the lowermost bone in the neck. That amounts to strange cervical ribs on about 16 percent of the creatures. For comparison, 56 specimens of the same vertebra from modern rhino skeletons had no such spots, says Frietson Galis, an evolutionary biologist at the Naturalis Biodiversity Center in Leiden, the Netherlands. Galis and paleontologist Alexandra van der Geer, also at Naturalis, report the findings August 29 in PeerJ. Found in what is now the North Sea and in adjacent Dutch deltas and coastal areas, the bones date from about 35,000 to 115,000 years ago, a time of changing climate and ecosystems. The woolly rhino, Coelodonta antiquitatis, probably disappeared from Western Europe sometime not long after roughly 35,000 years ago, although populations to the east survived longer.
9-7-17 Why do humans sweat?
Why do humans sweat?
The strange science of perspiration. Most furry mammals pant to regulate their body temperature. Other animals, like ectotherms — lizards, amphibians, and insects — have other behaviors that help keep them cool. Humans, however, are in a category of our own. We are the only mammal that relies on secreting water onto the surface of our skin to stay cool: We call it sweating. But how did we develop this ability? When did we ditch the fur of our primate ancestors in favor of sweaty skin? At some point in humanity's past, we, too, likely panted to thermoregulate. Our closest primate relatives — chimpanzees and gorillas — dump excess body heat by panting, so it stands to reason that early human ancestors would have panted, too, explains Yana Kamberov, assistant professor of genetics at the Perelman School of Medicine at the University of Pennsylvania. "Basically, all cooling in mammals involves, to a large extent, the heat that's needed to convert water from a liquid to a gas and the energy that's lost in doing that," Kamberov says. "Furry animals pant in order to take air in, and [they] use that air to dissipate body heat." For humans, however, something changed over the course of evolution that altered how we as a species thermoregulate and sent us down a unique path. The million-dollar question, Kamberov says, is why. "One possibility is that it enabled us to explore a niche that was free of predators," she suggests. "If you cool off the way a human does, you can go out during the hottest periods of the day, when most predators are going to be hiding themselves from heat ... We, on the other hand, are able, under very strong radiant heat, to sweat to cool ourselves off. This opens up an avenue for us ... to exploit a niche that otherwise wouldn't be available."
9-7-17 No, your genes don’t determine whether you love or hate Marmite
No, your genes don’t determine whether you love or hate Marmite
A nonsense PR stunt is doing the rounds, but finding snippets of DNA that are associated with whether you like a particular food doesn’t actually mean much. Yesterday New Scientist received a press release about a new piece of scientific research that was immediately, obviously silly. It was so egregiously wrong, we originally didn’t plan to cover it at all – beyond mocking it on social media – but since it has appeared in several other outlets, we thought it might be worth pointing out just why it is so bone-headed. The study was published by a genetic testing company called DNAFit. It purports to explain people’s reactions to Marmite, a yeast-based spread that is a popular breakfast food in the UK. For years Marmite has used advertising slogans along the lines of “you either love it or hate it”. Now DNAFit is claiming to understand why people have such polarised responses: apparently it’s all in the genes. DNAFit took genetic samples from 261 people, some of whom loved Marmite while others (you guessed it) hated it. They looked at single nucleotide polymorphisms (SNPs), which are bits of the genome where one letter varies from person to person. They found five SNPs that were statistically associated with Marmite preference: if you were a lover you were more likely to have one version, but if you were a hater you more likely had the other. Here’s the thing: this doesn’t tell you much. A genome association study like this cannot prove that your genes have an effect on breakfast spread preferences. If the effect exists, such a study can tell you where to find it – but it can also give you meaningless results.
9-6-17 Don’t quit now: Why you have more willpower than you think
Don’t quit now: Why you have more willpower than you think
Willpower is not the limited resource we once thought it was. A simple attitude-hack is all that stands between you and endless motivation. IT HAS been a long day. You’ve been squinting at spreadsheets since 9 am, but your boss keeps interrupting to ask how you’re getting on and colleagues insist on offloading their own problems. By 6 pm you’re exhausted. It’s a miracle that you even make it home before hitting the wine and chocolate. Psychologists used to have a convincing explanation for why days like these leave us weak in the face of temptation. Willpower is a limited resource that, like the cash you work so hard for, will eventually run out. Use it all up during the day and there’ll be none left by dinner time. This much has been received wisdom in psychology circles for nearly 20 years. Recently, though, that certainty has begun to fade. According to a series of newer findings, our levels of self-control are not so much a budget we have to eke out, but a renewable resource that can be powered up as we go along. “Instead of thinking of willpower as the amount of petrol in a car… think of it as the car’s battery,” says Krishna Savani at Nanyang Technological University in Singapore. “The more you drive, the more the battery gets charged, and the longer it will last.” In this view, your powers of concentration are only limited if you think they are. It raises the intriguing possibility that, if we can get into the right mindset, superhuman powers of motivation and self-control could be ours for the taking.
9-6-17 Need a creativity boost? Try listening to happy background music
Need a creativity boost? Try listening to happy background music
Listening to upbeat music has been found to boost people’s creativity – but silence is best for when you’re trying to decide on a solution for a problem. Need inspiration? Happy background music can help get the creative juices flowing. Simone Ritter, at Radboud University in the Netherlands, and Sam Ferguson, at the University of Technology in Sydney, Australia, have been studying the effect of silence and different types of music on how we think. “People in lots of contexts use music to help them work,” says Ferguson. A better understanding of how different types of music affect creativity is likely to be useful for many people, he says. They put 155 volunteers into five groups. Four of these were each given a type of music to listen to while undergoing a series of tests, while the fifth group did the tests in silence. The tests were designed to gauge two types of thinking: divergent thinking, which describes the process of generating new ideas, and convergent thinking, which is how we find the best solutions for a problem. Ritter and Ferguson found that people were more creative when listening to music they thought was positive, coming up with more unique ideas than the people who worked in silence. “We also tested other musical excerpts that were sad, anxious and calm, and didn’t see this effect,” says Ferguson. “It seems that the type of music present is important, rather than just any music.” However, happy music – in this instance, Antonio Vivaldi’s Spring – only boosted divergent thinking. No type of music helped convergent thinking, suggesting that it’s better to solve problems in silence.
9-6-17 A type of sleep therapy reduces depression, anxiety and paranoia
A type of sleep therapy reduces depression, anxiety and paranoia
Cognitive behavioural therapy for insomnia has been found to also help a range of mental health issues, including negative thoughts, hallucinations and psychosis. A type of therapy originally designed for insomnia has been found to also help a range of mental health issues, including negative thoughts, anxiety, depression and psychosis. Daniel Freeman, at the University of Oxford, and his colleagues have been testing Sleepio, a type of cognitive behavioural therapy available online. The ten-week course is intended to restore healthy sleep patterns in people with insomnia, and Freeman wanted to see if it could also relieve other problems. His team asked nearly 1900 students who have difficulty sleeping to try using Sleepio, and nearly 1870 others to try following standard advice for insomnia. Both groups filled in questionnaires beforehand that assessed their sleep patterns, as well as tendencies to experience paranoia and hallucinations. They repeated these questionnaires at three, ten and 22 weeks into the experiment. Overall, those using Sleepio slept 50 per cent better than the control group, says Freeman. Compared to this group, the Sleepio users also had a 30 per cent reduction in hallucinations, 25 per cent reduction in paranoia, and their anxiety and depression levels were 20 per cent lower. Statistical analysis revealed that improved sleep was itself accountable for up to 60 per cent of these additional benefits to mental health. “If you have problems sleeping, we know it affects the way you think, giving you more fearful and depressive thoughts and more rumination – all consistent with a dip in mood,” says Freeman.
9-6-17 Learning is a ubiquitous, mysterious phenomenon
Learning is a ubiquitous, mysterious phenomenon
I’ll admit it. I’m addicted to learning. There’s nothing quite like the thrill that comes with finding out something new. It’s no surprise I ended up this way. My parents were public school teachers. They instilled in me the belief that education not only opens up new opportunities but also is enjoyable in itself. My parents regularly took my siblings and me to museums, encouraged us to read widely and entertained our incessant “whys?” and “hows?” And though neither of my parents taught science, I remember studying constellations at night and experimenting with chemistry at the dining table. (My parents passed their passion for educating on to my younger brother and sister. One teaches math, the other biology and chemistry.) Perhaps it’s fitting, then, that as a new school year begins, I get to introduce Science News’ special report on learning. Or maybe not. After all, learning is something we all do. I share a newsroom with reporters and editors who also get a big kick out of learning every day. In truth, a love of learning is probably quite common. From birth, we learn — to recognize faces, to talk, to walk. We take the clues thrown at our senses and piece together an understanding of our world. Yes, we learn the three R’s in school, but we also learn (in and out of the classroom) how to build relationships, how to handle stress and what makes us happy. I’m currently learning how to prune my rosebush to get a great fall bloom, what makes an effective leader and the details of various cryptocurrencies. There’s an adage, occasionally attributed to Albert Einstein, that says something like: The day you stop learning is the day you start dying. That seems about right to me. (Webmaster's comment: Ditto!)
9-5-17 Alzheimer’s and smoking genes suggest we’re still evolving
Alzheimer’s and smoking genes suggest we’re still evolving
In the 20th century, people in the UK evolved to be less likely to smoke heavily and get Alzheimer’s, but the changes were subtle and may not last. We are still evolving – very slowly. In the 20th century, people in the UK evolved to be less likely to smoke heavily, but the effect was tiny. So claims a study of 200,000 genomes. A population can be described as evolving when the frequency of gene variants changes over time. Because most people in rich countries now live well beyond reproductive age, some argue that we have stopped evolving because natural selection has been weakened. But several recent studies claim we are still evolving, albeit slowly. Now Joseph Pickrell at Columbia University in New York and his team have analysed human genome sequences to spot gene variants that are becoming rarer. One variant, of a gene called CHRNA3, is associated with heavier smoking in those that smoke, raising their risk of a smoking-related death. Comparing people over the age of 80 with people over the age of 60, Pickrell estimates that the variant has declined by 1 per cent between generations. However, his team was not able to prove this, as they did not have any genomic data from people under the age of 40. A variant of the ApoE4 gene that is known to increase the risk of late-onset Alzheimer’s disease, as well as cardiovascular disease, may also be getting rarer. These variants might be becoming rarer because many people now have children in their 40s and 50s, when people with such variants are at greater risk of dying. Even a subtle impact on lifespan can have a relatively strong evolutionary effect over many generations, says Pickrell.
9-5-17 Learning takes brain acrobatics
Learning takes brain acrobatics.
When neural areas more easily switch communication partners, learning improves. In brains that learn with ease, groups of nerve cells can readily switch between conversations. Peer inside the brain of someone learning. You might be lucky enough to spy a synapse pop into existence. That physical bridge between two nerve cells seals new knowledge into the brain. As new information arrives, synapses form and strengthen, while others weaken, making way for new connections. You might see more subtle changes, too, like fluctuations in the levels of signaling molecules, or even slight boosts in nerve cell activity. Over the last few decades, scientists have zoomed in on these microscopic changes that happen as the brain learns. And while that detailed scrutiny has revealed a lot about the synapses that wire our brains, it isn’t enough. Neuroscientists still lack a complete picture of how the brain learns. They may have been looking too closely. When it comes to the neuroscience of learning, zeroing in on synapse action misses the forest for the trees. A new, zoomed-out approach attempts to make sense of the large-scale changes that enable learning. By studying the shifting interactions between many different brain regions over time, scientists are beginning to grasp how the brain takes in new information and holds onto it.
9-5-17 Zika could one day help combat deadly brain cancer
Zika could one day help combat deadly brain cancer
Virus infects and kills the stem cells that turn into glioblastomas. Zika virus infects and kills stem cells in human glioblastoma tissue, without infecting healthy brain cells. Because the stem cells generate the brain cancer cells, killing off the stem cells might prevent tumors from recurring. Zika’s damaging neurological effects might someday be enlisted for good — to treat brain cancer. In human cells and in mice, the virus infected and killed the stem cells that become a glioblastoma, an aggressive brain tumor, but left healthy brain cells alone. Jeremy Rich, a regenerative medicine scientist at the University of California, San Diego, and colleagues report the findings online September 5 in the Journal of Experimental Medicine. Previous studies had shown that Zika kills stem cells that generate nerve cells in developing brains (SN: 4/2/16, p. 26). Because of similarities between those neural precursor cells and stem cells that turn into glioblastomas, Rich’s team suspected the virus might also target the cells that cause the notoriously deadly type of cancer. In the United States, about 12,000 people are expected to be diagnosed with glioblastoma in 2017. (It’s the type of cancer U.S. Senator John McCain was found to have in July.) Even with treatment, most patients live only about a year after diagnosis, and tumors frequently recur.
9-5-17 We may be able to use Zika virus to attack brain cancer cells
We may be able to use Zika virus to attack brain cancer cells
Zika virus can infect and kill brain stem cells, causing neurological problems and microcephaly in babies. But this trait may also fight deadly glioblastoma. Zika can cause babies to be born with severe brain damage – but we may be able to harness the virus to fight brain tumours in adults. The virus, which arrived in South America from Polynesia around four years ago, is most dangerous in pregnant women. It can cause microcephaly – abnormally small heads – and associated neurological problems in the babies of women who were infected while pregnant, as well as a higher rate of miscarriage. The virus does this because, unlike most microbes, Zika can pass from blood into the brain, where it infects and kills stem cells, having severe effects on developing brains. But this ability to infect brain stem cells may prove useful for fighting deadly brain cancers, many of which are caused by mutated stem cells. Jeremy Rich at the University of California, San Diego, and his team have tested the Zika virus on glioblastoma, the most common kind of brain cancer. Glioblastoma is one of the most difficult cancers to treat – even after surgery and other therapies, it usually kills people within a year of diagnosis. The team found that exposing samples of human glioblastoma tumours grown in a dish to the Zika virus destroyed the cancer stem cells. It is these stem cells that usually kill a person, as they can become resistant to all available treatments.
9-5-17 Teaching methods go from lab to classroom
Teaching methods go from lab to classroom
Researchers are testing approaches to make learning stick. Moving education research into classrooms can be messy. But researchers are taking the plunge and finding some approaches that boost learning. Sure, students in the classroom have to remember facts, but they also have to apply them. Some research efforts to enhance learning zero in on methods to strengthen memory and recall, while others bolster students’ abilities to stay on task, think more fluidly and mentally track and juggle information. But there’s a catch. The science behind student learning is so far based on carefully controlled studies, primarily with college students. Do the same approaches work with younger students? Will they work in a classroom of 25 or 30 kids of varying abilities? These are questions researchers are asking now, says Erin Higgins of the U.S. Department of Education’s National Center for Education Research. Moving from the lab to a classroom, with all its disruptions and distractions, is key for pinning down what works, under what conditions and for whom. In the process of tweaking some of the most promising tools and strategies for classroom use, educators hope to find ways to help low-performing students gain skills that already pay off for their more successful peers. The efforts described here draw on new, innovative training methods to boost learning in K-12 classrooms. Higgins calls them “great examples” of the work under way.
9-5-17 People may have lived in Brazil more than 20,000 years ago
People may have lived in Brazil more than 20,000 years ago
Excavations at a Brazilian rock shelter near the center of South America suggest that humans hunted giant sloths there more than 20,000 years ago. Ancient people used some sloth bones unearthed at the site as personal ornaments, based on notches and holes in those finds. People hunted giant sloths in the center of South America around 23,120 years ago, researchers say — a find that adds to evidence that humans reached South America well before Clovis hunters roamed North America roughly 13,000 years ago. Evidence of people’s presence at Santa Elina rock shelter, located in a forested part of eastern Brazil, so long ago raises questions about how people first entered South America. Early settlers may have floated down the Pacific Coast in canoes before heading 2,000 kilometers east to the remote rock shelter, or they might have taken an inland route from North America, archaeologist Denis Vialou of the National Museum of Natural History in Paris and his colleagues report in the August Antiquity. Other South American sites reportedly occupied by Stone Age humans lie much closer to the coast than Santa Elina does. Excavations at Santa Elina from 1984 to 2004 revealed three sediment layers containing numerous stone artifacts and bones of giant sloths called Glossotherium. Sloth remains included small, bony plates from the skin that humans made into ornaments of some kind by adding notches and holes. Sediment layers also contained remains of hearths. Three dating methods, applied to charcoal particles, sediment and sloth bones, indicate that people first reached Santa Elina more than 20,000 years ago. Humans again visited the rock shelter from around 10,120 to 2,000 years ago, the researchers say.
9-4-17 Controversial footprints suggest we evolved in Europe not Africa
Controversial footprints suggest we evolved in Europe not Africa
A set of 5.7-million-year-old footprints, found on a Greek island, suggest that our earliest ancestors strayed far beyond their supposed African homeland. A set of ancient footprints has been found on a Greek island. They are extremely old – 5.7 million years – yet they seem to have been made by one of our hominin ancestors. At that time, hominins are thought to have been confined to Africa. The discovery supports the controversial suggestion that they may also have been living in eastern Europe. The earliest stages of hominin evolution are still mysterious. Our lineage split from chimpanzees, our closest living relatives, between 7 and 13 million years ago. The oldest undoubted hominin fossils were found in east Africa and date back about 4 million years – but there are a few older, possible hominin fossils from 6 to 7 million years ago. These include Orrorin from Kenya, and Sahelanthropus from Chad – locations that are roughly 2500 kilometres apart. The ancient footprints discovered by Gerard Gierlinski of the Polish Research Institute in Warsaw are a further 2500 kilometres away from Chad – this time to the north-east, on the tiny island of Trachilos near Crete. Gierlinski teamed up with colleagues, including Per Ahlberg at Uppsala University, Sweden, to analyse the tracks. The team found they could recognise two distinct sets of footprints, both apparently left by an animal that walked upright on two legs.
9-4-17 Weird fish fossil changes the story of how we moved onto land
Weird fish fossil changes the story of how we moved onto land
The 370-million-year-old fish Hongyu chowi doesn’t fit into the evolutionary picture we have created to explain our ancestor’s move from sea to land. The evolutionary story we have written to explain our ancestors’ move from sea to land may need a rethink. A fossil fish from this era has been discovered with several of the features of land animals – yet it was only distantly related to them. Roughly 360 million years ago, one group of lobe-finned fish began evolving into four-legged, land-living animals that resulted in reptiles, amphibians and mammals like us. Fossils have revealed many of the stages in this iconic evolutionary event. The evolutionary tree of species involved in the switch from sea to land has remained stable since the late 20th century, even as new fossils have come to light. However, a fossil discovered in a quarry in Ningxia, north China, now threatens that stability. It was discovered in 2002 by Min Zhu at the Institute of Vertebrate Paleontology and Paleoanthropology in Beijing and Per Ahlberg at Uppsala University in Sweden. The fossil belongs to a new species of lobe-finned fish, named Hongyu chowi. It was about 1.5 metres long, and lived 370 to 360 million years ago.
9-4-17 We ignore what doesn’t fit with our biases – even if it costs us
We ignore what doesn’t fit with our biases – even if it costs us
We tend to pay more attention to information that confirms our own beliefs and biases, and we are prepared to lose money to stick to our guns. We can’t help but be more welcoming of information that confirms our biases than facts that challenge them. Now an experiment has shown that we do this even when it means losing out financially. Most research on confirmation bias has focused on stereotypes that people believe to be true, says Stefano Palminteri at École Normale Supérieure (ENS) in Paris. In such experiments, people hold on to their beliefs even when shown evidence that they are wrong. “People don’t change their minds,” says Palminteri. But those kinds of beliefs tend not to have clear repercussions for the people who hold them. If our biases cost us financially, would we realise that they are not worth holding on to? To find out, Palminteri and his colleagues at ENS and University College London set 20 volunteers a task that involved learning to associate made-up symbols with financial reward. In the first of two experiments, the volunteers were shown two symbols at a time and had to choose between them. They then received a financial reward that varied depending on their choice. By repeating this multiple times, the volunteers found out how much some of the various symbols were worth. However, they could only see this information for symbols they had chosen.
9-3-17 How to fall to your death and live to tell the tale
How to fall to your death and live to tell the tale
From slips in the shower to stumbles down the stairs, falls kill more than 32,000 Americans every year. Doctors say learning how to take a spill might just save your life. Alcides Moreno and his brother Edgar were window washers in New York City. The two Ecuadoran immigrants worked for City Wide Window Cleaning, suspended high above the congested streets, dragging wet squeegees across the acres of glass that make up the skyline of Manhattan. On Dec. 7, 2007, the brothers took an elevator to the roof of Solow Tower, a 47-story apartment building on the Upper East Side. They stepped onto the 16-foot-long, 3-foot-wide aluminum scaffolding designed to slowly lower them down the black glass of the building. But the anchors holding the 1,250-pound platform gave way, plunging them 472 feet to the alley below. The fall lasted six seconds. Edgar, at 30 the younger brother, tumbled off the scaffolding, hit the top of a wooden fence, and was killed instantly. But rescuers found Alcides alive, sitting up amid the wreckage, breathing and conscious. Falls are one of life's great overlooked perils. We fear terror attacks, shark bites, Ebola outbreaks, and other minutely remote dangers, yet more than 420,000 people die worldwide each year after falling. Falls are the second-leading cause of death by injury, after car accidents. In the United States, falls cause 32,000 fatalities a year (more than four times the number caused by drowning and fires combined). Nearly three times as many people die in the U.S. after falling as are murdered by firearms.
9-1-17 Parabens tied to infertility
Parabens tied to infertility
Unregulated chemicals in everyday items such as toothpaste, soap, and deodorant could be causing fertility problems for men, a new study suggests. Parabens such as methylparaben and propylparaben are preservatives widely used in U.S. grooming products. To examine the effects of these chemicals on fertility, researchers in Poland studied the lab test results of 315 male fertility clinic patients, reports Reuters.com. They found that those with higher concentrations of parabens in their saliva, blood, urine, and semen had lower testosterone levels and a larger proportion of sperm that was abnormally shaped or slow moving—factors that reduce the likelihood of fertilization. Parabens were also linked to DNA damage in men’s sperm. The researchers remain unsure why the chemicals may affect fertility, or at what levels they can be harmful—but urge caution all the same. Study leader Joanna Jurewicz says avoiding parabens altogether would be “very difficult, because they are widespread,” but suggests checking labels on personal care products to limit consumption where possible.
9-1-17 A possible cure for peanut allergies
A possible cure for peanut allergies
A breakthrough new treatment for peanut allergies has enabled previously allergic children to eat the nuts without reaction for four years, raising hopes of a long-term cure for this increasingly common and sometimes life-threatening condition. About 1.4 percent of U.S. children were allergic to peanuts in 2008, up threefold from 1997, reports The Guardian (U.K.). Scientists have long been experimenting with peanut oral immunotherapy, in which sufferers are exposed to increasing doses of peanut protein in order to coax their immune system into developing a tolerance to the allergen. A team at Murdoch Childrens Research Institute in Australia took this treatment one step further, by combining the peanut protein with a probiotic. They assigned 56 children with peanut allergy to receive a daily dose of either the probiotic-protein combination, or a placebo. At the end of the 18-month study period, 82 percent of those given the treatment had gained tolerance to peanuts, compared with only 4 percent of the placebo group. When the kids were retested four years later, most of those who had gained the initial tolerance were still eating peanuts as part of their normal diet. The treatment needs further research, and won’t be publicly available for at least another five years. But study author Mimi Tang says her findings “show that the probiotic-peanut combination can actually change the immune response to peanuts and provide benefits, long-term, years after” the treatment is stopped.
9-1-17 We still don’t really know what CRISPR does to human embryos
We still don’t really know what CRISPR does to human embryos
A gene editing study made headlines last month, claiming the technique is safe for human embryos. But leading researchers don’t agree with the team’s findings. The results of a much-publicised study claiming mutations in human embryos can be safely corrected with CRISPR have been called into question by other researchers. The team behind the work say they stand by their findings, but at the very least the dispute shows there are still major issues that need to be resolved before anyone should attempt to use gene-editing to prevent children inheriting disease-causing mutations. “There are lots of unanswered questions,” says embryologist Anthony Perry of the University of Bath in the UK. The first studies to try using the CRISPR genome-editing technique to alter the DNA of human embryos revealed several major problems. For instance, it only corrected mutations in a small proportion of embryos. Last month, however, a team led by Shoukhrat Mitalipov of Oregon Health and Science University claimed they had managed to improve efficiency while avoiding other key problems such as unwanted alterations. The study was widely proclaimed as a breakthrough. Now doubts have been raised. Genome editing works by breaking DNA, and letting a cell’s natural repair mechanisms fix it. This is usually quite haphazard, and precise repairs were thought to be rare. But when Mitalipov’s team used CRISPR to try fixing a mutation that causes heart disease, they reported getting precise repairs in most of the embryos they tried it on. The team have claimed they have discovered a novel DNA repair mechanism in embryos, which uses egg DNA as a template for repairing the embryo’s DNA that originally came from sperm.
9-1-17 What happens in the brain to make us 'catch' yawns
What happens in the brain to make us 'catch' yawns
You may well be yawning just reading this - it's contagious. Now researchers have looked at what happens in our brains to trigger that response. A University of Nottingham team found it occurs in a part of the brain responsible for motor function. The primary motor cortex also plays a part in conditions such as Tourette's syndrome. So the scientists say understanding contagious yawning could also help understand those disorders too. Contagious yawning is a common form of echophenomena - the automatic imitation of someone else's words or actions. Echophenomena is also seen in Tourette's, as well as in other conditions, including epilepsy and autism. To test what's happening in the brain during the phenomenon, scientists monitored 36 volunteers while they watched others yawning. In the study, published in the journal Current Biology, some were told it was fine to yawn while others were told to stifle the urge. The urge to yawn was down to how each person's primary motor cortex worked - its "excitability". And, using external transcranial magnetic stimulation (TMS), it was also possible to increase "excitability" in the motor cortex and therefore people's propensity for contagious yawns.
9-1-17 Clues to why leaves come in many sizes
Clues to why leaves come in many sizes
The huge variety of leaves in the plant kingdom has long been a source of wonder and fascination. The leaves of a banana plant, for instance, are about a million times bigger than the leaves of heather. The conventional wisdom is that leaf size is limited by the balance between how much water is available to a plant and the risk of overheating. However, a study of more than 7,000 plant species around the world suggests the answer may be more complex. "A banana leaf is able to be so huge because bananas naturally grow in places that are very hot and very wet," said Ian Wright of Macquarie University in Sydney, Australia. "Our work shows that in fact that if there's enough water in the soil then there's almost no limit to how large leaves can be." He says this is only part of the puzzle of leaf size. "The other part is about the tendency for larger leaves to freeze at night," Dr Wright explained. "And, you put these two ingredients together - the risk of freezing and the risk of overheating - and this helps understand the pattern of leaf sizes you see across the entire world."
9-1-17 Pioneering gene therapy approved for leukaemia in the US
Pioneering gene therapy approved for leukaemia in the US
CAR-T treatments fight cancer by genetically modifying a person’s own immune cells. A CAR-T therapy has now been approved by the FDA – but it costs $475,000. A CAR-T treatment – a type of gene therapy for cancer – has been approved for use in the US. Announced by the US Food and Drug Administration (FDA) on Wednesday, this is the first approval anywhere in the world for a type of CAR-T therapy, although the techniques have been used experimentally for some time. CAR-T therapy made headlines earlier this year, when it was announced a CAR-T approach had saved the life of Layla, a young child in the UK who had leukaemia. The approach involves reprogramming a person’s own immune cells to make them better at targeting cancerous ones. The drug that has been approved by the FDA is Kymriah, a treatment for B-cell acute lymphoblastic leukaemia, the most common childhood cancer in the US. To synthesise Kymriah, a patient first has a type of immune cell, called T-cells, removed from their body and transported to a facility in New Jersey operated by the pharmaceutical firm Novartis. Here, viruses will be used to insert a gene into these cells. The gene codes for a protein called a chimeric antigen receptor (CAR). These cells are then reinfused back into the person. The added protein helps these modified T-cells home in on and fight leukemia cells. In a trial, this approach achieved an 83 per cent remission rate over a period of three months in people who hadn’t responded to other treatment options. The FDA has approved Kymriah for people aged 25 or under who have not responded to other treatments, or who have relapsed.
9-1-17 Rare vintages
Rare vintages, after archaeologists in Italy discovered a cache of ancient wine casks dating to 4000 B.C., some 3,000 years earlier than any previous evidence of wine making. The scientists are now trying to determine if the wine was red or white.
9-1-17 Binge watching impairs sleep
Binge watching impairs sleep
Binge watching shows on Netflix and other video on-demand services may take a significant toll on your sleep, reports Time?.com. An international team of researchers had 423 young adults complete a survey assessing their sleep habits and how often they watched TV. More than 80 percent were binge watchers, meaning they had within the previous month viewed back-to-back shows, on any type of screen, in one sitting. In most cases, these people didn’t set out to watch three or four consecutive installments of a series—it just happened. “The episode ends, a character may or may not have died, and we’re hooked,” says co-author Jan Van den Bulck, from the University of Michigan. Compared with the participants who didn’t get sucked into a show, the binge watchers reported more fatigue, more symptoms of insomnia, and heightened alertness at bedtime. Overall, they had a 98 percent higher risk for poor sleep than those who turned off the TV earlier. Van den Bulck suggests setting an episode limit before sitting down to watch a show, and doing meditation or relaxation exercises before bed.
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