9-30-20 Ruby Wax interview: We are addicted to bad news but we can break free
There is plenty to worry about right now, but that doesn't mean we should forget about the reasons for optimism, says comedian and mental health advocate Ruby Wax. RUBY WAX is on a serious mission to improve people’s mental health. The American-British TV star, comedian, author and mental health advocate found fame in the 1980s TV sitcom Girls on Top and went on to deploy her comic persona of a brash, overconfident American in multiple comedy interview shows. Yet it is her experience with depression and stress that has shaped much of her more recent career. Her encounter with major depression 15 years ago led her to earn a master’s degree in mindfulness-based cognitive therapy at the University of Oxford, an experience she incorporated into a stage show. For this, as well as her writing about depression and mindfulness, she was awarded an OBE, one of the highest civilian honours in the UK. Wax has also set up community groups where, before lockdown, people could meet up and chat; these have now moved online. In her fifth and latest book, And Now for the Good News… To the future with love, Wax goes on a whirlwind world tour to meet innovators in schools, businesses and communities whose work she believes shows things are looking up. Ruby Wax: We were besieged by bad news, even before covid. We were going on a drip feed, from one disaster to another, and we were getting addicted to it – at least, I was. I couldn’t wait for more bad news, and you could gossip about it. But where you pay your attention defines your reality. Your brain is shaped by what you look at. So I said, let’s move the lens, let’s break the habit. I went on a global hunt, to try to see the innovators, the people that are going to change the world. I also wanted to change my life – to see where I could live, what I could do, because I like reinvention. I did find some places I would like to live some of the time and people who I’d like to be around. The old model is we live in these dystopian islands of concrete. You live on the 87th floor, and if something terrible happens, you don’t know your neighbours. It’s built to isolate. But there are these places called intentional communities, where people share resources and responsibilities, like Findhorn in Scotland. I’ve just been there. It’s a community, there are little roads between the houses. People smile when they see you, even though they don’t know you. There’s a community room where you can eat with other people, although it’s not open now because of covid. I like the idea that everybody’s got your back – this is how humans were built, to have each other’s backs.
9-30-20 What should a second coronavirus lockdown look like in Europe?
IT IS no shock that many European countries are again facing rising coronavirus cases – this is exactly what researchers anticipated. Modelling in March by Mark Woolhouse at the University of Edinburgh, UK, suggested that a two-month UK lockdown would lead to low cases and an imperceptible rise over the summer before new measures were required at the end of September. Which is roughly what happened. Other models foresaw similar patterns. “I’m not claiming a prediction, but it’s a scenario that was predictable,” says Woolhouse. The speed and size of the wave in Europe has been a surprise though. “Every infectious disease epidemiologist has been expecting a big increase, but it’s been bigger and sooner than most of us would have expected,” says Paul Hunter at the University of East Anglia, UK. While we don’t know how big the epidemic will get this time round in the UK, he says it will probably dwarf the one in March and April. Deaths may be lower this time, Hunter adds, due to a higher proportion of younger people being affected and better treatments. The key question now is whether second national lockdowns are inevitable and, if so, will they differ from the first time? Israel is the only high-income country to have begun a full national second lockdown. It started on 18 September, with a further tightening of restrictions a week later. It is too soon to know the impact of this lockdown. Several countries, including Australia and the UK, have opted for local lockdowns as cases rise. On 22 September, England stopped far short of a second national lockdown, instead announcing modest measures around pub closing times and numbers at weddings. UK Prime Minister Boris Johnson made it clear that he didn’t want a full lockdown, but didn’t rule one out. The severity of a second lockdown may depend on how well countries managed their first one. The UK’s initial peak lasted longer than those in many other countries, and measures were relaxed when cases were still relatively high compared with other nations, says Stephen Griffin at the University of Leeds, UK.2R
9-30-20 Inside one of Australia's super-strict coronavirus quarantine hotels
A week ago, with an expired UK visa and after eight unsuccessful attempts to get home, I finally boarded a plane bound for Perth in Western Australia. I now find myself in quarantine, at the sharp end of the country’s tough policies to curb a second wave of covid-19 cases. Australia has limited the number of returning passengers since July, after security breaches in quarantine hotels in Melbourne, Victoria, led to another wave of infections. The city went into a second lockdown, imposing some of the strictest measures in the world, including a curfew between 9 pm and 5 am and hefty on-the-spot fines for people in breach of stay-at-home orders. The policies seem to have worked. After more than 11 gruelling weeks, cases dropped faster than expected, and the curfew was lifted on 28 September. On that day, there were just five new cases in the state of Victoria, down from a peak of 686 on 4 August. Compared with the UK, where travellers must quarantine at home for two weeks with little or no checks, Australia’s policies are extreme. With some celebrity exceptions – actor Tom Hanks and businessman Alan Sugar among them – only Australian citizens and permanent residents are currently allowed entry. Incoming flights are capped at around 50 passengers per plane, which led to one of the strangest flights I have ever taken. We were required to wear both a mask and face shield the entire time, except when eating. On the leg to Australia, I counted 22 of us in economy. As we descended into Perth, an announcement from the Australian government informed passengers that we would need to quarantine in a hotel for 14 days at our own expense. “Failure to do so may result in a fine or a prison sentence,” we were told. At the airport, temperatures were taken and we were asked about covid-19 symptoms. We were interviewed by state police to be granted permission to enter and were later bussed to a hotel with soldiers outside. “Enjoy that fresh air while you can,” a police officer told me as I was waiting to be assigned a room.
9-30-20 We may be able to tell someone's heart rate just by looking at them
We may be able to tell someone’s heart rate at a glance, which could help us interpret their emotional state. Alejandro Galvez-Pol at University College London and his colleagues showed 120 volunteers videos of two people positioned side-by-side. The heart rate of one of the individuals was shown on the screen, in the form of a square that changed colour from black to red with every heartbeat. The participants were then asked to say who they thought the heartbeat belonged to. On average, they guessed correctly 58 per cent of the time, more than would be expected by chance. Fatima Felisberti at Kingston University London says the findings are further evidence that humans have evolved to detect changes in blood flow in the faces of people we interact with – blushing being a classic example. We know that people can tell their own heart rate to some degree, says Micah Allen at Aarhus Institute of Advanced Studies, Sweden, “but it is really quite curious and fascinating to see that we can actually discern this information about other people, just by perceiving their faces”. This ability may aid in our understanding of the actions or intentions of other people, Galvez-Pol’s team suggests. “It could be that this ability to implicitly ‘read’ the heartbeats of other people from their face is something we evolved so that we can more easily align our beliefs and feelings with others, and also avoid being fooled by deception,” says Allen. One limitation is that the team didn’t test whether participants could detect a higher or lower heart rate without the help of an on-screen prompt. “It is still a bit unclear precisely what information participants use to complete the task, but that is an interesting research question itself,” says Allen.
9-29-20 Covid-19: Milestones of the global pandemic
The Covid-19 pandemic began last year in a city in central China, but has since grown to affect nearly every country on earth. The virus has put world leaders in hospital while exposing inequality. It has asked major questions of governments and encroached on the daily lives of billions. And it shows no signs of ending any time soon. As the number of deaths passes one million, we take a look at some of the landmarks along the way. 9 January 2020 - First reported death January was a big month for news - it saw the US assassinate an important Iranian general, rampant wildfires in Australia and the death of basketball great Kobe Bryant in a helicopter crash. We didn't know it at the time but the biggest story emerged from China, which the BBC first reported as a cluster of cases of a "mysterious viral pneumonia" in the city of Wuhan. On 11 January, China reported its first confirmed death from the virus - a 61-year-old male resident of the city. Chinese scientists identified the illness as a type of coronavirus, which cause different diseases from the common cold to more severe ones like Sars (severe acute respiratory syndrome). There were early signs of the kind of response that would later be commonplace around the world - the outbreak prompted Singapore and Hong Kong to bring in screening processes for travellers from Wuhan. There were also fears the virus could spread rapidly as hundreds of millions of people in China prepared to travel around the country for Chinese New Year. But it was still unclear how the illness was transmitted, with health officials saying no cases of human-to-human transmission had been confirmed. At that point, the World Health Organization (WHO) said it was aware of the outbreak, it was in contact with the Chinese government and it was closely monitoring the event.
9-29-20 Let the coronavirus spread among young people? It’s not a good idea
Coronavirus cases are rising again across the UK. Without urgent action, they could reach 50,000 per day by mid-October, health officials have warned. Many scientists are now calling for further measures, such as a short-term national lockdown to limit the virus’s spread. But others point out that restrictions cause their own harms, including impacts on other health services, economic hardship and a significant toll on mental health. Thousands of people attended a London protest last weekend against lockdown and related measures. Similar protests have taken place around the UK and the world. Meanwhile, a group of scientists have signed an open letter essentially arguing that the virus should be left to let rip through young and healthy populations. The open letter, by Sunetra Gupta at the University of Oxford and 31 of her colleagues, argues that lockdown and other restrictions have had a devastating impact on the wider delivery of healthcare. Cancer Research UK estimates that around 350,000 fewer people with suspected cancer symptoms were referred for a diagnosis between April and August, for example. However, others argue that the overwhelming of health services that occurred in the UK in April wasn’t solely because of the coronavirus epidemic, but was also due to years of underfunding of the National Health Service, which is often stretched beyond capacity during winter. The authors of the letter rightly point out that the pandemic has significantly worsened mental health, although anxiety and depression appeared to be rising before lockdowns came into effect. But their further points have come under fire from other scientists. Gupta and her co-authors argue that young people should be given age-specific advice on their individual level of risk because they are much less likely to die from covid-19. Older and vulnerable people should be shielded, while young and healthy people continue to live much as they used to. “The main concern is the destructive effect of lockdown and restrictions,” says Gupta.
9-29-20 The immune system: How to boost it and lower your immune age
Your immune system stands between you and deadly infections. But as you get older so does your immune age, making you more susceptible to disease. Fortunately, we are discovering plenty of things you can do to turn back the clock and stay healthy. In this episode of our video series Science with Sam, find out how your immune system works and how you can give it a boost. One of the most important things standing between you and a deadly infection is your immune system – the intricate, biological defence mechanism that protects your body from harmful invaders. And there’s a lot we can do to give our immune system a helping hand. Your immune system is made up of two divisions: the innate immune system and the adaptive immune system, each with its own battalion of specialist cells and defensive weapons. The innate immune system is the first line of defence. It’s made up of cells like the scary-sounding macrophage, and the less scary-sounding neutrophil. These general-purpose guards patrol the bloodstream on the lookout for anything that shouldn’t be there. When they detect an intruder, they neutralise the threat by engulfing it like Pac-Man, spraying it with deadly chemicals or suicidally expelling their DNA and throwing it around the invader like a net. Then there’s the adaptive immune system, which you can think of as the immune system’s special forces, elite agents trained to fight specific pathogens. Unlike the innate system, which can attack any invading cell or virus, these cells are only effective against one enemy, and they must be trained to fight them first. B cells fight bacteria and viruses by making Y-shaped proteins called antibodies that neutralise an invader or tag it for attack by other parts of the immune system. Then there are T cells. These coordinate and carry out attacks on infected cells. Helper T Cells call in reinforcements by sending out chemical messages known as cytokines. Killer T-Cells are the front line soldiers, trained, as the name suggests, to destroy the enemy.
9-29-20 50 years ago, an experimental drug hinted at serotonin’s many roles in the brain
Excerpt from the October 3, 1970 issue of Science News. An experimental drug’s effects on the sexual behavior of certain animals is arousing interest among investigators.… The drug, para-chlorophenylalanine … reduces the level of a naturally occurring neurochemical, serotonin, in the brain of rats, mice and dogs.… Little is known about how serotonin acts in the brain, and investigators quickly recognized that PCPA could be used to study this brain chemical. PCPA helped establish serotonin’s role in regulating sexual desire, as well as sleep, appetite and mood. The chemical messenger has become key to one common class of antidepressant drugs called selective serotonin reuptake inhibitors. Identified in 1974, SSRIs work by increasing the brain’s serotonin levels. But such drugs can hinder sexual desire. One SSRI that failed to relieve depression in humans found a second life as a treatment for sexual dysfunction. Approved by the U.S. Food and Drug Administration in 2015, this “little pink pill,” sold as Addyi, may boost sex drive in women by lowering serotonin in the brain’s reward centers.
9-28-20 The paleo diet may make your biological age older than your real age
A new way of calculating our biological age based on the bacteria in our gut has thrown up some surprising results. Among other things, it suggests that people following the paleo diet are nearly two years “older” on average compared with people not on the diet. “It is striking,” says Guruduth Banavar at Viome, a California-based company that sells tests that measure gut bacteria. “In our population, people on a paleo diet were younger, but their biological age is actually older.” In the past decade, many groups have developed ways of estimating people’s age based on biomarkers such as the length of telomeres. These estimated biological ages are thought to reveal whether people are ageing slower or faster than normal, though it has yet to be shown that biological age is an accurate predictor of life expectancy. Several groups have been trying to estimate age by using machine learning to analyse microbiome data. Viome’s approach involves looking at which genes are active in gut bacteria, not simply which genes are present, as other groups do, says Banavar. Its findings are based on 90,000 stool samples collected and analysed by the company, making it by far the largest such study to date. Another study out last year, for instance, was based on just 1165 samples. Because they have so many samples, the researchers have been able to look at how various lifestyle factors affect biological age as estimated by their method. For example, they could examine the effects of following the paleo diet, in which people eat as our Palaeolithic ancestors are supposed to have done. “For the paleo diet, the finding is quite strong,” says team member Hal Tily. “It’s unambiguous that something is going on.” However, this could be because people with poor health are more likely to try the paleo diet, rather than this being a result of the diet itself, cautions Cara Frankenfeld at George Mason University in Virginia. “We can’t identify whether something about a person’s health made them decide to change their diet or whether the diet preceded and influenced the biological age,” she says.
9-27-20 Brain-eating microbe: US city warned over water supply
Residents of Lake Jackson, Texas, have been warned about using tap water after a deadly brain-eating microbe was found in the city's public water supply. Tests confirmed the presence of Naegleria fowleri in the system. The amoeba can cause an infection of the brain, which is usually fatal. Infections are rare in the US, with 34 reported between 2009 and 2018. Officials in Lake Jackson said they were disinfecting the water supply but did not know how long this would take. Eight Texas communities were originally told on Friday night not to use their water supply for any reason except to flush toilets. The warning was lifted on Saturday for everywhere but Lake Jackson, a city of more than 27,000 residents. Authorities in Lake Jackson later said that people could begin using the water, but must boil it before drinking it. Residents were also told to take other measures, including not allowing water to go up their noses while showering or bathing. The city warned that children, elderly people, and people with weakened immune systems were "particularly vulnerable". Officials said they were flushing the water system, and would then carry out tests to ensure the water was safe to use. An investigation into the city's water supply began after a six-year-old boy contracted the microbe and died earlier this month, Lake Jackson City Manager Modesto Mundo told reporters. Naegleria fowleri occurs naturally in freshwater and is found around the world. It usually infects people when contaminated water enters the body through the nose and then travels to the brain. The Centers for Disease Control and Prevention (CDC) says infection typically occurs when people go swimming or diving in "warm freshwater places". The CDC says people cannot get infected by swallowing contaminated water, and it cannot be passed from person to person. Those infected with Naegleria fowleri have symptoms including fever, nausea and vomiting, as well as a stiff neck and headaches. Most die within a week.
9-26-20 Defects in early immune responses underlie some severe COVID-19 cases
Genetic flaws and rogue immune responses can cause life-threatening disease, studies find. COVID-19 kills some people and leaves others relatively unscathed. But why? Age and underlying health conditions are risk factors, but scientists are trying to tease out other differences, including in people’s genes or immune systems, that may play a role. Two new studies show that flaws in the body’s early response to viral infection, one caused by genetic defects and one by traitorous immune responses, are behind some severe COVID-19 cases. In one study, published online September 24 in Science, researchers identified certain genetic defects in some people with severe COVID-19 that make the body produce fewer interferons, proteins that are part of the immune system’s early warning system. In other people with severe disease, however, the body’s own immune responses disable interferons, a second study published online in Science the same day finds. These defects mean that the coronavirus that causes COVID-19, SARS-CoV-2, can infect cells without raising red flags, evading the usual onslaught of defenses brought on by interferons and leading to more severe disease, the researchers say. The results add to growing evidence that strong early immune responses to COVID-19 are crucial to protect people from becoming severely ill (SN: 9/23/20). The findings may eventually lead to treatments that can better help those people who do get very sick, says Brianne Barker, an immunologist at Drew University in Madison, N.J., who was not involved in either study. But “it’s really clear here that we can look at our severe patients and see that there’s not going to be a one-size-fits-all kind of treatment for them,” Barker says. For instance, while people with the genetic defects might benefit from receiving additional interferon early during an infection to boost their levels, those whose immune systems are going to mount a defense against the proteins would not.
9-26-20 Tiny, magnetically controlled robots coax nerve cells to grow connections
New research could point to additional treatments for people with nerve injuries. Tiny robots can operate as nerve cell connectors, bridging gaps between two distinct groups of cells. These microscopic patches may lead to more sophisticated ways to grow networks of nerve cells in the laboratory, and perhaps even illuminate ways to repair severed nerve cells in people, researchers report September 25 in Science Advances. Engineers Eunhee Kim and Hongsoo Choi, both of the Daegu Gyeongbuk Institute of Science and Technology in South Korea, and colleagues first built rectangular robots that were 300 micrometers long. Slender horizontal grooves, about the width of nerve cells’ tendrils that exchange messages with other cells, lined the top. These microrobots were fertile ground for rat nerve cells, the researchers found. As the cells grew, their message-sending axons and message-receiving dendrites neatly followed the robots’ lined grooves. Once laden with about 100 nerve cells, a microrobot’s objective was to nestle between two separate islands of nerve cells, grown on glass plates, and bridge the gap. Rotating magnetic fields sent the microrobot tumbling pell-mell toward its target. When the microrobot drew close, researchers used a steadier magnetic field to align the bot between the two clusters of cells. The nerve cells on the microrobot then grew out toward the clusters, while the cells in the clusters grew onto the bot. These new connections allowed neural signals to flow from one cluster of nerve cells to another, electrodes revealed. Creating these neural bridges might help researchers design better replicas of complex nerve cell networks in the brain. Similar systems could also lead to new ways of studying nerve cell growth, experiments that could ultimately point to therapies for people with nerve injuries (SN: 8/11/16). Such precision building could also be useful in computing, allowing scientists to design and build biological computers with nerve cells.
9-25-20 Magnetic microbots can hook up brain cells to make a neural network
Tiny robots that can transport individual neurons and connect them to form active neural circuits could help us study brain disorders such as Alzheimer’s disease. The robots, which were developed by Hongsoo Choi at the Daegu Gyeongbuk Institute of Science and Technology in South Korea and his colleagues, are 300 micrometres long and 95 micrometre wide. They are made from a polymer coated with nickel and titanium and their movement can be controlled with external magnetic fields. Each robot has a number of 5 micrometre-wide grooves that run along its length – similar to the width of a neuron’s axon and its dendrites, the projections that enable the cells to connect to each other. The grooves act as templates to guide the growth of the neurons. The team tested the robots using brain cells from rats, specifically neurons from the hippocampus, a region of the brain associated with learning and memory. The group created a 500 by 500 micrometre grid of two adjacent clusters of neurons on a glass surface, and used magnetic radiation to make the robot deliver a single neuron into the gap to between the two clusters so it could connect them. The microrobot could reach its target position within 10 seconds and connect the two neural clusters within 1 minute. The team believes the microrobots could be used to study the biological characteristics of neurons and neural networks, as well as to investigate brain conditions such as Alzheimer’s disease. It opens the possibility for neural networks that can be dynamically adjusted and enlarged, says Choi. For the moment, the microrobots have only been tested in a lab environment rather than in living tissues. The amount of magnetic radiation required to guide the robots is harmless – less than 100 milliTesla, compared with figures in the vicinity of 3 Tesla for MRI scans – but to be biocompatible, the robots would need to be constructed from different materials, says Choi.
9-25-20 Rapid evolution due to extreme climate events could lead to extinction
Evolution normally helps organisms positively adapt to changing circumstances, but climate change may turn that on its head. A model of how some species could rapidly evolve in response to increasingly extreme events, such as storms, has found that mutations could actually drive some small, vulnerable populations to extinction. This is because traits that help animals or plants that survive extreme events can be a disadvantage in normal situations. “By the next generation, the environment has already gone back to normal,” says Kelsey Lyberger at the University of California, Davis. “You never get to benefit from the change.” Many animals are already evolving in response to long-term global warming. For instance, owls in Finland are getting browner as snow cover declines and plants in California are flowering earlier as it gets drier. This process should help many populations adapt, but not all will be able to evolve fast enough. Climate change is expected to become a major cause of extinction along with habitat loss and over-exploitation. It is also clear that extreme events fuelled by global warming, such as more extensive wildfires, can drive vulnerable populations to extinction. For instance, in 2019, the category 5 Hurricane Dorian may have killed the last few individuals of a bird called the Bahama nuthatch. Such extreme events can also produce rapid evolution. Lizards on the Caribbean island of Dominica evolved a superstrong grip after category 5 Hurricane Maria in 2017 – likely because only lizards that managed to cling onto branches survived. But it is possible that these lizards have to consume more food to maintain this extra strength, making them a bit less likely to survive in normal conditions. Such observations inspired Lyberger and her colleagues to create a mathematical model that allows the effects of environmental changes of different duration to be compared. The results suggest that brief changes, such as storms, can reduce the fitness of survivors in normal conditions to such an extent that their numbers decline rather than recovering. The risk is greatest for small populations confined to a small area, such as an island.
9-24-20 A mother mouse’s gut microbes help wire her pup’s brain
Research in mice links mom’s gut microbes to her baby’s sensory connections. New findings in mice suggest yet another role for gut microbes, even before birth. The microbes residing in a female mouse’s gut help shape the wiring of her offspring’s brain, researchers report September 23 in Nature. While mouse and human development are worlds apart, the study hints at how a mother’s microbiome may have long-term consequences for her offspring. Scientists have previously found links between a mouse mother’s microbiome and her young’s brain and behavior, but many of those studies worked with animals that were stressed (SN: 7/9/18) or sick. Instead, Helen Vuong, a neurobiologist at UCLA, and her colleagues looked at what a mother’s microbial mix normally does for her pups’ brains. The new results point to the influence of specific microbes and the small molecules they produce, called metabolites. “Metabolites from the microbiome of the mother can influence the developing brain of the fetus,” says Cathryn Nagler, an immunologist at the University of Chicago who was not involved with the study. The metabolites do this by reaching a developing pup’s brain where they affect the growth of axons, she says. Axons are the threadlike signal-transmitters of nerve cells. Vuong and her team looked at the brains of fetuses from pregnant mice — some with their usual gut bugs, some raised without microbes and others ridded of their gut bacteria with antibiotics. When a mother’s microbes were missing, fetuses had shorter and fewer axons extending from the brain’s “relay station” to the cortex, Vuong says. These connections are important for processing sensory information. Those brain differences appear to have consequences for mice later in life. As adults, mice born to microbe-deficient mothers were less sensitive to touch than mice from mothers with a typical microbiome. For instance, in one of several sensory tests, mice from microbe-deficient mothers took longer to notice a small piece of tape stuck to one of their paws. But when microbe-lacking females were given Clostridia bacteria, their offspring’s brain and behavior developed normally. Clostridia are common gut microbes in humans and in mice, Nagler says, and their absence has been linked to some noncommunicable conditions, such as food allergies (SN: 8/26/14).
9-24-20 Life on Earth may have begun in hostile hot springs
Understanding how complex molecules formed on our planet could guide the search for life elsewhere in the solar system. At Bumpass Hell in California’s Lassen Volcanic National Park, the ground is literally boiling, and the aroma of rotten eggs fills the air. Gas bubbles rise through puddles of mud, producing goopy popping sounds. Jets of scorching-hot steam blast from vents in the earth. The fearsome site was named for the cowboy Kendall Bumpass, who in 1865 got too close and stepped through the thin crust. Boiling, acidic water burned his leg so badly that it had to be amputated. Some scientists contend that life on our planet arose in such seemingly inhospitable conditions. Long before creatures roamed the Earth, hot springs like Bumpass Hell may have promoted chemical reactions that linked together simple molecules in a first step toward complexity. Other scientists, however, place the starting point for Earth’s life underwater, at the deep hydrothermal vents where heated, mineral-rich water billows from cracks in the ocean floor. As researchers study and debate where and how life on Earth first ignited, their findings offer an important bonus. Understanding the origins of life on this planet could offer hints about where to search for life elsewhere, says Natalie Batalha, an astrophysicist at the University of California, Santa Cruz. “It has very significant implications for the future of space exploration.” Chemist Wenonah Vercoutere agrees. “The rules of physics are the same throughout the whole universe,” says Vercoutere, of NASA’s Ames Research Center in Moffett Field, Calif. “So what is there to say that the rules of biology do not also carry through and are in place and active in the whole universe?” At its biochemical core, the recipe for life relies on only a few ingredients: chemical elements, water or other media where chemical reactions can occur and an energy source to power those reactions. On Earth, all of those ingredients exist at terrestrial hot springs, home to some hardy creatures. Great Boiling Spring in Nevada, for example, is a scalding 77° Celsius, yet microbes manage to eke out an existence in water near the spring’s clay banks, researchers reported in 2016 in Nature Communications. Such conditions may reflect what it was like on early Earth, so these life-forms are most likely “related to some of the organisms that were originally on this planet,” says Jennifer Pett-Ridge, a microbial ecologist at Lawrence Livermore National Laboratory in California.
9-23-20 Hope Frozen review: The hard ethics of cryogenically freezing a child
Netflix’s Hope Frozen documentary follows a family in Thailand that cryogenically freezes their 2-year-old daughter’s brain after she dies, creating a controversy-fuelled media storm. THE world – including this magazine – hasn’t shied away from expressing opinions about the Alcor Life Extension Foundation, the US non-profit founded by Fred and Linda Chamberlain in 1972 to freeze corpses and body parts in the hope of one day resurrecting the dead. Most observers are content with interrogating Alcor’s bizarre mission by asking if technologies for resurrection will ever be viable. This, of course, is a non-question: who knows what is around the corner? The successful freezing and thawing of a whole rabbit brain in 2016 shows how careful we must be in dismissing such ideas. Mark O’Connell’s approach in To Be a Machine was more fruitful: he asked why people would want to freeze themselves or their loved ones at all. Hope Frozen, filmed in Thailand at around the time O’Connell was writing his book, goes some way towards an answer. Matheryn, nicknamed Einz, was born in 2013 to parents Nareerat and Sahatorn Naovaratpon. For more than two years, they and their besotted son, Matrix, filmed hour after hour of the little girl’s life. She was – and is still, in Pailin Wendel’s ravishing, painful documentary – captivating. Just before her third birthday, Einz died of ependymoblastoma. After 10 surgical operations, 12 bouts of chemotherapy and 20 rounds of radiation therapy, her family and the doctors knew it was coming: this highly aggressive brain cancer is a killer. “Some critics in Thailand, a mostly Buddhist country, felt the family had thwarted Einz’s reincarnation” At the eleventh hour, Sahatorn persuaded his family that on her death, her brain and some of her tissue should be frozen and transferred to Alcor’s Arizona facility. Einz became the youngest person to be cryonically preserved. The story created a media storm in Thailand. In the film, some critics in this mostly Buddhist country complained that her family had prevented Einz’s reincarnation and consigned her to limbo. (Webmaster's comment: I am 76 and a Alcor customer so I'll be joining her in a few years.)
9-23-20 How a 6-year-old had half his brain removed and recovered in 3 months
David Eagleman's book Livewired explores neuroplasticity, the brain's superpower, which lets it reshape after extreme surgery and adapt to losing a sense. IMAGINE if your 6-year-old son needed surgery to remove a staggering half of his brain. That was what faced Matthew, a boy with a rare condition triggering many epileptic seizures a day and that could only be treated with this drastic surgery. When he woke up afterwards, he was incontinent and couldn’t walk or speak. Yet with daily physical and language therapy, Matthew regained these abilities. In three months, he was almost back to normal, minus the seizures. Now an adult, brain scans show half of Matthew’s skull as a black void, yet the only visible effects are his slight limp and a little clumsiness in his right hand. How could someone lose half of their brain and recover almost all of their functioning in three months? For neuroscientist David Eagleman at Stanford University in California, this demonstrates one of the brain’s most remarkable qualities: neuroplasticity, or the ability to remake itself in response to changing circumstances. In Livewired, Eagleman explains why this ability is so fundamental to who we are that James Watson and Francis Crick’s claim to have discovered the “secret of life” with their work on DNA is only half of the story. The rest of what makes you who you are is “every bit of experience you have with the world: the textures and tastes, the caresses and car accidents, the languages and love stories… all of which sculpt the vast, microscopic tapestry of your brain cells and their connections,” he writes. In extreme cases, this brain resculpting is visible at the anatomical level through post-mortems or scans. Professional musicians develop a small bulge on a ridge of their motor cortex – a part of the brain that controls movement – revealing the effects of thousands of hours moving their fingers in complex choreographies. It is reminiscent of the way a large bicep may reflect the hours spent at the gym./p> 9-23-20
The theory of evolution is a vibrant, living entity still in its prime
THE theory of evolution is one of the greatest accomplishments of the human intellect. Some might argue that it is the greatest, although quantum theory or relativity would have their supporters too. But in the biological sciences, it stands unrivalled. It is no less than the grand unified theory of life. It is also a theory in the truest sense of the word: an interlocking and consistent system of empirical observations and testable hypotheses that has never failed scrutiny. Nothing has even been discovered that falsifies any part of it, despite strenuous efforts by detractors. It all stacks up. Yet we should resist the temptation to think that evolution is carved in tablets of stone. The radical but irresistible ideas put forward by Charles Darwin and Alfred Russel Wallace in 1859 remain the core of the theory, yet it has constantly accommodated new knowledge. This happened most conspicuously about a century ago, when the new science of genetics was melded with natural selection to create what became known as the “modern synthesis”. Today, we are arguably in the midst of another upgrade. Over the past 30 years, discoveries in developmental biology, epigenetics and elsewhere have needed to be brought under the wing of evolution. As our special report on Evolution is evolving: 13 ways we must rethink the theory of nature shows, they largely have been. Only hindsight will be able to judge whether what emerges is Evolution 3.0, or merely Modern Synthesis 1.1. If nothing else, the flurry of activity is proof that evolution – and hence biological science – is a vibrant, living-and-breathing entity still in its prime. Evolution has also achieved something that is arguably more important: it has seen off its culture warrior detractors. A decade ago, it was on the front line of the war on science, under attack from creationism and its pseudoscientific alter ego, intelligent design. Those voices have now largely fallen silent, worn down by the patient drumbeat of reason. Sadly, that remains an isolated victory in the wider anti-science culture war. But it shows that victories aren’t impossible. Evolution won because it is true. Eventually, truth will out.
9-23-20 Blood test could reveal if you will experience the placebo effect
The proteins in your blood could reveal whether or not you will experience the placebo effect. People who show a placebo response appear to have certain blood proteins – some of which are linked to inflammation, which could explain the healing powers of the placebo effect. A sugar pill or sham treatment can often make people feel better, but the reasons why have long been a mystery. Research over the past 20 years has focused on how specific brain regions might play a role and how genes could influence the response. Karin Meissner at the Ludwig Maximilian University of Munich in Germany and her colleagues looked for clues in blood instead, as it is much easier to access and study. The team induced nausea in 100 volunteers by asking them to sit in a small booth with moving black and white lines on two separate days. On the second day, 10 of the volunteers were given transcutaneous electrical nerve stimulation (TENS), in which a pressure point on the wrist was stimulated with electrodes placed on the skin. Sixty volunteers were given a sham TENS treatment that provided little or no electrical stimulation. The remaining 30 volunteers had no treatment at all. All the volunteers gave a blood sample before and after the nausea-inducing experience, and each person was asked to rate their level of nausea. People who had a 50 per cent reduction in their nausea on the second day, after receiving a sham treatment, were considered to have shown the placebo effect. From the samples, the researchers analysed differences in blood proteins before and after the nausea-producing experience, and whether these changed after a placebo treatment. They found 74 proteins that seem to be linked to the placebo effect. The levels of these proteins could predict who was likely to respond to a placebo, the team says.
9-23-20 When things look bleak, thinking in terms of ‘hope horizons’ can help
With wildfires raging, the outlook looks bleak from San Francisco. Thinking about the future in terms of “hope horizons” can help, writes Annalee Newitz. OUTSIDE my window, the skies are brown and the sun is a deep reddish-orange. Unfortunately, that isn’t because I’ve moved off-world to a beautiful alien planet orbiting a red dwarf star. This is simply what “outside” looks like in San Francisco when vast swathes of the western US are on fire. Even the light itself is alarming. Its Mordor-esque gloom makes everything seem like it is the wrong colour. (For a striking image of California’s Bidwell Bar Bridge against the backdrop of the state’s wildfires, (see “Wildfire nightmare captured in harrowing image of California burning“.) It has been a bad year for California. After years of drought, we started getting record high temperatures that were coupled with fierce winds. Back in 2018, our doddering old power lines, mismanaged and neglected, sparked a deadly fire that was supposed to be a once-in-a-lifetime Armageddon. It turns out that was merely a beta test. This year, the southern California desert reached 54.4°C. If verified, this is the hottest temperature ever reliably recorded on Earth. Then a rare lightning storm zapped the coast. The resulting wildfires have already burned more land than they did in all of 2018 – and the fire season has only just started. All this devastation comes on top of the coronavirus pandemic, which means that people fleeing the heat and fires can’t huddle in shelters together without risking a superspreader event. So, the future here is looking a little uncertain. At times like this, I find myself contemplating something I call a hope horizon, or how many years it might take before everything becomes alright again. My definition is deliberately open-ended. It raises questions like “What is ‘alright’?” and “What do you mean by ‘everything’?”
9-23-20 Spinosaurus dinosaur was 'enormous river-monster', researchers say
Palaeontologists believe they have settled a debate surrounding the largest ever carnivorous dinosaur. The researchers at the University of Portsmouth say their discovery of 1,200 dinosaur teeth "proves beyond reasonable doubt" that Spinosaurus was an "enormous river-monster". Its dental remains accounted for 45% of those found in a prehistoric river, they said. The findings have been published in the Cretaceous Research journal. Spinosaurus fossils were found in large numbers at the site of an ancient river bed in Morocco, which flowed through the Sahara Desert 100 million years ago. The scientists said their discovery meant the 15-metre (49ft) long, six-tonne dinosaur was not a land-based predator but a largely aquatic one. This backs up the latest findings made by researchers in April, following the analysis of a Spinosaurus tail. David Martill, professor of palaeobiology at the university, said: "We know of no other location where such a mass of dinosaur teeth has been found in bone-bearing rock. "The enhanced abundance of Spinosaurus teeth, relative to other dinosaurs, is a reflection of their aquatic lifestyle. "An animal living much of its life in water is much more likely to contribute teeth to the river deposit than those dinosaurs that perhaps only visited the river for drinking and feeding along its banks." Spinosaurus aegyptiacus remains were first discovered about 100 years ago in Egypt. They were moved to a museum in Munich but destroyed during World War Two. Since then only fragments of Spinosaurus bones have been found, including a giant fossil in 2014. Spinosaurus has enjoyed wider popular notoriety since 2001, when it bested a Tyrannosaurus rex in Jurassic Park III.
9-23-20 Evolution is evolving: 13 ways we must rethink the theory of nature
Do species really exist? Are genes destiny? Do only the fittest survive? Can we shape or stop evolution? New insights into nature are providing surprising answers, and a glorious new picture of life’s complexity. IN 1990, an international group of scientists embarked on one of the most ambitious research projects ever undertaken. They would sequence the entire human genome, determining the order of the 3.3 billion base pairs that code for the genes that make the proteins that each of us are built from. There was huge excitement at the prospect of decoding the “blueprint” of humanity. Given the complexity of our species, our genome was expected to contain at least 100,000 genes. What makes us human would finally be laid bare. It didn’t quite work out like that. The Human Genome Project was a resounding success, publishing its results in 2003, two years ahead of target. However, it revealed that humans only have around 22,000 genes, which is about the same number as other mammals. Meanwhile, the blueprint itself turned out to be encrypted in ways we are still trying to crack. The same thing is true of us that is true of every species: our DNA can be expressed in myriad different ways depending on which combination of sequences is activated. It is this, not the number of genes in the genome, that creates the complexity of life. The more we learn about genetics, the clearer it becomes that “genetic determinism” – the idea that genes and genes alone fix our destiny – is a myth. A given set of genes has the potential to produce a variety of observable characteristics, known as phenotypes, depending on the environment. An Arctic fox changes its coat colour with the seasons. The presence of predators causes water flea Daphnia longicephala to grow a protective helmet and spines. Even a change in social environment can prompt a shift. In the European paper wasp (Polistes dominula), for example, when the queen dies, the oldest worker transforms herself into a new queen. But she isn’t the only one to respond. Seirian Sumner at University College London and her colleagues found that the death of a colony’s queen results in temporary changes in the expression of genes in all workers, as though they are jostling genetically for succession. This flexibility is key to the survival of the colony and the species, says Sumner.
9-23-20 Some frogs have evolved eyes that are far too big for their bodies
Certain frogs have some of the biggest eyes of all vertebrates, relative to their body size, which is a significant evolutionary investment that has puzzled zoologists. Now, researchers have found that the eye size of these animals seems to scale depending on their environment. Eyesight is costly in biological terms because it requires a lot of energy to function, which explains why animals living in dark environments like caves often evolve to have smaller eyes. That means big-eyed frogs clearly need the ability to see contrasts, details, colours and rapid changes in order to thrive in their environment, says Kate Thomas at the Natural History Museum in London. “It’s not that they see any better than we do,” she says. “But compared to us, they’re investing a lot more of their total energy budget on vision.” Thomas and her fellow researchers measured the body length, total eye size and cornea size in thousands of fresh and conserved specimens representing 220 species and all 55 families of frogs worldwide. Their results showed that frogs’ active hours and how they reproduce affect eye size moderately, but the greatest factor linked to eye size is habitat. “Tree frogs have the biggest eyes, and they need to climb and jump and make quick decisions while jumping,” Thomas says. Their bright colours might also be a critical form of sexual signalling that other tree frogs need to be able to see. By contrast, Budgett’s frogs, which usually live in stagnant, murky waters and rely more on other senses for their survival, have very small eyes. This still leaves the question of what frogs are giving up in order to have large eyes, says Thomas. If they balance out their energy budget by reducing other senses, such as hearing, researchers have yet to identify which ones. Frogs generally hear very well, she says.
9-23-20 Early immune responses may be why younger people get less sick from COVID-19
The immune response of people over age 24 revs up more later in a coronavirus infection. One of the lingering questions of the pandemic is why COVID-19 symptoms tend to be milder in children and young adults than in older people. A new study suggests that the immune systems of people younger than 24 deal the coronavirus a strong first punch. Those early immune defenses, which set off alarm bells for the body to go on the attack no matter what the invader, may be weaker in older adults. Having more muted frontline defenses could allow an infection with SARS-CoV-2, the virus that causes COVID-19, get a foothold, resulting in worse symptoms for older people, researchers report September 21 in Science Translational Medicine. The results add to evidence that boosting early immune responses to the virus with a vaccine or drugs like interferons — which are based on proteins the body produces to stimulate immune cells — could help protect people (SN: 8/6/20). Researchers have had some ideas why younger people generally get less sick. It’s possible that compared with adults and older kids, younger children have lower amounts of the ACE2 protein in their upper respiratory tracts. That’s a protein that the virus uses to break into cells (SN: 8/4/20). Another explanation could have been that young people have less virus in their bodies, which could mean milder symptoms, although studies have shown that viral load is similar across people no matter their age. Or differences in the immune system, which tends to become less robust with age, could play a role. In the new study, pediatric infectious diseases physician and virologist Betsy Herold and colleagues divided 125 COVID-19 patients hospitalized at Montefiore Medical Center in New York City into five categories. People younger than 24 were split into three groups: those with symptoms who did not need a ventilator, those that did need ventilation and a third group that included kids who developed a coronavirus-related inflammatory syndrome that mainly affects children younger than 5 (SN:6/3/20). Adult patients older than 24 fell into two groups: people who needed a ventilator or died and those who recovered.
9-23-20 Antibodies made in the lab show some promise for treating COVID-19
New results hint that the proteins can reduce hospitalizations or need for ventilation. Amid the rush to test and develop potential treatments for COVID-19, lab-made antibodies are showing hints of success. In news releases, two companies announced preliminary results, though shared only limited data, that suggest the experimental drugs may help patients both early and late in infection. One clinical trial of monoclonal antibodies — human-made versions of immune system defenders produced by the body — suggests that the drugs can help keep people hospitalized with COVID-19 from needing a ventilator or from dying. And a second trial appears to show that the drugs can bring down levels of the coronavirus in recently infected people, and help reduce the chances that a person would need hospitalization. Antibodies are part of the body’s natural defense against infectious pathogens. The proteins typically attach to parts of bacteria or viruses to fight off infection. In the lab, scientists can engineer versions of antibodies to recognize specific targets in order to hinder the virus’ replication or prevent the body’s immune system from overreacting to the virus (SN: 2/21/20). A monoclonal antibody drug called tocilizumab is one of the latter types; it blocks a part of the immune response that can cause inflammation, a protein known as IL-6. By curbing inflammation, the drug could help people whose immune systems have become overactive through a process called a cytokine storm, which can cause severe COVID-19 symptoms (SN: 8/6/20). In a Phase III clinical trial of 389 people hospitalized with COVID-19, those who received tocilizumab were 44 percent less likely to need a ventilator or die compared with people who got a placebo, San Francisco–based biotechnology company Genentech announced September 17 in a news release. Of those who received the drug, 12.2 percent of people needed a ventilator or died, compared with 19.3 percent of patients who received a placebo. Still, when the researchers looked at death alone, the drug did not result in a statistically significant difference in mortality between the groups.
9-23-20 Doctor's diary: How can we deal with the long covid-19 symptoms?
THE first confirmed case of covid-19 in Brighton was around 1 February. I know this because I had been to a friend’s 50th birthday party that night. Having left early, I didn’t know anything was wrong until I received a cryptic text from the host, something about us meeting up “when this is all over”. I disregarded it. I later discovered that somebody at the party had been in contact with this first confirmed case, so several guests had to self-isolate. Many were doctors. It soon became clear that letting “hot” patients – those with a potential covid-19 infection – see their general practitioner (GP) might take many surgeries out of action, and money was made available for new solutions. That is how my organisation was tasked with setting up a “hot-hub” for the area. The challenge was: how can you see patients who aren’t sick enough to go to an accident and emergency department but who might have covid-19, yet make it as safe as possible for healthcare workers? What if someone has covid-19 symptoms, for instance, and is OK, but also has appendicitis? Our idea was to keep a patient in their car. You could recline them in the passenger seat and carry out a basic examination. So we decided to set up the hot-hub in a car park, inside a huge drive-in marquee. We paid scrupulous attention to infection control and conversations took place on the phone before and after the physical assessment, to minimise face-to-face contact. All the practices in the area were signed up, covering about 350,000 people. When we started, it felt as though every person we spoke to had covid-19. We didn’t have access to testing, but would advise patients on the basis of the phone call and physical examination. I became adept at recognising the “covid cough” over the phone.
9-22-20 Covid-19: Asymptomatic people may be more infectious than we thought
People who have the coronavirus without symptoms appear to have similar levels of the virus in their noses and throats to people with mild symptoms, a study has found. However, this doesn’t necessarily mean they are as likely to spread covid-19 as those who are sick. After much speculation early in the pandemic, a growing body of evidence suggests people can pass on the coronavirus even if they don’t have any symptoms. But it still isn’t clear how much virus these individuals carry in their upper airways and how infectious they might be. In particular it isn’t clear whether they are as contagious as those with symptoms. Sung-Han Kim at the University of Ulsan College of Medicine in South Korea and his colleagues took nose and throat swabs from 39 people with asymptomatic coronavirus infections as well as from 144 people with covid-19 who had mild symptoms. All the individuals had first tested positive for the virus an average of 13 days earlier. The researchers found that 64 per cent of the covid-19 patients and 54 per cent of those who were asymptomatic still had coronavirus-positive nose and throat swabs. They also discovered that levels of viral RNA were almost identical between these two groups. This was unexpected, says Kim, because for other viruses, such as influenza, the amount of virus an infected person harbours – known as the viral load – usually increases with the severity of symptoms. The detection of similar levels of viral RNA in mildly symptomatic and asymptomatic individuals suggests the coronavirus may be “unique”, he says. The study supports the idea that asymptomatic individuals have the potential to spread the virus regardless of symptoms, says Kim. “Normally with a virus infection, the symptoms give a way for the virus to exit your body and spread,” says Lucy Thorne at University College London, who wasn’t involved in the study. “But it seems from this and other studies that it’s still possible to spread [the coronavirus] when you don’t have symptoms,” she says. “I think the really strong public health message has to be that everyone has to take precautions even if they don’t have symptoms.”
9-22-20 People in Cape Verde evolved better malaria resistance in 550 years
Yes, we are still evolving. And one of the strongest examples of recent evolution in people has been found on the Cape Verde islands in the Atlantic, where a gene variant conferring a form of malaria resistance has become more common. Portuguese voyagers settled the uninhabited islands in 1462, bringing slaves from Africa with them. Most of the archipelago’s half a million inhabitants are descended from these peoples. Most people of West African origin have a variant in a gene called DARC that protects against malaria. This gene codes for a receptor that malaria parasites exploit to get inside cells; the variant reduces receptor levels. Amy Goldberg at Duke University in North Carolina and her colleagues analysed data on gene variants in 564 Cape Verdeans collected by another team. They found that around half the people on the outer islands have the protective DARC variant. However, on the more densely populated main island of Santiago, where there have been many malaria outbreaks over the centuries, about 80 per cent of people have the variant. Here, the protective variant is more common than other variants of West African origin, showing there has been strong selection for it. The local population’s resistance to malaria has long been noticed, the researchers point out. After visiting the islands in 1721, Captain George Roberts reported that, during the rainy season, a disease in Santiago is “dangerous to strangers”. The strength of selection for a particular gene variant – how fast a beneficial gene variant spreads per generation – can be calculated, and is called the selection coefficient. “We estimate the selection coefficient is approximately 0.08, one of the highest inferred in humans,” the researchers write.
9-21-20 Children’s allergic reactions to nuts spike at Halloween and Easter
On Easter and Halloween each year, severe allergic reactions to nuts spike in children, according to an analysis of data from emergency rooms across Canada. “I’m not so surprised,” says Moshe Ben-Shoshan at McGill University in Canada, who led the study. As a paediatric allergist who regularly works in the emergency room, Ben-Shoshan says he had already noticed that cases of severe allergic reactions among children tended to go up at certain times of the year. “I remember these cases of children coming in during Halloween after eating [nut] contaminated chocolate,” he says. He and his colleagues used records of emergency room visits to analyse the incidences of nut-induced anaphylaxis – a severe allergic reaction – in children across four Canadian provinces, including Quebec, Ontario, Newfoundland and Labrador, and British Columbia. The researchers looked at 1390 cases of anaphylaxis between 2011 and 2020 and found that the majority of cases occured in children under 11 years old, and rates of peanut-triggered anaphylaxis were 85 per cent higher than average on Halloween and 60 per cent higher than average during Easter. They saw a similar trend when they looked at anaphylaxis caused by other nuts. The team didn’t find a significant increase in nut-induced allergic reactions during other holidays such as Christmas, Diwali, Chinese New Year and Eid al-Adha. “Halloween and Easter involve social gatherings with other children in the presence of a lot of candy. These holidays may include interactions with other adults who may not be aware of the child’s food allergies,” says Tina Sindher at Stanford University in the US, who was not involved in the study. She adds that “a lot of ‘fun-size’ candy may not be labelled appropriately or may contain different ingredients.”
9-21-20 A tiny crustacean fossil contains roughly 100-million-year-old giant sperm
An ostracod encased in amber preserves what may be the oldest known fossilized sperm. Ostracods look like nothing more than seeds with legs. But some species of these tiny crustaceans have an outsize claim to fame: giant sperm. In the most extreme case, it can stretch 1.18 centimeters, over three times the length of an adult. A newfound collection of ostracods preserved in amber reveals that megasperm dates back to at least about 100 million years ago during the time of the dinosaurs, researchers report online September 16 in Proceedings of the Royal Society B. A tangle of sperm found inside a female is among the oldest, if not the oldest, fossilized sperm ever found. A single piece of amber from Myanmar held 39 ostracods, including many from a newly discovered species, Myanmarcypris hui. Using micro-CT scans, Dave Horne, a micropaleontologist at Queen Mary University of London, and colleagues peered inside a few of the tiny shelled animals. “We knew from looking at the piece of amber with an ordinary light microscope that there were antennae and legs sticking out of the shell, so we were hopeful of finding internal organs,” Horne says. If delicate parts like legs and antennae are preserved, it’s likely that other soft parts are too, he says. “But what we saw … exceeded expectations.” The layout of internal sex organs resembled that of their modern-day counterparts. And inside a M. hui female, the team found preserved giant sperm packing her seminal receptacles. Ostracods aren’t the only animal with giant sperm (SN: 7/23/12). Some fruit flies, for example, also rely on megasperm (SN: 5/25/16). In ostracods, giant sperm possibly resulted from “competition between sperms of two or more males trying to fertilize the eggs of the same female,” Horne says. “This must be a highly successful reproductive strategy to have lasted for a hundred million years.” Ostracod sperm must make a long, winding journey from the female’s vagina to her eggs, adds study coauthor Renate Matzke-Karasz, a geobiologist at Ludwig Maximilians University Munich. Spirals in the canal to the eggs make the distance longer than the entire length of the female. Shorter sperm might not be able to make the journey, Matzke-Karasz says.
9-20-20 The COVID 'long-haulers'
Even after supposedly recovering, thousands of Americans are suffering persistent and even disabling symptoms. Even after supposedly recovering, thousands of Americans are suffering persistent and even disabling symptoms. Here's everything you need to know:
- What is "long-haul" COVID? It's a persistent and wide-ranging set of symptoms that follow a coronavirus infection. Nearly 100 kinds of lingering symptoms and physical damage have been catalogued, including scarred lungs, chronic heart damage, severe headaches, kidney failure, bulging veins, hand tremors, debilitating fatigue, fever, nausea, stomach problems, hair loss, sensitivity to light and sound, blurry vision, loss of taste and smell, short-term memory loss, and a brain fog so dense it can be difficult to write even a simple email.
- What is causing these symptoms? Research indicates that the coronavirus is far more than a classic respiratory illness and can attack organs throughout the body. The virus binds itself to cells using a protein on the surface of the cells called ACE2. These ACE2 receptors are found inside blood vessels; on olfactory bulbs that provide a sense of smell; on kidneys; in the gastrointestinal tract; and, according to new research, in the brain.
- Are long-haulers generally old? Unlike the majority of people whom COVID kills, many long-haulers are relatively young: Putrino's survey of 1,400 patients found they are mostly female and have an average age of 44. Some were previously quite healthy and fit.
- How many long-haulers are there? Probably millions worldwide. A study in Italy found that 87 percent of COVID patients who were hospitalized still had symptoms two months after their release.
- Are all cases equal? No, there is a wide variation in severity. In milder cases, a handful of symptoms inexplicably come and go for months. In more severe cases, like Chimére Smith's, it becomes impossible to work. Smith, 38, a middle-school English teacher in Baltimore, has had COVID symptoms since March, including severe stomach problems and headaches, and has been to the emergency room a dozen times.
- Sick, but never diagnosed: Many COVID long-haulers complain that they were denied tests early on in the pandemic because of shortages in diagnostic swabs and restrictions placed on who was eligible for scarce tests. Boston resident Lauren Nichols, 32, got sick in March but was denied a test by her doctor, who said at her age she was in no danger. She finally tested positive, and has suffered a debilitating array of symptoms consistent with those experienced by other long-haulers, including nausea, brain fog, insomnia, and shortness of breath.
9-20-20 Coronavirus: WHO sets rules for testing African herbal remedies
The World Health Organization (WHO) has agreed rules for the testing of African herbal remedies to fight Covid-19. Sound science would be the sole basis for safe and effective traditional therapies to be adopted, it said. Any traditional remedies that are judged effective could be fast-tracked for large-scale manufacturing. Madagascar's leader has been promoting an untested product he says can cure the disease despite the WHO warning against using untested remedies. The WHO said the new rules were aimed at helping and empowering scientists in Africa to conduct proper clinical trials. The move comes as the number of confirmed cases of coronavirus worldwide passes 30 million, with reported global deaths standing at more than 957,000. In Africa there have been more than 1.3 million cases and than 33,000 reported deaths. Around 140 potential vaccines for Covid-19 are being developed around the world, with dozens already being tested on people in clinical trials. Alongside these efforts, the green light has now been given for phrase three clinical trials using African traditional medicines. A panel of experts, set up by the WHO, the Africa Centre for Disease Control and Prevention and the African Union Commission for Social Affairs, has agreed on the protocols. Phase three trials usually test the safety and efficacy of a drug on larger groups of participants. "The adoption of the technical documents will ensure that universally acceptable clinical evidence of the efficacy of herbal medicines for the treatment of Covid-19 is generated without compromising the safety of participants," said Prof Motlalepula Gilbert Matsabisa, the panel's chairman. "The onset of Covid-19, like the Ebola outbreak in West Africa, has highlighted the need for strengthened health systems and accelerated research and development programmes, including on traditional medicines," the WHO's Dr Prosper Tumusiime said in the statement.
9-19-20 What will happen when COVID-19 and the flu collide this fall?
The upcoming face-off in the U.S. could lead to one virus dominating or a deadly combo. The specter of a “twindemic” — two epidemics at the same time — looms as cold and flu season is set to start in October in the Northern Hemisphere. No one can predict what will happen when flu meets COVID-19, but public health officials are urging people to prepare for the worst. In this case, the worst would be a bad year for influenza, which in the United States has killed 12,000 to 61,000 people annually and hospitalized between 140,000 and 810,000 each year since 2010, combined with a resurgence of coronavirus infections. Together, the two could stress health care and public health systems beyond their limits. “We could see a perfect storm of accelerated COVID-19 activity as people gather more inside in particular, as they become increasingly fatigued with the mask wearing, social distancing and the hand hygiene, and as they are exposed to seasonal influenza,” said Jeanne Marrazzo, director of the infectious diseases division of the University of Alabama at Birmingham, during a news briefing from the Infectious Diseases Society of America, or IDSA, on September 10. Some states are getting coronavirus spread under control, but hospitalization levels haven’t gone down much, she said. “Overall, we still are on … a razor’s edge when it comes to COVID,” and influenza remains unpredictable. “We really can’t be complacent about this.” Infectious diseases experts worry about a conjunction of influenza and coronavirus for multiple reasons, beyond overburdened health systems. Teasing out whether a person has flu or coronavirus — which have very similar symptoms — will require testing for both viruses, at a time when turnaround for COVID-19 tests is often slow. And some people may get infected with multiple viruses simultaneously, which could make symptoms more severe.
9-18-20 The purpose of sleep appears to change when we are toddlers
Why do we sleep? The answer may depend on the person’s age, according to research that suggests the main role of sleep changes at the age of around two-and-a-half. Newborn babies spend a lot of time sleeping, and this gradually reduces as they get older. To find out why sleep changes as the brain develops, Van Savage at the University of California, Los Angeles, and his colleagues collected published data on brain activity and size and sleep duration across different age groups. They used this information to build a model of how these different aspects might be expected to change as we grow. This allowed them to swap in different figures to test various ideas. For example, if the brain is learning during rapid eye movement (REM) sleep, this would lead to a prediction that the duration of REM sleep is linked to aspects of brain development, which can then be tested against published findings. The group found that most of the brain processes associated with learning occur during REM sleep, and that this appears to be the most important function of sleep generally in young infants, who get much more REM sleep than adults. But there seems to be an abrupt shift in toddlers. “Before two-and-a-half, sleep is mainly about… rewiring the brain to learn and grow,” says Savage. But after this age, the main function of sleep appears to be the repair of any damage to the brain. “I was surprised that it was such a sharp transition point,” says Savage, who likens the sudden change to water freezing into ice. “There are tonnes of other things that are happening around this time,” says Marcos Frank at Washington State University. It is about this age that children start sleeping for longer throughout the night, for example, and the development of multiple systems, including vision and language, is well under way, he says.
9-18-20 50 years ago, scientists were on the trail of a brain-eating amoeba
Excerpt from the September 19, 1970 issue of Science News. A fearsome [disease] has been recognized in recent years, produced by a one-cell organism…. Mercifully, human invasion is rare, for the invader, an amoeba, destroys the brain tissue and produces death in from four to seven days. Only 50 cases are known.… This free-living amoeba, Naegleria gruberi, is not confined to tropical countries…. Four deaths traced to Naegleria occurred in 1967–69 in Virginia. The brain-eating amoeba, Naegleria fowleri — misidentified as its harmless cousin N. gruberi in Science News — causes a rare but deadly brain infection. Just four of 145 people infected with N. fowleri in the United States from 1962 to 2018 survived, reports the Centers for Disease Control and Prevention. The amoeba primarily infects people swimming in lakes and rivers, though several reported cases have been linked to contaminated tap water. Scientists are still trying to understand how the amoeba kills. “Brain-eating” may be a misnomer, recent research hints. Death could result from the immune system’s response to N. fowleri (SN: 8/22/15, p. 14).
9-18-20 Seven footprints may be the oldest evidence of humans on the Arabian Peninsula
The prints were likely made by people stopping to drink at an ancient lake, researchers say. Footprints discovered at what was once a rain-fed lake in Saudi Arabia’s Nefud Desert suggest that humans on the move made a pit stop there more than 100,000 years ago. The seven human footprints are likely the oldest evidence of Homo sapiens on the Arabian Peninsula, a new study finds. Dating sediment from above and below the foot impressions places them around 112,000 to 121,000 years old, researchers report September 18 in Science Advances. The previous oldest evidence of humans in the region dates to at least 86,000 years ago (SN: 4/9/18). Elsewhere in Saudi Arabia, researchers have found stone tools like those made by African H. sapiens that date to around 125,000 years ago (SN: 1/27/11), raising the likelihood that the newly discovered footprints were made by humans. Ancient H. sapiens groups likely used the site, known as Alathar, as a watering hole and place to forage for food in surrounding grasslands, say biologist Mathew Stewart of the Max Planck Institute for Chemical Ecology in Jena, Germany and colleagues. Sediment analyses suggest ancient people reached the lake during a dry stretch when the region’s rivers and lakes were shrinking. Other finds at the site dating to the same period include 107 camel footprints and 43 elephant footprints. Those impressions were made by herds of juvenile and adult animals, the scientists say. Fossils eroding out of footprint-bearing sediment included remains of elephants and large gazelles called oryxes, but not humans. Although humans might have hunted at the lake, the researchers found no stone tools or animal bones bearing butchery marks. Ancient people probably stopped briefly at Alathar, perhaps while following herds of elephants or other creatures through the region, the researchers say. Earlier members of the Homo genus, possibly Homo erectus, reached a grassy Arabian Peninsula at least 300,000 years ago and again around 240,000 years ago (SN: 11/29/18).
9-17-20 ‘The Origins of You’ explores how kids develop into their adult selves
Psychologists share what they’ve learned from long-term studies of human development. Everyone has an opinion about what makes people, especially the troublemakers, who they are. Bad parents, bad genes, bad society, bad luck, bad decisions — pick your poison. Starting several decades ago, four psychologists decided to examine how individuals flourish or flounder over the long run. Instead of jumping into a seemingly endless academic scrum over “nature versus nurture,” they studied how children actually develop over years and decades. Jay Belsky, Avshalom Caspi, Terrie Moffitt and Richie Poulton describe provocative insights from their investigations in The Origins of You. Developmental researchers acknowledge that many personal and social factors interact throughout life. No single factor can explain, say, why one person pursues a life of crime and another excels in college. Life events and random circumstances tug kids in different directions, making various outcomes more or less probable but never dictating outcomes, the authors emphasize. Only prospective studies can begin to illuminate the winding paths youngsters travel to become their adult selves. Much of The Origins of You concerns a project — now run by Caspi, Moffitt and Poulton — that has assessed about 1,000 New Zealanders in the town of Dunedin from birth to age 38 (data to age 45 is coming soon). The book also focuses on a study, started by Moffitt and Caspi, that has evaluated more than 1,000 pairs of British twins from ages 5 to 18, as well as another study, in which Belsky was involved, that followed about 1,300 U.S. children from birth to age 15. These investigations are among the few that have assessed a range of psychological and physical measures from childhood into adolescence and beyond.
9-17-20 Your shoes could be increasing the risk of a painful foot condition
Shoes that raise the toes make walking easier, according to a small study. The downside is that this might weaken the foot, increasing the risk of a common and painful condition known as plantar fasciitis. When Freddy Sichting at the Chemnitz University of Technology in Germany went running with Daniel Lieberman of Harvard University – whose work helped popularise barefoot running – the pair started talking about how shoes affect feet. In particular, they wondered about the way the sole of most shoes curves upwards under the toes, a feature called a toe spring. “It is such an obvious feature of nearly every shoe,” says Sichting. Despite this, he says, no one had studied its effect on the foot before. So Sichting, Lieberman and their colleagues got 13 volunteers aged between 19 and 33 to walk on a treadmill while barefoot or wearing simple sandals with a toe spring angle of 10, 20, 30 and 40 degrees. The researchers used sandals rather than shoes, so they could record the 3D motion of the foot, from which it was possible to work out how active the muscles in the foot were during walking. They didn’t test a sandal without a toe spring, as it is very different to walk in footwear with a completely flat sole. The results show that the muscles in the feet have to do a little less work per step to stabilise the foot while walking in footwear with a toe spring, Sichting says, with higher toe spring angles increasing the effect. “This sums up over thousands of steps, over days and years,” he says. “It’s this long-term effect that might be bad.” This could result in weaker foot muscles, which means there is more stress on other tissues such as the plantar fascia, a layer of connective tissue running under the foot from the toes to the heel. When people put a lot more stress on the foot than normal – when they go hiking, take up running, get a job that involves standing or put on weight – there is a higher risk of damaging the plantar fascia and developing plantar fasciitis, Sichting thinks.
9-17-20 Sound analysis hints sirens have an evolutionary link with wolf howls
There is an uncanny similarity between wolf howls and emergency sirens. The sound of a siren might be effective because we evolved to be alerted by howls, suggest researchers. Hynek Burda at the Czech University of Life Sciences and his colleagues compared several dozen recordings of wolf howls with the sounds made by various emergency sirens, such as those on ambulances and in tornado-warning systems. Their analysis looked at the most important acoustic components of these sounds – for example their initial and closing frequencies or how the sounds change from beginning to end. They found that most of the tested siren sounds “widely overlap” with the sounds of the wolf howls, which they call a “striking similarity”. The siren developers almost certainly didn’t deliberately model their sounds on wolf howls, says Burda. “But if they had looked for sound parameters that effectively propagate and effectively alert humans, then they may have found the same parameters as those of wolf howling.” Burda and his team suggest that wolf evolution has selected for the sound of the howls as the most effective way of communicating over long distances. These howls, in turn, may have formed a selection pressure for alertness to these sounds during the evolution of modern humans. Under this scenario, today’s sirens take advantage of our innate tendency to take note of these aposematic, or warning, sounds, as well as the fact that certain acoustic properties are ideally suited to effectively transmit sound over long distances. “Sirens also effectively provoke wolves and dogs to howl, indicating that the animals themselves consider them to be similar,” says Burda. Burda and his colleagues hope their work will inspire other researchers to investigate how naturally occurring aposematic sounds, such as wolf howls, the buzzing of hornets or the hissing of snakes, can be used to design new warning-sound systems.
9-17-20 Blood donations show that the United States is still nowhere near herd immunity
Less than 2 percent of nearly 1 million blood donors tested positive for coronavirus antibodies. To better understand how widely the coronavirus has spread in the United States, some researchers are turning to an unusual source of data: blood donations. In an effort to encourage more donations, many blood collection centers have been offering to test donated blood for antibodies to the coronavirus, which indicates a past infection with SARS-CoV-2, the virus that causes COVID-19. Of the nearly 1 million Americans who donated blood to the Red Cross from June 15 to August 23 and were tested, only 1.82 percent had the antibodies. That finding suggests that the vast majority of Americans have yet to be infected with the virus, researchers report September 14 in JAMA. Blood donations aren’t a random sample of the population, but the data can give researchers an idea how much of a population has been exposed to the virus, a concept known as seroprevalence, and how susceptible different populations remain to continuing outbreaks. While seroprevalence was generally low across the country, there was variation among different demographic groups. African-American and Hispanic donors had slightly higher seroprevalence, compared with white donors, which matches patterns seen in clinical diagnoses of COVID-19. Seroprevalence varied by region too. All regions except the Northeast experienced modest increases in seroprevalence over the course of the summer. By August 23, the South had a seroprevalence of about 2.9 percent, higher than the Midwest (about 2.7 percent) or West (about 2.4 percent) or Northeast (about 2.1 percent).
9-16-20 Apple’s new watch has a blood oxygen monitor – what is it good for?
Apple’s recently released Series 6 smart watch incorporates a new feature: it can measure your blood oxygen levels. The tech must have been years in the making, but the timing of its release worked well given we are in the middle of a global respiratory pandemic. The amount of oxygen in the blood is important medical information, and in hospitals it is usually measured with a device called a pulse oximeter, which shines a light through the finger or earlobe. Blood carrying more oxygen absorbs light differently. It is already possible to buy a fingertip pulse oximeter for use at home for about £20. Now Apple says it has replicated this function in its high-tech watch, which shines a light onto the back of the wrist and measures the light reflected back with embedded sensors. For a readout, the user must keep their arm still for 15 seconds, and the device will also take periodic background readings when the person happens to be still, day and night. In a press statement, Apple was vague about the purpose, saying it offers “insight into overall wellness”, and didn’t answer New Scientist’s requests for further details before publication. A spokesperson couldn’t share any published research showing how oxygen monitoring would help a typical healthy person. But tools to track personal health may come to the fore as the coronavirus pandemic continues. Home oxygen monitoring is in no way a test for infection with covid-19 – but it could help people who have already been diagnosed and aren’t sick enough to be in hospital but want reassurance about their condition. Some UK clinics are already piloting “virtual wards”, where people who might otherwise have been admitted to hospital stay at home with frequent telephone check-ups, and pulse oximetry is an important part of their monitoring.
9-16-20 Scientists dismiss new claims that the coronavirus was made in a lab
A research paper claiming to prove that the coronavirus was cooked up in a laboratory has been widely dismissed by mainstream scientists. The paper, which was posted online earlier this week and hasn’t been peer reviewed, says that “unusual features” of the virus’s genome suggest “sophisticated laboratory modification rather than natural evolution”. The authors allege that the modification of one or more bat viruses was carried out in a Chinese government laboratory in Wuhan. Experts poured scorn on the claim. The paper “does not provide any robust evidence of artificial manipulation and is highly speculative”, said Gkikas Magiorkinis at the National and Kapodistrian University of Athens, Greece, in a statement. “This preprint report cannot be given any credibility in its current form,” said Andrew Preston at the University of Bath, UK, in a statement. The claims in the paper are “unsubstantiated”, he added. The paper was co-authored by Li-Meng Yan, a self-styled whistle-blower from Hong Kong whose current affiliation is the non-profit Rule of Law Society and the Rule of Law Foundation, both in New York. The foundation’s website says its mission is “to expose corruption, obstruction, illegality, brutality, false imprisonment, excessive sentencing, harassment, and inhumanity pervasive in the political, legal, business and financial systems of China”. It was co-founded by US President Donald Trump’s former chief strategist, Steve Bannon. Yan did a series of media interviews in advance of the preprint being posted. She told the UK daytime TV show Loose Women that last year she was a medical doctor and PhD student at the University of Hong Kong (HKU) Medical Centre School of Public Health. In December, she was assigned to a secret investigation of the new disease that we now know as covid-19, she said. She said that in the course of her investigation, she discovered that it was caused by an unnatural coronavirus created in a Chinese government laboratory in Wuhan. She said she fled Hong Kong for the US in April after the Chinese government tried to make her “disappear”. HKU has confirmed that Yan was a post doctoral fellow and has since left the university. In a statement, it said that Yan did not conduct research into the coronavirus at HKU, and distanced itself from her comments. (Webmaster's comment: And what would be the Chinese motive for making this virus? They are a profit driven culture and there would be no profit in creating this virus. Killing off your customers makes no sense whatsoever!)
9-16-20 Five scientists tell us what happens next with the covid-19 pandemic
David Hunter, professor of epidemiology and medicine, University of Oxford, UK. There is a lot of discussion about a second wave, and when is a wave a wave, or will it be a ripple. Or some people suggest that a better analogy is tides. I sincerely hope there won’t be another pandemic like in March-April, that it would be much more attenuated. I suspect it will be, because we’ve got a lot of things in place: a better-educated population, social distancing, handwashing and mask-wearing. That should mean that the epidemic curve is attenuated. If we can, as the virus persists, do a better job of protecting the very old, there should be many fewer deaths, even if there are a lot of infections. So we’re in a much better place than we were six months ago, and even if there is a second wave or the tide comes in again, hopefully there’ll be a lower fatality rate. Benjamin Cowling, professor of epidemiology and biostatistics, University of Hong Kong, China. We are hoping to get a vaccine probably next April to June. We’ll vaccinate the most vulnerable people first. So what we may see is that we still have some social distancing, but maybe not as strict as right now – just trying to slow down the spread so that we can vaccinate everybody. And then things can go relatively more back to normal. But even after a whole population has been vaccinated, if the effectiveness isn’t as good as we hoped for, or if a strain of the virus emerges that can escape the vaccine protection, then we’re going to see winter epidemics of covid-19, like we do for flu. Even in a vaccinated population with partial protection, a winter outbreak of covid-19 could still cause more impact than a winter epidemic of flu because, on an individual basis, [covid-19] is 10 to 20 times more serious.
9-16-20 The way you walk may soon be used by authorities to identify you
Your walk is as unique as your fingerprint and harder to hide than your face. Now governments and companies are waking up to the power of gait analysis. LIAM GALLAGHER, formerly of the band Oasis, tends to stroll with a roll to his shoulders. John Wayne’s slow swagger has been linked to everything from a misaligned leg to small feet. Some say Vladimir Putin’s distinctive shuffle is thanks to KGB weapons training that encouraged operatives to dampen the swing of one arm to keep it closer to their gun. Considering that walking is such an everyday function of a bipedal species, it is incredible that we find so many different ways to do it. Perhaps that’s why our gaits – and what they say about us – are so fascinating. It takes dozens of muscles working together throughout the body to put one foot in front of the other. These subtle patterns of muscular flexes and strains are highly distinctive, so much so that scientists who study gait increasingly believe they are as unique to you as your fingerprint. Gait analysis has been around for years, but now it is going mainstream. China is using it to track its citizens. Transport companies want to use it to identify ticket holders. Doctors say an analysis of your strides might provide an early hint of health problems. But is this technology on a solid footing? And is it offering a step in the right direction or is it merely another worrisome invasion of our biometric privacy? We have watched other people walk for centuries. The ancient Greek philosopher Aristotle was one of the first to pay attention, but no one was more obsessed with the subject than the 19th-century French novelist Honoré de Balzac. He peppered his books with extravagant descriptions of how his characters got from A to B, often linking their walking style to their personalities, social status and occupation. Describing an elderly woman in his 1832 book The Vicar of Tours, he wrote that “her movements were not equally distributed over her whole person, as they are in other women… She moved, so to speak, in a single block.”
9-16-20 Bear from Ice Age found 'completely preserved' in Russian Arctic
The immaculately preserved remains of an Ice Age-era bear have been unearthed by reindeer herders in the Russian Arctic, researchers have said. The bear was revealed by the melting permafrost on the Lyakhovsky Islands in north-eastern Russia. With its teeth and nose intact, the bear is thought to be a species of brown bear that lived 22,000 to 39,500 years ago. It will be studied at the North-Eastern Federal University (NEFU) in the city of Yakutsk. Scientists at the university, known for its research into woolly mammoths and other prehistoric species, suggested the discovery was unprecedented. Dr Lena Grigorieva, a palaeontology researcher at the university, said the bear was "the first and only find of its kind" to be recovered in once piece with "soft tissue". It is completely preserved, with all internal organs in place, even including its nose," Dr Grigorieva said. "Previously, only skulls and bones were found. This find is of great importance for the whole world." Dr Grigorieva told the BBC the animal is believed to be an ancient relative of the brown bear, a large species found across Eurasia and North America today. Other Russian scientists will be invited to join the study, with more details to be announced soon, the NEFU said in a news release on Monday. "It is necessary to carry out radiocarbon analysis to determine the precise age of the bear," the university quoted Maxim Cheprasov of the Mammoth Museum laboratory as saying. The bear carcass was found by reindeer herders on Bolshoy Lyakhovsky Island, the largest of the Lyakhovsky Islands, which are part of the New Siberian Islands archipelago that lies between the Laptev Sea and the East Siberian Sea. Separately, the preserved carcass of a bear cub was found in Russia's far-eastern region of Yakutia, also known as the Sakha Republic. DNA testing will be carried out. Recent years have seen major discoveries of mammoths, woolly rhinos, foal, several puppies and cave-lion cubs as the permafrost melts across vast areas in the Russian region of Siberia. Last year, an 18,000-year-old puppy was found perfectly preserved with teeth and fur in the permafrost of Siberia.
9-16-20 Oldest animal sperm found in 100-million-year-old female seed shrimp
Dozens of perfectly preserved sperm coiled up inside the reproductive tract of a 100-million-year-old female microcrustacean have been identified as the oldest animal sperm ever found. This tiny crustacean (Myanmarcypris hui) had a sexual encounter just before getting trapped in resin that had flowed from a nearby tree which later turned to amber, says Renate Matzke-Karasz at Ludwig Maximilian University in Munich, Germany. The roughly 50 intact sperm cells nestled inside the organs of this newly discovered species of ostracod – small crustaceans known as “seed shrimp” that are usually about half a millimetre long – are considered giant, as they are at least as long as the adult animals’ body themselves, and probably much more, Matzke-Karasz says. the early Cretaceous period and found organs that would support giant sperm. But recently excavated amber from northern Myanmar has now allowed scientists to take direct images of well-preserved soft tissue in ostracods from this same period, including their sperm and eggs. The research team scanned the preserved animals using computed tomography and other imaging techniques. The eggs aren’t giant, Matzke-Karasz says, but the sperm are exceptionally long. “The difficulty of following individual sperm in the tangled mass makes precise length measurements impossible, but a minimum length of 200 nanometres can be estimated,” she says, adding that their arrangement suggests they are at least as long as the ostracod that produced them. Many species of ostracod, which live in most bodies of freshwater and saltwater throughout the world, still have giant sperm, says He Wang at the Chinese Academy of Sciences, who led the study. Some species of ostracods have shorter, quick-moving sperm. The fact that some ostracods had already evolved to produce slow, giant sperm rather than fast, tiny sperm by the age of the dinosaurs, and that they continue to do so today, suggests an important evolutionary advantage that merits further investigation, says Wang.
9-16-20 Ancient Lystrosaurus tusks may show the oldest signs of a hibernation-like state
These oddball ancestors of mammals might have slowed down to wait out the polar darkness. The earliest fossil evidence of the metabolic slowdowns known as torpor may come from tusks of ancient creatures called Lystrosaurus. Fossil signatures of hibernation, a form of torpor, have turned up in rodent teeth several million years old. Lystrosaurus species, however, flourished from about 252 million to 248 million years ago. These ancient relatives of mammals were “totally bizarre animals,” says paleontologist Megan Whitney at Harvard University’s Museum of Comparative Zoology. With short-legged bodies like a corgi, they sported tusks plus a bony turtlelike beak instead of a mouthful of teeth (SN: 12/13/69). Species ranged in size from smaller, doggish animals to somewhat cowlike creatures. Lystrosaurus lived in some of the most dramatic times on Earth. Unlike many creatures, it survived the massive volcanic eruptions in what’s now Siberia that upset the chemistry of Earth’s atmosphere and oceans and probably triggered the Permian mass extinction about 252 million years ago. Some 70 percent of species on land went extinct (SN: 8/28/15). Tusks of Lystrosaurus, like those of modern elephants, grow throughout the animals’ lives, recording a biography of sorts. Whitney examined six fossil tusks found in what is now Antarctica. In the Lystrosaurus heyday, those animals would have been far enough south to experience months of darkness in winter. She found some zones of closely spaced wide dark bands in the tusks that might indicate stress and seasons of torpor. Cells that normally add light-colored dentine material may have stalled for some period of time, creating only a dark mess. Thin, light stripes between dark ones indicate when cells may have been active again, and could signal brief warm-ups like those of modern hibernators, Whitney and paleontologist Christian Sidor of the University of Washington in Seattle report August 27 in Communications Biology.
9-15-20 Lung cell images show how intense a coronavirus infection can be
Microscopic views reveal virus particles coating the hairlike cilia of an airway cell. New closeup views of lung cells show just how prolifically the coronavirus that causes COVID-19 can replicate once it infiltrates the respiratory tract. In the lab, pediatric pulmonologist Camille Ehre and colleagues at the University of North Carolina at Chapel Hill infected cells that line the airways in the lungs with SARS-CoV-2, waited 96 hours and then snapped scanning electron micrograph images of the virus-laden cells. “Once a cell is infected, it is completely taken over by the virus, producing an astonishing number of viruses,” Ehre says. In a lab dish of about 1 million human cells, she says the viral load can skyrocket from about one thousand infectious viruses to 10 million in just two days. The new images were published September 3 in the New England Journal of Medicine. Cells that line the respiratory tract and their hairlike protrusions called cilia help clear airways of inhaled particles and pathogens. These types of cells are also specifically targeted by the coronavirus. Once infected, they churn out “astronomical numbers” of viral particles, Ehre says, potentially propelling the particles deeper into the lungs, which can cause pneumonia, or out into the air where they can infect others. “These images of airway cells jam-packed with viruses make a strong case for the use of masks to limit SARS-CoV-2 transmission whether an individual has symptoms or not,” Ehre says. Widespread mask wearing could help contain such explosive viral replication from spreading beyond a single individual.
9-15-20 The microbiome: How gut bacteria regulate our health
Our bodies contain almost as many microbial cells as human cells. This community of organisms is called the microbiome, and we are increasingly learning what a huge role they play in all aspects of our health. In this episode of our video series Science with Sam, find out what your microbiome does for you, and how to nurture a healthy internal ecology. Research has shown that having a diverse microbiome – particularly your gut bacteria – has benefits not only for your digestive health, but many other organ systems, and even your brain. That has led to the idea that treatments targeting the microbiome may be able to improve our mental health. Bacteria. Viruses. Fungi. We normally think of these organisms as our enemies. But they aren’t all bad. Our bodies are full of them and it turns out we can’t live without them. But what exactly are they and what do they do for us? From the moment we’re born, we acquire, and nurture an internal ecosystem of symbiotic bacteria and other microbes, trillions of them in all. In fact there are roughly as many microbial cells in our bodies as human cells. This thriving microbial world is called our microbiome. While some microbes can make us ill, we need our microbiome to survive. Combined, they are every bit as essential as our heart, our lungs or our brain. We have microbes living all over our skin and in every orifice of our bodies. But most of the microbiome is found in our gut. Our gut microbes are essential for digestion. They also help regulate hormones and they can boost our immune system. Our microbiome contains a wide range of microbes, some of which have beneficial effects on our health and some of which are detrimental. A healthy collection of microbes seems to be vital for our wellbeing, protecting against some of the biggest health threats, like heart disease, obesity, diabetes, arthritis and even depression.
9-14-20 Our sense of time may be warped because parts of our brain get tired
Time may sometimes seem slower than it is because part of our brain becomes fatigued. “One might have experienced this manipulation after hearing music with fast tempo,” says Masamichi Hayashi at Osaka University in Japan. “The next song with a slightly slower tempo will feel even slower.” Using a similar method of manipulation, Hayashi and his colleagues wanted to determine if there was a neural basis for our subjective sense of time. They focused their efforts on the brain’s supramarginal gyrus (SMG) after reading reports on how people with damage in that part of the brain had an impaired sense of time. The researchers scanned the brains of 20 people, with an average age of 21, as they were shown a quick succession of grey circles on a screen. The circles were used to manipulate the participants’ sense of time. Some participants only saw each circle for 250 milliseconds, whereas others saw them for 750ms. After this, each person was shown another grey circle, followed by a loud beep for 500 ms. These circles appeared for either 350, 450, 550 or 650ms and the participants were asked to judge whether this time period was shorter or longer than the beep. Participants who initially saw the grey circles for 250ms overestimated how long the new circle was on screen, while the other group underestimated. These findings were reflected in the brain scans, which showed that the participants who reported bigger time distortions had a greater reduction in the activity of the SMG. Hayashi speculates that this is because the first phase of the experiment fatigued the time-sensitive neurons in the SMG, making them less likely to fire as they became tuned to repeated stimuli. Hayashi says he is unsure why some people reported greater time distortions than others. “But I guess it makes sense when you think that some people are very good at timing, and other are not,” he says.
9-14-20 Treatments that target the coronavirus in the nose might help prevent COVID-19
Scientists and doctors want to interrupt the virus before it settles in. COVID-19 can ravage the body, targeting the lungs, heart and blood vessels. To curb this wide-ranging attack, scientists are focusing on another part of the body: the nose. The virus that causes the illness, SARS-CoV-2, gains its foothold by infecting certain nasal cells, studies suggest (SN: 6/12/20). As a result, the nose has emerged as a key battleground in the war against COVID-19. Slowing or stopping that nasal invasion might ultimately be powerful enough to change the course of the pandemic, some scientists suspect. So far, no such therapies exist. But people who study the nose and its contents bring fresh perspectives about the early stages of COVID-19 infections. Scientists are developing and testing ways to prevent the virus from settling in to prime nasal real estate. These include a nose spray that smothers and inactivates a key viral protein, disinfectants that are commonly used before sinus surgeries, and even dilute baby shampoo misted up the nose. “I’m a nose person,” says Andrew Lane, an otolaryngologist and rhinology specialist at Johns Hopkins School of Medicine. But to most people, noses don’t usually spark a lot of interest, he says. “Now it’s the center of people’s attention.” This nasal gazing makes perfect sense. “The nose is a place where the virus is setting up shop,” Lane says. In a recent study, he and colleagues measured levels of a protein on human cells called ACE2 that’s thought to be one of the ways the virus can infect the cells. Among a collection of human tissues taken from the noses and throats of people, the upper back part of the nasal cavity, known as the olfactory epithelium, was packed with ACE2. (This spot is also where smell cells dwell; SARS-CoV-2 infections there have been linked to loss of smell (SN: 5/11/20).
9-14-20 Coronavirus family tree reveals the virus is hardly mutating
Like any other biological entity, SARS-CoV-2 has a family tree. It isn’t a very old one – the virus has only been recognised since December – but it still has tales to tell. Most of what we know about this coronavirus comes from genetic analysis. The first complete SARS-CoV-2 genome sequence was read from a patient who worked at a seafood market in the Chinese city of Wuhan, and who was admitted to hospital on 26 December 2019 with symptoms of what turned out to be a new disease. Known as Wuhan-Hu-1, it is a bit like the type specimen of a species – the reference against which all others are compared. The sequence showed that the new disease was caused by a novel coronavirus closely related to a group found in bats. That was both good news and bad news. Coronaviruses are RNA viruses, which generally have the highest mutation rates of any known biological entity. RNA viruses are slippery customers, mutating often and hence evading drugs and immune defences. But most coronaviruses are an exception because their RNA-copying enzyme has a proofreading function. The assumption was that the new coronavirus would follow that rule and rarely mutate. But nobody knew. Tens of thousands of genomes from all over the world have since been sequenced, and are constantly slotted into an ever-growing family tree by the pathogen-tracking project Nextstrain at Fred Hutchinson Cancer Research Center in Seattle. At first all was quiet. Sequences seen in China in December and early January proved identical to the reference. So were the first sequences from outside China – three in Thailand and one in Nepal – that were analysed in early January. Then mutants started to appear. The first was collected in the Chinese province of Yunnan on 17 January. An identical one popped up in the US two days later. These were only two mutations away from the reference case, but in virology that is enough for them to be considered a new lineage. Lineages, however, aren’t necessarily biologically different. That proved to be the case with this new lineage, which had no reported differences in infectivity or virulence.
9-13-20 The origin of mud
For most of Earth's history, hardly any of the mucky stuff existed on land. It finally started piling up around 458 million years ago, changing life on the planet forever. Years ago, geologist Neil Davies traveled to Bolivia to pick through heaps of fossilized fish. He wanted to know more about the ancient shoreline these fish swam along roughly 460 million years ago, and perhaps learn how they died. The fish, he found, appeared to have been choked by muddy sand that rivers washed rapidly into the sea, maybe during a storm. Similar heaps of smothered fish appear elsewhere around the world in rocks of similar age. This was before plants had colonized continents, so riverbanks had no roots or stems that could trap muddy sediments on land. Magnify this effect globally, and the impacts would have been substantial — not just on coastal life but on the landscape of the entire planet. Before plants, rivers would have stripped continents of silt and clay — key constituents of mud — and sent these sediments to the seafloor. This would have left continents full of barren rock, and seas with smothered fish. Once plants arrived on land, things began to change. Mud clung to vegetation along riverbanks and stuck around rather than shuttling straight to the seafloor. Davies, now at the U.K.'s University of Cambridge, and his colleagues have found that the expansion of land plants between about 458 million and 359 million years ago coincides with a more than tenfold increase in mud on land — and a significant shift in the ways that rivers flowed. The arrival of first plants and then mud "fundamentally changed the way the world operates," he says. Life evolved tools to cope with the new muckiness and new river shapes, resulting in a diversification of life and landscapes that persists to this day. Plants are responsible for much of this change, but mud contributed too, by adding a cohesiveness to the continents — unlike sand, wet mud sticks together. Davies is now working to figure out whether early plants increased the creation of mud, trapped more of it in place, or played both roles. It's a story worth getting straight, says Woodward Fischer, a geobiologist at the California Institute of Technology in Pasadena. "Mud is one of the most common, abundant things you can think of," he says. "The recognition that for most of Earth's history it was not like that is a big deal." The research could also help inform modern-day decisions around river engineering projects like dam construction, Fischer says. Understanding the ways that vegetation manipulates river flow and sediment buildup could help prevent some of the failures that have contributed to flooding along the Mississippi River and other major waterways across the world. "Every little bit that we can do better there has huge impacts," he says. When geologists talk about mud, they're referring to tiny particles that stick together when wet. Those particles have often broken down from larger rocks over time due to the forces of wind, rain, ice, and snow. Fungi and microbes can break down rock and form mud, too. Before plants arrived on land, mud was around — it was just mostly sent to the seafloor by rivers. Once plants showed up, they not only held sediments in place but their roots also physically broke down rock and released chemicals that further crumbled it. In these ways, plants accelerated what geologists refer to as the "continental mud factory."
9-12-20 'Gentle medicine' could radically transform medical practice
The present state of medicine is in disrepair. Numerous criticisms of medical science have been articulated in recent years. Some critics argue that spurious disease categories are being invented, and existing disease categories expanded, for the aim of profit. Others say that the benefits of most new drugs are minimal and typically exaggerated by clinical research, and that the harms of these drugs are extensive and typically underestimated by clinical research. Still others point to problems with the research methods themselves, arguing that those once seen as gold standards in clinical research — randomized trials and meta-analyses — are in fact malleable and have been bent to serve the interests of industry rather than patients. Here is how the chief editor of The Lancet medical journal summarized these criticisms in 2015: Afflicted by studies with small sample sizes, tiny effects, invalid exploratory analyses, and flagrant conflicts of interest, together with an obsession for pursuing fashionable trends of dubious importance, science has taken a turn towards darkness. How should medicine face these problems? I coined the term "gentle medicine" to describe a number of changes that medicine could enact, with the hope that they would go some way to mitigating those problems. Some aspects of gentle medicine could involve small modifications to routine practice and present policy, while others could be more revisionary. Let's start with clinical practice. Physicians could be less interventionist than they currently are. Of course, many physicians and surgeons are already conservative in their therapeutic approach, and my suggestion is that such therapeutic conservatism ought to be more widespread. Similarly, the hopes and expectations of patients should be carefully managed, just as the Canadian physician William Osler counseled: "One of the first duties of the physician is to educate the masses not to take medicine." Treatment should, generally, be less aggressive, and more gentle, when feasible. Another aspect of gentle medicine is how the medical research agenda is determined. Most research resources in medicine belong to industry, and its profit motive contributes to that "obsession for pursuing fashionable trends of dubious importance." It would be great if we had more experimental antibiotics in the research pipeline, and it would be good to have high-quality evidence about the effectiveness of various lifestyle factors in modulating depression (for example). Similarly, it would be good to have a malaria vaccine and treatments for what are sometimes called "neglected tropical diseases," the disease burden of which is massive. The current coronavirus pandemic has displayed how little we know about some very basic but immensely important questions, such as the transmission dynamics of viruses, the influence of masks on mitigating disease transmission, and the kinds of social policies that can effectively flatten epidemic curves. But there is little industry profit to be made pursuing these research programs. Instead, great profit can be made by developing "me-too" drugs — a new token of a class of drugs for which there already exist multiple tokens. A new selective serotonin reuptake inhibitor (SSRI) could generate great profit for a company, though it would bring little benefit for patients, given that there are already many SSRIs on the market (and, in any case, their demonstrated effect sizes are extremely modest, as I argued in an Aeon essay).
9-12-20 College athletes show signs of possible heart injury after COVID-19
A small study found indicators of inflammation in images of some athletes’ hearts. Amid growing concerns that a bout of COVID-19 might damage the heart, a small study is reporting signs of an inflammatory heart condition in college athletes who had the infection. More than two dozen male and female competitive athletes at Ohio State University underwent magnetic resonance imaging of their hearts in the weeks to months after a positive test for SARS-CoV-2, the virus that causes COVID-19. The images indicated swelling in the heart muscle and possible injury to cells in four of the athletes, or 15 percent, researchers report online September 11 in JAMA Cardiology. That could mean the athletes had myocarditis, an inflammation of the heart muscle most frequently caused by viral infections. Heart images of eight additional athletes showed signs of possible injury to cells without evidence of swelling. It’s more difficult to interpret whether these changes in the heart tissue are due to coronavirus infection, says Saurabh Rajpal, a cardiologist at the Ohio State University Wexner Medical Center in Columbus. One limitation of the research is the lack of images of the athletes’ hearts prior to the illness for comparison, Rajpal and his colleagues write. None of the 26 athletes in the study, who play football, soccer, basketball, lacrosse or run track, were hospitalized due to COVID-19. Twelve of the 26, including two of the four with signs of inflamed hearts, reported mild symptoms during their infection, such as fever, sore throat, muscle aches and difficulty breathing. It will take more research to confirm the study’s findings and understand what they could mean for these young hearts. For now, the results suggest the heart may be at risk of injury, and serve as a reminder that after having COVID-19 — even with mild or no symptoms — young people need to pay close attention to how they are feeling when they return to exercise, says Rajpal. If they have symptoms like chest pain, shortness of breath or an abnormal heart beat, he says, they should see a doctor.
9-11-20 Why black Americans are more likely to be vegan
Black Americans are almost three times as likely to be vegan and vegetarian than other Americans. Why is giving up meat so popular? When Louis Hunter woke up on the morning of 31 May he didn't know what to do. His hometown of Minneapolis was in disarray after a week of protests following the death of George Floyd, and many businesses - including his own restaurant, Trio Plant-Based - were shut down. "God just touched me and told me to go out and pass out all the food that I had prepared the day before," he told the BBC. In total, Mr Hunter gave away 300 vegan meals and bottles of water to Black Lives Matter protesters. The cause and his restaurant are inextricable in his heart. In 2016 he was facing 20 years in jail on felony rioting charges after participating in a Black Lives Matter protest following the death of his cousin, Philando Castile. Mr Hunter has always maintained his innocence, and charges were eventually dismissed, but he lost his landscaping business and apartment while the sentence hung over his head for over a year. Through his legal battle, he met white activist Sarah Woodcock, who introduced him to the concept of veganism. He started reading about how reducing or eliminating animal products can help reduce the likelihood of developing chronic illnesses like diabetes and high blood pressure - illnesses that plague the black community in the US. He says he also started to connect how racial injustice contributes to the poor diet that many African Americans eat. "At first I knew nothing about vegan, plant-based food at all," he said. "After that I started seeing the other ways we were being treated wrongly, as far as our eating habits." Although he does not identify as a vegan, which the Vegan Society defines as an ethical lifestyle choice that eschews all animal products, he says he now eats largely a plant-based diet that consists mainly of vegetables, fruits and legumes.
9-11-20 Oxford vaccine trial pause isn’t bad news – it’s the process working
The has been great alarm over the news that a trial of a vaccine candidate for the coronavirus, from the University of Oxford and drug firm AstraZeneca, has had to be put on hold after a participant developed strange neurological symptoms. It might seem a cause for concern, but, in fact, it shows that research and development for this vaccine is proceeding exactly as it should do. It also highlights the danger of bypassing the normal stage of large safety trials, as Russia and China seem to be doing with their vaccines. We don’t yet know the full details, but AstraZeneca has said vaccination was paused due to a single “unexplained illness” in a UK participant. According to an anonymous source quoted in The New York Times, this illness is a condition called transverse myelitis. Rather than a precise diagnosis, transverse myelitis is more of a descriptive term for inflammation of the spinal cord. It can have many causes, but is sometimes triggered by a viral infection, which means it could be linked to the vaccine. On the other hand, it is also plausible that it isn’t. Many thousands of people have received this vaccine candidate so far, in the UK, US, Brazil and South Africa. Statistically, some of them are bound to develop new illnesses during the trial that are nothing to do with it. All we can do is wait as the researchers investigate. The alarm is perhaps inevitable given the stakes involved in coronavirus vaccine research. In the UK, the great attention paid to the Oxford vaccine trial seems to partly stem from national pride. But there are nine vaccine candidates around the world that have reached phase III trials: the large, final stage of testing that usually comes before regulatory approval. It is likely that not all of them will reach the clinic.
9-11-20 Coronavirus: How worried should we be about reports of reinfection?
In recent weeks, the first confirmed reports of people who have been re-infected with the coronavirus have begun to trickle in. Such cases suggest that, in some people at least, the immune system doesn’t develop lasting protection against the virus. How worried should we be? Immunologists weren’t surprised to see reinfection, as we see this all the time with many viruses, such as seasonal strains of the flu. This may be because the defences raised by our immune systems for one form of a virus don’t work as well for another. Long-lasting immunity is thought to be generated by memory immune cells. Some of these cells produce antibodies – molecules that can either prevent a future infection from occurring, or stop a second infection from causing disease. Memory T cells, on the other hand, guide the immune response or kill infected cells. So far, research in people and monkeys suggests that many people will have antibodies against the coronavirus for months. So why do some people appear to have caught it twice? Immunity might not last for everyone, while in other cases, it’s possible that the initial immune response wasn’t strong enough in the first place. Some immunologists predict that the current coronavirus is likely to trigger immunity in a similar way to the virus behind the SARS outbreak in 2003, as the two viruses are genetically similar. The SARS virus typically induces a long-lasting immunity, says Petter Brodin at the Karolinska Institute in Stockholm. One recent study found that people who had recovered from SARS still appear to have T cells for the virus 17 years later. But John Brooks at the US Centers for Disease Control cautions against assuming the viruses act in the same way. “The diseases they produce and the way they are being transmitted are remarkably different,” he says.
9-10-20 Some autistic children may prefer cats as they don’t hold eye contact
The fleeting way cats make eye contact may explain why some autistic children develop stronger relationships with pet cats than pet dogs. The “less intrusive glance” of cats, compared to the “long gazes” that dogs make, might align better with autistic children’s “social needs,” says Marine Grandgeorge at the University of Rennes in France. “Cats don’t hold a stare but tend to look away after short bouts of eye contact, and it’s possible that this feels more comfortable for people with autism,” she says. Previous research based on questionnaires with parents has shown that autistic children develop relationships with pets and often have “privileged” relationships with cats, says Grandgeorge. She and her colleagues visited 42 homes in western France and observed 23 autistic boys and 19 neurotypical boys and girls, all aged 6 to 12, who had either a pet cat or dog. By analysing the videos made during these visits, the researchers found that neurotypical children tended to gaze longer at their pets than children with autism did, she says. They noted that dogs – as well as children who aren’t autistic – tended to gaze for at least a second at a time during eye contact, says Grandgeorge. Cats – as well as autistic children – tended to give much shorter glances. “There’s this belief that autistic children don’t want social contact with humans, but maybe they just don’t want humans to insist on creating a connection through long gazes, because that feels too intrusive,” says Martine Hausberger at the French National Centre for Scientific Research, who worked on the study. “Cats glance, look away, then glance back again briefly, and what we see is the child then actively seeking attention from the cat,” says Hausberger. “That could be stimulating and developing social skills that are often considered lacking in autistic people.”
9-10-20 A sobering breakdown of severe COVID-19 cases shows young adults can’t dismiss it
A new study underscores the fact that people ages 18 to 34 can still get severely sick. Although older adults face the highest risk of being hospitalized with or dying from COVID-19, younger adults can also end up in the hospital (SN: 3/19/20). If they do, the outcome can be serious, and a new study is providing a look at just how severe the disease can be for those patients. Of roughly 3,200 people ages 18 to 34 who were admitted to 419 U.S. hospitals from early April to the end of June, 21 percent, or 684 people, landed in intensive care and 10 percent, or 331 patients, ended up on ventilators. Almost 3 percent, or nearly 90 people, died, researchers report September 9 in JAMA Internal Medicine. Those numbers are “alarming figures given that COVID-19 outbreaks are rampant in many U.S. colleges that have opened for in-person learning,” says Aubree Gordon, an epidemiologist at the University of Michigan in Ann Arbor. Younger adults now make up nearly a quarter of U.S. coronavirus cases. A 3 percent death rate is lower than what has been reported for hospitalized older adults with COVID-19 — which was more than 20 percent in two separate studies from the United States and Germany — but still higher than it is for some other illnesses. For instance, it’s more than twice the death rate for heart attacks in young adults, the researchers wrote. Underlying conditions like severe obesity or high blood pressure were linked to more serious illness or death. And the team found that younger adults who have multiple underlying conditions can face similar risks of serious illness and death as people 35 to 64 years old without those conditions. More than half of the hospitalized young adults were Black or Hispanic, although race or ethnicity was not associated with an increased risk of death or needing a ventilator.
9-10-20 Gallup Vault: New Vaccines Not Wildly Popular in U.S.
In 1954, shortly after the newly developed polio vaccine became available, Dr. George Gallup interpreted Americans' reaction to it positively, saying, "The public itself is very optimistic about the effectiveness of the Salk test. By more than a 13-to-1 ratio, the people interviewed who expressed an opinion feel that the new vaccine will work." To be precise, 53% thought the vaccine would work, 4% thought it would not, 33% were unsure and 10% were not familiar with the vaccine at all. That same year, Gallup found 60% of Americans saying they were willing to take the new vaccine themselves, while 31% said they would not. This level of skepticism about a new vaccine has proven not unique to polio, as similar percentages of Americans have expressed reluctance about four subsequent vaccines measured over the years. Three years later, in 1957, 20% said they would not take an Asian flu vaccine, with 15% saying they were unsure. Even higher percentages said they would not take new vaccines for smallpox in 2002 (45% would not or were unsure) and the swine flu in 2009 (45%). The 35% who now say they would not take a COVID-19 vaccine once it becomes available is right within the historical range. (Webmaster's comment: Many Americans are ignorant fools.)
9-10-20 Drones find signs of a Native American ‘Great Settlement’ beneath a Kansas pasture
The sprawling town may have been home to thousands before Spanish explorers arrived. Specially equipped drones flying over a Kansas cattle ranch have detected the buried remnants of a horseshoe-shaped ditch made more than 400 years ago by ancestors of today’s Wichita and Affiliated Tribes, scientists say. The find adds to suspicions that the Kansas site was part of a sprawling population center that Spanish explorers dubbed the Great Settlement in 1601, archaeologist Jesse Casana of Dartmouth College and his colleagues report August 24 in American Antiquity. Called Etzanoa by a captive the Spanish took from the Great Settlement, it could turn out to be one of the largest Native American settlements ever established north of Mexico, if confirmed by further research. The largest currently known is Cahokia, a site in what’s now Illinois where as many as 20,000 people lived between 1050 and 1150. Ancestral Wichita communities in Kansas and northern Oklahoma that date to between around 1425 and 1650 existed in a time frame during which South America’s Inca civilization rose and fell (SN: 8/3/20). In the 1800s, European settlers drove ancestral Wichita people from their native lands, leading to the destruction of their villages and communal traditions. The newly discovered earthwork, a 2-meter-wide ditch that forms a semicircle about 50 meters across, is similar to other circular earthworks known as council circles. Five council circles have been found among 22 ancestral Wichita sites excavated along an eight-kilometer stretch of the Walnut River. “We apparently have located the sixth council circle and the only one that has not been disturbed,” says anthropological archaeologist Donald Blakeslee of Wichita State University. Farming and construction projects have damaged or covered many ancestral Wichita sites.
9-10-20 How does a crop’s environment shape a food’s smell and taste?
Scientists explore whether terroir leaves a lasting imprint. About seven years ago, Kristin and Josh Mohagen were honeymooning in Napa Valley in California, when they smelled something surprising in their glasses of Cabernet Sauvignon: green pepper. A vintner explained that the grapes in that bottle had ripened on a hillside alongside a field of green peppers. “That was my first experience with terroir,” Josh Mohagen says. It made an impression. Inspired by their time in Napa, the Mohagens returned home to Fergus Falls, Minn., and launched a chocolate business based on the principle of terroir, often defined as “sense of place.” Different countries produce cocoa with distinct flavors and aromas, Kristin Mohagen says. Cocoa from Madagascar “has a really bright berry flavor, maybe raspberry, maybe citrus,” she says, while cocoa from the Dominican Republic “has a little more nutty, chocolaty taste.” The couple estimates that back in 2013, when they founded Terroir Chocolate, about 50 other small batch chocolate companies in the United States were also touting terroir as integral to their products’ flavors. Since then, terroir has continued to take hold as a marketing strategy — and not just for wine and chocolate. Terroir labels are also becoming more common for products like coffee, tea and craft beer, says Miguel Gómez, an economist at Cornell University who studies food marketing and distribution. Consumers “are increasingly interested in knowing where the products they are eating are produced — not only where but who is making them and how,” he says. People “value differences in the aromas, the flavors.” The definition of terroir is somewhat fluid. Wine enthusiasts use the French term to describe the environmental conditions in which a grape is grown that give a wine its unique flavor. The soil, climate and even the orientation of a hillside or the company of neighboring plants, insects and microbes play a role. Some experts expand terroir to include specific cultural practices for growing and processing grapes that could also influence flavor.
9-9-20 Don't Miss: Science Disrupt is about the people who bring about change
Contribute Love Letters to a Liveable Future charts the transformations in our lives following the covid-19 outbreak. Share your visions of the future by postcard or video link to ongoing work promoted by sci-art producers Artsadmin. Read Stephen Hawking: A memoir of friendship and physics describes how Leonard Mlodinow’s collaboration with Hawking on The Grand Design (a follow-up to A Brief History of Time) blossomed into a 15-year friendship with a giant of science. Listen Science Disrupt is a podcast about change-makers in science, from entrepreneurs and iconoclasts to smart outsiders. Guests include materials scientist Ainissa Ramirez and broadcaster Adam Hart.
9-9-20 Why there is no such thing as a healthy diet that works for everyone
What is good for us to eat varies so much from person to person that a universally wholesome diet is a fiction. Instead, the science of nutrition is hot on the heels of a new recipe for healthy eating. FOR about a decade, geneticist Tim Spector of King’s College London ate the same thing every day: a tuna and sweetcorn sandwich on brown bread, followed by a banana. He thought it was a healthy choice, until he turned the microscope on himself and discovered that it was about the worst possible thing he could eat. He was having huge post-lunch surges of sugar and fat in his bloodstream, both of which are known risk factors for diabetes, heart disease and obesity. But just because tuna sandwiches are bad for Spector doesn’t mean they are bad for everyone. Far from it: for some people, they are super healthy. The same is true of almost any food, even things like ice cream and white bread that have long been considered universally bad news. Recent research by Spector and others has revealed that our response to food is highly individualised and that, consequently, there is no such thing as a healthy diet that works for everybody. In fact, people respond to food in such idiosyncratic ways that everybody needs a personalised nutrition plan. Now he and others, including the US National Institutes of Health, are seeking to deliver such plans in a healthy eating revolution that is being called “precision nutrition”. The findings could also explain why decades of one-size-fits-all dietary advice has failed to halt the global epidemic of obesity and diabetes and why nutrition science has consistently failed to produce a straight answer to its most pressing question: what constitutes a healthy diet? The idea of diet as a major determinant of health goes back to at least the ancient world, with Hippocrates’ famous (but probably apocryphal) dictum “let food be your medicine”. Scientific attempts to define a healthy diet date back to the 1890s, when nutrition pioneer Wilbur Atwater at Wesleyan University in Connecticut published the first ever dietary guidelines. He recommended variety, moderation and the avoidance of too much fat, sugar and starch. That advice has largely stood the test of time, along with its underlying assumption that there is such a thing as a healthy diet. But now, 125 years of nutritional orthodoxy is being chewed up.
9-9-20 To curb obesity, we must pay heed to a revolution in nutrition science
IT WAS a tempting offer enjoyed by millions of people: as many cut-price restaurant meals as you could eat every Monday to Wednesday for a month. While the UK’s recent “eat out to help out” scheme may have saved jobs and boosted the hospitality industry after the coronavirus lockdown, it is unlikely to have done much for the country’s obesity crisis. The government’s own figures show meals from restaurants are on average twice as calorific as the equivalent dish prepared at home. For many years, the UK has laboured under the burden of having one of Europe’s fattest populations. Earlier this year, prime minister Boris Johnson – who blamed his brush with severe covid-19 on being overweight – swallowed his opposition to “nanny state” schemes and announced a national obesity strategy. It is likely to feature more calorie labelling, restrictions on junk food advertising and on BOGOF (buy-one, get-one-free) deals, along with nudge-style interventions to stop impulse purchases of calorific foods. None of these will do any harm, but as an anti-obesity strategy they fall well short of the latest science. As we report (see “Why there is no such thing as a healthy diet that works for everyone”), nutrition research is undergoing a much-needed revolution. It turns out that the way we respond to food varies so much from person to person that there is no such thing as a one-size-fits-all healthy diet. That may explain why science has failed to tackle the obesity epidemic. Consider a recent test of the efficacy of low-fat versus low-carb diets for weight loss. The DIETFITS study put more than 600 overweight people on one of the diets for a year. At the end, the average weight loss was the same in both groups, about 5.5 kilograms, but there was huge individual variation, ranging from much larger losses to significant weight gain.
9-9-20 How ancient proteins are untangling humanity's family tree
We can't extract DNA from some of the most perplexing ancient human fossils. But ancient proteins sometimes survive better, and they are finally starting to give up their secrets. IT WAS an astonishing discovery: a chamber deep underground, packed full of ancient human remains. The excavators who uncovered the fossils at South Africa’s Rising Star cave in 2013 described the experience as “breathtaking” and “emotional”. Then they took a proper look at the bones, and exhilaration gave way to bewilderment. This new species of ancient human, which the researchers called Homo naledi, had such an odd combination of primitive and modern features that it was impossible to know how it was related to other ancient humans and, ultimately, to us. About 20 years ago, it looked like the human evolutionary tree was coming into focus. Then palaeontologists started finding ancient humans, like H. naledi, that are so strange, it is as if they had walked off the pages of a Tolkien fantasy. We can’t expect ancient DNA to help resolve their place in the human family tree because most of these misfit cousins were found in places too warm for genetic material to survive. The trail seemed to have gone cold. In the past few years, however, we have learned to read the signals in other organic molecules that tend to survive longer than DNA and persist even in warm environments. Researchers have already analysed samples of proteins extracted from ancient bones and teeth to reveal relationships between ancient mammals. Now, some think they could reveal how archaic humans like H. naledi evolved and interacted. “I’m confident that it will be possible to put some of these very unusual hominins on the [family] tree,” says Matthew Collins at the University of Copenhagen in Denmark. It is no exaggeration to say ancient DNA has transformed our understanding of human evolution. It confirmed that our ancestors interbred with Neanderthals between about 100,000 and 50,000 years ago. It revealed the existence of a distinct group of Stone Age humans we had never recognised before – the Denisovans of east Asia – and showed that our ancestors interbred with them too, between about 50,000 and 15,000 years ago. More recently, ancient DNA studies have even begun to find evidence that Denisovans once interbred with a far more ancient group of humans, perhaps a species called Homo erectus that appeared almost 2 million years ago and vanished about 100,000 years ago.
9-9-20 What will happen to covid-19 cases in winter and how can we prepare?
WITH hindsight, we may come to see late summer in the northern hemisphere as the calm before the storm. While many countries in the north have suppressed the spread of covid-19 for now, there is growing evidence warning us that winter could undo that progress. Researchers are racing to pinpoint what role temperature and humidity may have in the spread and severity of the illness. They are exploring how SARS-CoV-2, the virus that causes covid-19, will interact with other seasonal respiratory viruses. And people are scouring data from winter in the southern hemisphere to see what the north might face. These questions are a matter of life and death. In the UK alone, a reasonable worst-case scenario in the event of a resurgence of the coronavirus this winter estimates that there could be as many as 251,000 deaths in hospitals – although the total under the range of possibilities within this scenario is more likely to be less than half that. Whatever the outcome, UK scientific advisers expect cases to increase this winter. The weather is the obvious change coming. To predict how this will influence the virus’s spread, we need to disentangle the effects of weather from other confounding factors, such as how countries have responded, different demographics and variation in testing rates. “Some of our motivation for studying this is, early in the pandemic, [US] President Trump and other global leaders were assuming, not backed up by evidence, that this would just go away in hot weather. That could have led to complacency,” says Rachel Lowe at the London School of Hygiene & Tropical Medicine. Trump’s claim that the virus would be halted by summer appears to have been proven wrong. A study by Lowe’s team found the virus spreading in different countries across the globe regardless of temperature.
9-9-20 Could the coronavirus merge with another virus to create a new threat?
DOCTORS may be fretting about concurrent outbreaks of flu and covid-19 (see “What will happen to covid-19 cases in winter and how can we prepare?”) but some virologists are worrying about another scenario: a Frankenvirus. SARS-CoV-2, the virus that causes covid-19, almost certainly originated from the hybridisation of two different coronaviruses. The details remain hazy, but the virus’s genome sequence suggests that this mash-up occurred in a bat about a decade ago. The bat was simultaneously infected with two closely related coronaviruses, which merged into a new one. Such recombination isn’t unusual for coronaviruses. “If you look in the family tree of coronavirus, there’s recombination everywhere,” says virologist Samuel Díaz-Muñoz at the University of California, Davis. It occurs for two reasons. First, coronaviruses are tolerant to co-infection. Unlike many other viruses, they allow co-infection of the same cell by other viruses. Second, the way coronaviruses replicate their genomes makes hybridisation not just possible but likely. They are RNA viruses, which usually have very high rates of mutation – the highest rate of any known biological entity – because the enzymes that copy their RNA don’t have a proofreading function. A high mutation rate can allow a virus to rapidly evolve resistance to the host’s immune response. Coronaviruses are the exception, because their replicase enzymes do proofread. SARS-CoV-2 has proved very resistant to mutation. According to Díaz-Muñoz, only six mutants have emerged thus far. The variability in coronaviruses comes from something else: recombination. Their replicase enzymes frequently jump from one part of the RNA template to another. This makes them adept at remixing their own genomes to create variation, and also allows them to steal genetic material from other closely related coronaviruses. “It is one of the things that facilitates jumping from one species to another. I think there’s no doubt that recombination in a bat was involved in the emergence of SARS-CoV-2,” says Díaz-Muñoz. The fear is that it could now happen again, inside a human.
9-9-20 Coronavirus: Oxford University vaccine trial paused after participant falls ill
Final clinical trials for a coronavirus vaccine, developed by AstraZeneca and Oxford University, have been put on hold after a participant had a suspected adverse reaction in the UK. AstraZeneca described it as a "routine" pause in the case of "an unexplained illness". The outcome of vaccine trials is being closely watched around the world. The AstraZeneca-Oxford University vaccine is seen as a strong contender among dozens being developed globally. Hopes have been high that the vaccine might be one of the first to come on the market, following successful phase 1 and 2 testing. Its move to Phase 3 testing in recent weeks has involved some 30,000 participants in the US as well as in the UK, Brazil and South Africa. Phase 3 trials in vaccines often involve thousands of participants and can last several years. The New York Times is reporting a volunteer in the UK trial has been diagnosed with transverse myelitis, an inflammatory syndrome that affects the spinal cord and can be caused by viral infections. However, the cause of the illness has not been confirmed and an independent investigation will now work out if there was any link to the vaccine. Wellcome Trust director Sir Jeremy Farrar, an expert in infectious disease control, said there were often pauses in vaccine trials and it was important any adverse reactions were taken seriously. "It is crucial that all that data is shared openly and transparently because the public must have absolute trust that these vaccines are safe and effective and, in the end, will hopefully bring the pandemic to a close," Sir Jeremy added. UK experts have said a temporary pause could be seen as a good thing because it showed the researchers are prioritising the safety of vaccine above everything else. People can develop side-effects from taking any drug but they can also fall ill naturally.
9-9-20 Coronavirus: Pharma firms unveil safety pledge over vaccine
A group of nine vaccine developers has announced a "historic pledge" to uphold scientific and ethical standards in the search for a coronavirus vaccine. The firms, including Pfizer and Merck, said they would only apply for regulatory approval after vaccines went through three phases of clinical study. It comes amid global debates about the safety of vaccines made this year. US President Donald Trump has said he wants one available in the US before November's election. No vaccine has yet completed clinical trials, according to the World Health Organization (WHO) - leading some scientists to fear the search for a vaccine is being politicised, and public trust could be damaged. In their pledge, the nine biopharmaceutical firms did not mention Mr Trump but said they believed their action would "ensure public confidence" in the development of any inoculation. They pledged to "always make the safety and well-being of vaccinated individuals our top priority". Other signatories were industry giants Johnson & Johnson, BioNTech, GlaxoSmithKline, AstraZeneca, Moderna and Novavax. "Together, these nine companies have collectively developed more than 70 novel vaccines that have helped to eradicate some of the world's most complex and deadly public health threats," the statement added. Nearly 180 vaccine candidates are being tested around the world, the WHO says. The organisation has said it does not expect a vaccine to meet its efficacy and safety guidelines in order to be approved this year because of the time it takes to test them safely. None of the candidate vaccines in advanced clinical trials have so far demonstrated a "clear signal" of efficacy at the level of at least 50% sought by the WHO, spokeswoman Margaret Harris said last week. "In terms of realistic timelines, we are really not expecting to see widespread vaccination until the middle of next year," she added. Similar sentiments have been shared by Thomas Cueni, director-general of the International Federation of Pharmaceutical Manufacturers. The industry body represents the companies that signed the pledge. "I think it's fairly unlikely that we will have a vaccine approved or in particular distributed at large scale before the end of this year," he told the BBC. "We may be surprised but clearly the manufacturers do not want speed above quality".
9-9-20 A stray molar is the oldest known fossil from an ancient gibbon
Ancestors of these small-bodied apes were in India roughly 13 million years ago, a study suggests. While searching for primate fossils in northern India, paleontologist Christopher Gilbert noticed something small and shiny poking out of the dirt. It turned out to be a roughly 13-million-year-old molar from a small-bodied ape related to modern gibbons. The tooth is the oldest known fossil from a gibbon ancestor, says Gilbert, of Hunter College at the City University of New York. He and colleagues assigned the fossil, which was eroding out of previously dated sediment at a site called Ramnagar, to a new genus and species, Kapi ramnagarensis. Until now, the oldest remains of an ancient gibbon species consisted of a small number of teeth found in China, which date from around 7 million to 9 million years ago. Possibly older fossils of a gibbonlike creature are controversial (SN: 10/29/15). Genetic studies of living primates have suggested that gibbon ancestors emerged by at least 20 million years ago in Africa. After finding the Ramnagar molar in 2015, Gilbert’s team compared it with corresponding teeth of living and extinct apes and monkeys. Features including low, rounded cusps on the edges of the chewing surface link the ancient tooth to modern gibbons and the gibbon predecessor in China, the scientists report September 9 in Proceedings of the Royal Society B. K. ramnagarensis comes from deposits that previously yielded fossils of an orangutan ancestor, suggesting to Gilbert that both apes reached South Asia from Africa around the same time. “We’re catching a window into that event” as small-bodied gibbons and large-bodied orangutans headed to their recent and current home ranges in East and Southeast Asia, he says.
9-8-20 We are finally unravelling the mystery of what causes severe covid-19
An out-of-control human peptide called bradykinin could be responsible for some of the varied and sometimes deadly symptoms seen in people who have contracted the coronavirus. We already have drugs to control bradykinin, which are being tested as treatments for people with covid-19. Bradykinin normally helps to regulate blood pressure, and in some people, the coronavirus seems to be pushing bradykinin production into overdrive. This would create a kind of “bradykinin storm” in the body that may lead to a number of symptoms common in covid-19. Renuka Roche at Eastern Michigan University says such a storm could explain many aspects of covid-19 that seem disjointed, such as muscle pain, women sometimes having milder illness than men, and African Americans being more likely to develop complications. In July, a team led by Daniel Jacobson at the Oak Ridge National Laboratory in Tennessee published a study in which they mined gene expression data in samples of lung fluid from nine people with covid-19 in China, and compared them with samples from a control group that didn’t have the disease. They found an over-expression of genes that are responsible for bradykinin production, along with under-expression of genes that produce enzymes to keep bradykinin levels in check. Because bradykinin dilates blood vessels and makes them more permeable, high levels of bradykinin could lead to fluid leakage in a blood-vessel-rich environment like the lungs. It can also break down the blood-brain barrier, suggesting a possible pathway for some of the coronavirus’s puzzling neurological symptoms. Josef Penninger at the University of British Columbia in Canada says the bradykinin hypothesis makes sense given what we know about the way the coronavirus works in the body. The virus invades human cells via ACE2 receptors, which, he says, also help keep bradykinin levels in check. But with the virus reducing the availability of these receptors, bradykinin levels could get out of control.
9-8-20 What is a vaccine and how do they work? Find out in Science with Sam
Since the first vaccine was developed in 1796, vaccinations have been phenomenally successful at preventing infectious diseases, and wiping out some altogether. The latest video in our new YouTube series, Science with Sam, explains how vaccines work by training your immune system to recognise viruses and bacteria. Ever wondered how flu vaccines are made or why you need a new one every year? Click play to find out. We also take a look at the unprecedented worldwide effort to develop a vaccine for the coronavirus, and consider the challenges involved in making, testing and distributing covid-19 vaccines. Most of us have never had to worry about getting smallpox, polio or diphtheria. A hundred years ago, these diseases were common killers. Now, smallpox is a thing of the past, while polio and diphtheria are very rare in most of the world. The reason? Vaccines. Vaccines are a way of training the immune system for a big fight, so that when it comes up against the same opponent in the future, it knows exactly how to defeat it. When you encounter a virus or bacterium for the first time, your body has a hard time fighting it. But over time, it learns to recognise the danger. Your immune system produces powerful proteins called antibodies that target and eliminate disease-causing microbes. After you recover from an infection, specialised cells remain in your blood and keep a memory of that pathogen – they’re called memory cells – so the next time you face the pathogen, your body can quickly produce the right antibodies to fight it off. Vaccines are a clever way of harnessing this mechanism to make us immune to a disease. They are made of weakened or killed viruses or bacteria that trigger an immune response, without making us ill.
9-7-20 Teens with asthma get tailored treatment thanks to cheap genetic test
A cheap and simple genetic test can guide the treatment of children with asthma, improving their quality of life, according to the results of the first clinical trial of personalised treatment of asthma. The treatment of asthma hasn’t changed much in the last 20 or 30 years. People who show symptoms of asthma tend to first be prescribed a drug that works on receptors in the airways and blood vessels, called beta-2 receptors. If that doesn’t work, they tend to be given inhaled steroids, which stop inflammation in the airways. But many people still struggle to manage their symptoms, says Somnath Mukhopadhyay, chair of paediatrics at the Royal Alexandra Children’s Hospital in Brighton, UK. About 17 per cent of people with asthma have a form that is “difficult to control”. Such individuals can end up having more severe and potentially life-threatening asthma attacks. “They can struggle to go up stairs, and have difficulty managing their social relationships,” says Mukhopadhyay. “They can have a very poor quality of life.” Previous research suggests that a genetic factor might explain why some people do better on certain treatments than others. A region of the genetic code for the beta-2 receptor can vary between individuals – people with different versions of this code tend to respond differently to treatments that target this receptor. This suggests that a genetic test to find out which form a person has could help guide an individual’s treatment, says Mukhopadhyay. To find out, Mukhopadhyay and his colleagues recruited 241 volunteers aged between 12 and 18 from 236 doctors’ surgeries around the UK. At the start of the study, all of the children were already being treated with a first-line drug that acts on beta-2 receptors, as well as inhaled steroids, but still found their asthma difficult to control. At that point, around half of the volunteers continued receiving the treatments selected by their family doctor (GP) based on their symptoms. The other half were given a genetic test, which involved sending a sample of spit to a lab.
9-7-20 Experimental drug boosts muscle and bone mass of mice in space
An experimental drug has dramatically increased muscle and bone mass in mice that spent a month on the International Space Station. The hope is that a human version could help people who spend long periods in bed due to illnesses, as well as astronauts. “It could help any condition, any prolonged illness, in which someone is bedridden,” says Emily Germain-Lee at the University of Connecticut. Maintaining muscle and bone is costly, so they lose mass when we don’t use them, whether due to spending time in bed or in microgravity. This effect is partly due to a protein called myostatin, which binds to receptors on the surface of muscle cells and blocks their growth. Many groups have been trying for decades to develop drugs that block myostatin’s effects, with little success. That may be because myostatin isn’t the only growth factor involved, says team member Se-Jin Lee at the Jackson Laboratory in Connecticut. Another protein, called activin A, binds to the same receptor and has similar effects. Disabling the myostatin gene in mice doubles muscle mass, says Lee, while disabling both the myostatin and activin A genes quadruples it. The experimental drug is a modified form of the receptor that both proteins bind to. When it is injected into the bloodstream, myostatin and activin A bind to it instead of the real receptors, reducing the inhibitory effect. “It acts as a decoy,” says Lee. High doses produce a 50 per cent increase in muscle mass throughout the bodies of mice in just two weeks. When mice were given a dose of the decoy receptor two days before being launched to the International Space Station, and then weekly while on the station, their muscle and bone mass increased by around 20 per cent, similar to ground-based mice given the same doses. In untreated mice, muscle mass fell around 10 per cent during the month in space.
9-6-20 'Super bacteria' survives for three years outside space station
Scientists who attached a strain of bacteria to the outside of the International Space Station have been stunned to find it survived for three years, in open space. The experiment, led by a team of Japanese researchers, involved the bacteria Deinococcus radiodurans, also known as Conan the Bacterium due to its extreme hardiness. Experts say the study could help shape our understanding of whether life might exist on other planets.
9-4-20 A Trump vaccine is still a vaccine
Now is not the time to drop your 'believe in science' mantra. COVID-19 vaccine could be here sooner than we thought. "I believe that by the time we get to the end of this calendar year that we will feel comfortable that we do have a safe and effective vaccine," Dr. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, said Wednesday. This is possible, he explained in another interview the day before, if two current trials with 30,000 volunteers produce such overwhelmingly positive results that researchers determine they have "a moral obligation" to accelerate the process of bringing the vaccine to the public. The Centers for Disease Control (CDC) issued guidance last week for all 50 states and several major cities to prepare for some vaccine administration as soon as the end of October. This should be heralded as good news, especially among those who have supported strict pandemic control measures. For many of that ilk, a vaccine was always the one acceptable end to broad shutdowns and rigorous social distancing. But now this very end may be nigh, and suspicion of the "Trump vaccine" is growing. The possible timing of an initial rollout near Election Day — paired with President Trump's transparent hope that a vaccine will help him win re-election — has people who long declared we must "trust science" about the pandemic now declaring this product of science is not to be trusted. As scads of tweeted objections argue, the fear is the administration will strong-arm the Food and Drug Administration (FDA) and CDC into pushing an ineffective or outright dangerous vaccine to early release for political gain. This isn't just a Twitter thing; though typically op-eds stop short of advising refusal of specific vaccines, worries about an unsafe, politically motivated vaccine have been raised repeatedly in The New York Times and other prominent outlets. Automatic rejection of a "Trump vaccine" is a mistake, and potentially a very serious one, which could help delay our desperately needed return to normal life by months. We already know a large portion of Americans will refuse even a free, FDA-approved COVID-19 vaccine. The plurality of that group is Republicans, many of whom may have previously been skeptical of vaccines and/or the necessity of any pandemic response at all. I don't think their skepticism of a COVID-19 vaccine is justifiable, but it is to be expected. Some of that group, however, are Democrats and independents who have spent the past half year defending vaccines and the medical establishment more generally against charges of undue political influence. Those same arguments should still apply. If public health experts like Fauci were trustworthy and impervious to political coercion before, they're still trustworthy now. Of course, an untested vaccine could be dangerous. And yes, the way Trump talks about the vaccine timeline is not reassuring. (How does he manage to make the assertion that he's "doing it not for the election" sound like an admission of exactly the opposite?) But if we know anything about Trump, it's that he says a lot of stuff that has no connection to reality — like his claim that the "deep state, or whoever, over at the FDA" is deliberately slowing vaccine trials to make him lose. Also not demonstrated is the opposite claim: that Trump forced the "deep state, or whoever, over at the FDA" to unsafe haste in vaccine creation. He talks as if he has, and an in-depth Washington Post story published Sunday indicates he has tried. Yet trying can mean nothing with someone as incompetent as Trump. In fact, the same story suggests the real crisis involving this vaccine is Trump's decimation of public confidence in its development, not the scientific soundness of the vaccine itself.
9-4-20 Strict new guidelines lay out a path to heritable human gene editing
But scientists say making changes in DNA that can be passed on isn’t yet safe and effective. Gene editing to make heritable changes in human DNA isn’t yet safe and effective enough to make gene-edited babies, an international scientific commission says. But in a Sept. 3 report, the group laid out a road map for rolling out heritable gene editing should society decide that kind of DNA alteration is acceptable. The International Commission on the Clinical Use of Human Germline Genome Editing formed after a Chinese scientist announced in 2018 that he had created two gene-edited baby girls, sparking outrage (SN: 11/27/18). In its first official weigh-in on the issue, the group lays out strict scientific criteria that would need to be met before heritable gene editing could be tried clinically. If countries can’t ensure that all of those criteria are met, heritable gene editing shouldn’t be approved, the commissioners say. Still, some critics charge that even presenting such criteria is premature. The science should wait until society decides whether to allow gene editing that can affect future generations, they say. Gene editing involves changing a single DNA letter, or base, in a gene. Many different technologies, including CRISPR/Cas9, base editors (SN: 3/5/19) and engineered proteins called zinc finger nucleases and TALENs (SN: 11/6/15), can be used to make edits at precise locations in DNA. Although accuracy of editing has improved, there are still concerns that gene editors will make unwanted, “off-target” changes elsewhere in DNA that might cause harm. Technologies to ensure every cell in an embryo contains the desired change — and only that change — also still need work, the commission says. “It’s accurate and efficient enough to do in animals,” but editing in human embryos requires much more precision, Haoyi Wang, a geneticist and molecular and stem cell biologist at the Chinese Academy of Sciences’ Institute of Zoology in Beijing said September 3 during a webinar to discuss the report.
9-3-20 Russian biologist still aims to make CRISPR babies despite the risks
Russian biologist Denis Rebrikov has told New Scientist that he still plans to use CRISPR genome editing to prevent children inheriting deafness, despite a major international report out today saying it isn’t yet safe enough to try in people. “We are still planning to correct the inherited hearing loss mutation in [the gene] GJB2, so that a hearing baby is born to a deaf couple,” says Rebrikov, who is at Pirogov Medical University in Moscow. Three children whose genomes were altered by CRISPR gene editing were born in China in 2018 and 2019. The unauthorised creation of those embryos caused concern around the world and spurred scientific institutes to set up the International Commission on the Clinical Use of Human Germline Genome Editing, a group of 18 doctors, biologists and ethicists from 10 countries tasked with drawing up guidelines for how to proceed in a responsible way. The main conclusion of its report, out today, is that genome editing isn’t yet safe and effective enough for altering human embryos before implantation in the uterus. “The criteria for safe and effective heritable human gene editing have not yet been met,” says Haoyi Wang at the Chinese Academy of Sciences, who is on the commission. The reason is that existing methods can cause unintended genetic mutations and also may not correct the condition-causing mutation in every cell, an issue known as mosaicism. However, the technology is advancing so fast that it might be ready for use in just a few years, says Wang. These problems aren’t a deal-breaker for using CRISPR as a treatment for serious conditions such as cancer or sickle cell, as the potential benefits outweigh the risks, and the changes CRISPR makes in these cases are not heritable. Many trials are already under way.
9-3-20 Steroids reduce deaths of critically ill COVID-19 patients, WHO confirms
The finding strengthens evidence that clinicians should give severely sick people the drugs. In June, a large study in the United Kingdom suggested that the steroid dexamethasone could help reduce the risk of death for critically ill COVID-19 patients. Now, more evidence suggests that steroids are an effective weapon against the coronavirus. Researchers from the World Health Organization combined data from seven randomized clinical trials for severely or critically ill COVID-19 patients treated with steroids versus standard care or a placebo up to June 9. The trials used the steroids hydrocortisone, dexamethasone or methylprednisolone. People who were on ventilators when their clinical trial started had a 30 percent chance of dying from the virus if given steroids compared with a 38 percent chance on standard care or a placebo, researchers report September 2 in JAMA. Results were even more promising for critically ill people who were not on ventilators: Those taking steroids had a 23 percent chance of death compared with a 42 percent for people taking a placebo or getting standard care. Results of three of the studies included in the combined analysis — one from France testing hydrocortisone, a trial of dexamethasone in Brazil and an international study of hydrocortisone — were published at the same time in JAMA. Those and other trials in the WHO analysis were stopped early because it wouldn’t have been ethical to continue and deny some sick patients steroids once the U.K. study found them effective. Based on the results of the combined analysis, the WHO recommended on September 2 that doctors give dexamethasone or hydrocortisone to severely and critically ill COVID-19 patients, but not to people with milder illness. Giving steroids to people with moderate or mild cases might dampen the immune system too much, allowing the virus to do more damage. The U.S. National Institutes of Health have also recommended use of steroids for hospitalized people who need extra oxygen or are on ventilators.
9-2-20 We could soon make cars stop people driving while drunk or on drugs
We are on the cusp of cars that automatically stop people driving while intoxicated. Embracing the technology will save lives, says Amie Hayley. THE message couldn’t be clearer: don’t drive under the influence of alcohol or drugs. Yet people still put themselves and others in danger by getting behind the wheel while intoxicated. Despite decades of education programmes and law enforcement, road collisions attributable to intoxicated driving remain unacceptably high. We need a better approach and we are in the middle of a technological boom that may just deliver one. Seat belts and airbags have dramatically reduced the number of lives lost on roads. However, they do little to prevent the cause of crashes. Someone dies every 25 seconds globally due to road traffic injuries, and one in five of the drivers involved will test positive for alcohol following the collision. Some cars already have intelligent driver monitoring systems that help to reduce deaths by human error, such as inattention. These use cameras to monitor drivers’ alertness. When there is a deviation from the behaviour it has been trained to recognise, such a system can either warn the driver or take complete control of the vehicle to stop a collision from occurring. These systems may reduce collisions by up to 20 per cent. Already, they must be installed in all new European vehicles. In 2024, they must be included in all new US vehicles. Australia and New Zealand will also follow suit. Now, a second wave of intelligent driver monitoring technology is on its way. Internal cameras can be combined with other biometric sensors, such as heart rate monitoring or skin conductibility, to determine a driver’s internal state in real time. In other words, a car could determine when its driver is impaired by drugs or alcohol.
9-2-20 E-cigarettes are no better than alternative aids to quit smoking
People who use e-cigarettes to help them stop smoking are no more likely to be abstinent a year later than those who use alternative aids or nothing at all. These individuals are also more likely to remain dependent on nicotine. That’s what John Pierce at the University of California, San Diego, and his colleagues found when they assessed attempts to quit smoking by thousands of people in the US. But the findings don’t necessarily mean that e-cigarettes won’t help some people quit, argue researchers who weren’t involved in the work. Pierce and his colleagues assessed data collected as part of a study that has recruited around 49,000 people across the US. In one piece of research, the team looked at the outcomes of 32,320 adults who were asked about their use of tobacco products. A year later, each person was asked if they had attempted to quit smoking, the methods they had used and whether they had been successful. The following year, they were asked whether they had remained abstinent for 12 months or more. Of the 9021 people who initially said they smoked on a daily basis, 2770 had attempted to quit. Around 24 per cent used e-cigarettes as a cessation aid, while about 19 per cent used other aids, such as clinically approved drugs and other nicotine replacement therapies, like patches, sprays and lozenges. The remainder of the group didn’t use any products. But the choice of product didn’t seem to make a difference to how successful their attempt to quit was. Only around 10 per cent of people managed to stay abstinent from tobacco products for 12 or more months by the end of the period, regardless of whether they had used e-cigarettes, other products or nothing at all. Around 82 per cent of those who had attempted to quit were still smoking by the end of the study period.
9-2-20 A lot of veg is 'toxic' but that doesn't mean you shouldn't eat it
There are claims online that most of the fruit and veg we eat is toxic. Though there is some truth to this, it doesn't mean you should stop eating your greens, writes James Wong. AFTER decades of celebrating the benefits of fruit and veg, some corners of the foodie media are voicing a radical new claim: fresh produce is not only unnecessary for human health, it is actually quite toxic. With countless devotees, this school of thought argues that most plants have evolved elaborate toxins to defend themselves from predation, which makes animal-based foods the safer and healthier choice. One statistic circulating on social media is that 98.8 per cent of plants are toxic whereas 99.9 per cent of animals are edible. As strange as it may seem, this narrative – at least, when it comes to plants – has a bit of truth to it, although that doesn’t mean you should stop eating plenty of fruit and vegetables. So let’s unpack the botany behind this claim. Unlike animals, plants can’t run away or hide from threats, so they use a different strategy: chemical weapons. They pack their cells with pungent, bitter-tasting compounds, caustic irritants and deadly nerve toxins to inflict damage on predators, humans included. This isn’t just exotic plants in far-off jungles either – in fact, a whole range of ordinary edible crops belong not only to the same genus, but even the same species as some proper toxic ones. Potatoes, courgettes and pumpkins are filled with such substances in the wild, and it was only after millennia of brilliant breeding work by the indigenous peoples of the Americas that they were rendered edible. Every now and then, some plants revert to their wild ways, meaning home growers can be poisoned by the cucurbitacins found in improperly grown courgettes, for example. You could add everything from carrots and rhubarb to kidney beans and nutmeg to the “toxic crops” list too, with literally hundreds of everyday examples. So how prevalent is this toxicity?
9-2-20 Joe Henrich interview: Psychology must look beyond Western cultures
Most psychology studies involve people living in Western, Educated, Industrialised, Rich and Democratic societies. But the pecularities of WEIRD thinking are far from universal. HOW does the culture we live in influence our psychology, motivation and decision making? Joe Henrich was a cultural anthropologist working in the Amazon when he first tried to find out. He pioneered the use of experimental cooperation games like the prisoner’s dilemma and the ultimatum game outside the lab. Later, he realised that his findings have big implications for psychological research, which tends to focus on students from Western backgrounds. In 2010, he introduced the “WEIRD” concept to describe the unusual psychology of the subjects in the vast majority of these studies. Now professor of human evolutionary biology at Harvard University, he tells New Scientist about the origins of WEIRDness, its impact on history and its role in the modern world. The WEIRD label emerged from a series of lunches I started having around 2006 with two cultural psychologists, Steven Heine and Ara Norenzayan. We had noticed that in the behavioural sciences and psychology in particular, about 96 per cent of study participants were from Western, Educated, Industrialised, Rich and Democratic societies – and that they were often psychological outliers in comparison with other populations. WEIRD people tend to show greater trust in strangers and fairness towards anonymous others; think more analytically rather than holistically; make more use of intentions in moral judgements; are more concerned with personality, the self and the cultivation of personal attributes; they are more individualistic and less loyal to their group; and they are more likely to judge the behaviour of others as reflecting some enduring disposition rather than temporary situational factors.It is important not to set up a dichotomy between the WEIRD and non-WEIRD. WEIRDness is a multi-dimensional continuum, and there is a lot of variation even within Western Europe. In a recent paper, we took data from the World Values Survey and, using techniques from population genetics, analysed the cultural distance of various populations from the US, the weirdest of WEIRD countries. This WEIRD scale shows New Englanders as the WEIRDest population in the world and substantially different to populations in the Middle East and Africa at the other end. Interestingly, although there is a huge body of research in social psychology setting up an East-West dichotomy, it turns out that the typical subjects studied in Japan or China are kind of in the middle of the WEIRD spectrum.
9-2-20 The moon really may have strange effects on our health
Any lunar influence on our health has long been dismissed as unscientific. But new evidence means it may be time to re-evaluate the moon’s subtle effects on our sleep and mental health. IN FEBRUARY 1954, biologist Frank Brown discovered something that made no sense. While investigating whether oysters can keep time, he had found that they open their shells to feed at high tide, roughly twice a day. Brown had a hunch they weren’t simply responding to changes in their environment but would continue the rhythm even if moved far from the sea. To find out, he shipped a batch of oysters from the ocean off New Haven, Connecticut, hundreds of kilometres inland to Northwestern University in Evanston, Illinois. Brown kept the shellfish in a sealed darkroom, shielded from changes in temperature, pressure, water currents and light. At first, the oysters kept their rhythm, feeding each day in time with the New Haven tides. Then, something strange happened – their feeding times gradually shifted until they lagged 3 hours behind. Brown was mystified, until he realised that they had adapted to the local state of the moon: they were feeding at times when Evanston, if it were by the sea, would experience high tide. Despite having no obvious environmental cues, it seemed these shellfish were somehow tracking lunar cycles. Brown became convinced that oysters, humans and all life forms are plugged into subtle cosmic cues, continuously sensing both lunar and solar movements to coordinate biological processes, from metabolism to reproduction. But his ideas seemed outlandish to his peers. Brown’s results were forgotten, and the notion of lunar influences was dismissed as pseudoscience. Now, growing evidence from a range of fields suggests he might have been right. Perhaps, hidden beneath our more obvious earthly rhythms, we are also creatures of the moon. The belief that the moon guides life on Earth goes back millennia. The ancient Greeks thought female fertility had a lunar source, noting that the menstrual cycle averages 29.5 days, the same as the period between consecutive full moons. The word “menstruation” is derived from the Greek mene, meaning moon. The moon has also traditionally been believed to influence mental health, hence the pejorative term “lunatic” (from the Latin luna, or moon). When the foundations for the modern field of chronobiology were laid in the 1950s and 60s, however, most researchers focused on daily rhythms. These appeared to be driven by internal, biochemical timers nudged by physical cues, especially sunlight.
9-2-20 Honeybee venom 'kills some breast cancer cells'
Australian scientists say the venom from honeybees has been found to destroy aggressive breast cancer cells in a lab setting. The venom - and a compound in it called melittin - were used against two cancer types which are hard to treat: triple-negative and HER2-enriched. The discovery has been described as "exciting", but scientists caution that further testing is needed. Breast cancer is the most common cancer affecting women around the world. While there are thousands of chemical compounds which can fight cancer cells in a lab setting, scientists say there are few which can be produced as treatment for humans. Bee venom has previously been found to have anti-cancer properties for other types of cancer such as melanoma. The study by the Harry Perkins Institute of Medical Research in Western Australia was published in Nature Precision Oncology, a peer-reviewed journal. It tested venom from over 300 honeybees and bumblebees. The honeybee extracts were found to be "extremely potent", said Ciara Duffy, a 25-year-old PhD researcher who led the study. One concentration of the venom was found to kill cancer cells within an hour, with minimal harm to the other cells. But the toxicity increased for other dosage levels. The researchers also found the melittin compound on its own was effective in "shutting down" or disrupting cancer cell growth. While melittin naturally occurs in honeybee venom, it can also be synthetically produced. Traditionally, triple-negative breast cancer - one of the most aggressive types - has been treated with surgery, radiotherapy and chemotherapy. It accounts for 10-15% of breast cancers. On Wednesday, Western Australia's chief scientist described the research as "incredibly exciting". "Significantly, this study demonstrates how melittin interferes with signalling pathways within breast cancer cells to reduce cell replication," said Prof Peter Klinken. "It provides another wonderful example of where compounds in nature can be used to treat human diseases."
9-1-20 What are T-cells and why have they become a political football?
Throughout the coronavirus pandemic there have been fierce debates over the science – when to lock down, whether face coverings help and whether children are less susceptible, for example. The latest row is over whether we have been ignoring a crucial part of our immune response to the virus: T-cells. This matters because if people have more immunity to the virus than we thought, then perhaps we could abandon some covid-19 countermeasures. This was the case made by US President Donald Trump’s newest adviser on covid-19, Scott Atlas at Stanford University in California. It has also been championed by others who argue against lockdowns. Is there any truth to the idea? The immune system has two main arms to fight off pathogens such as the coronavirus. The one we hear most about consists of antibodies, small molecules that can recognise specific pathogens and target them for destruction. Antibodies against the coronavirus can be measured in the blood and so surveys quickly began to gauge the proportion of people who have them. But even in places hit hard by the pandemic, antibody levels aren’t high enough to give herd immunity, which occurs when enough people are immune to the virus that it can no longer easily spread. Researchers have estimated that 65 per cent of a population would need to be immune to achieve herd immunity, based on how contagious the virus is. In London, antibody levels were about 10 per cent between 26 April to 9 August. For England as a whole, as with many European countries, it is in single digits. These levels are widely taken as indicating how many people have been infected by the coronavirus. But the picture is more complex than this because of the second arm of our immune system, T-cells. Antibodies are sometimes seen as more important because they can stop viruses from entering the body. But once viruses make it inside, only T-cells can kill infected cells.
9-1-20 Bronze Age tradition of keeping human remains uncovered
An "inconceivably macabre" tradition of keeping human remains as relics during the Bronze Age has been discovered by researchers. The discovery by University of Bristol archaeologists revealed how the dead were commemorated 4,500 years ago. In one case, a human thigh bone found in a grave near Stonehenge had been crafted into a musical instrument. The findings were made using radiocarbon dating and X-ray scanning techniques. Dr Thomas Booth, from the university, said: "Even in modern secular societies, human remains are seen as particularly powerful objects, and this seems to hold true for people of the Bronze Age. "However, they treated and interacted with the dead in ways which are inconceivably macabre to us today." In the discovery made in Wilsford, near Stonehenge, the carved and polished artefact was found with other items, including stone and bronze axes, a bone plate and a tusk. "Although fragments of human bone were included as grave goods with the dead, they were also kept in the homes of the living, buried under floors and even placed on display," said Professor Joanna Brück. "This suggests that Bronze Age people did not view human remains with the sense of horror or disgust that we might feel today." Researchers said the findings revealed human remains of those within living memory were regularly kept and circulated amongst the living. The team also used micro-computed tomography at the Natural History Museum to look at microscopic changes to the bone produced by bacteria, to learn how the body was treated while it was decomposing.