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134 Evolution News Articles
for July 2020
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Nature cares only that you reproduce and raise the kids.
After you've done that, get out of the way.


7-31-20 Sperm have a weird way of swimming and we only noticed after 300 years
Sperm swim differently to how we thought. Rather than undulating their tails symmetrically, like an eel, they have a lopsided wiggle that combines with spinning about their long axis to give an overall forward motion. “The asymmetry cancels out because of the rotation,” says Hermes Gadêlha at the University of Bristol, UK. “They are like otters when they swim in a corkscrew motion.” Human sperm were some of the first living cells to be seen under a microscope, by Dutchman Anton van Leeuwenhoek in 1677, when he viewed his own sperm retrieved after sex with his wife. The scientist later described them as having a “snakelike movement, like eels in water”. And this view persisted until now. Gadêlha’s team has made the best yet video of a sperm’s motion, by using a 3D camera recording at 55,000 frames a second combined with a microscope that moves the sample up and down very fast so all different parts of the tail come into focus. This showed that the whip-like tail beats asymmetrically, in that it only wiggles to one side. Alone, this would send the sperm swimming in circles – but the second aspect of sperm movement, spinning about their long axis, ensures they travel forwards. “Imagine you could only swim with one leg – you would swim in circles,” says Gadêlha. “But if you rotated from one side to another as you swam, you would balance out the asymmetry of your stroke.” The finding solves a puzzle, as the molecular machinery inside a sperm that makes its tail move is asymmetrical and it wasn’t known how this could produce the presumed symmetrical tail motion. A better picture of how sperm move could help us understand male infertility caused by sperm that can’t swim well, says Gadêlha.

7-31-20 Leonardo da Vinci saw a whale fossil that opened his mind to deep time
A young Leonardo da Vinci saw a fossil whale embedded in an Italian hillside – centuries before what is currently regarded as the first description of such a fossil. The experience may have given the Renaissance-era genius an intuitive appreciation of the vast age of Earth, long before geologists realised the planet’s antiquity. Leonardo da Vinci, born in 1452 in what is now Italy, wrote about many scientific subjects, centuries before the rise of organised research. The claim that he saw a fossil whale rests on passages in the Codex Arundel, a collection of scraps of his writings. On one page, he wrote of an unnamed animal with “branching, sturdy dorsal fins” that he imagined “tempestuously tearing open the briny waves”, causing “terrified shoals of dolphins and big tuna fish” to “flee”. For many years, scholars thought this was metaphorical, perhaps a rewriting of a passage from the Roman poet Ovid’s Metamorphoses. But in 2014, Kay Etheridge at Gettysburg College in Pennsylvania argued that it might be a description of something da Vinci actually saw. Italy has many whale fossils, especially in the hills of Tuscany where he spent his early years, so Etheridge suggested that he saw a fossil whale. A new study by Alberto Collareta at the University of Pisa in Italy and his colleagues largely backs Etheridge up, but they question one aspect of her interpretation. “Etheridge put the location of this encounter between Leonardo and a fossil whale in a cave,” says Collareta. This was because, on the neighbouring page of the Codex, da Vinci wrote: “Having wandered for some distance among overhanging rocks, I came to the entrance of a great cavern”. However, Collareta’s team says Italian fossil whales aren’t normally found in caves and the pages of the Codex aren’t in any particular order, so the two passages are probably unrelated.

7-30-20 These are the 12 ways you can drastically cut your dementia risk
Almost half of all dementia cases could potentially be prevented or delayed by adopting 12 health measures, a major review has found. The review identified the biggest known risk factors for dementia as smoking, excess alcohol consumption, high blood pressure, obesity, diabetes, head injury, depression, hearing loss and exposure to air pollution, as well as lack of exercise, education and social contact. Minimising these 12 risks could potentially prevent or delay up to 40 per cent of dementia cases globally, according to the review of the latest evidence by 28 leading dementia experts from around the world. “People who have family members with dementia often ask me, ‘Is there anything I can do to prevent myself from getting it?’,” says David Ames at the University of Melbourne in Australia, who was one of the authors of the review. “There are certainly some things you can do that might make a difference.” For example, the review finds that individuals can partially protect themselves by not smoking, drinking less than 21 units of alcohol per week, maintaining a systolic blood pressure of less than 130 mmHg, avoiding activities that could lead to head injuries, using hearing aids if needed, eating a healthy diet, and exercising and socialising regularly. Even older people can delay or possibly even prevent dementia by taking steps to improve their lifestyles, says Ames. “It’s never too early and it’s never too late to think about reducing your risk,” he says. In addition to making recommendations for individuals, the review calls on governments to protect their populations from dementia by providing primary and secondary education for all children, improving air quality, promoting healthy behaviours, and discouraging smoking and heavy drinking.

7-30-20 Seal lice can survive the pressure found 4000 metres under the sea
Seal lice – blood-sucking marine insects that live on seals, sea lions and walruses – can survive the crush of the deep ocean, withstanding the equivalent of pressures found 2000 metres deep for several minutes. One louse even survived the pressures found at 4000 metres deep. Seal lice (Lepidophthirus macrorhini) live out their entire lifecycle on their marine hosts, and previous research has shown that these insects survive being submerged in seawater for days by entering an immobile, low metabolism state to withstand the frigid cold, high salinity, and lack of oxygen. To find out how much pressure the lice could handle, Maria Leonardi at the Institute of Biology of Marine Organisms in Argentina, and her colleagues captured 15 elephant seal pups and collected lice from them with tweezers. The team then submerged the lice in seawater and placed them into a chamber where they were subjected to two rounds of varying hydrostatic pressures ranging from about 3 to 20 megapascals (MPa) for ten minutes at a time – that is about how long elephant seals spend on deep dives, some of which reach more than 2000 metres deep. All the adult lice and 89 per cent of nymphs survived pressures up to about 20 MPa, which you’d find 2000 metres beneath the surface of the water. During equipment calibration in the lab, one louse had the lousy luck of being accidentally subject to just over 44 MPa – equivalent to being more than 4000 metres underwater – for several minutes. It survived. “Here we have an example of an insect with nothing particular or special, with the build of any other insect, that is able to adapt to this condition,” says Claudio Lazzari at the University of Tours in France, who worked on the study. “The host is its environment,” says Katherine Moon at the University of California, Santa Cruz in the US who was not involved in the research. “Adaptation to the host or the way the host functions is exactly the way it’s going to go. Otherwise it won’t survive.”

7-30-20 How to convince teenagers to take COVID-19 seriously
This is not the time to be rebellious! s confirmed COVID-19 cases continue to rise across the U.S., it can be frustrating to see people dismiss the official advice for curbing the spread of the pandemic. And when the resistance is coming from within your own household, it's even more infuriating. Step forward Pandemic Teen — an even more irritating dependent than Regular Teen. It's natural for teenagers to push boundaries and question authority, of course. But if there's ever a time for them to skip the parties, stop sneaking out, and just do what you ask (i.e. wear the mask!), it's now. "Infection rates among teens are going up," says Carol Winner, MPH, public health expert and founder of social distancing brand Give Space. "States like Florida and California are seeing cases among those under age 18 on a rapid rise — California is at a rate of 8 percent infection in that age group." Indeed, recent research suggests that kids between ages 10 and 19 are catching and spreading COVID-19 at the same rate as adults. So how can parents get the message across to their teenagers that the pandemic is not to be taken lightly? Part of the problem is that teens are naturally inclined to break the rules and assert their individuality. Blame it on their brains. "This is their primary developmental task," says child and adolescent psychiatrist and author Gayani DeSilva, MD. "They're also developing higher cortical structures and the ability to make complex decisions. They may still be thinking in concrete terms, and not able to consider situations and decisions in abstract ways. This makes their decision making seem superficial, or immature. It is — but they can't help it." While the Centers for Disease Control and Prevention (CDC), and most state leaders, have issued rules regarding face coverings, social distancing, and hygiene, often the guidelines simply aren't clear enough for teenagers to understand. There's also the problem of information and guidance changing constantly, often without warning. "The information teens get is confusing," Dr. DeSilva says. "They are natural risk takers, so unless they get clear messages about how to be safe, they will take risks and shun some good advice." Part of a parent's role during the pandemic is helping their teen make sense of those conflicting messages. Dr. DeSilva recommends sitting down with them and explaining the risks of the pandemic in simple, straightforward terms, then telling them in clear language the behavior expected from them. And simple really does mean simple. Try something like: "We want you to wear a mask at all times when you're in public." Like all productive conversations with a teenager, the key is to listen. "Ask them what they think. Ask them if they have concerns and what scares them. Ask them if they have questions about the pandemic and guidelines. Ask them what they want to do, and how they want to keep themselves safe," Dr. DeSilva says. Then, when you have their attention, tell them what's at the root of all this — you want them to be safe and healthy. It's also important to remind teens of the greater good. They may perceive wearing a mask as a weakness because it doesn't look "cool," so emphasizing the sense of collective responsibility might be more effective than making it about them personally. "Social research tells us that although we may think of teens as being more self-absorbed than adults, they can often demonstrate empathy in a willingness to change their behavior for the betterment of the community," Winner says. Regular reminders that the sooner the virus is controlled, the sooner their freedoms will return could also help get the message across.

7-30-20 Finding coronavirus superspreaders may be key to halting a second wave
A skiing trip, a wedding, a choir practice: what these events have in common is that they were all occasions of coronavirus “superspreading”. This is when someone passes the virus on to an especially high number of people. While there is no universally agreed definition of a superspreading event, it is sometimes taken to be an incident in which someone passes on the virus to six or more other people. Getting to the bottom of why these puzzling clusters occur could be key to gaining control of the covid-19 pandemic and stopping a second wave of cases. For months, we have been hearing that the R number, or reproduction number, is what is needed to gauge the spread of covid-19. This is the average number of people that each infected person passes the virus on to. Before lockdown in the UK, the R number for coronavirus was estimated at somewhere between 2 and 3. It is now more appreciated that there is great variability in the number of new cases that each infected person generates. This can be described by the epidemic’s “K number” – the dispersion parameter – with a lower value of K signifying more variability. You need to know both R and K for a good picture of how the virus is spreading through a community. According to an analysis of how covid-19 had spread to other countries from China by the end of February, the K number was 0.1, an extremely low value. The researchers estimated that 80 per cent of cases were caused by about 10 per cent of infected people. Those 10 per cent could trigger a cluster of infections, while most other people would pass on coronavirus to no one else and a few would give it to just one other person. In other words, superspreading is integral to the pandemic, says Quentin Leclerc at the London School of Hygiene and Tropical Medicine.

7-30-20 How refugee camps in Bangladesh are being defended against covid-19
Coronavirus has begun spreading around refugee settlements, but in one of the world’s largest refugee camp complexes a worst-case scenario may have been avoided. A mathematical model run earlier this year by researchers at Johns Hopkins University – and now published following peer review – may have encouraged authorities to amplify measures that slowed the virus’s spread. The Kutupalong-Balukhali Expansion Site in Bangladesh, containing 23 separate camps, is home to about 600,000 Rohingya people who fled ongoing violence in neighbouring Myanmar. The population density surpasses that of many cities, with 46,000 people per square kilometre. The first case of coronavirus was reported there in mid-May. Months before the first cases appeared, Paul Spiegel at the Johns Hopkins Center for Humanitarian Health and his colleagues used what is called a “Susceptible Exposed Infectious Recovered” (SEIR) model to simulate how the virus might spread in the camp under different levels of transmission, interventions and precautions. Their simulation suggested that under a high transmission scenario with no interventions to slow the virus’s spread essentially all of the camps’ residents – 590,000 people – might have been infected within 12 months, with 2800 fatalities. Spiegel says the authorities were already planning interventions, but were given fresh impetus to do so when they were presented with his team’s results. “We have been told that the scenarios were a wake-up call and had a positive effect,” he says. To date, just 66 people in the camps have been confirmed to have coronavirus – although Spiegel says it is likely that there are more cases that haven’t been confirmed through testing. Measures to prevent and limit the spread of the coronavirus in the camps were implemented as early as March, says Catalin Bercaru, communications officer at the World Health Organization office in Dhaka, Bangladesh. Up to mid-July, the WHO trained 280 health facility staff and more than 1500 refugee community health work volunteers on how to deal with cooronavirus in the crowded conditions.

7-30-20 Lyme disease vaccine found to be safe and effective in clinical trial
A vaccine against Lyme disease has been shown to be safe and effective in a clinical trial and could be available by 2025. Tens of thousands of people in the US and Europe are diagnosed each year with Lyme disease, which is transmitted by tick bites and can cause lifelong health problems like joint and nerve pain if it isn’t treated early. French company Valneva has developed a vaccine that works by stopping Lyme-causing bacteria in ticks from passing into people’s bloodstreams when the ticks bite. It does this by targeting a protein on the bacteria called outer surface protein A. In a clinical trial involving 572 adults in the US and Europe, the vaccine was 82 to 96 per cent effective at stimulating immune protection against Lyme disease and caused no serious side effects. “The results are very promising,” says Maria Gomes-Solecki at the University of Tennessee. The next steps will be to test the vaccine in children and larger numbers of adults, and to determine whether booster shots will be necessary to provide long-lasting immunity, says Thomas Lingelbach, CEO of Valneva. “We hope the vaccine will be available within five years,” he says. Children are urgently in need of a vaccine because they are significantly more likely to get Lyme disease than adults, says Lingelbach. Research shows that children often don’t realise that they have been bitten by ticks, making early treatment harder. In the late 1990s, a Lyme disease vaccine that also targeted outer surface protein A became available, but it was discontinued after unfounded claims of serious side effects spread by anti-vaccination campaigners made people too scared to get it. Gomes-Solecki hopes the new vaccine won’t experience the same fate if it is approved. “In recent years, I do feel there has been a shift in public opinion because the need for a vaccine has increased given that Lyme disease keeps expanding into new geographic regions, and studies have been published supporting the safety of the original vaccine,” she says.

7-29-20 Sharon Moalem interview: Why women are genetically stronger than men
We know that women live longer and are less susceptible to certain diseases than men. That may be down to the benefits of having two X chromosomes. WOMEN generally outlive men and are less susceptible to certain illnesses – including covid-19, it now appears. Why health outcomes are so drastically different between the sexes is unclear. But Sharon Moalem, a doctor and genetic researcher based in New York, thinks he has the answer. It isn’t because women tend to go to the doctor more or have healthier habits, he says. Instead, it’s because they are typically better equipped, genetically speaking. In humans, sex is largely determined by chromosomes, the bundles of tightly coiled DNA that carry our genes. The cells of most women possess two X chromosomes while most men have one X and one Y. So that women’s cells don’t have to carry two versions of each gene on the X chromosome, one from each X, one of the Xs is mainly switched off. It appears that which one stays active in which cells is chosen seemingly at random some time during the first few weeks of pregnancy. The result is that half a women’s cells generally use the X chromosome she inherited from her mother, while the other half use the one from her father. It has long been known that if one X has a harmful mutation, cells that use the other X can compensate. That’s why, for instance, women are less likely to be colour-blind; a gene important for eye function resides on the X chromosome. Yet Moalem argues that the benefits are far more significant than this alone. He makes the case that even if there is no obviously harmful mutation, women tend to be at an advantage by having bodies made up of two populations of genetically different cells, and that this begins even before birth. He believes this is the reason why women are less vulnerable to certain congenital disorders and better at fighting off infections – including the coronavirus. As he sees it, women are simply genetically superior. Having two copies of an X chromosome has far more benefits than we realised, and serious implications for medicine. Clare Wilson: How can women be the stronger sex, when we are generally smaller and physically weaker? Sharon Moalem: All those things are true – on average, males have more muscle mass. But I am talking about genetic superiority, and the parameter is survival. We see the consequences in many areas of medicine. When you look at supercentenarians, those over the age of 110, they are 95 per cent female.But it isn’t just making it to old age – females have a survival advantage over the life course. When I was a physician at a neonatal intensive care unit, I saw that more girls make it to their first birthday than boys. And I was seeing lower rates of congenital malformations like tongue-tie and clubfoot. Anything that’s biologically difficult to form, females do better.

7-29-20 Boosting gut microbes helps protect mice against Alzheimer’s disease
A supplement that nourishes “good” bacteria in the gut seems to protect against an Alzheimer’s-like disease in mice and will soon be tested in a clinical trial. Growing evidence points to a link between Alzheimer’s disease and gut health. For example, studies have found that people with the condition tend to have more pro-inflammatory, or “bad”, bacteria and less anti-inflammatory, or “good”, bacteria in their guts. They also tend to have a less diverse mix of gut microbes overall. Chun Chen at Emory University in the US and her colleagues have added to this evidence by showing that mice engineered to have an Alzheimer’s-like disease also have more pro-inflammatory bacteria and less anti-inflammatory bacteria in their guts. In addition, they demonstrated that healthy mice housed with those with the Alzheimer’s-like disease were more likely to develop the condition themselves, possibly through exposure to their cagemates’ unhealthy gut microbes. To explore whether improving gut health may reduce the risk of developing Alzheimer’s disease, Chen and her colleagues gave mice a prebiotic supplement called R13 that is designed to promote a healthy mix of gut microbes. They found that mice treated with R13 were less likely to accumulate a protein called beta-amyloid in their guts. Beta-amyloid builds up in the brains of people with Alzheimer’s disease – forming sticky clumps that damage brain networks. Recent research in mice hints that this protein can travel from the gut to the brain and cause Alzheimer’s symptoms. R13 has recently been granted approval to be tested in a small clinical trial to see if it helps to slow or prevent Alzheimer’s disease in people. “It sounds really interesting, but we know from the history of Alzheimer’s drug trials that many promising treatments fail,” says Bryce Vissel at the University of Technology Sydney in Australia.

7-29-20 Covid-19 news: Young people may be driving spikes in cases, says WHO
The latest coronavirus news updated every day including coronavirus cases, the latest news, features and interviews from New Scientist and essential information about the covid-19 pandemic. WHO Europe director says young people may be driving recent spikes in cases. Rising coronavirus infections among young people could be driving recent spikes in cases across Europe, said Hans Kluge, the World Health Organization’s Europe regional director, in a BBC report today. Kluge said he has two daughters and understands that young people “do not want to miss a summer,” but added that they have a responsibility toward themselves, their family members and their communities. The Netherlands is among countries which have reported higher infection rates among younger people, with about a quarter of people who tested positive there last week aged 20 to 29. Earlier this week, officials in Brittany, France ordered curfews on beaches, parks and gardens in an attempt to prevent large gatherings of young people in particular, according to local leaders. Officials in Spain have also imposed similar curfews, with bars and nightclubs in Catalonia required to close by midnight since Friday. The US reported more than 1300 deaths from covid-19 yesterday, the highest daily death toll recorded in the country since May. More than 149,000 people in the US have now died from the disease and more than 4.3 million cases have been recorded there since the pandemic started. More than £4 million will go towards research aimed at understanding why people from Black, Asian and minority ethnic (BAME) backgrounds are disproportionately dying from covid-19. This funding will also go towards research on the risks posed to ethnic minority health workers, migrants and refugees, and the lack of representation from people in different ethnic groups in clinical trials testing new treatments and vaccines for covid-19. The funding comes from the UK Research and Innovation and the National Institute for Health Research.

7-29-20 We’ve finally figured out where Stonehenge’s giant boulders came from
The origins of the giant boulders at Stonehenge have long been a mystery – but now we have uncovered where they came from. David Nash at the University of Brighton in the UK and his colleagues have identified the source of 50 of the 52 large boulders, known as sarsens, that make up the monument’s iconic stone circle. By analysing the stones’ chemical composition, the team has traced their origins to 25 kilometres away from the monument, in the West Woods in Wiltshire. The sarsens comprise Stonehenge’s outer circle as well as a horseshoe-shaped inner ring. Many are in trilithons: two vertical stones topped with a horizontal lintel. Stonehenge also contains smaller rocks, known as bluestones, near its centre, the origins of which have previously been traced to Wales. The researchers analysed the chemistry of the sarsens via a technique called portable X-ray fluorescence spectrometry, essentially a handheld X-ray gun. With this, they took five readings at different positions for each stone. This revealed that 50 sarsens shared a common chemistry, containing more than 99 per cent silica, with trace elements including aluminium, calcium and iron. “Two, much to our surprise, were different to that main cluster, but also different to each other,” says Nash. This suggests they have two separate origins. Next, the researchers analysed a fragment of stone, taken from a collapsed sarsen when it was re-erected in 1958, to obtain a geochemical breakdown of the rock. They used this to sample areas of similar stone across southern Britain. The site in the West Woods, one of six the team sampled in the Marlborough Downs, turned up with a match. “We didn’t expect we would ever find the original source area,” says Nash.

7-29-20 The invisible superpower that helped dinosaurs conquer the world
From beginnings as skulking, cat-sized reptiles, dinosaurs came to rule Earth for 100 million years – but how? Their secret wasn’t teeth or claws, but something deep inside them. ABOUT 250 million years ago, a creature raced along the edge of a lake in what is now Poland, leaving prints behind it in the mud. It was a meek and forgettable animal called Prorotodactylus, about the size of a pet cat and with slender limbs. But those prints weren’t the only legacy it left: its descendants somehow became the rulers of Earth. Those descendants were the dinosaurs. The very word invokes majesty. These were among the most successful groups of animals ever, dominating the planet for more than 100 million years. They proliferated into creatures of all shapes and sizes, some even larger than a jet plane, and filled the land. Palaeontologists like me were long obsessed with understanding why these mighty animals were snuffed out 66 million years ago. We now know the answer: their days were ended by an enormous asteroid impact. Today, the greatest mystery of dinosaur evolution is how they rose to glory in the first place. The early descendants of Prorotodactylus would have stuck to the shadows, skulking away from much larger and more fearsome animals. So what was it that allowed them to take centre stage? Piecing together the answer is no easy matter. But over the past few years, a surprising new idea has gained traction. Perhaps the reason for the dinosaurs’ ascendency lies not in their teeth or claws or muscles. It may instead be thanks to a series of strange anatomical adaptations invisible from the outside – adaptations that allowed them to thrive in one of the most extreme periods of climate change the planet has seen up until now. The world was almost unrecognisable back when Prorotodactylus made those lakeside prints. Our planet had just experienced one of the worst mass extinctions ever. A blast of global warming, fuelled by volcanic eruptions of unimaginable scale in Siberia, had caused more than 95 per cent of Earth’s species to die. From this catastrophe sprang the dinosaurs’ ancestors and closest cousins, including Prorotodactylus. Within 20 million years, they had evolved and diversified into the three main subgroups of dinosaurs: the meat-eating theropods, the long-necked, plant-guzzling sauropodomorphs and the beaked, herbivorous ornithischians. Much later, these lineages would spawn recognisable dinosaurs: Tyrannosaurus, Brontosaurus and Triceratops, respectively (see “An interrupted reign”).

7-29-20 Social workers are masters at de-escalation. Here's what the police can learn from them.
Knowing how to peacefully resolve conflict, rather than exacerbate it, can save lives. First responders are often portrayed as the heroes of our society. Medical professionals, police officers, and firefighters are lauded with admiration and praise for their life-saving efforts, and for good reason. But there's one group of first responders that gets overlooked: social workers. These unsung heroes immerse themselves within communities to address systemic problems and improve the well-being of society as a whole. Sometimes they're called to hospitals or homes in emergencies to help police resolve conflict peacefully. That's because social workers are masters at de-escalation. As America is embroiled in protests against law enforcement, and people continue to be killed in police custody, the value of this skill — the ability to resolve conflict, rather than exacerbate it — is becoming increasingly apparent. Indeed, it can help save lives. "I've seen too many times when police use intimidation, or they lack empathy," says Tracie Simpson, a social worker in New Jersey. This can actually make a confrontation worse, and even deadly. Lisa Tyson, another New Jersey social worker, mentions the case of Elijah McClain, a 23-year-old Black man who died last year after police put him in a chokehold and then injected him with ketamine, a sedative, which ultimately sent him into cardiac arrest. Tyson says that, if a social worker had been present, non-physical methods of addressing conflict like "empathy, active listening, and I statements" may have been used. "We have to defuse conflicts with individuals that are involved in domestic violence, human trafficking, individuals with cognitive or physical disabilities, substance abuse issues or individuals who have experienced severe trauma," Tyson says. Still, some may be skeptical of a social worker's ability to be truly effective without a gun and a badge. This skepticism may be rooted in sexism: Social work is overwhelmingly dominated by women, who make up 83 percent of the field. Conversely, police work is 87 percent male-dominated. Are we exercising implicit bias when we doubt that a female social worker could be capable of disarming, say, a 6-foot-tall, 200-pound man? Tyson says that if her de-escalation tactics work, she doesn't even need to use physical restraint. "I typically use basic problem-solving skills to de-escalate any situation, and I'm always aware of a person's verbal and non-verbal cues," she explains. This can be important, considering that mentally ill individuals are 16 times more likely to die at the hands of law enforcement. One in four killed by the police have undiagnosed mental illnesses, and one in five inmates suffers from a mental illness. Tyson acknowledges that police have a tough job, but stresses that, "when mental health is a factor, it may be necessary to involve a mental health professional to ensure the safety of all involved." She recalls one incident in which police were called to a scene where a teenager who appeared to have a cognitive impairment was trying to run into traffic. "The store's security guard appeared to be inexperienced, and become physically aggressive, then called the police," Tyson says. When she arrived, she spoke to the teenager calmly until his parents could be located. "He ended up being safe and had the opportunity to receive the help he needed without being harmed or further traumatized," Tyson says. The teenager was Black, she notes, "which in many situations could lead to a fatal ending."

7-29-20 Close relatives of the coronavirus may have been in bats for decades
Viruses from the coronavirus lineage responsible for COVID-19 have been circulating in bats for decades, long before the virus started infecting people last year, a new study suggests. How exactly the virus jumped to humans is still a mystery. But the study suggests the coronavirus most likely evolved in bats — such as intermediate horseshoe bats (Rhinolophus affinis), the source of the coronavirus that caused the 2003–2004 SARS outbreak — not snakes or pangolins as some researchers have suggested (SN: 1/24/20). Pangolins or another animal might still have been an intermediate host before the virus made it to humans. Maciej Boni, an epidemiologist at Penn State, and his colleagues examined the genetic blueprints of the new coronavirus, or SARS-CoV-2, and 67 related viruses. The analysis aimed to uncover the evolutionary history of SARS-CoV-2 and see if the virus had exchanged bits of genetic material with other coronaviruses, a process called recombination, to become the formidable pathogen it is now. SARS-CoV-2 is not the result of genetic shuffling among known coronaviruses, the researchers report July 28 in Nature Microbiology. Previous studies had suggested that recombination with coronaviruses from pangolins may have contributed a portion of the virus’ spike protein, which is used to break into human cells (SN: 3/26/20). But the spike’s ability to attach to a protein on host cells called ACE2, which allows the virus to gain entry, appears to be an ancestral trait, rather than one gained from recombination. Based on the evolutionary relationship among the 68 coronaviruses, the researchers estimate that the branch of the virus family tree that leads to SARS-CoV-2 diverged from related viruses between 1948 and 1982. Those dates suggest that the coronavirus lineage that gave rise to the virus behind the pandemic has been present in bats for decades. That long period hints that more bat viruses with the potential to infect humans are circulating in horseshoe bats. Searching for such bat viruses can help identify potential threats before the pathogens make the jump, the team writes.

7-29-20 These ancient seafloor microbes woke up after over 100 million years
Scientists revived long-dormant organisms with carbon and nitrogen in the lab. Even after 100 million years buried in the seafloor, some microbes can wake up. And they’re hungry. An analysis of seafloor sediments dating from 13 million to nearly 102 million years ago found that nearly all of the microbes in the sediments were only dormant, not dead. When given food, even the most ancient microbes revived themselves and multiplied, researchers report July 28 in Nature Communications. Scientists have pondered how long energy-starved microbes might survive within the seafloor. That such ancient microbes can still be metabolically active, the researchers say, just goes to show that scientists are still fathoming the most extreme limits to life on Earth. The microbes’ patch of seafloor lies beneath a kind of ocean desert, part of a vast abyssal plain about 3,700 to 5,700 meters below sea level. Researchers, led by microbiologist Yuki Morono of the Japan Agency for Marine-Earth Science and Technology in Kochi, examined sediments collected in 2010 from part of the abyssal plain beneath the South Pacific Gyre. That region of the Pacific Ocean contains few nutrients that might fuel phytoplankton blooms and thereby support a cascade of ocean life. As a result, very little organic matter makes its way down through the water to settle on the seafloor. The extremely slow accumulation of organic material and other sediments in this region does allow oxygen in the water to seep deep into the sediments. So Morono and colleagues wondered whether any aerobic, or oxygen-liking, microbes found there might be revivable. After “feeding” microbes from the collected sediments with nutrients including carbon and nitrogen, the team tracked the organisms’ activity based on what was consumed.

7-28-20 Bacteria dug up from beneath the seabed may be 100 million years old
Microbes that have been hibernating deep below the Pacific Ocean since the reign of the dinosaurs have been revived in the lab. Some may be 100 million years old, perhaps making them the longest-lived life forms on Earth. We already know that microbes can survive deep below our planet’s surface, even though nutrients are generally scarce. Biologists suspect that the microbes enter a minimally active mode to stay alive. But whether they can emerge unscathed has been unclear. Now a team led by Steven D’Hondt at the University of Rhode Island and Yuki Morono at the Japan Agency for Marine-Earth Science and Technology has studied about 7000 individuals of a bacterium found living in mud 75 metres beneath the sea floor, 5700-metres-deep in the South Pacific Ocean. “We didn’t know whether we had fully functioning cells or zombies capable of doing very few things,” says D’Hondt. In the lab, the researchers gave the microbes nutrients laced with distinctive isotopes of carbon and nitrogen. Within 10 weeks, these isotopes began showing up inside the microbes, indicating that they had begun to feed like typical bacteria. That is remarkable considering what the bacteria have been through, says Jens Kallmeyer at the GFZ German Research Centre for Geosciences in Potsdam. He says the mud in which the bacteria were found is capped by layers of silicon dioxide that no microbe could penetrate. This implies that the microbial populations have been trapped since the mud was buried under the silicon dioxide an estimated 101.5 million years ago. Given that this mud contains few nutrients, survival must have been challenging. “Nowhere else on Earth do you find sediment as close to totally dead as this,” says Kallmeyer.

7-28-20 Which covid-19 treatments work and how close are we to getting more?
As the World Health Organization (WHO) baldly reminds us, “there are no specific vaccines or treatments for COVID-19”. However, trials of treatments are taking place. Some have shown promise in helping those infected by calming an overreacting immune system or targeting the coronavirus – either by destroying it or stopping it from replicating. Dexamethasone, a widely available steroid that dampens the immune response, became the first medicine shown to reduce deaths in covid-19 patients. The RECOVERY trial of more than 2000 people found that it reduced deaths in people on mechanical ventilators by a third – and by a fifth in those who received oxygen but not ventilation. “The trial showed it is beneficial to those who are severely affected,” says Sheuli Porkess at the Association of the British Pharmaceutical Industry. It is now being used by the National Health Service in the UK to treat covid-19. In June, the US bought up virtually all global stocks of the drug remdesivir, an antiviral that suggested promise against Ebola. The move came after one trial found that it reduced recovery time by four days in covid-19 patients. However, other studies have yielded mixed results: one in April showed no clinical benefit, while an analysis last month by Gilead, the company behind the drug, indicated a reduced risk of death in those severely affected by covid-19. Gilead cautions that more rigorous trials are needed. The drug has received emergency or conditional approval in a number of countries. The litmus test will come in a few weeks with the results of the international Solidarity trial. Trials are also looking at whether the anti-inflammatory tocilizumab, which is already used to treat arthritis, could be beneficial against covid-19.

7-28-20 Sarah Gilbert on how her team is making the Oxford coronavirus vaccine
Last week was a big one for Sarah Gilbert at the University of Oxford, leader of the team that created the “Oxford vaccine”, a front runner in the race for a coronavirus vaccine. On 20 July, her team published results showing that the vaccine produces the desired immune responses in people. Gilbert says she took a moment to pause ahead of the announcement – she had most of the day before, a Sunday, off. That is a rare luxury these days. She normally works long hours, including on weekends. “There is a lot going on during the week, so weekends are a time to catch up on more substantial pieces of work with fewer interruptions,” she says. Gilbert gradually moved into vaccine development after joining Oxford in 1994. Even so, she never imagined working on a vaccine to tackle a massive global pandemic. “We had been starting to prepare for a ‘disease X’ vaccine, but that was always envisaged as a novel pathogen that would cause an outbreak rather than a pandemic.” The type of vaccine she has been working on against coronavirus is known as a viral vector vaccine. The key component is DNA coding for a surface protein – which would normally trigger an immune response – from the virus you want to protect against. Like a Trojan Horse, this is put inside the shell of an adenovirus that causes colds in chimpanzees, which delivers it to human cells, where the protein is made. In response, the body produces both antibodies that circulate in the blood and bind to any matching viruses they encounter, and T-cells that destroy infected cells before they make more virus. To create the coronavirus vaccine, which is being developed in collaboration with drugs firm AstraZeneca, the researchers simply had to put DNA coding for the virus’s surface protein into the adenovirus “cassette” they had already created for other vaccines.

7-28-20 Coronavirus vaccine hope rises after a flurry of positive results
AMID rising global numbers of daily coronavirus infections, a fresh flush of vaccine trial results is offering hope for the longer run. There are more than 160 coronavirus vaccines in development around the world. About 140 of these are at the preclinical stage, meaning they are still being looked at in laboratories and in animal tests. Another 25 are already being tested in people. The rate at which the tally has risen to 160-plus is unusually fast. “What is phenomenal is the numbers changing over the past few months. The amount of research is incredible,” says Sheuli Porkess at the Association of the British Pharmaceutical Industry. As the candidates advance, the World Health Organization (WHO) last month started to convene a working group to prioritise the most promising vaccines. “Practical realities will require a process that focuses global efforts on a small handful of candidates that may have the highest impact,” the WHO said. Four vaccines have made big steps in development in the past few weeks. Initial trials show that they can trigger an immune response and appear safe – but it is too early to say if they will protect against coronavirus and whether they will work across many different groups of people, including older individuals and those with chronic health issues. On 20 July, a team led by Sarah Gilbert at the University of Oxford and pharmaceutical company AstraZeneca showed that their ChAdOx1 nCoV-19 vaccine produced the desired immune responses without showing sworkerious adverse reactions. That was in a combined phase I/II trial of 1077 volunteers. It is now being tested in many thousands more people. Six days earlier, US company Moderna and the US National Institute of Allergy and Infectious Diseases revealed that 45 people had received their mRNA-1273 vaccine and shown an antibody response. On Monday, they began a phase III trial intended to have 30,000 participants. The other two most promising candidates are from CanSino Biologics in China, which published encouraging phase II trial results on the same day as the Oxford team, and another from German company BioNTech with pharmaceutical giant Pfizer, which published a promising preliminary report on 14 July.

7-28-20 Tiny mammals once scavenged meat from giant dinosaur carcasses
The first mammals were small and elusive, but that didn’t stop them chowing down on dinosaur meat. A bone fragment from a giant dinosaur has bite marks that could only have been made by small mammals, which probably scavenged the carcass. “This is the earliest direct evidence for mammalian feeding behaviour,” says Felix Augustin at the Eberhard Karls University of Tübingen in Germany. The bone fragment came from the long neck of a sauropod dinosaur, which lived in what is now China in the late Jurassic around 160 million years ago. By this time dinosaurs had dominated ecosystems for tens of millions of years. Mammals lived alongside them, but most were small and unobtrusive while the dinosaurs ruled. Augustin and his colleagues had previously found bite marks on dinosaur bones from elsewhere, so they took a close look at the Chinese specimen. “I recognised small gnawing-like feeding traces,” says Augustin. To find out what made the traces, the team compared them to bite marks made by different kinds of animal and by other processes like trampling. Crucially, the teeth marks were often found in pairs. That matches the paired incisors mammals have at the front of their mouths. Meat-eating dinosaurs and other dinosaur-era animals don’t have paired incisors. No mammal remains were found with the sauropod bone, but a nearby bone bed held teeth from five Jurassic mammals. Only one species, Sineleutherus uyguricus, had an incisor preserved. In size, this matched the bite marks, says Augustin. However, he says it isn’t possible to say with confidence that S. uyguricus, and not another mammal, made the marks. The mammals must have been scavenging, says Augustin, as it isn’t possible that such tiny mammals could have taken down a huge sauropod dinosaur.

7-27-20 A popular heartburn medicine doesn’t work as a COVID-19 antiviral
New findings don’t rule out the chance the antacid might help in other ways. An over-the-counter heartburn remedy probably won’t directly stop coronavirus infections, a new study suggests. Anecdotal reports from China suggested people hospitalized with COVID-19 who were taking famotidine (sold under the brand name Pepcid) had better outcomes than people who took a different type of antacid called a proton pump inhibitor. But famotidine has no direct antiviral activity against SARS-CoV-2, the virus that causes COVID-19, according to preliminary results reported July 15 at bioRxiv.org. Those findings, which have not been reviewed by other scientists yet, suggest famotidine won’t help prevent coronavirus infections or illness. But they don’t rule out that the drug might help in other ways, says Mohsan Saeed, a virologist at Boston University School of Medicine. “We’re not challenging that famotidine might help,” he says. “We’re saying that the mechanism of action is not antiviral.” The result isn’t a complete surprise. “A compound of this nature having any role in infectious disease is kind of a head-scratcher,” Saeed says. But a couple pieces of evidence had hinted that it might help against the virus. Besides the reports out of China, two studies using computer simulations of coronavirus proteins predicted that famotidine might dock with and inhibit important viral enzymes called proteases that help the virus replicate. Based on those findings, Northwell Health in the New York City area began a clinical trial to test the antacid against the coronavirus in people. “We were kind of surprised, because there is no laboratory evidence to show that this compound might have some effect,” Saeed says. The data that originally suggested benefits from famotidine aren’t strong enough to justify basing treatments on the drug, says Tobias Janowitz, an oncologist and biomedical scientist at Cold Spring Harbor Laboratory in New York, who was not involved in the study. “Everything that has been published so far cannot be considered evidence for clinical efficacy,” he says. That includes a small study Janowitz was involved in which also found hints that over-the-counter Pepcid might improve symptoms for some people diagnosed with COVID-19.

7-27-20 The gravedigger’s truth: Hidden coronavirus deaths
Fewer than 100 people have died of Covid-19 in Somalia, according to official figures. But BBC Africa Eye has found that cemeteries are filling up fast in the country, whose healthcare system has been devastated by three decades of conflict. It's been looking into the reality of coronavirus in Somalia, following two young doctors in the fight of their lives.

7-26-20 Why are scientists creating genetically modified mosquitoes?
Creating these "Trojan horse" bugs could save human lives. But is it moral? Scientists plan to release altered mosquitoes designed to sabotage the species' ability to reproduce. Is this safe? Here's everything you need to know:

  1. Who's doing this? The federal Environmental Protection Agency has approved a plan by a British biotech company called Oxitec to release about 1 billion genetically modified (GM) mosquitoes in the Florida Keys and, next year, Texas. The mosquitoes (code-named OX5034) will only be male — the gender that does not bite humans — and will carry a new gene that will be passed on to their female offspring and cause them to die while they're still larvae.
  2. How does this technology work? Scientists first genetically modified an animal — a mouse — in 1974. But the process remained cumbersome and slow until the development of the CRISPR technique and other "gene-editing" technology this decade.
  3. Where do the plans stand? n May, the EPA greenlighted Oxitec's plans for both Florida and Texas, issuing the company an experimental use permit. Florida state authorities followed suit with their own approval.
  4. What could go wrong? Some geneticists, including Dr. Ricarda Steinbrecher of EcoNexus, a public-interest research organization, have raised alarms that Oxitec's altered mosquitoes haven't been adequately studied. The researcher said "the underlying mechanism(s) leading to cell death" in the larvae aren't "fully understood" and thus can't yield "precise and predictable results.
  5. What's the upside? Some see world-changing possibilities. Florida witnessed its first mosquito-to-human transmission of the Zika virus (which causes serious birth defects) in 2016, and West Nile is a perennial problem.
  6. Oxitec's modified moths: South Florida and Texas aren't the only places that Oxitec is testing its genetically modified insects. Earlier this year, Cornell University scientists announced the results of a project they had conducted with the company involving its genetically modified diamondback moths, or Plutella xylostella.

7-25-20 Donald Trump acts to cut prescription drug prices in US
President Donald Trump has signed four executive orders aimed at cutting prescription drug prices in the US. "The four orders I'm signing today will completely restructure the prescription drug market," said Mr Trump, who has long criticised "astronomical" prices. The measures would allow discounts and import of cheaper drugs from abroad. Mr Trump will meet pharmaceutical bosses on Tuesday, but some industry analysts have criticised the move, saying it would not have much effect. "This administration has decided to pursue a radical and dangerous policy to set prices based on rates paid in countries that he [President Trump] has labelled as socialist, which will harm patients today and into the future," Pharmaceutical Research and Manufacturers of America said in a statement. It said Mr Trump's move was "a reckless distraction that impedes our ability to respond to the current [coronavirus] pandemic - and those we could face in the future". President Trump's administration has been criticised for its response for the worsening Covid-19 crises, as the number of confirmed virus-related deaths in America has now topped 145,000. Since taking office, Mr Trump has made repeated attacks against those who set drug prices and has pledged to take radical steps to reduce them. But with the presidential election just several months away, industry experts have voiced doubts that any major decisions could come into force before the 3 November vote. They also say that the White House has limited power to implement drug pricing policies. Executive orders do not have any automatic legal force and can also be challenged in court. According to a 2019 report by the OECD group of industrialised nations, the US spends roughly twice the average amount spent by other member countries on pharmaceuticals per head.

7-25-20 Profit and risk in race for a vaccine
There's big money in creating the first COVID-19 vaccine. What will that mean for its safety? More than 100 separate labs are competing to develop the first COVID-19 vaccine, said Stephanie Baker at Bloomberg Businessweek, and a partnership between the University of Oxford and the pharma giant AstraZeneca is leading the race. A team of researchers at Oxford's Jenner Institute reported positive results this week from an early-stage human trial with more than 1,000 participants, and the stock market leaped at the news. The Oxford lab's vaccine is adenovirus-based; such vaccines have a small but critical "advantage over other candidates: They need only to be kept chilled rather than frozen." That could make worldwide distribution easier for Astra­Zeneca, which struck a manufacturing deal with ­Oxford — assisted by Bill Gates — "in about 10 days through a flurry of Zoom calls." After that deal was announced, "big money followed." The biggest patron: The United States' pandemic drug authority, BARDA, which handed Astra­Zeneca more than $1.2 billion; a test of 30,000 people in the U.S. is scheduled to start next month. The U.S. biotech upstart Moderna has also shown promising preliminary results, said Peter Loftus and Gregory Zuckerman at The Wall Street Journal, but "skepticism has dogged it since its creation in 2010." As its name suggests, the Cambridge, Massachusetts, biotech firm uses a novel process involving the creation of synthetic RNA. But while it has "more than 20 experimental drugs and vaccines" in development, "none are close to being commercially available." Since ­Mo­derna's COVID vaccine entered human ­trials, its stock has risen more than 230 percent. That has let some Mo­der­na executives profit, even though their vaccine has been tested on just a few human subjects, said Christopher Rowland and Carolyn Johnson at The Washington Post. CEO Stéphane Bancel and other executives have "picked up the pace" of their stock selling as the share price rises, and chairman Noubar Afeyan's venture capital firm sold $68 million of Moderna stock. The selling has continued even as Securities and Exchange Commission head Jay Clayton cautioned Moderna to "avoid even the appearance of impropriety." Also raising questions is a $1.6 billion federal contract awarded to Novavax, a company that has "never brought a vaccine to market," said Katie Thomas and Megan Twohey at The New York Times. The Trump administration wanted to "invest in a variety of vaccine technologies," and Novavax's approach holds out the possibility of faster vaccine production than some others. But critics see a second-tier player that has repeatedly "boosted its stock by promising vaccines for new outbreaks, yet never delivering." "Trump did promise America First," said The Economist, and his administration has "turned on the federal money hose" to achieve it. The U.S. has already cut deals for priority access to COVID treatments, causing alarm in countries that worry the U.S. will expect the same preference after "stumping up a lot of cash" in the vaccine race. Another concern is that the FDA will "cut corners" to make a vaccine ready before the election. The agency says that won't happen, but it's already been blasted for giving emergency approval as a COVID treatment to hydroxychloroquine "to avoid embarrassing the president," who endorsed the drug.

7-24-20 How a Jewish ghetto beat a typhus epidemic during the second world war
Jewish people confined inside a Nazi ghetto during the second world war were able to curb a massive typhus outbreak by introducing similar infection control measures to those being used to fight covid-19 today. Typhus, an often-fatal bacterial disease that is spread by body lice, swept through Europe during the second world war. Nazi propaganda portrayed Jews as major spreaders of the disease as a way of garnering public support for imprisoning them in ghettos. In November 1940, the Nazis walled more than 400,000 Jewish people inside a 3.4-square-kilometre ghetto in Warsaw, Poland. The overcrowded conditions, lack of sewage maintenance and inadequate food and hospital resources meant that typhus rapidly infected about 100,000 people and caused 25,000 deaths. However, by October 1941, just before the following winter, new infections suddenly ground to a halt. This was unexpected, because typhus normally accelerates at the start of winter, and ghettos in other places like Ukraine were still being ravaged by the disease. “Many thought it was a miracle,” says Lewi Stone at RMIT University in Australia. To find out how the Warsaw ghetto stamped out typhus, Stone and his colleagues trawled through historical documents from libraries around the world, including some kept by doctors who lived in the Warsaw ghetto. They discovered that doctors imprisoned there – including eminent microbiologist and Nobel prize nominee Ludwik Hirszfeld who helped discover blood types – helped lead community efforts to stop the disease from spreading. Hundreds of lectures were held to educate the public about the importance of personal hygiene, social distancing and self-isolating when sick. A secret university was also set up to train medical students in infection control, and community leaders helped to organise elaborate sanitation programmes and soup kitchens.

7-24-20 Masks help new moms with COVID-19 safely breastfeed their babies
Wearing a mask and hand-cleaning prevented the coronavirus from spreading from mom to baby. Mothers with COVID-19 at delivery can breastfeed their newborns without passing along the infection, as long as they take certain safety precautions. Wearing a surgical mask while nursing and cleaning hands before handling their babies kept the coronavirus from spreading from mothers to their infants, a new study finds. It adds to a growing body of evidence that suggests babies are rarely becoming infected after birth and getting severely ill from the virus. The study took place at three hospitals in New York City, the initial epicenter of the U.S. outbreak. Doctors identified 120 babies born from late March to mid-May to 116 women who were positive for SARS-CoV-2, the virus that causes COVID-19. After donning surgical masks (SN: 6/26/20) and cleaning hands, the mothers could hold their babies within the first hour of birth. Early skin-to-skin contact promotes bonding and breastfeeding and has other health benefits. None of the babies were positive for SARS-CoV-2 when tested a day after they were born, researchers report online July 23 in the Lancet Child & Adolescent Health. Seventy-nine of the babies were tested for the virus five to seven days after birth, by which time many had been discharged to their homes, with guidance for parents on continuing infection control. All of these infants tested negative. At this point, 64 were still breastfeeding or getting breastmilk from a bottle. At two weeks after birth, 70 of 72 infants tested negative for SARS-CoV-2, while two had invalid test results; none of the babies had COVID-19 symptoms. The 53 infants that had a one-month telemedicine visit continued to show no signs of the illness.

7-24-20 Coronavirus: My pregnancy in a pandemic
Coronavirus has meant pregnant women around the world have had to face additional challenges – like changing birth plans, social isolation, and financial challenges. Two women in Vancouver and London have documented their birth stories for the BBC, to show what it’s like to have a baby in a pandemic.

7-24-20 Ancient DNA suggests Vikings may have been plagued by smallpox
Viral genetic material in human remains pushes infections back to the 600s. Some Vikings may have died from now-extinct strains of one of humankind’s deadliest pathogens: smallpox. Researchers collected DNA from viruses in the remains of northern Europeans living during the Viking Age, some of whom were likely Vikings themselves, and found that they were infected with extinct but related versions of the variola virus that causes smallpox, the team reports in the July 24 Science. The new finding pushes back the proven record of smallpox infecting people by almost 1,000 years, to the year 603. Researchers had previously discovered ancient traces of variola virus DNA in a mummy from the mid-1600s, which put the common origin of modern strains in the 16th or 17th century (SN: 12/8/16). It is still uncertain when the virus that causes smallpox first began to infect people. The disease is estimated to have killed as many as 500 million people and is the only human pathogen to have been eradicated globally. Written records from more than 3,000 years ago have documented smallpox-like symptoms, and scientists have identified possible smallpox skin lesions on mummified remains. But it’s difficult to prove that the smallpox virus was the cause. “This is really exciting work,” says Ana Duggan, an evolutionary geneticist at McMaster University in Hamilton, Canada, who was not involved in the study. “Our understanding of this historical and devastating disease just got a lot wider. We are uncovering [variola virus] diversity that was unknown and unappreciated until right now.” Martin Sikora, a computational biologist at the University of Copenhagen, and his colleagues isolated viral DNA from the teeth and bones of 1,867 humans who lived approximately 31,000 to 150 years ago. Of those people, 13 had remnants from the variola virus. Eleven remains belonged to people — including some thought to be Vikings — who had lived in northern Europe, western Russia and the United Kingdom during the Viking Age more than 1,000 years ago. Two others lived in western Russia during the 19th century and were infected with variola virus strains closely related to modern versions.

7-24-20 Genetic impact of colonial-era slave trade revealed in DNA study
A major DNA study has shed new light on the fate of millions of Africans who were traded as slaves to the Americas between the 16th and 19th centuries.More than 50,000 people took part in the study, which was able to identify more details of the "genetic impact" the trade has had on present-day populations in the Americas. It lays bare the consequences of rape, maltreatment, disease and racism. More than 12.5m Africans were traded between 1515 and the mid-19th Century. Some two million of the enslaved men, women and children died en route to the Americas. The DNA study was led by consumer genetics company 23andMe and included 30,000 people of African ancestry on both sides of the Atlantic. The findings were published in the American Journal of Human Genetics. Steven Micheletti, a population geneticist at 23andMe told AFP news agency that the aim was to compare the genetic results with the manifests of slave ships "to see how they agreed and how they disagree". While much of their findings agreed with historical documentation about where people were taken from in Africa and where they were enslaved in the Americas, "in some cases, we see that they disagree, quite strikingly", he added. The study found, in line with the major slave route, that most Americans of African descent have roots in territories now located in Angola and the Democratic Republic of Congo. What was surprising was the over-representation of Nigerian ancestry in the US and Latin America when compared with the recorded number of enslaved people from that region. Researchers say this can be explained by the "intercolonial trade that occurred primarily between 1619 and 1807". They believe enslaved Nigerians were transported from the British Caribbean to other areas, "presumably to maintain the slave economy as transatlantic slave-trading was increasingly prohibited". (Webmaster's comment: Slave women and girl children were constantly being raped and impregnated by their owners! They did this to improve the stock! And they made sure they got to the girl children before the African males could!)

7-23-20 How the slave trade left its mark in the DNA of people in the Americas
A study of the DNA of people in the Americas with African heritage has revealed overlooked details about the transatlantic slave trade.-how-the-slave-trade-left-its-mark-in-the-dna-of-people-in-the-americas/#ixzz6T7z6V86g. “This gives some clarity and some sense of individual history,” says historian Linda Heywood of Boston University in Massachusetts, who wasn’t involved in the research. DNA evidence means African Americans can pinpoint where their ancestors were abducted from and reclaim aspects of their heritage that were hidden by the slave trade, she says. “It broadens the way in which identity and personal history can be thought about.” An estimated 12.5 million people were taken from Africa to the Americas between the 1500s and 1800s, according to historical texts like shipping documents and records of people being sold. To fill out the picture, Steven Micheletti of consumer genetics firm 23andMe in Sunnyvale, California, and his colleagues looked at DNA from 50,281 people, including 27,422 people from across the Americas with a minimum of 5 per cent African ancestry, 20,942 Europeans and 1917 Africans. This allowed them to identify stretches of DNA that are unique to people from particular regions of Africa. The data came from 23andMe customers, along with public genome databases. Studies like this are becoming possible because African people, who were previously under-represented in genome databases, are now being asked to take part in research, says Joanna Mountain, also of 23andMe. Nevertheless, gaps remain. “I’m hoping we get some data from Mozambique sometime soon. It was involved in the slave trade, but we didn’t have enough data to include it in this study,” she says. In line with historical records of where slaves were taken from, the African DNA in people in the Americas was most similar to that of people living in west African countries like Senegal, the Democratic Republic of the Congo and Angola.

7-23-20 DNA from Viking people reveals the unexpected history of smallpox
The DNA of ancient smallpox viruses has been found in the bones and teeth of a dozen or so people who lived in northern Europe during the Viking age. Unexpectedly, these smallpox strains are quite different to the strain that was eliminated in the 20th century – and possibly far less deadly. Historical accounts and lesions found on Egyptian mummies suggest that the Variola virus, which causes smallpox, has plagued people for thousands of years. Barbara Mühlemann at the University of Cambridge and her colleagues now have the first unambiguous evidence. They started by looking for viral sequences in previously sequenced DNA from nearly 2000 individuals who lived in Eurasia and the Americas between 30,000 and 150 years ago. “Presumably many people died of the virus,” she says. In these people, viral DNA might be present in their remains and could have been sequenced along with their own DNA. Sure enough, the team found signs of Variola DNA in 26 individuals. They then looked for more viral DNA in the original samples. They found it in 13 individuals, 11 of whom died between AD 600 and AD 1050 – overlapping with the Viking age from AD 793 to AD 1066. Most of these individuals died in Scandinavia or what is now western Russia. Three were found on an island in the Baltic Sea called Öland, one in a boat burial around AD 700 and two others in separate burials around AD 1000. The last two probably died in the same outbreak. The Variola virus was also found in a man in a mass grave in Oxford, UK, which is odd given that all 35 men in this grave were violently killed. They are thought to be Viking warriors killed in AD 1002 after Ethelred the Unready ordered the death of all Danes in England – the St Brice’s Day massacre.

7-23-20 Does your blood type influence how susceptible you are to covid-19?
You may have heard that your blood type can protect you against covid-19, or make you more vulnerable. The science suggests that it can do both, a bit, but researchers say that it is too soon to make decisions about personal risk based on your blood group. The idea that blood type might influence susceptibility to infection by the coronavirus that causes covid-19 began circulating in March after researchers in China posted some preliminary results online. Their starting point was the fact that susceptibility to the virus behind SARS is influenced by blood group, with type O somewhat protective against catching the virus. Other viruses are also blood-group dependent; people with type A blood have been found to be more susceptible to hepatitis B and HIV. The Chinese team blood-typed 2173 people in hospital with covid-19 and compared them with the general population. This revealed that among people in hospital there were more in blood group A and fewer in blood group O than the general population, which suggests type A was associated with a higher risk of infection and type O with a lower risk. A few weeks later, researchers in New York found a similar pattern, but only among patients whose blood type was rhesus positive. How so? The earlier work on the SARS virus had shown that the protection enjoyed by people with type O blood was due to them already having protective antibodies, which may have been created in response to immunogenic molecules, or antigens, from other pathogens. These antibodies inhibited the SARS virus from latching onto a cell receptor called ACE2, which it uses to break into human cells. Those antibodies seen in people with type O blood appear to have been elicited by antigens very similar to those on type A blood cells. This could explain why people in the type A blood group don’t have these antibodies: even if they had been exposed to the same pathogens as those people with type O blood, their immune systems would recognise the antigens as “self”.

7-23-20 Mosquitoes evolved to suck human blood when they couldn’t find water
Mosquitoes evolved to bite humans if they lived in places with intense dry seasons, according to a study of African mosquitoes. The insects need water to breed and may have latched onto people because we store it in large quantities. Many mosquitoes bite a wide range of animals, but some have specialised in biting humans and nobody knew why until now. Aedes aegypti mosquitoes often specialise in humans, bringing diseases like Zika, dengue and yellow fever with them. But some African populations of the species have a wider diet. “No one had actually gone through and systematically characterised behavioural variation in Africa,” says Noah Rose at Princeton University in New Jersey. To do this, he and his colleagues captured A. aegypti eggs from 27 sites in sub-Saharan Africa and raised them in a lab. They then put the mosquitoes in a chamber where they could catch a whiff of either a human or an animal – a guinea pig or a quail – to see which they would move towards to attempt to bite. A huge range of preferences was found. The researchers then built a model to determine which factors affected the mosquitoes’ preferences. Those living in areas where the dry season was long and intense were much more likely to prefer humans. There was also a smaller effect of urbanisation: mosquitoes in cities tended to prefer humans. A long dry season is a problem for A. aegypti, says Rose, because these mosquitoes depend on standing water to rear their young. But humans often create sources of standing water, whether by storing rainwater in barrels or by irrigating crop fields. Mosquitoes that lived thousands of years ago may have been drawn to these places and thus evolved to bite humans. The story may well be different for Anopheles mosquitoes, which spread malaria, says Rose. These mosquitoes are only distantly related to A. aegypti and have a different life cycle. “The adults can go into a state called aestivation, where they dry out through the dry season,” says Rose.

7-23-20 An ancient skull hints crocodiles swam from Africa to the Americas
Features of a fossil from what’s now Libya tie the animal closely to its extant American kin. A resemblance between a long-lost African crocodile and modern American crocs goes beyond the shared bump on their snouts. New analyses of a roughly 7-million-year old skull from the extinct Crocodylus checchiai suggest that crocodiles journeyed from Africa to the Americas millions of years ago, researchers report July 23 in Scientific Reports. Unearthed in the 1930s, the fossil came from what’s now Libya and sat for decades in a museum. With CT scanning, scientists have now mapped the skull’s structure, revealing hidden anatomical features that tie the animal closely to the four species of American crocodiles alive today. “It really looks like an American true crocodile, but it comes from Africa,” says Massimo Delfino, a paleoherpetologist at the University of Turin in Italy. Genetic analyses had already linked the Nile crocodile with its American kin. Though scientists suspected that crocs long ago colonized one of the locales before journeying to the other, the fossil record hadn’t painted a clear picture of which came first. This C. checchiai specimen predates the earliest known crocodile in the Americas (from roughly 5 million years ago) by about 2 million years. The skull’s structural features place C. checchiai at the base of the American crocs’ branch of the crocodile family tree. But the animal was also a close relative of the Nile crocodile, the researchers found. As a result, the newly described fossil “fills a gap between the Nile crocodile in Africa and the four extant American species,” Delfino says. The continents would have been in roughly the same place as now when C. checchiai or a close relative may have been on the move. So the new finding suggests that a group of crocs, or at least one pregnant female, may have made a transatlantic journey from Africa to the Americas, Delfino says. “It’s not so surprising,” he says, given today’s crocodilians’ ability to survive saltwater and travel hundreds of kilometers when helped by ocean currents.

7-23-20 Stone artifacts hint that humans reached the Americas surprisingly early
Archaeologists date their finds in Mexico to as early as about 33,000 years ago. Humans may have arrived in North America way earlier than archaeologists thought. Stone tools unearthed in a cave in Mexico indicate that humans could have lived in the area as early as about 33,000 years ago, researchers report online July 22 in Nature. That’s more than 10,000 years before humans are generally thought to have settled North America. This controversial discovery enters a new piece of evidence into the fierce debate about when and how the Americas were first populated. “A paper like this one is really stirring up the pot,” says coauthor Eske Willerslev, an evolutionary biologist at the University of Cambridge. It “will no doubt get a lot of arguments going.” For decades, archaeologists thought the Americas’ first residents were the Clovis people — big game hunters known for their well-crafted spearpoints who crossed a land bridge from Asia to Alaska about 13,000 years ago (SN: 8/8/18). Recent, well-accepted archaeological discoveries suggest that North America’s first settlers actually arrived a few thousand years before the rise of the Clovis culture, by about 16,000 years ago (SN: 10/24/18), says Vance Holliday, an archaeologist the University of Arizona in Tucson not involved in the new work. If the new finds really are human tools, Holliday says, this would be the oldest evidence for a human-inhabited site anywhere in the Americas. At Chiquihuite Cave in central Mexico, archaeologists unearthed what appear to be over 1,900 stone tools. Using radiocarbon dating to determine the ages of charcoal, bone and other detritus surrounding the artifacts, the researchers determined that more than 200 of the tools were embedded in a layer of earth as old as 33,150 to 31,400 years. Other artifacts were found in a layer as fresh as about 13,000 years old.

7-22-20 Humans reached the Americas 15,000 years earlier than thought
HUMANS seem to have been living in the Americas as early as 33,000 years ago – 15,000 years before the most widely accepted date. The finding implies that people arrived there before the peak of the last glacial period and there is a long American prehistory we are yet to uncover. The first American settlers were probably Homo sapiens, but we can’t rule out extinct groups like Neanderthals and Denisovans. The settlers probably entered from north-east Asia across a land bridge linking Asia and Alaska. This was submerged by rising seas when the ice sheets melted at the end of the last glacial period. Most archaeologists accept that humans were in the Americas 18,000 years ago. Now two studies bolster the idea that people got there much earlier. Ciprian Ardelean at the Autonomous University of Zacatecas in Mexico and his colleagues have spent the past decade excavating Chiquihuite cave in Zacatecas. They have found almost 2000 stone tools buried in sediments in the cave, including blades, points and scrapers. No human remains or DNA have been found. The youngest samples of sediment are at least 12,200 years old, and the oldest may be 33,150 years old (Nature, DOI: 10.1038/s41586-020-2509-0). This suggests that people lived in the Americas before a crucial event: the last glacial maximum – the peak of the last glaciation. Between 26,500 and 19,000 years ago, ice sheets extended across much of North America. This was thought to make condition too harsh for people to enter the Americas, but the new findings suggest humans were already present. The second study compiles reliably dated archaeological sites to track the spread of people across North America. Lorena Becerra-Valdivia at the University of New South Wales in Australia and Thomas Higham at the University of Oxford, who are also on Ardelean’s team, assembled dates from 42 sites in North America and north-east Asia. Chiquihuite cave was the oldest reliably dated site (Nature, DOI: 10.1038/s41586-020-2491-6).

7-22-20 Earliest evidence for humans in the Americas
Humans settled in the Americas much earlier than previously thought, according to new finds from Mexico. They suggest people were living there 33,000 years ago, twice the widely accepted age for the earliest settlement of the Americas. The results are based on work at Chiquihuite Cave, a high-altitude rock shelter in central Mexico. Archaeologists found nearly 2,000 stone tools, suggesting the cave was used by people for at least 20,000 years. During the second half of the 20th Century, a consensus emerged among North American archaeologists that the Clovis people had been the first to reach the Americas, about 11,500 years ago. The ancestors of the Clovis were thought to have crossed a land bridge linking Siberia to Alaska during the last ice age. This land bridge - known as Beringia - subsequently disappeared underwater as the ice melted. And these big-game hunters were thought to have contributed to the extinction of the megafauna - large mammals such as mammoth, mastodon and various species of bear that roamed the region until the end of the last ice age. As the "Clovis First" idea took hold, reports of earlier human settlement were dismissed as unreliable and archaeologists stopped looking for signs of earlier occupation. But in the 1970s, this orthodoxy started to be challenged. In the 1980s, solid evidence for a 14,500-year-old human presence at Monte Verde, Chile, emerged. And since the 2000s, other pre-Clovis sites have become widely accepted - including the 15,500-year-old Buttermilk Creek Complex in central Texas. Now, Ciprian Ardelean, from the Universidad Autónoma de Zacatecas, Mexico, Tom Higham, from the University of Oxford, and colleagues have found evidence of human occupation stretching back far beyond that date, at the Chiquihuite site in the central-northern Mexican Highlands. The results have been published in the journal Nature.

7-22-20 Coronavirus: Cracking the secrets of how bats survive viruses
Scientists have deciphered the genetic blueprints of six of the world's bats. Their codes of life contain genetic clues to their "exceptional immunity", which protects them against deadly viruses. Researchers hope to use the information to crack the secrets of how bats carry coronaviruses without getting sick. They say this may ultimately provide solutions to help human health during this and future pandemics. Prof Emma Teeling of University College Dublin said the "exquisite" genome sequences they have unravelled suggest bats have "unique immune systems". And understanding how bats can tolerate viruses without getting sick could help in the development of new treatments for viruses such as Covid-19. "If we could mimic the immune response of bats to viruses, that allows them to tolerate them, then you could look to nature to find a cure," she told BBC News. "It's already evolved, we don't need to reinvent the wheel. We now have the tools to be able to understand the steps we need to take; we need to develop the drugs to do it." Prof Teeling is the co-founder of the Bat1K project, which aims to decode the genomes of all 1,421 living bat species. "These genomes are the tools needed to identify the genetic solutions evolved in bats that ultimately could be harnessed to alleviate human ageing and disease," she said. Covid-19 is thought to have arisen in bats, passing to humans through another, as yet unidentified, animal. A number of other diseases, including Sars, Mers and Ebola, are thought to have jumped to humans this way. Ecologists and conservationists have warned that bats should not be persecuted; when left undisturbed in their natural habitats, they pose little risk to human health. And they are vital for the balance of nature. Many are pollinators, dispersing the seeds from fruit, and others are insectivores, eating millions of tons of insects a night.

7-22-20 UK could eliminate the coronavirus but it might do more harm than good
BECOMING a covid-19-free zone sounds like the ultimate goal for any nation. Several countries around the world have come pretty close and, according to a group of independent scientists, the UK could join them. The group says that, as an island nation, the UK could introduce specific measures over the next year and follow in the footsteps of other island success stories, such as Iceland, Taiwan and New Zealand. But closer scrutiny reveals that no country has truly eliminated the coronavirus from its shores and that doing so would mean making such large sacrifices in other areas of public well-being that it might not be worth it. Earlier this month, Independent SAGE – a self-appointed group of scientists that provides advice with the intention of guiding UK government policy on the coronavirus – published a report recommending that the UK aims for zero reported cases, known as elimination, within the next 12 months. “Achieving elimination would allow all social distancing measures to be lifted, schools to be fully open, the hospitality and entertainment industries to reopen fully, revitalisation of the economy and a sense of much needed normality for the population,” the report said. All the researchers New Scientist contacted agreed that elimination is a worthy goal. Most say it is theoretically possible for many countries, including the UK, to rid themselves of the virus even without a vaccine. Success would require tough measures, however. The steps suggested in the Independent SAGE report are familiar ones. They include boosting test, trace and isolate programmes, maintaining lockdown policies and strictly restricting travel. Such measures would be a departure from the current phased return to normal life proposed by the UK government. It recently advised people to return to office working and will soon offer discounts on restaurant meals to encourage dining out. Recent figures suggest England’s test and trace programme is only reaching about 80 per cent of infected people’s contacts, and it is unclear how many of those told to isolate are doing so. Tight restrictions on travel and border control would have costs for business, tourism and the broader economy.

7-22-20 Research is our best weapon in the fight against covid-19 and obesity
The obesity and covid-19 pandemics have been shown to be interlinked, and both urgently require more research to provide clear evidence on how best to beat them. FOR months now, UK prime minister Boris Johnson and his ministers have been repeating a mantra for tackling the coronavirus pandemic: follow the science. Debates about “the” science aside – the UK government seems to have had too many modellers and not enough public health experts advising it – an approach based on evidence is always a good one. Evidence, however, can sometimes be lacking. On 29 January, early in the pandemic, the World Health Organization published a guide on the use of medical masks by the general public to slow the spread of the virus. It said that compulsory mask wearing shouldn’t be required, as “no evidence is available on its usefulness to protect non-sick persons”. It is easy to read those words and assume that face coverings of any kind are pointless – indeed, that is precisely what many people have done. But as the saying goes, absence of evidence is not evidence of absence. Rigorous studies on mask wearing have simply not been done, so we cannot say for sure that they work. We also cannot say that they don’t. Now, though, new evidence is trickling in. As a result, official policy in many countries, including in England (see “What are face covering rules in England and why did the policy change?”), is changing. We still don’t have the gold standard of medical evidence – a randomised trial – but as we learn more about how the coronavirus is transmitted, face coverings seem a sensible idea. Not content with fighting one pandemic, Johnson has also signalled his intention to begin battle with another: obesity. Of course, the two pandemics have become interlinked, with obesity a factor in the development of some cases of severe covid-19. However, despite obesity having been around for a great deal longer than covid-19, the evidence on what to do about it remains surprisingly contradictory, with dieticians at loggerheads over whether the most effective approach is to reduce how much fat or carbohydrate we eat (see “What is the best way to lose weight and keep it off for good?”). To find out, we need more long-term research. Only then can we follow the science.

7-22-20 Hearing restored in rats by modifying ear cells to respond to light
Cochlear implants that restore hearing could be improved by genetically modifying the nerve cells in people’s ears so that they respond to light instead of electricity, a study in rats has shown. “This is so much better than what we currently have with electrical implants,” says Tobias Moser at the University Medical Center Göttingen in Germany. Our hearing relies on hair cells inside the cochlea of our ears detecting sounds of different frequencies and then stimulating the right auditory nerve cells. Damage to these hair cells is a common cause of deafness. Cochlear implants can partly restore hearing by electrically stimulating nerve cells, bypassing the hair cells. But the electrical signals stimulate lots of nerve cells at once, meaning the resulting sound is less detailed – the audio equivalent of a low-resolution image. People with cochlear implants may not understand speech in noisy environments or enjoy music in the way they did before, says Moser. The problem is that the salty fluid inside the cochlear conducts electricity, so it is hard to confine the signal. Instead, Moser’s team is developing optical cochlear implants that use light to stimulate the nerve cells. Of course, nerve cells don’t usually respond to light. But they can be genetically modified to respond to it. Optogenetics, as this is called, is widely used for research and is also being tested as a way to restore sight or treat neural conditions. It appears to be safe from the animal and human studies done so far. Moser’s team has previous shown that the concept works by using a single optical fibre to stimulate the cochlea in deaf animals that have modified auditory nerve cells. Now the researchers have tested an implant with 10 LED chips in rats. After the implant was inserted into deaf rats with modified auditory nerve cells the animals responded to a sound they had been trained to respond to before being deafened. This shows that what they heard via the implant was sufficiently similar, says Moser. “I think this is a great achievement.” For people, the team will create implants with 64 light sources, or channels. The sound clip below starts with a spoken sentence and then simulates how it would sound with a standard cochlear implant and then with an optical implant with 64 channels.

7-22-20 COVID-19 vaccines by Oxford, CanSino and Pfizer all trigger immune responses
Volunteers who got the vaccine candidates made antibodies and T cells against the coronavirus. More coronavirus vaccine candidates have passed initial safety tests and induce immune responses that might protect against the virus. All volunteers in a small clinical trial who were given an experimental vaccine developed by researchers at the University of Oxford made antibodies against a protein the virus uses to break into cells. Those participants also produced immune cells called T cells that are important for long-lived immunity, the researchers, working with the global pharmaceutical company AstraZeneca, report July 20 in the Lancet. Levels of neutralizing antibodies, which can block viral entry into cells, were at levels on par with those from people who have recovered from COVID-19. No serious side effects were seen, particularly when volunteers took acetaminophen after getting an injection. “The results so far are encouraging,” says Mark Poznansky, a vaccinologist who directs the Vaccine & Immunotherapy Center at Massachusetts General Hospital in Boston who was not involved in the study. The researchers won’t truly know whether the vaccine is safe and effective until many more people get it. Work on other viruses suggests that neutralizing antibodies and T cells in people’s blood should offer protection against infection or serious illness. But “a fundamental point about COVID-19 is that we don’t yet know what constitutes a protective [immune] response to the virus,” Poznansky says. “We’re not yet 100 percent clear about how those antibodies contribute to protection in the context of a vaccine.” The AstraZeneca/Oxford vaccine starts with a chimpanzee adenovirus engineered so that it cannot replicate itself, making it safe to use. The virus can infect human cells, and delivers DNA instructions for making the coronavirus’ spike protein — the knobby protein studding the virus’s outer shell. Once inside a human cell, the DNA integrates, and the cell produces the spike protein, which the immune system then gears up to attack by producing antibodies and training white blood cells known as T cells to recognize the coronavirus.

7-22-20 A blood test may show which COVID-19 patients steroids will help — or harm
Treatment timing can dramatically lower risk of death or needing a ventilator, or raise it. A cheap and easy blood test for inflammation may help determine which COVID-19 patients will benefit from getting steroids. In an observational study of people hospitalized with COVID-19, those with high levels of an inflammation indicator called C-reactive protein in their blood had a reduced chance of dying or being put on a ventilator when treated with steroids. But steroid treatment more than doubled the risk of needing a ventilator or dying for people with low levels of the inflammation-indicating protein, researchers report July 22 in the Journal of Hospital Medicine. “Steroids are Goldilocks drugs: They need to be given at the just right time,” says Luis Ostrosky, an infectious diseases doctor at the University of Texas Health Science Center at Houston who was not involved with the work. Giving steroids too early may rein in the immune system too much so that it can’t effectively fight the coronavirus, leading to the virus doing more damage. And “if you give steroids too late, the damage is already done.” Using C-reactive protein as guide “may be the key to starting [steroids] at the right time,” Ostrosky says. A large clinical trial in the United Kingdom called the RECOVERY trial has shown that the steroid dexamethasone can reduce the risk of death among COVID-19 patients who need extra oxygen or who are on ventilators (SN: 6/16/20). In that study, there was no benefit — and maybe a hint of harm — for patients who don’t need extra oxygen to breathe. The new results are in line with those from the RECOVERY trial and may help explain why some patients do better on steroids than others, Ostrosky says. Shitij Arora, a hospital physician at Albert Einstein College of Medicine and Montefiore Medical Center in New York City, noticed in mid-March that some patients coming into the hospital with COVID-19 had intense inflammation in their lungs, while others didn’t. Arora treated a handful of patients who had lung inflammation with steroids and saw some of them dramatically improve.

7-22-20 What is the best way to lose weight and keep it off for good?
HOW can countries become more resilient to the coronavirus? You may have heard about face masks, hand-washing and avoiding crowds. But as UK Prime Minister Boris Johnson was recovering from covid-19 in May, he announced another tactic: targeting the nation’s waistlines. People who are overweight are certainly at a higher risk of developing severe covid-19, especially if they also have type 2 diabetes, which is linked to obesity. Around a third of UK adults are overweight, and roughly another third are obese. Johnson has blamed his own weight for how severely he was affected by coronavirus when he was admitted to hospital in April. England’s deputy chief medical officer, Jenny Harries, also said this month that losing weight would reduce people’s chances of a severe case of covid-19 if there is a second wave in the country this winter and advised that people should get “as fit as possible”. There is just one problem: we don’t actually know the best way for people to lose weight and keep it off. Many initiatives have been tried, but very few have been shown to work. “There’s no country in the world that has solved this,” says Michael Lean at the University of Glasgow, UK. People in most countries have been getting gradually heavier over the past few decades, with the UK one of the heaviest countries in Europe. This seems to be exacerbating the severity of the covid-19 outbreak, researchers argued in a recent editorial in the medical journal BMJ. “While exercise seems to help prevent weight gain, it doesn’t cause people to lose weight” The UK government hasn’t yet released specifics of how it plans to reverse this trend, but it is unlikely to be as simple as people getting fitter, as Harries implied. While exercise seems to help prevent weight gain, studies have shown that it doesn’t cause people to lose weight, perhaps because it is hard to achieve the levels necessary to burn off a significant amount of fat. It may also make people hungrier. Physical activity seems to have a host of health benefits, including protecting against heart disease and boosting mental health, but weight loss isn’t one of them.

7-22-20 Hidden nutrition: We don't know what makes up 99 per cent of our food
We know next to nothing about the vast majority of compounds in our diet. Now researchers are finding ways to study this "nutritional dark matter" – and what it could mean for our health. TODAY I searched my kitchen cupboards for dark matter, and found it in a packet of Korean instant noodles. The food label ran to 38 ingredients, many of them additives. But it also listed some real foods, including soy, chilli, sesame, shrimp, cabbage, seaweed, mushroom, anchovy and cuttlefish. And also the one I was looking for, garlic. To be clear, I’m not suggesting that garlic contains actual dark matter, the 85 per cent or so of material in the universe that physicists say is there but cannot observe directly. But it does contain what has been called “nutritional dark matter”: the thousands and thousands of compounds that are in food but which, until recently, were totally unknown, and which may be affecting our health. Given that eating is one of the big human universals, that’s a mind-boggling oversight. “Our understanding of how diet affects health is limited to 150 key nutritional components,” says Albert-László Barabási at Harvard Medical School, who coined the term nutritional dark matter. “But these represent only a small fraction of the biochemicals present in our food.” It is time, he says, for nutritionists to go dark-matter hunting, to massively expand our knowledge of what is on our plate and its impact on us. The idea that food is a rich and complex mix of biochemicals is hardly news. Even the well-known macronutrients – proteins, carbohydrates and fats – are hugely diverse. There’s also a vast supporting cast of micronutrients: minerals, vitamins and other biochemicals, many of which are only present in minuscule quantities, but which can still have profound health effects. The official source of information on this complex biochemical soup is the National Nutrient Database for Standard Reference, maintained by the US Department of Agriculture (USDA). It contains information on the composition of hundreds of thousands of foods, broken down into 188 different nutritional components.

7-22-20 Mexico archaeology: Pre-Hispanic ruins found on mountaintop
Two pre-Hispanic carved stone monuments believed to date back more than 1,500 years have been uncovered on a mountaintop in central Mexico. Archaeologists say the site - which in its heyday would have had seven pyramids, a ceremonial area and a games court - was found by villagers. It is thought to have been built by the Zapotecs, who lived in the southern highlands of what is now Mexico. The carvings suggest it may have been dedicated to the god of the underworld. The site is at a strategic point on top of the Cerro de Peña mountain in Puebla state at a height of 1,845m (6,000ft). Archaeologists think it lay hidden since the 6th Century. Access to the site is along a rocky path, which takes two and a half hours to climb. It was found by residents of the nearby village of Santa Cruz Huehuepiaxtla. So far, two stelae (etched stone panels), as well as smaller carved stones, have been found. One of the carvings is of a figure with horns and claws wearing a loincloth. Others are believed to represent an iguana, an eagle and female figure thought to be a deity resembling a bat. José Alfredo Arellanes, from Mexico's National Institute of Anthropology and History (INAH), says 87 glyphs, or symbols, have been found so far. Mr Arellanes says initial investigations suggest a ceremonial area, flanked by temples and the homes of the rulers, would have been located at the top of the mountain. The archaeologist thinks the site would have also had seven pyramids and a court to play pelota, a game in which players used their hips to propel a rubber ball through stone hoops. Puebla is an area rich with archaeological ruins but locals said they were proud to have led archaeologists to this latest find. Experts are still analysing the finds but said the site could have been built by people belonging to the Zapotec civilization, also known as the "Cloud People", which originated in the area 2,500 years ago and had a sophisticated architecture and style of writing based on glyphs. Those following the Zapotec religion believed in lots of gods, many of them associated with agriculture or animals.

7-21-20 Everything you need to know about the Oxford coronavirus vaccine
An experimental coronavirus vaccine developed at the University of Oxford produces the hoped for immune responses in people. Even though it isn’t yet clear if this means the vaccine will prevent infections, the group that made it has struck deals for companies to make 2 billion doses of it within a year. “It’s a really important day today,” says team leader Sarah Gilbert. “But there’s still a long way to go.” At least 23 experimental vaccines are being tested in people. The aim of these trials is to prove that the vaccines work, but that will take time, because it requires giving the vaccine or a placebo to many thousands of people in a region where there are lots of coronavirus cases. The latest findings were the result of a smaller trial intended to study the immune response to find out if the vaccine is safe and produces the intended effect. About 1000 volunteers were given the Oxford vaccine, which uses a chimpanzee cold virus to deliver the gene for the coronavirus spike protein to human cells. The modified virus can’t replicate, so can’t cause infection itself. No serious adverse effects were reported in the study, published this week. The volunteers did generate lots of antibodies, proteins that circulate in the blood and bind to viruses. Not all antibodies bind in a way that renders the virus harmless, but after one dose most volunteers produced neutralising antibodies, which do prevent viruses infecting cells. After two doses, all the volunteers generated neutralising antibodies. Their bodies also made immune cells known as T-cells that seek out and destroy infected cells before they produce more viruses. This cellular response is thought to be an important part of immunity to the coronavirus. “We are super-excited by these results,” says team member Teresa Lambe. The antibody response is comparable to that seen in natural infections, but the cellular response is stronger. However, it remains to be seen whether this response is sufficient to protect against infection and how long this protection lasts.

7-21-20 The millennial pandemic
Young people are by far the majority of COVID-19 cases — but should we blame them? The first time I heard COVID-19 referred to as "the boomer remover" was in February, during those eerie early days of the pandemic when we still had the capacity to marvel at the novelty of ideas like "quarantine" and "self-isolation" and "flattening the curve." Though the phrase originated with Gen Z TikTok teens, being a millennial — and therefore embarrassingly invested in what the generation directly below mine is "up to" — I found it irreverent and cheeky and the tiniest bit worrisome. My parents are boomers! The phrase also reflected a surface-level truth: Older generations were largely the ones who were dying from the novel disease. At first this information was used dismissively, to downplay the pandemic deaths as being largely confined to nursing homes and health-care facilities. But the focus on who was dying also obscured another more complicated generational picture of who was catching and spreading the disease. Now, amid a resurgence of the COVID-19 around the country, it's become clear it isn't the boomers or their parents who are driving the pandemic. It's us, the millennials. The reason recent deaths are relatively low, at least in part, is owed to younger people being the ones overwhelmingly testing positive for COVID-19 at the moment; the 18-34 age group in California, for example, is by far the largest demographic to test positive so far, followed by the 35-49 age group. Nationwide, that trend appears to hold: in Arizona, over 60 percent of new infections are in people under the age of 45, and in Texas' two largest counties, half of the emergent cases are in people under 40. (The standard definition of millennials, as people born between 1980 and 1994, puts the generation in the range of 26 to 40 years old). Speaking in late June, Vice President Mike Pence went as far as to call it "very encouraging news" that "roughly half of the new cases are Americans under the age of 35." But it's not "very encouraging" at all. For one thing, while millennials, teens, and children don't tend to get as sick as older generations, they are not invincible. Many have died (there are around 3,000-plus confirmed COVID-19 deaths of people under the age of 45 in the U.S. so far) or been hospitalized, or will otherwise live with lifelong health complications as a result of surviving the disease. "I was laughing at all the memes and the jokes [about the coronavirus], and now I'm not," one 27-year-old coronavirus survivor told Kaiser Health News. "It's real." Even more to the point, though, is the fact that "people between the ages 18 and 50 don't live in some sort of a bubble," as Oklahoma City Mayor David Holt recently put it to The Associated Press. "They are the children and grandchildren of vulnerable people. They may be standing next to you at a wedding. They might be serving you a meal in a restaurant." While it is still early, it appears that outbreaks among young people tend to foreshadow subsequent outbreaks in vulnerable populations, which leads to spikes in deaths. "We first see it in the community, and then we see it in the residents and staff [at nursing homes], and then you see the deaths," David Grabowski, a professor at Harvard Medical School, told The Wall Street Journal. The emergence of cases in younger populations shouldn't be written off; it's a grave omen of what's coming. A Japanese study shared by the CDC and cited by USA Today even "traced half the COVID-19 clusters in a community back to someone under the age of 40. Forty-one percent [of] the original cases did not show symptoms at the time of transmission."

7-21-20 Coronavirus-infected cells sprout filaments that may spread the virus
Tiny projections may serve as highways to new cells to infect. Like a scene out of a sci-fi movie, cells invaded by the coronavirus can sprout probing appendages bedecked with viral bits. Human cells infected with SARS-CoV-2, the coronavirus that causes COVID-19, formed more numerous and longer extremities, called filopodia, than uninfected cells, researchers report online June 28 in Cell. High-resolution electron microscopy confirmed the presence of these filopodia in infected monkey cells and captured SARS-CoV-2 viral particles budding from the projections. These protrusions may have unexplored roles in spreading the virus, and could serve as targets for future antiviral therapies. Similar spindly projections are found on some healthy cells, where the structures serve different roles. Repair cells, for example, send out filopodia to detect chemical cues to navigate to wound sites. Other viruses, including the coronavirus behind the SARS epidemic, also can cause cells to sprout filopodia. Some viruses, such as Marburg and Ebola, travel along filopodia of infected cells and may use the structures to move directly from one cell to another. The extensions “are highways for transport,” says Robert Grosse, a cell biologist at the University of Freiburg in Germany. More work is needed to confirm what role filopodia play in a COVID-19 infection. Microscopy of infected cells over time would provide insight into whether these cell-to-cell connections affect viral spread, says Mark Denison, a virologist at Vanderbilt University Medical Center in Nashville not involved in the study. The filopodia observed in the new study contained a protein called CK2. Cells dosed with silmitasertib, a CK2-inhibiting molecule in clinical trials for various cancers, were more resistant to a SARS-CoV-2 infection than untreated counterparts. That suggests that CK2 could be a target for future coronavirus drug treatments, Grosse says (SN: 3/10/20)

7-21-20 Scientists stumbled across the first known manganese-fueled bacteria
Two species of bacteria left telltale manganese metal pebbles in a dirty lab jar left to soak. Scientists have discovered the first bacteria known to use the metal manganese to grow. And the researchers had to look only as far as the office sink. “It’s definitely an interesting story about serendipity,” says Jared Leadbetter, an environmental microbiologist at Caltech. He and Hang Yu, also an environmental microbiologist at Caltech, report their fortuitous find in the July 16 Nature. Leadbetter had been working with a pink compound called manganese carbonate in a glass jar. After having trouble cleaning the jar, he filled it with tap water and left it to soak. When he returned 10 weeks later, after an out-of-town teaching stint, the contents of the jar had transformed into a dark, crusty material. Leadbetter knew that scientists had long suspected that bacteria could use manganese to fuel growth. Over a century ago, researchers discovered that bacteria could borrow electrons from chemical elements like nitrogen, sulfur, iron — and manganese. In some cases, bacteria could even use these electrons to fuel growth in much the same way that humans use electrons from carbohydrates in the diet for energy. But no one had identified bacteria that could turn electrons from manganese into energy. When bacteria do borrow electrons from manganese, they convert the metal to a dark material called manganese oxide. Manganese oxide is found all over the planet — from deposits in Earth’s crust to the seafloor to drinking water. And, as it turned out, in Leadbetter’s glass jar. He wondered if the bacteria that had oxidized his manganese might be the elusive species that actually use manganese to grow. “Maybe I better not pour this down the sink,” he thought.

7-20-20 Covid-19 news: Oxford vaccine is safe and induces immune response
The latest coronavirus news updated every day including coronavirus cases, the latest news, features and interviews from New Scientist and essential information about the covid-19 pandemic. Oxford’s coronavirus vaccine candidate appears safe and induces immune response. A coronavirus vaccine candidate being developed by the University of Oxford in partnership with pharmaceutical company AstraZeneca is safe and activates an immune response in people, according to preliminary results from trials involving 1077 volunteers. People injected with the vaccine, called ChAdOx1 nCoV-19, made antibodies and immune cells against the coronavirus. The trial results were published today in The Lancet. No serious side effects were found, although 70 per cent of people developed a fever or headache which could be managed with painkillers. It is not yet clear whether this vaccine candidate offers protection against infection with the coronavirus, and we won’t know whether it can stop people from becoming ill with covid-19 until we see the results of larger trials. Those trials will involve 10,000 people in the UK, 30,000 people in the US, 2,000 in South Africa and 5,000 in Brazil. The UK government has secured access to 100 million doses of the vaccine candidate, in addition to 90 million doses of other coronavirus vaccine candidates from US and European companies. Globally, more than 140 coronavirus vaccines are currently in development, with 23 candidates being tested in people. The seven-day average for daily new coronavirus cases in the US has risen for the 41st consecutive day, mostly due to ongoing spikes in the number of cases in Florida, Texas and California. Los Angeles mayor Eric Garcetti said the county is “on the brink” of shutting down again due to the recent rise in cases. France has made face coverings mandatory in all enclosed public spaces, with those who fail to adhere to the rules facing fines of €135 (£123). Coronavirus cases are on the rise in the north-west and eastern parts of the country, with health minister Olivier Véran warning that France has between 400 and 500 active coronavirus clusters. Anti-mask activists gathered in London’s Hyde Park on Sunday to protest the introduction of new legislation on face coverings. It will be mandatory to wear them in shops and supermarkets in England from 24 July. A survey by the Office for National Statistics conducted between 8 and 12 July found that 61 per cent of people said they used face coverings outside their homes in the previous week.

7-20-20 Coronavirus: Did 'herd immunity' change the course of the outbreak?
On Thursday 12 March, everyday life remained relatively normal across the UK. The back pages of the newspapers were dominated by the victory of Atletico Madrid over Liverpool - 50,000 fans had crammed into Anfield stadium. Throughout that day shoppers shopped, while millions drove to work or poured out of trains into city centres. And in the evening, people went out. At Wembley Arena, Lewis Capaldi sang to an audience of 12,000 fans - having urged them to bring hand sanitiser with them. Around the UK people headed for events big and small. But these were not normal times. A new coronavirus was spreading across the globe. On that day, Italy was shutting all non-essential shops and the Republic of Ireland announced that schools would close. But looking back, the question that will always be asked is - did the UK go into lockdown too slowly? Should those crowds have been out that day? The World Health Organization (WHO) had been asking countries to do everything they could to contain the infection since late February. And some countries were scaling up test and trace to try to suppress the virus. But on 12 March, the UK had all but abandoned community testing to focus on those sick enough to be admitted to hospital. At the time, there were 590 known cases of coronavirus in the UK - more than four times the number in the previous week. The government announced it was moving out of the "contain" phase into the "delay" phase. The risk level was raised to high, and anyone with symptoms was asked to self-isolate for a week. The lockdown was yet to start. At a press conference Prime Minister Boris Johnson, his chief scientific adviser Sir Patrick Vallance and chief medical officer Prof Chris Whitty explained the policy to keep schools open and to allow major public events to go ahead. Johnson said that according to scientific advice, banning major public events would have little effect on the spread of the disease. Prof Whitty argued that beginning social distancing measures "too early" would risk people becoming tired of them and public compliance waning. And Sir Patrick began to talk about the concept of herd immunity. Speaking about the coronavirus he said: "It's not possible to stop everybody getting it and it's also actually not desirable because you want some immunity in the population. We need immunity to protect ourselves from this in the future."

7-20-20 Coronavirus: Why are Americans so angry about masks?
In the midst of the pandemic, a small piece of cloth has incited a nationwide feud about public health, civil liberties and personal freedom. Some Americans refuse to wear a facial covering out of principle. Others in this country are enraged by the way that people flout the mask mandates. Bob Palmgren tried to be polite - at first. He told a customer he had to wear a mask inside his restaurant, RJ's Bob-Be-Que Shack in Mission, Kansas. The customer, a man in his forties in a Make America Great Again (MAGA) cap, had flashed a gun and said that he was exempt from a state-wide mask requirement. He said that he could explain the exemption in the law to Mr Palmgren. Mr Palmgren, a former marine, told the customer that he was not interested in continuing the conversation. Mr Palmgren was not swayed by the customer's gun, either. "Coronavirus doesn't care if you have a gun or not," said Mr Palmgren, describing his conversation with the customer. "I said: 'Now get the hell out of here.'" The argument in the restaurant reflected a deep divide over requirements to wear masks in this country. People in Kansas, along with those who live in more than half of the country, are now required to wear masks in public as part of an ongoing effort to slow down the spread of the virus. But some people have been fighting against the mandate. The wearing of masks has become a catalyst for political conflict, an arena where scientific evidence is often viewed through a partisan lens. Most Democrats support the wearing of masks, according to a poll conducted by researchers at the Pew Research Center. Most Republicans do not. The Republicans are following the lead of the president: Trump has been reluctant to wear a mask, saying that it did not seem right to wear one while he was receiving heads of state at the White House. He put a mask on in public for the first time during a visit to a military hospital earlier this month.

7-20-20 Quadruple-stranded DNA seen in healthy human cells for the first time
The world’s most famous molecule – the DNA double helix – sometimes doubles up again. Researchers have now found this quadruple-stranded form in healthy human cells for the first time. Four-stranded DNA has been seen before in some cancer cells and in lab-based chemistry experiments, but this is the first time the molecule has been visualised in healthy, living human cells, as a stable structure created by normal cellular processes. “We’ve undoubtedly demonstrated that the quadruple-strand DNA forms in living cells,” says Marco Di Antonio at Imperial College London. “This forces us to rethink the biology of DNA.” The DNA molecule is made up of four nucleobases – adenine, cytosine, guanine and thymine – and can configure itself in a number of ways. It creates a four-stranded structure when four guanine bases form a square – guanine is the only base able to bond with itself. Di Antonio, who conducted the work while at the University of Cambridge, and his colleagues were able to visualise the quadruple form within human tissue by attaching a new kind of fluorescent marker to DNA in living cells. He says the discovery may improve our understanding of how the genetic material divulges its information. “We know exactly what DNA does,” says Di Antonio, “but how does the cell know where to express genes and how much protein to make?” The researchers speculate that the quadruplex structure forms to hold the molecule open and facilitate the reading of the genetic code and thus the production of proteins. It may also influence the amount of each protein that is made. Usually, this function is performed by epigenetic markers – chemical tags on DNA that increase or decrease the activity of genes – and it seems that the quadruplex form of DNA has a similar role. “There is a sort of crosstalk between the formation of quadruplex DNA and epigenetic markers,” says Di Antonio. “The quadruplex form is an epigenetic mark in its own right.”

7-20-20 Coronavirus: Oxford vaccine can train immune system
A coronavirus vaccine developed by the University of Oxford appears safe and trains the immune system. Trials involving 1,077 people showed the injection led to them making antibodies and white blood cells that can fight coronavirus. The findings are hugely promising, but it is still too soon to know if this is enough to offer protection and larger trials are under way. The UK has already ordered 100 million doses of the vaccine. The vaccine - called ChAdOx1 nCoV-19 - is being developed at unprecedented speed. It is made from a genetically engineered virus that causes the common cold in chimpanzees. It has been heavily modified, first so it cannot cause infections in people and also to make it "look" more like coronavirus. Scientists did this by transferring the genetic instructions for the coronavirus's "spike protein" - the crucial tool it uses to invade our cells - to the vaccine they were developing. This means the vaccine resembles the coronavirus and the immune system can learn how to attack it. Much of the focus on coronavirus so far has been about antibodies, but these are only one part of our immune defence. Antibodies are small proteins made by the immune system that stick onto the surface of viruses. Neutralising antibodies can disable the coronavirus. T-cells, a type of white blood cell, help coordinate the immune system and are able to spot which of the body's cells have been infected and destroy them. Nearly all effective vaccines induce both an antibody and a T-cell response. Levels of T cells peaked 14 days after vaccination and antibody levels peaked after 28 days. The study has not run for long enough to understand what long-term immunity may look like. There were no dangerous side-effects from taking the vaccine, however, 70% of people on the trial developed either fever or headache. The researchers say this could be managed with paracetamol.

7-20-20 Smallpox vaccination kits from the US civil war reveal historic virus
Strains of viruses used for smallpox vaccines in the US during the civil war have been identified and their genomes reconstructed. “The successful eradication of smallpox via vaccination shows the crucial importance that that practice has had within human history,” says Ana Duggan, who led a team of researchers to analyse smallpox vaccines while at McMaster University in Canada. Smallpox, caused by the variola virus, killed approximately 30 per cent of the people it infected. It was officially eradicated in 1980 after concerted global vaccination efforts. Early protective practices against smallpox involved infecting people with related viruses to induce a milder case of disease that would inoculate them against variola. This was usually done by applying some infected pus or scabs to a cut in the skin, a process known as variolation. Duggan and her colleagues gathered genetic material from US civil war-era vaccination kits to identify the viruses used for smallpox vaccinations at the time. The team analysed five kits, part of a museum collection, that had been used by doctors in the greater Philadelphia area in the mid to late 19th century. The kits contained lancets, tin boxes that held scab material and small glass plates for mixing fluid that had been collected from the blisters of infected people. The team reconstructed the genomes of any viruses present by analysing the scabs and dried blister material from four kits. In one kit, which contained no direct evidence of biological material, the researchers soaked a tin box in a solution with enzymes that essentially hoover up the virus fragments without damaging the box. All five of the viruses identified were strains of the vaccinia virus, which is only distantly related to variola, and is the cause of cowpox. None of the viral genetic material was intact, meaning that it wasn’t infectious. The team then pieced together the viral fragments like a jigsaw puzzle, with the aid of a computer algorithm as well as the genetic sequence of an intact vaccinia virus as a reference.

7-19-20 Coronavirus face masks: Why men are less likely to wear masks
After much squabbling, Monica* took a drastic decision. Her husband Eduardo had repeatedly refused to wear a face mask as the Covid-19 pandemic grew in Brazil - the country with the second-highest number of coronavirus deaths, behind only the US. So she decided to leave the family apartment in Niteroi (a city of 480,000 people near Rio de Janeiro), and move to her parents' house with their seven-year-old son. "I am asthmatic and that makes me particularly vulnerable to the coronavirus. But my husband thought I was being paranoid," she tells the BBC. "His reasoning was that he didn't need a mask because when he left home he didn't go to enclosed spaces. "He wasn't thinking that he was putting me and our son at a higher risk." More men die of Covid-19... but more of them refuse to wear masks. Monica and Eduardo's story lays bare a gender divide that has been widely observed during the pandemic. Studies have found that men are more reluctant than women to wear personal protective equipment and face covers - a trend also seen in previous epidemics. That's despite the fact that Covid-19 has infected more than 13.8 million people and killed more than 590,000 according to the widely-used Johns Hopkins University database. And in the vast majority of countries where data is available, death rates are notably higher among men. The scientific advice has been shifting in favour of masks as evidence emerges that the coronavirus is airborne - and may spread via tiny particles suspended in the air as well as larger droplets from coughs or sneezes. The World Health Organization (WHO), which initially suggested they weren't useful in stopping the spread of the virus, now recommends face coverings in indoor spaces and when social distancing is not possible. And in a number of countries, masks are now mandatory in shops and on public transport. So, if masks can help fight the coronavirus, why is it that men are less prone to wear them? The academics surveyed nearly 2,500 people in the US and found that men were not only less inclined to wear face masks than women. They also considered that donning a mask was "shameful, not cool and a sign of weakness". (Webmaster's comment: Male macho bullshit!)

7-17-20 An asteroid impact, not volcanism, may have made Earth unlivable for dinosaurs
New simulations add to evidence that the Chicxulub strike is what killed T. rex and its kin. For decades, scientists have gone back and forth about whether massive volcanic eruptions or an asteroid impact — or maybe both — caused a mass extinction that saw the demise of all nonbird dinosaurs about 66 million years ago. Now, geologic evidence and data on dinosaur habitats, combined with climate and ecological simulations, suggest it wasn’t the volcanism. Instead, a decades-long cold winter triggered by the giant impact wiped out dinosaur habitats and made it impossible for the creatures to survive, researchers report June 29 in Proceedings of the National Academy of Sciences. In a plot twist, volcanism at the Deccan Traps, in what is now India, may have actually ameliorated the negative effects of the long winter, warming the planet quicker than would have occurred otherwise and allowing mammals room to thrive, the researchers say. “It’s a complete change in the narrative of Deccan volcanism … [which] may well have been the benevolent hero of the time,” says Alexander Farnsworth, a paleoclimatologist at the University of Bristol in England. The new research adds to a growing body of evidence that suggests the impact, not the eruptions, caused the die-off, including a recent study suggesting the bulk of volcanic outgassing happened either too early or too late to have caused the mass extinction (SN: 1/16/20). An estimated 75 percent of the planet’s plant and animal species disappeared in a relative blink of an eye during the extinction event at the end of the Cretaceous Period. Previous research has indicated that a giant asteroid impact, at Chicxulub in what’s now the Yucatán Peninsula in Mexico, released enough ash, dust and gases to block out the sun and dramatically cool the planet for an extended period of time (SN: 11/2/17), possibly causing the extinction.

7-17-20 This dinosaur may have shed its feathers like modern songbirds
The first fossilized signs of sequential molting support the idea that Microraptor was a flyer. A patch of three oddly short feathers spotted among the fossilized plumage of Microraptor may be the first evidence of a nonbird dinosaur molting. The fossil find further suggests that Microraptor, which lived 120 million years ago, may have shed only a few feathers at a time — just like modern songbirds, researchers report July 15 in Current Biology. Such “sequential molting,” they say, suggests that Microraptor was an adept and frequent flyer. Unlike many aquatic birds, modern songbirds lose only a few feathers at a time, enabling them to stay aloft year-round for foraging or to escape predators. Microraptor’s shorter feathers appear in just a small patch on one of the dinosaur’s four wings — suggesting that the dinosaur molted sequentially, too, bird ecologist Yosef Kiat at the University of Haifa in Israel and colleagues report. All modern, adult birds molt at least once a year to replace old, damaged feathers, or to exchange their bright summer colors for drab winter camouflage. Genetic reconstructions of bird lineages have previously suggested that sequential molting has existed in birds for at least 70 million years, and was a trait of the common ancestor of all modern birds. But this is the first fossil evidence of a nonbird dinosaur exhibiting this behavior. Furthermore, the researchers say, the find would push back the estimated origins of sequential molting by 50 million years or so. Microraptor may have been one of the earliest flyers — depending on how one defines flying. Previous analyses have suggested that the dinosaur didn’t just glide from tree to tree, but was able to launch itself from the ground using its wings and back legs (SN: 10/28/16).

7-16-20 Covid-19 news: Scientists suggest young volunteers could test vaccines
The latest coronavirus news updated every day including coronavirus cases, the latest news, features and interviews from New Scientist and essential information about the covid-19 pandemic. Scientists suggest young, healthy people could test coronavirus vaccine candidates. A group of scientists are calling for young, healthy people to help accelerate vaccine research by volunteering to be exposed to the coronavirus in so-called “challenge trials.” The process might make it easier to see how effective different vaccine candidates are at providing protection against covid-19. Challenge trials have been used in the past to test vaccines, but they raise ethical questions about exposing healthy people to a disease for which we have no treatment to guarantee their safety. “If challenge trials can safely and effectively speed the vaccine development process, then there is a formidable presumption in favour of their use, which would require a very compelling ethical justification to overcome,” said an open letter signed by more than 100 prominent figures, including 15 Nobel laureates, which was sent to the US National Institutes of Health, a medical research organisation. UK security officials said information about coronavirus vaccines being developed in UK, US and Canadian organisations were targeted by Russian state-sponsored hackers. The UK’s National Cyber Security Centre said a group called APT29, which it said was “almost certainly” part of Russia’s intelligence services, were targeting research groups and drug companies. Phase III clinical trials of a coronavirus vaccine candidate developed by Chinese state-owned company Sinopharm have begun in the United Arab Emirates. The government of the UAE says 15,000 volunteers will be recruited in the country over three to six months. There are currently 23 coronavirus vaccine candidates in human trials, with three of them in or close to entering phase III, the final stage of testing.

7-16-20 Mental health toll of the coronavirus pandemic is now becoming clear
“Everything just went haywire. My moods were all over the place,” says Black actor and producer Dami Adeyeye, as he describes the perfect storm of living with his family under lockdown in the UK, watching police brutality in the US after the killing of George Floyd and seeing a UK government report showing that covid-19 is deadlier if you are from a black, Asian and minority ethnic (BAME) background. The 27-year-old Adeyeye has experienced depression in the past and isn’t alone in grappling with his mental health during the pandemic. Across the UK, a greater percentage of people from a BAME background said concerns over jobs, housing and money had damaged their mental health during the pandemic than white people, according to a survey of 14,000 adults with an existing mental health condition by the UK charity Mind. The research is part of a growing wave revealing the contours of the mental health crisis many experts predicted would come to pass because of the pandemic. Tom Dening at the University of Nottingham in the UK notes that covid-19 itself causes neuropsychiatric problems such as delirium. People treated for the illness in intensive care units are left with a higher risk of depression and anxiety, with around 40 per cent likely to have post-traumatic stress disorder (PTSD). That could eventually amount to tens of thousands of people in the UK, says Dening. Indirectly, the coronavirus has also had sweeping effects on the mental health of many. “The general population is suffering the effects of uncertainty, isolation, disruption of their social networks, fear of getting the illness, worrying about family, concerns about employment, education and money,” says Dening. Anxiety and depression levels rose in the UK and other countries in the run-up to covid-19 restrictions being implemented and have stayed above average during lockdowns.

7-15-20 Covid-19 news: US vaccine candidate set to enter final trials
The latest coronavirus news updated every day including coronavirus cases, the latest news, features and interviews from New Scientist and essential information about the covid-19 pandemic. Moderna coronavirus vaccine candidate deemed safe in first human trial A coronavirus vaccine candidate developed by US company Moderna and the US National Institutes of Health, a medical research organisation, is expected to become the first in the US to enter the final stage of clinical testing. Preliminary results suggested it is safe and able to induce an immune response against the virus. Moderna plans to enter phase III clinical trials on 27 July, and hopes to test the vaccine on 30,000 people, including those whose circumstances put them at high-risk of getting infected with the coronavirus. All 45 volunteers who received the experimental vaccine as part of the phase I trial for safety were found to have developed antibodies against the coronavirus in their blood, and none had serious side effects. These volunteers were younger adults, and preliminary tests on older adults are currently under review. “No matter how you slice this, this is good news,” US government health advisor Anthony Fauci told the Associated Press. There are currently 23 coronavirus vaccine candidates in clinical trials around the world. Face coverings will not be mandatory in offices in England, the UK’s health minister Matt Hancock told MPs on Tuesday. This followed the government’s earlier announcement that people in England will be required to wear face coverings in shops and supermarkets starting on 24 July. “The reason is that in offices you tend to spend a lot of time with the same people, and so the way to stop the spread of the virus in offices is to have social distancing, either two metres or one metre plus mitigations in place,” Hancock said on BBC Radio 4 today. Epidemiologist Rowland Kao at the University of Edinburgh says contact tracing is also more straightforward in offices. “Contact tracing is going to be vital in preventing a large outbreak,” says Kao, adding that reducing infections due to casual contact will play a big role in allowing contact tracing to work well. New Zealand must be prepared for new coronavirus outbreaks, the country’s prime minister Jacinda Ardern told journalists today. She said New Zealand would use local lockdowns to contain any new outbreaks, with nationwide lockdowns imposed if necessary. New Zealand’s strategy is aimed at completely eliminating the virus from the country.

7-15-20 The secret power of the tequila plant that could help feed the world
Agave uses a turbocharged version of photosynthesis that works in even the driest spots. As climate change threatens our food supply, the race is on to harness its power in more resilient crops. CLOSE to the town of Ayr in Queensland, Australia, there is a field of unusual crops. The plants are a silvery shade of teal, with long fleshy leaves splaying out in all directions like thin, serrated knives. When Daniel Tan walks among them, the tallest stand two heads taller than him. There are thousands of these blue agaves here. Best known as the raw ingredient needed to make the fiery spirit tequila, they are more commonly found in Mexico than on Australia’s Pacific coast. Yet for Tan, a researcher at the University of Sydney, they are part of an impending global revolution. We certainly need one. Plants provide us with food, fuel, building materials and natural beauty, all while locking away untold volumes of carbon dioxide that would otherwise crank up the planet’s thermostat. But as Earth’s population and temperature continue to rise, we will need more from our green allies. Our food requirements alone will be eye-watering. In 30 years, we may need to produce about 50 per cent more food to feed nearly 10 billion people – just as global warming is predicted to slash the yield of many major grain crops. Researchers like Tan are looking to a radical solution, involving plants’ not-so-secret weapon: photosynthesis. We ultimately depend on this process, by which plants store energy from sunlight for everything that nourishes us. So it might seem odd to say it is scandalously inefficient. But it is – for most species. By understanding the secrets of plants such as agave with supercharged versions of photosynthesis, the hope is we can create a greener, cleaner, more secure future for us all. Photosynthesis captures the power of sunlight to convert CO2 and water into sugars, which plants then use to fuel their growth. It is a wondrous thing. Yet despite the fact that evolution has had at least 2 billion years to perfect it, we have to content ourselves with the wonder that it is done at all, not that it is done well. The maximum conversion efficiency of solar energy to biomass in most plants is a disappointing 4.6 per cent.

7-15-20 How children in the UK are coping with the coronavirus lockdown
SINCE lockdown began in the UK, Cathy Creswell at the University of Oxford and her colleagues have been surveying thousands of families to find out how they are affected by the covid-19 pandemic. The Co-SPACE Study has now published its first findings from a longitudinal study that questioned people over several months. What has your survey of families during lockdown shown? More than 10,000 people have now taken part. Our first report was at the beginning of April, looking at the first 1500 people. What we saw then has remained pretty consistent all the way through, which was that families were certainly feeling under a great deal of stress. Parents were particularly struggling with balancing work and childcare, and the most common concern they were reporting was about their children’s emotional wellbeing. We could see that very early on, but we couldn’t obviously see the direct impact that lockdown had. Now you have data over a longer period, how have young people changed during the lockdown?From our longitudinal data in June, that was from about 3000 people, so far we are seeing significant increases in behavioural problems, emotional symptoms and attention and impulsivity problems in primary school age children [age 4 to 10]. In secondary school age students [age 11 to 16], based on parent reports, we actually saw a reduction in emotional symptoms over time and no change in behavioural problems. We only have a small subset of teenagers who are self-reporting, but again they weren’t reporting an increase in difficulties either. We need to keep looking at it carefully, but it does fit with what many families have told us, which is that, for many young people of secondary school age, not having the pressures of school does seem to have brought some benefits in terms of their mental health.

7-15-20 Children missing out on vaccinations due to virus
The number of children worldwide getting life-saving vaccinations has declined amid the pandemic, the UN and WHO say. The drop in routine immunisations could cause more harm than Covid-19 itself, the World Health Organization head warns. US pharmaceutical company Moderna says it is entering final testing phase for its coronavirus vaccine. Phase one testing has proved safe and provoked an immune response, it says. UK Health Minister Matt Hancock says masks will not be made compulsory in offices. Hong Kong is bringing in strict new measures to counteract a virus surge, including closing all bars. NZ PM Jacinda Ardern says they must prepare for new outbreaks, as the virus "explodes" globally. Globally, there have been 13.3m confirmed cases since the outbreak began, and 578,000 deaths.

7-15-20 What are face covering rules in England and why did the policy change?
Since the start of the coronavirus pandemic, face coverings and masks have become ubiquitous in some Asian countries, but the UK public has generally been more reluctant to adopt them. Now the law is about to change. What are the new rules? People will have to wear face coverings inside shops and supermarkets in England from 24 July, unless they have certain disabilities or are under the age of 11. They already have to wear coverings while using public transport and in hospitals. Although store workers aren’t expected to enforce the rule, people who break it could face a fine of up to £100 if police get involved. This brings England more into line with restrictions in Scotland and many other European countries. At the start of the covid-19 pandemic, many scientists said there was not enough evidence to support their use. There were two big concerns: they could encourage people to take risks such as getting closer to others, and as masks still let in some virus, overall exposure could increase. There were also fears that the public would buy medical-grade masks when hospitals were already going short. What has changed? UK prime minister Boris Johnson said earlier this week: “The scientific evidence of face coverings, and the importance of stopping aerosol droplets… that’s been growing.” His spokespeople haven’t clarified which studies he was referring to, but noted that the World Health Organization recently changed its advice on face coverings, saying new information showed they could provide “a barrier for potentially infectious droplets”. We still don’t have the best kind of medical evidence: large randomised trials showing that people who cover their face are less likely to catch coronavirus than those who don’t. But other kinds of evidence have been emerging over the past few months. For instance, a study last month showed that in a coronavirus outbreak on a US aircraft carrier, those who wore face coverings had a lower chance of infection than others, at 56 per cent compared with 81 per cent. There is also clear evidence that face coverings stop people from spraying droplets into the air when talking. The UK’s Royal Society recently reviewed all the evidence and concluded that face coverings are effective for protecting both the wearer and those around them from transmission in either direction, as long as the covering is of good quality.

7-15-20 TAlzheimer’s disease may start in the gut and spread to the brain
Alzheimer’s disease may be caused by the abnormal build-up of a protein in the gut that gradually spreads to the brain, according to research in mice. In people with Alzheimer’s disease, a protein called beta-amyloid clumps together in the brain to form plaques that disrupt normal brain processes. Beta-amyloid deposits have also been found in the guts of people who died with the condition, but they have been largely overlooked. John Rudd at the Chinese University of Hong Kong and his colleagues wondered if the beta-amyloid found in the brains of people with Alzheimer’s disease may originally have come from their guts. To test this idea, the researchers injected small amounts of the protein into the gastrointestinal tracts of mice. The beta-amyloid had a fluorescent marker attached so they could see where it ended up. The protein was rapidly taken up by the complex cluster of neurons that line the guts, which are sometimes referred to as the body’s “second brain”. One year later, the beta-amyloid had migrated up the vagus nerve, which connects the gut and the brain, and into the brains of the mice. After the beta-amyloid entered the brains, the mice displayed short-term and long-term memory problems reminiscent of those seen in people with Alzheimer’s disease. The exact role beta-amyloid in the brain plays in causing Alzheimer’s symptoms is still unclear, but if the protein is migrating from the gut in people, it may be possible to prevent or delay the condition by removing beta-amyloid before it spreads to the brain, says Rudd. “Even if only some of the beta-amyloid load in the brain comes from the gastrointestinal tract, stopping or slowing that could give people an extra one or two years,” he says.

7-15-20 Fertility rate: 'Jaw-dropping' global crash in children being born
The world is ill-prepared for the global crash in children being born which is set to have a "jaw-dropping" impact on societies, say researchers. Falling fertility rates mean nearly every country could have shrinking populations by the end of the century. And 23 nations - including Spain and Japan - are expected to see their populations halve by 2100. Countries will also age dramatically, with as many people turning 80 as there are being born. The fertility rate - the average number of children a woman gives birth to - is falling. If the number falls below approximately 2.1, then the size of the population starts to fall. In 1950, women were having an average of 4.7 children in their lifetime. Researchers at the University of Washington's Institute for Health Metrics and Evaluation showed the global fertility rate nearly halved to 2.4 in 2017 - and their study, published in the Lancet, projects it will fall below 1.7 by 2100. As a result, the researchers expect the number of people on the planet to peak at 9.7 billion around 2064, before falling down to 8.8 billion by the end of the century. "That's a pretty big thing; most of the world is transitioning into natural population decline," researcher Prof Christopher Murray told the BBC. "I think it's incredibly hard to think this through and recognise how big a thing this is; it's extraordinary, we'll have to reorganise societies. It has nothing to do with sperm counts or the usual things that come to mind when discussing fertility. Instead it is being driven by more women in education and work, as well as greater access to contraception, leading to women choosing to have fewer children. In many ways, falling fertility rates are a success story. Japan's population is projected to fall from a peak of 128 million in 2017 to less than 53 million by the end of the century. Italy is expected to see an equally dramatic population crash from 61 million to 28 million over the same timeframe. They are two of 23 countries - which also include Spain, Portugal, Thailand and South Korea - expected to see their population more than halve.

7-15-20 How changing the way you sit could add years to your life
Our bodies evolved to take rest breaks, but sitting on chairs and couches can cause long-term damage. Here’s how to change the way you sit and boost your health. ANOTHER blistering afternoon in northern Tanzania, another high-stakes game of musical chairs. Stumbling back into camp to escape the sun, desperate for a seat, we glanced at each other and then at the single unoccupied camp chair. In the other, grinning, sat Onawasi, a respected elder with a mischievous bent. He seemed to be enjoying this. We were spending our summer with the Hadza community, one of the last populations of hunter-gatherers on the planet. Hadza men and women manage to avoid heart disease and other diseases of the more industrialised world, and we wanted to understand why. Our small research team had come in two Land Cruisers loaded with tech to measure every movement made and calorie burned as Hadza men and women scoured the landscape every day for wild game, honey, tubers and berries. After a long morning, we felt drained by the inescapable heat and humidity. All we wanted to do was sit. Onawasi seemed to feel the same way. He had spent the morning hunting, and certainly deserved the chair more than we did. But this was getting out of hand. Our precious camp chairs that we took into the bush despite their weight were Hadza magnets. Every visitor to our little research area seemed drawn to them like moths to a porch light. We knew we had a lot to learn from the Hadza about staying physically active. It turns out they also had something important to teach us about resting. Together, over the next 10 years, we would come to understand why chairs are so irresistible, and why they seem to make us ill. In a simpler time, before Brexit, Donald Trump was US president or covid-19, way back in 2012, the world was alerted to a new and insidious danger, an invisible pandemic. I-Min Lee, an epidemiologist at Harvard University, analysed mortality data from heart disease, diabetes and cancer and found a common culprit: sitting. In a landmark paper in The Lancet, Lee and her colleagues concluded that prolonged periods of inactivity killed more than 5 million people every year globally, making the health risks “similar to… smoking and obesity”. In the media, sitting became the new smoking. Even more alarming for those of us who spend our lives in front of a screen, exercise doesn’t fully undo the dangers of sitting. Long hours spent in a chair or on the sofa steal years from our lives, even if we hit the gym religiously. Sitting is different, and maybe worse, than just a lack of exercise.

7-15-20 Competitive hot dog eaters may be nearing humans’ max eating speed
A new analysis sets the limit at about eight franks per minute. In the race to scarf down as many hot dogs as possible in 10 minutes, competitive eaters may have a limit: 83 franks, buns and all. That’s according to an analysis of nearly 40 years of the storied Nathan’s Famous Coney Island Hot Dog Eating Contest. Started in the 1970s in New York City, the contest now is a televised international event. The current record of 75 hot dogs — set in July — is an improvement over the competition’s early days, where winners were crowned after eating a measly dozen or so dogs. James Smoliga, a physiologist at High Point University in North Carolina, was watching the hot dog eating contest in 2019 when an idea struck him: Could he apply the mathematical equations used to estimate the limits of athletic performance to feats of gluttony? Smoliga dug into the hot dog record books. Based on data from 152 competitors over 39 years, he calculated an upper hot dog limit of about 83 hot dogs in 10 minutes. That translates to a consumption rate of about 832 grams per minute (and more than 23,000 calories total), Smoliga reports online July 15 in Biology Letters. Whether or not competitive eaters ever reach that limit, the scale of improvement “completely dwarfs other athletic achievements,” Smoliga says. Record performances in sports like track and field have improved about 40 percent since record keeping began, whereas hot dog eating prowess has improved approximately 700 percent. Humans even hold their own, pound for pound, against other meat-eating animals. When normalized for body mass, competitive hot dog eaters have a consumption rate that bests that of grizzly bears and coyotes, Smoliga reports, though wolves lead the pack. Eating large quantities of food quickly can be a useful strategy for carnivores when food is scarce. And Smoliga says humans’ capacity for a relatively high consumption rate may have proved useful at some point in our evolutionary past. But nowadays, inhaling six or seven hot dogs a minute for 10 minutes mostly leads to digestive problems, and if you’re lucky, the coveted Mustard Belt of champions.

7-14-20 Remdesivir may work even better against COVID-19 than we thought
Data suggest antiviral can cut death risk in people, and stop virus growth in cells and mice. Remdesivir can not only speed recovery, but may cut the chance of dying of COVID-19, preliminary data released by the drug’s maker suggest. Among severely sick people, the antiviral drug reduced the risk of dying by 62 percent compared with standard care, the Foster City, Calif., drugmaker Gilead Sciences Inc. reported at a virtual scientific conference on July 10. Hospitalized people taking remdesivir had a 7.4 percent death rate two weeks after treatment started, while those not taking the drug had a 12.5 percent mortality rate, the company reported. The new data, along with another newly reported study in mice and human cells, add to evidence that remdesivir is effective as a treatment for the coronavirus. In a previous clinical trial run by the U.S. National Institute of Allergy and Infectious Diseases, the drug shortened hospital stays by about four days, and showed a trend toward lower death rates that was not statistically meaningful (SN: 4/29/20). The new data come from two studies: a Phase III study of 312 patients, which was aimed at studying the efficacy of the drug, and a study that retrospectively examined the effect of the drug in 818 people with COVID-19. The company also found that 74.4 percent of people taking remdesivir recovered by day 14, compared with 59 percent of those getting standard care. Gilead also reported data on remdesivir given for “compassionate use” to children and pregnant women, meaning no other treatment was available and the individuals could not join a clinical trial. Of 77 pediatric patients taking remdesivir, 73 percent, or 56 kids, were released from the hospital by day 28. Twelve percent remained hospitalized but breathing on their own without needing extra oxygen, and 4 percent died. Among 86 infected women, the drug helped lessen the amount of extra oxygen needed in 96 percent of pregnant women and 89 percent of women who had newly given birth.

7-14-20 Coronavirus: Why attitudes to masks have changed around the world
In the past few days, both US President Donald Trump and UK Prime Minister Boris Johnson have been seen wearing masks in public for the first time. It's a dramatic turnaround - Mr Trump previously mocked others for wearing masks, and suggested some might wear such personal protective equipment to show their disapproval of him, even after the US Centers for Disease Control recommended face coverings. Meanwhile, the UK government was initially reluctant to advise the general public to wear face coverings, even as other countries in Europe did. It introduced rules requiring people to wear face coverings on public transport in June, and now says people in England must wear face coverings in shops or face a fine. Globally, many authorities - including the World Health Organization (WHO) - initially suggested that masks were not effective in preventing the spread of the coronavirus. However, they are now recommending face coverings in indoor spaces, and many governments have even made them mandatory. What's changed - and why? The number of governments recommending face coverings has gone up significantly over the past six months. As of mid-March, about 10 countries had policies recommending face coverings - now more than 130 countries and 20 US states do, says Masks4All, an activist group of researchers that advocates the use of homemade masks during the pandemic. Some studies also suggest that people's attitudes have changed. "Countries with no previous history of wearing face masks and coverings amongst the general public rapidly adopted usage such as in Italy (83.4%), the United States (65.8%) and Spain (63.8%)," says a report by the Royal Society - one of the leading science bodies in the UK. The changes appear to be partly due to a better understanding of how Covid-19 spreads.

7-14-20 A bad UK winter could cause 120,000 hospital deaths linked to covid-19
A particularly “challenging” winter could bring a second wave of coronavirus infections that leads to around 120,000 deaths in UK hospitals, twice as many as the first wave, according to an estimate of a reasonable worst-case scenario. Assuming people acted as though the coronavirus were no longer a threat, the average number of people one person with the virus goes on to infect – known as the R number – could rise from the current estimate of between 0.7 and 0.9 to 1.7 by September, say scientists behind the report, which was requested by the UK government’s chief scientific officer, Patrick Vallance. This would lead to a second wave of infections, peaking in January and February next year. “A peak of coronavirus infection in the winter could be more serious than the one we’ve just been through,” report chair Stephen Holgate at the University of Southampton, UK, told a press briefing. “We’re anticipating the worst, which is the best we can do.” Holgate is one of 37 scientists behind the Academy of Medical Sciences report. The group considered what might happen if people went back to a typical way of life, and didn’t factor in the use of new medicines, including dexamethasone, or a potential vaccine. But members also assumed that the UK government would step in to prevent the R number reaching 3, as it did back in March. To build a picture of what might happen, the team considered the known impact of covid-19 on healthcare resources, combined with that of flu and other seasonal infections, during a time when health services are often overstretched. The researchers also looked to the experiences of other countries, particularly what happened to the R number in US states that have recently eased lockdown restrictions.

7-14-20 Aztec palace's remains uncovered off Mexico City's main Zócalo plaza
The remains of an ancient Aztec palace have been discovered under a stately building in Mexico City. During renovations at the building off the capital's central Zócalo plaza, workers found basalt slab floors. The floors were part of an open space in the palace of Aztec ruler Axayácatl, Mexico's National Institute of Anthropology and History (INAH) said. The palace was also used as the home of Spanish conquistador Hernán Cortés after the fall of the Aztec empire. Excavators have found evidence of the home Cortés had at the palace site. Archaeologists say it is likely to have reused materials from Axayácatl's palace - which, like other sacred Aztec buildings, was razed by the Spanish conquistadors. Axayácatl reigned between 1469 and 1481 and was the father of Montezuma, one of the empire's last rulers. "Below the subflooring of the house of Cortés, more than three metres deep, the remains of another floor of basalt slabs, but from pre-Hispanic times, were detected," INAH said. "Given its characteristics, the specialists deduced that it was part of an open space in the former palace of Axayácatl, probably a courtyard." Cortés arrived in what is now Mexico in 1518 as commander of a mission to explore the region - rumoured among Europeans to hold great wealth - for Spanish colonisation. He and his men laid siege to the Aztec capital Tenochtitlán in 1521. When the city surrendered, the Spanish colonisers destroyed it. The building which stands on the site now - the Nacional Monte de Piedad - is a historic pawnshop that was built in 1755.

7-14-20 This 1.4-million-year-old hand ax adds to Homo erectus’ known toolkit
East African find shows ancient hominids crafted a range of simple and more complex tools. Homo erectus, a possible direct ancestor of people today, crafted a surprisingly cutting-edge tool out of a hippo’s leg bone around 1.4 million years ago, researchers say. This find is a rare example of an ancient type of hand ax made out of bone rather than stone, reports a team led by paleoanthropologists Katsuhiro Sano of Tohoku University in Sendai, Japan, and Gen Suwa of the University of Tokyo. The tool was discovered at Ethiopia’s Konso-Gardula site (SN: 1/2/93), which has produced stone tools and fossils attributed to H. erectus. Along with a variety of stone tools now recognized at several East African sites (SN: 3/4/20), the bone hand ax “suggests that Homo erectus technology was more sophisticated and versatile than we had thought,” Suwa says. Taken together, these finds show that, perhaps several hundred thousand years earlier than previously known, the H. erectus toolkit consisted of items requiring a series of precise operations to manufacture, such as stone and bone hand axes, as well as simpler tools that could be made relatively quickly. H. erectus at Konso-Gardula modified a chunk of a hippo’s leg bone so that a roughly 13-centimeter-long oval piece with a sharp edge near the tip could be struck off in one blow from a stone or bone hammer, the researchers conclude July 13 in the Proceedings of the National Academy of Sciences. One or more toolmakers then chipped off bone from the artifact to render its final shape. Signs of wear indicate that the hand ax was used in cutting or sawing activities. Only one other bone hand ax of comparable age has been found. That roughly 1.3- to 1.6-million-year-old implement, from Tanzania’s Olduvai Gorge, contains fewer signs of chipping and shaping than the Konso-Gardula hand ax does, the scientists say.

7-13-20 Coronavirus immunity: Can you catch it twice?
A new study of people who have caught and recovered from coronavirus raises the prospect that immunity to the virus may be short-lived. Scientists at King's College London studied how the body naturally fights off the virus by making antibodies, and how long these last in the weeks and months after recovery. Almost all of the 96 people in the study had detectable antibodies that could neutralise and stop coronavirus. But levels began to wane over the three months of the study. Our immune system is the body's defence against infection and it comes in two parts. The first is always ready to go and leaps into action as soon as any foreign invader is detected in the body. It is known as the innate immune response and includes the release of chemicals that cause inflammation and white blood cells that can destroy infected cells. But this system is not specific to coronavirus. It will not learn and it will not give you immunity to the coronavirus. Instead you need the adaptive immune response. This includes cells that produce targeted antibodies that can stick to the virus in order to stop it and T cells that can attack just the cells infected with the virus, called the cellular response. This takes time - studies suggest it takes around 10 days to start making antibodies that can target the coronavirus and the sickest patients develop the strongest immune response. If the adaptive immune response is powerful enough, then it could leave a lasting memory of the infection that will give protection in the future. It is not known if people who have only mild symptoms, or none at all, will develop a sufficient adaptive immune response. Understanding of the role of T-cells is still developing. But a recent study found people testing negative for coronavirus antibodies may still have some immunity. For every person testing positive for antibodies, it was found two had specific T-cells which identify and destroy infected cells. The immune system's memory is rather like our own - it remembers some infections clearly, but has a habit of forgetting others.

7-13-20 How the covid-19 pandemic is making malaria and HIV more deadly
The coronavirus pandemic’s effects on healthcare for tuberculosis (TB), malaria and HIV could lead to deaths of an order of magnitude similar to those from covid-19 itself in some parts of the world, a new analysis finds. In a worst-case scenario, malaria deaths were projected to rise by 36 per cent over the next five years as malaria net campaigns are affected in the sub-Saharan countries where the disease is most prevalent. Over the same period, deaths from TB could rise by a fifth as new cases go undetected and deaths from HIV by a tenth as access to life-saving drugs is hit. Although the team behind the research doesn’t give absolute figures, such extreme disruption would lead to hundreds of thousands of extra deaths each year. For countries with high HIV, TB and malaria rates and weak healthcare systems, “this is right up there in terms of a major priority for how we’re going to combat and minimise the entire risk that the covid-19 pandemic brings”, says Timothy Hallett at Imperial College London, who led the study. “It’s not piddly in comparison to covid-19, it’s absolutely a priority.” The new warning is one part of emerging evidence revealing the death and hardship that covid-19 could wreak because of its impact on healthcare services vital for preventing and treating other major epidemics. Malaria, TB and HIV kill around 2.6 million people a year combined. The analysis came up with four hypothetical scenarios, based on different interventions in low and middle-income countries. Hallett points out that these scenarios may not come to pass and it is hard to predict how the covid-19 pandemic will unfold. However, recent history holds precedent for possible knock-on effects. The research was inspired by what was seen during the Ebola outbreak in West Africa between 2014 and 2016, where around half of the deaths were from other diseases as healthcare systems buckled.

7-13-20 Covid-19 news: Face coverings may become mandatory in shops in England
The latest coronavirus news updated every day including coronavirus cases, the latest news, features and interviews from New Scientist and essential information about the covid-19 pandemic. People may soon have to wear face coverings in shops in England, says Boris Johnson. Antibodies against the coronavirus in a person’s blood may peak about three weeks after symptoms first appear, then decline rapidly, according to a preliminary study that hasn’t been peer-reviewed. The study, led by researchers at King’s College London, monitored antibody levels in the blood of 65 covid-19 patients and 31 healthcare workers who’d had a positive coronavirus antibody test, between March and June. Three months after antibody levels peaked, only 17 per cent of people tested still had an antibody response with the same level of potency against the virus, the study found. In some people, antibody levels fell 23-fold over the same time period. One concern is that a short-lived antibody response might limit the ability of a coronavirus vaccine to induce immunity. But alongside antibodies, there’s evidence that other parts of the body’s immune system – such as immune cells called T-cells – may also contribute to immunity against the coronavirus and could be harnessed by a future vaccine. Scotland reported no deaths from covid-19 today for the fifth consecutive day, the nation’s first minister Nicola Sturgeon announced during a press briefing. But there are concerns that people travelling across the border from England may make it difficult for Scotland to achieve full elimination of the virus. Mexico saw record daily numbers of new coronavirus cases last week and now has the fourth-highest number of recorded deaths from covid-19, after the US, Brazil and the UK. There have been more than 299,000 coronavirus cases and more than 35,000 deaths from covid-19 in Mexico since the pandemic began. Officials in Mexico say these numbers are probably a significant underestimate, because of a limited testing capacity.

7-13-20 Damaged human lungs revived for transplant by connecting them to a pig
Donated lungs that are too damaged to be used in transplants have been revived after being connected to the blood supply of a live pig. The technique could potentially triple the number of lungs available for transplant, say the researchers behind the work. As soon as someone dies, their lungs begin to deteriorate. If the person has chosen to donate their lungs, the race is on to get the organs to a recipient as soon as possible. “The lung is very delicate,” says James Fildes at the University of Manchester, UK, who wasn’t involved in the work. “It is one of the most difficult organs to preserve.” Most donated lungs are only outside the body for a matter of hours. But even then, the majority will have deteriorated so much that they cannot safely be used for transplantation. Only around 28 per cent of donated lungs meet the criteria for transplantation in the US, according to the American Lung Association. Doctors can attempt to “recondition” damaged lungs using ex vivo lung perfusion (EVLP) devices that pump oxygenated air and fluid through the lungs, but even then, many fail, says Gordana Vunjak-Novakovic at Columbia University in New York. Vunjak-Novakovic and her colleagues wondered whether the lungs might do better if they were connected to a living body, with other working organs able to deliver nutrients and remove harmful substances. To find out, the team obtained lungs that had been rejected for transplantation from six human donors, both single lungs and pairs. One lung had failed even after 5 hours on an EVLP device, and had been outside the body for around 24 hours before the team received it. The team connected each lung to the circulatory system of an anaesthetised pig for 24 hours, with tubes feeding the blood vessels of the human lung from those in the neck of the pig. At the same time, the lung was pumped with air using a ventilator. Immunosuppressant drugs, which prevent “foreign” tissues from being rejected by the immune system, were added to the circulatory system, infiltrating both the pig and the human lung.

7-13-20 Lab-grown sperm could let infertile men have gene-edited children
The first reliable way of isolating sperm stem cells from the testes and growing them outside the body could help infertile men have genetic children of their own. A few teams have claimed to have isolated sperm stem cells before, but haven’t been able to repeat the results. “The general feeling is that there is no reliable method,” says Miles Wilkinson at the University of California, San Diego. His team has been studying the cells in the testes. By sequencing the RNA in single cells, they identified different cell types and found a marker protein on the surface of the stem cells that give rise to sperm, known as spermatogonial stem cells. Using this marker, they isolated these cells from biopsies of testes. The resulting sets of cells don’t consist solely of sperm stem cells, but are far more highly enriched in them than anyone has achieved before. The team found a way to keep these cells alive and growing for at least a month. The key is blocking something called the ATK pathway. In mice, blocking ATK makes stem cells differentiate, but Wilkinson found that the opposite is true in humans. “I think this is a really big step forward in our field,” says Ans van Pelt at the University of Amsterdam in the Netherlands, who wasn’t involved in the study. This could lead to treatments for those who have mutations that stop these stem cells turning into sperm. For example, CRISPR gene editing has been used to correct these mutations in mouse sperm stem cells, which have restored fertility in mice once the stem cells were put back into the same animals. These stem cells have also been used to produce sperm outside the body for in vitro fertilisation (IVF). The biggest obstacle to doing this in people is the lack of a reliable way of isolating human sperm stem cells. Wilkinson says his team is focused on the basic science rather than the clinical applications, but that it would be feasible to gene-edit the stem cells.

7-13-20 America the unhealthy: Inequality kills
Smoking, poor diet, lack of exercise? Yes, but that's not all. A researcher tells us what really hurts U.S. life expectancy. n the United States, life expectancy at birth, a common way to measure a country's health, rose steadily for decades — it was 69.9 years for a baby born in 1959 and 79.1 years for one born in 2014. Then it dropped for three consecutive years. That did not surprise Stephen Bezruchka, a University of Washington health services researcher who wrote about the deterioration of U.S. health status, as compared with other nations, in the 2012 Annual Review of Public Health. Nearly two decades ago, Bezruchka came up with the idea of a "Health Olympics," in which the nations of the world compete on life expectancy. Japan is the current champion, with a life expectancy of 84.5 years, far ahead of the U.S. Earlier this year, new data from the Centers for Disease Control and Prevention showed that U.S. life expectancy ticked up slightly — by 0.1 year — in 2018. (There are several ways to estimate life expectancy, which yield slightly different numbers. But the trends remain consistent.) We checked in with Bezruchka, who is also a medical doctor, for an update on his perspective. Have we turned the corner? The discussion has been edited for length and clarity.

  1. How are we doing in the Health Olympics? If the race is how long we will live, the most recent data published last December in the United Nations Human Development Report, which ranks countries by length of life, puts us at number 36, meaning that 35 nations have longer lives than the U.S.
  2. A baby born in the U.S. in 2018 has a life expectancy of 78.9 years. Is life expectancy the most important indicator of a nation's health? It's the easiest one for most people to understand. I think infant mortality — death under the age of 1 — may be a better indicator. But since everybody that you talk to has survived infancy, that's not so meaningful to them. It's the same with child mortality.
  3. The U.S. has a child mortality problem? In the U.S., the child mortality rate — that is, the proportion of children who die before their fifth birthday per 1,000 live births — is 6. Compare that with Slovenia's child mortality rate of 2.6, which shows what is achievable.
  4. How does life expectancy for whites in the U.S. compare with that of other racial and ethnic groups? Do you see the same pattern in other countries? Hispanic or Latinx life expectancy in the U.S. is a little better than that of non-Latinx whites. African-American life expectancy is lower than for whites although the gap has been narrowing. The difference is now about three years, and that has come down from much higher.
  5. In the 1950s, the U.S. was one of the top 10 nations for life expectancy. What happened? We have changed from a country that, in the 1950s, believed in economic justice. We had high tax rates on the rich, and we had welfare programs for other people. But we have changed from a community focus, or a collective focus, to one in which today we have to pursue our health as individuals.
  6. Inequality kills? The higher the income gap between the rich and the poor, the more stress we feel if we're not on top. There are studies in the U.S. showing, at the county level, that if you have a big gap between the rich and poor and you have high incomes in a county, you're going to have more mass shootings, defined as four or more victims.
  7. Do your fellow doctors agree with you that inequality is to blame for America's poor health status? I think that has changed over time. When I first presented this at a conference of doctors in 1995, it made sense to some, and to some it was nonsense. About 10 years ago, these ideas became more acceptable. More doctors recognize our poor health status and some know it's due to more than personal behavior. We have the health of a middle-income or poor country, in many respects.
  8. If income inequality is the culprit, does that mean well-off Americans with good health habits are protected from our nation's relatively short life expectancy? There are a couple of ways to look at this. Yes, richer people are going to have longer lives than poorer people. But studies comparing richer people in Europe versus richer people in the United States show longer life expectancy among the richer in Europe than here.

7-13-20 Coronavirus: Llamas provide key to immune therapy
As Fifi the llama munches on grass on a pasture in Reading, her immune system has provided the template for a coronavirus treatment breakthrough. Scientists from the UK's Rosalind Franklin Institute have used Fifi's specially evolved antibodies to make an immune-boosting therapy. The resulting llama-based, Covid-specific "antibody cocktail" could enter clinical trials within months. The development is published in Nature Structural and Molecular Biology. It involves "engineering" llama antibodies, which are relatively small, and much more simply structured than the antibodies in our own blood. That size and structure means they can be "redesigned" in the lab. Professor James Naismith, director of the Rosalind Franklin Institute - and the lead researcher - described the technique as akin to cutting a key that fits the coronavirus lock. "With the llama's antibodies, we have keys that don't quite fit - they'll go into the lock but won't turn all the way round," he said. "So we take that key and use molecular biology to polish bits of it, until we've cut a key that fits." Antibodies are part of what is known as the adaptive immune system; they are molecules that essentially morph in response to an invading virus or bacteria. "Then if you get re-infected," explained Prof Naismith, "your body looks for any [virus particles] with antibodies stuck around them and destroys them." This type of immune therapy essentially boosts a sick person's immune system with antibodies which have already adapted to the virus. There is already evidence that antibody-rich blood, taken from people who have recently recovered from the coronavirus, could be used as a treatment. But the key trick with this llama-derived antibody therapy is that the scientists can produce coronavirus-specific antibodies to order. The small re-engineered part of the llama antibody is also known as a nanobody, said Prof Naismith. "In the lab, we can make nanobodies that kill the live virus extremely well - better than almost anything we've seen," he added. "They're incredibly good at killing the virus in culture."

7-13-20 A bacterial toxin enables the first mitochondrial gene editor
Researchers can now change DNA in a previously inaccessible organelle. Bacterial weaponry has an unexpected use in human cells. A protein secreted by bacteria to kill other microbes has been re-engineered to tweak DNA inaccessible to other gene editors, scientists report online July 8 in Nature. The advance paves the way for one day fixing mutations in mitochondria. Those energy-producing organelles are inherited from a mother and have their own DNA, distinct from the genetic information — from both parents — that’s stored in a cell’s nucleus. “I’ve been a mitochondrial biologist for 25 years, and I view this as an extremely important advance for the field,” says Vamsi Mootha, a Howard Hughes Medical Institute investigator at Massachusetts General Hospital in Boston and the Broad Institute of MIT and Harvard. Mutations in mitochondrial DNA cause over 150 distinct syndromes and affect 1,000 to 4,000 children born in the United States each year. There are no cures for these diseases and currently, the only way to prevent a child from inheriting dysfunctional mitochondria is a controversial “three-parent baby” method (SN: 12/14/16). This in vitro fertilization technique requires mitochondria from a donor egg, in addition to genetic information from a mother and father. An approach for developing cures for genetic diseases is gene editing, a technique that makes changes directly to DNA. Perhaps the most famous gene editor, CRISPR/Cas9 is a molecular scissors that cuts DNA. Researchers have also previously used molecules called TALENs to cut up mitochondrial DNA in mice and eliminate defective organelles (SN: 4/23/15). A newer technology, called base editors, bolts proteins that can change DNA bases — represented by the letters A, C, G and T — to a modified version of the CRISPR-associated protein Cas9 (SN: 10/25/17). These editors chemically transform one DNA base into another, essentially fixing typos that can lead to disease. This technology, however, works only on DNA in nuclei, not mitochondria.

7-13-20 India's growing Covid-19 waste challenges workers
India's Covid-19 caseload is rising, and people have been urged to wear face masks even when they are outdoors. But the directive has created another problem - there is no system of safely discarding Covid-19 waste. Rubbish collectors have complained that people are mixing used gloves and masks with other waste, and it's putting the waste collectors lives at risk. Workers say that they need training and safety gear to properly handle hazardous waste.

7-11-20 The struggle to keep India's Covid-19 patients breathing
In April, a sprawling hospital in a village in western India was directed to quickly set up an additional 200-bed ward for coronavirus patients. Infections were surging in Maharashtra state, where the 934-bed Kasturba Hospital is located in Sevagram village, some 50 miles south of the city of Nagpur. The busy not-for-profit hospital was already getting a million patient visits every year. Most of the Covid beds - including the 30 in critical care - needed piped oxygen supply. Over the next few weeks, the hospital spent $40,000 (£32,000), to connect a bank of cylinders to the new beds using copper pipes. "It was a huge challenge," Dr SP Kalantri, medical superintendent of the hospital, told me. "Ideally you'd need to plan and execute well ahead to create additional beds with access to piped oxygen. Oxygen is the key to survival for coronavirus patients." Some 15% of Covid-19 patients see rapid lung failure and require help with breathing, according to the World Health Organisation (WHO). Some patients appear in no evident respiratory distress, but are found to have dangerously low oxygen levels - a condition called silent hypoxia. A fraction of critically ill patients require a ventilator. "Demand for high-flow oxygen has shot through the roof after the pandemic," Dr Muzzafal Lakdawala, who runs a Mumbai-based rock concert venue-turned-600-bed Covid facility with its own oxygen tank, told me. The WHO estimates that with a million new Covid-19 infections a week, the world will require some 620,000 cubic meters of oxygen a day, or 88,000 large cylinders. Some 80% of the market is owned by a handful of companies, and demand in many countries is outstripping supplies, it says. With more than 800,000 reported infections and rising, demand for oxygen has also risen in India. Hospitals and care centres are consuming up to 1,300 tonnes of oxygen every day, compared to 900 tonnes before the pandemic.

7-11-20 Iron Age 'mystery' murder victim found in Wendover
An Iron Age skeleton with his hands bound has been discovered by HS2 project archaeologists, who believe he may be a murder victim. The remains of the 2,000-year-old adult male were found face down at Wellwick Farm near Wendover in Buckinghamshire. Project archaeologist Dr Rachel Wood described the death as "a mystery" and hopes further analysis will shed light on the "potentially gruesome" find. A Stonehenge-style wooden formation and Roman burial have also been discovered. They are among a number of finds ranging from the Neolithic Age to the Medieval period unearthed ahead of construction work for the 225mph (362 km/h) rail line. Dr Wood, who works for Fusion JV, said: "Discovering a site showing human activity spanning 4,000 years came as a bit of a surprise to us." A large Neolithic circular monument of wooden posts 65m (213 ft) in diameter and aligned with the winter solstice, "similar to Stonehenge", was uncovered. The site also has evidence of domestic occupation during the Bronze to Iron Ages (3000BC to AD43), including a roundhouse and animal pits. During the Roman era it was used for burials and a "high status" skeleton buried in an "expensive" lead coffin was unearthed. Dr Wood said the fascinating thing about the site was its "persistent use over centuries for the burial of specific, high status people". The only exception was the Iron Age skeleton. Dr Wood said: "The death of the Wellwick Farm man remains a mystery to us, but there aren't many ways you end up in a bottom of a ditch, face down, with your hands bound. "We hope our osteologists will be able to shed more light on this potentially gruesome death."

7-10-20 A COVID-19 vaccine may come soon. Will the blistering pace backfire?
In the rush to bring vaccines to market, any misstep could erode the public’s trust. In January, vaccine researchers lined up on the starting blocks, waiting to hear a pistol. That shot came on January 10, when scientists in China announced the complete genetic makeup of the novel coronavirus. With that information in hand, the headlong race toward a vaccine began. As the virus, now known as SARS-CoV-2, began to spread like wildfire around the globe, researchers sprinted to catch up with treatments and vaccines. Now, six months later, there is still no cure and no preventative for the disease caused by the virus, COVID-19, though there are glimmers of hope. Studies show that two drugs can help treat the sick: The antiviral remdesivir shortens recovery times (SN: 4/29/20) and a steroid called dexamethasone reduces deaths among people hospitalized with COVID-19 who need help breathing (SN: 6/16/20). But the finish line in this race remains a safe and effective vaccine. With nearly 180 vaccine candidates now being tested in lab dishes, animals and even already in humans, that end may be in sight. Some experts predict that a vaccine may be available for emergency use for the general public by the end of the year even before it receives expedited U.S. Food and Drug Administration approval. Velocity might come at the expense of safety and efficacy, some experts worry. And that could stymie efforts to convince enough people to get the vaccine in order to build the herd immunity needed to end the pandemic. “We’re calling for transparency of data,” says Esther Krofah, executive director of FasterCures, a Washington, D.C.-based nonprofit. “We want things to accelerate meaningfully in a way that does not compromise safety or the science, but we need to see the data,” she says.

7-10-20 These cells slow an immune response. Derailing them could help fight tumors
Drug combinations that release multiple brakes on the defense system curbed cancer in mice. Drugs that release brakes on the immune system have helped thousands of people with cancers that were previously untreatable. Yet these therapies, known as checkpoint blockers (SN: 10/1/18), fail in many patients and work poorly for some cancers. That’s because the body’s defense system can stall in more than one way. Checkpoint blockers traditionally target a particular set of brakes: protein interactions that disarm the body’s T cells, allowing cancer to grow unchecked. But an additional brake may be at work as well — an immune cell population called myeloid-derived suppressor cells, or MDSCs. These cells reach unusually high levels in people with cancer. Now, experiments in mice suggest that immune checkpoint therapies could get a boost if paired with other drugs targeting MDSCs. Researchers reported their initial findings at the annual meeting of the American Association for Cancer Research, held virtually in late June. MDSCs are a mix of immature cells from the same family as neutrophils and macrophages, which act as general first responders in the immune system. MDSCs caught scientists’ attention decades ago, but it wasn’t until the last several years that their importance in cancer came into focus. “Their normal function is to slow things down,” says William Carson III, a surgical oncologist at Ohio State University in Columbus. Disabling them, Carson thought, might allow the immune system to launch a speedier attack on cancer cells. In a 2016 study of people who received checkpoint blockers for advanced melanoma, patients with lower levels of MDSCs in their blood responded better to the immune therapy and lived longer. That made Carson and his colleagues wonder if getting rid of the suppressor cells could create an environment for checkpoint blockers to work better. And they knew a class of drugs that could potentially achieve this: Brd4 inhibitors.

7-10-20 Sperm swim up to 70 per cent faster when they have a lazy tail
A human sperm can move up to 70 per cent faster if it has a lazy tail, a finding that could pave the way for new fertility diagnostic tests. Sperm cells use their tails to swim, though some don’t use the whole tail – leaving a piece at the end inactive. This part only constitutes about 3 to 5 per cent of a normal sperm tail – which is usually between 50 and 55 micrometres long – and doesn’t actively bend like the rest of the tail. But it may be key to gaining speed. The tail makes a shape a bit like a sine wave to propel the sperm, says Meurig Gallagher at the University of Birmingham in the UK, who worked on the study. “The tail moves left and right, but when you get to the end, that part is also trying to move this way in the fluid.” “We found that when the end piece instead relaxes with the tail – it generates a shape that allows the tail to swim more efficiently.” Gallagher and his colleagues, led by Cara Neal also at the University of Birmingham, devised mathematical models for how sperm swim. Unlike previous models, the team included the end piece of a sperm’s tail that had been historically overlooked. “Nobody has looked at the end piece because it’s effectively at the limit of light microscopy,” says Neal. The researchers modelled sperm swimming in a range of environments, including in semen and in the female reproductive tract, including in cervical mucus. They found that sperm with an inactive end piece swam more efficiently and faster than sperm with tails which were completely active. Depending on the environment, this type of tail was found to propel sperm 20 to 70 per cent faster and was between 1.5 and 4.5 times more energy efficient when swimming. The team suggests that sperm with an inactive or relaxed, tail end swim quicker because this results in the tail taking up a more efficient shape. The researchers hope this finding could help doctors determine why someone is fertile or infertile on a more detailed level.

7-10-20 'I can recover at home': Cosmetic surgeons see rise in patients amid pandemic
A number of cosmetic surgery clinics around the world are reporting a rise in people getting treatment during the coronavirus outbreak as they can hide their treatment behind a mask or work from home. Despite the virus shutting businesses across the globe, a number of plastic surgery clinics have remained open, adopting stricter measures such as Covid-19 tests and more frequent cleaning. Clinics in the US, Japan, South Korea and Australia have all seen a rise in patients coming in for treatment including lip fillers, botox, face lifts and nose jobs. "I decided to get procedures done during quarantine because it allowed me to heal at my own pace," Aaron Hernandez, who had lip fillers and buccal (cheek) fat removal in Los Angeles, told the BBC. "Getting my lips done is not something that all men tend to do, so some people might find it different. Therefore I preferred to stay home and recover fully and people not know what work I had done once I'm out." The last time he had the procedure done before quarantine, he said, he had to go out in public for work and his lips were "extremely swollen and bruised". Rod J Rohrich, a cosmetic surgeon based in Texas, said he was seeing a lot more patients. "Even more than I would say is normal. We could probably operate six days a week if we wanted to. It's pretty amazing," he told the BBC. He said usually people would have to factor in recovery at home when considering surgery but now that many people are working from home, this doesn't need to be considered. "They can actually recover at home and also they can have a mask that they wear when they go outside after a rhinoplasty or facelift. People want to resume their normal lives and part of that is looking as good as they feel." It's not just the US that is seeing a rise in patients during the outbreak. South Korea, well-known for its cosmetic surgery, was one of the first countries to see cases of the virus. Instead of enforcing a nationwide lockdown, it had a social distancing plan with people encouraged to work from home. Cosmetic clinics have seen a decline in foreign visitors however locals have been coming to clinics for treatments. A number of clinics chose to offer a discount to locals.

7-9-20 Boosting a liver protein may mimic the brain benefits of exercise
Liver-made proteins that circulate in the blood improved memories, a mouse study suggests. Exercise’s power to boost the brain might require a little help from the liver. A chemical signal from the liver, triggered by exercise, helps elderly mice keep their brains sharp, suggests a study published in the July 10 Science. Understanding this liver-to-brain signal may help scientists develop a drug that benefits the brain the way exercise does. Lots of studies have shown that exercise helps the brain, buffering the memory declines that come with old age, for instance. Scientists have long sought an “exercise pill” that could be useful for elderly people too frail to work out or for whom exercise is otherwise risky. “Can we somehow get people who can’t exercise to have the same benefits?” asks Saul Villeda, a neuroscientist at the University of California, San Francisco. Villeda and colleagues took an approach similar to experiments that revealed the rejuvenating effects of blood from young mice (SN: 5/5/14). But instead of youthfulness, the researchers focused on fitness. The researchers injected sedentary elderly mice with plasma from elderly mice that had voluntarily run on wheels over the course of six weeks. After eight injections over 24 days, the sedentary elderly mice performed better on memory tasks, such as remembering where a hidden platform was in a pool of water, than elderly mice that received injections from sedentary mice. Comparing the plasma of exercised mice with that of sedentary mice showed an abundance of proteins produced by the liver in mice that ran on wheels. The researchers closely studied one of these liver proteins produced in response to exercise, called GPLD1. GPLD1 is an enzyme, a type of molecular scissors. It snips other proteins off the outsides of cells, releasing those proteins to go do other jobs. Targeting these biological jobs with a molecule that behaves like GPLD1 might be a way to mimic the brain benefits of exercise, the researchers suspect.

7-9-20 Dolphins and whales separately evolved the same speedy swimming bones
A 24-million-year-old fossil of a giant tusked dolphin lacks several features common to modern dolphins and baleen whales. The discovery shows that the common ancestor of dolphins and whales lacked these features, meaning the same adaptations for swimming must have evolved independently in both lineages. “We were surprised to find so many archaic features in an extinct dolphin,” says Robert Boessenecker at the College of Charleston in South Carolina. Ankylorhiza tiedemani was one of the top predators in the sea from around 30 to 23 million years ago. The 5-metre-long dolphin would have looked much like a bottlenose dolphin, says Boessenecker, apart from its front teeth. These stick straight out and may have been used for ramming prey. Boessenecker’s team has been studying an A. tiedemani fossil found in the 1990s. “No one had found such a complete skeleton before,” he says. It revealed an unexpected lack of modern features. Compared to ancient ancestors all modern whales and dolphins have extra vertebrae in their tails, giving them more flexibility and swimming power, and a very narrow base to the tail, just before the tail flukes. The “upper arm” bone in their pectoral flippers is very short relative to the other bones, and they have two or three extra finger bones. This helps make the flippers larger and stiffer, improving manoeuvreability. It has been assumed that these features all evolved before the ancestors of baleen whales split from the ancestors of echolocating dolphins around 35 million years ago, says Boessenecker, but the fossil shows these features are instead a result of convergent evolution. “All these features evolved at least twice,” he says. We don’t know what Ankylorhiza preyed on. But if it lived in pods it would have been able to eat just about anything it wanted, says Boessenecker – including the 13-metre-long predecessors of megalodon sharks that lived at this time.

7-9-20 There’s little evidence showing which police reforms work
Rapid research is needed to find out what efforts are most effective. When criminologist Robin Engel suddenly found herself leading the effort to reform a police department under fire after a white police officer killed an unarmed Black man in July 2015, she looked for some kind of road map to follow. Instead, she found herself in poorly charted territory. A professor at the University of Cincinnati, Engel had been called on frequently to help police departments around the country manage their response to acts of police violence. This time, the call came from close to home. Campus Officer Ray Tensing, 25, had shot and killed 43-year-old musician Samuel DuBose during an off-campus traffic stop. Engel recommended that the university hire a high-ranking official to oversee the police department and its immediate response to the crisis, and initiate longer term, comprehensive reforms to prevent future incidents. Within days, Engel had become that official, reporting directly to the university president and outranking the university’s police chief, despite lacking police experience herself. She sought input from various community stakeholders, many of whom had been rankled by her appointment to lead the police division. She also turned to her best-known tool — research. She began probing for studies to guide her on the sorts of reforms she could institute, ones with proven track records of changing police behavior in the field. Her search was unfruitful. “I thought most certainly we would have an evidence base that I could follow,” Engel says. “I was incredibly disappointed at the lack of evidence that was available. I was really disappointed in my own field.” (Webmaster's comment: They will only work when we get rid of all the racists, white nationalists, Klan, and Neo-Nazis in our police departments.)

7-9-20 Calculating a dog’s age in human years is harder than you think
Sorry, your 4-year-old Lab isn’t 28 in human years. She’s 53. To estimate your dog’s age in human years, multiply the dog’s age by seven, right? Wrong. A more accurate conversion isn’t so easy to do in your head: Multiply the natural logarithm of the dog’s age by 16, then add 31. Researchers report this new canine age formula online July 2 in Cell Systems. As animals get older, tiny chemical tags called methyl groups get added and removed from DNA. These changes track with different stages of growth and can be used to determine biological age. Scientists can even compare changes across species. In this case, the researchers compared the methylation states of 320 humans, ages 1 to 103 years, with those of 104 Labrador retrievers, ages 5 weeks to 16 years. The relationship between human and dog years changes over time, the scientists found. Early in life, puppies develop much faster than humans, but as dogs get older, their aging curve begins to flatten. An 8-week-old puppy is roughly the same age as a 9-month-old human. A 1-year-old dog corresponds to around 31 human years, and a 4-year-old dog is closer to a 53-year-old human. The new equation also lines up the average life span of a Lab — 12 years — with the average 70-year human life span. The study focused only on yellow Labrador retrievers. Since the life spans of other breeds vary, further studies are needed to find out the real age of every very good dog, the scientists say.

7-9-20 Ancient mammoth tusk found in Siberia is engraved with fighting camels
Ancient engravings etched onto a mammoth tusk discovered in Siberia reveal the oldest known images of camels in Asia. Images of two-humped camels have been found etched onto a 1.5-metre mammoth tusk discovered in the lower Tom river in western Siberia. The tusk is about 13,000 years old and also has an etching of what researchers call an anthropomorphic image, which may portray a human wearing a camel disguise. “Stylistic features of the images on the tusk date them to the final stage of the Upper Palaeolithic as well,” says Yury Esin at the Khakassian Research Institute for Language, Literature, and History in Russia. Esin and his colleagues carbon-dated the tusk, and say the engravings are consistent with images of camels painted in caves around the same time. The oldest camel image was found in Kapova cave in the Ural mountains and dates to between 16,000 and 19,000 years ago. The images on the tusk (see below) show camels with wounds fighting, neck to neck, and one pair of camels has arrows and wounds, indicating they were hunted. “Perhaps the reason for creating this imagery was the importance of the camel fights and camel hunting in the culture of a particular community,” says Esin. “It is likely that this hunting was seasonal.” Esin speculates that since these fights would have happened at the beginning of the mating season, they could mark an important point in the annual cycle of the people who lived in the area. The only camel bones found near the Tom river area date mostly to about 30,000 to 55,000 years ago. Although one dates to the same time period as the mammoth tusk Esin’s team analysed, the bones were found several hundred kilometres to the south of the tusk, lending some weight to the idea that the people were nomadic, says Esin. The tusk also shows an image of what appears to be a human with a camel hump on their body. Esin says this could represent a hunter wearing a skin cloak as a disguise to help approach camels. The tusk was initially found in 1988 during a construction project, but remained nearly unstudied until now. Esin says that researchers know very little about the people who lived in this area of Siberia at the time. Other evidence shows that they hunted mammoths, although this tusk may also have been collected from an animal killed in another fashion.

7-9-20 South Americans may have traveled to Polynesia 800 years ago
DNA suggests people from the Americas had a role in the peopling of Pacific islands. More than 800 years ago, Indigenous people in South America traversed more than 7,000 kilometers of open sea to reach eastern Polynesia, a new study suggests. There, the South Americans mated with Polynesian inhabitants during the initial period of discovery and settlement of those remote islands, researchers say. Genetic analyses show that initial DNA swaps between the voyagers and people on a still-undetermined eastern Polynesian island were followed by the spread of the South American ancestry to other eastern Polynesian islands. Eventually that ancestry spread as far east as Easter Island, also known as Rapa Nui, a team led by computational biologist Alexander Ioannidis and population geneticist Andrés Moreno-Estrada reports online July 8 in Nature. The study offers the first genetic glimpse of “a prehistoric event that left no conclusive trace, except for the one recorded in the DNA of those who had contact 800 years ago in one of the most remote places on Earth,” says Moreno-Estrada, of the National Laboratory of Genomics for Biodiversity in Irapuato, Mexico. Ideas about how remote Polynesia came to be populated have long inspired scientific debate. Norwegian explorer Thor Heyerdahl’s 1947 Kon-Tiki expedition tested his idea that South American seafarers settled the Pacific islands, including Rapa Nui, showing that it was possible to drift by wooden raft from about 129 kilometers off Peru’s coast to Polynesia. But most scholars at that time assumed Asians had voyaged east as early as around 3,500 years ago to relatively close-by western Polynesia, eventually populating eastern Polynesia by around 1,000 years ago without having any contacts with people from South America. Computer simulations since have indicated that winds and currents would carry a vessel from northern South America to the Polynesian islands. But the idea of seafaring South Americans having an early role in the peopling of Polynesia hasn’t been widely accepted.

7-8-20 Polynesians and Native Americans met 800 years ago after epic voyage
Polynesians and Native Americans met and had children together around AD 1200, according to a study of modern Polynesian peoples’ DNA. But the encounter didn’t take place on Rapa Nui (Easter Island), the island closest to South America, as has long been suggested. Instead, the Polynesians in question were from islands hundreds of kilometres further away. The Pacific islands of Polynesia were some of the last places to be settled by humans. Beginning about 5000 years ago, people sailed east from South-East Asia into the Pacific, and found hundreds of islands including Samoa and the Marquesas. The easternmost island, Rapa Nui, was the last to be settled. This story is supported by genetic, archaeological and linguistic evidence linking Polynesian people with South-East Asians. But some anthropologists have long argued that Polynesians might also have some Native American ancestry, pointing to other factors, such as crops. “There is the sweet potato in Polynesia, even though it was domesticated in, and is native to, the Americas,” says Alexander Ioannidis at Stanford University in California. It has also been claimed that the famous statues on Rapa Nui resemble ancient Peruvian statues. Geneticists have found evidence of Native American genes in Polynesian people, but the results are disputed. Now Ioannidis and his colleagues have sequenced the full genomes of 354 Polynesian people from 17 islands, as well as 453 Native Americans from 15 groups from the Pacific coast. They found small amounts of Native American DNA in Polynesians from the eastern islands: not just Rapa Nui, but also the Palliser islands, the Marquesas and Mangareva. We don’t know exactly which islanders were the point of contact, says the team, but they were almost certainly from one of the more westerly of the group. Later settlers carried the genes to the easterly islands, including Rapa Nui.

7-8-20 Evidence found of epic prehistoric Pacific voyages
New evidence has been found for epic prehistoric voyages between the Americas and eastern Polynesia. DNA analysis suggests there was mixing between Native Americans and Polynesians around AD 1200. The extent of potential contacts between the regions has been a hotly contested area for decades. In 1947, Norwegian explorer Thor Heyerdahl made a journey by raft from South America to Polynesia to demonstrate the voyage was possible. Until now, proponents of Native American and Polynesian interaction reasoned that some common cultural elements, such as a similar word used for a common crop, hinted that the two populations had mingled before Europeans settled in South America. Opponents pointed to studies with differing conclusions and the fact that the two groups were separated by thousands of kilometres of open ocean. Alexander Ioannidis from Stanford University in California and his international colleagues analysed genetic data from more than 800 living indigenous inhabitants of coastal South America and French Polynesia. They were looking for snippets of DNA that are characteristic of each population and for segments that are "identical by descent" - meaning they are inherited from the same ancestor many generations ago. "We found identical-by-descent segments of Native American ancestry across several Polynesian islands," said Mr Ioannidis. "It was conclusive evidence that there was a single shared contact event." In other words, Polynesians and Native Americans met at one point in history, and during that time children with both Native American and Polynesian ancestry were born. Statistical analyses confirmed the event occurred around AD 1200, at about the time Pacific islands were originally being settled by Polynesians. Asked who he thought made contact first, Mr Ioannidis ventured that it may have been Polynesian navigators reaching South America.

7-8-20 How to stop the coronavirus: What we've learned six months in
SINCE the first reports of the novel coronavirus, the list of known symptoms has changed, as has our understanding of what the virus does to the body. Health advice, for both governments and individuals, has evolved, too. And although some countries claim to have virtually eliminated the virus, others are only now seeing cases beginning to spike and some are seeing what looks like a “second wave” of infections. What can we learn from the countries that got it right – and those that got it so very wrong? One major early fumble was the incorrect assumption that the virus was like the flu. Many nations already had a plan in place for dealing with a pandemic flu. “It inhibited their ability to think about how to respond to another virus,” says Jennifer Nuzzo at Johns Hopkins University in Maryland. The coronavirus required a different response, says Michael Baker at the University of Otago in Wellington, who advised the New Zealand government on the country’s covid-19 response. Flu typically has an incubation period – the time between someone becoming infected and showing symptoms – of around one to two days. This makes it extremely difficult to trace the contacts of an infected person before they get sick themselves. The coronavirus, on the other hand, appears to have an incubation period of about five to six days, but potentially several weeks. “It means that it’s a slower moving wave and there are more opportunities to use contact tracing and isolation and quarantine,” says Baker. “We know that’s the case because [the] SARS [coronavirus] was contained and eliminated with those traditional measures.” In addition, while flu can “sweep through a population in a matter of weeks”, he says, the coronavirus can stick around for much longer and can have lasting health effects for those who survive covid-19. This is one reason why the idea of waiting to achieve herd immunity rather than taking action to limit the impact of the virus – a strategy the UK and Swedish governments initially considered – was widely dismissed by the scientific community. Today, the UK has the highest number of recorded coronavirus cases in western Europe, probably in part due to the UK government’s delayed response to the outbreak. One factor that unites the nations that have done a better job at limiting case numbers is a quick initial response. “In countries like China, South Korea, Japan, the initial response was quite rapid, so the containment phase worked really well for them,” says Rajiv Chowdhury at the University of Cambridge. By quickly identifying new cases and where they were coming from, these countries stood a much better chance of interrupting the ongoing transmission of the virus, he says.

7-8-20 Grief over covid-19 deaths may be unusually severe and long-lasting
Since losing her mother to covid-19 in April, Helen Stoba, who lives in Liverpool, UK, has been racked with guilt, anger and confusion. She struggles to focus and has nightmares. “No one truly understands how different the grieving process is at the moment,” she says. Psychiatrists are observing similar emotions in others who have lost loved ones to covid-19 (see “Stories of loss,” below). They warn that the unique challenges of coming to terms with these deaths could lead to a rise in a condition known as prolonged grief disorder. Grief tends to ease with time as people adapt to life without the deceased. But about 10 per cent of bereaved individuals develop prolonged grief disorder – severe, unrelenting grief that lasts for six months or more and makes it difficult to function. Previous research has found that people are more likely to develop the condition if a death is sudden and unexpected, they are experiencing other stressors or they lack social support. More people are experiencing these risk factors during the pandemic, since the coronavirus often kills swiftly, many bereaved people have additional stressors, such as the loss of their job, and social structures are undermined. “Grieving people tend to appreciate a hug, which is impossible when we are required to adhere to physical distancing,” says psychologist Lauren Breen at Curtin University in Australia. Many covid-19 deaths also come with extra challenges that could further increase the risk of prolonged grief disorder, says Joseph Goveas, a psychiatrist at the Medical College of Wisconsin. These include not being able to say goodbye in person, covid-19 specific restrictions on rituals like washing, kissing or viewing the body and limits on the number of people who can attend funerals. These may all derail the healing process, he says. Goveas is also seeing high levels of guilt in patients who have lost loved ones to covid-19. “They feel like they didn’t do enough or they have survivor’s guilt and wonder why they were spared,” he says.

7-8-20 Can a young person's genes really set them up for a life of crime?
Most adolescents dabble in delinquency, but few become lifetime offenders. Long-running studies can help tell us why and improve policing, says psychologist Terrie Moffitt. OUR attitudes towards crime and punishment are highly political. They often come down to how much we believe a person’s particular life circumstances should be taken into account when deciding whether their punishment fits the crime they committed. But criminal justice isn’t an evidence-free zone. Behavioural scientist Terrie Moffitt at King’s College London has spent her career trying to uncover biological and environmental roots to criminal behaviour. Now she has evidence from brain imaging and genetics to support her idea that there are generally two groups of people who persistently commit crime, each with different causes for their behaviour and different prospects for reform. Dan Jones: How has the nature-nurture debate influenced views on criminal behaviour? Terrie Moffitt: Our thinking about the roots of antisocial behaviour has followed pendulum swings between putting nature or nurture centre stage. Writing in the late 17th century, philosopher John Locke came down on the side of nurture, arguing that we are born as blank slates and learn all our behaviours, bad ones included. Then in the 19th century, Cesare Lombroso, the founder of criminology, suggested that bad people were born that way and could be identified by the shape of their eyes, ears, teeth and eyebrows. By the 1960s, after John Watson and B. F. Skinner developed behaviourism, the pendulum had swung back to nurture. Everything changed in the 1980s and 90s, and the debates really heated up. Scientists started reporting studies of crime drawing on thousands of twins and adoptees in Scandinavian registers, which seemed to point to genetic transmission of criminal behaviour from parent to child. This was like pouring petrol on a fire, and the nature-nurture debate got vicious. But these studies also made clear that over half the variation in antisocial and criminal behaviour couldn’t be explained by genetics, and provided some of the first really solid evidence for the social transmission of crime in families. Since then, nearly everyone has come to agree that crime involves both nature and nurture. (Webmaster's comment: Male violence has at least a 50% component! It is built in! Those with it should be neutered!)

7-8-20 The powerhouses inside cells have been gene-edited for the first time
Mitochondria, the structures inside our cells that use food to produce energy, have been gene-edited for the first time. A new kind of “base editor” was used, opening the door to treating disorders related to faulty mitochondria. These organelles have their own genomes and mutations in this DNA can lead to everything from muscle weakness to intellectual disability. Some inherited mitochondrial mutations result in death in early childhood, while an accumulation of mitochondrial mutations may be one of the causes of age-related diseases. Two problems have thwarted previous attempts to gene-edit mitochondria. The first is that most gene editors work by cutting DNA, but mitochondrial genomes break down if cut. In 2016, David Liu at the Broad Institute of MIT in Massachusetts developed base editors that change one DNA letter – or base pair – to another without cutting DNA. “You are directly rearranging the atoms in one base pair to become another, without cutting the double helix,” says Liu. But these base editors consist of proteins adapted from the CRISPR gene-editing method, which need an RNA molecule to guide them to their target. That brings up the second problem: no one has managed to get RNA into mitochondria. Now Liu’s team has collaborated with two other groups to create an entirely new kind of base editor that doesn’t rely on CRISPR. The researchers, including Beverly Mok at Harvard and Marcos de Moraes at the University of Washington, in Seattle, fused proteins that can make the necessary chemical changes to mitochondrial DNA with proteins that bind to specific sequences. They added a kind of delivery address to get them into mitochondria. In tests in human cells growing in a dish, this base editor made the desired change in up to 50 per cent of mitochondrial genomes. “If true, that’s quite impressive,” says Nick Lane at University College London.

7-8-20 How we make decisions during a pandemic
Behavioral experts reveal what might be prompting people to act — or not. As strict stay-at-home orders are lifted, people face a number of decisions. Mundane logistical questions — Should I go get my hair cut? When can I picnic with friends? What should I wear to the hardware store? — during the COVID-19 pandemic carry implications for personal and public health, in some cases life-or-death ones. When multiplied through the population, seemingly small decisions can either dramatically slow or accelerate this pandemic. So we might like to think that our behavioral choices are based purely on the best information we have. But that isn't the case, experts say. In fact, we are all susceptible to biases that push and pull our brains in invisible ways. This happens in part because of overconfidence in our ability to know why we make the choices we do. "There's a powerful belief in the value of introspection, which much of social psychology and psychological science has shown is a mistake," says psychologist Jennifer Lerner of the Harvard Kennedy School. "We are not good at understanding what our brains are doing." Research by Lerner and others can help us better understand how our decision-making processes are affected in these unprecedented times — and perhaps how we can inoculate ourselves and others against unwise decisions. Here are six factors that can sway how we choose to behave during the pandemic:

  1. Bias of the here and now: In many ways, we are creatures of the present. "We tend to make decisions based on the information that is most resonant, closest at hand, most recent," says Nicholas King, a biomedical ethicist at McGill University in Montreal.
  2. Colored by emotions: Research shows that even the most minor of choices can be colored by our mood. "Emotions have a profound effect on the process with which people make decisions," says Lerner, who coauthored an article about emotion and decision-making in the 2015 Annual Review of Psychology.
  3. Searching for certainty: Another prevailing force right now is extreme uncertainty, which, as King puts it, "sucks." This instability can lead people to seek narrow ranges of information in order to confirm their perspectives.
  4. Peer pressure: We rarely make decisions in a vacuum — even if they seem entirely personal. And we are influenced by those around us more than we might think.
  5. When healthy is easy: To understand how to help people make better decisions in this pandemic, scientists are looking to insights gained from previous work on pro-social health behaviors. Gretchen Chapman, who studies social and decision sciences at Carnegie Mellon University, has done decades of research in this field, such as on people's decisions to get vaccines.
  6. What we can learn, how we can do better: A better understanding of how we make decisions can also help experts learn how to nudge us toward healthy behaviors. Chapman and colleagues, for example, are studying how different messages — straight informational versus one that includes an estimate of how popular something is (how many Americans are wearing masks, for example) — change people's intended behavior.

7-8-20 What you need to know about the airborne transmission of COVID-19
Some scientists argue the virus can float in the air for extended lengths of time. The scientific debate over evidence that the coronavirus can float in the air for extended periods of time is intensifying. The World Health Organization has repeatedly downplayed the importance of such airborne transmission, instead emphasizing, with substantial evidence, the risks of close contact with infected people. But now, over 200 experts have signed an open letter to the WHO saying it’s time to recognize evidence that the coronavirus is airborne. The letter, published July 6 in Clinical Infectious Diseases, argues that the public health institution must update its prevention recommendations to help people avoid those risks. The WHO is aware of the letter and reviewing its contents, according to a July 6 Reuters report. Here’s what you need to know about the ongoing debate and what it means for fighting the spread of COVID-19. At the beginning of the outbreak, scientists thought that the virus was spread largely through bits of spit or mucus that people coughed or sneezed. Those droplets, up to roughly a millimeter across, would fall from the air within a short amount of time. The WHO has long maintained that the coronavirus spreads primarily via these larger droplets, which don’t easily travel farther than about six feet. But researchers increasingly think that the coronavirus can stay in the air longer and travel farther in tinier bits, called aerosols, that can be generated by people talking, breathing or singing (SN:4/2/20). These aerosols, which are less than 5 microns in diameter, can linger in the air for extended periods in places without ventilation, possibly infecting people long after the infected person has left. Laboratory studies have found that infectious coronavirus can persist in the air for at least three hours when artificially aerosolized, though these results are hard to translate to real-world conditions. But evidence from “superspreader” events also point to airborne transmission. For example, a single infected person at a choir practice in Mount Vernon, Wash., infected at least 45 other people, many of whom were farther than six feet from the sick singer (SN: 4/17/20).

7-7-20 Let us test for COVID-19 at home
One of the great frustrations of the coronavirus era is that most discrete acts of social distancing are objectively pointless. At any given moment, even if you live somewhere cases are spiking, you are probably not transmitting the coronavirus. Yet you don't know that — asymptomatic infection is not only possible but common — so you act as if you are contagious all the time. But what if you could know? That's the possibility raised by the launch of a new antigen test from a New Jersey company, Becton Dickinson (BD), which announced Monday that the Food and Drug Administration (FDA) had granted emergency approval for facilities like pharmacies and doctors' offices to offer this quick screening. The BD test is easy, cheap, fast, and accurate. It could change everything about how we handle this pandemic. It could re-open schools, churches, and restaurants and allow us to visit elderly family with minimal concern. If only the FDA would allow everyone to use it. Libertarians like me are always going on about how the government needs to get out of the way and let people make their own choices, but really, this time, the government needs to get out of the way. Widespread, rapid testing is now possible, and it is unconscionable for the FDA to prevent it. This BD antigen test is remarkable in four ways: One, it's performed by swabbing the inside of the nose — there's no blood draw, and the swab isn't that long one that practically reaches into your brain — meaning it doesn't require laboratory personnel. Most people can learn to do this, contrary the FDA's repeated expressions of doubt in the average American's competency. (That doubt is why the FDA has only approved a few COVID-19 tests with at-home sample collection and none with at-home results processing. Meanwhile, average Americans somehow manage to self-administer tests, many with at-home results, for pregnancy, ovulation, ketosis, colon cancer, blood glucose, UTIs, HIV, Lyme Disease, Chlamydia, strep throat, and the composition of our genomes, among other things.) Two, it only takes about 15 minutes to produce a result. Three, it costs just $20 per test with an initial platform cost of around $300, and it's plausible that price could be lowered at scale. Another, similar test, from a company called Quidel Corp., can already be run for as little as $5 per use. Other, cheaper tests intended for daily home use are in development, too. These paper strip tests, even simpler to administer than the swab, would run as low as $1 per use. We'd need them in production to implement the kind of testing I'm suggesting; Becton Dickinson aims to ramp up to making 2 million tests per week by the end of September, which by itself is not nearly enough. And four, the BD test is capable of 84 percent sensitivity and 100 percent specificity, which means it correctly identifies positive cases 84 percent of the time and negative cases all the time. A few false negatives will slip through, but this is high enough accuracy to make the test enormously useful. It gets us to a risk level that will be acceptable to the vast majority of people. (Frequent testing can also help catch the false negatives.)

7-7-20 Risk of airborne coronavirus spread being underplayed, say researchers
Over 200 scientists have called for the world to take more precautions against the airborne transmission of the coronavirus. While the virus is known to spread through the air via large droplets produced when people cough or sneeze, they say it can also be spread by smaller droplets known as aerosols that can linger in the air. Preventing this means ventilating buildings and avoiding overcrowding. “Hand-washing and social distancing are appropriate, but, in our view, insufficient to provide protection from virus-carrying respiratory microdroplets released into the air by infected people,” states a letter written by Lidia Morawska at Queensland University of Technology in Australia. It has been signed by 239 researchers. The letter also calls for international bodies such as the World Health Organization (WHO) to acknowledge the possibility of this type of airborne spread and suggests precautions against it. Morawska and others have made similar calls in recent months, but it is especially important to address the issue now that people in many countries are returning to workplaces, restaurants and pubs, says signatory Julian Tang at the University of Leicester in the UK. Improving ventilation will reduce the risk, he says. “You can’t rely on people wearing masks.” The letter has been attacked by some researchers. “I don’t think the overall conclusions are correct,” says Paul Hunter at the University of East Anglia, UK. “They are potentially damaging.” He says the letter could cause confusion among the public and that taking measures to prevent aerosol spread could give people a false sense of security, making them less likely to take other steps, such as washing their hands. The WHO uses the term “airborne spread” only for transmission by droplets that are less than 5 micrometres in diameter. These can remain aloft for longer than the larger droplets produced by an infected person coughing or sneezing.

7-7-20 Covid-19 news: Everyone should wear face coverings, says Royal Society
The latest coronavirus news updated every day including coronavirus cases, the latest news, features and interviews from New Scientist and essential information about the covid-19 pandemic.Everyone in the UK should wear a face covering, says Royal Society president. Everyone in the UK should wear a face covering, the president of the Royal Society has said. In a statement published today, Venki Ramakrishnan said people should have face coverings with them when they leave their home and should always wear them in crowded public spaces, “particularly indoors in enclosed public spaces where physical distancing is often not possible.” Brazil’s president Jair Bolsonaro said he has tested positive for coronavirus in an announcement on live TV to a group of reporters. Bolsanaro has repeatedly underplayed the risks of the pandemic and has publicly flouted social distancing rules, including attending anti-lockdown protests and vetoing changes to the law requiring people to wear face coverings. Brazil has recorded more than 1.6 million coronavirus cases, the second-highest number after the US, and more than 65,000 deaths from covid-19. Only 5 per cent of Spain’s population has antibodies against the coronavirus, according to a study of more than 61,000 people published yesterday in The Lancet – the largest such study in Europe so far. The findings cast further doubt on the already problematic idea that countries could naturally achieve herd immunity – a situation where a sufficient number of people within the population have been infected or vaccinated against a pathogen to limit it from spreading further. It still isn’t clear how long any form of immunity against the coronavirus might last, and accuracy of covid-19 antibody tests have been called into question. An estimated 60 per cent of people would need to have antibodies to reach herd immunity within a population. “We are very far from achieving that number,” Marina Pollán, who led the study in Spain, told CNN. Even if that number were achieved, it would lead to 30 million deaths from the virus worldwide. The Australian state of Victoria has reimposed stay-at-home orders in Melbourne and the Mitchell Shire for the next six weeks in an effort to tackle a new coronavirus outbreak. 191 new cases were confirmed in Victoria today – the highest number of daily new cases there since the start of the pandemic. The reimposed restrictions are expected to affect 5 million people.

7-6-20 Ultrasound tweezers could help remove kidney stones without surgery
Beams of ultrasound could be used to remove kidney stones by steering them through the body. In experiments on pigs, a team using the approach was able to move glass beads along a predefined course. Kidney stones arise when minerals dissolved in urine form crystals. They can get stuck inside the kidneys or in the ureter, the narrow tube that leads from the kidneys to the bladder, becoming painful. One treatment involves breaking the stones up into smaller pieces, so they can more easily exit the body in urine. This may be done by pushing a long thin tube up into the ureter from the bladder, or by firing ultrasound shock waves from outside the body, but both methods can leave fragments behind that encourage more stones to grow. More severe cases require surgery. A team led by Michael Bailey at the University of Washington in Seattle has been exploring a different approach, using gentler ultrasound waves to release stones from where they have got stuck. The first idea the team tried was giving a stone a small nudge, to boost its chances of moving along naturally. The first test of this, in 15 people, suggests that smaller stones can usually be made to move a little using this approach, helping them to be cleared from the body, although it wasn’t a placebo-controlled trial. Now Bailey’s group has found a way to better control how the stone moves, using carefully targeted sound waves to create a ring of high pressure around the stone, trapping it in place. If the ring is moved, it drags the stone along with it. “Even moving it just a small distance will help,” says Bailey. The team tested the approach on three anaesthetised pigs, using glass beads that had been placed inside their bladders to stand in for kidney stones. The beads were successfully steered along pre-chosen routes with over 90 per cent accuracy. “It’s really quite controllable,” says Bailey, who consults for US firm SonoMotion, which has licensed the technology.

7-7-20 All kinds of outbreaks, from COVID-19 to violence, share the same principles
Adam Kucharski discusses his new book The Rules of Contagion. Epidemiologists like to say, “If you’ve seen one pandemic, you’ve seen … one pandemic.” But behind each outbreak lie core principles that help explain why the outbreak began, why it grew, why it peaked when it did and why it ended. In The Rules of Contagion, mathematician and epidemiologist Adam Kucharski of the London School of Hygiene & Tropical Medicine outlines those principles and shows how they apply beyond infectious disease, to the spread of ideas, financial crises, violence and more. Kucharski hardly mentions the novel coronavirus sweeping the globe. He was just wrapping up final edits when the first cases of COVID-19 appeared in Wuhan, China. But the book still feels extraordinarily prescient. Kucharski provides context for readers to understand the current pandemic, as well as a framework for thinking about other types of contagious spread. Science News spoke with Kucharski about the principles of contagion, disease modeling and misinformation. The following conversation has been edited for length and clarity. I’ve noticed that the same mistakes get made repeatedly across fields. For example, after the 2008 financial crisis, a lot of people realized that the network structure between banks and loans and exposure to risk was very similar to a lot of the network features that caused problems with sexually transmitted infections in the 1970s and ’80s. If there are a lot of “loops” in the network, with people connected to each other in multiple ways, it makes it harder to stop the spread. If the network is structured so that highly connected individuals are disproportionately linked to less-connected individuals, it can result in an outbreak that spreads slower at first, but eventually reaches more of the network. Pre-2008, the financial network had both of these features. It’s also important to understand the underlying network. When looking at violence, it might be tempting to think the events are random, but there is often a series of connections that link them, and targeting these links with interventions can help prevent future incidents.

7-7-20 How making a COVID-19 vaccine confronts thorny ethical issues
A shot at COVID-19 vaccine development shows the ethical issues behind commonly used cell lines. Ethical concerns abound in the race to develop a COVID-19 vaccine. How do we ethically test it in people? Can people be forced to get the vaccine if they don’t want it? Who should get it first? Tackling those questions demands that a vaccine exist. But a slew of other ethical questions arise long before anything is loaded into a syringe. In particular, some Catholic leaders in the United States and Canada are concerned about COVID-19 vaccine candidates made using cells derived from human fetuses aborted electively in the 1970s and 1980s. The group wrote a letter to the commissioner of the U.S. Food and Drug Administration in April, expressing concern that several vaccines involving these cell lines were selected for Operation Warp Speed — a multibillion-dollar U.S. government partnership aimed at delivering a COVID-19 vaccine by January 2021. The group urged the FDA to instead provide incentives for COVID-19 vaccines that do not use fetal cell lines. But, as virologist Angela Rasmussen of Columbia University pointed out on Twitter, those other vaccines are being developed with scientific input from research using HeLA cells — which come with their own thorny ethical issues of consent. Here’s how scientists and bioethicists are thinking about the cell lines they use as they develop COVID-19 vaccines. Cell lines are cultures of human or other animal cells that can be grown for long periods of time in the lab. Some of these cultures are known as immortalized cell lines because the cells never stop dividing. Most cells can’t perform this trick — they eventually stop splitting and die. Immortal cell lines have cheated death. Some are more than 50 years old. Cell lines can be manipulated to become immortal. Or sometimes, immortality arises by chance. “Whenever people make primary cell cultures from different organs of different animals, every so often you just get … lucky, and some cultures just won’t die,” explains Matthew Koci, a viral immunologist at North Carolina State University in Raleigh. Such long-lasting cell lines go on to get studied, and studied some more. Some end up being used in labs around the world.

7-7-20 Mysterious Stone Age flint artefacts may be crude sculptures of humans
More than 100 distinctive flint artefacts from a Stone Age village in Jordan may be figurines of people used in funeral rituals, according to a team of archaeologists. However, other researchers aren’t convinced that the objects represent people at all. Since 2014, Juan Jose´ Iba´n~ez at the Milá and Fontanals Institution for Humanities Research in Spain and his colleagues have been excavating a site called Kharaysin in Jordan. It was occupied from around 9000 BC until at least 7000 BC. At this time, people who were previously hunter-gatherers were taking up settled farming. Kharaysin is one of the oldest examples of a village where people built houses and lived year-round. “We were excavating funerary areas, a cemetery,” says Iba´n~ez. This is where the researchers found the flint objects, each with the same distinctive shape and with two pairs of notches carved into it on either side. “We know very well the tools that are made at that period,” says Iba´n~ez. These artefacts didn’t look like any of them. The objects don’t seem to have been used as tools, as they show no signs of wear from use. This suggests they were decorative or symbolic, says Iba´n~ez. When a team member first proposed that the artefacts were figurines representing humans, “we were kind of sceptical”, says Iba´n~ez. However, the team has since become convinced that they are depictions of people, albeit crude ones. “They made two notches in one side, one representing the neck probably and the other the hip,” says Iba´n~ez (Antiquity, DOI: 10.15184/aqy.2020.78). “This is an intriguing hypothesis, but humans are very good at seeing faces in natural objects,” says April Nowell at the University of Victoria in Canada. “That is why there are so many stories about the man in the moon, and why every now and again people see Jesus in a piece of toast. If someone showed you that photograph of the ‘figurines’ without knowing the subject of the paper, you would most likely have said that this is a photograph of stone tools.”

7-7-20 Dinosaur ancestors 'may have been tiny'
Dinosaurs are often thought of as giant creatures, but new research adds to evidence they started out small. The evidence comes from a newly described fossil relative found on Madagascar that lived some 237 million years ago and stood just 10cm tall. The specimen may also help clarify the currently murky origins of pterosaurs, the winged reptiles that ruled the skies at the time of the dinosaurs. The work appears in the Proceedings of the National Academy of Sciences. "There's a general perception of dinosaurs as being giants," said co-author Christian Kammerer, from the North Carolina Museum of Natural Sciences. "But this new animal is very close to the divergence of dinosaurs and pterosaurs, and it's shockingly small." The specimen, named Kongonaphon kely, or "tiny bug slayer", was found in 1998 in Madagascar by a team of palaeontologists, led by John Flynn from the American Museum of Natural History in New York. Dinosaurs and pterosaurs both belong to the group Ornithodira. Their origins, however, are poorly known, as few specimens from near the root of this lineage have been found. Kongonaphon is not the first small fossil animal known near the root of the ornithodiran family tree but, previously, such specimens were considered isolated exceptions. In general, scientists thought body size remained similar among the first archosaurs - the larger reptile group that includes birds, crocodilians, non-avian dinosaurs, and pterosaurs - and the earliest ornithodirans. They are then thought to have increased to gigantic proportions in the dinosaur lineage. "Analysing changes in body size throughout archosaur evolution, we found compelling evidence that it decreased sharply early in the history of the dinosaur-pterosaur lineage," Dr Kammerer said. Wear on the teeth of Kongonaphon suggests it ate insects. A shift to this kind of diet, which is associated with small body size, may have helped early ornithodirans survive by occupying a niche different from their mostly meat-eating contemporaneous relatives.

7-6-20 Self-destructive civilizations may doom our search for alien intelligence
A lack of signals from space may also be bad news for Earthlings. On Earth, civilizations have limited lifetimes. Roman civilization, for instance, lasted less than a thousand years from the founding of its republic to the fall of its empire (after a long decline). In the New World, Maya civilization spanned roughly two millennia (maybe a little longer depending on when you date its beginning). In the late Bronze Age, the Greek Mycenaean civilization lasted a mere five centuries or so. As for American civilization (as in the United States of), at the rate things are going it won’t last even that long. For some reason, civilization is not a self-perpetuating state of affairs on this planet. And perhaps not on other planets, either. In fact, limits to civilization lifetimes may explain why extraterrestrial aliens have not yet communicated with Earthlings. A new analysis suggests that the entire Milky Way galaxy currently houses only a few dozen worlds equipped with sufficiently sophisticated technology to send us a message. They are probably scattered at such great distances that any signals sent our way haven’t had time to get here. And by the time a signal arrives, there may be nobody here around to hear it. “We may imagine a galaxy in which intelligent life is widespread, but communication unlikely,” write Tom Westby and Christopher Conselice in the June 10 Astrophysical Journal. Westby and Conselice, of the University of Nottingham in England, base their analysis on a modified version of the Drake equation, proposed nearly 60 years ago by the astronomer Frank Drake. At a time when most scientists didn’t take communicating with E.T. seriously, Drake identified the factors that would, in principle, permit an estimate of how many communicating civilizations might exist in the galaxy. His equation provided the framework for all subsequent scientific assessment of the prospects for extraterrestrial intelligence. (Webmaster's comment: To become the dominate species of this planet human beings are in the process using up all the resources, destroying the environment, and killing every other thing that lives. In less than another 2,000 years we will be gone!)

7-6-20 Hair sample tests may give women more accurate fertility predictions
Women wanting to know how many eggs they have left may in future be able to have their hair tested to reveal their hormone levels. A signalling chemical related to women’s fertility called anti-Müllerian hormone (AMH) is incorporated into hair shafts while they are still underneath the skin. Testing the hair may give a better indication of fertility than current blood tests. AMH is released by eggs in the ovaries, the number of which decline with age. Blood AMH levels broadly correlate with how many eggs a woman has left, and therefore how long it will be before she stops being fertile. Some firms offer AMH blood testing for any woman trying to get pregnant – although doctors’ bodies have warned that for the general population, it isn’t a good indicator of how likely someone is to conceive. But for people having IVF, it does predict which women are likely to respond well or poorly to stimulation of their ovaries, according to the European Society of Human Reproduction and Embryology. In future, women may be able to send off a hair sample for testing, instead of having a blood sample taken. In a group of 152 women aged between 18 and 65, hair AMH levels correlated with levels in their blood, and with the number of eggs present in their ovaries as seen by an ultrasound scan – but hair levels of the hormone tracked age better than blood levels, suggesting the hair test may be more accurate. Hormone levels in hair may be a better indicator of longer-term average blood levels than a one-off blood sample, says Sarthak Sawarkar at US fertility company MedAnswers, who did the study. “Hair is a medium that can accumulate biomarkers over several weeks, while hormone levels in blood can fluctuate rapidly in response to stimuli,” he said in a statement. The work was presented at this year’s online meeting of the European Society of Human Reproduction and Embryology.

7-6-20 Brain-eating amoeba: Warning issued in Florida after rare infection case
A case of a rare brain-eating amoeba has been confirmed in Florida, according to health officials in the US state. The Florida Department of Health (DOH) said one person in Hillsborough County had contracted Naegleria fowleri. The microscopic, single-celled amoeba can cause an infection of the brain, and is usually fatal. Commonly found in warm freshwater, the amoeba enters the body through the nose. The DOH did not outline where the infection was contracted, or the patient's condition. The amoeba cannot be passed from person to person. Infections are typically seen in southern US states. They are rare in Florida, where only 37 cases have been reported since 1962. But given the potentially deadly consequences of infection, the DOH issued a warning to residents of Hillsborough County on 3 July. Health officials urged locals to avoid nasal contact with water from taps and other sources. This includes bodies of open water such as lakes, rivers, ponds and canals, where infections are more likely in the warmer summer months of July, August and September. 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. The DOH has urged people who experience those symptoms to "seek medical attention right away, as the disease progresses rapidly". "Remember, this disease is rare and effective prevention strategies can allow for a safe and relaxing summer swim season," the DOH said. Naegleria fowleri infections are rare in the US, according to the US Centers for Disease Control and Prevention (CDC). Between 2009 and 2018, only 34 infections were reported in the country. Of those cases, 30 people were infected by recreational water, three after performing nasal irrigation with contaminated tap water, and one person was infected by contaminated tap water used on a backyard slip-n-slide, the CDC said.

7-6-20 China bubonic plague: Inner Mongolia takes precautions after case
Authorities in China have stepped up precautions after a city in the Inner Mongolia autonomous region confirmed one case of bubonic plague. According to state reports, the Bayannur patient - a herdsman - is in quarantine and in a stable condition. Officials said they were also investigating a second suspected case, according to China's Global Times. The bubonic plague was once the world's most feared disease, but can now be easily treated. The first case was reported as suspected bubonic plague on Saturday at a hospital in Urad Middle Banner, in Bayannur city. It is not yet clear how or why the patient might have become infected. The second suspected case involves a 15-year-old, who had apparently been in contact with a marmot hunted by a dog, a tweet from Global Times said. A level 3 alert, which forbids the hunting and eating of animals that could carry plague and calls on the public to report suspected cases, has been put in place until the end of the year. Bubonic plague, caused by bacterial infection, was responsible for one of the deadliest epidemics in human history - the Black Death - which killed about 50 million people across Africa, Asia and Europe in the 14th Century. There have been a handful of large outbreaks since. It killed about a fifth of London's population during the Great Plague of 1665, while more than 12 million died in outbreaks during the 19th Century in China and India. But nowadays it can be treated by antibiotics. Left untreated, the disease - which is typically transmitted from animals to humans by fleas - has a 30-60% fatality rate. Symptoms of the plague include high fever, chills, nausea, weakness and swollen lymph nodes in the neck, armpit or groin. Bubonic cases are rare, but there are still a few flare-ups of the disease from time to time. Madagascar saw more than 300 cases during an outbreak in 2017. However, a study in medical journal The Lancet found less than 30 people died

7-6-20 What is bubonic plague?
A suspected case of bubonic plague has been reported to Chinese authorities. It is not known how the patient became infected, but the country is on alert for more cases. Plague is one of the deadliest diseases in human history - but it can now be easily treated with antibiotics. Plague is a potentially lethal infectious disease that is caused by bacteria called Yersinia pestis that live in some animals - mainly rodents - and their fleas. Bubonic plague is the most common type of the disease that people can get. The name comes from the symptoms it causes - painful, swollen lymph nodes or 'buboes' in the groin or armpit. From 2010 to 2015 there were 3,248 cases reported worldwide, including 584 deaths. Historically, it has also been called the Black Death, in reference to the gangrenous blackening and death of body parts, such as the fingers and toes, that can happen with the illness. A person usually becomes ill with bubonic plague between two and six days after being infected. Along with the tender, enlarged lymph nodes, that can be as large as a chicken egg, other symptoms include fever, chills, headache, muscle aches and tiredness. Plague can also affect the lungs, causing a cough, chest pain and difficulty breathing. The bacteria can also enter the bloodstream and cause a condition called septicaemia or sepsis, which can lead to tissue damage, organ failure and death. Domestic cats and dogs can become infected from flea bites or from eating infected rodents. The infection could also enter the body through a cut in the skin if the person came in close contact with an infected animal's blood. The current alert in China forbids the hunting and eating of animals that could carry plague. The body of someone who has died after being infected with plague can infect people who are in close contact, such as those who are preparing the body for burial.

7-5-20 Underwater cave in Mexico reveals ancient Mayan secrets
Cave divers on Mexico's Yucatan Peninsula have found evidence of a mining operation started 12,000 years ago. It is thought the cave was mined for red ochre, a pigment associated with ancient paintings.

7-4-20 Coronavirus: What makes a gathering a ‘superspreader’ event?
Now months into the US coronavirus outbreak, safety precautions have become routine: stand 6ft (2m) apart, wear a mask, and wash your hands. But still, certain 'superspreader' events - birthday parties, bar nights, and even choir practice - seem to be the culprits in an outsized number of Covid-19 infections. So how can one night out, or a single infected person, lead to dozens of cases? We asked Dr Abraar Karan, a physician and public health researcher at Harvard Medical School, to look at three different cases since the US outbreak began to understand how some events can shift from low to high risk, and how to avoid attending a superspreader event yourself. At a superspreading event, the number of cases transmitted will be disproportionately high compared to general transmission, Dr Karan says. And the risk of these superspreading events may balloon in the presence of superspreading people, who pass on their infection more widely either by being in contact with more people or emitting more of the virus. "I tend to think of it as this: the vast majority of people may not infect any other people, and some people in certain situations infect a lot of people," he says. "One person may infect 10 people, or 15 people or 20 people." Research is still being done, Dr Karan says, but early results indicate that coronavirus spread is primarily powered by these supercharged events. "Different models have looked at this and they suggest that 20% of people account for 80% of spread." And while risk profiles will vary widely between similar events, Dr Karan says there are certain factors that should raise a red flag. "If you have any of the following in combination: indoors, crowded, closed spaces, without any sort of personal protective equipment like masks, which you're not going to have eating - I think those are all high-risk," he says.

7-4-20 Underwater caves once hosted the Americas’ oldest known ochre mines
Now-submerged Mexican caves hold signs of red pigment extraction as early as 12,000 years ago. Ancient Americans ventured deep into caves along a stretch of Mexico’s Yucatán Peninsula to mine a red pigment that could have had both practical and ritual uses, researchers say. Discoveries of mining-related artifacts and digging areas by divers in three now-submerged cave systems indicate that people there removed a natural pigment called red ochre, say archaeologist Brandi MacDonald of the University of Missouri in Columbia and her colleagues. Radiocarbon dates of burned wood from fires used to illuminate mining areas place humans at these sites between roughly 12,000 and 10,000 years ago, making it the oldest evidence of ochre mining in the Americas, the investigators report July 3 in Science Advances. Previous finds have suggested that ancient Americans used red ochre in many ways, including as an antiseptic, sunscreen, hide-tanning agent and for body painting and other symbolic purposes (SN: 2/12/14). Remnants of ancient pigment mining uncovered by MacDonald’s team raise the possibility that some miners may have died and been left where they perished. Divers previously found at least 10 human skeletons in Yucatán caves dating to as early as around 12,000 years ago, before rising seas inundated the underground chambers (SN: 2/6/20). In one cave system, an approximately 900-meter-long series of tunnels dubbed La Mina contained extensive evidence of red ochre extraction. Several narrow passages leading into La Mina contained piles of stones and broken pieces of cave growths that miners apparently used as navigation guides. Other broken-off cave growths had been wielded as digging tools. Most of the 352 pits and other intentionally disturbed areas in La Mina contain remnants of ochre deposits, the researchers say. Ochre samples from La Mina were bright red and chemically suitable for making paint, they add.

7-3-20 Coronavirus: Testing sewage an 'easy win'
A sewage-based coronavirus test could be an "easy win" that would pick up infection spikes up to 10 days earlier than with existing medical-based tests. Scientists led by UK's Centre for Ecology and Hydrology are working on a standardised test to "count" the amount of coronavirus in a wastewater sample. "The earlier you find [a signal], the earlier an intervention can happen," says lead researcher Dr Andrew Singer. "That means lives will be made much more liveable in the current crisis." A network of scientists from universities including Newcastle, Bangor and Edinburgh have already teamed up with local water companies to collect samples of untreated sewage from treatment plants; the first stage in mapping the outbreak through the sewers. Early in the Covid-19 pandemic, research revealed that people infected with the virus "shed" viral material in their faeces. That insight prompted an interest in "sewage epidemiology". "By sampling wastewater at different parts of the sewerage network, we can gradually narrow an outbreak down to smaller geographical areas, enabling public-health officials to quickly target interventions in those areas at greatest risk of spreading the infection," said Dr Singer. "Our network already has six labs that are capable of doing that work, so a national surveillance system could happen tomorrow." So while the researchers say they already have a reliable test that can show the presence or absence of the coronavirus, they are now working on a way to measure levels of infection regularly and reliably across the water-treatment network. "It's easy to say whether something's there or not with genetic fingerprinting," explained Newcastle University's Prof David Graham, who is involved in the development of that test. "But for the sake of epidemiology - which has life-and-death impacts - we wanted to be more exact." Prof Graham and his colleagues have now developed a way to quantify the genetic material from the coronavirus.

7-3-20 Eating seaweed can genetically modify the bacteria in our guts
Eating seaweed can genetically alter the bacteria in your gut as they can acquire genes from marine bacteria for digesting substances unique to seaweeds. It isn’t known if this affects people’s health, but having gut bacteria that can digest carrageenan, a common food additive derived from seaweed, might be harmful. “Our microbes are naturally genetically engineering themselves,” says Eric Martens at the University of Michigan. Seaweeds contain unique dietary fibres – large carbohydrate molecules – that neither we nor the bacteria in our guts can normally digest. For instance, the nori wrappers used for sushi are rich in porphyran. In 2012, however, a team including Martens found that one gut bacterium had acquired the genes needed to digest porphyran, probably from a bacterium that lives in the sea. Now a team led by Martens has found several more examples. The researchers started by seeing if any bacteria present in faecal samples from a few hundred volunteers could grow if fed only carbohydrates unique to certain seaweeds. They then sequenced the genomes of these bacteria. The team found two strains of Bacteroides gut bacteria that can digest carrageenan, which is found in red seaweeds traditionally eaten in parts of Europe and Asia. It is added to many foods to thicken them, and is also found in some sex lubricants. There has been controversy over the safety of carrageenan because it can break down into a substance called poligeenan, which is toxic. Full-size carrageenan molecules should normally pass through the gut intact, but people with bacteria that can digest carrageenan might produce poligeenan in their guts. “Whether this happens in enough abundance, we don’t know,” says Martens. Even if poligeenan is produced, it might remain safely inside bacteria. This issue should be investigated further, he says.

7-3-20 A sugary diet changes gut bacteria and worsens brain function in rats
We know diets can shape the billions of bacteria that live in your gut. Now, research in rats suggests the gut bacteria may, in turn, affect brain function by changing the way genes are expressed in areas important for memory. Scott Kanoski at the University of Southern California and his colleagues fed young rats a high-sugar diet while a separate group of rats were only fed standard chow. Around a month later, the team tested the rats’ memory. Specifically, rats performed a task designed to measure their ability to tell whether or not they had seen an item before, in a specific context. This type of memory is thought to rely on a brain structure called the hippocampus. The rats on a high-sugar diet performed significantly worse than those that had been given healthy food. The two groups of rats also appeared to have differences in their gut microbiomes. An analysis of the animals’ faeces found that the guts of the sugar-fed rats had higher levels of several types of bacteria. The levels of one of these types of bacteria seem to correspond to memory performance. Rats with higher levels of Parabacteroides bacteria performed worst on the memory task. To find out if Parabacteroides bacteria might be influencing brain function, Kanoski’s team delivered the bacteria directly to the guts of a separate group of rats that had been fed a cocktail of antibiotics to kill off previous communities of bacteria. Rats given Parabacteroides performed worse in the same memory tasks compared with rats that had just been treated with antibiotics. The hippocampi of the rats also appear to express genes differently. This brain region had a pattern of gene expression that suggested alterations in the way certain groups of neurons fire in both rats that were fed sugar and those treated with Parabacteroides. There are several different ways gut bacteria might influence the brain, says Ted Dinan at University College Cork, Ireland. The vagus nerve, for example, provides a direct connection between the gut and brain. Preliminary evidence suggests that some types of gut bacteria can alleviate anxiety in mice – but only if the vagus nerve is intact. Gut bacteria also produce a variety of compounds that might affect brain function.

7-3-20 4 reasons not to worry about that ‘new’ swine flu in the news
While similar to H1N1, it has shown no signs of spreading rapidly or causing severe disease. It may feel odd to be thinking ahead to the next potential pandemic when the world is far from finished with the current one. But reports of a newly identified swine influenza virus that shows hints of being able to spread among humans have raised that specter — although public health officials say it’s not an imminent threat. That virus, identified in pigs in some parts of China, has characteristics similar to a strain that caused the 2009 H1N1 swine flu pandemic (SN: 12/18/09), a new study finds. But just identifying such a flu virus circulating in pigs does not mean it poses an immediate threat to people. Rather it signals to researchers that they should monitor sick people for similar viruses. “It’s not an immediate threat where you’re seeing infections,” Anthony Fauci, director of the U.S. National Institute of Allergy and Infectious Diseases in Bethesda, Md., said in a U.S. Senate hearing on June 30. “But it’s something we need to keep our eye on, just the way we did in 2009 with the emergence of the swine flu.” Influenza viruses bind to a protein called sialic acid to break into cells. Birds and people have different types of this protein in their upper airway, but pigs have both. That makes pigs not only susceptible to swine-specific flu strains but also to flu viruses from birds and humans. As a result, the animals often become influenza mixing pots. Once in pigs, bird, swine and human flu viruses can exchange genetic material — called reassortment — giving rise to new strains (SN: 2/12/10). If some of those new strains can infect people and make them sick, the virus might go on to cause larger outbreaks. Like the 2009 H1N1 virus, a newly identified pig virus, called G4 EA H1N1, or G4 for short, can attach to the type of sialic acid that lines a person’s respiratory tract, and it can also replicate in human cells grown in a dish, researchers report June 29 in the Proceedings of the National Academy of Sciences. Infected ferrets — an animal commonly used to study influenza because ferrets exhibit similar symptoms as people — can also get sick and pass the virus to other ferrets. The findings hint that the virus has the potential to cause disease and be transmitted among people.

7-3-20 Medics who changed history wouldn't get into modern medical schools
Many of the people behind the most significant medical discoveries of the past 300 years wouldn’t have got into medical school by today’s standards, because they either studied the “wrong” subjects, got low grades or didn’t follow the rules. The finding highlights how the education system wrongly favours academic achievement over other important traits, like persistence and creativity, says David Jenkins at the University of Toronto, Canada. “We have to be much more flexible in how we accept young people into medical school or any other profession or activity that is their goal,” says Jenkins. Jenkins’s research was born out of his own frustration with being penalised because he “couldn’t read very quickly”. He has since noticed how would-be medical students spend hours memorising passages from physics textbooks that they will never use in clinical practice. To find out if this academic focus might rule out potential students who might otherwise be destined for greatness, Jenkins and his colleagues looked at the early academic achievements of 100 people considered to be among the greatest innovators in medicine. The list of innovators included Edward Jenner, who discovered the world’s first vaccine – for smallpox, which has since been eradicated worldwide. Frederick Banting was another example, who conducted Nobel prizewinning research on the role that insulin can play in treating diabetes. Specifically, the team looked at which subjects the innovators had studied at school, and their grades, as well as the comments of their teachers, and whether they had ever failed or been expelled. “We assume all great medical innovators would certainly be accepted to medical school,” says Jenkins. But his team found that, by today’s standards, only 24 per cent would meet entry requirements.

7-2-20 Why COVID-19 is both startlingly unique and painfully familiar
The coronavirus has a lot of tricks up its sleeve, but not all of them are new. For Abby Knowles, a headache and fatigue was just the start. She soon felt like she had a tight band across her chest, making it difficult to breathe. She developed pain in her upper body, which led doctors to check if she was having a heart attack (she wasn’t). Her blood pressure began to oscillate — too low, too high — leaving her lightheaded and nauseous. Her mind became so foggy she couldn’t read a book. A symptom might taper off, only to return. “You’ll think, ‘Oh I’m done with that bit, brilliant,’” Knowles says, “and then three days later it will be back.” After more than three months of illness, Knowles — who is 38 and lives in Reading, England — has been referred for an evaluation for long-term complications from COVID-19, the disease caused by the virus SARS-CoV-2. Meanwhile, her husband Dan, who also became sick toward the end of March, had a high fever and more typical COVID-19 symptoms for a few days but soon recovered. The experiences of the Knowles and many COVID-19 patients point to the ways that the coronavirus can be maddeningly unpredictable. Some people have debilitating illness, while others barely feel sick, if at all. For some, it’s mostly a respiratory illness, while others have neurological symptoms (SN: 6/12/20), such as loss of smell (SN: 5/11/20). Severely ill patients may develop life-threatening blood clots (SN: 6/23/20), adding vascular symptoms to the list. Some patients are struggling to get back to normal long after being sick. And the way the disease plays out by age can be baffling. Severe cases of COVID-19 have been rare among children, but some have suffered a dangerous inflammatory syndrome that can appear weeks after an infection (SN: 6/3/20). Older people remain at highest risk for hospitalizations and death from COVID-19, but young adults are getting seriously ill, too (SN: 3/19/20). That group generally tends to fare better than the very young and very old with viral infections (one glaring exception: the 1918 flu pandemic, which killed healthy, young adults at a high rate). In the six months since China reported a pneumonia of unknown cause, doctors have described a burgeoning catalog of health harms from what’s now called COVID-19. In some ways, the disease stands apart: The range of COVID-19’s effects and the difficulty in predicting how severely it will hit any one person is out of the ordinary. But some of the symptoms and patterns associated with COVID-19 are painfully familiar.

7-2-20 Horror movie fans are better at coping with the coronavirus pandemic
Everyone is entitled to one good scare – and it may be good for us. People who watch a lot of horror films and those who are morbidly curious about unpleasant subjects seem to be more psychologically resilient to the covid-19 pandemic, a study reveals. “Horror users tended to have less psychological distress,” says Coltan Scrivner at the University of Chicago. The research was prompted by a question from New Scientist news editor Penny Sarchet. In a Twitter conversation with horror researcher Mathias Clasen at Aarhus University in Denmark, Sarchet asked “if people who like apocalyptic/horror movies (which I’ve always hated!) will be more resilient to the trauma of this pandemic”. Scrivner, Clasen and their colleagues decided to find out. They asked 310 US volunteers which film genres they liked, including horror and other “prepper” genres such as post-apocalyptic and alien invasion. They also asked whether people had seen pandemic-themed films such as Contagion. The volunteers then took personality tests and a questionnaire designed to measure their morbid curiosity: their motivation to seek out information about dangerous situations or phenomena. Alongside this, the volunteers were asked how well they were coping with the covid-19 pandemic, both whether they were still having positive experiences despite the crisis, and whether they were experiencing unusually severe negative states like anxiety. Participants were also asked how well-prepared they had been – for instance, whether the pandemic’s consequences took them by surprise. Fans of horror movies were less prone to negative mental states. “Which suggested to us, maybe with horror it’s about emotion regulation,” says Scrivner. Watching scary movies “allows me to give myself the experience of being afraid and then conquering that fear”. This may be one of the underlying reasons for people’s fascination with scary stories.

7-1-20 The way our bodies remember coronavirus should make a vaccine possible
THROUGHOUT the pandemic, SARS-CoV-2 has proved full of surprises, most of them nasty. Initially regarded as a respiratory virus, we now know it infects other organ systems, and can linger for months. It disproportionally kills people from poor and ethnic minority backgrounds and also men, for reasons that still aren’t fully understood. It doesn’t seem to be suppressed by warm weather or climates. But the latest surprise is a nice one. Initial fears that the virus would fail to raise immune memory – the lengthy, sometimes lifelong, protection that we get from exposure to many viruses including measles – look exaggerated. It is still early days, but signs from patients point to a strong and long-lasting immune response (see “Can we become immune to the coronavirus? What the evidence says so far”). That is welcome news for two reasons. It makes a vaccine more likely, and means that people who have recovered from the virus almost certainly can’t get it again, at least in the short term. But it also brings complications. One is that governments will be tempted to introduce “immunity passports” for people who have recovered, perhaps permitting them to travel or attend large gatherings, which those without passports would be banned from. That may seem like a good idea, but bioethicists warn that it could backfire, for example by creating perverse incentives to get infected and a black market in stolen or forged passports. It could also be the start of a slippery slope to a more comprehensive system of health passports and surveillance. The other fear is that it revives the canard that naturally acquired herd immunity will save us. That this was ever on the table beggars belief: without knowing whether natural immunity exists, positing herd immunity as an exit strategy is scientifically illiterate. Even now, natural herd immunity is for the birds. The levels of infection required would kill millions and devastate health services. But herd immunity does remain the way out, if it is artificially created by vaccination. On that front, the latest science looks good. With infections rising globally (see “Lockdown measures return as covid-19 cases spike in several countries”), we badly need it.

7-1-20 Evolution tells us why there are two types of leader in today's world
The leadership styles of Donald Trump and Jacinda Ardern are dramatically different, but our evolutionary history explains both – and why our preferences have changed. DONALD TRUMP in the US and Jacinda Ardern in New Zealand. Vladimir Putin in Russia and Sanna Marin in Finland. It is hard to imagine more drastically different political figures. Yet each of these individuals has reached the highest office in their country. Given the vast differences in their personal qualities, behaviour and rhetoric, can we ever understand what makes for a successful leader? How is it that Trump, Ardern, Putin and Marin can all become leaders of their nations? If you have had any exposure to business leadership theories, you may see a pattern here. Many identify two main ways that leaders exert their influence over groups. These dichotomies go by names such as democratic versus autocratic, participative versus directive and personalised versus positional. This sort of analysis may be helpful in characterising leadership styles, but it can only take us so far in understanding why we have the leaders we do. Now, an idea emerging from evolutionary biology promises to do much more. This approach connects the two distinct leadership styles with deeper human drives and motivations. Its proponents argue that through this perspective, we can explain a lot about the state of the world today, from the US-China trade war to the success of countries such as New Zealand, Germany and Taiwan in responding to covid-19, and from Boris Johnson’s victory in last year’s UK general election to the under-representation of women in boardrooms. Some believe this model can even predict the outcome of the forthcoming US presidential election. Can they be right? Evolutionary biologists call the two styles of leadership “dominance” and “prestige”. A prestige leader influences people through their superior personal attributes, such as knowledge, wisdom and vision. These leaders may also be charismatic and use their skill at rhetoric to win over followers: think of Jesus or Confucius. Or, for a more contemporary case, take the German chancellor Angela Merkel. Women aren’t restricted to prestige leadership alone, but it is thought by some that female leaders generally operate this way because women’s responsibilities for childcare and food-gathering throughout most of human history have left them with an “evolved psychology” that is more cooperative, in general, than men’s. At least, that’s how prestige leadership is depicted by Mark van Vugt at Vrije University in Amsterdam, the Netherlands, and Jennifer Smith at Mills College in Oakland, California, in a paper published last year that sets out this evolutionary model.

7-1-20 Coronavirus: What does Covid-19 do to the brain?
Stroke, delirium, anxiety, confusion, fatigue - the list goes on. If you think Covid-19 is just a respiratory disease, think again. As each week passes, it is becoming increasingly clear that coronavirus can trigger a huge range of neurological problems. Several people who've contacted me after comparatively mild illness have spoken of the lingering cognitive impact of the disease - problems with their memory, tiredness, staying focused. But it's at the more severe end that there is most concern. Chatting to Paul Mylrea, it's hard to imagine that he had two massive strokes, both caused by coronavirus infection. The 64-year-old, who is director of communications at Cambridge University, is eloquent and, despite some lingering weakness on his right side, able-bodied. He has made one of the most remarkable recoveries ever seen by doctors at the National Hospital for Neurology and Neurosurgery (NHNN) in London. His first stroke happened while he was in intensive care at University College Hospital. Potentially deadly blood clots were also found in his lungs and legs, so he was put on powerful blood-thinning (anticoagulant) drugs. A couple of days later he suffered a second, even bigger stroke and was immediately transferred to the NHNN in Queen Square. Consultant neurologist Dr Arvind Chandratheva was just leaving hospital when the ambulance arrived. "Paul had a blank expression on his face," he says. "He could only see on one side and he couldn't figure out how to use his phone or remember his passcode. "I immediately thought that the blood thinners had caused a bleed in the brain, but what we saw was so strange and different." Paul had suffered another acute stroke due to a clot, depriving vital areas of the brain of blood supply. Tests showed that he had astonishingly high levels of a marker for the amount of clotting in the blood known as D-dimer. Normally these are less than 300, and in stroke patients can rise to 1,000. Paul Mylrea's levels were over 80,000. "I've never seen that level of clotting before - something about his body's response to the infection had caused his blood to become incredibly sticky," says Dr Chandratheva.

7-1-20 Coronavirus: Immunity may be more widespread than tests suggest
People testing negative for coronavirus antibodies may still have some immunity, a study has suggested. For every person testing positive for antibodies, two were found to have specific T-cells which identify and destroy infected cells. This was seen even in people who had mild or symptomless cases of Covid-19. But it's not yet clear whether this just protects that individual, or if it might also stop them from passing on the infection to others. Researchers at the Karolinksa Institute in Sweden tested 200 people for both antibodies and T-cells. Some were blood donors while others were tracked down from the group of people first infected in Sweden, mainly returning from earlier affected areas like northern Italy. This could mean a wider group have some level of immunity to Covid-19 than antibody testing figures, like those published as part of the UK Office for National Statistics Infection Survey, suggest. It's likely those people did mount an antibody response, but either it had faded or was not detectable by the current tests. And these people should be protected if they are exposed to the virus for a second time. Prof Danny Altmann at Imperial College London described the study as "robust, impressive and thorough" and said it added to a growing body of evidence that "antibody testing alone underestimates immunity". This doesn't necessarily get us any closer to herd immunity, though, according to assistant professor Marcus Buggert, one of the study's authors. More analysis needs to be done to understand whether these T-cells provide "sterilising immunity", meaning they completely block the virus, or whether they might protect an individual from getting sick but not stop them from carrying the virus and transmitting it. Much of the discussion around Covid-19 immunity has focused on antibodies - Y-shaped proteins which act like "missiles shooting down a target", assistant Prof Buggert explained. They bind to the virus before it can enter your cells, and neutralise it. If antibodies fail to neutralise the virus, it can enter your cells and turn them into virus-making factories. T-cells, on the other hand, target already-infected cells and completely destroy them, stopping them from spreading to other, healthy cells.

7-1-20 Can we become immune to the coronavirus? What the evidence says so far
WHEN the novel pneumonia circulating in China was confirmed to be caused by a coronavirus, an already troubling situation suddenly got that bit worse. As a rule, coronaviruses don’t produce a very strong “immune memory”: the long-lasting response that allows our bodies to thwart a subsequent attack, and which makes vaccines possible. When reports emerged from Japan and China of people who had been given the all-clear catching the virus again, immunologists’ worst fears seemed to be confirmed. But seven months later, hopes are rising. There is no longer any serious doubt that our bodies can form an immune memory to the SARS-CoV-2 virus – although we still don’t know how effective that memory will be. “That is the main outstanding question for covid-19,” says Nicolas Vabret at the Icahn School of Medicine at Mount Sinai in New York. “It’s absolutely the right question to be asking now because so many things depend on it,” says Paul Klenerman at the University of Oxford. That includes the prospect of developing vaccines, therapies and herd immunity, but also decisions on whether to issue immunity passports to people who have recovered from the virus, and how and when to ease lockdown measures. Immune memory can be an incredibly powerful and durable force. Immunologists like to tell the story of a measles epidemic on the Faroe Islands in 1846. When Danish doctor Peter Panum went to investigate, he discovered that the disease was raging, but also that 98 older people were immune to it. They turned out to be the survivors of the islands’ previous outbreak in 1781. A single encounter with the measles virus had endowed them with lifelong protection. Other viruses, however, don’t generate such a strong immune response, which can make them difficult to vaccinate against. Respiratory syncytial virus, for example, has thus far resisted all efforts to develop a vaccine. Other viruses elicit a moderate immune response and weak, brief memory. Vaccines for these viruses are possible, but often require regular boosters to maintain immunity.


134 Evolution News Articles
for July 2020

Evolution News Articles for June 2020