Hollows in the ground to catch and store heavy rain water are among projects that will get cash.

The United Arab Emirates is sending a satellite to the Red Planet to study its weather and climate.

If the 2010s were the decade when small satellites revolutionized the space industry, the 2020s will be when commercial space odysseys finally go mainstream. At least that's the gamble that Jason Andrews, the co-founder and former CEO of Seattle-based Spaceflight Industries, is taking with French-born tech entrepreneur Nicolas Gaume. Today Andrews and Gaume are taking the wraps off Orbite, a Seattle startup that will focus on getting would-be spacefliers ready for those future odysseys. "You're going to go to a space camp for the next generation," Gaume said. Andrews, who's been in the space business for more than two decades,… Read More

A New York court hearing accepts the plan to pull the OneWeb satellite company out of bankruptcy.

The US space agency's next rover is placed atop of the rocket that will send it to the Red Planet.

MPs warn some regions will run out of water within the next 20 years unless "urgent action" is taken.

The majority of emissions cuts from electric cars will be wiped out by new road-building.

An all-electric construction vehicle from the Staffordshire firm wins this year's MacRobert Award.

A third of all the lemur species on Earth are "one step from extinction".

New evidence has been found for epic prehistoric voyages between the Americas and eastern Polynesia.

The chance of breaching one of the Paris accord goals in the next five years has doubled, a study says.

Monica Coenraads had a terrible feeling something was wrong with her 14-month-old baby, Chelsea. She had not learned to walk. She had one word, duck, and then lost it.During a family vacation to Barbados more than 20 years ago, Chelsea cried the whole time. She bit her parents so hard they bled. She was only happy in the hotel room with the shades drawn."I got home and said: 'That's it. We have to figure out what is wrong.'"What happened upended Coenraads' life.Chelsea, it turned out, had a rare genetic disease, Rett syndrome. It's one of about 7,000 rare or orphan diseases -- defined in the United States as an illness that affects fewer than 200,000 people nationwide -- with more such diseases being identified every day. Ninety-five percent of them have no known therapies. They are overlooked by most scientists, and some illnesses may be untreatable, even if they are understood. And what research there was has largely been halted as labs closed in response to coronavirus fears.Coenraads, 57, who lives in Trumbull, Connecticut, has encouraged research into Rett syndrome where there had been none, providing hope for her daughter and the small number of people who live with the disease, and showing one way that a determined person can succeed against such odds.When frantic parents of children with other rare disorders ask how she did it and what they can do, Coenraads recognizes the fear in their voices."We have no choice," she said. "We are desperate parents. We have children with horrible diseases."She talks to every parent who calls, but, she said, "I always get off the phone thinking: 'You don't know what you're up against. It is daunting, and it will consume your life.'"What follows are the stories of Coenraads and three people who have succeeded in promoting research on uncommon diseases, but in very different ways.'Single-Minded Advocacy'Coenraads is not extraordinarily wealthy and had no science background when she started searching for help for Chelsea, who is now 23. She ran an Italian restaurant in Stamford, Connecticut, but sold it when she was pregnant, intending to be a stay-at-home mother for a year or two.She was, and then some.The Coenraads had never heard of Rett syndrome when they received that diagnosis for Chelsea, at age 2. It is a neurological disorder caused by a mutated gene on the X chromosome that destroys a child's abilities to walk, talk, eat and even breathe easily. There was no treatment, no cure. And because it is so rare -- it affects only 1 in 10,000 girls and almost no boys -- it seemed destined to languish as a research curiosity, not something companies would pursue.Coenraads refused to accept that situation. She started the Rett Syndrome Research Trust in 2007. It has since raised $70 million, nearly all from private donations and galas with silent and live auctions -- "typical nonprofit fundraising," Coenraads said.But money was not enough."I wasn't going to sit back and assume research was happening and things would work out," she said. She wanted to figure out the bottlenecks and what would be needed to move the work forward.She began by looking for scientists who knew about Rett and calling them."Everyone helped," she said. "Everyone gave me the names of a few others. Within six months, I had a plan."She explained what was involved:"You have to get up to speed on the science, which is no easy feat. And after that, you must understand what has been done and, more important, what has to be done."If that weren't daunting enough, she said, "you have to learn the basics of drug development and how to recruit scientists and companies to work on your disease." And she cautioned that with researchers, "you have to recognize when a project sure is interesting but isn't necessarily going to move the needle closer to a cure."Even after a breakthrough, academics usually are not able to initiate the sort of clinical studies that are needed to show a research discovery can help patients."Ninety-nine percent of the time, the discovery will languish," Coenraads said. "Scientists will move on to their next discovery."Once she had gathered enough academic research, she was able to "hit the ground running," she said, contacting companies and telling them what they wanted to hear: Yes, there was a mouse model of the disease. Yes, there were so-called natural history studies that illustrate what to expect if the disease was not treated.She interested one company, Avexis, in starting a gene therapy trial. Then Avexis was bought by Novartis, which has said it hopes to do the trial after more preliminary work.One scientist, Sir Adrian Bird at the University of Edinburgh, described Coenraads' work in a ceremony when his university conferred her an honorary degree: "For what started as a tiny charity to inspire world-class research on a disorder that initially languished in obscurity and ignorance, and take it all the way to the brink of clinical application in less than 20 years is an amazing achievement."He added, "There is no doubt that it would not have happened without Monica's single-minded advocacy."At 23, Chelsea is in a wheelchair, unable to speak, stand, eat or use her hands, and she needs a feeding tube. She has scoliosis and intractable seizures, as well as tight, painful muscles. But Chelsea is aware and loving, Coenraads said, with, "a beautiful and engaging personality."The coronavirus has presented new challenges for her care. Because she's at such high risk, caregivers cannot enter the Coenraads' home. Coenraads' husband, Pieter, who owns a store that sells uniforms and medical scrubs, has to go to work every day, so Monica Coenraads is now on her own to care for Chelsea.She helps her daughter stretch every day and exercise on a treadmill, using a device that supports her and holds her upright."It was very hard in the beginning, but we found our rhythm," Coenraads said. "Now I can get work done and care for her."She Became Her Own ExpertMost seeking a cure for a rare genetic disease hope to recruit scientists and companies to do the work. But one determined couple took another route. They went back to school and became scientists themselves.The journey of Sonia Vallabh, 36, and her husband, Eric Minikel, began in December 2011. She was living in Cambridge, Massachusetts, and had just graduated from Harvard Law School. Her mother died the year before, at age 52, from Gerstmann-Straussler-Scheinker syndrome, a degenerative and uniformly fatal brain disease caused by misfolded prion proteins.It is estimated that no more than 10 out of every 100 million people have GSS. Symptoms begin subtly, progressing from clumsiness to an inability to walk and developing slurred speech that eventually inhibits talking. Late stages often result in dementia.Knowing there was a 50-50 chance, Vallabh took a genetic test that gave her the bad news that she was going to develop GSS, and probably around the same age as her mother.Vallabh had just started work at a small consulting company, and her husband, now 36, had recently gotten a degree in urban planning from MIT. The couple decided they had to learn more. They knew there was no treatment or cure for GSS. Was there any promising research?They realized they didn't understand enough about the science to ask the right questions."There was a certain amount of vocabulary needed," Vallabh said. "I didn't want to call people and have them say: 'Oh yeah, we're working on a cure. We will call you in five years.'"She started night classes in molecular biology, biochemistry, cell biology and genetics at the Harvard Extension School and audited courses at MIT.Then she decided she needed to see how things were done in a lab. So she got a job as a research technician at Massachusetts General Hospital, quitting her day job as a lawyer. Her husband soon followed, quitting his urban-planning job and starting a position there in bioinformatics.Soon they decided they had to study prion diseases, so they enrolled as Ph.D. students at Harvard. After receiving their degrees, they were hired at the Broad Institute in Cambridge with a laser focus on finding a treatment that might work in Vallabh's lifetime.They decided their best bet was molecules that can block the production of prion proteins called antisense oligonucleotides. Drugs based on the molecules work in other genetic disorders; they enter the brain by being injected into the spinal fluid, and appear to be safe.In October 2014, the couple met with Ionis, a small biotechnology firm, to see if the company would develop a prion antisense oligonucleotide.Vallabh learned from the meeting that the rules are different for rare diseases. For common diseases, companies do the preliminary work. But with rare diseases, "the burden shifts," she said.It is not enough to have data supporting an idea for an effective treatment. Vallabh and Minikel had to develop a test to show the drug was working. They had to do studies showing the treatment changed the disease's course in animals. They had to sign up more than 200 people willing to participate in research or clinical trials. And they had to meet with the Food and Drug Administration."We took on a lot," Vallabh said.But in 2018, Ionis agreed to work toward a clinical trial.A preparatory step was to recruit and study people who have the gene but do not yet have symptoms and others without the gene. The aim was to see if those with the gene have subtle markers of disease progression. That study began in 2017, but recruitment was suspended in March because of coronavirus."I believe in the drug; I believe in the strategy," Vallabh. And, she said, once the trial starts, "I do think we can get a rigorous answer in a relatively short time frame, within a year."But is it really feasible for others to take the path Vallabh and Minikel took?"I know, I know," Vallabh said. "We are and aren't all in the same boat. Every disease has its own landscape."It is almost, but not quite, unheard-of for people with a rare disease mutation to do their own research, Vallabh said.People like her "are rare," she added.'Working Against the Clock'Neena Nizar, 42, grew up in Dubai, United Arab Emirates, knowing something was wrong with her but unable to find out what. One doctor after another proposed an incorrect diagnosis. She was told she had rickets, then that she had polio. She had a series of useless surgeries.She eventually learned the diagnosis: Jansen's metaphyseal chondrodysplasia, a genetic disease so rare only about 30 cases have been reported since it was first described in 1970. Patients have deformed bones, short limbs, small hands with clubbed fingers, dwarfism and a large upper face but a tiny jaw.Today, Nizar has a Ph.D. in educational leadership and lives in Elkhorn, Nebraska, where she is married and has two boys, now 11 and 9. Her search for a diagnosis began when she realized her sons, as they were growing up, shared her affliction."I sent X-rays around the world of my kids and myself," she said. "I sent them to all of the skeletal dysplasia experts, but no one knew what it was."She also contacted more than 50 geneticists. Most didn't know what their condition was. But a pediatric geneticist in India, Dr. Sheela Nampoothiri, figured it out after taking one look at Nizar's sons' X-rays. She remembered seeing a slide in a medical school class. The professor said he was going to skip right over that slide, the doctor told Nizar, explaining to students that "you will never see this."The doctor sent Nizar's DNA for genetic testing. She had chondrodysplasia, and by then, the boys' bones were already badly bent."I knew we had to get the kids treatment," she said.Dr. Harald Jueppner, a pediatric nephrologist at Massachusetts General, was the researcher who first identified the mutation that caused the condition. Nizar learned that he had been studying the mutated gene, called a PTH/PTHrP receptor, for 20 years out of scientific interest. But he had never seen a patient. She told him he could now see three -- herself and her two sons.She also learned that Jueppner and a colleague, Thomas Gardella, had found in experiments that certain peptides, or short chains of amino acids, looked promising as possible treatments for Jansen's. At that point Nizar latched onto the researchers, urging them to study the peptides for Jansen's. They tried one of them in animal experiments. It partly reversed some of the abnormalities, Jueppner said, but, he added, "remember, this mouse model of Jansen's is far from being ideal."Nizar stayed in constant contact with Jueppner and Gardella prodding them to not lose sight of the work."Working with Neena has been an incredible experience," Jueppner said. "She is a force of nature."In 2017, Nizar set up a foundation to support research. But she was not in a good position to fundraise. "We only had eight patients, and I couldn't go to GoFundMe," she said. "My family and friends are tired of giving me money."So Nizar spoke to experts at conferences hosted by the National Institutes of Health, hoping to find a way to receive research funds. With her prodding, Jueppner and Gardella received a grant to study and improve the peptides they'd found as a possible Jansen's treatment.In 2018, Nizar asked the FDA for guidance. "They were surprised we didn't have a drug company, " she said. "I told the lady at the FDA that, at this point, I am the drug company."The researchers at Massachusetts General, she said, "have something we can try, and I want to get it to our kids." Time is limited, she stressed. "Once they hit puberty, some of their bones set. We are working against the clock."The FDA told her and the researchers at Massachusetts General what preclinical data would be required before testing in patients would be allowed.At the time, Jueppner estimated that the data might be available in a year or two. But the coronavirus changed all that. The lab shut down on March 20 and is slowly reopening, he said.If the research does proceed and if all goes well, Nizar said, she will be faced with a new set of problems."How can we make it in the absence of a pharmaceutical company?" she asked. Her tiny foundation certainly cannot manufacture the drug, and no one even holds patent rights."No matter how good your science is, you or your scientists can only take it so far," Nizar said.Building His Own CompanyMatt Wilsey knew a lot about what it takes for a company to succeed. Wilsey, a 42-year-old tech entrepreneur and investor, had a wide array of friends in California's Silicon Valley. But he never thought he'd have to use his business savvy to try to save his own child.When Grace Wilsey was born in 2009, Wilsey and his wife, Kristen, now 39, knew right away she had some problems. She was floppy and did not seem to be alert. She did not develop normally -- she did not sit up, or crawl. She did not learn to walk or talk.When Grace was 3, Matt and Kristen Wilsey found out why -- Grace had a genetic disorder so rare only one other child in the world, a little boy in Utah, was known to have it. It was caused by a mutation in a gene, NGLY1, but scientists did not know what that gene did or why a mutation would result in such devastating effects. They didn't know how the disease would progress or if Grace would die young.Matt Wilsey sprung into action. He asked Stanford physicians for guidance and was told he needed a foundation with a good advisory committee. Having money is great, they said, but you have to know whom and what to spend it on.He started a foundation and began cold calling and emailing scientific luminaries, asking if they would talk to him and agree to work on the project. So far, the foundation has raised $9 million, mostly from friends and family.Carolyn Bertozzi, a chemist at Stanford, was one of his initial recruits."He is really good at forming personal relationships," Bertozzi said. "That allowed him to convince total strangers to join his team and work on his cause."She was also touched by Wilsey's story and intrigued by the scientific challenge."Imagine you are a parent," she said. "No one had ever had this diagnosis before, and you have no idea what to expect."She was not alone. Wilsey managed to recruit about 150 eminent scientists as advisers, with some actively working on the research problem.Wilsey understands that it might appear his success is a result of his money and connections. But, he said, they have little to do with it. "Many of the people we work with don't even receive funding from us," he said. The "magic sauce," he said, is "hard work, time and constant relationship building."In 2017, he also invited patients from around the world to come to Palo Alto for a conference, and 21 families attended. He hopes to repeat the conferences every few years for the growing number of identified NGLY1 patients, now up to 70.The scientific team finally figured out that the mutated gene controls the way other genes function. Now they hope to develop a treatment -- gene therapy, or anything else that works.To move along whatever treatment looks promising, Wilsey and Bertozzi formed a company, Grace Science LLC.Wilsey realizes he has advantages others do not. He and his wife have the luxury of being able to work full time on their project. He has wealthy friends and relatives who donated generously to their foundation.And they can afford intensive therapy for Grace, who is now 10 years old. Wilsey said Grace's doctors told him his daughter probably was at the level of an 18-month-old. But he thinks she understands more than that. She can't talk, but he thinks she can communicate with her hands and eyes.Wilsey knows the disease seems to accelerate once children hit puberty, with an increase in seizures and greater risk of aspiration and choking, as well as more sleep disturbances. Children die, although he tries not to think about that."That's a constant reminder that the clock is ticking," Wilsey said. "You really can't give up. Even if the idea creeps into your mind, you push it right out."This article originally appeared in The New York Times.(C) 2020 The New York Times Company

Aligning polar satellites will enable the first ever reliable maps of Antarctic sea-ice thickness.

Dinosaurs are thought of as giant creatures, but new work adds to evidence they started out small.

Traders in India are being denied the "right to shade" under trees, threatening food security.

A stretch of DNA linked to COVID-19 was passed down from Neanderthals 60,000 years ago, according to a new study.Scientists don't yet know why this particular segment increases the risk of severe illness from the coronavirus. But the new findings, which were posted online Friday and have not yet been published in a scientific journal, show how some clues to modern health stem from ancient history."This interbreeding effect that happened 60,000 years ago is still having an impact today," said Joshua Akey, a geneticist at Princeton University who was not involved in the new study.This piece of the genome, which spans six genes on chromosome 3, has had a puzzling journey through human history, the study found. The variant is now common in Bangladesh, where 63% of people carry at least one copy. Across all of South Asia, almost one-third of people have inherited the segment.Elsewhere, however, the segment is far less common. Only 8% of Europeans carry it, and just 4% have it in East Asia. It is almost completely absent in Africa.It's not clear what evolutionary pattern produced this distribution over the past 60,000 years. "That's the $10,000 question," said Hugo Zeberg, a geneticist at the Karolinska Institute in Sweden who was one of the authors of the new study.One possibility is that the Neanderthal version is harmful and has been getting rarer overall. It's also possible that the segment improved people's health in South Asia, perhaps providing a strong immune response to viruses in the region."One should stress that at this point this is pure speculation," said Zeberg's co-author, Svante Paabo, the director of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany.Researchers are only beginning to understand why COVID-19 is more dangerous for some people than others. Older people are more likely to become severely ill than younger ones. Men are at more risk than women.Social inequality matters, too. In the United States, Black people are far more likely than white people to become severely ill from the coronavirus, for example, most likely due in part to the country's history of systemic racism. It has left Black people with a high rate of chronic diseases such as diabetes, as well as living conditions and jobs that may increase exposure to the virus.Genes play a role as well. Last month, researchers compared people in Italy and Spain who became very sick with COVID-19 to those who had only mild infections. They found two places in the genome associated with a greater risk. One is on chromosome 9 and includes ABO, a gene that determines blood type. The other is the Neanderthal segment on chromosome 3.But these genetic findings are being rapidly updated as more people infected with the coronavirus are studied. Just last week, an international group of scientists called the COVID-19 Host Genetics Initiative released a new set of data downplaying the risk of blood type. "The jury is still out on ABO," said Mark Daly, a geneticist at Harvard Medical School who is a member of the initiative.The new data showed an even stronger link between the disease and the chromosome 3 segment. People who carry two copies of the variant are three times more likely to suffer from severe illness than people who do not.After the new batch of data came out Monday, Zeberg decided to find out if the chromosome 3 segment was passed down from Neanderthals.About 60,000 years ago, some ancestors of modern humans expanded out of Africa and swept across Europe, Asia and Australia. These people encountered Neanderthals and interbred. Once Neanderthal DNA entered our gene pool, it spread down through the generations, long after Neanderthals became extinct.Most Neanderthal genes turned out to be harmful to modern humans. They may have been a burden on people's health or made it harder to have children. As a result, Neanderthal genes became rarer, and many disappeared from our gene pool.But some genes appear to have provided an evolutionary edge and have become quite common. In May, Zeberg, Paabo and Dr. Janet Kelso, also of the Max Planck Institute, discovered that one-third of European women have a Neanderthal hormone receptor. It is associated with increased fertility and fewer miscarriages.Zeberg knew that other Neanderthal genes that are common today even help us fight viruses. When modern humans expanded into Asia and Europe, they may have encountered new viruses against which Neanderthals had already evolved defenses. We have held onto those genes ever since.Zeberg looked at chromosome 3 in an online database of Neanderthal genomes. He found that the version that raises people's risk of severe COVID-19 is the same version found in a Neanderthal who lived in Croatia 50,000 years ago. "I texted Svante immediately," Zeberg said in an interview, referring to Paabo.Paabo was on vacation in a cottage in the remote Swedish countryside. Zeberg showed up the next day, and they worked day and night until they posted the study online Friday."It's the most crazy vacation I've ever had in this cottage," Paabo said.Tony Capra, a geneticist at Vanderbilt University who was not involved in the study, thought it was plausible that the Neanderthal chunk of DNA originally provided a benefit -- perhaps even against other viruses. "But that was 40,000 years ago, and here we are now," he said.It's possible that an immune response that worked against ancient viruses has ended up overreacting against the new coronavirus. People who develop severe cases of COVID-19 typically do so because their immune systems launch uncontrolled attacks that end up scarring their lungs and causing inflammation.Paabo said the DNA segment may account in part for why people of Bangladeshi descent are dying at a high rate of COVID-19 in the United Kingdom.It's an open question whether this Neanderthal segment continues to keep a strong link to COVID-19 as Zeberg and other researchers study more patients. And it may take discoveries of the segment in ancient fossils of modern humans to understand why it became so common in some places but not others.But Zeberg said that the 60,000-year journey of this chunk of DNA in our species might help explain why it's so dangerous today."Its evolutionary history may give us some clues," Zeberg said.This article originally appeared in The New York Times.(C) 2020 The New York Times Company

An Electron rocket launched from New Zealand's North Island fails in flight, destroying its satellites.

If a worm and a snake had a slimy, scandalous love child, it might look something like a caecilian: a legless creature that's actually neither worm nor snake but a soil-dwelling amphibian found in tropics across the globe.Content to spend most of their time beneath the forest floor, caecilians are elusive and poorly understood. Which is why Carlos Jared, a biologist at the Butantan Institute in Sao Paulo, Brazil, has spent a good part of the last three decades hot on their trail.Bagging a caecilian specimen, he said, often takes hours of laborious digging, carefully executed so a poorly aimed shovel doesn't cleave the creature in two. Once a specimen is spotted, "you have to jump on it," Jared said, and then wrestle the wriggly amphibian -- which, depending on the species, can range in length from a couple inches to 5 feet -- into a sack. Many caecilians have squirmed out of Jared's grasp at the last moment, gleefully greased by a gelatinous goo that oozes out of their skin.But Jared said the animals' fascinating and sometimes baffling biology makes the incessant chasing more than worth it. His team's latest discovery, published Friday in iScience, shows caecilians' mouths might be rimmed by venom-tipped teeth, not unlike those found in some snakes.The discovery would mark the first time venom glands have been found in the mouth of an amphibian -- one whose evolutionary history predates the appearance of snakes by more than 100 million years. That could make little-known caecilians among the oldest venomous biters on Earth.Like most other amphibians, caecilians have long been thought to produce only poisons, which, unlike venoms, aren't actively injected into other creatures. So Pedro Luiz Mailho-Fontana, a postdoctoral scholar working with Jared, was baffled when he discovered a series of fluid-filled ducts lining the teeth of a ringed caecilian specimen in the lab. "This is a very different thing here," he recalled thinking.After searching the mouths of newly hatched caecilians, Mailho-Fontana determined that the tooth-cradling glands grow out of the same tissue that gives rise to teeth.Dental tissue also happens to be the point of origin for venom glands in snakes, which could help explain the purpose of the newfound ducts, Jared said. Without legs or arms to parry with predators or prey, animals like snakes and caecilians must rely heavily on their heads.Caecilians, like some snakes, are equipped with impressive teeth, and can get pretty "bitey," said Emma Sherratt, an evolutionary biologist at the University of Adelaide who wasn't involved in the study.If caecilians also pack a venomous bite, they may have independently stumbled upon a strategy that's worked out well for many snakes. That would be "really interesting and remarkable," said Shab Mohammadi, an evolutionary biologist at the University of Nebraska-Lincoln who wasn't involved in the study. Perhaps limblessness is an important impetus for the evolution of tooth-borne toxins.But Mohammadi also noted that it's still unclear how noxious the glands' contents are or how toxic they are to the insects and worms that caecilians nosh on. Jared and his team have yet to do an in-depth chemical analysis of the caecilian's glandular goop, although early tests show it's full of a protein that's also present in venoms from insects and snakes. Caecilians' mouths seem to teem with slime at mealtimes, but the secretions have proved to be stubbornly viscous and tough to extract, Mailho-Fontana said.The researchers are also unsure how widespread venom glands are among caecilian species, which currently number more than 200 (with many more likely unknown). If the ducts are found in ancient lineages, it could indicate that caecilians were among the first land-living vertebrates to lace their bites with venom.Jared's team is planning to snag a few more specimens, but even once they manage to get them, it won't be easy.A few years ago, during a visit to a collaborator's lab in London, Marta Maria Antoniazzi, a co-author of the study also of the Butantan Institute, picked up a tiny caecilian that promptly sank its teeth into her hand."It hurt a lot," she said.And the wound took a surprisingly long time to close up. Now, Antoniazzi wonders if she was an unwitting victim of venom."At the time, we couldn't have even imagined," she said.This article originally appeared in The New York Times.(C) 2020 The New York Times Company

Can hydrogen - a relatively clean source of fuel - help power the economy of the future?

The launch of Nasa's Mars rover Perseverance is delayed again to 30 July at the earliest.