19 articles from TUESDAY 5.11.2019

Study reveals which conditions can render basaltic volcanoes highly destructive

More than half of the world’s volcanoes are basaltic. Most basaltic eruptions tend to ooze their magma out in a relatively benign way, producing a thick, sticky flow. But occasionally they go off with a big bang, like the eruption of Mount Etna in 122BC, which destroyed the Roman town of Catania. Now a study reveals what makes some basaltic eruptions so explosive.

By cooking up miniature volcanoes in the lab, analysing rock samples flung from explosive basaltic eruptions and numerically modelling the eruption process, Dr Fabio Arzilli, from the University of Manchester, and colleagues showed that low temperature magma and fast ascent up the pipes are key conditions for an explosive basaltic eruption.

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Bradley Doorn has worked at NASA for 10 years. Credit: NASA/Bradley Doorn.

Brad Doorn, program manager for NASA Earth Applied Sciences Water Resources Program and Food Security Program, is receiving NASA’s prestigious Exceptional Service Medal for his committed work to advance NASA’s goals. This award is granted to NASA civil servants for “sustained performance that embodies multiple contributions” to NASA’s programs and goals, and whose “record of achievements sets a benchmark for others to follow.”

Doorn got his start in science in the Black Hills of South Dakota, and has seen the value of NASA Earth observations throughout his career. Now, he is responsible for developing the strategy to enhance these NASA capabilities for water resources and agriculture applications, including drought monitoring and crop management.

Lawrence Friedl, director of NASA’s Applied Sciences Program within the Earth Science division, remarked that the award is well-deserved. “Brad’s decade of service has ensured the Water Resources and Food Security Programs’ success,” Friedl said. “He’s built a standout team who's worked hand-in-hand with partners to ensure our Earth observations and research are benefitting communities around the world. He's a great leader – we wouldn’t be where we are today without him.”

Doorn said he is honored to receive the award, and is inspired daily by his team. “This award is a tremendous honor and wouldn’t have been possible without the Water Resources and Agriculture program management teams that develop and lead an inspired portfolio of applied research.  I am humbled by this recognition and thank the Applied Sciences Program, Earth Science Division and NASA for this opportunity to serve my country.” He will receive the award on November 5, 2019 at a ceremony in Washington, D.C.

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Tuesday, November 5, 2019 - 13:00
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The glow of the Milky Way — our galaxy seen edgewise — arcs across a sea of stars in a new mosaic of the southern sky produced from a year of observations by NASA’s Transiting Exoplanet Survey Satellite (TESS). Constructed from 208 TESS images, the panorama reveals both the beauty of the cosmic landscape and the reach of TESS’s cameras.
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If there is any field of science that understands the doctrine of unintended consequences, it’s medicine. We rely on antibiotics to wipe out infections, and in the process breed a class of superbugs resistant to the drugs. We develop powerful medications that can control chronic pain, and in the U.S., have a nationwide addiction crisis to show for that breakthrough.

Now, it appears, we can add asthma control to the list pharmaceutical blowbacks we didn’t see coming. According to a new study published in BMJ Open, the familiar lightweight, pocket-sized aerosolized inhalers that make breathing easier for so many of the 235 million people worldwide who suffer from asthma may be choking the planet on a powerful greenhouse gas they release in the process.

The study, led by Dr. Alexander JK Wilkinson, a respiratory specialist with Britain’s National Health Service, focused on the 4.67 million people diagnosed with asthma in the United Kingdom, but it has implications for treatment worldwide, including in the U.S., where 22.6 million people (6.1 million of them children) are afflicted with the condition. The researcher compared the greenhouse gas emissions of aerosol pumps—known as metered dose inhalers (MDI)—with dry powder inhalers (DPI), which are shaped something like a hockey puck and are activated simply by inhaling. The two weren’t even close.

The problem with MDIs is not carbon dioxide (the most common greenhouse gas), but rather two types of hydrofluoroalkane (HFA) gas, which represents a far smaller share of greenhouse emissions, but a much more powerful one. Even the least polluting inhaler was found to emit HFAs at levels equal to up to 10 kg (22 lbs.) of carbon dioxide into the air over the course of its 200-puff lifetime. The worst emitted the equivalent of more than 36 kg (79 lbs) of CO2.

Dry powder inhalers, by comparison, use no HFA propellants at all. To the extent that they have any carbon footprint, it’s mostly from their manufacture and disposal, and the numbers are comparatively small—from 1.5 kg to 6 kg (3.3 lbs to 13 lbs) CO2 equivalent depending on brand.

In the U.K., MDIs represent about 70% of all inhaler prescriptions and the researchers estimate they are responsible for releasing the equivalent of 635,000 metric tons of carbon dioxide each year. If just 10% of those patients switched to DPIs, the equivalent of 58,000 metric tons of CO2 could be kept out of the atmosphere. That, Britain’s Sky News pointed out, is the same carbon footprint as 180,000 gas-powered cars driving making the round-trip journey between London and Edinburgh—about 1,300 km (or approximately 800 miles) each.

What makes such a switchover especially important, the study argues, is that many of the people who are hurt most by all this MDI outgassing are the very people the inhalers are designed to help. “Climate change is a huge and present threat to health which will disproportionately impact the poorest and most vulnerable people on the planet,” the researchers wrote, “including people with pre-existing lung disease.”

Across the rest of Europe, less than 50% of inhalers prescribed are MDIs and in Scandinavia it’s barely 10%. The difference, in most cases, is less about pharmaceutical efficacy than simply local medical custom and practice.

The authors are not calling for a blanket elimination of MDIs. Dry powder inhalers require patients to have at least enough lung strength to draw in the medication, and many do not. For them, the forced puff of an MDI is the only way to administer the drug.

“We recognize the need to protect the environment,” said Jesica Kirby, head of health advice for the advocacy group Asthma UK, in a statement responding to the study, “but it’s critically important that people with asthma receive the medicines they need to stay well and avoid a life-threatening asthma attack.”

As with so many things medical, the right solution is all about finding the proper balance between cost and benefits. In the case of asthma, the benefit of dialing back the aerosols and turning to alternatives whenever possible can accrue to not just individual patients, but the planet at large.

Editor’s note, Nov. 7:

The original headline on this story has been updated to clarify that it is one commonly used type of inhaler—not all inhalers—that emits significant greenhouse gases.

Correction, Nov. 9:

An earlier version of this story misstated the greenhouse gas in the inhalers; it is hydrofluoroalkane, not methane.

Statement sets out ‘vital signs’ as indicators of magnitude of the climate emergency

The world’s people face “untold suffering due to the climate crisis” unless there are major transformations to global society, according to a stark warning from more than 11,000 scientists.

“We declare clearly and unequivocally that planet Earth is facing a climate emergency,” it states. “To secure a sustainable future, we must change how we live. [This] entails major transformations in the ways our global society functions and interacts with natural ecosystems.”

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Tuesday, November 5, 2019 - 09:30
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A new NASA study shows that over the last 20 years, the atmosphere above the Amazon rainforest has been drying out, increasing the demand for water and leaving ecosystems vulnerable to fires and drought. It also shows that this increase in dryness is primarily the result of human activities.
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Why Didn't She Get Alzheimer's? The Answer Could Hold a Key to Fighting the DiseaseThe woman's genetic profile showed she would develop Alzheimer's by the time she turned 50.A member of the world's largest family to suffer from Alzheimer's, she, like generations of her relatives, was born with a gene mutation that causes people to begin having memory and thinking problems in their 40s and deteriorate rapidly toward death around age 60.But remarkably, she experienced no cognitive decline at all until her 70s, nearly three decades later than expected.How did that happen? New research provides an answer, one that experts say could change the scientific understanding of Alzheimer's disease and inspire new ideas about how to prevent and treat it.In a study published Monday in the journal Nature Medicine, researchers say the woman, whose name they withheld to protect her privacy, has another mutation that has protected her from dementia even though her brain has developed a major neurological feature of Alzheimer's disease.This ultra rare mutation appears to help stave off the disease by minimizing the binding of a particular sugar compound to an important gene. That finding suggests that treatments could be developed to give other people that same protective mechanism."I'm very excited to see this new study come out -- the impact is dramatic," said Dr. Yadong Huang, a senior investigator at Gladstone Institutes, who was not involved in the research. "For both research and therapeutic development, this new finding is very important."A drug or gene therapy would not be available any time soon because scientists first need to replicate the protective mechanism found in this one patient by testing it in laboratory animals and human brain cells.Still, this case comes at a time when the Alzheimer's field is craving new approaches after billions of dollars have been spent on developing and testing treatments and some 200 drug trials have failed. It has been more than 15 years since the last treatment for dementia was approved, and the few drugs available do not work very well for very long.The woman is entering her late 70s now and lives in Medellin, the epicenter for an extended Colombian family of about 6,000 people whose members have been plagued with dementia for centuries, a condition they called "La Bobera" -- "the foolishness" -- and attributed to superstitious causes.Decades ago, a Colombian neurologist, Dr. Francisco Lopera, began painstakingly collecting the family's birth and death records in Medellin and remote Andes mountain villages. He documented the sprawling family tree and took dangerous risks in guerrilla and drug-trafficking territory to cajole relatives of people who died with dementia into giving him their brains for analysis.Through this work, Lopera, whose brain bank at the University of Antioquia now contains 300 brains, helped discover that their Alzheimer's was caused by a mutation on a gene called Presenilin 1.While this type of hereditary early-onset dementia accounts for only a small proportion of the roughly 30 million people worldwide with Alzheimer's, it is important because unlike most forms of Alzheimer's, the Colombian version has been traced to a specific cause and a consistent pattern. So Lopera and a team of American scientists have spent years studying the family, searching for answers both to help the Colombians and to address the mounting epidemic of the more typical old-age Alzheimer's disease.When they found that the woman had the Presenilin 1 mutation, but had not yet even developed a pre-Alzheimer's condition called mild cognitive impairment, the scientists were mystified."We have a single person who is resilient to Alzheimer's disease when she should be at high risk," said Dr. Eric Reiman, executive director of the Banner Alzheimer's Institute in Phoenix and a leader of the research team.The woman was flown to Boston, where some of the researchers are based, for brain scans and other tests. Those results were puzzling, said Yakeel Quiroz, a Colombian neuropsychologist who directs the familial dementia neuroimaging lab at Massachusetts General Hospital.The woman's brain was laden with the foremost hallmark of Alzheimer's: plaques of amyloid protein."The highest levels of amyloid that we have seen so far," said Quiroz, adding that the excessive amyloid probably accumulated because the woman has lived much longer than other family members with the Alzheimer's-causing mutation.But the woman had few other neurological signs of the disease -- not much of a protein called tau, which forms tangles in Alzheimer's brains, and little neurodegeneration or brain atrophy."Her brain was functioning really well," said Quiroz, who, like Reiman, is a senior author of the study. "Compared to people who are 45 or 50, she's actually better."She said the woman, who raised four children, had only one year of formal education and could barely read or write, so it was unlikely her cognitive protection came from educational stimulation."She has a secret in her biology," Lopera said. "This case is a big window to discover new approaches."Quiroz consulted Dr. Joseph Arboleda-Velasquez, who, like her, is an assistant professor at Harvard Medical School (he is also Quiroz's husband). Arboleda-Velasquez, a cell biologist at Massachusetts Eye and Ear, conducted extensive genetic testing and sequencing, determining that the woman has an extremely rare mutation on a gene called APOE.APOE is important in general-population Alzheimer's. One variant, APOE4, present in about 14% of people, greatly increases risk and is present in 40% of people with Alzheimer's. People with another variant, APOE2, occurring in about 7% of the population, are less likely to develop Alzheimer's, while those with the most common variant, APOE3, are in the middle.The Colombian woman has two copies of APOE3, but both copies have a mutation called Christchurch (for the New Zealand city where it was discovered). The Christchurch mutation is extremely rare, but several years ago, Reiman's daughter Rebecca, a technologist, helped determine that a handful of Colombian family members have that mutation on one of their APOE genes. They developed Alzheimer's as early as their relatives, though -- unlike the woman with mutations on both APOE genes."The fact that she had two copies, not just one, really kind of sealed the deal," Arboleda-Velasquez said.The woman's mutation is in an area of the APOE gene that binds with a sugar-protein compound called heparan sulfate proteoglycans (HSPG), which is involved in spreading tau in Alzheimer's disease.In laboratory experiments, the researchers found that the less a variant of APOE binds to HSPG, the less it is linked to Alzheimer's. With the Christchurch mutation, there was barely any binding.That, said Arboleda-Velasquez, "was the piece that completed the puzzle because, 'Oh, this is how the mutation has such a strong effect.'"Researchers were also able to develop a compound that, in laboratory dish experiments, mimicked the action of the mutation, suggesting it's possible to make drugs that prevent APOE from binding to HSPG.Dr. Guojun Bu, who studies APOE, said that while the findings involved a single case and more research is needed, the implications could be profound."When you have delayed onset of Alzheimer's by three decades, you say wow," said Bu, chairman of the neuroscience department at the Mayo Clinic in Jacksonville, Florida, who was not involved in the study.He said the research suggests that instead of drugs attacking amyloid or tau, which have failed in many clinical trials, a medication or gene therapy targeting APOE could be promising.Reiman, who led another newly published study showing that APOE has a bigger impact on a person's risk of getting Alzheimer's than previously thought, said potential treatments could try to reduce or even silence APOE activity in the brain. People born without APOE appear to have no cognitive problems, but they do have very high cholesterol that requires treatment.Huang, who wrote a commentary about the study and is affiliated with two companies focusing on potential APOE-related treatments, said the findings also challenge a leading Alzheimer's theory about the role of amyloid.Since the woman had huge amounts of amyloid but few other Alzheimer's indicators, "it actually illustrates, to my knowledge for the first time, a very clear dissociation of amyloid accumulation from tau pathology, neurodegeneration and even cognitive decline," he said.Lopera said the woman is just beginning to develop dementia, and he recently disclosed her genetic profile to her four adult children, who each have only one copy of the Christchurch mutation.The researchers are also evaluating a few other members of the Colombian family, who appear to also have some resistance to Alzheimer's. They are not as old as the woman, and they do not have the Christchurch mutation, but the team hopes to find other genetic factors from studying them and examine whether those factors operate along the same or different biological pathways, Reiman said."We've learned that at least one individual can live for very long having the cause of Alzheimer's, and she's resistant to it," Arboleda-Velasquez said. "What this patient is teaching is there could be a pathway for correcting the disease."This article originally appeared in The New York Times.(C) 2019 The New York Times Company