scientificamerican--2020-09-08--Jupiter's Ocean Moons Raise One Another's Tides

Jupiter ’ s four largest moons may be conspiring to maintain their subsurface oceans .
Long thought to arise from heat generated by the crust-flexing pull of Jupiter , these oceans may also owe their existence to immense subsurface tidal waves generated by gravitational interactions among the moons .
Measuring such tides can provide insights about the depths of these lunar abysses—environments that may offer the best chances for finding extraterrestrial life in our solar system .
Observations of Jupiter ’ s Galilean satellites—Europa , Callisto , Ganymede and Io—have long hinted at the presence of subsurface liquid layers .
@ @ @ @ @ @ @ have a water-rich mantle , while Io may instead have a magma ocean driving its extreme volcanic activity .
As the moons move around the planet , its gravitational tugging on their interior and the heat from the slow decay of radioactive elements have kept the liquid material from solidifying .
Less attention has been paid to how the moons pull at one another .
All objects in the universe exert a gravitational tug in proportion to their mass , and it attenuates across distances .
Jupiter , for instance , pulls on @ @ @ @ @ @ @ the effect is negligible .
Because of their small size , the Galilean satellites ’ tug on one another has long been considered irrelevant as well .
When Hamish Hay , then a graduate student at the University of Arizona , found himself working on a side project involving the tidal pull of exoplanets , he began to wonder more about the way an ocean layer could change the equation .
Hay , now a researcher at NASA ’ s Jet Propulsion Laboratory , decided to look at the tides of the ocean-rich @ @ @ @ @ @ @ he found that when the orbits of the natural satellites lined up just right , their relatively small pull could be amplified by the behavior of their oceans .
Under those special conditions , known as resonances , the tidal effects could grow significantly larger , even exceeding those produced by the much more massive Jupiter .
“ It 's quite interesting because the effects can be strong , ” says Mikael Beuthe , who studies subsurface oceans at the Royal Observatory of Belgium .
Beuthe reviewed Hay ’ s study but was @ @ @ @ @ @ @ High Seas in the Dark Below When NASA ’ s Voyager 1 spacecraft arrived at Jupiter in 1979 , it spotted volcanic plumes rising from Io that hinted at a buried magma ocean .
Further observations from Voyager 1 and other missions showed telltale fissures on the surface of Europa , revealing the icy moon ’ s crust was more active and mobile than previously realized , likely because of a subsurface ocean .
In recent years such oceans have been found on many other worlds—even tiny , cold Pluto may boast one @ @ @ @ @ @ @ , and many scientists suspect Ganymede and Callisto house their own deep , watery inner layers .
The oceans of Jupiter ’ s moons differ from those found on our planet .
Whereas Earth ’ s oceans have an average depth of about 3.7 kilometers—and plunge to 11 kilometers at their deepest point in the Mariana Trench—the Galilean satellites ’ oceans are thought to reach hundreds of kilometers .
That arrangement gives them an advantage for tidal changes .
“ Thick , [ or deep ] , oceans ... can respond very quickly @ @ @ @ @ @ @ .
The speed of a wave is controlled by the depth of its ocean , because a thick liquid reservoir can change more quickly than a thin one .
It seems counterintuitive , but a shallow ocean must push water from a wider region to form a wave as high as one created by a smaller area on a deep-ocean world .
Enter resonances , which behave somewhat like a child on a swing .
A push at just the right moment in the swing ’ s arc—or , in actuality , at @ @ @ @ @ @ @ s orbit—can give the swing a much greater boost than a push at another time .
Spurred by resonances stirred up by the pull of its Galilean neighbors , each moon ’ s liquid layer sloshes around higher and faster than it would otherwise .
The resulting tidal waves surge through that moon ’ s subsurface , never crashing against continents but instead continuing in a perpetual wave front that extends across half of the natural satellite ’ s circumference .
Resonances raised by Jupiter would be most potent in seas that are @ @ @ @ @ @ @ unrealistic assumption for the Galilean oceans .
The moons , however , can trigger resonances in deeper oceans as they twirl in their orbits , making the resulting waves more likely to surge higher than those caused by the planet itself .
According to Hay , this intramoon tidal pull should manifest most strongly near each Galilean satellite ’ s equator , potentially allowing water or magma to push through more easily there .
Greater levels of geologic activity at the equators could therefore be a possible signal of strong moon-on-moon tides .
@ @ @ @ @ @ @ although many other possible explanations exist for apparent enhancements to equatorial upwelling .
Much of Io ’ s volcanic activity seems to happen near its equator rather than its poles , although Hay cautions that appearance could be a result of observational bias : the equatorial region has been imaged more frequently than the poles .
NASA ’ s Juno mission is in the process of changing that imbalance and should provide more insights about Io ’ s polar regions .
That information is expected to help to determine the true frequency and @ @ @ @ @ @ @ .
Europa also appears to have an especially jumbled “ chaotic terrain ” near its equator that could come from material being squeezed to the surface by the tides .
Eventual measurements of the strength of any Galilean tides should be straightforward , however .
Above the waves , a moon ’ s crust rises and falls by several meters , too—much like the deck of a ship on a storm-tossed sea .
That movement could allow spacecraft such as the European Space Agency ’ s Jupiter Icy Moons Explorer ( JUICE ) @ @ @ @ @ @ @ tides .
Toward the end of its multi-year mission in the Jovian system , which is slated to begin in late 2029 , JUICE will orbit Ganymede in hopes of determining whether or not the moon has a liquid ocean .
Mission scientists already plan to measure Ganymede ’ s tidal amplitudes with two of the spacecraft ’ s instruments : 3GM and GALA .
“ If there are dynamical tides due to resonances , the signal due to moon-moon tides will be even more detectable , ” says 3GM ’ s principle @ @ @ @ @ @ @ part of Hay ’ s study .
Hauke Hussmann , principle investigator of GALA , who was also not involved in the paper , says that his instrument should be able to spot changes caused by the moons .
NASA ’ s Europa Clipper spacecraft , another mission slated to study Jupiter ’ s icy moons , may not be able to match JUICE ’ s measurements .
According to Clipper team member and Stanford University geophysicist Gregor Steinbrügge , the spacecraft ’ s ice-penetrating radar will be capable of measuring the large @ @ @ @ @ @ @ will struggle to see the subtler , more transient effects of intramoon tides .
If either mission manages to properly measure the rise and fall of the crust on a Galilean moon , those data could help in determining the depths of that moon ’ s ocean .
Because the resonance changes based on the thickness of the ocean , the frequency of the waves can provide a rough estimate .
A crust that crests 20 times per Europan day would have a thinner ocean , for instance , than one that does @ @ @ @ @ @ @ says .
By probing an oft-neglected quantity in the study of the Galilean satellites , Hay ’ s research has provided a new way to look at them .
“ We have to take this into account and do something about it , ” Beuthe says .
“ It could be an important factor ” in understanding these moons , he says .

Jupiter’s four largest moons may be conspiring to maintain their subsurface oceans. Long thought to arise from heat generated by the crust-flexing pull of Jupiter, these oceans may also owe their existence to immense subsurface tidal waves generated by gravitational interactions among the moons. Measuring such tides can provide insights about the depths of these lunar abysses—environments that may offer the best chances for finding extraterrestrial life in our solar system.
Observations of Jupiter’s Galilean satellites—Europa, Callisto, Ganymede and Io—have long hinted at the presence of subsurface liquid layers. Three of the moons are thought to have a water-rich mantle, while Io may instead have a magma ocean driving its extreme volcanic activity. As the moons move around the planet, its gravitational tugging on their interior and the heat from the slow decay of radioactive elements have kept the liquid material from solidifying.
Less attention has been paid to how the moons pull at one another. All objects in the universe exert a gravitational tug in proportion to their mass, and it attenuates across distances. Jupiter, for instance, pulls on Earth but is so far away that the effect is negligible. Because of their small size, the Galilean satellites’ tug on one another has long been considered irrelevant as well.
When Hamish Hay, then a graduate student at the University of Arizona, found himself working on a side project involving the tidal pull of exoplanets, he began to wonder more about the way an ocean layer could change the equation. Hay, now a researcher at NASA’s Jet Propulsion Laboratory, decided to look at the tides of the ocean-rich Galilean moons.
To his surprise, he found that when the orbits of the natural satellites lined up just right, their relatively small pull could be amplified by the behavior of their oceans. Under those special conditions, known as resonances, the tidal effects could grow significantly larger, even exceeding those produced by the much more massive Jupiter.
“It's quite interesting because the effects can be strong,” says Mikael Beuthe, who studies subsurface oceans at the Royal Observatory of Belgium. Beuthe reviewed Hay’s study but was not directly involved in the work.
High Seas in the Dark Below
When NASA’s Voyager 1 spacecraft arrived at Jupiter in 1979, it spotted volcanic plumes rising from Io that hinted at a buried magma ocean. Further observations from Voyager 1 and other missions showed telltale fissures on the surface of Europa, revealing the icy moon’s crust was more active and mobile than previously realized, likely because of a subsurface ocean. In recent years such oceans have been found on many other worlds—even tiny, cold Pluto may boast one. Ocean worlds seem to be widespread, and many scientists suspect Ganymede and Callisto house their own deep, watery inner layers.
The oceans of Jupiter’s moons differ from those found on our planet. Whereas Earth’s oceans have an average depth of about 3.7 kilometers—and plunge to 11 kilometers at their deepest point in the Mariana Trench—the Galilean satellites’ oceans are thought to reach hundreds of kilometers. That arrangement gives them an advantage for tidal changes. “Thick, [or deep], oceans ... can respond very quickly to tidal effects,” Hay says.
The speed of a wave is controlled by the depth of its ocean, because a thick liquid reservoir can change more quickly than a thin one. It seems counterintuitive, but a shallow ocean must push water from a wider region to form a wave as high as one created by a smaller area on a deep-ocean world.
Enter resonances, which behave somewhat like a child on a swing. A push at just the right moment in the swing’s arc—or, in actuality, at the proper point in a moon’s orbit—can give the swing a much greater boost than a push at another time. Spurred by resonances stirred up by the pull of its Galilean neighbors, each moon’s liquid layer sloshes around higher and faster than it would otherwise. The resulting tidal waves surge through that moon’s subsurface, never crashing against continents but instead continuing in a perpetual wave front that extends across half of the natural satellite’s circumference.
Resonances raised by Jupiter would be most potent in seas that are only a few hundreds of meters deep—an unrealistic assumption for the Galilean oceans. The moons, however, can trigger resonances in deeper oceans as they twirl in their orbits, making the resulting waves more likely to surge higher than those caused by the planet itself.
According to Hay, this intramoon tidal pull should manifest most strongly near each Galilean satellite’s equator, potentially allowing water or magma to push through more easily there. Greater levels of geologic activity at the equators could therefore be a possible signal of strong moon-on-moon tides. Observations already tentatively support this scenario, although many other possible explanations exist for apparent enhancements to equatorial upwelling. Much of Io’s volcanic activity seems to happen near its equator rather than its poles, although Hay cautions that appearance could be a result of observational bias: the equatorial region has been imaged more frequently than the poles. NASA’s Juno mission is in the process of changing that imbalance and should provide more insights about Io’s polar regions. That information is expected to help to determine the true frequency and distribution of the moon’s volcanoes. Europa also appears to have an especially jumbled “chaotic terrain” near its equator that could come from material being squeezed to the surface by the tides.
Plumbing the Depths
Eventual measurements of the strength of any Galilean tides should be straightforward, however. Above the waves, a moon’s crust rises and falls by several meters, too—much like the deck of a ship on a storm-tossed sea. That movement could allow spacecraft such as the European Space Agency’s Jupiter Icy Moons Explorer (JUICE) to measure the surges caused by resonant tides.
Toward the end of its multiyear mission in the Jovian system, which is slated to begin in late 2029, JUICE will orbit Ganymede in hopes of determining whether or not the moon has a liquid ocean. Mission scientists already plan to measure Ganymede’s tidal amplitudes with two of the spacecraft’s instruments: 3GM and GALA. “If there are dynamical tides due to resonances, the signal due to moon-moon tides will be even more detectable,” says 3GM’s principle investigator Luciano Iess, who was not part of Hay’s study. Hauke Hussmann, principle investigator of GALA, who was also not involved in the paper, says that his instrument should be able to spot changes caused by the moons.
NASA’s Europa Clipper spacecraft, another mission slated to study Jupiter’s icy moons, may not be able to match JUICE’s measurements. According to Clipper team member and Stanford University geophysicist Gregor Steinbrügge, the spacecraft’s ice-penetrating radar will be capable of measuring the large tidal deformations caused by Jupiter but will struggle to see the subtler, more transient effects of intramoon tides.
If either mission manages to properly measure the rise and fall of the crust on a Galilean moon, those data could help in determining the depths of that moon’s ocean. Because the resonance changes based on the thickness of the ocean, the frequency of the waves can provide a rough estimate. A crust that crests 20 times per Europan day would have a thinner ocean, for instance, than one that does so 21 times a day, Hay says.
By probing an oft-neglected quantity in the study of the Galilean satellites, Hay’s research has provided a new way to look at them. “We have to take this into account and do something about it,” Beuthe says. “It could be an important factor” in understanding these moons, he says.


scientificamerican--2020-09-09--Some Dinosaurs Probably Nested in Arctic

“ Those vicious , predatory dinosaurs that tended to be fairly small—six to nine , ten feet long snout to tail .
They ’ re certainly in the Jurassic Park movies , the things that terrorize people.
” Anthony Fiorillo , a paleontologist at Southern Methodist University in Dallas , Texas .
For more than two decades now , Fiorillo has been digging up dinosaur fossils hundreds of miles north of the Arctic Circle in Alaska .
“ So one of the fundamental questions about dinosaurs in Alaska , in the Ancient Arctic , is did they live there all @ @ @ @ @ @ @ how did they get there ?
” “ This fossil that ’ s the subject of this story is a baby dinosaur .
It ’ s a predatory dinosaur and it is a baby , it ’ s not just a juvenile and given the size estimate of this thing , this probably was not far from where the nesting ground was , so this is the first physical proof that at least some dinosaurs nested in the arctic ” Some of the first Arctic dinosaur remains ever found were discovered back in @ @ @ @ @ @ @ an archipelago north of mainland Norway .
Since then researchers have theorized that dinosaurs must have migrated to avoid deeply cold winters .
But Fiorillo says this new discovery disproves that idea .
“ Well , you know the classic stereotype for dinosaurs is that , had been that they were living in tropical and subtropical environments , sometimes somewhat swampy .
If you look at the various artworks over generations that was quite often how these dinosaurs were reconstructed.
” In reality , the climate north of Alaska ’ s Brooks range @ @ @ @ @ @ @ what we might see today in Portland Oregon or Calgary , Alberta .
“ Certainly a place where things were capable of being cool at times but certainly warmer than the Arctic today.
” The fossil find is a piece of jawbone , with a tooth , from a Dromaeosaur .
Fiorillo and colleagues unearthed it along the banks of the Colville River , not too far from the Arctic Ocean .
The bone is the first non-dental evidence of that species in the Far North .
The researchers report their discovery in @ @ @ @ @ @ @ Alessandro Chiarenza et al , The first juvenile dromaeosaurid ( Dinosauria : Theropoda ) from Arctic Alaska ] “ How did they do what they did ?
Because even with the warmer temperatures , at the latitude that these dinosaurs were living , which is at least 70 degrees north , if not even farther north , how did they endure long periods of light and dark ?
” And that ’ s where the research will go next .
For now , Fiorillo says the new discovery proves that these giant reptiles @ @ @ @ @ @ @ of the Late Cretaceous that we still experience today in the Arctic .

Full Transcript
“Those vicious, predatory dinosaurs that tended to be fairly small—six- to nine-, 10-feet-long, snout to tail—they’re certainly in the Jurassic Park movies, the things that terrorize people.”
Anthony Fiorillo, a paleontologist at Southern Methodist University in Dallas, Tex. For more than two decades now, Fiorillo has been digging up dinosaur fossils hundreds of miles north of the Arctic Circle in Alaska.
“So one of the fundamental questions about dinosaurs in Alaska, in the ancient Arctic, is: Did they live there all year round? Did they migrate? How did they get there?”
A recent discovery sheds light on those questions.
“This fossil that’s the subject of this story is a baby dinosaur. It’s a predatory dinosaur, and it is a baby; it’s not just a juvenile. And given the size estimate of this thing, this probably was not far from where the nesting ground was, so this is the first physical proof that at least some dinosaurs nested in the Arctic.”
Some of the first Arctic dinosaur remains ever found were discovered back in the 1960s in Svalbard, an archipelago north of mainland Norway. Since then researchers have theorized that dinosaurs must have migrated to avoid deeply cold winters. But Fiorillo says this new discovery disproves that idea.
“Well, you know, the classic stereotype for dinosaurs is that—had been that—they were living in tropical and subtropical environments, sometimes somewhat swampy. If you look at the various artworks over generations, that was quite often how these dinosaurs were reconstructed.”
In reality, the climate north of Alaska’s Brooks Range 70 million years ago was similar to what we might see today in Portland, Ore., or Calgary, Alberta.
“Certainly a place where things were capable of being cool at times but certainly warmer than the Arctic today.”
The fossil find is a piece of jawbone, with a tooth, from a dromaeosaur. Fiorillo and colleagues unearthed it along the banks of the Colville River, not too far from the Arctic Ocean. The bone is the first nondental evidence of that species in the far north. The researchers report their discovery in the journal PLOS ONE. [Alfio Alessandro Chiarenza et al., The first juvenile dromaeosaurid (Dinosauria: Theropoda) from Arctic Alaska]
Of course, questions remain:
“How did they do what they did? Because even with the warmer temperatures, at the latitude that these dinosaurs were living, which is at least 70 degrees north, if not even farther north, how did they endure long periods of light and dark?”
And that’s where the research will go next. For now, Fiorillo says the new discovery proves that these giant reptiles were well adapted to the highly seasonal environments of the Late Cretaceous that we still experience today in the Arctic.
—Emily Schwing
[The above text is a transcript of this podcast.]


scientificamerican--2020-09-08--Smoking or Vaping May Increase the Risk of a Severe Coronavirus Infection

Editor ’ s Note ( 9/8/20 ) : This article has been updated and republished in light of findings suggesting a higher rate of COVID-19 diagnoses among young adult e-cigarette users .
Smoking or vaping could make you more vulnerable to a severe infection with the novel coronavirus , some experts say .
Although there have not been many studies investigating this link specifically , a wealth of evidence suggests that smoking suppresses immune function in the lungs and triggers inflammation .
There have been far fewer investigations of vaping , but preliminary research suggests it may do similar damage @ @ @ @ @ @ @ users are at a heightened risk of developing chronic lung conditions , which have been associated with more severe cases of COVID-19 , as the disease caused by the new virus is called .
Scientists say it therefore seems reasonable to assume that smoking—and possibly vaping—could increase the risk of developing a serious infection from the coronavirus .
“ All these things make me believe that we are going to have more severe cases—especially [ in ] people who are [ long-term ] smokers or vapers , ” says Melodi Pirzada , chief @ @ @ @ @ @ @ on Long Island .
* She has not treated COVID-19 patients herself , “ but it is definitely common sense to think that once you have a history of smoking or vaping , the whole airways , the defense mechanism of your lungs—everything changes , ” she says .
Only a handful of studies have looked directly at whether smoking or vaping increases a person ’ s risk of severe COVID-19 .
A preprint study in China found that men were slightly more likely than women to be hospitalized for coronavirus infections , @ @ @ @ @ @ @ related to the fact that in the country , vastly more men than women smoke .
( The paper , which has not been peer-reviewed , has been withdrawn because it was based on early data .
It will be replaced with a more up-to-date version soon , the authors write . )
Another study , which has been published online in the Chinese Medical Journal , involved 78 patients with COVID-19 and found that those with a history of smoking were 14 times as likely to develop pneumonia .
** There is @ @ @ @ @ @ @ the lungs and suppresses immune function .
“ For regular smoking , we know it inhibits the ciliary clearance of the airways , ” Pirzada says .
“ We have these little [ hairlike ] structures known as cilia , and they are responsible for taking the toxins and the mucus out of our airways and clearing the lungs when we cough .
We know that that is affected when you smoke and when you vape.
” During a respiratory infection in the lungs , there tends to be an influx of white @ @ @ @ @ @ @ start killing the pathogen—followed by an influx of lymphocytes—which are responsible for clearing the infection .
“ There ’ s a very coordinated series of events that take place when you do become infected with a virus , ” says Ray Pickles , an associate professor of microbiology and immunology at the University of North Carolina at Chapel Hill .
“ These are probably the events that take place in the vast majority of us as individuals , whether we ’ re infected by influenza or whether we ’ re infected by SARS-CoV-2 @ @ @ @ @ @ @ known .
“ I think once you start perturbing this sequence of events in any which way or direction , that ’ s when things can go awry.
” Smoking is a known risk factor for influenza , says Robert Tarran , a professor of cell biology and physiology at Chapel Hill .
“ People who smoke are immunosuppressed to some degree , ” Tarran says .
“ They make more mucus .
It doesn ’ t clear the lungs as well .
There are pro-inflammatory changes ; immune cells are changed as @ @ @ @ @ @ @ to , basically , they ’ re more likely to get viruses and have a worse outcome.
” Vapers ’ risk of viral infections has not been studied as much , although there are some epidemiological studies suggesting they are more likely to get respiratory infections , Tarran says .
Five months after this story was first published , a national survey published in the Journal of Adolescent Health found that adolescents and young adults who reported vaping e-cigarettes were five times more likely to be diagnosed with COVID-19 than nonusers .
Those @ @ @ @ @ @ @ were seven times more likely to receive a positive diagnosis .
And animal studies provide some clues .
Mice that were exposed to e-cigarette aerosol and then inoculated with Streptococcus pneumoniae bacteria or influenza A were less likely to survive .
And vaping may interfere with neutrophil function , some studies suggest .
Scientists at Chapel Hill have shown that e-cigarette use suppresses the activity of immune- and inflammatory-response genes in nasal cells—more so even than smoking .
And a preprint study found that the gene that encodes the receptor ACE2 , which @ @ @ @ @ @ @ , is more active in smokers than nonsmokers .
Of course , none of these studies directly show that smoking or vaping increases the severity of COVID-19 infections , and it is not clear to what extent prior research can be extrapolated to the current pandemic .
But given that smoking and vaping do well-established harm to the immune system , it seems prudent to assume they might make coronavirus infections worse .
“ I think that a sensible thing to do for people is to stop smoking and stop vaping—and avoid secondhand @ @ @ @ @ @ @ director of the Center for Tobacco Control Research and Education at the University of California , San Francisco .
“ We don ’ t have every little detail on this nailed down , ” he says .
“ But based on what we know , generally , about smoking and e-cigarettes—and in particular about smoking and COVID-19 from people who are already sick , from one study in China—it stands to reason that you would lower your risk if you stopped doing these things.
” After all , Glantz adds , “ what @ @ @ @ @ @ @ ’ s Note ( 3/17/20 ) : This sentence was edited after posting to update Melodi Pirzada ’ s title .
**Editor ’ s Note ( 3/19/20 ) : This sentence was edited after posting to correct the figure for the increased risk of pneumonia .
Read more about the coronavirus outbreak here .

Editor’s Note (9/8/20): This article has been updated and republished in light of findings suggesting a higher rate of COVID-19 diagnoses among young adult e-cigarette users.
Smoking or vaping could make you more vulnerable to a severe infection with the novel coronavirus, some experts say.
Although there have not been many studies investigating this link specifically, a wealth of evidence suggests that smoking suppresses immune function in the lungs and triggers inflammation. There have been far fewer investigations of vaping, but preliminary research suggests it may do similar damage. And both long-term smokers and e-cigarette users are at a heightened risk of developing chronic lung conditions, which have been associated with more severe cases of COVID-19, as the disease caused by the new virus is called. Scientists say it therefore seems reasonable to assume that smoking—and possibly vaping—could increase the risk of developing a serious infection from the coronavirus.
“All these things make me believe that we are going to have more severe cases—especially [in] people who are [long-term] smokers or vapers,” says Melodi Pirzada, chief of pediatric pulmonology at NYU Winthrop Hospital on Long Island.* She has not treated COVID-19 patients herself, “but it is definitely common sense to think that once you have a history of smoking or vaping, the whole airways, the defense mechanism of your lungs—everything changes,” she says.
Only a handful of studies have looked directly at whether smoking or vaping increases a person’s risk of severe COVID-19. A preprint study in China found that men were slightly more likely than women to be hospitalized for coronavirus infections, and scientists say this observation could be related to the fact that in the country, vastly more men than women smoke. (The paper, which has not been peer-reviewed, has been withdrawn because it was based on early data. It will be replaced with a more up-to-date version soon, the authors write.) Another study, which has been published online in the Chinese Medical Journal, involved 78 patients with COVID-19 and found that those with a history of smoking were 14 times as likely to develop pneumonia.**
There is substantial scientific literature showing that smoking inflames the lungs and suppresses immune function. “For regular smoking, we know it inhibits the ciliary clearance of the airways,” Pirzada says. “We have these little [hairlike] structures known as cilia, and they are responsible for taking the toxins and the mucus out of our airways and clearing the lungs when we cough. We know that that is affected when you smoke and when you vape.”
During a respiratory infection in the lungs, there tends to be an influx of white blood cells called neutrophils—the first responders that start killing the pathogen—followed by an influx of lymphocytes—which are responsible for clearing the infection. “There’s a very coordinated series of events that take place when you do become infected with a virus,” says Ray Pickles, an associate professor of microbiology and immunology at the University of North Carolina at Chapel Hill. “These are probably the events that take place in the vast majority of us as individuals, whether we’re infected by influenza or whether we’re infected by SARS-CoV-2,” as the new coronavirus is known. “I think once you start perturbing this sequence of events in any which way or direction, that’s when things can go awry.”
Smoking is a known risk factor for influenza, says Robert Tarran, a professor of cell biology and physiology at Chapel Hill. “People who smoke are immunosuppressed to some degree,” Tarran says. “They make more mucus. It doesn’t clear the lungs as well. There are pro-inflammatory changes; immune cells are changed as well. And all that leads up to, basically, they’re more likely to get viruses and have a worse outcome.”
Vapers’ risk of viral infections has not been studied as much, although there are some epidemiological studies suggesting they are more likely to get respiratory infections, Tarran says. Five months after this story was first published, a national survey published in the Journal of Adolescent Health found that adolescents and young adults who reported vaping e-cigarettes were five times more likely to be diagnosed with COVID-19 than nonusers. Those who reported using both cigarettes and e-cigarettes were seven times more likely to receive a positive diagnosis. And animal studies provide some clues. Mice that were exposed to e-cigarette aerosol and then inoculated with Streptococcus pneumoniae bacteria or influenza A were less likely to survive. And vaping may interfere with neutrophil function, some studies suggest. Scientists at Chapel Hill have shown that e-cigarette use suppresses the activity of immune- and inflammatory-response genes in nasal cells—more so even than smoking. And a preprint study found that the gene that encodes the receptor ACE2, which the novel coronavirus uses to infect cells, is more active in smokers than nonsmokers.
Of course, none of these studies directly show that smoking or vaping increases the severity of COVID-19 infections, and it is not clear to what extent prior research can be extrapolated to the current pandemic. But given that smoking and vaping do well-established harm to the immune system, it seems prudent to assume they might make coronavirus infections worse.
“I think that a sensible thing to do for people is to stop smoking and stop vaping—and avoid secondhand exposure,” says Stanton Glantz, director of the Center for Tobacco Control Research and Education at the University of California, San Francisco. “We don’t have every little detail on this nailed down,” he says. “But based on what we know, generally, about smoking and e-cigarettes—and in particular about smoking and COVID-19 from people who are already sick, from one study in China—it stands to reason that you would lower your risk if you stopped doing these things.” After all, Glantz adds, “what’s the downside?”
*Editor’s Note (3/17/20): This sentence was edited after posting to update Melodi Pirzada’s title.
**Editor’s Note (3/19/20): This sentence was edited after posting to correct the figure for the increased risk of pneumonia.
Read more about the coronavirus outbreak here.


scientificamerican--2020-09-08--Mountain Peaks Seem to Shape Personality Traits in the American West

The designation “ mountain man ” conjures an image of a rough , bearded , possibly grimy white man living ruggedly and adventurously amid trees , snow , deer and the occasional bear .
Although most people who live in the U.S. ’ s mountain states today do not reflect this narrow , stereotypical extreme , the peaks that surround them may shape personality traits that resonate with the persona .
Findings published in Nature Human Behaviour on September 7 suggest that mountainous landscapes may promote openness to new experiences among the people who live in them .
But the @ @ @ @ @ @ @ slopes scored lower for other traits , such as agreeableness and extraversion—in keeping with the stereotype of the laconic individualist that has often been portrayed in Westerns .
The spirit of adventure seems to come with an embrace of solitude and isolation , all traits that may help adaptation to these harsh environments .
Although the results seem to confirm that mountains can shape some aspects of a “ mountain adventurer , ” the impact—what researchers call the effect size—for any one individual might be small , says the study ’ s first @ @ @ @ @ @ @ and psychologist at the University of Cambridge .
Not every single person living along the Colorado Front Range is a wild-haired , adventurous loner .
But mountains may draw out these traits to different degrees in people who live there , creating a sort of broad regional tendency .
Even if the effects are relatively small , Götz says , this geographical influence could “ scale up to produce consequential outcomes on the regional level.
” The exploration of the “ frontier ” mystique in the western U.S. needs to be revisited in @ @ @ @ @ @ @ about whether “ physical topography is associated with personality , ” says Michele Gelfand , a distinguished university professor in the department of psychology at the University of Maryland , who was not involved in the study .
Gelfand also raises the question of whether the findings apply primarily to the U.S. and its “ loose and individualistic culture.
” For example , the study results suggested that mountains might underlie lower scores for conscientiousness , a measure of conformity .
If researchers were to look at Switzerland , which is more close-knit @ @ @ @ @ @ @ might find that “ conscientiousness is higher in mountainous regions ” there , she says .
To examine the relationship between mountain living in the western U.S. and personality , Götz and his colleagues used self-reported data for about 3.39 million people aged 10 to 99 distributed across 37,227 zip codes in the 48 contiguous states , Alaska and Washington , D.C .
Almost three quarters of the respondents were white .
The investigators evaluated the “ mountainousness ” of the zip codes using both elevation and change in elevation .
And they @ @ @ @ @ @ @ five ” markers of personality traits : agreeableness ( trust and altruism ) , conscientiousness ( responsibility and adherence to social rules ) , extraversion ( sociability ) , neuroticism ( anxiety or emotional instability ) and openness to experience ( curiosity and creativity ) .
Then they compared how topography and these personality traits tracked with each other .
The team found that mountains tend to draw out openness to new experiences , emphasizing people ’ s tendencies toward originality and adventurousness .
But they seem to decrease the other four traits @ @ @ @ @ @ @ the West ” is long past—at least in terms of European settlement of lands taken from Native Americans in the region—its rugged mountains have “ acquired a unique sociocultural meaning ” that has lingered even as they have ceased to be the “ frontier , ” Götz says .
That persistent mystique and cultural legacy may still influence people even in the 21st century .
Götz is careful to emphasize that mountains ’ effect on personality is only one of many factors that shape broadly regional traits .
Just as many gene variants @ @ @ @ @ @ @ several influences , including “ mountainousness , ” act in concert to shape personality .
People living in cities might also embrace openness as a personality trait but with more of a social emphasis , Gelfand observes .
“ In cities , this trait may be adaptive because you are constantly meeting new people , and there are many weak ties and social networks , ” she says .
So “ while mountainous regions may be also high on openness , that could be for different reasons.
” Although the big five personality @ @ @ @ @ @ @ not without flaws ” and may not “ yield perfectly comparable results across cultures , ” Götz says .
Given the study ’ s focus on the sociocultural constructs around settlers moving west across the American landscape , the “ cross-cultural generalizability remains an open question , ” he says .
It ’ s a question he and his colleagues intend to pursue , examining cultures with populated mountain areas but without the colonialist American frontier legacy .
Because the effects of mountainousness are consistent but small , many other factors need to @ @ @ @ @ @ @ .
The big data sets and machine-learning approaches Götz and his colleagues used are excellent tools to search for these small but important factors .
Götz says that sorting through the massive amounts of information “ will be a long and tedious journey , ” not unlike an adventurous trek westward .

The designation “mountain man” conjures an image of a rough, bearded, possibly grimy white man living ruggedly and adventurously amid trees, snow, deer and the occasional bear. Although most people who live in the U.S.’s mountain states today do not reflect this narrow, stereotypical extreme, the peaks that surround them may shape personality traits that resonate with the persona.
Findings published in Nature Human Behaviour on September 7 suggest that mountainous landscapes may promote openness to new experiences among the people who live in them. But the authors also reported that denizens of the slopes scored lower for other traits, such as agreeableness and extraversion—in keeping with the stereotype of the laconic individualist that has often been portrayed in Westerns. The spirit of adventure seems to come with an embrace of solitude and isolation, all traits that may help adaptation to these harsh environments.
Although the results seem to confirm that mountains can shape some aspects of a “mountain adventurer,” the impact—what researchers call the effect size—for any one individual might be small, says the study’s first author Friedrich Götz, a Ph.D. candidate and psychologist at the University of Cambridge. Not every single person living along the Colorado Front Range is a wild-haired, adventurous loner. But mountains may draw out these traits to different degrees in people who live there, creating a sort of broad regional tendency. Even if the effects are relatively small, Götz says, this geographical influence could “scale up to produce consequential outcomes on the regional level.”
The exploration of the “frontier” mystique in the western U.S. needs to be revisited in other mountainous settings before making broader statements about whether “physical topography is associated with personality,” says Michele Gelfand, a distinguished university professor in the department of psychology at the University of Maryland, who was not involved in the study.
Gelfand also raises the question of whether the findings apply primarily to the U.S. and its “loose and individualistic culture.” For example, the study results suggested that mountains might underlie lower scores for conscientiousness, a measure of conformity. If researchers were to look at Switzerland, which is more close-knit and collectivist in its culture, they might find that “conscientiousness is higher in mountainous regions” there, she says.
To examine the relationship between mountain living in the western U.S. and personality, Götz and his colleagues used self-reported data for about 3.39 million people aged 10 to 99 distributed across 37,227 zip codes in the 48 contiguous states, Alaska and Washington, D.C. Almost three quarters of the respondents were white.
The investigators evaluated the “mountainousness” of the zip codes using both elevation and change in elevation. And they looked at the commonly used “big five” markers of personality traits: agreeableness (trust and altruism), conscientiousness (responsibility and adherence to social rules), extraversion (sociability), neuroticism (anxiety or emotional instability) and openness to experience (curiosity and creativity). Then they compared how topography and these personality traits tracked with each other.
The team found that mountains tend to draw out openness to new experiences, emphasizing people’s tendencies toward originality and adventurousness. But they seem to decrease the other four traits.
Even though the “opening of the West” is long past—at least in terms of European settlement of lands taken from Native Americans in the region—its rugged mountains have “acquired a unique sociocultural meaning” that has lingered even as they have ceased to be the “frontier,” Götz says. That persistent mystique and cultural legacy may still influence people even in the 21st century.
Götz is careful to emphasize that mountains’ effect on personality is only one of many factors that shape broadly regional traits. Just as many gene variants can contribute to who we are, several influences, including “mountainousness,” act in concert to shape personality.
People living in cities might also embrace openness as a personality trait but with more of a social emphasis, Gelfand observes. “In cities, this trait may be adaptive because you are constantly meeting new people, and there are many weak ties and social networks,” she says. So “while mountainous regions may be also high on openness, that could be for different reasons.”
Although the big five personality construct is useful, it is “not without flaws” and may not “yield perfectly comparable results across cultures,” Götz says. Given the study’s focus on the sociocultural constructs around settlers moving west across the American landscape, the “cross-cultural generalizability remains an open question,” he says. It’s a question he and his colleagues intend to pursue, examining cultures with populated mountain areas but without the colonialist American frontier legacy.
Because the effects of mountainousness are consistent but small, many other factors need to be assessed as candidates for shaping personality. The big data sets and machine-learning approaches Götz and his colleagues used are excellent tools to search for these small but important factors. Götz says that sorting through the massive amounts of information “will be a long and tedious journey,” not unlike an adventurous trek westward.


scientificamerican--2020-09-08--COVID-19's Disparate Impacts Are Not a Story about Race

George Floyd could not breathe .
Like other Americans now numbering in the hundreds of thousands , he gasped horribly for air before his world went dark .
Unlike them , his agony was not born from a lung-ravaging virus .
He was strangled .
He was killed in public , with the weight of anti-Black hatred kneeling terribly—almost boastfully—down on his neck .
Weeks before , and miles away , a comparison of public parks in New York shows the tale of two cities .
In some , uniformed officers protect groups of friends basking in the sunlight by @ @ @ @ @ @ @ , they patrol .
With eyebrows narrowed , they brutally arrest grieving folks of color for disobedience .
Near Sacramento , a 14-year-old child is pinned to asphalt and beaten in the face .
In Manhattan , a Black man is ground into asphalt for violating the six-feet social distancing order .
An officer slaps him , kneels terribly down on his neck .
In the Emergency Department , a patient ’ s father halts me with a fanned palm a foot from my chest—prevents me from examining his child even though I @ @ @ @ @ @ @ inquires if I ’ ve “ been home recently.
” My ability to take care of a gasping boy is questioned on account of my Taiwanese ethnicity .
A week later , a triage nurse asks a new patient why he has come to the hospital .
He responds , simply , that he had recently been “ coughed on by [ an ] Asian.
” In this pandemic , data are taking a back seat to racial prejudice .
The irrational racist surveillance that leads to the brutalization of Black Americans in @ @ @ @ @ @ @ and medical care .
Fueled by a president who continues to blame a faceless China for the pandemic ’ s miseries , citizens and caregivers of color face fear and disdain .
Simultaneously , re-emerging myths of genetic racial differences scrutinize bodies of color as sources of disease , all while obscuring the deadly climate of injustice that hastens breathlessness .
America ’ s racism is rampant , and it ’ s shaping the response to this pandemic to the detriment of us all .
Travel bans missed the mark .
Travelers from @ @ @ @ @ @ @ to at least 93 countries across five continents .
Voyages from Italy were responsible for bringing COVID-19 to 46 nations , while travel from China is responsible for just 27 index cases .
Yet , while the United States issued a travel ban on China at the end of January , it took another month and a half to limit European travel .
During that time , an estimated two million people flew from Europe to the land of the free .
As with the greater globe , a majority of U.S. index @ @ @ @ @ @ @ But stigma has not followed these lines of export the way it sticks to Asia and other “ aliens.
” Conservative legislators call for deportations and stronger defenses at the Southern border , while the “ normal reaction ” of anti-Asian hatred skyrockets .
Public political displays urging citizens to eat at empty Chinatown restaurants do little to stem the Sinophobia , but no such exhibition has been necessary to demonstrate the safety of spaghetti and meatballs .
The widespread media narrative is similarly skewed .
German Chancellor Angela Merkel ’ s pedigree @ @ @ @ @ @ @ in quantum chemistry was celebrated as an explanation for the prowess of her pandemic response .
But the reported success of Germany—a country of 83 million people , $ 3.9 trillion GDP , and over 9,300 COVID-19 deaths—does not seem so successful when compared to Vietnam , a country of 96 million people and $ 245 billion GDP , with zero COVID-19 deaths even in May .
Though East Asia had fewer deaths in total than Europe had every day throughout the early months of the pandemic , a New York Times list @ @ @ @ @ @ @ said an essay in Medium , “ exactly one sentence on Asia and the rest on white leaders that mostly did worse than Iran ” ( a country that , according to the New York Times , “ Completely and Utterly Botched Its Response to Coronavirus ” ) .
The same New York Times article praised the heroics of Italian leaders—who bore responsibility for a death toll 115 times that of South Korea ’ s count of 310 COVID-19 deaths—and focused on Western leadership without mentioning the relative summer success of countries in @ @ @ @ @ @ @ in Taiwan—just seven as of this writing .
We are supposed to use data to mitigate bias—to be objective—but we are picking and choosing what information we digest to fit our own narratives about who is to blame , where sickness comes from .
These statistics that we look to in order to be empirical , are actually imperial .
On the front lines , I order a chest x ray to investigate a man ’ s shortness of breath .
He clutches my protective yellow gown and asks , anxiously , if @ @ @ @ @ @ @ three weeks ago could be the culprit .
Later , he mentions that a close family friend recently traveled in Europe .
He does not connect this information to COVID-19—offers it only in passing to tell me where to buy good chocolates .
Later , a woman screams in my direction that she wants to f—ing destroy China .
The increasingly overt racism against Asian Americans—who today are broadly seen as “ Chinese ” —is a rehash of the historic entanglement of pandemic xenophobia with disease , genes , race , and risk @ @ @ @ @ @ @ and dangerous sources of disease .
Medical texts , like Arthur Stout ’ s 1862 publication on “ Chinese Immigration and the Physiologic Causes of the Decay of the Nation , ” add legitimacy to this racist folktale , which contends that foreigners , in addition to their biologic lowliness , also possess behavioral inferiority as evidenced by lack of sanitation and strange foods .
This fable is being told anew ; this February , the governor of Veneto , Italy—which grieves over 2,000 COVID-19 deaths amongst a population of 4.9 million—argued that @ @ @ @ @ @ @ since Italians have “ culturally strong attention to hygiene , washing hands ... whereas we have all seen the Chinese eating mice alive.
” President Trump—in direct violation of WHO guidelines for naming new pandemics—continues to reference COVID-19 as the Wuhan or Chinese Virus , even using the phrase “ kung flu ” at a campaign rally in Tulsa , Okla. , this June .
The idea that the color of someone ’ s skin determines their capacity for intelligence , health , and morality , is the same idea that leads some @ @ @ @ @ @ @ assault Black bodies deemed suspicious , even if they ’ re just jogging through the neighborhood .
Already in this pandemic , the same false ideas about biologic susceptibility have entered public discussion to skew national conversation .
On February 29 , Trump mega-fan Bill Mitchell tweeted to 550,000 followers : “ I read that Asian lungs have more receptors and are therefore more susceptible to this kind of virus .
Is this true or urban myth ?
” In June , during a legislative briefing on COVID-19 , Democratic Representative Bill Foster @ @ @ @ @ @ @ genetic component ” to racial disparities seen during the pandemic , and suggested the need for altering policy responses and “ genetic engineering ” to accommodate for potential differences in racial biology .
Taken in its worst form , these suggestions are redolent of Nazi-era scientific racism .
But these ideas , in fact , came from a non-peer reviewed 2020 study—already referenced in the Journal of the American Medical Association—which postulated that increased expression of specific lung cell receptors might explain why COVID-19 is “ concentrated in the Asian area.
” American @ @ @ @ @ @ @ skin color are perishing from COVID-19 at shockingly inordinate numbers .
Data show that Black Americans face excess COVID-19 death as a result of disparate access to testing , high levels of underlying health conditions , greater occupational exposure , and lower rates of medical insurance coverage .
Black bodies have been wounded and strained by decades of discriminatory housing policies , mass incarceration , malnutrition , and trauma .
Their lungs cough disproportionately with asthma because they ’ ve been forced to live near disease-producing highways and toxic landfills ; because they @ @ @ @ @ @ @ business strategies to drive profits up for the tobacco industry .
These are the injustices that make them unable to breathe .
And yet , Trump ’ s Surgeon General Jerome Adams ordered communities of color to “ step up ” and avoid drugs and alcohol during the pandemic , as if the individual behavior of Black people is to blame .
Ohio state senator and emergency medicine physician Steve Huffman wondered aloud during a hearing , if “ African Americans or the colored population ” face disparate coronavirus deaths because they “ @ @ @ @ @ @ @ as other groups.
” Simultaneously , publications in prestigious medical journals such as Health Affairs and the British Medical Journal continue to hypothesize that the disproportionate severity of COVID-19 in African American communities may be as result of yet unfound genetic factors .
Like the work of Stout , these theories—backed by the weight of physician and legislative authority—guide endeavors to focus on internal deficiencies within bodies of color , instead of intervening on the stark inequities of social treatment that leave them gasping for air .
We can not allow fables of @ @ @ @ @ @ @ burden of COVID-19 on people of color , as if the excess death of 13,000 Black people came from the consent of their genomes .
Still , the biology and behavior of people are color are being made into scapegoats for systemic suffering .
So while COVID-19 is not a story about race , it is a story about racism .
One that judges bodies of color as preordained sources of disease and menace—dangerous even down to their DNA .
It is the same gaze that indicted George Floyd as a worthy target @ @ @ @ @ @ @ , helpless , unable to breathe .
Floyd was not genetically predisposed to breathlessness .
He , like thousands of other Black patients , died because the color of his skin made him susceptible to inequity .
Today , no one suspects that Italy was terrorized by COVID-19 because Italian genes incline the population to respiratory illness .
Researchers understand that low COVID-19 mortality rates in New Zealand are not explained by beneficial polymorphisms .
We reach for fantasies of physiologic dissent only when it supports our existing biases .
We see how @ @ @ @ @ @ @ easily and automatically onto Asia , while Europe—buffered by its perceived whiteness , normalcy , and health—does not seem like a site of sickness or genetic variation .
This isn ’ t scientific .
This is a manifestation of the racist enterprise that registers certain groups as more diseased , more threatening , more worthy of policing .
It leads to irrational travel restrictions , public brutality .
The degree to which these reactionary impulses can influence decision-making—even in the face of logical , factual information—is indication of how strong these implicit biases @ @ @ @ @ @ @ .
The disparate travel bans on the East and West were a terrible mistake that shows how the massive gap between our biased narratives and our reality generates enormous anguish .
Systemic racism—and the hubris and blindness it bears—has hampered our ability to formulate cogent decisions at prodigious cost .
COVID-19 trekked , unchecked , on the backs of the assumed benign : the rich , the white , the wealthy .
But that ’ s not whom it hurt .
The people who suffered the most are the most vulnerable : the @ @ @ @ @ @ @ ’ t afford the hospital bill , the children without internet or clean water .
It ’ s the men and women who can not shelter in place because they have no refuge to crouch in .
The locked-up folks who don ’ t have six feet to give , the transplanted asylum-seekers who can not escape despair or disease .
They are the ones who pay .
They even the ledger , dripping in red .
The power that permitted the murder of George Floyd has inflicted a lethal shortness of breath @ @ @ @ @ @ @ his skin tone .
COVID-19 has burned through the country , abetted by a racist gaze that arbitrates bodies of color as cesspools of disease and danger .
This prejudiced contemplation has distorted our attention to focus on Asia , on DNA , despite clear testimony that indicts major , preexisting health inequities for the undue burden of pandemic suffering in communities of color .
This bigotry endangers the people who are thought to look dangerous , while waving through threats that do not fit the preordained description of a hazard—the European traveler @ @ @ @ @ @ @ cop .
At a time when predominantly Black U.S. counties are experiencing COVID-19 death rates six times higher than everyone else , it is impossible not to remember Eric Garner , choking , gasping .
It is impossible not to remember Ahmaud Arbery , whose sunny jog should not have robbed him of his breath .
It is impossible not to remember how George Floyd struggled against a knee to tell the world he could not breathe .
How he died , months before his 47th revolution around the sun .

George Floyd could not breathe. Like other Americans now numbering in the hundreds of thousands, he gasped horribly for air before his world went dark. Unlike them, his agony was not born from a lung-ravaging virus. He was strangled. He was killed in public, with the weight of anti-Black hatred kneeling terribly—almost boastfully—down on his neck.
Weeks before, and miles away, a comparison of public parks in New York shows the tale of two cities. In some, uniformed officers protect groups of friends basking in the sunlight by handing out masks and water. Elsewhere, they patrol. With eyebrows narrowed, they brutally arrest grieving folks of color for disobedience. Near Sacramento, a 14-year-old child is pinned to asphalt and beaten in the face. In Manhattan, a Black man is ground into asphalt for violating the six-feet social distancing order. An officer slaps him, kneels terribly down on his neck.
In the Emergency Department, a patient’s father halts me with a fanned palm a foot from my chest—prevents me from examining his child even though I’ve introduced myself as the doctor—and inquires if I’ve “been home recently.” My ability to take care of a gasping boy is questioned on account of my Taiwanese ethnicity. A week later, a triage nurse asks a new patient why he has come to the hospital. He responds, simply, that he had recently been “coughed on by [an] Asian.”
In this pandemic, data are taking a back seat to racial prejudice. The irrational racist surveillance that leads to the brutalization of Black Americans in their neighborhoods is spilling into public health and medical care. Fueled by a president who continues to blame a faceless China for the pandemic’s miseries, citizens and caregivers of color face fear and disdain. Simultaneously, re-emerging myths of genetic racial differences scrutinize bodies of color as sources of disease, all while obscuring the deadly climate of injustice that hastens breathlessness. America’s racism is rampant, and it’s shaping the response to this pandemic to the detriment of us all.
Travel bans missed the mark. Travelers from Europe—not Asia—brought the first cases of COVID-19 to at least 93 countries across five continents. Voyages from Italy were responsible for bringing COVID-19 to 46 nations, while travel from China is responsible for just 27 index cases. Yet, while the United States issued a travel ban on China at the end of January, it took another month and a half to limit European travel. During that time, an estimated two million people flew from Europe to the land of the free.
As with the greater globe, a majority of U.S. index cases came coughing, from Europe. But stigma has not followed these lines of export the way it sticks to Asia and other “aliens.” Conservative legislators call for deportations and stronger defenses at the Southern border, while the “normal reaction” of anti-Asian hatred skyrockets. Public political displays urging citizens to eat at empty Chinatown restaurants do little to stem the Sinophobia, but no such exhibition has been necessary to demonstrate the safety of spaghetti and meatballs.
The widespread media narrative is similarly skewed. German Chancellor Angela Merkel’s pedigree as a scientist with an advanced degree in quantum chemistry was celebrated as an explanation for the prowess of her pandemic response. But the reported success of Germany—a country of 83 million people, $3.9 trillion GDP, and over 9,300 COVID-19 deaths—does not seem so successful when compared to Vietnam, a country of 96 million people and $245 billion GDP, with zero COVID-19 deaths even in May. Though East Asia had fewer deaths in total than Europe had every day throughout the early months of the pandemic, a New York Times list of “true leaders” spent, said an essay in Medium, “exactly one sentence on Asia and the rest on white leaders that mostly did worse than Iran” (a country that, according to the New York Times, “Completely and Utterly Botched Its Response to Coronavirus”).
The same New York Times article praised the heroics of Italian leaders—who bore responsibility for a death toll 115 times that of South Korea’s count of 310 COVID-19 deaths—and focused on Western leadership without mentioning the relative summer success of countries in Africa, or the pandemic death count in Taiwan—just seven as of this writing.
We are supposed to use data to mitigate bias—to be objective—but we are picking and choosing what information we digest to fit our own narratives about who is to blame, where sickness comes from. These statistics that we look to in order to be empirical, are actually imperial.
On the front lines, I order a chest x ray to investigate a man’s shortness of breath. He clutches my protective yellow gown and asks, anxiously, if I think a package delivered from China three weeks ago could be the culprit. Later, he mentions that a close family friend recently traveled in Europe. He does not connect this information to COVID-19—offers it only in passing to tell me where to buy good chocolates. Later, a woman screams in my direction that she wants to f—ing destroy China.
The increasingly overt racism against Asian Americans—who today are broadly seen as “Chinese”—is a rehash of the historic entanglement of pandemic xenophobia with disease, genes, race, and risk. Immigrants are caricaturized as innately disposed and dangerous sources of disease. Medical texts, like Arthur Stout’s 1862 publication on “Chinese Immigration and the Physiologic Causes of the Decay of the Nation,” add legitimacy to this racist folktale, which contends that foreigners, in addition to their biologic lowliness, also possess behavioral inferiority as evidenced by lack of sanitation and strange foods.
This fable is being told anew; this February, the governor of Veneto, Italy—which grieves over 2,000 COVID-19 deaths amongst a population of 4.9 million—argued that Italy would fare better than Wuhan, since Italians have “culturally strong attention to hygiene, washing hands ... whereas we have all seen the Chinese eating mice alive.” President Trump—in direct violation of WHO guidelines for naming new pandemics—continues to reference COVID-19 as the Wuhan or Chinese Virus, even using the phrase “kung flu” at a campaign rally in Tulsa, Okla., this June.
The idea that the color of someone’s skin determines their capacity for intelligence, health, and morality, is the same idea that leads some people to feel the innate entitlement—the birthright—to assault Black bodies deemed suspicious, even if they’re just jogging through the neighborhood. Already in this pandemic, the same false ideas about biologic susceptibility have entered public discussion to skew national conversation.
On February 29, Trump mega-fan Bill Mitchell tweeted to 550,000 followers: “I read that Asian lungs have more receptors and are therefore more susceptible to this kind of virus. Is this true or urban myth?” In June, during a legislative briefing on COVID-19, Democratic Representative Bill Foster noted that there may be a “genetic component” to racial disparities seen during the pandemic.
These ideas came, in part, from a non-peer reviewed 2020 study—already referenced in the Journal of the American Medical Association—which postulated that increased expression of specific lung cell receptors might explain why COVID-19 is “concentrated in the Asian area.”
American citizens who share George Floyd’s skin color are perishing from COVID-19 at shockingly inordinate numbers. Data show that Black Americans face excess COVID-19 death as a result of disparate access to testing, high levels of underlying health conditions, greater occupational exposure, and lower rates of medical insurance coverage. Black bodies have been wounded and strained by decades of discriminatory housing policies, mass incarceration, malnutrition, and trauma. Their lungs cough disproportionately with asthma because they’ve been forced to live near disease-producing highways and toxic landfills; because they’ve been maliciously targeted by predatory business strategies to drive profits up for the tobacco industry. These are the injustices that make them unable to breathe.
And yet, Trump’s Surgeon General Jerome Adams ordered communities of color to “step up” and avoid drugs and alcohol during the pandemic, as if the individual behavior of Black people is to blame. Ohio state senator and emergency medicine physician Steve Huffman wondered aloud during a hearing, if “African Americans or the colored population” face disparate coronavirus deaths because they “do not wash their hands as well as other groups.”
Simultaneously, publications in prestigious medical journals such as Health Affairs and the British Medical Journal continue to hypothesize that the disproportionate severity of COVID-19 in African American communities may be as result of yet unfound genetic factors. Like the work of Stout, these theories—backed by the weight of physician and legislative authority—guide endeavors to focus on internal deficiencies within bodies of color, instead of intervening on the stark inequities of social treatment that leave them gasping for air.
We cannot allow fables of inherent racial difference to sanction the disproportionate burden of COVID-19 on people of color, as if the excess death of 13,000 Black people came from the consent of their genomes. Still, the biology and behavior of people are color are being made into scapegoats for systemic suffering.
So while COVID-19 is not a story about race, it is a story about racism. One that judges bodies of color as preordained sources of disease and menace—dangerous even down to their DNA. It is the same gaze that indicted George Floyd as a worthy target of violence even as he was handcuffed, helpless, unable to breathe.
Floyd was not genetically predisposed to breathlessness. He, like thousands of other Black patients, died because the color of his skin made him susceptible to inequity.
Today, no one suspects that Italy was terrorized by COVID-19 because Italian genes incline the population to respiratory illness. Researchers understand that low COVID-19 mortality rates in New Zealand are not explained by beneficial polymorphisms.
We reach for fantasies of physiologic dissent only when it supports our existing biases. We see how ideas of danger and biologic difference map easily and automatically onto Asia, while Europe—buffered by its perceived whiteness, normalcy, and health—does not seem like a site of sickness or genetic variation.
This isn’t scientific. This is a manifestation of the racist enterprise that registers certain groups as more diseased, more threatening, more worthy of policing. It leads to irrational travel restrictions, public brutality. The degree to which these reactionary impulses can influence decision-making—even in the face of logical, factual information—is indication of how strong these implicit biases are, how muscular this inequity is.
The disparate travel bans on the East and West were a terrible mistake that shows how the massive gap between our biased narratives and our reality generates enormous anguish. Systemic racism—and the hubris and blindness it bears—has hampered our ability to formulate cogent decisions at prodigious cost.
COVID-19 trekked, unchecked, on the backs of the assumed benign: the rich, the white, the wealthy. But that’s not whom it hurt. The people who suffered the most are the most vulnerable: the essential workers, the elders who can’t afford the hospital bill, the children without internet or clean water. It’s the men and women who cannot shelter in place because they have no refuge to crouch in. The locked-up folks who don’t have six feet to give, the transplanted asylum-seekers who cannot escape despair or disease. They are the ones who pay. They even the ledger, dripping in red.
The power that permitted the murder of George Floyd has inflicted a lethal shortness of breath on thousands of other citizens who share his skin tone. COVID-19 has burned through the country, abetted by a racist gaze that arbitrates bodies of color as cesspools of disease and danger. This prejudiced contemplation has distorted our attention to focus on Asia, on DNA, despite clear testimony that indicts major, preexisting health inequities for the undue burden of pandemic suffering in communities of color. This bigotry endangers the people who are thought to look dangerous, while waving through threats that do not fit the preordained description of a hazard—the European traveler, the international businessman, the uniformed cop.
At a time when predominantly Black U.S. counties are experiencing COVID-19 death rates six times higher than everyone else, it is impossible not to remember Eric Garner, choking, gasping. It is impossible not to remember Ahmaud Arbery, whose sunny jog should not have robbed him of his breath. It is impossible not to remember how George Floyd struggled against a knee to tell the world he could not breathe. How he died, months before his 47th revolution around the sun.
Editor’s Note (9/11/20): This article has been edited after posting to correct the description of Representative Bill Foster’s comments.


scientificamerican--2020-09-07--The Idea That a Scientific Theory Can Be 'Falsified' Is a Myth

J.B.S .
Haldane , one of the founders of modern evolutionary biology theory , was reportedly asked what it would take for him to lose faith in the theory of evolution and is said to have replied , “ Fossil rabbits in the Precambrian.
” Since the so-called “ Cambrian explosion ” of 500 million years ago marks the earliest appearance in the fossil record of complex animals , finding mammal fossils that predate them would falsify the theory .
But would it really ?
The Haldane story , though apocryphal , is one of many in the scientific folklore @ @ @ @ @ @ @ characteristic of science .
As expressed by astrophysicist Mario Livio in his book Brilliant Blunders : `` [ E ] ver since the seminal work of philosopher of science Karl Popper , for a scientific theory to be worthy of its name , it has to be falsifiable by experiments or observations .
This requirement has become the foundation of the ‘ scientific method.
’ ” But the field known as science studies ( comprising the history , philosophy and sociology of science ) has shown that falsification can not work even in @ @ @ @ @ @ @ result is not a simple fact obtained directly from nature .
Identifying and dating Haldane 's bone involves using many other theories from diverse fields , including physics , chemistry and geology .
Similarly , a theoretical prediction is never the product of a single theory but also requires using many other theories .
When a “ theoretical ” prediction disagrees with “ experimental ” data , what this tells us is that that there is a disagreement between two sets of theories , so we can not say that any particular theory @ @ @ @ @ @ @ other philosophy of science—is not necessary for the actual practice of science .
The physicist Paul Dirac was right when he said , `` Philosophy will never lead to important discoveries .
It is just a way of talking about discoveries which have already been made.
” Actual scientific history reveals that scientists break all the rules all the time , including falsification .
As philosopher of science Thomas Kuhn noted , Newton 's laws were retained despite the fact that they were contradicted for decades by the motions of the perihelion of @ @ @ @ @ @ @ .
It is the single-minded focus on finding what works that gives science its strength , not any philosophy .
Albert Einstein said that scientists are not , and should not be , driven by any single perspective but should be willing to go wherever experiment dictates and adopt whatever works .
Unfortunately , some scientists have disparaged the entire field of science studies , claiming that it was undermining public confidence in science by denying that scientific theories were objectively true .
This is a mistake since science studies play vital roles @ @ @ @ @ @ @ that it gives scientists a much richer understanding of their discipline .
As Einstein said : `` So many people today—and even professional scientists—seem to me like somebody who has seen thousands of trees but has never seen a forest .
A knowledge of the historic and philosophical background gives that kind of independence from prejudices of his generation from which most scientists are suffering .
This independence created by philosophical insight is—in my opinion—the mark of distinction between a mere artisan or specialist and a real seeker after truth . ''
The @ @ @ @ @ @ @ in inspiring more confidence in science , not less .
The second is that this knowledge equips people to better argue against antiscience forces that use the same strategy over and over again , whether it is about the dangers of tobacco , climate change , vaccinations or evolution .
Their goal is to exploit the slivers of doubt and discrepant results that always exist in science in order to challenge the consensus views of scientific experts .
They fund and report their own results that go counter to the scientific consensus in @ @ @ @ @ @ @ argue that they have falsified the consensus .
In their book Merchants of Doubt , historians Naomi Oreskes and Erik M. Conway say that for these groups “ [ t ] he goal was to fight science with science—or at least with the gaps and uncertainties in existing science , and with scientific research that could be used to deflect attention from the main event.
” Science studies provide supporters of science with better arguments to combat these critics , by showing that the strength of scientific conclusions arises because credible experts use @ @ @ @ @ @ @ consensus judgments about whether a theory should be retained or rejected in favor of a new one .
These consensus judgments are what have enabled the astounding levels of success that have revolutionized our lives for the better .
It is the preponderance of evidence that is relevant in making such judgments , not one or even a few results .
So , when anti-vaxxers or anti-evolutionists or climate change deniers point to this or that result to argue that they have falsified the scientific consensus , they are making a meaningless statement @ @ @ @ @ @ @ produce a preponderance of evidence in support of their case , and they have not done so .
Falsification is appealing because it tells a simple and optimistic story of scientific progress , that by steadily eliminating false theories we can eventually arrive at true ones .
As Sherlock Holmes put it , “ When you have eliminated the impossible , whatever remains , however improbable , must be the truth.
” Such simple but incorrect narratives abound in science folklore and textbooks .
Richard Feynman in his book QED , right after @ @ @ @ @ @ @ quantum electrodynamics came about , said , `` What I have just outlined is what I call a “ physicist ’ s history of physics , ” which is never correct .
What I am telling you is a sort of conventionalized myth-story that the physicists tell to their students , and those students tell to their students , and is not necessarily related to the actual historical development which I do not really know ! ''
But if you propagate a “ myth-story ” enough times and it gets passed on from @ @ @ @ @ @ @ into a fact , and falsification is one such myth-story .
It is time we abandoned it .

J.B.S. Haldane, one of the founders of modern evolutionary biology theory, was reportedly asked what it would take for him to lose faith in the theory of evolution and is said to have replied, “Fossil rabbits in the Precambrian.” Since the so-called “Cambrian explosion” of 500 million years ago marks the earliest appearance in the fossil record of complex animals, finding mammal fossils that predate them would falsify the theory.
But would it really?
The Haldane story, though apocryphal, is one of many in the scientific folklore that suggest that falsification is the defining characteristic of science. As expressed by astrophysicist Mario Livio in his book Brilliant Blunders: "[E]ver since the seminal work of philosopher of science Karl Popper, for a scientific theory to be worthy of its name, it has to be falsifiable by experiments or observations. This requirement has become the foundation of the ‘scientific method.’”
But the field known as science studies (comprising the history, philosophy and sociology of science) has shown that falsification cannot work even in principle. This is because an experimental result is not a simple fact obtained directly from nature. Identifying and dating Haldane's bone involves using many other theories from diverse fields, including physics, chemistry and geology. Similarly, a theoretical prediction is never the product of a single theory but also requires using many other theories. When a “theoretical” prediction disagrees with “experimental” data, what this tells us is that that there is a disagreement between two sets of theories, so we cannot say that any particular theory is falsified.
Fortunately, falsification—or any other philosophy of science—is not necessary for the actual practice of science. The physicist Paul Dirac was right when he said, "Philosophy will never lead to important discoveries. It is just a way of talking about discoveries which have already been made.” Actual scientific history reveals that scientists break all the rules all the time, including falsification. As philosopher of science Thomas Kuhn noted, Newton's laws were retained despite the fact that they were contradicted for decades by the motions of the perihelion of Mercury and the perigee of the moon. It is the single-minded focus on finding what works that gives science its strength, not any philosophy. Albert Einstein said that scientists are not, and should not be, driven by any single perspective but should be willing to go wherever experiment dictates and adopt whatever works.
Unfortunately, some scientists have disparaged the entire field of science studies, claiming that it was undermining public confidence in science by denying that scientific theories were objectively true. This is a mistake since science studies play vital roles in two areas. The first is that it gives scientists a much richer understanding of their discipline. As Einstein said: "So many people today—and even professional scientists—seem to me like somebody who has seen thousands of trees but has never seen a forest. A knowledge of the historic and philosophical background gives that kind of independence from prejudices of his generation from which most scientists are suffering. This independence created by philosophical insight is—in my opinion—the mark of distinction between a mere artisan or specialist and a real seeker after truth." The actual story of how science evolves results in inspiring more confidence in science, not less.
The second is that this knowledge equips people to better argue against antiscience forces that use the same strategy over and over again, whether it is about the dangers of tobacco, climate change, vaccinations or evolution. Their goal is to exploit the slivers of doubt and discrepant results that always exist in science in order to challenge the consensus views of scientific experts. They fund and report their own results that go counter to the scientific consensus in this or that narrow area and then argue that they have falsified the consensus. In their book Merchants of Doubt, historians Naomi Oreskes and Erik M. Conway say that for these groups “[t]he goal was to fight science with science—or at least with the gaps and uncertainties in existing science, and with scientific research that could be used to deflect attention from the main event.”
Science studies provide supporters of science with better arguments to combat these critics, by showing that the strength of scientific conclusions arises because credible experts use comprehensive bodies of evidence to arrive at consensus judgments about whether a theory should be retained or rejected in favor of a new one. These consensus judgments are what have enabled the astounding levels of success that have revolutionized our lives for the better. It is the preponderance of evidence that is relevant in making such judgments, not one or even a few results.
So, when anti-vaxxers or anti-evolutionists or climate change deniers point to this or that result to argue that they have falsified the scientific consensus, they are making a meaningless statement. What they need to do is produce a preponderance of evidence in support of their case, and they have not done so.
Falsification is appealing because it tells a simple and optimistic story of scientific progress, that by steadily eliminating false theories we can eventually arrive at true ones. As Sherlock Holmes put it, “When you have eliminated the impossible, whatever remains, however improbable, must be the truth.” Such simple but incorrect narratives abound in science folklore and textbooks. Richard Feynman in his book QED, right after “explaining” how the theory of quantum electrodynamics came about, said, "What I have just outlined is what I call a “physicist’s history of physics,” which is never correct. What I am telling you is a sort of conventionalized myth-story that the physicists tell to their students, and those students tell to their students, and is not necessarily related to the actual historical development which I do not really know!"
But if you propagate a “myth-story” enough times and it gets passed on from generation to generation, it can congeal into a fact, and falsification is one such myth-story.
It is time we abandoned it.


scientificamerican--2020-09-04--Coronavirus News Roundup: August 29-September 4

The items below are highlights from the free newsletter , “ Smart , useful , science stuff about COVID-19.
” To receive newsletter issues daily in your inbox , sign up here .
Please consider a monthly contribution to support this newsletter .
Several media outlets this week have covered hints and speculation that two SARS-CoV-2 vaccines—probably ones being tested by Moderna and by Pfizer in thousands of people—could be approved on an emergency basis in October or November by the U.S. federal government .
Groups reported to be prioritized to receive these vaccines include health care workers , essential @ @ @ @ @ @ @ over 65 , Native Americans , prisoners , and people in some other racial and ethnic categories .
It ’ s probably wise to pay attention to recently reported statements by Dr. Anthony Fauci , the top infectious disease official in the U.S. , on this topic .
In a 9/1/20 story by Liz Szabo at Kaiser Health News , Fauci says that indeed a vaccine could be available “ earlier than expected if ongoing clinical trials produce overwhelmingly positive results.
” An independent board called the Data and Safety Monitoring Board has @ @ @ @ @ @ @ short if strong results come in , Szabo reports .
Fauci says he trusts this board to eschew political influence , the story states .
And people also should trust the vaccine approval process because the experimental data behind any recommendations or decisions will be made public , Fauci is described as saying .
Others quoted in the story raise concerns about stopping these large-scale efficacy and safety studies early .
A string of new research and an editorial all published in the medical journal JAMA suggest that inexpensive , widely available anti-inflammatory @ @ @ @ @ @ @ and methylprednisolone—reduce deaths among people with severe COVID-19 , reports Roni Caryn Rabin at The New York Times ( 9/2/20 ) .
These anti-inflammatory compounds are often just called “ steroids , ” but they are not the same as the anabolic steroids that can be misused by athletes .
The new findings prompted the World Health Organization to update its COVID-19 treatment advice and strongly recommend the corticosteroids for `` severely and critically ill patients , but not to those with mild disease , ” Rabin writes .
JAMA ’ s editor @ @ @ @ @ @ @ as saying , “ Clearly , now steroids are the standard of care [ for severe and critical COVID-19 ] .
” COVID-19 patients often die of the body ’ s extreme immune response to the virus , which leads to inflammation , the story states : https : //www.nytimes.com/2020/09/02/health/coronavirus-steroids.html .
My ears perked up a month or so ago when a children ’ s hospital infectious-diseases pediatrician told me she treated the first reported case in her state of the rare multi-system inflammatory syndrome affecting some children exposed to the new coronavirus @ @ @ @ @ @ @ is known as MIS-C ; it ’ s called PIMS in the UK and some other places .
The pediatrician said it 's difficult to determine how to treat children with MIS-C because there are no senior colleagues to draw on who have in-depth experience with the syndrome—COVID-19 is only 8 or so months old and doctors only described MIS-C in late April .
I grew curious about how doctors solve that problem with this dangerous condition , which it turns out is more life-threatening and potentially harmful to kids than COVID-19 is @ @ @ @ @ @ @ children ’ s hearts .
So , I reported and wrote a story for Scientific American about what is known so far about diagnosing and treating MIS-C ( 9/1/20 ) .
Corticosteroids are among the treatments that some doctors have prescribed , but their true effectiveness is unclear because there are no randomly assigned , controlled experiments under way yet to test this treatment and others for MIS-C.
It ’ s well-known by now that COVID-19 also damages the hearts of many of its adult victims .
In a 8/31/20 essay for Scientific @ @ @ @ @ @ @ Barber describes a related phenomenon—new findings of potentially fatal heart damage in people of all ages , including some previously healthy college and professional athletes , weeks or even months after a symptom-free infection with the new coronavirus .
These patients come to suffer from myocarditis , or inflammation of the heart , which often manifests with shortness of breath , a racing heartbeat , chest pain , fever , or fatigue , Barber writes .
The long-term impact could be significant , according to a cardiologist at the DZHK Centre for Cardiovascular @ @ @ @ @ @ @ from an email ) in the piece .
He writes : “ My personal take is that COVID will increase the incidents of heart failure over the next decades.
” Some cases resolve on their own , the story states , but the best defense for now is not getting the virus .
Testing for SARS-CoV-2 and then isolating people who test positive have proven key to gaining control over the pandemic in many countries .
In an excellent , in-depth piece in The New Yorker ( 9/2/20 ) , surgeon , writer @ @ @ @ @ @ @ lays out the morass of issues that make it difficult to obtain such a test in the U.S. As part of the solution , he proposes a “ national grid , ” as we have for the nation ’ s electricity , `` for the generation , transmission , or distribution of our testing supply.
” Currently , he notes , “ the vast majority of infected Americans , including those with symptoms , never get tested . ''
To be effective for controlling outbreaks , tests should be repeated at least weekly @ @ @ @ @ @ @ The problem is not a lack of technology for testing , he states .
It ’ s that there has been no coordinated implementation to effectively deploy all this technology .
Better logistics to manage billing systems , the flow of people at test sites , and of swab , reagent , and test tube supplies will be key to fixing coronavirus testing in the U.S. , he writes .
And better logistics also could improve the logjams that occur with the four companies that process most test samples in the U.S. , @ @ @ @ @ @ @ pick up the slack , but currently go largely unused , he reports .
The piece concludes with a forecast for “ one of the worst falls and winters in American history , ” but Gawande also notes some collaborative advances and communities that are doing things right , recognizing that public health is part of health care .
You might enjoy “ Updated guidelines for what not to wear after Labor Day , ” by Caroline Doyle and Ginny Hogan , for McSweeney ’ s ( 9/2/20 ) .

The items below are highlights from the free newsletter, “Smart, useful, science stuff about COVID-19.” To receive newsletter issues daily in your inbox, sign up here. Please consider a monthly contribution to support this newsletter.
Several media outlets this week have covered hints and speculation that two SARS-CoV-2 vaccines—probably ones being tested by Moderna and by Pfizer in thousands of people—could be approved on an emergency basis in October or November by the U.S. federal government. Groups reported to be prioritized to receive these vaccines include health care workers, essential workers, national security employees, people over 65, Native Americans, prisoners, and people in some other racial and ethnic categories. It’s probably wise to pay attention to recently reported statements by Dr. Anthony Fauci, the top infectious disease official in the U.S., on this topic. In a 9/1/20 story by Liz Szabo at Kaiser Health News, Fauci says that indeed a vaccine could be available “earlier than expected if ongoing clinical trials produce overwhelmingly positive results.” An independent board called the Data and Safety Monitoring Board has the authority to recommend cutting vaccine experiments short if strong results come in, Szabo reports. Fauci says he trusts this board to eschew political influence, the story states. And people also should trust the vaccine approval process because the experimental data behind any recommendations or decisions will be made public, Fauci is described as saying. Others quoted in the story raise concerns about stopping these large-scale efficacy and safety studies early.
A string of new research and an editorial all published in the medical journal JAMA suggest that inexpensive, widely available anti-inflammatory drugs called corticosteroids—specifically dexamethasone, hydrocortisone, and methylprednisolone—reduce deaths among people with severe COVID-19, reports Roni Caryn Rabin at The New York Times (9/2/20). These anti-inflammatory compounds are often just called “steroids,” but they are not the same as the anabolic steroids that can be misused by athletes. The new findings prompted the World Health Organization to update its COVID-19 treatment advice and strongly recommend the corticosteroids for "severely and critically ill patients, but not to those with mild disease,” Rabin writes. JAMA’s editor in chief is quoted in the story as saying, “Clearly, now steroids are the standard of care [for severe and critical COVID-19].” COVID-19 patients often die of the body’s extreme immune response to the virus, which leads to inflammation, the story states: https://www.nytimes.com/2020/09/02/health/coronavirus-steroids.html.
My ears perked up a month or so ago when a children’s hospital infectious-diseases pediatrician told me she treated the first reported case in her state of the rare multi-system inflammatory syndrome affecting some children exposed to the new coronavirus. In the U.S., the syndrome is known as MIS-C; it’s called PIMS in the UK and some other places. The pediatrician said it's difficult to determine how to treat children with MIS-C because there are no senior colleagues to draw on who have in-depth experience with the syndrome—COVID-19 is only 8 or so months old and doctors only described MIS-C in late April. I grew curious about how doctors solve that problem with this dangerous condition, which it turns out is more life-threatening and potentially harmful to kids than COVID-19 is. MIS-C can cause long-term damage to children’s hearts. So, I reported and wrote a story for Scientific American about what is known so far about diagnosing and treating MIS-C (9/1/20). Corticosteroids are among the treatments that some doctors have prescribed, but their true effectiveness is unclear because there are no randomly assigned, controlled experiments under way yet to test this treatment and others for MIS-C.
It’s well-known by now that COVID-19 also damages the hearts of many of its adult victims. In a 8/31/20 essay for Scientific American, emergency department physician Dr. Carolyn Barber describes a related phenomenon—new findings of potentially fatal heart damage in people of all ages, including some previously healthy college and professional athletes, weeks or even months after a symptom-free infection with the new coronavirus. These patients come to suffer from myocarditis, or inflammation of the heart, which often manifests with shortness of breath, a racing heartbeat, chest pain, fever, or fatigue, Barber writes. The long-term impact could be significant, according to a cardiologist at the DZHK Centre for Cardiovascular Imaging in Germany who is quoted (from an email) in the piece. He writes: “My personal take is that COVID will increase the incidents of heart failure over the next decades.” Some cases resolve on their own, the story states, but the best defense for now is not getting the virus.
Testing for SARS-CoV-2 and then isolating people who test positive have proven key to gaining control over the pandemic in many countries. In an excellent, in-depth piece in The New Yorker (9/2/20), surgeon, writer, and public health researcher Atul Gawande lays out the morass of issues that make it difficult to obtain such a test in the U.S. As part of the solution, he proposes a “national grid,” as we have for the nation’s electricity, "for the generation, transmission, or distribution of our testing supply.” Currently, he notes, “the vast majority of infected Americans, including those with symptoms, never get tested." To be effective for controlling outbreaks, tests should be repeated at least weekly and possibly daily, he reports. The problem is not a lack of technology for testing, he states. It’s that there has been no coordinated implementation to effectively deploy all this technology. Better logistics to manage billing systems, the flow of people at test sites, and of swab, reagent, and test tube supplies will be key to fixing coronavirus testing in the U.S., he writes. And better logistics also could improve the logjams that occur with the four companies that process most test samples in the U.S., Gawande writes. Some U.S. labs could pick up the slack, but currently go largely unused, he reports. The piece concludes with a forecast for “one of the worst falls and winters in American history,” but Gawande also notes some collaborative advances and communities that are doing things right, recognizing that public health is part of health care.
You might enjoy “Updated guidelines for what not to wear after Labor Day,” by Caroline Doyle and Ginny Hogan, for McSweeney’s (9/2/20).


scientificamerican--2020-09-09--Coronavirus: How It Infects Us and How We Might Stop It

How does SARS-CoV-2 sneak into our body ?
What can our immune system do and how can the virus sometimes @ @ @ @ @ the leading drug and vaccine candidates work ?
Will the virus plague us forever ?
@ @ @ @ @ about these burning questions with Britt Glaunsinger , a virologist at the University of California @ @ @ @ @ Howard Hughes Medical Institute who is a specialist in viral infection .

How does SARS-CoV-2 sneak into our body? What can our immune system do and how can the virus sometimes defeat it? How do the leading drug and vaccine candidates work? Will the virus plague us forever? Scientific American presents a conversation about these burning questions with Britt Glaunsinger, a virologist at the University of California, Berkeley, and the Howard Hughes Medical Institute who is a specialist in viral infection.