Mighty Mice in Space

Friday, September 18th, 2020

A research team led by Dr. Se-Jin Lee of the Jackson Laboratory in Connecticut sent 40 young female black mice to the International Space Station in December, to study muscle loss:

In a paper published in the Proceedings of the National Academy of Sciences, Lee said the 24 regular untreated mice lost considerable muscle and bone mass in weightlessness as expected — up to 18%. But the eight genetically engineered “mighty mice” launched with double the muscle maintained their bulk. Their muscles appeared to be comparable to similar “mighty mice” that stayed behind at NASA’s Kennedy Space Center.

The PNAS abstract explains:

Among the physiological consequences of extended spaceflight are loss of skeletal muscle and bone mass. One signaling pathway that plays an important role in maintaining muscle and bone homeostasis is that regulated by the secreted signaling proteins, myostatin (MSTN) and activin A.

Here, we used both genetic and pharmacological approaches to investigate the effect of targeting MSTN/activin A signaling in mice that were sent to the International Space Station.

Wild type mice lost significant muscle and bone mass during the 33 d spent in microgravity. Muscle weights of Mstn -/- mice, which are about twice those of wild type mice, were largely maintained during spaceflight.

Systemic inhibition of MSTN/activin A signaling using a soluble form of the activin type IIB receptor (ACVR2B), which can bind each of these ligands, led to dramatic increases in both muscle and bone mass, with effects being comparable in ground and flight mice.

It’s not just mice who have muscle-building myostatin-related mutations, but Belgian Blue cattle, Flex Wheeler, a German toddler, a Michigan toddler, and “bully” whippets.

Rarely are science fiction stories written by credentialed scientists

Wednesday, September 16th, 2020

John C. Wright highly recommends The Hidden Truth by Hans G. Schantz:

It is a gem of a book, a rare find, combining a charming coming of age story, diamond-hard science fiction speculation, a conspiracy thriller, a touch of trenchant political commentary, and, uniquely, a challenge written into a science fiction book of the reigning scientific orthodoxy of the day.

Rarely are science fiction stories written by credentialed scientists. Even more rare is one that proposes a revolutionary theory that questions the historical and theoretical roots of the standard model of modern physics, and no other book does so in the context of an action thriller.


If you liked Heinlein style juveniles, with their young men learning lessons about personal responsibility and integrity of character, and seasoned with brief avuncular lectures on topics ranging from electromagnetic theory to economic reality, then you are likely to enjoy this book.


Rumor has it that the author, Hans Schantz, is hard at work on the final volume, A HELL OF AN ENGINEER, but a hefty amount of public interest, and some book sales of the first three in the series, might stoke the fires under this boiler, and give him the spirit needed to complete the work in a reasonable time.

Acetaminophen increases risk-taking

Monday, September 14th, 2020

Acetaminophen, also known as paracetamol and sold widely under the brand names Tylenol and Panadol, also increases risk-taking:

In a series of experiments involving over 500 university students as participants, Way and his team measured how a single 1,000 mg dose of acetaminophen (the recommended maximum adult single dosage) randomly assigned to participants affected their risk-taking behaviour, compared against placebos randomly given to a control group.

In each of the experiments, participants had to pump up an uninflated balloon on a computer screen, with each single pump earning imaginary money. Their instructions were to earn as much imaginary money as possible by pumping the balloon as much as possible, but to make sure not to pop the balloon, in which case they would lose the money.

The results showed that the students who took acetaminophen engaged in significantly more risk-taking during the exercise, relative to the more cautious and conservative placebo group. On the whole, those on acetaminophen pumped (and burst) their balloons more than the controls.

Cable bacteria overcome a lack of oxygen

Saturday, September 12th, 2020

For Lars Peter Nielsen, it all began with the mysterious disappearance of hydrogen sulfide.

The microbiologist had collected black, stinky mud from the bottom of Aarhus Harbor in Denmark, dropped it into big glass beakers, and inserted custom microsensors that detected changes in the mud’s chemistry. At the start of the experiment, the muck was saturated with hydrogen sulfide—the source of the sediment’s stink and color. But 30 days later, one band of mud had become paler, suggesting some hydrogen sulphide had gone missing. Eventually, the microsensors indicated that all of the compound had disappeared. Given what scientists knew about the biogeochemistry of mud, recalls Nielsen, who works at Aarhus University, “This didn’t make sense at all.”

The first explanation, he says, was that the sensors were wrong. But the cause turned out to be far stranger: bacteria that join cells end to end to build electrical cables able to carry current up to 5 centimeters through mud. The adaptation, never seen before in a microbe, allows these so-called cable bacteria to overcome a major challenge facing many organisms that live in mud: a lack of oxygen. Its absence would normally keep bacteria from metabolizing compounds, such as hydrogen sulfide, as food. But the cables, by linking the microbes to sediments richer in oxygen, allow them to carry out the reaction long distance.


Most cells thrive by robbing electrons from one molecule, a process called oxidation, and donating them to another molecule, usually oxygen—so-called reduction. Energy harvested from these reactions drives the other processes of life. In eukaryotic cells, including our own, such “redox” reactions take place on the inner membrane of the mitochondria, and the distances involved are tiny—just micrometers. That is why so many researchers were skeptical of Nielsen’s claim that cable bacteria were moving electrons across a span of mud equivalent to the width of a golf ball.

The vanishing hydrogen sulfide was key to proving it. Bacteria produce the compound in mud by breaking down plant debris and other organic material; in deeper sediments, hydrogen sulfide builds up because there is little oxygen to help other bacteria break it down. Yet, in Nielsen’s laboratory beakers, the hydrogen sulfide was disappearing anyway. Moreover, a rusty hue appeared on the mud’s surface, indicating that an iron oxide had formed.

(Hat tip to Hans G. Schantz.)

Any virus that can make people sick has to have at least one good trick for evading the immune system

Saturday, August 29th, 2020

The immune system is very complicated, Ed Yong notes, but it works, roughly, like this:

The first of three phases involves detecting a threat, summoning help, and launching the counterattack. It begins as soon as a virus drifts into your airways, and infiltrates the cells that line them.

When cells sense molecules common to pathogens and uncommon to humans, they produce proteins called cytokines. Some act like alarms, summoning and activating a diverse squad of white blood cells that go to town on the intruding viruses — swallowing and digesting them, bombarding them with destructive chemicals, and releasing yet more cytokines. Some also directly prevent viruses from reproducing (and are delightfully called interferons). These aggressive acts lead to inflammation. Redness, heat, swelling, soreness — these are all signs of the immune system working as intended.

This initial set of events is part of what’s called the innate immune system. It’s quick, occurring within minutes of the virus’s entry. It’s ancient, using components that are shared among most animals. It’s generic, acting in much the same way in everyone. And it’s broad, lashing out at anything that seems both nonhuman and dangerous, without much caring about which specific pathogen is afoot. What the innate immune system lacks in precision, it makes up for in speed. Its job is to shut down an infection as soon as possible. Failing that, it buys time for the second phase of the immune response: bringing in the specialists.

Amid all the fighting in your airways, messenger cells grab small fragments of virus and carry these to the lymph nodes, where highly specialized white blood cells — T-cells — are waiting. The T-cells are selective and preprogrammed defenders. Each is built a little differently, and comes ready-made to attack just a few of the zillion pathogens that could possibly exist. For any new virus, you probably have a T-cell somewhere that could theoretically fight it. Your body just has to find and mobilize that cell. Picture the lymph nodes as bars full of grizzled T-cell mercenaries, each of which has just one type of target they’re prepared to fight. The messenger cell bursts in with a grainy photo, showing it to each mercenary in turn, asking: Is this your guy? When a match is found, the relevant merc arms up and clones itself into an entire battalion, which marches off to the airways.

Some T-cells are killers, which blow up the infected respiratory cells in which viruses are hiding. Others are helpers, which boost the rest of the immune system. Among their beneficiaries, these helper T-cells activate the B-cells that produce antibodies — small molecules that can neutralize viruses by gumming up the structures they use to latch on to their hosts. Roughly speaking — and this will be important later — antibodies mop up the viruses that are floating around outside our cells, while T-cells kill the ones that have already worked their way inside. T-cells do demolition; antibodies do cleanup.

Both T-cells and antibodies are part of the adaptive immune system. This branch is more precise than the innate branch, but much slower: Finding and activating the right cells can take several days. It’s also long-lasting: Unlike the innate branch of the immune system, the adaptive one has memory.

After the virus is cleared, most of the mobilized T-cell and B-cell forces stand down and die off. But a small fraction remain on retainer — veterans of the COVID-19 war of 2020, bunkered within your organs and patrolling your bloodstream. This is the third and final phase of the immune response: Keep a few of the specialists on tap. If the same virus attacks again, these “memory cells” can spring into action and launch the adaptive branch of the immune system without the usual days-long delay. Memory is the basis of immunity as we colloquially know it — a lasting defense against whatever has previously ailed us.

In general, the immune system’s reaction to SARS-CoV-2 is what you would expect:

Still, “any virus that can make people sick has to have at least one good trick for evading the immune system,” [Shane Crotty from the La Jolla Institute of Immunology] says. The new coronavirus seems to rely on early stealth, somehow delaying the launch of the innate immune system, and inhibiting the production of interferons — those molecules that initially block viral replication. “I believe this [delay] is really the key in determining good versus bad outcomes,” says Akiko Iwasaki, an immunologist at Yale. It creates a brief time window in which the virus can replicate unnoticed before the alarm bells start sounding. Those delays cascade: If the innate branch is slow to mobilize, the adaptive branch will also lag.


Immune responses are inherently violent. Cells are destroyed. Harmful chemicals are unleashed. Ideally, that violence is targeted and restrained; as Metcalf puts it, “Half of the immune system is designed to turn the other half off.” But if an infection is allowed to run amok, the immune system might do the same, causing a lot of collateral damage in its prolonged and flailing attempts to control the virus.

This is apparently what happens in severe cases of COVID-19. “If you can’t clear the virus quickly enough, you’re susceptible to damage from the virus and the immune system,” says Donna Farber, a microbiologist at Columbia. Many people in intensive-care units seem to succumb to the ravages of their own immune cells, even if they eventually beat the virus. Others suffer from lasting lung and heart problems, long after they are discharged. Such immune overreactions also happen in extreme cases of influenza, but they wreak greater damage in COVID-19.

There’s a further twist. Normally, the immune system mobilizes different groups of cells and molecules when fighting three broad groups of pathogens: viruses and microbes that invade cells, bacteria and fungi that stay outside cells, and parasitic worms. Only the first of these programs should activate during a viral infection. But Iwasaki’s team recently showed that all three activate in severe COVID-19 cases. “It seems completely random,” she says. In the worst cases, “the immune system almost seems confused as to what it’s supposed to be making.”

Magnetometer readings are much less easy to jam than GPS signaling

Tuesday, August 25th, 2020

The U.S. Air Force is looking into using Earth’s magnetic field as an alternative to GPS:

Magnetic fields emanating from the earth’s surface vary in intensity, just like topography, and so-called magnetic anomaly maps of those fields have existed for years. Back in 2017, Aaron Canciani, an assistant professor of electrical engineering at the Air Force Institute of Technology, set out to see if magnetic sensors (magnetometers) affixed to aircraft could measure the intensity of those magnetic fields and, thus, locate the plane based on where it was in relation to those “landmarks.” His paper (and this video) shows how to outfit a Cessna plane with magnetometers in the rear and the front. Forty flight-hours worth of data and a lot of work reducing noise from the readings proved the idea viable.

But swapping magnetic fields for GPS isn’t easy. Unlike a crisp clear signal from space, factors such as the electrical operations of the plane itself can interfere with a sensor’s ability to detect the strength of the field. This is where artificial intelligence comes in, canceling out the noise from the sensor readings to allow for a better signal and more accuracy.

Researchers in the Air Force’s-MIT Artificial Intelligence Accelerator. community, working with scientists at MIT, continued to work on the problem, publishing their own paper in July. They showed that magnetic field readings can be accurate to ten meters, only slightly inferior to GPS, which is accurate down to three meters. But magnetometer readings are much less easy to jam than GPS signaling. GPS readings rely on a signal sent along a specific wavelength across vast distances. Magnometers just have to read the magnetic environment around the vehicle.

Science is probably the best thing humans ever invented

Sunday, August 9th, 2020

Zach Weinersmith (the cartoonist behind Saturday Morning Breakfast Cereal and Soonishillustrates the ideas in Stuart Ritchie’s new book, Science Fictions: How Fraud, Bias, Negligence and Hype Undermine the Search for Truth.

(Ritchie’s previous book was Intelligence: All that Matters.)

Here are a few of my favorite panels:

Science is probably the best thing

Massage Their Statistics

This is what a kiloton looks like

Wednesday, August 5th, 2020

If you haven’t seen the massive explosion in Beirut, it is legitimately terrifying:

That’s thousands of tons of ammonium nitrate going off, with roughly the energy of kilotons of TNT.

There’s not much left.

(Hat tip to our Slovenian Guest.)

Closer threats inspire a more primitive kind of fear

Saturday, August 1st, 2020

Your brain handles a perceived threat differently depending on how close it is to you;

“Clinically, people who develop PTSD are more likely to have experienced threats that invaded their personal space, assaults or rapes or witnessing a crime at a close distance. They’re the people that tend to develop this long-lasting threat memory,” said Kevin LaBar, a professor of psychology and neuroscience at Duke University who is the senior author on a paper appearing this week in the Proceedings of the National Academy of Sciences.

“We’ve never been able to study that in the lab because you have a fixed distance to the computer screen,” LaBar said.

But Duke graduate student Leonard Faul and postdoc Daniel Stjepanovic figured out a way to do it, using a 3D television, a mirror and some MRI-safe 3D glasses.

“It’s like an IMAX experience,” LaBar said. “The threatening characters popped out of the screen and would either invade your personal space as you’re navigating this virtual world, or they were farther away.”

The VR simulation put 49 study subjects into a first-person view that had them moving down either a dark alley or a brighter, tree-lined street as they lay in the MRI tube having their brains scanned. Ambient sound and visual backgrounds were altered to provide some context for the threat versus safe memories.

On the first day of testing, subjects received a mild shock when the “threat avatar” appeared, either two feet away or 10 feet away, but not when they saw the safe avatar at the same distances.

The data from the first day showed that near threats were more frightening and they engaged limbic and mid-brain “survival circuitry,” in a way that the farther threats did not.

The following day, subjects encountered the same scenarios again but only a few shocks were given initially to remind them of the threatening context. Once again, the subjects showed a greater behavioral response to near threats than to distant threats.

“On the second day, we got fear reinstatement, both near and far threats, but it was stronger for the near threat,” LaBar said.

Tellingly, the nearby threats that engaged the survival circuits also proved harder to extinguish after they no longer produced shocks. The farther threats that engaged more higher-order thinking in the cortex were easier to extinguish. The near threats engaged the cerebellum, and the persistence of this signal predicted how much fear was reinstated the next day, LaBar said. “It’s the evolutionarily older cortex.”

The more distant threats showed greater connectivity between the amygdala, hippocampus and ventral medial prefrontal cortex and the areas of the cortex related to complex planning and visual processing, areas the researchers said are more related to thinking one’s way out of a situation and coping.

(Hat tip to Greg Ellifritz.)

Most studies put the rate between 0.5% and 1.0%

Thursday, July 30th, 2020

Covid-19 kills from around 0.3% to 1.5% of people infected:

Most studies put the rate between 0.5% and 1.0%, meaning that for every 1,000 people who get infected, from five to 10 would die on average.

COVID-19 IFR by Study

More than 14.7 million people have been infected with SARS-CoV-2 across the globe, and over 609,000 people have died, with nearly a quarter of the fatalities in the U.S., according to data compiled by Johns Hopkins University. That means that among confirmed global cases, roughly 4.2% of those people died.

The percentage of deaths among people with confirmed infections is higher than the percentage of deaths among infections overall, researchers say, because so many milder and asymptomatic Covid-19 cases go missed.

The U.S. Centers for Disease Control and Prevention has estimated that for every known case of Covid-19, roughly 10 more went unrecorded through the beginning of May. From March to early May, the total number of infections was likely six to 24 times greater than the number of reported cases depending on the state, the agency said Tuesday in a paper published in the journal JAMA Internal Medicine.


An analysis of 26 different studies estimating the infection-fatality rate in different parts of the globe found an aggregate estimate of about 0.68%, with a range of 0.53% to 0.82%, according to a report posted in July on the preprint server medRxiv, which hasn’t yet been reviewed by other researchers.

Cholesterol drug fenofibrate may downgrade Covid-19 to common cold

Wednesday, July 29th, 2020

A study conducted by professor Yaakov Nahmias at Hebrew University in Israel has found that an existing cholesterol drug, fenofibrate, could ‘downgrade’ Covid-19 threat level to that of a common cold:

According to the research, the virus leads to deposits of lipids in the lungs. Nahmias partnered with Mount Sinai Medical Center researcher Dr Benjamin tenOever to gain better insights into SARS-CoV-2 mechanism of attack on the human body.

The researchers observed that the virus changes lipid metabolism in human lungs. They believe that halting this process could help prevent the onset of problems that increase the severity of the disease.

While SARS-CoV-2 hinders the ability of the body to break down fat, fenofibrate starts this process by binding and activating the DNA site that is blocked by the virus.

Covid-19 measures have all but wiped out the flu

Tuesday, July 28th, 2020

Countries in the Southern Hemisphere are reporting far lower numbers of influenza and other seasonal respiratory viral infections this year, due to measures meant to corral the coronavirus, like mask use and restrictions on air travel:

“We keep checking for the other viruses, but all we’re seeing is Covid,” said Dr. Cortés, the Chilean doctor. Of roughly 1,300 Covid-19 patients she has treated since late March, only a handful had the flu. “We were surprised by the decline in the other viruses like influenza. We never dreamed it would practically disappear,” she said.

Chile's Influenza Cases

Chile has recorded only 1,134 seasonal respiratory infections so far this year, compared with 20,949 during the same period last year. In the first two weeks of July—the equivalent to early January in the Northern Hemisphere and the height of the local flu season—the country reported no new confirmed influenza cases.

Trans men should be allowed to play against biological men

Sunday, July 26th, 2020

World Rugby is considering banning trans women from playing women’s rugby because of significant safety concerns that have emerged following recent research:

The Guardian can reveal that in a 38-page draft document produced by its transgender working group, it is acknowledged that there is likely to be “at least a 20-30% greater risk” of injury when a female player is tackled by someone who has gone through male puberty. The document also says the latest science shows that trans women retain “significant” physical advantages over biological women even after they take medication to lower their testosterone.

As a result, World Rugby’s working group suggests that its current rules, which allow trans women to play women’s rugby if they lower their testosterone levels for at least 12 months in line with the International Olympic Committee’s guidelines, are “not fit for the purpose”.


It also recommends that trans men should be allowed to play against biological men, provided they have undergone a physical assessment and have signed a consent form.


As World Rugby’s working group notes, players who are assigned male at birth and whose puberty and development is influenced by androgens/testosterone “are stronger by 25%-50%, are 30% more powerful, 40% heavier, and about 15% faster than players who are assigned female at birth (who do not experience an androgen-influenced development).”

Heat is the poor man’s altitude

Sunday, July 12th, 2020

This is the time of year, Alex Hutchinson reminds us, when fitness journalists write articles about how the miserable heat that’s ruining your workouts is actually doing you a big favor:

You’re lucky to be dripping buckets of sweat and chafing up a storm, because heat is the “poor man’s altitude,” ramping up the physiological demands of your workout and triggering a series of adaptations that enhance your endurance.


Heat training works differently [from altitude training]. The most notable change, after just a few days, is a dramatic increase—of up to 20 percent—in the volume of plasma coursing through your veins. That’s the part of the blood that doesn’t include hemoglobin-rich red blood cells, so it’s not immediately obvious whether more plasma will enhance your endurance under moderate weather conditions.


If heat training causes your plasma volume to increase, that will lower your hematocrit.

Lundby’s hypothesis is based on the idea that your kidneys are constantly monitoring hematocrit, trying to keep it in a normal range. If your hematocrit has a sustained decrease, the kidney responds by producing EPO to trigger the production of more hemoglobin-rich red blood cells. Unlike the rapid increase in plasma volume, this is a slower process. Lundby and his colleagues figure it could take about five weeks.


The 11 cyclists in the heat group did those sessions in about 100 degrees and 65 percent humidity; the 12 cyclists in the control group did the same sessions at 60 degrees and 25 percent humidity, aiming for the same subjective effort level. During the heat sessions, the cyclists were limited to half a liter of water to ensure mild dehydration, which is thought to be one of the triggers for plasma volume expansion.

The key outcome measure: total hemoglobin mass increased 893 to 935 grams in the heat group, a significant 4.7 percent increase. In the control group, hemoglobin mass stayed essentially unchanged, edging up by just 0.5 percent.

Army halts SERE course after 90 soldiers test positive for coronavirus

Thursday, July 2nd, 2020

Out of the 110 students participating in the Survival, Evasion, Resistance and Escape (SERE) course at Fort Bragg, North Carolina, 82 — along with eight instructors — tested positive for COVID-19:

The course was terminated and all 110 soldiers are being quarantined for 14 days, Burton said.