Any conflict in space will be much slower and more deliberate than a Star Wars scene

Saturday, November 14th, 2020

When considering how to control space , Rebecca Reesman and James Wilson lay out the ways in which space combat is counter-intuitive for policymakers and strategists:

Satellites move quickly, but predictably:  Satellites in commonly used circular orbits move at speeds between 3km/s and 8km/s, depending on their altitude. By contrast, an average bullet only travels about 0.75km/s. They are here, and then gone.

Space is big: The volume of space between low-earth orbit and geostationary orbit is about 200 trillion cubic kilometers. That is 190 times larger than the volume of Earth.

Timing is everything: Within the confines of the atmosphere, airplanes, tanks, and ships can nominally move in any direction. Satellites do not have that freedom. Due to the gravitational pull of Earth, satellites are always moving in either a circular or elliptical path, constantly in free-fall around the Earth. Getting two satellites in the same spot is not intuitive. Therefore, it requires careful planning and perfect timing.

Satellites maneuver slowly: While satellites move quickly, space is big, and that makes purposeful maneuvers seem relatively slow. Once a satellite is in orbit, it requires time and a large amount of delta-V to perform phasing maneuvers.

Given all of this, for engagements in space, maneuvers and actions will have to be planned far in advance, Reesman said in an interview. “Any conflict in space will be much slower and more deliberate than a Star Wars scene,” she said. “It requires a lot more long-term thinking and strategic placement of assets.


Radio signals can be used to jam an opponent’s satellites, or spoof them by sending harmful commands. This would be an extension of electronic warfare already used in naval and air battles.

Some nations, such as France, have gone so far as to talk about deploying weapons in space to protect their own satellites. However, the authors suggest that satellites using kinetic weapons to shoot down opposing satellites seems unlikely for now, given the extraordinary energy required to maneuver an orbital weapon into a proper trajectory. More likely would be a “T-bone” collision between satellites, which does not require plane matching but rather occurs when two orbits cross.

Nations do have a strong incentive to not destroy other satellites because of the potential to create hazardous debris that would potentially affect all nations’ assets in space—and debris generated in space has a lasting effect. However, in the immediacy of war, a nation may decide it is worth permanently losing access to some slots in geostationary orbit, due to debris, in order to win a ground-based war.

All of the studies on face masks and social distancing are based on preventing flu transmission

Wednesday, October 28th, 2020

In the Southern Hemisphere, where the flu season happens during our summer months, the WHO data suggests it never took off at all:

In Australia, just 14 positive flu cases were recorded in April, compared with 367 during the same month in 2019 — a 96 per cent drop.

By June, usually the peak of its flu season, there were none. In fact, Australia has not reported a positive case to the WHO since July.

In Chile, just 12 cases of flu were detected between April and October. There were nearly 7,000 during the same period in 2019.

And in South Africa, surveillance tests picked up just two cases at the beginning of the season, which quickly dropped to zero over the following month — overall, a 99 per cent drop compared with the previous year.

In the UK, our flu season is only just beginning. But since Covid-19 began spreading in March, just 767 cases have been reported to the WHO compared with nearly 7,000 from March to October last year.

And while lab-confirmed flu cases last year jumped by ten per cent between September and October, as a new season gets under way this year they’ve risen by just 0.7 per cent so far.


‘All of the studies on face masks and social distancing are based on preventing flu transmission and have shown huge reductions,’ he adds. ‘So it’s no surprise it worked.’

Oxophilicity of the surface plays a very important role in electrolysis

Monday, October 26th, 2020

Chemist Ian McCrum used a special platinum crystal to bring sustainable hydrogen one step closer:

To understand what is so special about this crystal, we need to zoom in on the surface of the platinum. This is not flat and smooth, but irregular with tiny steps and kinks. And it is precisely at these irregularities that chemical reactions take place. McCrum designed the special crystal in such a way that the surface has the same number of these irregularities throughout the crystal. He then decorated the edges with different metals, such as ruthenium and molybdenum. In this way, he ensured that all the electrodes had exactly the same atomic structure, but each time with a different metal in the edges. This enabled him to vary the interaction of the electrode with the oxygen atom of water in a systematic and well-defined way.

Measurements then began, with a surprising outcome. Marc Koper says, “Our breakthrough is that there appears to be a clear link between the activity of the electrode for making hydrogen and the degree to which the metal in the edge binds to the oxygen atom of water.” The latter is also known as oxophilicity, with oxophilic literally meaning oxygen-loving. “We have even found an optimum for this oxophilicity,” says Koper. “We have now definitively established that the oxophilicity of the surface plays a very important role in electrolysis.”

Not every maverick is a new Galileo

Tuesday, October 20th, 2020

One of the hardest questions a science commentator faces, Matt Ridley says, is when to take a heretic seriously:

It’s tempting for established scientists to use arguments from authority to dismiss reasonable challenges, but not every maverick is a new Galileo. As the astronomer Carl Sagan once put it, “Too much openness and you accept every notion, idea and hypothesis—which is tantamount to knowing nothing. Too much skepticism—especially rejection of new ideas before they are adequately tested—and you’re not only unpleasantly grumpy, but also closed to the advance of science.” In other words, as some wit once put it, don’t be so open-minded that your brains fall out.

Peer review is supposed to be the device that guides us away from unreliable heretics. A scientific result is only reliable when reputable scholars have given it their approval. Dr. Yan’s report has not been peer reviewed. But in recent years, peer review’s reputation has been tarnished by a series of scandals. The Surgisphere study was peer reviewed, as was the study by Dr. Andrew Wakefield, hero of the anti-vaccine movement, claiming that the MMR vaccine (for measles, mumps and rubella) caused autism. Investigations show that peer review is often perfunctory rather than thorough; often exploited by chums to help each other; and frequently used by gatekeepers to exclude and extinguish legitimate minority scientific opinions in a field.

Herbert Ayres, an expert in operations research, summarized the problem well several decades ago: “As a referee of a paper that threatens to disrupt his life, [a professor] is in a conflict-of-interest position, pure and simple. Unless we’re convinced that he, we, and all our friends who referee have integrity in the upper fifth percentile of those who have so far qualified for sainthood, it is beyond naive to believe that censorship does not occur.” Rosalyn Yalow, winner of the Nobel Prize in medicine, was fond of displaying the letter she received in 1955 from the Journal of Clinical Investigation noting that the reviewers were “particularly emphatic in rejecting” her paper.

The health of science depends on tolerating, even encouraging, at least some disagreement. In practice, science is prevented from turning into religion not by asking scientists to challenge their own theories but by getting them to challenge each other, sometimes with gusto. Where science becomes political, as in climate change and Covid-19, this diversity of opinion is sometimes extinguished in the pursuit of a consensus to present to a politician or a press conference, and to deny the oxygen of publicity to cranks. This year has driven home as never before the message that there is no such thing as “the science”; there are different scientific views on how to suppress the virus.

Researchers synthesize room temperature superconducting material

Friday, October 16th, 2020

When I heard that a team from the University of Rochester had synthesized a room-temperature superconductor, I was not expecting this footnote:

The carbonaceous sulfur hydride exhibited superconductivity at about 58 degrees Fahrenheit and a pressure of about 39 million psi.

Dias’s lab at Rochester used hydrogen-rich materials that metalize at lower pressures than pure hydrogen, producing picoliters of superconductor in a diamond anvil cell:

First the lab combined yttrium and hydrogen. The resulting yttrium superhydride exhibited superconductivity at what was then a record high temperature of about 12 degrees Fahrenheit and a pressure of about 26 million pounds per square inch.

Next the lab explored covalent hydrogen-rich organic-derived materials.

This work resulted in the carbonaceous sulfur hydride. “This presence of carbon is of tantamount importance here,” the researchers report. Further “compositional tuning” of this combination of elements may be the key to achieving superconductivity at even higher temperatures, they add.

Vitamin D reduced a patient’s risk of needing intensive care 25-fold

Monday, October 12th, 2020

In May, Matt Ridley notes, arguments on the link between Vitamin D deficiency and poor Covid outcomes started to gather speed:

That month, the Health Secretary’s attention was drawn to two studies showing a strong association between the incidence and severity of Covid-19 with vitamin D deficiencies in the patients. Vadim Backman of Northwestern University, one of the authors of one of those studies, said about healthy levels of vitamin D that “Our analysis shows that it might be as high as cutting the mortality rate in half.”

When asked to look at the evidence, Matt Hancock perfectly reasonably handed the question to Public Health England to answer. They attempted to analyse the statistical data and came up unconvinced. The problem is that a correlation is not a proof of cause and effect, and a correlation (albeit a very strong one) is all that we had at that point. Or almost all that we had.

The gold standard of medical research is the randomised controlled trial. Back in May, we had no such test for vitamin D and Covid-19. Now we do. The world’s first randomised control trial on vitamin D and Covid has just been published. The results are clear-cut. The trial, which took place in Spain at the Reina Sofía University Hospital, involved 76 patients suffering from Covid-19. Fifty of those patients were given vitamin D. The remaining 26 were not. Half of those not given Vitamin D became so sick that they needed to be put on intensive care. By comparison, only one person who was given Vitamin D requiring ICU admission.

Put another way, the use of Vitamin D reduced a patient’s risk of needing intensive care 25-fold.

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.)