That’s one small stem for a plant, one giant leap for plant science.

In a tiny, lab-grown garden, the first seeds ever sown in lunar dirt have sprouted. This small crop, planted in samples returned by Apollo missions, offers hope that astronauts could someday grow their own food on the moon.

But plants potted in lunar dirt grew more slowly and were scrawnier than others grown in volcanic material from Earth, researchers report May 12 in Communications Biology. That finding suggests that farming on the moon would take a lot more than a green thumb.
“Ah! It’s so cool!” says University of Wisconsin–Madison astrobotanist Richard Barker of the experiment.

“Ever since these samples came back, there’s been botanists that wanted to know what would happen if you grew plants in them,” says Barker, who wasn’t involved in the study. “But everyone knows those precious samples … are priceless, and so you can understand why [NASA was] reluctant to release them.”

Now, NASA’s upcoming plans to send astronauts back to the moon as part of its Artemis program have offered a new incentive to examine that precious dirt and explore how lunar resources could support long-term missions (SN: 7/15/19).

The dirt, or regolith, that covers the moon is basically a gardener’s worst nightmare. This fine powder of razor-sharp bits is full of metallic iron, rather than the oxidized kind that is palatable to plants (SN: 9/15/20). It’s also full of tiny glass shards forged by space rocks pelting the moon. What it is not full of is nitrogen, phosphorus or much else plants need to grow. So, even though scientists have gotten pretty good at coaxing plants to grow in fake moon dust made of earthly materials, no one knew whether newborn plants could put down their delicate roots in the real stuff.

To find out, a trio of researchers at the University of Florida in Gainesville ran experiments with thale cress (Arabidopsis thaliana). This well-studied plant is in the same family as mustards and can grow in just a tiny clod of material. That was key because the researchers had only a little bit of the moon to go around.

The team planted seeds in tiny pots that each held about a gram of dirt. Four pots were filled with samples returned by Apollo 11, another four with Apollo 12 samples and a final four with dirt from Apollo 17. Another 16 pots were filled with earthly volcanic material used in past experiments to mimic moon dirt. All were grown under LED lights in the lab and watered with a broth of nutrients.
“Nothing really compared to when we first saw the seedlings as they were sprouting in the lunar regolith,” says Anna-Lisa Paul, a plant molecular biologist. “That was a moving experience, to be able to say that we’re watching the very first terrestrial organisms to grow in extraterrestrial materials, ever. And it was amazing. Just amazing.”

Plants grew in all the pots of lunar dirt, but none grew as well as those cultivated in earthly material. “The healthiest ones were just smaller,” Paul says. The sickliest moon-grown plants were tiny and had purplish pigmentation — a red flag for plant stress. Plants grown in Apollo 11 samples, which had been exposed on the lunar surface the longest, were most stunted.

Paul and colleagues also inspected the genes in their mini alien Eden. “By seeing what kind of genes are turned on and turned off in response to a stress, that shows you what tools plants are pulling out of their metabolic toolbox to deal with that stress,” she says. All plants grown in moon dirt pulled out genetic tools typically seen in plants struggling with stress from salt, metals or reactive oxygen species (SN: 9/8/21).

Apollo 11 seedlings had the most severely stressed genetic profile, offering more evidence that regolith exposed to the lunar surface longer — and therefore littered with more impact glass and metallic iron — is more toxic to plants.

Future space explorers could choose the site for their lunar habitat accordingly. Perhaps lunar dirt could also be modified somehow to make it more comfortable for plants. Or plants could be genetically engineered to feel more at home in alien soil. “We can also choose plants that do better,” Paul says. “Maybe spinach plants, which are very salt-tolerant, would have no trouble growing in lunar regolith.”

Barker isn’t daunted by the challenges promised by this first attempt at lunar gardening. “There’s many, many steps and pieces of technology to be developed before humanity can really engage in lunar agriculture,” he says. “But having this particular dataset is really important for those of us that believe it’s possible and important.”

For millennia, the universe did a pretty good job of keeping its secrets from science.

Ancient Greeks thought the universe was a sphere of fixed stars surrounding smaller spheres carrying planets around the central Earth. Even Copernicus, who in the 16th century correctly replaced the Earth with the sun, viewed the universe as a single solar system encased by the star-studded outer sphere.

But in the centuries that followed, the universe revealed some of its vastness. It contained countless stars agglomerated in huge clusters, now called galaxies.

Then, at the end of the 1920s, the cosmos disclosed its most closely held secret of all: It was getting bigger. Rather than static and stable, an everlasting and ever-the-same entity encompassing all of reality, the universe continually expanded. Observations of distant galaxies showed them flying apart from each other, suggesting the current cosmos to be just the adult phase of a universe born long ago in the burst of a tiny blotch of energy.

It was a surprise that shook science at its foundations, undercutting philosophical preconceptions about existence and launching a new era in cosmology, the study of the universe. But even more surprising, in retrospect, is that such a deep secret had already been suspected by a mathematician whose specialty was predicting the weather.
A century ago this month (May 1922), Russian mathematician-meteorologist Alexander Friedmann composed a paper, based on Einstein’s general theory of relativity, that outlined multiple possible histories of the universe. One such possibility described cosmic expansion, starting from a singular point. In essence, even without considering any astronomical evidence, Friedmann had anticipated the modern Big Bang theory of the birth and evolution of the universe.

“The new vision of the universe opened by Friedmann,” writes Russian physicist Vladimir Soloviev in a recent paper, “has become a foundation of modern cosmology.”

Friedmann was not well known at the time. He had graduated in 1910 from St. Petersburg University in Russia, having studied math along with some physics. In graduate school he investigated the use of math in meteorology and atmospheric dynamics. He applied that expertise in aiding the Russian air force during World War I, using math to predict the optimum release point for dropping bombs on enemy targets.

After the war, Friedmann learned of Einstein’s general theory of relativity, which describes gravity as a manifestation of the geometry of space (or more accurately, spacetime). In Einstein’s theory, mass distorts spacetime, producing spacetime “curvature,” which makes masses appear to attract each other.

Friedmann was especially intrigued by Einstein’s 1917 paper (and a similar paper by Willem de Sitter) applying general relativity to the universe as a whole. Einstein found that his original equations allowed the universe to grow or shrink. But he considered that unthinkable, so he added a term representing a repulsive force that (he thought) would keep the size of the cosmos constant. Einstein concluded that space had a positive spatial curvature (like the surface of a ball), implying a “closed,” or finite universe.

Friedmann accepted the new term, called the cosmological constant, but pointed out that for various values of that constant, along with other assumptions, the universe might exhibit very different behaviors. Einstein’s static universe was a special case; the universe might also expand forever, or expand for a while, then contract to a point and then begin expanding again.

Friedmann’s paper describing dynamic universes, titled “On the Curvature of Space,” was accepted for publication in the prestigious Zeitschrift für Physik on June 29, 1922.

Einstein objected. He wrote a note to the journal contending that Friedmann had committed a mathematical error. But the error was Einstein’s. He later acknowledged that Friedmann’s math was correct, while still denying that it had any physical validity.

Friedmann insisted otherwise.

He was not just a pure mathematician, oblivious to the physical meanings of his symbols on paper. His in-depth appreciation of the relationship between equations and the atmosphere persuaded him that the math meant something physical. He even wrote a book (The World as Space and Time) delving deeply into the connection between the math of spatial geometry and the motion of physical bodies. Physical bodies “interpret” the “geometrical world,” he declared, enabling scientists to test which of the various possible geometrical worlds humans actually inhabit. Because of the physics-math connection, he averred, “it becomes possible to determine the geometry of the geometrical world through experimental studies of the physical world.”

So when Friedmann derived solutions to Einstein’s equations, he translated them into the possible physical meanings for the universe. Depending on various factors, the universe could be expanding from a point, or from a finite but smaller initial state, for instance. In one case he envisioned, the universe began to expand at a decelerating rate, but then reached an inflection point, whereupon it began expanding at a faster and faster rate. At the end of the 20th century, astronomers measuring the brightness of distant supernovas concluded that the universe had taken just such a course, a shock almost as surprising as the expansion of the universe itself. But Friedmann’s math had already forecast such a possibility.
No doubt Friedmann’s deep appreciation for the synergy of abstract math and concrete physics prepared his mind to consider the notion that the universe could be expanding. But maybe he had some additional help. Although he was the first scientist to seriously propose an expanding universe, he wasn’t the first person. Almost 75 years before Friedmann’s paper, the poet Edgar Allan Poe had published an essay (or “prose poem”) called Eureka. In that essay Poe described the history of the universe as expanding from the explosion of a “primordial particle.” Poe even described the universe as growing and then contracting back to a point again, just as envisioned in one of Friedmann’s scenarios.

Although Poe had studied math during his brief time as a student at West Point, he had used no equations in Eureka, and his essay was not recognized as a contribution to science. At least not directly. It turns out, though, that Friedmann was an avid reader, and among his favorite authors were Dostoevsky and Poe. So perhaps that’s why Friedmann was more receptive to an expanding universe than other scientists of his day.

Today Friedmann’s math remains at the core of modern cosmological theory. “The fundamental equations he derived still provide the basis for the current cosmological theories of the Big Bang and the accelerating universe,” Israeli mathematician and historian Ari Belenkiy noted in a 2013 paper. “He introduced the fundamental idea of modern cosmology — that the universe is dynamic and may evolve in different manners.”

Friedmann emphasized that astronomical knowledge in his day was insufficient to reveal which of the possible mathematical histories the universe has chosen. Now scientists have much more data, and have narrowed the possibilities in a way that confirms the prescience of Friedmann’s math.

Friedmann did not live to see the triumphs of his insights, though, or even the early evidence that the universe really does expand. He died in 1925 from typhoid fever, at the age of 37. But he died knowing that he had deciphered a secret about the universe deeper than any suspected by any scientist before him. As his wife remembered, he liked to quote a passage from Dante: “The waters I am entering, no one yet has crossed.”

Deep in the human brain, a very specific kind of cell dies during Parkinson’s disease.

For the first time, researchers have sorted large numbers of human brain cells in the substantia nigra into 10 distinct types. Just one is especially vulnerable in Parkinson’s disease, the team reports May 5 in Nature Neuroscience. The result could lead to a clearer view of how Parkinson’s takes hold, and perhaps even ways to stop it.

The new research “goes right to the core of the matter,” says neuroscientist Raj Awatramani of Northwestern University Feinberg School of Medicine in Chicago. Pinpointing the brain cells that seem to be especially susceptible to the devastating disease is “the strength of this paper,” says Awatramani, who was not involved in the study.

Parkinson’s disease steals people’s ability to move smoothly, leaving balance problems, tremors and rigidity. In the United States, nearly 1 million people are estimated to have Parkinson’s. Scientists have known for decades that these symptoms come with the death of nerve cells in the substantia nigra. Neurons there churn out dopamine, a chemical signal involved in movement, among other jobs (SN: 9/7/17).

But those dopamine-making neurons are not all equally vulnerable in Parkinson’s, it turns out.

“This seemed like an opportunity to … really clarify which kinds of cells are actually dying in Parkinson’s disease,” says Evan Macosko, a psychiatrist and neuroscientist at Massachusetts General Hospital in Boston and the Broad Institute of MIT and Harvard.
The tricky part was that dopamine-making neurons in the substantia nigra are rare. In samples of postmortem brains, “we couldn’t survey enough of [the cells] to really get an answer,” Macosko says. But Abdulraouf Abdulraouf, a researcher in Macosko’s laboratory, led experiments that sorted these cells, figuring out a way to selectively pull the cells’ nuclei out from the rest of the cells present in the substantia nigra. That enrichment ultimately led to an abundance of nuclei to analyze.

By studying over 15,000 nuclei from the brains of eight formerly healthy people, the researchers further sorted dopamine-making cells in the substantia nigra into 10 distinct groups. Each of these cell groups was defined by a specific brain location and certain combinations of genes that were active.

When the researchers looked at substantia nigra neurons in the brains of people who died with either Parkinson’s disease or the related Lewy body dementia, the team noticed something curious: One of these 10 cell types was drastically diminished.

These missing neurons were identified by their location in the lower part of the substantia nigra and an active AGTR1 gene, lab member Tushar Kamath and colleagues found. That gene was thought to serve simply as a good way to identify these cells, Macosko says; researchers don’t know whether the gene has a role in these dopamine-making cells’ fate in people.

The new finding points to ways to perhaps counter the debilitating diseases. Scientists have been keen to replace the missing dopamine-making neurons in the brains of people with Parkinson’s. The new study shows what those cells would need to look like, Awatramani says. “If a particular subtype is more vulnerable in Parkinson’s disease, maybe that’s the one we should be trying to replace,” he says.

In fact, Macosko says that stem cell scientists have already been in contact, eager to make these specific cells. “We hope this is a guidepost,” Macosko says.

The new study involved only a small number of human brains. Going forward, Macosko and his colleagues hope to study more brains, and more parts of those brains. “We were able to get some pretty interesting insights with a relatively small number of people,” he says. “When we get to larger numbers of people with other kinds of diseases, I think we’re going to learn a lot.”

There have been suggestions that our solar system might have a tenth planet…. In the April Publications of the Astronomical Society of the Pacific, a mathematician … presents what he says is “some very interesting evidence of a planet beyond Pluto.” The evidence comes from calculations of the orbit of Halley’s comet.

Update
The 1972 evidence never yielded a planet, but astronomers haven’t stopped looking — though it became a search for Planet 9 with Pluto’s 2006 switch to dwarf status. In the mid-2010s, scientists hypothesized that the tug of a large planet 500 to 600 times as far from the sun as Earth could explain the peculiar orbits of some objects in the solar system’s debris-filled Kuiper Belt (SN: 7/23/16, p. 7). But that evidence might not stand up to further scrutiny (SN: 3/13/21, p. 9). Researchers using the Atacama C­osmology Telescope in Chile to scan nearly 90 percent of the Southern Hemisphere’s sky had no luck finding the planet, the team reported in December 2021.

Booster shots against COVID-19 are once again on my mind. The U.S. Food and Drug Administration says that older people and immunocompromised people are eligible for a second booster shot provided it has been at least four months since their last shot. After I got over the shock of the FDA calling me “older” — meaning anyone 50 and up — I’ve been pondering whether to get a second booster (otherwise known as a fourth dose of an mRNA vaccine, or third dose of any vaccine if you initially got the Johnson & Johnson vaccine), and if so, when.

Peter, a 60-year-old acquaintance who asked me not to use his last name to protect his privacy, told me he’s going to get a second booster, but not now. He’s holding out for fall and hoping for a variant-specific version of the vaccine. Right now, he and his wife “are vaxxed out,” he says. And he worries that getting boosted too often could hurt his immune system’s ability to respond to new variants. “I just think it’s the law of diminishing returns,” he says.

Lots of scientists and policy makers are thinking about these issues, too. For instance, last week an advisory committee to the U.S. Centers for Disease Control and Prevention met to discuss boosters. And a bevy of studies about how well boosters work and how they affect the immune system have come out in recent weeks, some of them peer-reviewed, some still preliminary.
In making my own decision, I wanted to know several things. First, does a second booster really provide additional protection from the coronavirus beyond what I got from my first booster (SN: 11/8/21)? Second, are there downsides to getting boosted again? And finally, if I’m going to do it, when should that be and which vaccine will I get?

To get a handle on the first question, I need to know how much protection the first booster actually gave me. I’m not immunocompromised, so there’s no reason for me to get an antibody test to see if I have enough of those defenders to fend off the coronavirus. I just have to assume that my immune system is behaving normally and that what’s true for others in my age group also goes for me.

How long does COVID-19 booster immunity last?
Although the exact numbers vary, several studies have found that a third dose of the Pfizer COVID-19 vaccine gave higher levels of protection against the omicron variant than two doses did (SN: 3/1/22). But that protection wanes after a few months.

Data from Israel, where some people have been getting fourth doses for months, suggest that a second booster does indeed bolster protection, but again only temporarily. In health care workers who got a fourth dose, antibody levels shot up above levels achieved after the third jab, researchers reported April 7 in the New England Journal of Medicine. Vaccine effectiveness against infection was 30 percent with the Pfizer shot and 11 percent with Moderna. Both were better at preventing symptomatic disease, with Pfizer weighing in at 43 percent and Moderna at 31 percent. But those who did get infected produced high levels of the virus, suggesting they were contagious to others.

In a separate study published in the same journal, researchers looking at people 60 and older found that a fourth dose gave protection against both infection and severe disease, but the protection against infection began to decline after about five weeks.

There’s more data on protection against severe illness from a study of more than 11,000 people admitted for COVID-19 to a hospital or emergency department in the Kaiser Permanente Southern California health care system. At nine months after the second shot, two doses of the Pfizer vaccine were 31 percent effective at keeping people out of the emergency room with omicron, researchers reported April 22 in Lancet Respiratory Medicine. The shots were 41 percent effective at preventing more severe illness resulting in hospitalizations from the omicron variant.

The third dose (first booster) bumped the effectiveness way up to 85 percent against hospitalization and 77 percent against ER visits, the team found. But the effect was temporary. By three months after the booster, effectiveness had declined to 55 percent against hospitalization and 53 percent against emergency room visits. The same jump in protection and quick waning from the first booster has also been noted in the United Kingdom and Qatar.

It’s been about six months since my first booster shot, so any extra protection I got from it is probably gone by now. But will a fourth dose restore protection?

The CDC calculates that for every million people 50 and older who get a fourth dose of vaccine, 830 hospitalizations, 183 intensive care unit admissions and 85 deaths could be prevented. Those are impressive numbers, but many people think efforts should be focused more on getting still-unvaccinated people immunized instead of worrying about additional shots for the already vaxxed. CDC’s numbers support that. Because unvaccinated people are so vulnerable to the coronavirus, you would need to vaccinate just 135 people aged 50 and older with two shots to prevent one hospitalization. But already vaccinated people still have quite a bit of immunity, so you’d need to vaccinate 1,205 older people with a fourth dose to prevent one hospitalization.
How does my health factor in?
Of course, that’s data concerning populations. I and millions of others are trying to make individual calculations. “People need to make decisions based on their health condition as well as their exposure levels,” says Prakash Nagarkatti, an immunologist at the University of South Carolina School of Medicine Columbia. For instance, people whose jobs or other activities put them in contact with lots of people have higher exposure risks than someone who works at home. People who are older or have underlying health conditions, such as diabetes, obesity, high blood pressure, or lung, kidney, liver and heart diseases are all at higher risk. Those people might benefit from a shot now. “But if you’re 50 to 60 and very healthy, I don’t know if you need it right away,” Nagarkatti says. “You could maybe wait a few months.”

I’ve got some health risks that may make me more likely to get severely ill, and I have a couple of big events coming up this summer where I could get exposed to the virus. So getting boosted now to get a little bump in immunity that should last for a few months seems like a good idea. I’m also basing that decision about when to get a booster on what’s happening with the virus.

Case counts in my county are on the upswing. Nationally, BA.2.12.1, a potentially even wilier subvariant of the already slippery BA.2 omicron variant, is on the rise, making up almost 29 percent of cases in the week ending April 23. South Africa is experiencing a rise in cases caused by the omicron subvariants BA.4 and BA.5. It could be the start of a fifth wave of infection in that country, something researchers thought wouldn’t happen because so many people there were previously infected and vaccinated, Jacob Lemieux, an infectious disease researcher at Massachusetts General Hospital in Boston said April 26 in a news briefing. “It has the flavor of, ‘Here we go, again,’” he said. “So much for the idea of herd immunity.”

Are there any downsides to a second booster?
But would I be harming my immune system if I get a booster shot now? Previous experience with vaccines against other viruses suggests repeated boosting isn’t always a good thing, Galit Alter, codirector of the Harvard University Center for AIDS Research said in the news briefing. For instance, in one HIV vaccine trial, people were boosted six times with the same protein. Each time their antibody levels went up, but the researchers found that the immune system was making nonfunctional, unhelpful antibodies that blocked the action of good ones. So far, that hasn’t happened with the COVID-19 vaccines, but it could be important to space out doses to prevent such a scenario.

Another worry for immunologists is original antigenic sin. That has nothing to do with apples, serpents and gardens. Instead it happens when the immune system sees a virus or portion of the virus for the first time and trains memory cells to make antibodies against the virus. The next time the person encounters the virus or another version of it, instead of adding to the antibody arsenal, it continues to make only those original antibodies.

With the coronavirus, though, “what’s happened is the opposite of antigenic sin,” says Michel Nussenzweig, an immunologist and Howard Hughes Medical Institute investigator at Rockefeller University in New York City. He and colleagues examined what happens to the immune response after a third dose of vaccine, focusing especially on very long-lived immune cells called memory B cells. Those memory cells still made new antibodies when they got a third look at the vaccine, Nussenzweig and colleagues reported April 21 in Nature. That wouldn’t happen if antigenic sin were a problem. And it’s great news since an ever-growing repertoire of antibodies may help defend against future variants.

A separate Nature Immunology study found that other immune cells called T cells also learn new tricks after a booster dose or a breakthrough infection. Those and other studies seem to indicate that getting a booster isn’t bad for my immune system and could help me against future variants.

Is it okay to mix and match COVID-19 booster shots?
Now the question is, which booster to get? Mixing vaccines doesn’t seem to push the immune system toward making the unhelpful antibodies, Alter said. It “tantalizes the immune system with different flavors of vaccines, and seems to reawaken it,” she said. “Even mixing and matching mRNAs may be highly advantageous to the immune system.” She and colleagues found that the Moderna vaccine may make more IgA antibodies, the type that help protect mucous membranes in the nose, mouth and other slick surfaces in the body from infection, than the Pfizer vaccine does. Pfizer’s makes more of the IgM and IgG antibodies that circulate in the blood, data published March 29 in Science Translational Medicine show.

Since I got the Pfizer vaccine for my first three doses, it seems wise to shake things up with Moderna this time. I’ve already booked my shot.

As for Peter, after I laid out the evidence, he said he was convinced that he should probably get a shot now, as his doctor recommends. But he admitted he might just wait to see if Moderna comes out with an updated version of its vaccine.

What’s really needed, all the experts tell me, is to better understand how the immune system operates so researchers can build better vaccines with longer-lasting protection so we won’t be facing needles multiple times per year.

Taking antibiotics in the first two years of life can prevent babies from developing a robust immune response to certain vaccines. The new finding provides another cautionary tale against overusing antibiotics, researchers say.

Babies get immunized in their first six months, and receive booster doses in their second year, to protect against certain infectious diseases. Antibiotic use during that time was associated with subpar immune responses to four vaccines babies receive to ward off whooping cough, polio and other diseases, researchers report online April 27 in Pediatrics.

And the more rounds of antibiotics a child received, the more antibody levels to the vaccines dropped below what’s considered protective. Levels induced by the primary series of shots for the polio, diphtheria-tetanus-pertussis, Haemophilus influenzae type b and pneumococcal vaccines fell 5 to 11 percent with each antibiotic course. In the children’s second year, antibody levels generated by booster shots of these vaccines dropped 12 to 21 percent per course.
“If anyone needed yet another reason why overprescription of antibiotics is not a good thing, this paper offers that reason,” says immunologist Bali Pulendran of Stanford University School of Medicine, who was not involved in the study.

Taking antibiotics disrupts the population of bacteria that live in the gut. That’s well known, but researchers are still learning about how that disruption can affect a person’s health. The new study adds to evidence that diminishing the amount and diversity of gut bacteria impacts vaccination. In studies in mice, antibiotics hampered the immune system’s response to vaccines. And a small study in humans found that antibiotics dampened adults’ response to the flu vaccine in those whose prior immune memory for influenza had waned, Pulendran and colleagues reported in 2019.

The study in Pediatrics is the first to report an association between antibiotic use and compromised vaccine responses in children. Michael Pichichero, a pediatric infectious diseases specialist at the Rochester General Hospital Research Institute in New York, and colleagues collected blood samples taken from 560 children during routine visits with their pediatricians. Of those, 342 children had been prescribed close to 1,700 courses of antibiotics and 218 children had not gotten the drugs. The team analyzed whether antibody levels induced by the four vaccines met the threshold considered protective and found levels more often fell short for the kids who had gotten antibiotics.

The type and length of antibiotic treatment also made a difference. Broad spectrum drugs were associated with antibody levels below what is protective, while a more targeted antibiotic was not. Furthermore, a 10-day course, but not a five-day course, reduced vaccine-induced antibody levels.

The researchers didn’t look at whether children in the study with diminished antibody levels were more likely to develop vaccine-preventable diseases. But there has been concern about outbreaks of whooping cough, says Pichichero, which have occurred in the the United States despite vaccination (SN: 4/4/14). Perhaps antibiotic use can help explain these outbreaks, he says.

To see what kinds of changes are occurring in the gut bacteria, Pichichero and colleagues are beginning a study with a new group of children. The researchers will collect stool samples along with blood draws and antibiotic use records. They’d like to follow the children past age 5, beyond the time kids receive another round of booster shots, to learn whether antibiotics also interfere with this next opportunity to develop antibodies.

“Antibiotics are miracle medicines,” says Pichichero. “In no way does this study imply that children who need an antibiotic shouldn’t get it.” But if possible, it should be a narrowly targeted antibiotic for a shorter course, he says. Along with the risk of antibiotic resistance that comes with overuse of the drugs (SN: 1/24/22), the impact antibiotics could have on vaccine-induced immunity “has clinical implications for every individual child.”

Leonardo da Vinci was wrong about trees.

The multitalented, Renaissance genius wrote down his “rule of trees” over 500 years ago. It described the way he thought that trees branch. Though it was a brilliant insight that helped him to draw realistic landscapes, Leonardo’s rule breaks down for many types of trees. Now, a new branching rule — dubbed “Leonardo-like” — works for virtually any leafy tree, researchers report in a paper accepted April 13 in Physical Review E.

“The older Leonardo rule describes the thickness of the branches, while the length of the branch was not taken into account,” says physicist Sergey Grigoriev of the Petersburg Nuclear Physics Institute in Gatchina, Russia. “Therefore, the description using the older rule is not complete.”
Leonardo’s rule says that the thickness of a limb before it branches into smaller ones is the same as the combined thickness of the limbs sprouting from it (SN: 6/1/11). But according to Grigoriev and his colleagues, it’s the surface area that stays the same.

Using surface area as a guide, the new rule incorporates limb widths and lengths, and predicts that long branches end up being thinner than short ones. Unlike Leonardo’s guess, the updated rule works for slender birches as well as it does for sturdy oaks, the team reports.

The connection between the surface area of branches and overall tree structure shows that it’s the living, outer layers that guide tree structure, the researchers say. “The life of a tree flows according to the laws of conservation of area in two-dimensional space,” the authors write in their study, “as if the tree were a two-dimensional object.” In other words, it’s as if just two dimensions — the width of each limb and the distance between branchings on a limb — determine any tree’s structure. As a result, when trees are rendered in two dimensions in a painting or on a screen, the new rule describes them particularly well.
The new Leonardo-like rule is an improvement, says Katherine McCulloh, a botanist at the University of Wisconsin–Madison who was not involved with this study. But she has her doubts about the Russian group’s rationale for it. In most trees, she says, the living portion extends much deeper than the thin surface layer.

“It’s really species-dependent, and even age-dependent,” McCulloh says. “A giant, old oak tree might have a centimeter of living wood … [but] there are certainly tropical tree species that have very deep sapwood and may have living wood for most of their cross sections.”

Still, the fact that the Leonardo-like rule appears to hold for many trees intrigues McCulloh. “To me, it drives home the question of why are [trees] conserving this geometry for their external tissue, and how is that related to the microscopic level differences that we observe in wood,” she says. “It’s a really interesting question.”

To test their rule, Grigoriev and colleagues took photographs of trees from a variety of species and analyzed the branches to confirm that the real-world patterns matched the predictions. The photos offer “a direct measurement of the characteristics of a tree without touching it, which can be important when dealing with a living object,” Grigoriev says.

Though the team hasn’t studied evergreens yet, the rule holds for all of the deciduous trees that the researchers have looked at. “We have applied our methodology to maple, linden, apple,” Grigoriev says, in addition to oak, birch and chestnut. “They show the same general structure and obey the Leonardo-like rule.”

While it’s possible to confirm the rule by measuring branches by hand, it would require climbing into trees and checking all the limbs — a risky exercise for trees and scientists alike. “Note,” the researchers write, “that not a single tree was harmed during these experiments.”