A new species of hulking ancient herbivore would have overshadowed its relatives.

Fossils found in Poland belong to a new species that roamed during the Late Triassic, a period some 237 million to 201 million years ago, researchers report November 22 in Science. But unlike most of the enormous animals who lived during that time period, this new creature isn’t a dinosaur — it’s a dicynodont.

Dicynodonts are a group of ancient four-legged animals that are related to mammals’ ancestors. They’re a diverse group, but the new species is far larger than any other dicynodont found to date. The elephant-sized creature was more than 4.5 meters long and probably weighed about nine tons, the researchers estimate. Related animals didn’t become that big again until the Eocene, 150 million years later.
“We think it’s one of the most unexpected fossil discoveries from the Triassic of Europe,” says study coauthor Grzegorz Niedzwiedzki, a paleontologist at Uppsala University in Sweden. “Who would have ever thought that there is a fossil record of such a giant, elephant-sized mammal cousin in this part of the world?” He and his team first described some of the bones in 2008; now they’ve made the new species — Lisowicia bojani — official.

The creature had upright forelimbs like today’s rhinoceroses and hippos, instead of the splayed front limbs seen on other Triassic dicynodonts, which were similar to the forelimbs of present-day lizards. That posture would have helped it support its massive bodyweight.

WASHINGTON — After a stunningly explosive summer, Kilauea, the world’s longest continuously erupting volcano, finally seems to have taken a break. But the scientists studying it haven’t. Reams of new data collected during an unprecedented opportunity to monitor an ongoing, accessible eruption are changing what’s known about how some volcanoes behave.

“It was hugely significant,” says Jessica Larsen, a petrologist at the University of Alaska Fairbanks, and “a departure from what Kilauea had been doing for more than 35 years.”
The latest eruption started in May. By the time it had ended three months later, over 825 million cubic meters of earth had collapsed at the summit. That’s the equivalent of 300,000 Olympic-sized swimming pools, Kyle Anderson, a geophysicist with the U.S. Geologic Survey in Menlo Park, Calif., said December 11 in a news conference at the annual meeting of the American Geophysical Union.

As the summit crater deflated, magma gushed through underground tunnels, draining out through fissures along an area called the lower eastern rift zone at a rate of roughly 50 meters per day. That lava eventually covered 35.5 square kilometers of land, Anderson and his colleagues reported in a study published December 11 in Science.

The volcano also taught scientists a thing or two.
Scientists previously believed that groundwater plays a big role in how a caldera collapses. When craters were drained of their magma, “cooling, cracking depressurized the caldera, allowing groundwater to seep in and create a series of explosive eruptions,” Anderson said. “But groundwater did not play a significant role in driving the explosions this summer.”

Instead, the destruction of Kilauea’s crater is what’s called a piston-style caldera collapse, he said. Sixty-two small collapse events rattled the volcano from mid-May to late August, with each collapse causing the crater to sink and pushing the surrounding land out and up. By the end, the center of the volcano sank by as much as 500 meters — more than the height of the Empire State Building.

That activity didn’t just destroy the crater. “We could see surges in the eruption rate 40 kilometers away whenever there was a collapse,” Anderson said.
Life finds a way
Under the sea, life moved in around the brand-new land surprisingly quickly. Using a remotely operated vehicle to explore the seafloor, researchers in September found evidence of hydrothermal activity along newly deposited lava flows about 650 meters deep. More surprising, bright yellow, potentially iron-oxidizing microbes had already moved in.

“There’s no reason why we should have expected there would be hydrothermal activity that would be alive within the first 100 days,” Chris German, a geologist at Woods Hole Oceanographic Institution in Falmouth, Mass., said at the news conference. “This is actually life here!”

The discovery suggests “how volcanism can give rise to the chemical energy that can drive primitive microbial organisms and flower a whole ecosystem,” he said.

Studying these ecosystems can provide insight into how life may form in places like Enceladus, an icy moon of Saturn. Hydrothermal activity is common where Earth’s tectonic plates meet. But alien worlds don’t show evidence of plate tectonics, though they can be volcanically active, German says. Studying how hydrothermal life forms near volcanoes that aren’t along tectonic boundaries on Earth could reveal a lot about other celestial bodies.

“This is a better analog of what we expect to them to be like,” says German, but “it is what’s least studied.”

What comes next
As of December 5, Kilauea had not erupted for three months, suggesting it’s in what’s called a pause – still active but not spewing lava. Observations from previous eruptions suggest that the next phase of Kilauea’s volcanic cycle may be a quieter one. But the volcano likely won’t stay quiet forever, says Christina Neal, the head scientist at the USGS Hawaiian Volcano Observatory and a coauthor of the Science paper. “We’re in this lull and we just don’t know what is going to happen next,” she says.Life finds a way
Under the sea, life moved in around the brand-new land surprisingly quickly. Using a remotely operated vehicle to explore the seafloor, researchers in September found evidence of hydrothermal activity along newly deposited lava flows about 650 meters deep. More surprising, bright yellow, potentially iron-oxidizing microbes had already moved in.

“There’s no reason why we should have expected there would be hydrothermal activity that would be alive within the first 100 days,” Chris German, a geologist at Woods Hole Oceanographic Institution in Falmouth, Mass., said at the news conference. “This is actually life here!”

The discovery suggests “how volcanism can give rise to the chemical energy that can drive primitive microbial organisms and flower a whole ecosystem,” he said.

Studying these ecosystems can provide insight into how life may form in places like Enceladus, an icy moon of Saturn. Hydrothermal activity is common where Earth’s tectonic plates meet. But alien worlds don’t show evidence of plate tectonics, though they can be volcanically active, German says. Studying how hydrothermal life forms near volcanoes that aren’t along tectonic boundaries on Earth could reveal a lot about other celestial bodies.
Scientists are tracking ground swelling near the Puu Oo vent, where much of Kilauea’s lava has flowed from during the volcano’s 35-year eruption history. That inflation is an indication that magma may still be on the move deep below.

The terrain surrounding this remote region is dense with vegetation, making it a difficult area to study. But new methods tested during the 2018 eruption, such as the use of uncrewed aerial vehicles, for example, could aid in tracking the recent deformation.

Scientists are also watching the volcano next door: Mauna Loa. History has shown that Mauna Loa can act up during periods when Kilauea sleeps. For the past several years, volcanologists have kept an eye on Kilauea’s larger sister volcano, which went silent last fall, after a period with few earthquakes and intermittent deformation. “We’re seeing a little bit of inflation at Mauna Loa and some earthquake swarms where it had been active, Neal says. “So that’s another issue of concern for us going into the future.”

When an outbreak of a viral hemorrhagic fever hit Nigeria in 2018, scientists were ready: They were already in the country testing new disease-tracking technology, and within weeks managed to steer health workers toward the most appropriate response.

Lassa fever, which is transmitted from rodents to humans, pops up every year in West Africa. But 2018 was the worst season on record for Nigeria. By mid-March, there were 376 confirmed cases — more than three times as many as by that point in 2017 — and another 1,495 suspected. Health officials weren’t sure if the bad year was being caused by the strains that usually circulate, or by a new strain that might be more transmissible between humans and warrant a stronger response.
New technology for analyzing DNA in the field helped answer that question mid-outbreak, confirming the outbreak was being caused by pretty much the same strains transmitted from rodents to humans in past years. That rapid finding helped Nigeria shape its response, allowing health officials to focus efforts on rodent control and safe food storage, rather than sinking time and money into measures aimed at stopping unlikely human-to-human transmission, researchers report in the Jan. 4 Science.

While the scientists were reporting their results to the Nigeria Centre for Disease Control, they were also discussing the data with other virologists and epidemiologists in online forums. This kind of real-time collaboration can help scientists and public health workers “see the bigger picture about pathogen spread,” says Nicholas Loman, a microbial genomicist at the University of Birmingham in England who was not involved in the research.

Portable DNA sequencers, some as small as a cell phone, have allowed scientists to read the genetic information of viruses emerging in places without extensive lab infrastructure. Looking for genetic differences between patient samples can give clues to how a virus is being transmitted and how quickly it’s changing over time — key information for getting outbreaks under control. If viral DNA from several patients is very similar, that suggests the virus may be transmitted between people; if the DNA is more distinct, people might be picking up the virus independently from other animals.

The technology has also been used amid recent Ebola and Zika outbreaks. But the Lassa virus presents a unique challenge, says study coauthor Stephan Günther, a virologist at the Bernhard-Nocht-Institute for Tropical Medicine in Hamburg, Germany. Unlike Ebola or Zika, Lassa has a lot of genetic variation between strains. So while the same small regions of DNA from various strains of Ebola or Zika can be identified for analysis, it’s hard to accurately target similar regions for comparison among Lassa strains.
Instead, Günther and his team used a tactic called metagenomics: They collected breast milk, plasma and cerebrospinal fluid from patients and sequenced all the DNA within — human, viral and anything else lurking. Then, the team picked out the Lassa virus DNA from that dataset.

All told, the scientists analyzed Lassa virus DNA from 120 patients, far more than initially intended. “We went to the field to do a pilot study,” Günther says. “Then the outbreak came. And we quickly scaled up.” Preexisting relationships in Nigeria helped make that happen: The team had been collaborating for a decade with researchers at the Irrua Specialist Teaching Hospital and working alongside the World Health Organization and the Nigeria Centre for Disease Control.

Analyzing and interpreting the massive amounts of data generated by the metagenomics approach was a challenge, especially with limited internet connection, Günther says. Researchers analyzed 36 samples during the outbreak — less than a third of their total dataset, but still enough to guide the response. The full analysis, completed after the outbreak, confirmed the initial findings.

A metagenomics approach could be useful in disease surveillance more broadly. Currently, “we look for things that we know about and expect to find. Yet evidence from Ebola in West Africa and Zika in the Americas is that emerging pathogens can pop up in unexpected places, and take too long to be recognized,” Loman says. Sequencing all DNA in a sample, he says, could allow scientists to detect problem pathogens before they cause outbreaks.Instead, Günther and his team used a tactic called metagenomics: They collected breast milk, plasma and cerebrospinal fluid from patients and sequenced all the DNA within — human, viral and anything else lurking. Then, the team picked out the Lassa virus DNA from that dataset.

All told, the scientists analyzed Lassa virus DNA from 120 patients, far more than initially intended. “We went to the field to do a pilot study,” Günther says. “Then the outbreak came. And we quickly scaled up.” Preexisting relationships in Nigeria helped make that happen: The team had been collaborating for a decade with researchers at the Irrua Specialist Teaching Hospital and working alongside the World Health Organization and the Nigeria Centre for Disease Control.

Analyzing and interpreting the massive amounts of data generated by the metagenomics approach was a challenge, especially with limited internet connection, Günther says. Researchers analyzed 36 samples during the outbreak — less than a third of their total dataset, but still enough to guide the response. The full analysis, completed after the outbreak, confirmed the initial findings.

A metagenomics approach could be useful in disease surveillance more broadly. Currently, “we look for things that we know about and expect to find. Yet evidence from Ebola in West Africa and Zika in the Americas is that emerging pathogens can pop up in unexpected places, and take too long to be recognized,” Loman says. Sequencing all DNA in a sample, he says, could allow scientists to detect problem pathogens before they cause outbreaks.

Approval of the first and only treatment in the United States specifically targeting postpartum depression offers hope for millions of women each year who suffer from the debilitating mental health disorder after giving birth.

The new drug brexanolone — marketed under the name Zulresso and approved on March 19 by the U.S. Food and Drug Administration — is expected to become available to the public in late June. Developed by Sage Therapeutics, based in Cambridge, Mass., the drug is costly and treatment is intensive: It’s administered in the hospital as a 60-hour intravenous drip, and a treatment runs between $20,000 and $35,000. But researchers say that it could help many of the estimated 11.5 percent of U.S. new moms each year who experience postpartum depression, which can interfere with normal bonding between mothers and infants and lead to feeling hopeless, sad or overly anxious.
Here’s a closer look at the drug, its benefits and some potential drawbacks.

How does the new drug work?
How exactly brexanolone works is not known. But because the drug’s chemical structure is nearly identical to the natural hormone allopregnanolone, it’s thought that brexanolone operates in a similar way.

Allopregnanolone enhances the effects of a neurochemical called gamma-aminobutyric acid, or GABA, which stops nerve cells in the brain from firing. Ultimately this action helps quell a person’s anxiety or stress.
During pregnancy, the concentration of allopregnanolone in a woman’s brain spikes. This leads some neurons to compensate by temporarily tuning out GABA so that the nerve cells don’t become too inactive. Levels of the steroid typically return to normal quickly after a baby is born, and the neurons once again responding to GABA shortly thereafter. But for some women, this process can take longer, possibly resulting in postpartum depression.

Brexanolone temporarily elevates the brain’s allopregnanolone levels again, which results in a patient’s mood improving. But it’s still not clear exactly why the drug has this effect, says Samantha Meltzer-Brody, a reproductive psychiatrist at the University of North Carolina School of Medicine in Chapel Hill and the lead scientist of the drug’s clinical trials. Nor is it clear whether allopregnanolone’s, and thus possible brexanolone’s, influence on GABA is affecting only postpartum depression. But the drug clearly “has this incredibly robust response,” she says, “unlike anything currently available.”

How effective was the drug in clinical trials?
Brexanolone went through three separate clinical trials in which patients were randomly given either the drug or a placebo: one Phase II trial, which tests the drug’s effectiveness and proper dosage, and two Phase III trials, which tested the drug’s effects on moderate or severe postpartum depression and were necessary to gain approval for the drug’s commercial use in people.

Of 234 people who completed the trials, 94 received the suggested dosage of brexanolone. About 70 of those patients, or 75 percent, had what Meltzer-Brody described as a “robust response” to just one course of treatment. And of those patients with positive responses, 94 percent continued to feel well 30 days after the treatment. The results suggest that the drug may be most effective for those with severe postpartum depression; among those with moderate symptoms, the drug and the placebo had a fairly similar impact.

Can people take the drug again?
“There’s nothing prohibiting” a second course of brexanolone, but the effects of a repeat course have not been studied, Meltzer-Brody says. The drug was designed to be taken in tandem with the start of antidepressants, which take effect after about two to four weeks. So by the time the brexanolone wears off, the antidepressants would have kicked in.

It’s not clear yet if some patients could need a second dose. The clinical trials compared a group of women taking both antidepressants and brexanolone with another group taking only brexanolone and found no difference in the two group’s response 30 days after tests ended, Meltzer-Brody says. Because the study ended at 30 days, it’s unclear if the effects of brexanolone on its own last longer.

Can women breastfeed while taking brexanolone?
As a precaution, treated women did not breastfeed until six days after taking the drug. But in tests of breastmilk from 12 treated, lactating women, concentrations of brexanolone in breastmilk were negligible — less than 10 nanograms per millileter — in most of the women 36 hours after they received the infusion, according to Sage’s briefing document for the FDA. The FDA has yet to issue guidance on breast feeding.

Are there side effects?
About a third of the trial patients experienced sleepiness, sedation or headaches. The possibility of drowsiness led to the FDA’s requirement that the drug be administered by IV drip in a supervised setting. “If someone isn’t supervised, then there would be the risk that someone could get sleepy and pass out,” Meltzer-Brody says.

Are there plans for different versions of the drug?
Sage Therapeutics is developing a pill version of a drug called SAGE-217. It’s chemically similar to brexanolone and has similar antidepressant effects. Early results from a Phase III trial reported by the company in January show that, of 78 women treated with the pill, 72 percent responded favorably within two weeks, and 53 percent had not experienced a recurrence of symptoms four weeks later.

Is it worth the price and time?
Setting aside 60 hours to be hospitalized for an expensive drug could be discouraging for some. “It’s going to be very important for insurance to cover it in order for it be accessible,” Meltzer-Brody says. “I’m hoping that will be the case.” But based on the reaction of women with severe postpartum depression who participated in the trials, “two-and-a-half days seems like nothing if your debilitating, depressive symptoms will be gone.”

These are wondrous times for space exploration. Just when you think exploring the cosmos couldn’t possibly get more fun, another discovery delivers a new “oh wow” moment.

Consider the asteroid Bennu. It’s an unprepossessing space rock that drew scientists’ curiosity because it is among the most pristine objects in our solar system, and it might provide clues to the origins of life. But checking out Bennu is no trip to Paris; it’s about 130 million kilometers from Earth. NASA launched its OSIRIS-REx probe to Bennu in 2016, and it didn’t arrive until last December. The spacecraft is currently orbiting its quarry in preparation for an attempt at gathering samples from the asteroid’s surface in 2020 and then toting them back to Earth. Estimated delivery date: September 24, 2023. Clearly, asteroid science is not a discipline for those with short attention spans.
So imagine scientists’ delight when OSIRIS-REx already had news to share: Bennu is squirting jets of dust into space. It’s an asteroid behavior no one had ever seen before. Astronomy writer Lisa Grossman learned all about Bennu’s surprise jets while attending the Lunar and Planetary Science Conference in March. She reports that the dusty fountains may be the work of volatile gases beneath Bennu’s surface. The presence of volatiles would suggest that the rock wandered into the inner solar system relatively recently. But astronomers still have a lot to figure out about Bennu’s history, and they couldn’t be happier.

In other surprising space rock news from the conference, astronomers analyzing the much-more-distant object dubbed Ultima Thule now think it’s an agglomeration of mini-worlds that stuck together in the early days of the solar system — as Grossman terms it, a “Frankenworld.” That’s just the latest unexpected news from this Kuiper Belt denizen. If you’re as space rock obsessed as we are, you may recall that the first fuzzy images from NASA’s New Horizons spacecraft, which flew by Ultima Thule on January 1, suggested that the rock looked like a bowling pin or a snowman spinning in space. More recent images reveal not a snowman, but instead two pancakes or hamburger patties glued end to end (SN: 3/16/19, p. 15). That has scientists scrambling to figure out what forces could create such an oddly shaped object.

We’ll be hearing more about Bennu, Ultima Thule and other residents of our solar system in the months to come. I’m particularly looking forward to news from the Parker Solar Probe, which is tightening its orbit around the sun. I’m the one who is going to have to be patient in this case, though that’s not an attribute typically associated with journalists. The spacecraft won’t make its closest encounter with the sun until 2024, before ending its mission the following year. But the probe will be reporting in, and we’ll be reporting, too, as it makes this historic journey (SN: 1/19/19, p. 7).

Open your Web browser or your trusty print magazine and join us for the adventure. We hope you’ll enjoy the journey as much as we do.

Hayabusa2 has blasted the asteroid Ryugu with a projectile, probably adding a crater to the small world’s surface and stirring up dust that scientists hope to snag.

The projectile, a two-kilogram copper cylinder, separated from the Hayabusa2 spacecraft at 9:56 p.m. EDT on April 4, JAXA, Japan’s space agency, reports.

Hayabusa2 flew to the other side of the asteroid to hide from debris that would have been ejected when the projectile hit (SN: 1/19/19, p. 20). Scientists won’t know for sure whether the object successfully made a crater, and, if so, how big it is, until the craft circles back. But by 10:36 p.m. EDT, Hayabusa2’s cameras had captured a blurry shot of a dust plume spurting up from Ryugu, so the team thinks the attempt worked.
“This is the world’s first collision experiment with an asteroid!” JAXA tweeted.

Hayabusa2 plans to briefly touch down inside the crater to pick up a pinch of asteroid dust. The spacecraft has already grabbed one sample of Ryugu’s surface (SN Online: 2/22/19). But dust exposed by the impact will give researchers a look at the asteroid’s subsurface, which has not been exposed to sunlight or other types of space radiation for up to billions of years.

If all goes as planned, Hayabusa2 will return to Earth with both samples in late 2020. A third planned sample pickup has been scrapped because Ryugu’s boulder-strewn surface is so hazardous for the spacecraft.
Comparing the two samples will reveal details of how being exposed to space changes the appearance and composition of rocky asteroids, and will help scientists figure out how Ryugu formed (SN Online: 3/20/19). Scientists hope that the asteroid contains water and organic material that might help explain how life got started in the solar system.

A skull found in a cliffside cave on Greece’s southern coast in 1978 represents the oldest Homo sapiens fossil outside Africa, scientists say.

That skull, from an individual who lived at least 210,000 years ago, was encased in rock that also held a Neandertal skull dating to at least 170,000 years ago, contends a team led by paleoanthropologist Katerina Harvati of the University of Tübingen in Germany.

If these findings, reported online July 10 in Nature, hold up, the ancient Greek H. sapiens skull is more than 160,000 years older than the next oldest European H. sapiens fossils (SN Online: 11/2/11). It’s also older than a proposed H. sapiens jaw found at Israel’s Misliya Cave that dates to between around 177,000 and 194,000 years ago (SN: 2/17/18, p. 6).

“Multiple Homo sapiens populations dispersed out of Africa starting much earlier, and reaching much farther into Europe, than previously thought,” Harvati said at a July 8 news conference. African H. sapiens originated roughly 300,000 years ago (SN: 7/8/17, p. 6).
A small group of humans may have reached what’s now Greece more than 200,000 years ago, she suggested. Neandertals who settled in southeastern Europe not long after that may have replaced those first H. sapiens. Then humans arriving in Mediterranean Europe tens of thousands of years later would eventually have replaced resident Neandertals, who died out around 40,000 years ago (SN Online: 6/26/19).

But Harvati’s group can’t exclude the possibility that H. sapiens and Neandertals simultaneously inhabited southeastern Europe more than 200,000 years ago and sometimes interbred. A 2017 analysis of ancient and modern DNA concluded that humans likely mated with European Neandertals at that time.

The two skulls were held in a small section of wall that had washed into Greece’s Apidima Cave from higher cliff sediment and then solidified roughly 150,000 years ago. Since one skull is older than the other, each must originally have been deposited in different sediment layers before ending up about 30 centimeters apart on the cave wall, the researchers say.
Earlier studies indicated that one Apidima skull, which retains the face and much of the braincase, was a Neandertal that lived at least 160,000 years ago. But fossilization and sediment pressures had distorted the skull’s shape. Based on four 3-D digital reconstructions of the specimen, Harvati’s team concluded that its heavy brow ridges, sloping face and other features resembled Neandertal skulls more than ancient and modern human skulls. An analysis of the decay rate of radioactive forms of uranium in skull bone fragments produced an age estimate of at least 170,000 years.

A second Apidima fossil, also dated using uranium analyses, consists of the back of a slightly distorted braincase. Its rounded shape in a digital reconstruction characterizes H. sapiens, not Neandertals, the researchers say. A bunlike bulge often protrudes from the back of Neandertals’ skulls.
But without any facial remains to confirm the species identity of the partial braincase, “it is still possible that both Apidima skulls are Neandertals,” says paleoanthropologist Israel Hershkovitz of Tel Aviv University. Hershkovitz led the team that discovered the Misliya jaw and assigned it to H. sapiens.

Harvati and her colleagues will try to extract DNA and species-distinguishing proteins (SN: 6/8/19, p. 6) from the Greek skulls to determine their evolutionary identities and to look for signs of interbreeding between humans and Neandertals.

The find does little to resolve competing explanations of how ancient humans made their way out of Africa. Harvati’s suggestion that humans trekked from Africa to Eurasia several times starting more than 200,000 years ago is plausible, says paleoanthropologist Eric Delson of City University of New York’s Lehman College in an accompanying commentary. And the idea that some H. sapiens newcomers gave way to Neandertals probably also applied to humans who reached Misliya Cave and nearby Middle Eastern sites as late as around 90,000 years ago, before Neandertals occupied the area by 60,000 years ago, Delson says.

Hershkovitz disagrees. Ancient humans and Neandertals lived side-by-side in the Middle East for 100,000 years or more and occasionally interbred, he contends. Misliya Cave sediment bearing stone tools dates to as early as 274,000 years ago, Hershkovitz says. Since only H. sapiens remains have been found in the Israeli cave, ancient humans probably made those stone artifacts and could have been forerunners of Greek H. sapiens.

Bacteria can slip into the brain by commandeering cells in the brain’s protective layers, a new study finds. The results hint at how a deadly infection called bacterial meningitis takes hold.

In mice infected with meningitis-causing bacteria, the microbes exploit previously unknown communication between pain-sensing nerve cells and immune cells to slip by the brain’s defenses, researchers report March 1 in Nature. The results also hint at a new way to possibly delay the invasion — using migraine medicines to interrupt those cell-to-cell conversations.
Bacterial meningitis is an infection of the protective layers, or meninges, of the brain that affects 2.5 million people globally per year. It can cause severe headaches and sometimes lasting neurological injury or death.

“Unexpectedly, pain fibers are actually hijacked by the bacteria as they’re trying to invade the brain,” says Isaac Chiu, an immunologist at Harvard Medical School in Boston. Normally, one might expect pain to be a warning system for us to shut down the bacteria in some way, he says. “We found the opposite…. This [pain] signal is being used by the bacteria for an advantage.”

It’s known that pain-sensing neurons and immune cells coexist in the meninges, particularly in the outermost layer called the dura mater (SN: 11/11/20). So to see what role the pain and immune cells play in bacterial meningitis, Chiu’s team infected mice with two of the bacteria known to cause the infection in humans: Streptococcus pneumoniae and S. agalactiae. The researchers then observed where that bacteria ended up in mice genetically tweaked to lack pain-sensing nerve cells and compared those resting spots to those in mice with the nerve cells intact.

Mice without pain-sensing neurons had fewer bacteria in the meninges and brain than those with the nerve cells, the team found. This contradicts the idea that pain in meningitis serves as a warning signal to the body’s immune system, mobilizing it for action.

Further tests showed that the bacteria triggered a chain of immune-suppressing events, starting with the microbes secreting toxins in the dura mater.

The toxins hitched onto the pain neurons, which in turn released a molecule called CGRP. This molecule is already known to bind to a receptor on immune cells, where it helps control the dura mater’s immune responses. Injecting infected mice with more CGRP lowered the number of dural immune cells and helped the infection along, the researchers found.

The team also looked more closely at the receptor that CGRP binds to. In infected mice bred without the receptor, fewer bacteria made it into the brain. But in ones with the receptor, immune cells that would otherwise engulf bacteria and recruit reinforcements were disabled.
The findings suggest that either preventing the release of CGRP or preventing it from binding to immune cells might help delay infection.

In humans, neuroscientists know that CGRP is a driver of headaches — it’s already a target of migraine medications (SN: 6/5/18). So the researchers gave five mice the migraine medication olcegepant, which blocks CGRP’s effects, and infected them with S. pneumoniae. After infection, the medicated mice had less bacteria in the meninges and brain, took longer to show symptoms, didn’t lose as much weight and survived longer than mice that were not given the medication.

The finding suggests olcegepant slowed the infection. Even though it only bought mice a few extra hours, that’s crucial in meningitis, which can develop just as quickly. Were olcegepant to work the same way in humans, it might give doctors more time to treat meningitis. But the effect is probably not as dramatic in people, cautions Michael Wilson, a neurologist at the University of California, San Francisco who wasn’t involved with the work.

Scientists still need to determine whether pain-sensing nerve cells and immune cells have the same rapport in human dura mater, and whether migraine drugs could help treat bacterial meningitis in people.

Neurologist Avindra Nath has doubts. Clinicians think the immune response and inflammation damage the brain during meningitis, says Nath, who heads the team investigating nervous system infections at the National Institute of Neurological Disorders and Stroke in Bethesda, Md. So treatment involves drugs that suppress the immune response, rather than enhance it as migraine medications might.

Chiu acknowledges this but notes there might be room for both approaches. If dural mater immune cells could head the infection off at the pass, it may keep some bacteria from penetrating the defenses, minimizing brain inflammation.

This study might not ultimately change how clinicians treat patients, Wilson says. But it still reveals something new about one of the first lines of defense for the brain.

The Milky Way is churning out far more stars than previously thought, according to a new estimate of its star formation rate.

Gamma rays from aluminum-26, a radioactive isotope that arises primarily from massive stars, reveal that the Milky Way converts four to eight solar masses of interstellar gas and dust into new stars each year, researchers report in work submitted to arXiv.org on January 24. That range is two to four times the conventional estimate and corresponds to an annual birthrate in our galaxy of about 10 to 20 stars, because most stars are less massive than the sun.
At this rate, every million years — a blink of the eye in astronomical terms — our galaxy spawns 10 million to 20 million new stars. That’s enough to fill roughly 10,000 star clusters like the beautiful Pleiades cluster in the constellation Taurus. In contrast, many galaxies, including most of the ones that orbit the Milky Way, make no new stars at all.

“The star formation rate is very important to understand for galaxy evolution,” says Thomas Siegert, an astrophysicist at the University of Würzburg in Germany. The more stars a galaxy makes, the faster it enriches itself with oxygen, iron and the other elements that stars create. Those elements then alter star-making gas clouds and can change the relative number of large and small stars that the gas clouds form.

Siegert and his colleagues studied the observed intensity and spatial distribution of emission from aluminum-26 in our galaxy. A massive star creates this isotope during both life and death. During its life, the star blows the aluminum into space via a strong wind. If the star explodes when it dies, the resulting supernova forges more. The isotope, with a half-life of 700,000 years, decays and gives off gamma rays.

Like X-rays, and unlike visible light, gamma rays penetrate the dust that cloaks the youngest stars. “We’re looking through the entire galaxy,” Siegert says. “We’re not X-raying it; here we’re gamma-raying it.”

The more stars our galaxy spawns, the more gamma rays emerge. The best match with the observations, the researchers find, is a star formation rate of four to eight solar masses a year. That is much higher than the standard estimate for the Milky Way of about two solar masses a year.

The revised rate is very realistic, says Pavel Kroupa, an astronomer at the University of Bonn in Germany who was not involved in the work. “I’m very impressed by the detailed modeling of how they account for the star formation process,” he says. “It’s a very beautiful work. I can see some ways of improving it, but this is really a major step in the absolutely correct direction.”

Siegert cautions that it is difficult to tell how far the gamma rays have traveled before reaching us. In particular, if some of the observed emission arises nearby — within just a few hundred light-years of us — then the galaxy has less aluminum-26 than the researchers have calculated, which means the star formation rate is on the lower side of the new estimate. Still, he says it’s unlikely to be as low as the standard two solar masses per year.
In any event, the Milky Way is the most vigorous star creator in a collection of more than 100 nearby galaxies called the Local Group. The largest Local Group galaxy, Andromeda, converts only a fraction of a solar mass of gas and dust into new stars a year. Among Local Group galaxies, the Milky Way ranks second in size, but its high star formation rate means that we definitely try a lot harder.

Psychedelics go beneath the cell surface to unleash their potentially therapeutic effects.

These drugs are showing promise in clinical trials as treatments for mental health disorders (SN: 12/3/21). Now, scientists might know why. These substances can get inside nerve cells in the cortex — the brain region important for consciousness — and tell the neurons to grow, researchers report in the Feb. 17 Science.

Several mental health conditions, including depression and post-traumatic stress disorder, are tied to chronic stress, which degrades neurons in the cortex over time. Scientists have long thought that repairing the cells could provide therapeutic benefits, like lowered anxiety and improved mood.
Psychedelics — including psilocin, which comes from magic mushrooms, and LSD — do that repairing by promoting the growth of nerve cell branches that receive information, called dendrites (SN: 11/17/20). The behavior might explain the drugs’ positive outcomes in research. But how they trigger cell growth was a mystery.

It was already known that, in cortical neurons, psychedelics activate a certain protein that receives signals and gives instructions to cells. This protein, called the 5-HT2A receptor, is also stimulated by serotonin, a chemical made by the body and implicated in mood. But a study in 2018 determined that serotonin doesn’t make these neurons grow. That finding “was really leaving us scratching our heads,” says chemical neuroscientist David Olson, director of the Institute for Psychedelics and Neurotherapeutics at the University of California, Davis.

To figure out why these two types of chemicals affect neurons differently, Olson and colleagues tweaked some substances to change how well they activated the receptor. But those better equipped to turn it on didn’t make neurons grow. Instead, the team noticed that “greasy” substances, like LSD, that easily pass through cells’ fatty outer layers resulted in neurons branching out.

Polar chemicals such as serotonin, which have unevenly distributed electrical charges and therefore can’t get into cells, didn’t induce growth. Further experiments showed that most cortical neurons’ 5-HT2A receptors are located inside the cell, not at the surface where scientists have mainly studied them.

But once serotonin gained access to the cortical neurons’ interior — via artificially added gateways in the cell surface — it too led to growth. It also induced antidepressant-like effects in mice. A day after receiving a surge in serotonin, animals whose brain cells contained unnatural entry points didn’t give up as quickly as normal mice when forced to swim. In this test, the longer the mice tread water, the more effective an antidepressant is predicted to be, showing that inside access to 5-HT2A receptors is key for possible therapeutic effects.

“It seems to overturn a lot about what we think should be true about how these drugs work,” says neuroscientist Alex Kwan of Cornell University, who was not involved in the study. “Everybody, including myself, thought that [psychedelics] act on receptors that are on the cell surface.”
That’s where most receptors that function like 5-HT2A are found, says biochemist Javier González-Maeso of the Virginia Commonwealth University in Richmond, who was also not involved in the work.

Because serotonin can’t reach 5-HT2A receptors inside typical cortical neurons, Olson proposes that the receptors might respond to a different chemical made by the body. “If it’s there, it must have some kind of role,” he says. DMT, for example, is a naturally occurring psychedelic made by plants and animals, including humans, and can reach a cell’s interior.

Kwan disagrees. “It’s interesting that psychedelics can act on them, but I don’t know if the brain necessarily needs to use them when performing its normal function.” Instead, he suggests that the internal receptors might be a reserve pool, ready to replace those that get degraded on the cell surface.

Either way, understanding the cellular mechanisms behind psychedelics’ potential therapeutic effects could help scientists develop safer and more effective treatments for mental health disorders.

“Ultimately, I hope this leads to better medicines,” Olson says.