It was one of the biggest climate change questions of the early 2000s: Had the planet’s rising fever stalled, even as humans pumped more heat-trapping gases into Earth’s atmosphere?

By the turn of the century, the scientific understanding of climate change was on firm footing. Decades of research showed that carbon dioxide was accumulating in Earth’s atmosphere, thanks to human activities like burning fossil fuels and cutting down carbon-storing forests, and that global temperatures were rising as a result. Yet weather records seemed to show that global warming slowed between around 1998 and 2012. How could that be?
After careful study, scientists found the apparent pause to be a hiccup in the data. Earth had, in fact, continued to warm. This hiccup, though, prompted an outsize response from climate skeptics and scientists. It serves as a case study for how public perception shapes what science gets done, for better or worse.

The mystery of what came to be called the “global warming hiatus” arose as scientists built up, year after year, data on the planet’s average surface temperature. Several organizations maintain their own temperature datasets; each relies on observations gathered at weather stations and from ships and buoys around the globe. The actual amount of warming varies from year to year, but overall the trend is going up, and record-hot years are becoming more common. The 1995 Intergovernmental Panel on Climate Change report, for instance, noted that recent years had been among the warmest recorded since 1860.

And then came the powerful El Niño of 1997–1998, a weather pattern that transferred large amounts of heat from the ocean into the atmosphere. The planet’s temperature soared as a result — but then, according to the weather records, it appeared to slacken dramatically. Between 1998 and 2012, the global average surface temperature rose at less than half the rate it did between 1951 and 2012. That didn’t make sense. Global warming should be accelerating over time as people ramp up the rate at which they add heat-trapping gases to the atmosphere.
By the mid-2000s, climate skeptics had seized on the narrative that “global warming has stopped.” Most professional climate scientists were not studying the phenomenon, since most believed the apparent pause fell within the range of natural temperature variability. But public attention soon caught up to them, and researchers began investigating whether the pause was a real thing. It was a high-profile shift in scientific focus.

“In studying that anomalous period, we learned a lot of lessons about both the climate system and the scientific process,” says Zeke Hausfather, a climate scientist now with the technology company Stripe.

By the early 2010s, scientists were busily working to explain why the global temperature records seemed to be flatlining. Ideas included the contribution of cooling sulfur particles emitted by coal-burning power plants and heat being taken up by the Atlantic and Southern oceans. Such studies were the most focused attempt ever to understand the factors that drive year-to-year temperature variability. They revealed how much natural variability can be expected when factors such as a powerful El Niño are superimposed onto a long-term warming trend.

Scientists spent years investigating the purported warming pause — devoting more time and resources than they otherwise might have. So many papers were published on the apparent pause that scientists began joking that the journal Nature Climate Change should change its name to Nature Hiatus.
Then in 2015, a team led by researchers at the U.S. National Oceanic and Atmospheric Administration published a jaw-dropping conclusion in the journal Science. The rise in global temperatures had not plateaued; rather, incomplete data had obscured ongoing global warming. When more Arctic temperature records were included and biases in ocean temperature data were corrected, the NOAA dataset showed the heat-up continuing. With the newly corrected data, the apparent pause in global warming vanished. A 2017 study led by Hausfather confirmed and extended these findings, as did other reports.

Even after these studies were published, the hiatus remained a favored topic among climate skeptics, who used it to argue that concern over global warming was overblown. Congressman Lamar Smith, a Republican from Texas who chaired the House of Representatives’ science committee in the mid-2010s, was particularly incensed by the 2015 NOAA study. He demanded to see the underlying data while also accusing NOAA of altering it. (The agency denied fudging the data.)

“In retrospect, it is clear that we focused too much on the apparent hiatus,” Hausfather says. Figuring out why global temperature records seemed to plateau between 1998 and 2012 is important — but so is keeping a big-picture view of the broader understanding of climate change. The hiccup represented a short fluctuation in a much longer and much more important trend.
Science relies on testing hypotheses and questioning conclusions, but here’s a case where probing an anomaly was taken arguably too far. It caused researchers to doubt their conclusions and spend large amounts of time questioning their well-established methods, says Stephan Lewandowsky, a cognitive scientist at the University of Bristol who has studied climate scientists’ response to the hiatus. Scientists studying the hiatus could have been working instead on providing clear information to policy makers about the reality of global warming and the urgency of addressing it.

The debates over whether the hiatus was real or not fed public confusion and undermined efforts to convince people to take aggressive action to reduce climate change’s impacts. That’s an important lesson going forward, Lewandowsky says.

“My sense is that the scientific community has moved on,” he says. “By contrast, the political operatives behind organized denial have learned a different lesson, which is that the ‘global warming has stopped’ meme is very effective in generating public complacency, and so they will use it at every opportunity.”

Already, some climate deniers are talking about a new “pause” in global warming because not every one of the past five years has set a new record, he notes. Yet the big-picture trend remains clear: Global temperatures have continued to rise in recent years. The warmest seven years on record have all occurred since 2015, and each decade since the 1980s has been warmer than the one before.

As health officials continue their investigation of unexplained cases of liver inflammation in children, what is known is still outpaced by what isn’t.

At least 500 cases of hepatitis from an unknown cause have been reported in children in roughly 30 countries, according to health agencies in Europe and the United States. As of May 18, 180 cases are under review in 36 U.S. states and territories.

Many of the children have recovered. But some cases have been severe, with more than two dozen of the kids needing liver transplants. At least a dozen children have died, including five in the United States.
The illnesses have mainly been seen in children under age 5. So far, health agencies have ruled out common causes of hepatitis, while reporting that some of the children have tested positive for adenovirus. That pathogen — which infects basically everyone, usually without serious issues — is not known as a primary cause of liver damage. For some children who are positive, officials have identified the particular adenovirus: type 41.

But there are several reasons why pinning an adenovirus as the sole hepatitis culprit doesn’t fully add up, researchers say. Nor is it clear whether the recent cases indicate an uptick in hepatitis illnesses, or just more attention. Though the cases seem to have popped up out of nowhere, “we’ve seen similar rare severe liver disease like this in children,” says Anna Peters, a pediatric transplant hepatologist at the Cincinnati Children’s Hospital Medical Center.

Most of all, it’s important for parents to remember that the cases described so far “are a rare phenomenon,” Peters says. “Parents shouldn’t panic.”

Hepatitis in children
Hepatitis is an inflammation of the liver that can interfere with the organ’s many functions, including filtering blood and regulating clotting. Three hepatitis viruses, called hepatitis A, B and C, are common causes of the illness in the United States. Hepatitis A is spread when infected fecal material reaches the mouth. Children can get B and C when it’s transmitted from a pregnant person to an infant. There are vaccines available for A and B but not C. An excessive dose of acetaminophen can also cause hepatitis in children.

The signs of hepatitis can include nausea, fatigue, a yellow tinge to skin and eyes, urine that’s darker than usual and stools that are light-colored, among other symptoms. Hepatitis that arises quickly usually resolves, whereas some cases progress more slowly and lead to liver damage over time.

It’s rare for a child to develop sudden liver failure. An estimated 500 to 600 cases occur each year in the United States, and around 30 percent of those are “indeterminate,” meaning a cause isn’t found, according to the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition.

The indeterminate category of sudden liver failure has been known for some time, Peters says, and that subset of cases has similarities to the hepatitis under investigation. There hasn’t been data reported yet on whether the recent cases represent an increase over what’s been seen in prior years, Peters says. “Maybe this is just increased recognition of something that’s been going on.”

Adenovirus as a suspect
Not all of the children with hepatitis have been positive for adenovirus, nor have they all been tested. The European Centre for Disease Prevention and Control, or ECDC, has reported that of 151 cases tested, 90 were positive, or 60 percent. The last dispatch from the U.K. Health Security Agency, from early May, noted that 126 samples out of 163 had been tested, with 91, or 72 percent, positive. Further analysis of 18 cases identified adenovirus type 41.

Adenoviruses commonly infect people, typically causing colds, bronchitis or other respiratory illnesses. Two types, adenovirus 40 and 41, target the intestines, leading to gastrointestinal symptoms such as vomiting and diarrhea.

“All of these types, including this prime suspect type 41, have been detected everywhere continuously,” says virologist Adriana Kajon of the Lovelace Biomedical Research Institute in Albuquerque. “All of them have existed and have been reported continuously for decades.”

People usually recover from an adenovirus infection. The exception is those whose immune systems aren’t functioning properly — then, an infection can be serious. There have been cases of hepatitis from adenovirus in immunocompromised children, but the kids under investigation are not immunocompromised.

There are several curious details about the adenovirus findings. For example, the children who have tested positive for the virus had low levels in their blood. In cases of hepatitis from adenovirus, “the virus levels are very, very high,” Peters says.

Nor has adenovirus been found in the liver. In a study of nine children with the hepatitis in Alabama who were positive for adenovirus in blood samples, researchers studied liver tissue from six of the kids. There was no sign of the virus in the liver, the researchers report May 6 in Morbidity and Mortality Weekly Report.

“It’s very hard to implicate a virus that you cannot find in the crime scene,” Kajon said May 3 at a symposium for clinical virology in West Palm Beach, Fla.

Another oddity: There doesn’t seem to be a path of viral spread from one location to another. That’s unlike SARS-CoV-2, the virus that causes COVID-19, “where there was quite clearly a spread from some epicenter originally,” says virologist and clinician Andrew Tai of the University of Michigan Medical School in Ann Arbor, who treats patients with liver disease.

An adenovirus culprit is not out of the realm of possibility, but “virus associations with diseases are always hard to really nail down and prove,” says virologist Katherine Spindler, also of the University of Michigan Medical School. “We’re going to be hard pressed to say this is due to adenovirus 41, let alone adenovirus.”

Considering COVID-19
Looming over all of this is the possibility that a many-magnitudes-larger infectious disease outbreak, COVID-19, could have a part.

Researchers have found that SARS-CoV-2 impacts the liver in milder and more severe cases of COVID-19. There is evidence that the liver becomes inflamed in children and adults during an infection. Liver failure can occur with a severe bout of COVID-19. And children who develop multisystem inflammatory syndrome in children, or MIS-C, after COVID-19 can have hepatitis as part of that syndrome.

Peters and her colleagues have described yet another way SARS-CoV-2 could put the liver at risk. The team reported the case of a young female patient from the fall of 2020, who had sudden liver failure about three weeks after a SARS-CoV-2 infection. She did not have MIS-C. A liver biopsy showed signs of autoimmune hepatitis, a type in which the body attacks its own liver, Peters and colleagues report in the May Journal of Pediatric Gastroenterology and Nutrition Reports. The patient recovered after treatment with anti-inflammatory medication.

Some of the children with hepatitis have tested positive for SARS-CoV-2, but more haven’t. The ECDC has reported that 20 of 173 cases tested were positive for SARS-CoV-2, while the U.K. Health Security Agency detected the virus in 24 of 132 samples tested.

However, there have been very little data reported on whether the children have antibodies to SARS-CoV-2, which would be evidence of a past infection. (Vaccination hasn’t been available to most of these young children.) The ECDC found that of 19 cases tested, 14 were positive for antibodies to the virus.

One theory is that an earlier SARS-CoV-2 infection has set the stage for an unexpected response to an adenovirus or other infection. With people no longer minimizing contact, the spread of adenoviruses and other respiratory viruses is returning to prepandemic levels.

“We are possibly seeing the return of these forgotten pathogens, so to speak, aggravating disease or eliciting severe inflammation resulting from some kind of preexisting condition,” which could be COVID-19, Kajon said on May 3.

“I cannot think of anything else that has had a worldwide impact that can explain cases of hepatitis in places as distant as the U.K. and Argentina,” Kajon says.

With SARS-CoV-2, researchers have a good sense of how it causes disease during an active infection, Peters says. But for the longer-term effects, “everybody is still sorting things out.”

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.”

One common chemical in sunscreen can have devastating effects on coral reefs. Now, scientists know why.

Sea anemones, which are closely related to corals, and mushroom coral can turn oxybenzone — a chemical that protects people against ultraviolet light — into a deadly toxin that’s activated by light. The good news is that algae living alongside the creatures can soak up the toxin and blunt its damage, researchers report in the May 6 Science.

But that also means that bleached coral reefs lacking algae may be more vulnerable to death. Heat-stressed corals and anemones can eject helpful algae that provide oxygen and remove waste products, which turns reefs white. Such bleaching is becoming more common as a result of climate change (SN: 4/7/20).
The findings hint that sunscreen pollution and climate change combined could be a greater threat to coral reefs and other marine habitats than either would be separately, says Craig Downs. He is a forensic ecotoxicologist with the nonprofit Haereticus Environmental Laboratory in Amherst, Va., and was not involved with the study.

Previous work suggested that oxybenzone can kill young corals or prevent adult corals from recovering after tissue damage. As a result, some places, including Hawaii and Thailand, have banned oxybenzone-containing sunscreens.

In the new study, environmental chemist Djordje Vuckovic of Stanford University and colleagues found that glass anemones (Exaiptasia pallida) exposed to oxybenzone and UV light add sugars to the chemical. While such sugary add-ons would typically help organisms detoxify chemicals and clear them from the body, the oxybenzone-sugar compound instead becomes a toxin that’s activated by light.

Anemones exposed to either simulated sunlight or oxybenzone alone survived the length of the experiment, or 21 days, the team showed. But all anemones exposed to fake sunlight while submersed in water containing the chemical died within 17 days.
The anemones’ algal friends absorbed much of the oxybenzone and the toxin that the animals were exposed to in the lab. Anemones lacking algae died days sooner than anemones with algae.

In similar experiments, algae living inside mushroom coral (Discosoma sp.) also soaked up the toxin, a sign that algal relationships are a safeguard against its harmful effects. The coral’s algae seem to be particularly protective: Over eight days, no mushroom corals died after being exposed to oxybenzone and simulated sunlight.

It’s still unclear what amount of oxybenzone might be toxic to coral reefs in the wild. Another lingering question, Downs says, is whether other sunscreen components that are similar in structure to oxybenzone might have the same effects. Pinning that down could help researchers make better, reef-safe sunscreens.

For many recreational runners, taking a jog is a fun way to stay fit and burn calories. But it turns out an individual has a tendency to settle into the same, comfortable pace on short and long runs — and that pace is the one that minimizes their body’s energy use over a given distance.

“I was really surprised,” says Jessica Selinger, a biomechanist at Queen’s University in Kingston, Canada. “Intuitively, I would have thought people run faster at shorter distances and slow their pace at longer distances.”

Selinger and colleagues combined data from more than 4,600 runners, who went on 37,201 runs while wearing a fitness device called the Lumo Run, with lab-based physiology data. The analysis, described April 28 in Current Biology, also shows that it takes more energy for someone to run a given distance if they run faster or slower than their optimum speed.
“There is a speed that for you is going to feel the best,” Selinger says. “That speed is the one where you’re actually burning fewer calories.”

The runners ranged in age from 16 to 83, and had body mass indices spanning from 14.3 to 45.4. But no matter participants’ age, weight or sex — or whether they ran only a narrow range of distances or runs of varying lengths — the same pattern showed up in the data repeatedly.

Researchers have thought that running was performance-driven, says Melissa Thompson, a biomechanist at Fort Lewis College in Durango, Colo., who was not involved in the new study. This new research, she says, is “talking about preference, not performance.”

Most related research, Selinger says, has been done in university laboratories, with study subjects who are generally younger and healthier than the general population. By using wearable devices, the researchers could track many more runs, across more real-life conditions than is possible in a lab. That allowed the scientists to look at a “much broader cross section of humanity,” she says. Treadmill tests measuring energy use at different paces with people representative of those included in the fitness tracker data were used to determine optimum energy-efficient speeds.

Because the study includes a wide range of conditions and doesn’t control for things like fasting before running, it’s messier than data gathered in labs. Still, the sheer volume of real-world runs recorded by the wearable devices supports a convincing general rule about how humans run, says Rodger Kram, a physiologist at the University of Colorado Boulder not involved with the study. “I think the rule’s right.”

The results don’t apply to very long runs when fatigue starts to set in, or to race performance by elite athletes or others consciously training for speed. And a runner’s optimum pace can change over time, with training or age for instance.

There are quick tricks for those who want to speed up and go for a little more calorie burn to temporarily trump their body’s natural inclinations: Listen to upbeat music or jog alongside someone with a faster pace, Selinger says. “But it seems like your preference is actually to sink back into that optimum.”

The results match observations of optimum pacing from animals like horses and wildebeests, and also correspond to the way humans tend to walk at a speed that minimizes their individual energy use (SN: 9/10/15).

It does make sense that humans would be adapted to run at an optimum speed for minimizing energy use, says coauthor Scott Delp, a biomechanist at Stanford University. Imagine being an early human ancestor going out to hunt difficult prey. “It might be days before I get my next food,” he says. “So I want to spend the least energy en route to getting that food.”

An act of acrobatics keeps males of one orb-weaving spider species from becoming their mates’ post-sex snack.

After mating, Philoponella prominens males catapult away from females at speeds up to nearly 90 centimeters per second, researchers report April 25 in Current Biology. Other spiders jump to capture prey or avoid predators (SN: 3/16/19). But P. prominens is unique among spiders in that males soar through the air to avoid sexual cannibalism, the researchers say.

P. prominens is a social species that’s native to countries such as Japan and Korea. Up to 300 individual spiders can come together to weave an entire neighborhood of webs. While studying P. prominens’ sexual behavior, arachnologist Shichang Zhang and colleagues noticed that sex seemed to always end with a catapulting male. But the movement was “so fast that common cameras could not record the details,” says Zhang, of Hubei University in Wuhan, China.

High-resolution video of mating partners clocked the male arachnids’ speed from around 32 cm/s to 88 cm/s, the researchers report. That’s equal to just under 1 mile per hour to nearly 2 mph.
The jump looks a little like the start of a backstroke swimming race, Zhang says. Males hold the tips of their front legs against a female’s body. The spiders then use hydraulic pressure to extend a joint in those legs, quickly launching a male off a female before she can capture and eat him.

Of 155 successful mating rituals that the researchers observed, 152 males catapulted to survival. The remaining three that didn’t fell victim to their partner. Female spiders also ate all 30 males that the team stopped from jumping to freedom with a paintbrush.

These male orb weavers probably acquired their jumping abilities to counter females’ cannibalistic tendencies, Zhang says. The spiders’ leap to survival is a “fantastic kinetic performance.”

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.”