It’s possible that I shall make an ass of myself. But in that case one can always get out of it with a little dialectic. I have, of course, so worded my proposition as to be right either way (K.Marx, Letter to F.Engels on the Indian Mutiny)
Wednesday, December 10, 2025
A new ‘hypertropical’ climate is emerging in the Amazon
Unprecedented hot drought conditions are becoming more common, exposing trees to deadly stress
The Amazon rainforest is being hit with more days of extreme drought that is leading to tree die-offs that will change the nature of these tropical sinks of carbon dioxide produced by the burning of fossil fuels.
The Amazon rainforest is slowly transitioning to a new, hotter climate with more frequent and intense droughts — conditions that haven’t been seen on Earth for tens of millions of years.
The conclusions come from a new study led by the University of California, Berkeley, involving a large team of national and international scientists.
The researchers predict that, if society continues to emit high levels of greenhouse gases, “hot drought” conditions could become more prevalent across the Amazon by 2100, occurring even during the wet season. This could lead to widespread tree dieoffs and impair Earth’s ability to deal with increasing levels of atmospheric carbon dioxide, since tropical forests worldwide absorb more human carbon emissions than any other biome. Recent reports found an increase in atmospheric carbon dioxide after severe droughts in the Amazon, showing that weather in the tropics has a measurable impact on the planet’s carbon budget.
The new study, to be published Dec. 10 in the journal Nature, explains why these severe tropical droughts are reducing the global uptake of carbon dioxide from the atmosphere.
The scientists refer to the new climate regime, or biome, as the hypertropics. It is emerging because of global warming, which is extending the typical July-to-September dry season as it also brings hotter-than-normal temperatures. In their study, the researchers document that hot drought conditions stress the trees and increase the normal tree mortality rate by 55%.
“When these hot droughts occur, that’s the climate that we associate with a hypertropical forest, because it's beyond the boundary of what we consider to be tropical forest now,” said study leader Jeff Chambers, a UC Berkeley professor of geography. By 2100, hot drought conditions could occur as many as 150 days each year.
Chambers and his team also discovered why the trees are dying under hypertropical conditions, which now only occur a few days to weeks during extreme droughts. Once the soil moisture content by volume decreases to about one-third, the trees either shut down carbon capture, starving to death, or develop air bubbles in their sap, akin to embolisms that cause strokes in humans.
This affects faster-growing species of trees more than slow-growing trees, the researchers found. That means that as the number of high heat-stress days increases, Amazon forests will experience a shift in tree species to those less susceptible — if that shift can take place fast enough in a rapidly changing environment.
“We showed that the fast-growing, low wood-density trees were more vulnerable, dying in greater numbers than high wood-density trees,” he said. “That implies that secondary forests might be more vulnerable to drought-induced mortality, because secondary forests have a larger fraction of these types of trees.”
Since the annual tree mortality is slightly more than 1%, an extra 0.55% may not seem like much, but it has a cumulative impact on the forest, Chambers said. Hypertropical conditions also are likely to appear outside the Amazon in rainforests in western Africa and across Southeast Asia.
Chambers emphasized that the direst outcome is predicted if society does very little to reduce carbon dioxide emissions that drive climate change.
“It all depends on what we do,” he said. “It's up to us to what extent we're actually going to create this hypertropical climate. If we're just going to emit greenhouse gasses as much as we want, without any control, then we're going to create this hypertropical climate sooner.”
Monitoring tree sap
Chambers has been conducting research in the Amazon since his graduate school days in 1993, much of that time with the Instituto Nacional de Pesquisas da Amazônia (INPA) in Manaus. His earliest research first established that the average age of rainforest trees 10 centimeters (4 inches) in diameter is about 180 years, making the region one of Earth’s longest-term storage areas for carbon. Some trees are more than 1,000 years old.
Since then, he has conducted studies to understand carbon cycling in tropical forests and forest-climate interactions. He and his international group of collaborators installed instruments on two approximately 50-meter-tall towers at two study sites north of Manaus to record temperature and humidity at different levels above the ground, as well as sunlight intensity at the top of the tree canopy and soil moisture in the forest floor. The oldest of the towers was visited in November by California Governor Gavin Newsom during his attendance at the COP30 climate summit in Belém, Brazil.
Chambers also collaborated with a team to install sensors in the trees themselves to record the flux of water from the soil up the stem and out to the atmosphere. These sensors measure sap flow, leaf temperature, water transpiration from leaves and the water potential of the soil — that is, how difficult it is for the tree to draw water from the soil to its topmost leaves through transpiration.
Using more than 30 years of data from the oldest of the two plots, which had previously been selectively logged, he and his team demonstrated a significant increase in tree die-offs the year after intense droughts. The highest tree mortality rates were among fast-growing species that are the first to sprout in logged areas and which have a low wood density.
Chambers and his colleagues also combined data from the two sites during droughts in 2015 and 2023 caused by El Niño. At both sites, they found that when the soil moisture content dropped below a threshold of about 0.32 — meaning about a third of the soil’s pores were filled with water — transpiration rates in the trees dropped rapidly, leading to increased hydraulic stress.
“The really remarkable thing is that the threshold soil moisture content in a different plot with different trees for droughts in different years — 2015 and 2023 — were essentially the same: 0.32 and 0.33,” he said. “That was really surprising to everyone.”
Eventually, when high heat continued under extended drought conditions, trees began to experience hydraulic collapse — the formation of embolisms or bubbles in the fluid-filled xylem.
“Normally, plants are pretty good at trying to compartmentalize and just say, OK, I'm willing to sacrifice that branch to keep this core piece alive,” he said. “But if there are enough embolisms, the tree just dies.”
The trees also began to starve; as the leaves closed their pores to prevent water loss, they also shut off their supply of carbon dioxide, which they need to build and repair tissue.
Finally, after exploring the changing climate conditions using published data from five different Earth system models, the researchers realized that the tropical forest was shifting to a hotter state that has no analog today, though it was found in the tropics when the Earth was much hotter between 10 and 40 million years ago. They define the hypertropics as regions that are warmer than the 99th percentile of historical tropical climates, with more frequent and intense droughts.
With more warming predicted for the future, this climate state will become more common and, depending on how quickly climate changes, may lead to broader forest die-back processes as the climate continues to warm. The hot drought conditions that drive elevated tree mortality are projected to frequently emerge during a typical dry season 20 to 40 years from now, Chambers said. But by 2100, they predicted, extreme hot drought days will no longer be confined to the peak of the dry season but will increasingly occur throughout the entire year, including during the wettest months.
“Present-day hot droughts are harbingers of this emerging climate, providing windows of opportunity to better understand tropical forest responses to increasingly extreme future conditions,” the authors wrote.
UC Berkeley co-authors of the paper include Bruno Oliva Gimenez, a former UC Berkeley postdoctoral fellow now at INPA; Anna Weber and integrative biology professor Paul Fine. Other co-authors include Adriano José Nogueira, Lima Cristina Santos da Silva, Regison Costa de Oliveira, Gustavo C. Spanner, Tatiana D. Gaui, Daisy Celestina Souza, Joaquim dos Santos and Niro Higuchi of INPA and collaborators from the U.S., United Kingdom, Brazil, Germany and Norway. The research was funded by numerous U.S. and international agencies over the past 30 years.
UC Berkeley graduate student Daisy Souza working in a lift basket among the leaves high in the rainforest canopy to study photosynthesis.
The newly described pumpkin toadlet Brachycephalus lulai, discovered in the mountain forests of Serra do Quiriri, southern Brazil, and named in honor of Brazil’s President Luiz Inácio Lula da Silva. Photo: Luiz Fernando Ribeiro.
Article title: A new species of Brachycephalus (Anura: Brachycephalidae) from Serra do Quiriri, northeastern Santa Catarina state, southern Brazil, with a review of the diagnosis among species of the B. pernix group and proposed conservation measures
Author countries: Brazil, U.S., Germany
Funding: The field work was funded by Fundação Grupo Boticário de Proteção à Natureza (through grant 1149_20191) through project conducted by Mater Natura – Instituto de Estudos Ambientais. MRP received a grant from CNPq/MCT (301636/2016-8). GS-S received grant from São Paulo Research Foundation (FAPESP; processes #2022/04847-7 and # 2023/09718-3). There was no additional external funding received for this study. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
A new species of Brachycephalus (Anura: Brachycephalidae) from Serra do Quiriri, northeastern Santa Catarina state, southern Brazil, with a review of the diagnosis among species of the B. pernix group and proposed conservation measures
Article Publication Date
10-Dec-2025
COI Statement
The authors have declared that no competing interests exist.
Brachycephalus lulai is a tiny pumpkin toadlet measuring less than 14 mm in length. Photo: Luiz Fernando Ribeiro.
Credit
Image credit 1: Luiz Fernando Ribeiro, CC-BY 4.0 (https://creativecommons.org/licenses/by/4.0/)
A new species of Brachycephalus (Anura: Brachycephalidae) from Serra do Quiriri, northeastern Santa Catarina state, southern Brazil, with a review of the diagnosis among species of the B. pernix group and proposed conservation measures
Divergent color variation ofBrachycephalusspecies.
Credit
Bornschein et al., 2025, PLOS One, CC-BY 4.0 (https://creativecommons.org/licenses/by/4.0/)
For millions suffering from long COVID, their persistent breathlessness, brain fog and fatigue remain a maddening mystery, but a group of leading microbiologists think they may have cracked the case.
The culprit for some long COVID cases, they suggest, might be other infections that accompany SARS-CoV-2.
A review published in eLife by 17 experts, including those from Rutgers Health, argues that co-infections acquired before or during COVID could cause symptoms to persist indefinitely for many people.
"This is an aspect of long COVID that is not talked about a lot," said Maria Laura Gennaro, a microbiologist at the Rutgers New Jersey Medical School who chaired the Microbiology Task Force for the National Institutes of Health's Researching COVID to Enhance Recovery initiative, a large-scale study of long COVID.
Long COVID symptoms, which have affected up to 400 million people worldwide, range from mild impairment to severe disability, striking the brain, heart, lungs and digestive system. Yet no proven treatments exist because the underlying causes remain unknown.
The new review synthesizes existing research and expert judgment to make a case that has received little attention: Infections beyond the coronavirus may be critical players.
The most compelling evidence involves Epstein-Barr virus (EBV), the pathogen that causes mononucleosis. About 95% of adults carry latent EBV, typically without symptoms until an immune disruption such as COVID awakens the dormant virus.
Researchers of one early study found that two-thirds of people with long COVID showed signs of recent EBV activity, and those with more symptoms had higher antibody levels. Later research linked EBV reactivation to long COVID hallmarks such as fatigue and cognitive problems.
Tuberculosis (TB) is another potential culprit. About one-quarter of the world's population carries latent TB. Evidence suggests COVID can deplete the immune cells that normally keep TB in check, potentially triggering reactivation. The relationship runs both ways: TB infection also may worsen COVID outcomes.
The timing of co-infections matters, the researchers said. Infections before COVID could leave the immune system compromised. Infections during acute illness could compound tissue damage. Infections afterward could exploit post-COVID immune dysfunction.
The authors noted that 44 nations have experienced tenfold increases in at least 13 infectious diseases compared with pre-pandemic levels. One explanation they cite, called "immunity theft," describes heightened vulnerability to other infections following acute COVID.
If co-infections contribute to long COVID, existing drugs might help. Antibiotics and antivirals could potentially be repurposed to target underlying infections. Clinical trials could test whether treating specific co-infections relieves symptoms.
But the authors acknowledge their argument's limits. The associations they discuss are biologically plausible but remain speculative. No one has established a causal link between any co-infection and long COVID.
"Everyone has heard it a million times, but it bears repeating: Correlation doesn't equal causation," Gennaro said.
She said proving the hypothesis would require large epidemiological studies and animal experiments, which is complicated by the absence of good animal models for long COVID.
The researchers hope their work will open new lines of investigation. For the millions living with long COVID, the review offers no immediate answers, but its authors suggest that effective treatment may require looking beyond COVID itself.
Stanford Medicine investigators have unearthed the biological process by which mRNA-based vaccines for COVID-19 can cause heart damage in some young men and adolescents — and they’ve shown a possible route to reducing its likelihood.
Using advanced but now common lab technologies, along with published data from vaccinated individuals, the researchers identified a two-step sequence in which these vaccines activate a certain type of immune cell, in turn riling up another type of immune cell. The resulting inflammatory activity directly injures heart muscle cells, while triggering further inflammatory damage.
The mRNA vaccines for COVID-19, which have now been administered several billion times, have been heavily scrutinized for safety and have been shown to be extremely safe, said Joseph Wu, MD, PhD, the director of the Stanford Cardiovascular Institute.
“The mRNA vaccines have done a tremendous job mitigating the COVID pandemic,” said Wu, the Simon H. Stertzer, MD, Professor and a professor of medicine and of radiology. “Without these vaccines, more people would have gotten sick, more people would have had severe effects and more people would have died.”
mRNA vaccines are viewed as a breakthrough because they can be produced quickly enough to keep up with sudden microbial strain changes and they can be rapidly adapted to fight widely divergent types of pathogens. But, as with all vaccines, not everyone who gets the shot experiences a purely benign reaction.
One rare but real risk of the mRNA-based COVID-19 vaccines is myocarditis, or inflammation of heart tissue. Symptoms — chest pain, shortness of breath, fever and palpitations — appear in the absence of any viral infection. And they happen quickly: within one to three days after a shot. Most of those affected have high blood levels of a substance called cardiac troponin, a well-established clinical indicator of heart-muscle injury. (Cardiac troponin is normally found exclusively in the heart muscle. When found circulating in blood, it indicates damage to heart muscle cells.)
Vaccine-associated myocarditis occurs in about one in every 140,000 vaccinees after a first dose and rises to one in 32,000 after a second dose. For reasons that aren’t clear, incidence peaks among male vaccinees age 30 or below, at one in 16,750 vaccinees.
Fortunately, most of these cases end well, Wu said, with full heart function retained or restored. Recovery is typically swift.
“It’s not a heart attack in the traditional sense,” he said. “There’s no blockage of blood vessels as found in most common heart attacks. When symptoms are mild and the inflammation hasn’t caused structural damage to the heart, we just observe these patients to make sure they recover.”
However, Wu noted, if the inflammation is severe the resulting heart injury can be quite debilitating, leading to hospitalizations; ICU admissions for critically ill patients; and deaths, albeit rarely.
“But COVID’s worse,” he added. A case of COVID-19 is about 10 times as likely to induce myocarditis as an mRNA-based COVID-19 vaccination, Wu said. That’s in addition to all the other trouble it causes.
Wu shares senior authorship of a study describing his team’s findings, to be published Dec. 10 in Science Translational Medicine, with former Stanford Medicine postdoctoral scholar Masataka Nishiga, MD, PhD, now an assistant professor at The Ohio State University. The study’s lead author is current postdoctoral scholar Xu Cao, PhD.
“Medical scientists are quite aware that COVID itself can cause myocarditis,” Wu said. “To a lesser extent, so can the mRNA vaccines. The question is, why?”
Suspects identified
To find out, he and his colleagues first analyzed data from blood draws of individuals vaccinated for COVID-19, some of whom developed myocarditis. Comparing those who did with those who didn’t, they noticed high levels of a couple of proteins in the blood of vaccinees who wound up with myocarditis.
“Two proteins, named CXCL10 and IFN-gamma, popped up. We think these two are the major drivers of myocarditis,” Wu said. They operate like a tag team.
CXCL10 and IFN-gamma both belong to a class of proteins called cytokines: signaling substances that immune cells secrete to carry on chemical conversations with one another.
Hoping to listen in on these communications, the scientists generated human immune cells called macrophages — fierce first-responder cells of the immune system — in a dish and incubated them with mRNA vaccines.
The macrophages responded by pumping out various cytokines but, most notably, pronounced amounts of CXCL10. They also otherwise generally mimicked the vaccine responses of macrophages reported in humans, as shown by comparison with published data from vaccinated individuals.
When the scientists further supplied the dish with an additional kind of immune cell — T cells, roving sentinels that can recognize and mount immune attacks on specific pathogens but can also incite general arousal of the immune system — or even when they merely steeped T cells in the solution in which vaccine-administered macrophages had bathed, they saw a marked uptick in the T cells’ output of IFN-gamma. But T cells incubated with mRNA vaccine in the absence of macrophages or their bathwater produced only standard amounts of IFN-gamma. These results showed that macrophages are the chief source of CXCL10 and that T cells are the chief source of IFN-gamma in response to mRNA vaccination.
Tag-teaming
But did the two cytokines, together, contribute directly to cardiac injury? The researchers vaccinated young male mice, then found heightened levels of cardiac troponin, the widely used clinical marker of heart muscle damage.
The investigators also noticed infiltration of macrophages and another frontline take-no-prisoners immune-cell type, neutrophils — short-lived first responders that live to die in glorious battle (typically with bacterial or fungal pathogens) and are the main component of pus — into the mice’s cardiac tissue. This also occurs in post-vaccination myocarditis patients.
This macrophage and neutrophil infiltration into the heart — which comes at a cost, as these shoot-first-and-ask-questions-later warrior immune cells often unload friendly fire, causing collateral damage to healthy tissue, including heart muscle — could be minimized by blocking CXCL10 and IFN-gamma activity.
Also seen in the mice’s hearts were increased populations of cell-surface molecules that snag macrophages, neutrophils and other white-blood-cell types, causing them to adhere to endothelial cells, which line all blood vessels including those in the heart.
So, yes, CXCL10 and IFN-gamma did contribute directly to cardiac injury in these mice. And blocking them largely preserved the immune response to the vaccination while lowering levels of cardiac troponin induced by vaccination.
Wu’s lab excels at a technology involving the transformation of human skin cells or blood cells into blank cells that can then be guided to differentiate into cardiomyocytes, macrophages and endothelial cells and to coalesce into spherical structures that mimic the heart’s rhythmic contractions.
The researchers treated these “cardiac spheroids” with CXCL10- and IFN-gamma-enriched bathwater from vaccine-stimulated macrophages and T cells, respectively. They witnessed a significant increase in markers of cardiac stress, rescued by inhibitors of the two cytokines.
The cardiac spheroids’ squeezing capacity, beating rate and other measures of healthy heart function were all impaired but, again, partially restored by the cytokine inhibitors.
Saved by a soybean
Wu had a hunch that a common dietary supplement could help prevent such damage. Given higher myocarditis rates among males and estrogen’s known anti-inflammatory properties, he revisited a compound he’d studied a few years earlier.
In a 2022 paper published in Cell, Wu’s team had identified genistein, a mild estrogen-like substance derived from soybeans, as having anti-inflammatory activity and the ability to counter marijuana-induced damage to blood vessels and heart tissue.
“Genistein is only weakly absorbed when taken orally,” Wu said. “Nobody ever overdosed on tofu.”
Wu and his colleagues conducted a series of experiments closely paralleling those described above, pre-treating cells, cardiac spheres and mice (the latter by oral administration of large quantities) with genistein. Doing this prevented much of the deleterious effects of mRNA vaccines or the CXCL10/IFN-gamma combo to heart cells and tissue.
The genistein Wu and his associates used was purer and more concentrated than the dietary supplement found in health food stores.
“It’s reasonable to believe that the mRNA-vaccine-induced inflammatory response may extend to other organs,” Wu said. “We and others have seen some evidence of this in lung, liver and kidney. It’s possible that genistein may also reverse these changes.”
Elevated inflammatory cytokine signaling could be a class effect of mRNA vaccines. Notably, IFN-gamma signaling is a fundamental defense mechanism against foreign DNA and RNA molecules, including viral nucleic acids, Wu said.
“Your body needs these cytokines to ward off viruses. It’s essential to immune response but can become toxic in large amounts,” he said. IFN-gamma secreted in large amounts, however lofty its purpose, can trigger myocarditis-like symptoms and degradation of structural heart muscle proteins.
That risk probably extends beyond mRNA-based COVID-19 vaccines.
“Other vaccines can cause myocarditis and inflammatory problems, but the symptoms tend to be more diffuse,” Wu said. “Plus, mRNA-based COVID-19 vaccines’ risks have received intense public scrutiny and media coverage. If you get chest pains from a COVID vaccine you go to the hospital to get checked out, and if the serum troponin is positive, then you get diagnosed with myocarditis. If you get achy muscles or joints from a flu vaccine, you just blow it off.”
The study was funded by the National Institutes of Health (grants R01 HL113006, R01 HL141371, R01 HL141851, R01 HL163680 and R01 HL176822) and the Gootter-Jensen Foundation.
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About Stanford Medicine
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