Fike is co-author of a new study published July 20 in Nature Communications.

“Our previous work identified the role that changing sedimentation rates had on local versus global controls on geochemical signatures that we use to reconstruct environmental change,” said Fike, professor of earth and planetary sciences and director of environmental studies in Arts & Sciences.

“In this study, we investigated organic carbon loading, or how much organic matter — which drives subsequent microbial activity in the sediments — is delivered to the seafloor,” Fike said. “We are able to show that this, too, plays a critical role in regulating the types of signals that get preserved in sediments.

“We need to be aware of this when trying to extract records of past ‘global’ environmental change,” he said.

Scientists have long used information from sediments at the bottom of the ocean — layers of rock and microbial muck — to reconstruct the conditions in oceans of the past.

A critical challenge in understanding Earth’s surface evolution is differentiating between signals preserved in the sedimentary record that reflect global processes, such as the evolution of ocean chemistry, and those that are local, representing the depositional environment and the burial history of the sediments.

The new study is based on analyses of a mineral called pyrite (FeS₂) that is formed in marine sediments influenced by bacterial activity. The scientists examined concentrations of carbon, nitrogen and sulfur and stable isotopes of glacial-interglacial sediments on the seafloor along the continental margin off of modern-day Peru.

Varying rates of microbial metabolic activity, regulated by regional oceanographic variations in oxygen availability and the flux of sinking organic matter, appear to have driven the observed pyrite sulfur variability on the Peruvian margin, the scientists discovered.

The study was led by Virgil Pasquier, a postdoctoral fellow at the Weizmann Institute of Sciences in Israel, and co-authored by Itay Halevy, also of the Weizmann Institute. Pasquier previously worked with Fike at Washington University. Together, the collaborators have raised concerns about the common use of pyrite sulfur isotopes to reconstruct Earth’s evolving oxidation state.

“We seek to understand how Earth’s surface environment has changed over time,” said Fike, who also serves as director of Washington University’s International Center for Energy, Environment and Sustainability. “In order to do this, it’s critical to understand the kinds of processes that can influence the records we use for these reconstructions.”

“In this study, we have identified an important factor — local organic carbon delivery to the seafloor — that modifies the geochemical signatures preserved in sedimentary pyrite records,” he said. “It overprints potential records of global biogeochemical cycling with information about changes in the local environment.

“This observation provides a new window to reconstruct past local environmental conditions, which is quite exciting,” Fike said.

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Materials provided by Washington University in St. Louis. Original written by Talia Ogliore. Note: Content may be edited for style and length.

Spider silk is said to be one of the strongest, toughest materials on the Earth. Now engineers at Washington University in St. Louis have designed amyloid silk hybrid proteins and produced them in engineered bacteria. The resulting fibers are stronger and tougher than some natural spider silks.

Their research was published in the journal ACS Nano.

To be precise, the artificial silk — dubbed “polymeric amyloid” fiber — was not technically produced by researchers, but by bacteria that were genetically engineered in the lab of Fuzhong Zhang, a professor in the Department of Energy, Environmental & Chemical Engineering in the McKelvey School of Engineering.

Zhang has worked with spider silk before. In 2018, his lab engineered bacteria that produced a recombinant spider silk with performance on par with its natural counterparts in all of the important mechanical properties.

“After our previous work, I wondered if we could create something better than spider silk using our synthetic biology platform,” Zhang said.

The research team, which includes first author Jingyao Li, a PhD student in Zhang’s lab, modified the amino acid sequence of spider silk proteins to introduce new properties, while keeping some of the attractive features of spider silk.

A problem associated with recombinant spider silk fiber — without significant modification from natural spider silk sequence — is the need to create β-nanocrystals, a main component of natural spider silk, which contributes to its strength. “Spiders have figured out how to spin fibers with a desirable amount of nanocrystals,” Zhang said. “But when humans use artificial spinning processes, the amount of nanocrystals in a synthetic silk fiber is often lower than its natural counterpart.”

To solve this problem, the team redesigned the silk sequence by introducing amyloid sequences that have high tendency to form β-nanocrystals. They created different polymeric amyloid proteins using three well-studied amyloid sequences as representatives. The resulting proteins had less repetitive amino acid sequences than spider silk, making them easier to be produced by engineered bacteria. Ultimately, the bacteria produced a hybrid polymeric amyloid protein with 128 repeating units. Recombinant expression of spider silk protein with similar repeating units has proven to be difficult.

The longer the protein, the stronger and tougher the resulting fiber. The 128-repeat proteins resulted in a fiber with gigapascal strength (a measure of how much force is needed to break a fiber of fixed diameter), which is stronger than common steel. The fibers’ toughness (a measure of how much energy is needed to break a fiber) is higher than Kevlar and all previous recombinant silk fibers. Its strength and toughness are even higher than some reported natural spider silk fibers.

In collaboration with Young- Shin Jun, professor in the Department of Energy, Environmental & Chemical Engineering, and her PhD student Yaguang Zhu, the team confirmed that the high mechanical properties of the polymeric amyloid fibers indeed come from the enhanced amount of β-nanocrystals.

These new proteins and the resulting fibers are not the end of the story for high-performance synthetic fibers in the Zhang lab. They are just getting started. “This demonstrates that we can engineer biology to produce materials that beat the best material in nature,” Zhang said.

This work explored just three of thousands of different amyloid sequences that could potentially enhance the properties of natural spider silk. “There seem to be unlimited possibilities in engineering high-performance materials using our platform,” Li said. “It’s likely that you can use other sequences, put them into our design and also get a performance-enhanced fiber.”

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Materials provided by Washington University in St. Louis. Original written by Brandie Jefferson. Note: Content may be edited for style and length.

Triggered by the 2015-16 El Niño, extreme drought and associated mega-wildfires caused the death of around 2.5 billion trees and plants and emitted 495 million tonnes of CO₂ from an area that makes up just 1.2 per cent of the entire Brazilian Amazon rainforest, and 1 per cent of the whole biome.

The stark findings, discovered by an international team of scientists working for more than eight years on a long-term study in the Amazon before, during and after the El Niño, have significant implications for global efforts to control the atmospheric carbon balance.

In normal circumstances, because of high moisture levels, the Amazon rainforest does not burn. However, extreme drought makes the forest temporarily flammable. Fires started by farmers can escape their land and trigger forest fires.

According to climate predictions, extreme droughts will become more common and, until now, the long-term effects of drought and fires on the Amazon rainforest, and particularly within forests disturbed by people through activities such as selective or illegal logging, were largely unknown.

Examining the Amazonian epicentre of the El Niño — Brazil’s Lower Tapajós, an eastern Amazonia area around twice the size of Belgium — the research team, led by scientists from Lancaster University, the University of Oxford, and The Brazilian Agricultural Research Corporation found the damage lasts for multiple years.

The study revealed that trees and plants in drought-affected forests, as well as burned forests, continued to die at a rate above the norm for up to three years after the El Niño drought — releasing more CO₂.into the atmosphere.

The total carbon emissions from the drought and fires in the Lower Tapajós region alone were higher than a whole year’s deforestation within the entire Amazon. And, as a result of the drought and fires, the region released as much over a three-year period as some of the world’s worst polluting countries’ yearly carbon emissions — exceeding the emissions of developed countries such as the UK and Australia.

After three years, only around a third (37%) of the emissions were re-absorbed by plant growth in the forest. This shows that the Amazon’s vital function as a carbon sink can be hampered for years following these drought events.

Dr Erika Berenguer, lead author of the report from Lancaster University and the University of Oxford, said: “Our results highlight the enormously damaging and long-lasting effects fires can cause in Amazonian forests, an ecosystem that did not co-evolve with fires as a regular pressure.”

The scientists gathered data by regularly revisiting 21 plots across a mixture of primary forest, secondary re-growing forest and forests where people have selectively logged. The results from these plots were then extrapolated to the region.

Although previous research has shown human-disturbed forests are more susceptible to fires, it was unknown if there was any difference in the vulnerability and resilience of trees and plants in these forests when drought and fires happen.

The study showed that while many trees died in primary forest affected by drought, the loss of trees was much worse in secondary and other human-disturbed forests. The researchers found that trees and plants with lower wood density and thinner barks were more prone to dying from the drought and fires. These smaller trees are more common in human-disturbed forests.

The researchers estimate that around 447 million large trees (greater than 10cm Diameter at Breast Height) died, and around 2.5 billion smaller trees (less than 10cm DBH) died across the Lower Tapajós region.

The researchers also compared the effect on different forest types from drought alone, as well as the combined stresses of drought and fire.

Tree and plant mortality was higher in secondary forests from drought alone when compared with primary forests. Impact from drought was not higher in human-modified forests, but was significantly greater in those human-modified forests that experienced a combination of drought and fire.

Carbon emissions from those forests burned by wildfires were almost six times higher than forests affected by drought alone.

These findings highlight how interference by people can make the Amazon forests more vulnerable and underline the need to reduce illegal logging and other large-scale human disturbances of forests in the Amazon, as well as investments in fire-fighting capabilities in the Amazon.

Professor Jos Barlow of Lancaster University and the Universidade Federal de Lavras, and Principal Investigator of the research, said: “The results highlight the need for action across different scales. Internationally, we need action to tackle climate change, which is making extreme droughts and fires more likely. At the local level, forests will suffer fewer negative consequences from fires if they are protected from degradation.”

The link between on-road traffic and air pollution is well-known, as are the negative health impacts of pollution exposure. However, the many factors that may influence commuters’ exposure to pollutants — such as frequency, time, and duration of commute — and the overall impact of commuting remains a matter of on-going scientific discovery.

Dr. Jenna Krall, assistant professor at the George Mason University College of Health and Human Services, is using statistical methods to better understand exposure to air pollution. Krall studies how commuting patterns impact exposure to fine particulate matter (PM2.5) from various traffic-related sources such as tailpipe emissions, road salts, and brake wear.

New research from Krall and colleagues published in Environmental Research examines commuter characteristics to better understand how factors such as departure time, commute length, and number of trips are associated with exposure to PM2.5. Building on a study of 46 women’s exposure to PM2.5 using personal air pollution monitors, the new research clustered commuters to determine whether these clusters were associated with traffic pollution exposures. The new study reveals that commuters that travel to work during rush hour have higher overall exposure to traffic-related air pollution compared to sporadic commuters, though the difference was not statistically significant.

As COVID-19 infection rates decline in most areas of the country and employers weigh whether to continue work-from-home policies, studies such as this provide important insight into the role that daily commutes can play in personal air pollution exposure and the public’s health.

“This is one of the first studies to utilize in-vehicle monitoring, specifically on-board diagnostics data loggers, to understand real-world commuting behaviors for environmental health,” said Krall, “Linking these data with personal air pollution monitoring allowed us to better understand how commuter characteristics are associated with sources of air pollution exposures.”

“The current research cannot tell us whether modifying commutes, for example by avoiding highways or commuting outside of rush hour, will lower traffic pollution exposures for commuters. More research is needed to determine what changes would be effective to lower exposures,” says Krall.

Krall’s on-going research seeks to distinguish between similar sources of traffic pollution, such as pollution generated by brake wear or from tailpipe emissions, and to develop statistical methods to better estimate exposure to pollution sources.

Study participants included 46 women commuters in northern Virginia who were exposed to pollution generated by mobile vehicles, road salts, and other sources throughout a 48-hour period.

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Materials provided by George Mason University. Note: Content may be edited for style and length.

A growing body of studies suggests COVID-19 emulates many aspects of systemic autoimmune disorders, including the release of a flurry of overactive immune cells that produce toxic webs of proteins and DNA called neutrophil extracellular traps, or NETs.

For this study, the team analyzed serum from over 300 hospitalized COVID patients, searching for a novel autoantibody that shields the toxic NETs from being destroyed and produces a lasting noxious effect in a patient’s body.

The results, published in JCI Insight, reveal markedly elevated levels of the anti-NET antibodies in many of the participants. Those with higher levels of the autoantibodies were more likely to develop severe COVID-19 symptoms.

“We see a slew of different antibodies produced in COVID-19 patients, and now we discovered another clinically significant one that is likely contributing to severe COVID,” said Yu (Ray) Zuo, M.D., lead author and a rheumatologist at Michigan Medicine. “They feed into the inflammatory storm that we’re seeing in the most serious cases of viral infection.”

Researchers generated NETs in the lab and incubated them with COVID patient serum. They found the serum from patients with higher levels of anti-NET antibodies struggled to degrade the toxic traps.

The team also spiked healthy serum with anti-NETs purified from the infected patients. While a healthy person’s serum should completely disintegrate the extracellular traps, the purified anti-NET antibodies significantly hindered the process.

“We knew that people with severe forms of COVID have higher amounts of these neutrophil extracellular traps, which amplify inflammation and promote blood clot formation,” said Jason Knight, M.D., corresponding author of the paper and an associate professor of rheumatology at Michigan Medicine. “We’ve now found that this process is exacerbated by the anti-NET antibodies, which disrupt our body’s immune homeostasis during COVID-19 infection.”

Similarities to another autoimmune disease

Zuo and the Michigan Medicine team previously reported the presence of anti-NETs in patients with antiphospholipid syndrome, a systemic autoimmune condition characterized by severe blood clots and recurring pregnancy loss.

The anti-NET antibodies, which are likely associated with the development of recurrent blood clots and more severe disease in antiphospholipid syndrome, showed remarkably similar function in this study of COVID-19 patients, said corresponding author Yogen Kanthi, M.D., a cardiologist and vascular medicine specialist at the National Heart, Lung, and Blood Institute and Lasker Investigator at the National Institutes of Health.

“In both diseases, the anti-NET antibodies coat the surface of the neutrophil extracellular traps, making it much harder for the body to clear out this web that causes inflammation and clotting,” Kanthi said. “Knowing their function is likely to help physicians design more targeted COVID-19 treatments and also for other inflammatory diseases.”

How COVID-19 manages to trigger the production of a variety of autoantibodies, including anti-NETs, remains unknown. Further study of the virus’ autoimmune aspects, Zuo noted, will not only lead to better understanding of the disease, but will also likely shed light onto the origins of autoimmune diseases.

Future research and “long COVID”

The paper’s findings may also unlock other COVID mysteries, including the persistence of symptoms in some people months after clearing the virus, a phenomenon known as long COVID, Zuo said.

The team is currently conducting a follow-up study, calling back patients who were previously hospitalized to repeat testing for the anti-NETs and other autoantibodies that formed during their hospitalizations.

Previously, they found durable anti-NET antibodies that persisted in antiphospholipid syndrome patients for up to four years. The team will investigate if and how the autoantibodies influence long COVID, the post-acute sequalae of the virus marked by symptoms like brain fog, fatigue and shortness of breath.

While vaccination is doing its job to limit severe infections and hospitalizations, millions still feel the effects of long COVID, which is why this research is so important, Zuo said.

“The better we understand these COVID-induced autoantibodies such as anti-NET antibodies, the more equipped we will be to fight COVID-19 at every stage of viral infection,” Zuo said. “Studying these antibodies will also teach us about the mechanisms of autoimmunity in general, especially in the field of rheumatology.”