Culture

A team of Colorado State University scientists, led by veterinary postdoctoral fellow Dr. Anna Fagre, has detected Zika virus RNA in free-ranging African bats. RNA, or ribonucleic acid, is a molecule that plays a central role in the function of genes.

According to Fagre, the new research is a first-ever in science. It also marks the first time scientists have published a study on the detection of Zika virus RNA in any free-ranging bat.

The findings have ecological implications and raise questions about how bats are exposed to Zika virus in nature. The study was recently published in Scientific Reports, a journal published by Nature Research.

Fagre, a researcher at CSU's Center for Vector-Borne Infectious Diseases, said while other studies have shown that bats are susceptible to Zika virus in controlled experimental settings, detection of nucleic acid in bats in the wild indicates that they are naturally infected or exposed through the bite of infected mosquitoes.

"This provides more information about the ecology of flaviviruses and suggests that there is still a lot left to learn surrounding the host range of flaviviruses, like Zika virus," she said. Flaviviruses include viruses such as West Nile and dengue and cause several diseases in humans.

CSU Assistant Professor Rebekah Kading, senior author of the study, said she, Fagre and the research team aimed to learn more about potential reservoirs of Zika virus through the project.

The team used 198 samples from bats gathered in the Zika Forest and surrounding areas in Uganda and confirmed Zika virus in four bats representing three species. Samples used in the study date back to 2009 from different parts of Uganda, years prior to the large outbreaks of Zika virus in 2015 to 2017 in North and South Americas.

"We knew that flaviviruses were circulating in bats, and we had serological evidence for that," said Kading. "We wondered: Were bats exposed to the virus or could they have some involvement in transmission of Zika virus?"

The virus detected by the team in the bats was most closely related to the Asian lineage Zika virus, the strain that caused the epidemic in the Americas following outbreaks in Micronesia and French Polynesia. The first detection of the Asian lineage Zika virus in Africa was in late 2016 in Angola and Cape Verde.

"Our positive samples, which are most closely related to the Asian lineage Zika virus, came from bats sampled from 2009 to 2013," said Fagre. "This could mean that the Asian lineage strain of the virus has been present on the African continent longer than we originally thought, or it could mean that there was a fair amount of viral evolution and genomic changes that occurred in African lineage Zika virus that we were not previously aware of."

Fagre said the relatively low prevalence of Zika virus in the bat samples indicates that bats may be incidental hosts of Zika virus infection, rather than amplifying hosts or reservoir hosts.

"Given that these results are from a single cross-sectional study, it would be risky and premature to draw any conclusions about the ecology and epidemiology of this pathogen, based on our study," she said. "Studies like this only tell one part of the story."

The research team also created a unique assay for the study, focusing on a specific molecular component that flaviviruses possess called subgenomic flavivirus RNA, sfRNA. Most scientists that search for evidence of Zika virus infection in humans or animals use PCR, polymerase chain reaction, to identify bits of genomic RNA, the nucleic acid that results in the production of protein, said Fagre.

Kading said her team will continue their research to try and learn more about how long these RNA fragments persist in tissues, which will allow them to approximate when these bats were infected with Zika virus.

"There is always a concern about zoonotic viruses," she said. "The potential for another outbreak is there and it could go quiet for a while. We know that in the Zika forest, where the virus was first found, the virus is in non-human primates. There are still some questions with that as well. I don't think Zika virus has gone away forever."

URBANA, Ill. -When pigs get hit with significant illnesses during key stages of pregnancy, their immune response may negatively affect developing piglets, making them less productive on the farm. New research from the University of Illinois shows that when those piglets - especially males - experience a second stressor in early life, they are at higher risk of neurodevelopmental and other neurological anomalies, putting them at an even greater disadvantage in production settings.

"With more information about maternal illness, what we call maternal immune activation, we can make better decisions about how to handle these types of immune challenges within animal production settings," says Marissa Keever-Keigher, doctoral student in the Department of Animal Sciences at Illinois and lead researcher on the study.

Studying brain development in the domestic pig is relevant on the farm, of course, but pig studies can also inform human neurodevelopmental research. That's because the pig's development, genetics, brain structure, and more are very similar to our own.

In previous pig studies looking at the effects of maternal immune activation, Keever-Keigher and her colleagues showed important genetic changes occur in the piglet amygdala, a brain structure that plays an important role in learning, social behavior, and stress response in both humans and pigs.

The researchers also knew from primate and rodent studies that a second immune challenge, known as a double hit, can further disrupt typical brain development in young animals. To test the double hit hypothesis in pigs, the team chose weaning as the second challenge.

"While weaning is not itself an immune challenge, it is an extremely stressful time during a piglet's life and can elicit an immune response," says Haley Rymut, doctoral student in animal sciences and co-author on the study. "Piglets have to deal with a broad array of stressors, including physical stressors from being handled and moved, and emotional stressors from being taken away from the mom and placed with their peers. Any of those physical or emotional stressors can kick off an immune response."

The researchers looked at a combination of factors for piglets in the study: whether or not their moms were infected with porcine reproductive and respiratory syndrome virus (PRRSV) during gestation, and whether or not they were weaned at 21 days of age, the typical age in production settings. They also noted the sex of the piglets, as their earlier research indicated male piglets showed more changes in the amygdala as a result of maternal illness.

"Using high throughput sequencing technologies, we were able to monitor the levels of more than 16,000 genes in the pigs. We uncovered more than 100 genes and molecular pathways affected by either maternal immune activation, weaning, sex, or a combination of factors in the amygdala on day 22 for all piglets. The effect of pre- and postnatal stressors on neuropeptide genes confirms the plasticity of the infant brain during development to respond and adapt to challenges," says Sandra Rodriguez-Zas, professor in animal sciences and faculty advisor to Keever-Keigher and Rymut. Rodriguez-Zas is principal investigator of the U.S. Department of Agriculture-funded study.

Many of the genes expressed at higher or lower-than-typical rates in weaned piglets from virus-infected mothers have been associated with autism spectrum disorder (ASD) and schizophrenia spectrum disorder (SSD) in previous studies. But genes relevant to other neurological disorders were affected too.

"We also found changes in expression of genes associated with neurodegenerative diseases like Huntington's and Alzheimer's disease," Keever-Keigher says.

As in the scientists' previous work, the double hit affected male piglets more than females, with greater dysregulation of genes in the amygdala. The researchers found evidence of more protective pathways in female brains, giving them an advantage in handling stressful events.

The study provides valuable clues for researchers studying ASD, SSD, and neurodegenerative disorders in humans, even though some aspects might not translate directly.

Rymut says, "For most children, weaning isn't nearly as stressful as it is for pigs in a production setting. But many other traumatic events early in childhood could set up that double hit."

On the farm, pigs from virus-infected mothers often show anti-social behaviors. Because pigs are typically group-housed and fed via communal feeders, pigs that don't like being around their peers are often last to feed and generally more stressed, leading to slower growth rates and lower overall body condition scores.

"The lesson for swine producers, I think, is to be really mindful of stressful conditions in the production cycle, and try to mitigate those as much as we can in order to create the most productive and healthy livestock animals and benefit producers' bottom lines," Keever-Keigher says.

Rymut adds, "Also, knowing how the different sexes respond could help producers manage animals that are less likely to be productive as a result of maternal immune activation."

In a new study, University of Maine researchers found that culture helps humans adapt to their environment and overcome challenges better and faster than genetics.

After conducting an extensive review of the literature and evidence of long-term human evolution, scientists Tim Waring and Zach Wood concluded that humans are experiencing a "special evolutionary transition" in which the importance of culture, such as learned knowledge, practices and skills, is surpassing the value of genes as the primary driver of human evolution.

Culture is an under-appreciated factor in human evolution, Waring says. Like genes, culture helps people adjust to their environment and meet the challenges of survival and reproduction. Culture, however, does so more effectively than genes because the transfer of knowledge is faster and more flexible than the inheritance of genes, according to Waring and Wood.

Culture is a stronger mechanism of adaptation for a couple of reasons, Waring says. It's faster: gene transfer occurs only once a generation, while cultural practices can be rapidly learned and frequently updated. Culture is also more flexible than genes: gene transfer is rigid and limited to the genetic information of two parents, while cultural transmission is based on flexible human learning and effectively unlimited with the ability to make use of information from peers and experts far beyond parents. As a result, cultural evolution is a stronger type of adaptation than old genetics.

Waring, an associate professor of social-ecological systems modeling, and Wood, a postdoctoral research associate with the School of Biology and Ecology, have just published their findings in a literature review in the Proceedings of the Royal Society B, the flagship biological research journal of The Royal Society in London.

"This research explains why humans are such a unique species. We evolve both genetically and culturally over time, but we are slowly becoming ever more cultural and ever less genetic," Waring says.

Culture has influenced how humans survive and evolve for millenia. According to Waring and Wood, the combination of both culture and genes has fueled several key adaptations in humans such as reduced aggression, cooperative inclinations, collaborative abilities and the capacity for social learning. Increasingly, the researchers suggest, human adaptations are steered by culture, and require genes to accommodate.

Waring and Wood say culture is also special in one important way: it is strongly group-oriented. Factors like conformity, social identity and shared norms and institutions -- factors that have no genetic equivalent -- make cultural evolution very group-oriented, according to researchers. Therefore, competition between culturally organized groups propels adaptations such as new cooperative norms and social systems that help groups survive better together.

According to researchers, "culturally organized groups appear to solve adaptive problems more readily than individuals, through the compounding value of social learning and cultural transmission in groups." Cultural adaptations may also occur faster in larger groups than in small ones.

With groups primarily driving culture and culture now fueling human evolution more than genetics, Waring and Wood found that evolution itself has become more group-oriented.

"In the very long term, we suggest that humans are evolving from individual genetic organisms to cultural groups which function as superorganisms, similar to ant colonies and beehives," Waring says. "The 'society as organism' metaphor is not so metaphorical after all. This insight can help society better understand how individuals can fit into a well-organized and mutually beneficial system. Take the coronavirus pandemic, for example. An effective national epidemic response program is truly a national immune system, and we can therefore learn directly from how immune systems work to improve our COVID response."

People of color are more than twice as likely to die after a traumatic brain injury as white people, according to a new retrospective review from Oregon Health & Science University.

The study published today in the journal Frontiers in Surgery.

In the report, "Racial and Ethnic Inequities in Mortality During Hospitalization for Traumatic Brain Injury: A Call to Action," the researchers analyzed more than a decade of data related to the health outcomes and demographics of thousands of patients treated for traumatic head injuries at OHSU Hospital, one of two Level 1 trauma centers in the state.

They found a clear delineation of worse outcomes for people of color.

"We have a societal and professional duty to recognize and accept that the effects of structural racism have taken hold of our patients' health long before they arrive in our trauma bays, ICU beds, and operating tables," they write. "These disparities permeate our society and contribute to inequitable health outcomes, and we must take action to identify the factors which perpetuate this disproportionate suffering."

The researchers found no bias in the treatment patients received while in the hospital. Measurements including the number of days spent in intensive care and charges for hospital services were similar between groups.

Rather, they say the findings highlight underlying disparities in health that disproportionately affect people of color.

"If you ran the same analysis with patients with pneumonia, you might find the same results," said senior author Ahmed M. Raslan, M.D., FAANS, associate professor of neurological surgery in the OHSU School of Medicine. "Our findings point to the problem in a more robust and clear way. The problem is rooted in social determinants of health, including factors such as diet, lifestyle, occupations and access to health care."

The study is the first to review racial and ethnic disparities in the field of neurosurgical trauma.

Researchers reviewed outcomes for 6,352 patients treated for traumatic brain injuries between 2006 and 2017. The overall mortality rate was 9.9% among all patients. Among the 1,504 patients who identified as racial or ethnic minorities, 14.6% died.

Weighted for severity of injury, age and other factors, researchers calculated an in-hospital mortality hazard ratio of 2.21 for minority patients compared to white patients.

"Dr. Raslan's research is incredibly important in highlighting disparities in health outcomes experienced by people of color," said Nathan Selden, M.D., Ph.D., professor and chair of neurological surgery in the OHSU School of Medicine. "Together with our department's efforts to improve the care of traumatic brain injuries, and more broadly to improve diversity in medicine, I am confident OHSU can really make a difference."

Hydrogels are commonly used inside the body to help in tissue regeneration and drug delivery. However, once inside, they can be challenging to control for optimal use. A team of researchers in the Department of Biomedical Engineering at Texas A&M University is developing a new way to manipulate the gel -- by using light.

Graduate student Patrick Lee and Dr. Akhilesh Gaharwar, associate professor, are developing a new class of hydrogels that can leverage light in a multitude of ways. Light is a particularly attractive source of energy as it can be confined to a predefined area as well as be finetuned by the time or intensity of light exposure. Their work was recently published in the journal Advanced Materials.

Light?responsive hydrogels are an emerging class of materials used for developing noninvasive, noncontact, precise and controllable medical devices in a wide range of biomedical applications, including photothermal therapy, photodynamic therapy, drug delivery and regenerative medicine.

Lee said light-responsive biomaterials are often used in biomedical applications; however, current light sources, such as ultraviolet light and visible light, cannot sufficiently penetrate the tissue to interact with the hydrogel. Instead, the team is researching near-infrared (NIR) light, which has a higher penetration depth.

The team is using a new class of two-dimensional nanomaterials known as molybdenum disulfide (MoS2), which has shown negligible toxicity to cells and superior NIR absorption. These nanosheets with high photothermal conversion efficiency can absorb and convert NIR light to heat, which can be developed to control thermoresponsive materials.

In the group's previous study published in Advanced Materials, certain polymers react with MoS2 nanosheets to form hydrogels. Building on this discovery, the team further utilizes MoS2 nanosheets and thermoresponsive polymers to control the hydrogel under NIR light by photothermal effect.

"This work leverages light to activate the dynamic polymer-nanomaterials interactions," Gaharwar said. "Upon NIR exposure, MoS2 acts as a crosslink epicenter by connecting with multiple polymeric chains via defect?driven click chemistry, which is unique."

NIR light allows internal formation of therapeutic hydrogels in the body for precise drug delivery. For cancer therapy, most of the drugs can be retained within the tumor, which will ease the side effects of chemotherapy. Moreover, NIR light can generate heat inside the tumors to ablate cancer cells, known as photothermal therapy. Therefore, a synergetic combination of photothermal therapy and chemotherapy has shown a higher efficacy in destroying cancer cells.

The Permian Basin, located in western Texas and southeastern New Mexico, is the largest oil- and gas-producing region in the U.S. The oilfield operations emit methane, but quantifying the greenhouse gas is difficult because of the large area and the fact that many sources are intermittent emitters. Now, researchers reporting in ACS' Environmental Science & Technology Letters have conducted an extensive airborne campaign with imaging spectrometers and identified large methane sources across this area.

According to the U.S. Energy Information Administration, 38% of the nation's total oil and 17% of natural gas production took place in the Permian Basin in 2020. Therefore, quantifying emissions from these operations, which continue to expand rapidly, is of great interest to environmental scientists. Previous studies have tried to estimate methane leakage in the Permian Basin through satellite images or mobile field studies, but either the spatial resolution was too coarse to quantify methane coming from individual sources, or the studies were limited to small areas or timeframes. So Daniel Cusworth and colleagues from the NASA Jet Propulsion Laboratory, the University of Arizona and Arizona State University formed a collaboration. They wanted to quantify strong methane point source emissions (greater than 22-44 pounds of methane per hour) in the Permian Basin using airborne imaging spectrometry, a technology that would allow high-resolution mapping of those sources across large areas and multiple overflights.

From September to November 2019, the researchers conducted repeated flights in airplanes carrying imaging spectrometers, covering about 21,000 square miles and 60,000 active wells in the Permian Basin. The spectrometers detected 1,100 unique large methane point sources that were sampled at least three times. Most of these sources were highly intermittent (detected 25% or fewer of the times sampled). However, sources that were routinely persistent (detected 50-100% of the time) comprised 11% of the methane emitters but 29% of the total detected emissions, possibly indicating leaking equipment that needs repair. Half of the detected methane came from oil and gas production wells, 38% from pipelines and other equipment used to collect and transport oil and gas, and 12% from processing plants. These results show that frequent, high-resolution monitoring is necessary to understand intermittent methane emitters across large areas and to pinpoint persistent leaks for mitigation, the researchers say.

Jack Tseng loves bone-crunching animals -- hyenas are his favorite -- so when paleontologist Joseph Peterson discovered fossilized dinosaur bones that had teeth marks from a juvenile Tyrannosaurus rex, Tseng decided to try to replicate the bite marks and measure how hard those kids could actually chomp down.

Last year, he and Peterson made a metal replica of a scimitar-shaped tooth of a 13-year-old juvie T. rex, mounted it on a mechanical testing frame commonly used in engineering and materials science, and tried to crack a cow legbone with it.

Based on 17 successful attempts to match the depth and shape of the bite marks on the fossils -- he had to toss out some trials because the fresh bone slid around too much -- he determined that a juvenile could have exerted up to 5,641 newtons of force, somewhere between the jaw forces exerted by a hyena and a crocodile.

Compare that to the bite force of an adult T. rex -- about 35,000 newtons -- or to the puny biting power of humans: 300 newtons.

Previous bite force estimates for juvenile T. rexes -- based on reconstruction of the jaw muscles or from mathematically scaling down the bite force of adult T. rexes -- were considerably less, about 4,000 newtons.

Why does it matter? Bite force measurements can help paleontologists understand the ecosystem in which dinosaurs -- or any extinct animal -- lived, which predators were powerful enough to eat which prey, and what other predators they competed with.

"If you are up to almost 6,000 newtons of bite force, that places them in a slightly different weight class," said Tseng, UC Berkeley assistant professor of integrative biology. "By really refining our estimates of juvenile bite force, we can more succinctly place them in a part of the food web and think about how they may have played the role of a different kind of predator from their larger, adult parents."

The study reveals that juvenile T. rexes, while not yet able to crush bones like their 30- or 40-year-old parents, were developing their biting techniques and strengthening their jaw muscles to be able do so once their adult teeth came in.

"This actually gives us a little bit of a metric to help us gauge how quickly the bite force is changing from juvenile to adulthood, and something to compare with how the body is changing during that same period of time," said Peterson, a professor at the University of Wisconsin in Oshkosh and a paleopathologist -- a specialist on the injuries and deformities visible in fossil skeletons. "Are they already crushing bone? No, but they are puncturing it. It allows us to get a better idea of how they are feeding, what they are eating. It is just adding more to that full picture of how animals like tyrannosaurs lived and grew and the roles that they played in that ecosystem."

Tseng, Peterson and graduate student Shannon Brink of East Carolina University in Greenville, North Carolina, will publish their findings this week in the journal PeerJ.

Teeth marks galore, but who was the biter?

Experiments using metal casts of dinosaur teeth to match observed bite marks are rare, not because bite marks on dinosaur fossils are rare, but because the identity of the biter is seldom clear.

Two dinosaur fossils that Peterson excavated years earlier from the Hell Creek Formation of eastern Montana, however, proved ideal for such an experiment. One, the skull of a juvenile T. rex, had a healed bite mark on its face. "What, other than another T. rex, would be able to chomp another T. rex and puncture its skull?" he reasoned. Tyrannosaurs, like crocodiles today, played rough, and the wound was likely from a fight over food or territory.

In addition, the puncture holes in the skull, which had healed, were the size and shape of juvenile T. rex teeth, and the spacing fit a juvenile's tooth gap. Juvenile T. rexes have teeth that are oval in cross section: more knife-like, presumably to cut and tear flesh. Adult T. rexes have teeth with round cross sections: more like posts, to crush bone. Both juveniles and adults could replace lost or broken teeth from spares buried in the jaw that emerged once the socket was empty.

Because skull bone is harder than other bone, Peterson said, matching these holes with punctures made by the metal tooth in a cow bone provided an upper limit to the bite force.

The other fossil was a tail vertebra from a plant-eating, duckbilled dinosaur, an Edmontosaurus. It had two puncture marks from teeth that matched those of a juvenile T. rex. Peterson said that T. rex was the only predator around at that time -- the late Cretaceous Period, more than 66 million years ago -- that could have bitten that hard on the tailbone of a duckbill. The juvenile likely punctured the bone when chomping down on a meaty part of the tail of the already dead animal.

Because vertebrae are softer, experimentally creating similar punctures in a cow bone gave the researchers a lower limit on bite force.

Tseng employed a testing technique that was used in 2010 by researchers who measured the bite force of a much older and smaller dinosaur from the early Cretaceous: a Deinonychus, made famous under a different name -- Velociraptor -- in the 1993 movie Jurassic Park. Its bite force was between 4,000 and 8,000 newtons.

Tseng, then at the University at Buffalo in New York, and Peterson made a replica of a juvenile T. rex tooth from the middle of the jaw using a dental-grade cobalt chromium alloy, which is much harder than dinosaur tooth enamel, Tseng said.

They then mounted the metal tooth in a mechanical testing frame and pushed it slowly, at a millimeter per second, into a fresh-frozen and thawed humerus of a cow. Bones are easier to fracture at low speed than with a rapid chomp. Because the middle of the humerus has a thicker cortex than the bone near the joint ends, the middle was used to replicate the facial punctures. The ends were used to simulate the vertebra punctures.

"What we did, an actualistic study, is to say, 'Let's actually stab the thing with a tooth and see what it does,'" Peterson said. "What we are finding is that our estimates are slightly different than other models, but they are within a close enough range -- we are on the same page."

Tseng emphasized that there is no one number describing the bite force of any animal: it depends on how the creature bites and adjusts the prey in its mouth for the best leverage.

"They probably were not just chomping down. If you look at modern predators, even reptilian predators, sometimes there is adjustment. Maybe they are finding the most mechanically advantageous place, or the strongest tooth to make their bite," said Tseng, who is a 2004 graduate of UC Berkeley's Department of Integrative Biology and an assistant curator in the University of California Museum of Paleontology. "Presumably, there is some tuning involved before they make that bite, so they can literally take the best bite forward to make that kill or to damage whatever they are trying to get into."

Nevertheless, the measurements are a start in charting the increase in tyrannosaurs' bite force as they mature, similar to how paleontologists have charted T. rex size and weight with age.

"Just as you can do a growth curve for such an organism, you can also do a strength curve for their bite force -- what was their bite force at 12 or 13 years old, what was it at 30, 35 or 40 years old. And what does that potentially mean about the role that those animals played in that ecosystem at the time?" Peterson said. "What's cool about finding bite marks in bone from a juvenile tyrannosaur is that it is tells us that at 13 years old, they weren't capable of crushing bone yet, but they were already trying, they were puncturing bone, pretty deep. They are probably building up their strength as they get older."

Tseng, whose primary interest is mammals, is eager to resume studies interrupted by the pandemic to measure the bite force of various living and extinct animals in order to infer the ecosystem niches of predators no longer alive. For those creatures, fossils are all that paleontologists have, in order to "interpret behavior and breathe some life into these extinct animals," said Peterson.

"I use a biomechanical lens when I look at everything, living or extinct," Tseng added. "Ecologists today studying food webs and ecosystems don't rely much on bones; they have physical animals and plants. It is really the paleontologists who are interested in this approach, because the majority of what we have to study are bones and bite marks."

A large group of iconic fossils widely believed to shed light on the origins of many of Earth's animals and the communities they lived in may be hiding a secret.

Scientists, led by two from the University of Portsmouth, UK, are the first to model how exceptionally well preserved fossils that record the largest and most intense burst of evolution ever seen could have been moved by mudflows.

The finding, published in Communications Earth & Environment, offers a cautionary note on how palaeontologists build a picture from the remains of the creatures they study.

Until now, it has been widely accepted the fossils buried in mudflows in the Burgess Shale in Canada that show the result of the Cambrian explosion 505 million years ago had all lived together but that's now in doubt.

The Cambrian explosion was responsible for kick-starting the huge diversity of animal life now seen on the planet.

Now, Dr Nic Minter and Dr Orla Bath Enright have found that some of the animals which became fossils could have remained well preserved even after being carried large distances, throwing doubt on the idea the creatures all lived together.

Dr Minter said: "This finding might surprise scientists or lead to them striking a more cautionary tone in how they interpret early marine ecosystems from half a billion years ago.

"It has been assumed that because the Burgess Shale fossils are so well preserved, they couldn't have been transported over large distances. However, this new research shows that the general type of flow responsible for the deposits in which they were buried does not cause further damage to deceased animals. This means the fossils found in individual layers of sediment, and assumed to represent animal communities, could actually have been living far apart in distance."

Drs Minter and Bath Enright, of the University of Portsmouth's School of the Environment, Geography and Geosciences, studied the Burgess Shale area of British Columbia, both on location in the field and with laboratory experiments.

The site is an area rich in fossils entombed in the deposits of mudflows and is one of the world's most important fossil sites, with more than 65,000 specimens already collected and, so far, more than 120 species counted.

The Burgess Shale area has been fundamental to scientists in understanding the origins of animal groups and the communities they lived among and has been closely studied multiple times.

The researchers, together with collaborators from the Universities of Southampton and Saskatchewan in Canada, used fieldwork to identify how the mudflows would have behaved, and then used flume tank laboratory tests to mimic the mudflows and are confident that the bodies of certain creatures could have been moved over tens of kilometres without damage, creating the illusion of animal communities which never existed.

The Burgess Shale was discovered in the early 1900s and led to the idea of the 'Cambrian explosion' of life, with the appearance of animals representing almost all the modern phyla, and inspiring copious research and discoveries.

Dr Bath Enright said: "Many would argue that it is fundamental, even ground zero for scientists in understanding the diversity of life."

It's not known precisely what caused the mudflows which buried and moved the animals which became fossilised, but the area was subject to multiple flows, causing well preserved fossils to be found at many different levels in the shale.

"We don't know over what kind of overall time frame these many flows happened, but we know each one produced an 'event bed' that we see today stacked up on top of one another. These flows could pick up animals from multiple places as they moved across the seafloor and then dropped them all together in one place," said Dr Bath Enright.

"When we see multiple species accumulated together it can give the illusion we are seeing a single community. But we argue that an individual 'event bed' could be the product of several communities of animals being picked up from multiple places by a mudflow and then deposited together to give what looks like a much more complicated single community of animals.

"Palaeontologists need to appreciate the nature of the sediments that fossils are preserved within and what the implications of that are. We could be overestimating the complexity of early marine animal communities and therefore the patterns and drivers of evolution that have led to our present day diversity and complexity."

The researchers hope to do further study to investigate whether differences in the species that are present in other fossil sites are due to evolutionary changes through time or the nature of the flows and the effects of transport and preservation of the fossils.

CRISPR-based technologies offer enormous potential to benefit human health and safety, from disease eradication to fortified food supplies. As one example, CRISPR-based gene drives, which are engineered to spread specific traits through targeted populations, are being developed to stop the transmission of devastating diseases such as malaria and dengue fever.

But many scientists and ethicists have raised concerns over the unchecked spread of gene drives. Once deployed in the wild, how can scientists prevent gene drives from uncontrollably spreading across populations like wildfire?

Now, scientists at the University of California San Diego and their colleagues have developed a gene drive with a built-in genetic barrier that is designed to keep the drive under control. Led by molecular geneticist Omar Akbari's lab, the researchers engineered synthetic fly species that, upon release in sufficient numbers, act as gene drives that can spread locally and be reversed if desired.

The scientists describe their SPECIES (Synthetic Postzygotic barriers Exploiting CRISPR-based Incompatibilities for Engineering Species) development as a proof-of-concept innovation that could be portable to other species such as insect disease vectors. Spreading gene drives that limit pests that feast on valuable food crops is another example of a potential SPECIES application.

"Gene drives can potentially spread beyond intended borders and be hard to control. SPECIES offers a way to control populations in a very safe and reversible manner," said Akbari, a UC San Diego Division of Biological Sciences associate professor and senior author of the paper, which is published in the journal Nature Communications.

The idea behind the creation of SPECIES is reflective of the formation of new species in nature. As members of a single species separate over time, due to, for example, a new land formation, earthquake separation or other geological event, a new species eventually can evolve from the physical disconnection. If the new species eventually returns to mate with the original species, they could produce unviable offspring due to biological changes following the separation through a natural phenomenon known as reproductive isolation.

Working in the fly species Drosophila melanogaster, UC San Diego researchers and their colleagues at the California Institute of Technology, UC Berkeley and the Innovative Genomics Institute used CRISPR genetic-editing technologies to develop flies encoding SPECIES systems that are reproductively incompatible with wild versions of D. melanogaster.

"Even though speciation happens consistently in nature, creating a new artificial species is actually a pretty big bioengineering challenge," said Anna Buchman, the lead author of the paper. "The beauty of the SPECIES approach is that it simplifies the process, giving us a defined set of tools we need in any organism to elegantly bring about speciation."

Conceptually, when SPECIES are deployed in the wild in sufficient numbers, they can controllably drive through a population and replace all of their wild counterparts as they spread. Using malaria as an example, SPECIES mosquitoes could be developed with a genetic element that makes them incapable of transmitting malaria.

"You can spread an anti-malaria SPECIES into a target population in a confinable and controllable way," said Akbari. "Since SPECIES are incompatible with wild-type mosquitoes, their populations can be controlled and reversed by limiting their threshold population below 50 percent. This gives you the ability to confine and reverse its spread if desired."

As the SPECIES barrier completes its role in temporarily replacing wildtype populations, their numbers can be reduced with the reintroduction of wild type populations.

"This essentially allows us to harness all of the power of gene drives--like disease elimination or crop protection--without the high risk of uncontrollable spread," said Akbari.

Twice a day, at dusk and just before dawn, a faint layer of sodium and other metals begins sinking down through the atmosphere, about 90 miles high above the city of Boulder, Colorado. The movement was captured by one of the world's most sensitive "lidar" instruments and reported today in the AGU journal Geophysical Research Letters.

The metals in those layers come originally from rocky material blasting into Earth's atmosphere from space, and the regularly appearing layers promise to help researchers understand better how earth's atmosphere interacts with space, even potentially how those interactions help support life.

"This is an important discovery because we have never seen these dusk/dawn features before, and because these metal layers affect many things. The metals can fall into the ocean and act as fertilizer for ecosystems, the ionized metals can affect GPS radio signals," said Xinzhao Chu, CIRES Fellow, CU Boulder professor of Aerospace Engineering Sciences, and lead author of the new assessment.

It is the first time that the metal layers--which are not harmful to people--have been seen so regularly at these extreme heights in the atmosphere. Such high-altitude metal layers were discovered by Chu's group just 10 years ago above McMurdo, Antarctica, but there they occur more sporadically. Above Boulder, they're consistent, daily, and synched with winds that occur high in the atmosphere.

"Consistent daily patterns seen in our Boulder observations tell us that there are unknown processes at play, a golden opportunity for atmospheric scientists," said Jackson Jandreau who worked alongside Chu and Yingfei Chen in this study. Chen and Jandreau are both PhD students in Chu's group.

The discovery also gives researchers a window into a crucial part of the atmosphere that is challenging to observe. It's a complicated region where interactions between the sun, earth and our planet's magnetic field can end up creating the environmental conditions in which surface life can thrive, protected from the harsh space environment.

"There are metals in the atmospheres of other planetary bodies, such as Mars, and researchers look for Earth-like features on exoplanets as indicators for hospitable environments," Chu said. "Can these metal layers be one of these features?"

A new study led by researchers at Washington State University has identified a protein that could be the key to improving treatment outcomes after a heart attack.

Published in the Journal of Biological Chemistry, the research suggests that protein kinase A (PKA) plays a role in heart muscle cell necrosis, a major type of cell death that commonly occurs after reperfusion therapy, the treatment used to unblock arteries and restore blood flow after a heart attack.

"Our study has found that turning off a gene that controls this protein activity increased necrotic cell death and led to more heart injury and worse heart function following heart attack in a rodent model," said study author Zhaokang Cheng, an assistant professor in the WSU College of Pharmacy and Pharmaceutical Sciences. "With further research, this discovery could ultimately lead to the development of a small-molecule drug that could intervene in that pathway to limit or prevent heart muscle cell death after reperfusion therapy."

Such a drug could help reduce heart injury and increase the survival and lifespan of heart attack victims, Cheng said. Every year, about 800,000 people in the U.S. have a heart attack, which amounts to one heart attack occurring every 40 seconds.

Reperfusion therapy, which uses clot-dissolving drugs or mechanical means to unblock clogged arteries, has long been the most effective treatment for heart attack. Though it significantly reduces heart damage, patients treated with this therapy still experience some damage, about half of which actually results from the treatment itself. This is because the rapid restoration of blood flow into oxygen-deprived heart tissues can lead to a swift rise in free radicals. When left unchecked, this surge of free radicals induces oxidative stress, which can cause heart muscle cell death and heart injury as part of a condition known as ischemia/reperfusion injury.

Though scientists have long considered necrosis to be a passive, unavoidable form of cell death, recent studies have suggested that some forms of it happen in a highly regulated manner that could potentially be targeted for treatment. Little has been known about how this type of cell death is regulated, however, which is what prompted Cheng to take a closer look.

He and his team had previously screened more than 20,000 genes to look for ones that appeared to either suppress or promote necrotic cell death. One gene that stood out to them as warranting further study was PRKAR1A, which helps regulate PKA activity by encoding a protein known as PKA regulatory subunit R1alpha.

So the researchers conducted a series of experiments to validate whether the R1alpha protein can regulate necrotic cell death in a rodent model. They found that turning off the PRKAR1A gene increased cell death, both in cultured cells and in mice. Mice lacking the gene also had more heart injury and worse heart function after heart attack, as compared to wild-type mice.

Cheng explained that, under normal circumstances, the rapid increase of free radicals after heart attack treatment triggers the heart to launch its antioxidant defense system, the built-in protective mechanism that helps keep free radicals in check. What their new study findings suggest is that the antioxidant defense system cannot be launched as effectively when the R1alpha protein is removed from the heart, resulting in more oxidative stress, which leads to cell death and heart injury.

He explained that the R1alpha protein binds to another type of protein known as PKA catalytic subunits to keep PKA activity in check. When R1alpha is removed, the catalytic subunits are uncontrolled and PKA activity increases, which Cheng believes is what prevents the activation of the antioxidant defense system. This suggests that use of a small-molecule compound that selectively inhibits PKA activity could potentially block necrotic cell death and lead to better outcomes after heart attack treatment.

Though Cheng said he hoped their research would eventually allow them to test such a compound in an animal model, the next step they are pursuing is to determine whether there are other mechanisms by which PKA regulates necrotic cell death aside from the antioxidant defense system.

Doctors have hoped that antibiotics could benefit patients with chronic lung diseases, but a new study has found no benefit for patients with life-threatening idiopathic pulmonary fibrosis in preventing hospitalization or death.

While there were no statistical benefits for patients with the lung-scarring disease, the new research will prevent unnecessary antibiotic use that could contribute to the growing problem of antibiotic resistance. The nationwide clinical trial - believed to be the largest idiopathic pulmonary fibrosis trial ever conducted - also collected biological samples that will advance the understanding and treatment of the mysterious and ultimately fatal illness.

"We were certainly disappointed in the results. But we remain hopeful that in further downstream analyses, we may yet find groups of patients that were potentially benefiting. In the meantime, this study will make sure that no one takes antibiotics without need," said researcher Imre Noth, MD, the chief of UVA Health's Division of Pulmonary and Critical Care Medicine. "We did view the study as great success as an NIH [National Institutes of Health] initiative, in that the pragmatic design, without blinding patients to treatment, led to rapid enrollment, ahead of schedule and basically ahead of budget, showing that large studies can be accomplished in this uncommon disease."

About Idiopathic Pulmonary Fibrosis

In idiopathic pulmonary fibrosis, scar tissue builds up in the lungs over time, preventing them from supplying adequate oxygen to the body. It typically affects people over age 50, mostly men. Patients typically survive only two to five years after diagnosis, though some live much longer.

Doctors are uncertain what triggers idiopathic pulmonary fibrosis. ("Idiopathic" means "unknown cause.") However, environmental and genetic factors may play a part, as may lung infections.

Doctors also suspect that changes in the microorganisms that naturally live in our lungs may be a factor. Scientists have increasingly come to appreciate the importance of the tiny organisms that live in our bodies and on our skin. In idiopathic pulmonary fibrosis, the thinking goes, the natural state of the microorganisms in the lungs may become unbalanced - perhaps there are too many of one type or a general loss of variety. Lab work in mice has suggested that antimicrobials may be able to help fix the problem.

To see if antimicrobial treatments could benefit idiopathic pulmonary fibrosis, researchers at 35 sites around the country conducted a randomized clinical trial with volunteers age 40 or older. A total of 513 patients enrolled between August 2017 and June 2019. Half received antimicrobial drugs, choosing between co-trimoxazol or doxycycline, while the other half received the standard care.

After a median follow-up time of 12.7 months, there was no statistically significant benefit from the antimicrobials. The time to both breathing-related hospitalization or death was unchanged.

The findings echoed those of a previous study, and the researchers say the results show that treatment with antibiotics is ineffective and unwarranted as a general treatment for idiopathic pulmonary fibrosis. They do not rule out, however, that it may be useful in a limited number of patients with known disruptions to their lung microorganisms.

"As the largest single study in IPF ever conducted, I think we are going to learn a lot as we look at things more closely. Might our choice of antibiotics have been the right ones? Were there some patients that did better than others? Who should we be targeting for treatment? All things this study will help in the future," said Noth, a top expert on the disease. "I am heartened and hopeful moving forward as this study teaches us a lot for the next one, and each study gets us closer to better treatments and a cure."

(Carlisle, Pa.) -- A new study published in the American Journal of Lifestyle Medicine finds critical links between job loss and physical inactivity in young adults during the U.S. Great Recession of 2008-09 that can be crucial to understanding the role of adverse economic shocks on physical activity during the COVID-19 pandemic. It is the first study to examine how job losses during the Great Recession affected the physical activity of young adults in the United States.

The study by Dickinson College economist Shamma Alam and Harvard T. H. Chan School of Public Health economist Bijetri Bose looked at Panel Study of Income Dynamics (PSID) data for young adults age 18 to 27--a phase of development associated with maturation and significant social, psychological and economic changes. They found that job losses experienced by the individual during the Great Recession reduce the likelihood of physical exercise by a significant 6.3 percentage points. This as action plans established by the World Health Organization and United Nations call for a 10 percent reduction in physical inactivity by 2025 and 2030, respectively.

"Our study finds that young adults from the Great Recession, who form the core part of the millennial generation today, suffered from significantly lower physical activity, which typically leads to worse physical health outcomes such as increased obesity," said Alam. "The Great Recession--considered the longest since the Great Depression--presents enormous economic implications and lessons that are relevant for the current COVID-19 induced economic downturn."

While the Great Recession had a disproportionately high 19% unemployment rate among young adults, unemployment for young adults during the COVID-19 pandemic has been much higher, peaking in 2020 at approximately 33 percent for those age 16-19; 26 percent for those age 20-24; and 16 percent for those age 25-29. Additionally, according to Pew Research, young adults age 18-29 also have--more than any other age group-- used money from their savings or retirement account, borrowed money from friends or family and received unemployment benefits since the coronavirus hit in February 2020.

Alam suggested these known decreases in physical activity during significant economic downturns also could have implications for the mental health of young adults. "Physical activity significantly went down following job losses during a major recession like the Great Recession likely because of negative mental health outcomes suffered by the individuals. When individuals are worried about their jobs and livelihood, they do not feel like exercising. Therefore, we are likely to see similar effects on physical activity during the current COVID-19 induced recession," said Alam, adding that in addition to job losses, stay-at-home orders had negative effect on young adults' mental health, which may then negatively affect physical activity.

Professor Tetsuo Endoh's Group at Tohoku University's Center for Innovative Integrated Electronics has announced a new magnetic tunnel junction (MTJ) quad-technology that provides better endurance and reliable data retention - over 10 years - beyond the 1X nm generation.

This novel Quad technology meets the design requirements for the state-of-the-art X nm complementary metal-oxide semiconductor (CMOS) node and will pave the way for ultra-low-power consumption for Internet of Things (IoT) edge-devices in mobile communication, the automotive industry, consumer electronics, and industrial/infrastructure equipment.

The results will be presented in June at an international conference on semiconductor ultra-large scale integrated circuits entitled "2021 Symposia on VLSI Technology and Circuits." The conference takes place from June 13 to 19.

Developing smart societies through the use of the IoT, AI, and networks based on the next-generation mobile communication systems requires edge devices to be more power-efficient. A greater power efficiency also aids the goal of becoming carbon neutral.

Many logic circuits embedded with spin transfer-torque magnetoresistive random access memory (STT-MRAM) as a low power consumption technology. However, meeting the design rules of the X nm CMOS requires the MTJ diameter to be formed using the back end of line (BEOL) process and must fabricate at 1X nm generation.

The developed Quad-interface MTJ (Quad MTJ) - the first of its kind - has three new technologies: (i) a low RA technology, (ii) a low damping material in the recording layer, and (iii) a stable reference layer.

This enabled it to have (1) better retention characteristics of over 10 years, (2) endurance that exceeded at least 6 X 1011, (3) a high-speed write operation of 10 nanoseconds, (4) a low power consumption operation of 20%, and (5) a low write error rate combined with a circular diameter of 18 nm. Additionally, the Quad-MTJ has high retention and high endurance characteristics at a 10 ns high-speed operation. This is the first time in the world that severe conditions 1 - 5 have been realized at the 1X nm generation.

The 18nm Quad-MTJ possesses a large capacity STT-MRAM technology that is smaller than static random access memory (SRAM). As such, it is expected to replace SRAM for the X nm generation in CMOS logic. This means that STT-MRAM's application can expand to the leading-edge logic, achieving ultra-power consumption, excellent scalability and high reliability in application processors.

Treating patients with acute respiratory failure is a constant challenge in intensive care medicine. In most cases, the underlying cause is lung inflammation triggered by a bacterial infection or - more rarely, despite being frequently observed at present due to the corona pandemic - a viral infection. During the inflammation, cells of the immune system - the white blood cells - migrate to the lungs and fight the pathogens. At the same time, however, they also cause "collateral damage" in the lung tissue. If the inflammatory reaction is not resolved in time, this can result in chronic inflammation with permanent impairment of lung function. Together with colleagues from London, Madrid and Munich, a research team at the University of Münster headed by Prof Jan Rossaint and Prof Alexander Zarbock, two specialists in anaesthesiology and intensive care medicine, has gained new insight into the cellular processes involved in bacterial lung inflammation. In a study on mice, the researchers found that the interaction between platelets and certain white blood cells - the regulatory T cells - play a significant role in resolving the inflammation. The study has been published in the Journal of Experimental Medicine.

Platelets partner with regulatory T cells and send signals to scavenger cells

It was already known that, at the beginning of an inflammatory reaction in the lungs, as is the case with other organs, platelets work together with neutrophil granulocytes - a subgroup of white blood cells that specialize in fighting off pathogens. However, for the first time, the team of scientists has now shown that, as the inflammation progresses, platelets bind to regulatory T cells and that this binding is needed for the migration of the T cells, together with the platelets, to the site of inflammation in the lungs. Upon their arrival, they work together secreting anti-inflammatory messenger substances which "reprogramme" the macrophages in the lungs. These white blood cells, also known as scavenger cells, then stop directing neutrophil granulocytes to the site of inflammation, instead eliminating the neutrophil granulocytes that are no longer needed. This helps the inflammation subside and prevents further tissue damage.

Search for new therapy concepts

"When treating patients with acute lung failure, we have various measures we can take to support lung function and focus on combating the causative pathogens with antibiotics, for example," explains Jan Rossaint. "However, we lack other therapeutic options which can be used to target the causes and regulate the course of the inflammation." These latest investigations have provided a basis for such therapy concepts. In further steps, the researchers will examine whether the inflammatory mechanisms they observed in mice also occur in humans and look for starting points to test specific therapies.