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On April 28, a supermagnetized stellar remnant known as a magnetar blasted out a simultaneous mix of X-ray and radio signals never observed before. The flare-up included the first fast radio burst (FRB) ever seen from within our Milky Way galaxy and shows that magnetars can produce these mysterious and powerful radio blasts previously only seen in other galaxies.

"Before this event, a wide variety of scenarios could explain the origin of FRBs," said Chris Bochenek, a doctoral student in astrophysics at Caltech who led one study of the radio event. "While there may still be exciting twists in the story of FRBs in the future, for me, right now, I think it's fair to say that most FRBs come from magnetars until proven otherwise."

A magnetar is a type of isolated neutron star, the crushed, city-size remains of a star many times more massive than our Sun. What makes a magnetar so special is its intense magnetic field. The field can be 10 trillion times stronger than a refrigerator magnet's and up to a thousand times stronger than a typical neutron star's. This represents an enormous storehouse of energy that astronomers suspect powers magnetar outbursts.

The X-ray portion of the synchronous bursts was detected by several satellites, including NASA's Wind mission.

The radio component was discovered by the Canadian Hydrogen Intensity Mapping Experiment (CHIME), a radio telescope located at Dominion Radio Astrophysical Observatory in British Columbia and led by McGill University in Montreal, the University of British Columbia, and the University of Toronto.

A NASA-funded project called Survey for Transient Astronomical Radio Emission 2 (STARE2) also detected the radio burst seen by CHIME. Consisting of a trio of detectors in California and Utah and operated by Caltech and NASA's Jet Propulsion Laboratory in Southern California, STARE 2 is led by Bochenek, Shri Kulkarni at Caltech, and Konstantin Belov at JPL. They determined the burst's energy was comparable to FRBs.

By the time these bursts occurred, astronomers had already been monitoring their source for more than half a day.

Late on April 27, NASA's Neil Gehrels Swift Observatory spotted a new round of activity from a magnetar called SGR 1935+2154 (SGR 1935 for short) located in the constellation Vulpecula. It was the object's most prolific flare-up yet - a storm of rapid-fire X-ray bursts, each lasting less than a second. The storm, which raged for hours, was picked up at various times by Swift, NASA's Fermi Gamma-ray Space Telescope, and NASA's Neutron star Interior Composition Explorer (NICER), an X-ray telescope mounted on the International Space Station.

About 13 hours after the storm subsided, when the magnetar was out of view for Swift, Fermi and NICER, one special X-ray burst erupted. The blast was seen by the European Space Agency's INTEGRAL mission, the China National Space Administration's Huiyan X-ray satellite, and the Russian Konus instrument on Wind. As the half-second-long X-ray burst flared, CHIME and STARE2 detected the radio burst, which lasted only a thousandth of a second.

"The radio burst was far brighter than anything we had seen before, so we immediately knew it was an exciting event," said Paul Scholz, a researcher at the University of Toronto's Dunlap Institute for Astronomy & Astrophysics and a member of the CHIME/FRB Collaboration. "We've studied magnetars in our galaxy for decades, while FRBs are an extragalactic phenomenon whose origins have been a mystery. This event shows that the two phenomena are likely connected."

Papers from both the CHIME/FRB Collaboration and the STARE2 team were published on Nov. 4 in the journal Nature.

SGR 1935's distance remains poorly established, with estimates ranging from 14,000 to 41,000 light-years. Assuming it lies at the nearer end of this range, the X-ray portion of the simultaneous bursts carried as much energy as our Sun produces over a month. Intriguingly, however, it was not as powerful as some of the flares in the magnetar's storm eruption.

"The bursts seen by NICER and Fermi during the storm are clearly different in their spectral characteristics from the one associated with the radio blast," said George Younes, a researcher at George Washington University in Washington and the lead author of two papers analyzing the burst storm that are now undergoing peer review. "We attribute this difference to the location of the X-ray flare on the star's surface, with the FRB-associated burst likely occurring at or close to the magnetic pole. This may be key to understanding the origin of the exceptional radio signal."

SGR 1935's radio burst was thousands of times brighter than any radio emissions from magnetars in our galaxy. If this event had occurred in another galaxy, it would have been indistinguishable from some of the weaker FRBs observed.

In addition, the radio pulse arrived during an X-ray burst, something that has never before been seen in association with FRBs. Taken together, the observations strongly suggest that SGR 1935 produced the Milky Way's equivalent of an FRB, which means magnetars in other galaxies likely produce at least some of these signals.

For ironclad proof of the magnetar connection, researchers ideally would like to find an FRB outside of our galaxy that coincides with an X-ray burst from the same source. This combination may only be possible for nearby galaxies, which is why CHIME, STARE2 and NASA's high-energy satellites will keep watching the skies.

It is an experience we all share, as miraculous as it is mysterious. Birth.

Today, roughly one in three births in the United States occurs via cesarean section or C-section. In some other countries across the globe, like Brazil and Turkey, this percentage is even higher.

Yet little is known about how delivery by C-section affects an individual's long-term development.

As these interventions become more common in health care to foster positive outcomes for both mothers and babies, it is important to understand these long-term effects, both positive and negative, according to William Kenkel, an assistant professor of psychological and brain sciences at the University of Delaware.

Specifically, Kenkel is interested in understanding how different birth experiences, including vaginal delivery, emergency C-section and scheduled C-section, affect the developing nervous system. He also wants to know whether these changes occur through hormones that surge during birth.

"The body is set up in very redundant ways, and it reuses the same set of hormones for multiple things," said Kenkel, who studies the way hormones affect the brain to shape behavior.

This made Kenkel wonder if the disruption of these naturally occurring hormones during C-section could be a contributing factor in known health effects associated with cesarean. Previous peer-reviewed research, by multiple authors, has identified links between C-section and negative health outcomes in children, including obesity, asthma and autism. For example, studies have shown that delivery by C-section increases a child's risk for obesity by age 5 by an astounding 55%.

"We don't know why these links exist," he said. "Hormones provide a new way to look at these problems."

Understanding the body's stress response
During birth, hormones in the body surge in both mother and baby, sent along by the nervous system. These stress hormones are there to spur delivery and to help a baby adapt to living outside the womb. Some of the transitions babies accomplish at birth include starting to breathe, setting the body's internal temperature and responding to microbes passed along by the mother that help us regulate our immune system, digestion and more.

Looking across the research literature, however, Kenkel found that how one is born can have an effect on the amount of stress hormones released at the time of delivery. For example, vaginal delivery had the highest presence of birth signaling hormones, followed by emergency cesarean, then scheduled cesarean with the lowest levels.

He pointed out, too, that when babies are delivered by cesarean section, some of these normal hormonal signals are disrupted, or, in the case of scheduled C-section, never even started. How long these hormonal differences last remains unknown. This led Kenkel to question whether research should be looking at this more closely because these hormones acting in early life are capable of developmental programming, meaning they can cause permanent changes.

"Most likely there is a very broad, but shallow effect occurring," said Kenkel, who is among only a handful of researchers considering the hormonal implications of birth and the brain.

Other research, particularly related to a healthy microbiome, has focused on whether procedures should be used to reintroduce microbes that babies delivered by cesarean may have missed out on.

Kenkel wonders if the same idea could be used to introduce hormones in children that might not be activated by cesarean delivery. This is not necessarily a new idea. For example, premature infants are often given a hormone called cortisol to help the lungs mature.

"We may want to investigate whether doing a similar intervention makes sense in cesarean for any number of other hormones to get the body off on the right foot," he said.

While a lot of research has looked at the hormone oxytocin and whether or not it could play a role in the causes of autism, according to Kenkel, cesarean delivery and obstetric interventions more broadly, are all things that affect oxytocin signaling during this sensitive period around birth.

"There are times in our development where hormones have long-lasting consequences," said Kenkel. "For example, if I were to experience stress right now, I would generally recover quickly. In early life, however, we are sensitive because we are still trying to learn what the environment is going to be like. So, if my mom experienced high stress levels while I was in utero, that tells me that this environment that I'm going to be born into is a rough one, so I may want to change my development to anticipate that."

These hormones are versatile, too. Oxytocin is well known for its role in social bonding and helping mom bond with her baby, but evolution has found a lot of other uses for it. Oxytocin is also really good at regulating appetite, temperature and stress response.

"These seemingly disconnected aspects of life share connections using the same hormone; and when seemingly unrelated medical interventions affect those hormones, it can translate into surprising outcomes," he said.

If he can establish that hormones during birth play a long-lasting role in life, Kenkel said, it would lend evidence for research to explore possible interventions that could be applied at birth to ensure development that more closely resembles outcomes associated with a vaginal delivery.

Kenkel published his findings in a paper in the Journal of Neuroendocrinology.

He hopes the paper will open the door to new research ideas or directions in this area, particularly greater collaborative research between the fields of neuroscience and obstetrics, given the shared interest in hormone mechanisms and early life.

"At this stage of our understanding, we just need a lot more information," Kenkel said.

Support staff and Black and Latinx hospital employees with and without patient care responsibilities are at highest risk for SARS-CoV-2 infection in health care settings, a Rutgers study found.

After screening 3,904 employees and clinicians at a New Jersey hospital between late April and late June for the SARS-CoV-2 virus and for lgG-antibodies to the virus, whose presence suggests past recent infection, the study, published in the journal Open Forum Infectious Diseases, found that these employees are at higher risk than previously thought.

"The risk to workers in health care settings with little or no patient contact has attracted relatively little attention to date, but our results suggest potentially high infection rates in this group," said lead author Emily S. Barrett, an associate professor at Rutgers School of Public Health and a member of the Environmental and Occupational Health Sciences Institute. "By contrast and to our surprise, physicians, nurses and emergency medical technicians showed much lower infection rates."

Health care workers who live in highly impacted communities may have been susceptible to becoming infected outside of the hospital during the early surge of COVID-19, according to co-lead author Daniel B. Horton, an assistant professor at Rutgers Robert Wood Johnson Medical School and a member of the Institute for Health, Health Care Policy and Aging Research.

"In the early phase of the pandemic, support staff in the hospital may also have had less access to personal protective equipment or less enforcement of safety protocols," he said. "Going forward, as cases of COVID-19 in the hospital rise again, protecting these and all hospital workers from infection both in and out of the hospital is critical."

In the hospital-based study, researchers found that 13 participants tested positive for the virus and 374 tested positive for the antibody, which suggests recent past infection -- nearly 10 percent of those studied -- and that Black and Latinx workers had two times the odds of receiving a positive test for the virus or antibody compared to white workers.

Phlebotomists had the highest proportionate rate of positive tests--nearly 1 in 4 tested--followed by those employed in maintenance/housekeeping, dining/food services and interpersonal/support roles. By comparison, positivity rates were lower among doctors (7 percent) and nurses (9 percent).

Regardless of whether the infections originated in the hospital or in the community, Barrett said, the results suggest a need to enact safety protocols for hospital employees to protect the health care workforce from future waves of infection.

"The 40 percent of infected health care workers who reported having had no symptoms of infection could be a potential source of SARS-CoV-2 spread in hospitals even if their infections were initially acquired in the community," she said.

The very heart of inpatient care for psychiatric patients is socialization, group therapy, shared meals, and a standard two people per room. Then COVID-19 hit with the accompanying public health warnings to isolate, socially distance, and wear masks.

That sent clinicians and staff from The University of Texas Health Science Center at Houston (UTHealth) moving quickly to create a strategy for the UTHealth Harris County Psychiatric Center (UTHealth HCPC) that provided the best psychiatric care within a safe environment in the middle of an epic pandemic. That strategy was published in the October issue of Psychiatry Research.

"When COVID-19 began, we were left with the question of how to manage a highly infectious virus in a freestanding psychiatric hospital. There was no existing published guideline on how to do this," said first author Lokesh Shahani, MD, MPH, assistant professor in the Louis A. Faillace, MD, Department of Psychiatry and Behavioral Sciences at McGovern Medical School at UTHealth and chief medical officer of UTHealth HCPC.

The largest provider of inpatient psychiatric care in the Greater Houston area, the center is a 274-bed, safety-net hospital that provides care to around 9,000 patients each year. It is led by Executive Director Jair C. Soares, MD, PhD, senior author of the paper, and Pat R. Rutherford, Jr. Chair in Psychiatry in the Faillace Department of Psychiatry and Behavioral Sciences.

By mid-March, with rising Harris County cases, hospital leaders realized that the chances of a patient arriving who was infected with COVID-19 were rapidly growing.

"Our mission is to treat patients in the community who have psychiatric conditions and we didn't want to turn anyone away," said Stephen Glazier, COO of the hospital. "The only way to do that was to create an isolated COVID-19 unit."

To create the space, new patients were not admitted to that unit and remaining patients were moved into other units as spots became available. Glazier asked for volunteers willing to staff the unit day and night. Shahani, who is board certified in infectious disease as well as psychiatry, decided to lead the infection control initiative.

"I am honored to work alongside our dedicated nursing staff who stepped up and volunteered to take care of our COVID-19 patients," Shahani said. "Staff safety was our priority and we made sure everyone was trained in appropriately using PPE and had access to the same."

The team turned for advice and leadership from co-author Luis Ostrosky, MD, professor of infectious diseases at McGovern Medical School, and vice chair of Healthcare Quality at McGovern Medical School. "We had to keep staff safe as well as patients," Shahani said. "Being a part of UTHealth and able to consult with Dr. Ostrosky was invaluable for us."

Ostrosky is the COVID-19 Incident Commander for UTHealth. "COVID-19 continues to challenge the way we work. Knowledge acquisition and flexibility have been key in making changes and adapting to our new reality," Ostrosky said. "From transporting patients in helicopters, to figuring out waiting rooms, to making psychiatric care safe, UTHealth is here for our community's needs."

Complicating the process for the team were patients who refused to be tested for the coronavirus or understand why they had to wear a mask.

"In a medical hospital, patients are able to have a private room with attached bathroom, which we don't have, and they are tested for the virus. Psychiatric patients don't always consent for testing because of their severe mental illness, and 40% refused testing," Shahani said. "Wearing a face mask and adhering to hand hygiene are other measures needed to keep people safe, but people with chronic severe mental illness don't have the ability to always follow guidelines such as that."

The team decided to focus on screening for symptoms, fever, contact, and travel history. They used extreme caution: anyone who was suspected of having the virus was isolated.

The first test for the new unit came April 17 when an asymptomatic patient required isolation because of recent travel and exposure. Since then, over 100 patients have been treated in the COVID-19 unit, with 52% of them testing positive for the virus.

"We've had community partners who needed a safe place to treat patients and we have been able to step in and accept these patients," Shahani said. "We have been safely delivering psychiatric care during the pandemic."

"We could not be any prouder of the outstanding team of very committed, compassionate clinicians and staff we have at UTHealth HCPC," Soares said. "They stepped up to help us continue to function at very high levels through this unprecedented crisis with the pandemic."

GRAND RAPIDS, Mich. (Nov. 4, 2020) -- For the first time, scientists have visualized a new class of molecular gates that maintain pH balance within brain cells, a critical function that keeps cells alive and helps prevent stroke and other brain injuries.

These gates, called proton-activated chloride channels (PAC), nest within cell membranes and regulate the passage of small molecules called chloride ions into and out of cells. This allows cells to sense and respond to their environment.

"Proton-activated chloride channels have only recently been described but they are critical for cell survival, particularly in the brain," said Wei Lü, Ph.D., a Van Andel Institute assistant professor and co-corresponding author of the study, which was published today in Nature. "Our new images, coupled with our findings into how these channels work, provide much-needed molecular blueprints that will help answer long-standing questions in the field and provide new insights into how these channels may be therapeutically targeted in disease."

The images reveal a wedding bouquet-like structure, with parts that change configuration in response to environmental pH. When pH shifts from alkaline to acidic, a key pH sensor moves from its "resting" location and is inserted in an "acidic pocket," which signals that the gate allowing ions in and out of the cell should be open. This specific mechanism has never before been described.

This study is a collaboration between the Lü Lab at Van Andel Institute and a group led by Zhaozhu Qiu, Ph.D., an assistant professor at Johns Hopkins University School of Medicine and co-corresponding author of the paper. The Johns Hopkins team first reported the discovery of PAC in Science last year.

Solving PAC structures are another important, early step toward an understanding that may one day impact human health.

A new University of Colorado Boulder-led study sheds light on a protein key to controlling how cells grow, proliferate and function and long implicated in tumor development.

The findings, published this week in the journal Genes and Development, could lead not only to new therapies for hard-to-treat cancers, but also inform novel treatments for neurological diseases and rare developmental disorders, the authors say.

"These findings could have broad biomedical application," said lead author Dylan Taatjes, a professor in the Department of Biochemistry.

For decades, scientists have known that the protein Cyclin Dependent Kinase 7 (CDK7) plays an instrumental role in helping all cell types transcribe, or decode, the genetic instructions provided by their DNA.

As Taatjes explains, each cell contains the same vast library, or genome. But a kidney cell may turn to different sections of that library for instructions than, say, a skin cell or a heart cell. Like a librarian, CDK7 helps ensure that each cell accesses the right instructions at the right time, guiding which genes get flipped on and off.

While that's important during human development and for normal cell function, CDK7 can be exploited by cancer cells to drive runaway growth. In recent years, scientists have discovered that the protein can fuel certain cancers to proliferate out of control, including "triple negative" breast cancers, which are more aggressive and don't respond well to common treatments.

That finding has inspired growing interest in the development of so-called "CDK7-inhibitors" but due to a lack of understanding of what the CDK7 does, early clinical trials have been disappointing.

"We wanted to find out exactly how it's really working inside human cells," Taatjes said.

To that end, the Taatjes lab teamed up with scientists from two pharmaceutical companies, Syros and Paraza, as well as colleagues in other CU Boulder labs, the University of Colorado School of Medicine and the BioFrontiers Institute.

Using sophisticated analytical techniques, basic biochemistry and next-generation genetic sequencing, the team identified, for the first time, the hundreds of specific proteins that CDK7 switches on or off, providing unprecedented insight into its role in cells.

The study also revealed that:

CDK7 plays a role in multiple stages of transcription (decoding the genome), shaping what is known as "transcriptional splicing"--in which unneeded parts of the transcribed genome are pruned away to leave only those necessary for the cellular task at hand. Notably, errors in splicing have been linked to myriad diseases, including blood cancers.

CDK7 serves as a "master regulator" of other key enzymes, turning them on to further drive transcriptional programs. Defects in the execution of such programs have been linked to cognitive diseases, including Alzheimer's disease and rare developmental disorders, including head and facial deformities.

The function of CDK7 is controlled by the company it keeps. When attached to a larger 10-protein complex, known as TFIIH, it is largely inactive. But when it breaks off on its own, its activity ramps way up.

Phase 1 trials are currently underway administering the latest version of CDK7 inhibitors to drug-resistant breast, colorectal, lung, ovarian and pancreatic cancer patients.

The findings of the new study suggest such drugs hold promise, Taatjes said.

"In biology, it is widely recognized that cells will compensate by activating other enzymes if one specific enzyme is inhibited," he said, explaining the mechanism behind drug resistance. "Our results suggest that CDK7 inhibitors could have distinct therapeutic advantages, given that they would not only block CDK7, but would impact the function of other enzymes."

The research could also lead to next-generation therapeutics, which--instead of silencing the protein completely--would target it only in its liberated, most active phase. This could result in more selective inhibitors that would be less damaging to healthy cells, with fewer side effects.

And because of its many roles in shaping how human cells develop and function, other applications may be possible.

"Cancer is an obvious application but it is by no means the only one," Taatjes said.

The ability of SARS-CoV-2 to infect cells depends on interactions between the viral spike protein and the human cell surface protein ACE2. To enable the virus to hook onto the cell surface, the spike protein binds ACE2 using three finger-like protrusions, called the receptor binding domains (RBDs). Blocking the RBDs therefore has the potential to stop the virus from entering human cells. This can be done using antibodies.

Nanobodies, small antibodies found in camels and llamas, are promising as tools against viruses due to their high stability and small size. Although obtaining them from animals is time consuming, technological advances now allow for rapid selection of synthetic nanobodies, called sybodies. A technology platform to select sybodies from large synthetic libraries was recently developed in the lab of Markus Seeger at the University of Zurich, and made available for this study.

In search of the best sybody against SARS-CoV-2

EMBL Hamburg's Christian Löw group searched through the existing libraries to find sybodies that could block SARS-CoV-2 from infecting human cells. First, they used the viral spike protein's RBDs as bait to select those sybodies that bind to them. Next, they tested the selected sybodies according to their stability, effectiveness, and the precision of binding. Among the best binders, one called sybody 23 turned out to be particularly effective in blocking the RBDs.

To learn exactly how sybody 23 interacts with the viral RBDs, researchers in the group of Dmitri Svergun at EMBL Hamburg analysed the binding of sybody 23 to the RBDs by small-angle X-ray scattering. In addition, Martin Hällberg at CSSB and Karolinska Institutet used cryo-EM to determine the structure of the full SARS-CoV-2 spike bound to sybody 23. The RBDs switch between two positions: in the 'up' position the RBDs poke out, ready to bind ACE2; in the 'down' position they are furled to hide from the human immune system. The molecular structures revealed that sybody 23 binds RBDs in both 'up' and 'down' positions, and blocks the areas where ACE2 would normally bind. This ability to block RBDs regardless of their position might explain why sybody 23 is so effective.

Finally, to test if sybody 23 can neutralise a virus, the group of Ben Murrell at Karolinska Institutet used a different virus, called a lentivirus, modified such that it carried SARS-CoV-2's spike protein on its surface. They observed that sybody 23 successfully disabled the modified virus in vitro. Additional tests will be necessary to confirm whether this sybody could stop SARS-CoV-2 infection in the human body.

Scientific collaboration during lockdown

"The collaborative spirit has been enormous in these times, and everybody was motivated to contribute," says Christian Löw, one of the lead scientists in the study. The researchers started the project as soon as they received approval from EMBL leadership to reopen their laboratories during the COVID-19 lockdown. They managed to select the candidate sybodies and perform the analyses in just a few weeks.

"Getting the results so quickly was only possible because the methodologies we used had already been established for other research projects unrelated to SARS-CoV-2. Developing these tools would have taken significantly more time and resources," says Löw.

The results of this project hold out the promise of a potential way to treat COVID-19. In future work, the scientists will perform further analyses to confirm whether sybody 23 could be an effective COVID-19 treatment.

Nara, Japan - Mutants that reveal the secrets of how plants attack? No, it's not a scene from a science fiction movie, but you could be forgiven for thinking that. Instead, it's a scene from real life:

Researchers at Nara Institute of Science and Technology in Japan report in a new study in Science Advances that parasitic plants use the plant hormone ethylene as a signal to invade the roots of host plants.

To develop a successful parasitic relationship, parasitic plants form a specialized structure, the haustorium which attaches to and invades the host plant. The formation of haustoria is regulated by signal molecules derived from the host plant and allows the parasitic plant to absorb water, nutrients, and small materials from the host plant.

"To understand the genetic programs for haustorium development, we identified mutants that displayed haustorial defects on host invasion," says lead author of the study Songkui Cui. "Genome sequencing showed that these mutants have defective ethylene signaling, and it turned out that ethylene signaling genes are crucial for the parasitic plant to infect its host plant."

Ethylene is a gaseous plant hormone that is involved in fruit ripening, aging of leaves, and the formation of root nodules. Ethylene is also widely involved in plant interactions with viruses and numerous organisms, such as insects and bacteria, lending either resistance or susceptibility to plants depending on the types of pathogens.

"Our results indicate that ethylene mediates host recognition in parasitic plants for host invasion," explains project leader Satoko Yoshida. "This is the first time that the mediation of host invasion by parasitic plant genes has been identified via forward genetics. Our findings offer a new understanding of how a parasitic plant uses the ethylene molecule to tweak haustorium development and host invasion."

Forward genetics is used to identify genes, or sets of genes, that produce a particular characteristic in an organism. The model species used in this study is from a family of parasitic plants that includes destructive weeds. But the molecular basis for their parasitism has been largely unexplored until now.

"Our results suggest that parasitic plants have taken over ethylene signaling for parasitism at multiple stages of their life cycle, such as germination, haustorium growth termination, and host invasion. This knowledge could provide new ways to use ethylene and ethylene inhibitors to control a broader range of parasitic weeds, including those that don't rely entirely on hosts to complete their life cycle, by manipulating haustorial function," says Cui.

Fossilized jaw bone fragments of a rat-like creature found at the Petrified Forest National Park in Arizona last year by a Virginia Tech College of Science Ph.D. candidate are in fact a newly discovered 220-million-year-old species of cynodont or stem-mammal, a precursor of modern-day mammals.

The finding of this new species, Kataigidodon venetus, has been published today in the journal Biology Letters by lead author Ben Kligman, a doctoral student in the Department of Geosciences.

"This discovery sheds light on the geography and environment during the early evolution of mammals," Kligman said. "It also adds to evidence that humid climates played an important role in the early evolution of mammals and their closest relatives. Kataigidodon was living alongside dinosauromorphs and possibly early dinosaurs related to Coelophysis -- a small bipedal predator -- and Kataigidodon was possibly prey of these early dinosaurs and other predators like crocodylomorphs, small coyote-like quadrupedal predators related to living crocodiles."

Kligman added that finding a fossil that is part of Cynodontia, which includes close cousins of mammals, such as Kataigidodon, as well as true mammals, from Triassic rocks is an extremely rare event in North America. Prior to Kligman's discovery, the only other unambiguous cynodont fossil from the Late Triassic of western North America was the 1990 discovery of a braincase of Adelobasileus cromptoni in Texas. Note that 220 million years ago, modern day Arizona and Texas were located close to the equator, near the center of the supercontinent Pangaea. Kataigidodon would have been living in a lush tropical forest ecosystem.

Kligman made the discovery while working as a seasonal paleontologist at Petrified Forest National Park in 2019. The two fossil lower jaws of Kataigidodon were found in the Upper Triassic Chinle Formation. Because only the lower jaws were discovered and are quite small -- half an inch, the size of a medium grain of rice -- Kligman only has a semi-picture of how the creature looked, roughly 3.5 inches in total body size, minus the tail.

Along with the jawbone fossils, Kligman found incisor, canine, and complex-postcanine teeth, similar to modern day mammals. Given the pointed shape of its teeth and small body size, it likely fed on a diet of insects, Kligman added. (Why are jaw fossils commonly found, even among small specimens? According to Kligman, the fossil record is "biased" toward only preserving the largest and most robust bones in a skeleton. The other smaller or more fragile bones -- ribs, arms, feet -- disappear.)

Kligman carried out field work, specimen preparation, CT scanning, conception, and design of the study
and drafting of the manuscript. He added that he and his collaborators only discovered the fossils were of a new species after reviewing the CT scan dataset of the jaws and comparing it to other related species.

"It likely would have looked like a small rat or mouse. If you were to see it in person you would think it is a mammal," Kligman added. Does it have fur? Kligman and the researchers he worked with to identify and name the creature actually don't know. "Triassic cynodonts have not been found from geological settings which could preserve fur if it was there, but later nonmammalian cynodonts from the Jurassic had fur, so scientists assume that Triassic ones did also."

The name Kataigidodon venetus derives from the Greek words for thunderstorm, "kataigidos," and tooth, "odon," and the Latin word for blue, "venetus," all referring to the discovery location of Thunderstorm Ridge, and the blue color of the rocks at this site. Kligman didn't name the creature, though. That task fell to Hans Dieter-Sues, coauthor and curator of vertebrate paleontology at the Smithsonian National Museum.

Additional collaborators include Adam Marsh, park paleontologist at Petrified Forest National Park, who found the jaw fossils with Kligman, and Christian Sidor, an associate professor at the University of Washington's Department of Biology. The research was funded by the Petrified Forest Museum Association, the Friends of Petrified Forest National Park, and the Virginia Tech Department of Geosciences.

"This study exemplifies the idea that what we collect determines what we can say," said Michelle Stocker, an assistant professor of geosciences and Kligman's doctoral advisor. "Our hypotheses and interpretations of past life on Earth depend on the actual fossil materials that we have, and if our search images for finding fossils only focuses on large-bodied animals, we will miss those important small specimens that are key for understanding the diversification of many groups."

With Kataigidodon being only the second other unambiguous cynodont fossil from the Late Triassic found in western North America, could there be more new species out there waiting to be found?

Kligman said most likely. "We have preliminary evidence that more species of cynodonts are present in the same site as Kataigidodon, but we are hoping to find better fossils of them," he added.

A world-first study on the Great Barrier Reef shows crown-of-thorns starfish have the ability to find their own way home--a behaviour previously undocumented--but only if their neighbourhood is stocked with their favourite food: corals.

Australian researchers observed the starfish emerging from their shelters in the afternoons so they could feed on coral during the night before returning home at dawn.

"The crown-of-thorns starfish often partied all night, slept-in and only those with a well-stocked larder found their way home--so it's very much a teenager model of behaviour," said lead author Dr Scott Ling from the Institute for Marine and Antarctic Studies at the University of Tasmania.

"Their preferred prey is Acropora corals," said co-author Professor Morgan Pratchett from the ARC Centre of Excellence for Coral Reef Studies at James Cook University (CoralCoE at JCU). Acropora is an important coral species--for the past two million years they have been the building blocks of reefs across the world.

"When populations of Acropora dropped, the starfish didn't return home," Prof Pratchett said. "Their behaviour is directly linked to the local abundance of Acropora."

The results of the study show healthy reefs with a high cover of these corals may encourage crown-of-thorns aggregations and outbreaks. The outbreaks cause extensive, widespread and sustained coral loss throughout the Indo-Pacific region.

Similar examples of predator infestations driving environmental devastation include sea urchins overgrazing on kelp forests and coral reef fishes munching through patches of seagrass.

The researchers used in-situ time-lapse photography to track the movements of 58 starfish in the northern and southern Great Barrier Reef during an outbreak in 2015. In the absence of their preferred Acropora coral prey, starfish were typically homeless and instead roamed up to 20 metres per day.

"Unlike sea urchins that can switch diet once they overgraze kelp forests, results of the time-lapse monitoring indicate that the starfish will consume available Acropora and ultimately eat themselves out of house and home before dispersing in search of new feeding grounds," Dr Ling said.

Previous outbreaks on the Great Barrier Reef were recorded in 1962, 1979, 1993 and 2009. Though mass-coral bleaching due to global warming is now the greatest threat to coral reefs worldwide, the combined impact of mass-bleaching and crown-of-thorns outbreaks is potentially catastrophic for coral reefs.

"By better understanding the behaviour of these starfish we can help prevent and control their outbreaks, which will help alleviate the pressures on coral reefs," Prof Pratchett said.

Gentoo penguins should be reclassified as four separate species, say scientists at the Milner Centre for Evolution at the University of Bath, after analysing the genetic and physical differences between populations around the southern hemisphere.

The researchers say that counting them as four separate species will aid in their conservation because it will make it easier to monitor any decline in numbers.

Gentoo penguins, with the Latin name Pygoscelis papua, live in a range of latitudes in the southern hemisphere and are currently split into two subspecies, P. p. ellsworthi and P. p. papua.

The researchers suggest these two sub species should be raised to species level and two new species created, which they have named P. poncetii after the Australian seabird conservationist Sally Poncet, and P. taeniata in recognition of a former proposal for this name dating to the 1920s.

Their study, published in the journal Ecology and Evolution, looked at the genomes of populations living in the Falkland Islands and South Georgia in the southern Atlantic Ocean, the South Shetland Islands in the Antarctic and Kerguelen Islands in the Indian Ocean.

They used genome data to create an evolutionary tree to understand the relationship between the different populations. When they combined these data with measurements of museum specimens from each of the populations, they found clear morphological (physical) and genetic differences between the four populations.

Dr Jane Younger, Prize Fellow from the Milner Centre for Evolution at the University of Bath, led the study. She said: "For the first time, we've shown that these penguins are not only genetically distinct, but that they are also physically different too.

"Gentoos tend to stick close to their home colonies, and over hundreds of thousands of years have become geographically isolated from each other to the point where they don't interbreed with each other, even though they could easily swim the distance that separates them.

"The four species we propose live in quite different latitudes - for example P. ellsworthi lives on the Antarctic continent whereas P. poncetii, P. taeniata and P. papua live further north where conditions are milder, and so it's not that surprising that they have evolved to adapt to their different habitats."

PhD student Josh Tyler said: "They look very similar to the untrained eye, but when we measured their skeletons we found statistical differences in the lengths of their bones and the sizes and shape of their beaks.

"It's a similar story to giraffes, which were revealed in 2016 to be four genetically distinct species."

The scientists say that regarding the four populations as separate species, gives conservationists a better chance of protecting their diversity because if there's a decline in one of them it will change the threat status as defined by the IUCN Red List.

Dr Younger said: "Currently gentoo penguins are fairly stable in numbers, however there is some evidence of the northern populations moving further south as the climate gets warmer, so we need to watch them closely."

The proposed changes to the classification of gentoos will be reviewed by an international committee of scientists which will assess all the evidence in the scientific literature before the new taxonomy is accepted.

Investigations of deceased COVID-19 patients have shed light on possible lung damage caused by the virus.

The study, published today in The Lancet's eBioMedicine, by King's College London in collaboration with University of Trieste and the International Centre for Genetic Engineering and Biology in Italy, shows the unique characteristics to the SARS-CoV-2 virus and may explain why patients suffer from 'long COVID'.

Patients with COVID-19 can experience symptoms such as blood clotting and loss of smell and taste. Some who survive the infection can experience the effects of the disease for months - known as 'long COVID' - with a feeling of fatigue and lack of breath. There have been a limited number of studies that have analysed the organs of COVID-19 patients which means the characteristics of the disease are still largely unknown.

Researchers analysed the organs of 41 patients who died of COVID-19 at the University Hospital of Trieste, Italy, from February to April 2020, at the start of the pandemic. The team took lung, heart, liver, and kidney samples to examine the behaviour of the virus.

Findings show extensive lung damage in most cases, with patients experiencing profound disruption of the normal lung structure and the transformation of respiratory tissue into fibrotic material.

Almost 90% of patients showed two additional characteristics that were quite unique to COVID-19 compared to other forms of pneumonia. First, patients showed extensive blood clotting of the lung arteries and veins (thrombosis). Second, several lung cells were abnormally large and had many nuclei, resulting from the fusion of different cells into single large cells. This formation of fused cells (syncytia) is due to the viral spike protein, which the virus uses to enter the cell. When the protein is present on the surface of cells infected by the COVID-19 virus, it stimulates their fusion with other normal lung cells, which can be a cause for inflammation and thrombosis.

Additionally, research showed the long-term persistence of the viral genome in respiratory cells and in cells lining the blood vessels, along with the infected cell syncytia. The presence of these infected cells can cause the major structural changes observed in lungs, which can persist for several weeks or months and could eventually explain 'long COVID'.

The study found no overt signs of viral infection or prolonged inflammation detected in other organs.

Professor Mauro Giacca, at the British Heart Foundation Centre at King's College London, said: "These findings are very exciting. The findings indicate that COVID-19 is not simply a disease caused by the death of virus-infected cells but is likely the consequence of these abnormal cells persisting for long periods inside the lungs."

The team is now actively testing the effect of these abnormal cells on blood clotting and inflammation and are searching for new drugs that can block the viral spike protein which causes cells to fuse.

Over the course of only a century, humanity has made an observable impact on the genetic diversity of the lion population. That's the conclusion of a recently published study by Drs. Caitlin Curry and James Derr from the Texas A&M University College of Veterinary Medicine & Biomedical Sciences.

By comparing the DNA of lions today to lions from 100 years ago, they found that there is clear genetic evidence of recent population fragmentation, which is when groups of a species are isolated from each other. This fragmentation could ultimately have a long-term impact on the genetic health of the iconic species. The research was published in the journal Molecular Biology and Evolution.

"I was surprised at what we found -- surprised and disappointed, because it's not what I wanted to see," Derr said. "I really wanted to be able to tell everyone that the management we've been doing for the last 100 years is perfect and to keep doing what we've been doing and everything will be fine. But that's not the take-home lesson; unfortunately, that's not the story we can tell.

Curry and Derr started their study with one overarching question: Has the genetic structure of lion populations changed over the last 100 years?

There have been several studies on modern lions, so gathering data for the modern populations was straightforward. Curry pulled together DNA data from three previously published studies on lions that lived between 1990-2012.

The historical populations, against which they wanted to compare the modern lion DNA, provided more of a challenge. Fortunately, scientists have a way to turn back time. Many of those lion remains still reside perfectly preserved in collections around the world. Curry used DNA extracted from bones, teeth and hides of 143 lions that lived between 1880-1949 to create a historical population data set.

Both population data sets cover the same geographical range from India to Southern Africa where lions are found. Scientists call this type of analysis, comparing data from the same space at different times, a spatiotemporal study.

No Room To Roam

It has been understood for a long time that female lions tend to stay close to the pride in which they were born, while males travel great distances to find new prides. Therefore, males are almost exclusively responsible for the movement of genes in the population, which helps keep genetic diversity within the species high.

As the human population continues to rapidly grow across Africa and more and more barriers to lion movement have gone up in the form of cities, fences and farmland, male lions haven't been able to travel the distances they once could.

According to Curry, while lions are still genetically diverse right now, the results in the DNA were more pronounced than she expected.

"In the historical population, you couldn't easily identify where a lion was from based on its nuclear DNA. This is due to high historical levels of gene flow across the population," she said. "But in the modern population, you can determine the general area, or sub-population, for most of the lions. But, even with sub-populations being more isolated, the overall level of genetic diversity is still considered high across all lion populations."

Consequences Of Low Genetic Diversity

If lions are still generally genetically healthy today, then why does this matter?

"Over the last 100 years or so, we have restricted the natural movements of many species," Derr said. "This isolation leads to reduced gene flow and ultimately may result in reducing genetic diversity to a level that threatens the survival of local populations."

Perhaps the most well-known example of what happens with a lack of genetic diversity is another large cat, the African cheetah.

According to genetic analysis, scientists believe cheetahs have suffered two large bottleneck events, or events that lead to a rapid shrinking of the gene pool. When these events happen, it results in the breeding of closely related individuals in the population, or inbreeding, creating very low genetic diversity.

This has led to a current cheetah population that, even in the wild, struggles to fend off new diseases, has difficulty breeding, and faces other significant health problems.

A Story Of Hope

But that fate can still be avoided in lions, especially now that experts are armed with proof that lion populations have been significantly impacted by isolation and subdivision.

"This should not be a disheartening story but rather one of hope," Curry said. "Yes, we see a decrease in genetic diversity across lion populations over the past century. But, currently, compared with other mammalian species, lion genetic diversity is still considered high across all lion populations.

"With responsible management focused on giving prides enough space to breed and allowing males to move more freely between isolated pockets, it is possible to increase the genetic diversity and reduce population sub-division across lion populations."

There have been multiple reintroduction programs bringing lions back to areas where lions once roamed, and coexistence strategies are increasingly being integrated into wildlife conservation programs.

"The positive take-home message is now that we've documented this and we understand it, policies can be tailored to manage these populations differently," Derr said. "We know now that you can't treat all lions the same. Now we have the responsibility to manage these animals, and many other managed wildlife species, in ways that better reflects their current biology."

The advent of genome science has given researchers an unprecedented ability to understand the root causes of a host of conditions. Justin Cotney, assistant professor of genetics and genome sciences in the UConn School of Medicine, has used this technology to identify a suite of genes and regulatory elements critical to normal heart development.

In a paper published in the October issue of Circulation Research, Cotney outlines the importance of "hub genes" in heart development. Hub genes operate like the hub of a wheel; they serve as the center from which many other "spokes" radiate and follow their lead in terms of when and to what extent they are expressed.

By studying a massive dataset of 125,000 control patients' genomes amassed from other studies in the Genome Aggregation Database (gnomAD), Cotney and his team identified a set of genes and regulators critical for heart development. These genes experience infrequent mutations, leading the researchers to conclude they are important to healthy development.

"You can't be a normal, healthy human with a mutation in these genes," Cotney says.

The heart develops between the first four to eight weeks of embryonic development. The researchers isolated this timeframe and looked at which parts of the genome were active.

"If you want to understand how the heart is built, that's where you need to look," Cotney says.

The genome contains approximately three meters of DNA within the six-micrometer nucleus. This means the DNA must be tightly packed when it is not in use. The researchers used machine learning to determine which sections of the DNA unraveled during this timeframe as indicated by histone modifications.

Cotney's team identified more than 100,000 regulatory sequences that are active during human heart development. More than 13,000 of these, around 10% of the total, had never been annotated as active in any human tissue or developmental stage. Their analysis of these regulatory elements and gene expression implicated more than 200 novel genes for heart development many likely to involved in congenital heart defects.

"There's still a lot about the genome we don't know," Cotney says.

Since these genes are involved in heart-specific expression, they also play a key role in the development of congenital heart defects, one of the most common birth defects. Other studies of the genetic mechanisms responsible for congenital heart defects have highlighted other genes than the ones captured by Cotney's study.

"These genes were generally being ignored to date, but we're saying it's something people should pay attention to," Cotney says.

By flagging these genetic elements, clinicians looking at a congenital heart defect patient's genome can identify which parts of their genome are likely responsible for the condition.

It is unlikely a single mutation causes a congenital heart defect. These genes are part of gene expression networks meaning when a defect occurs, it is likely the result of several related mutations.

Other studies have shown disrupting a single regulator rarely has a noticeable effect on an organism. Many regulatory elements are redundant, so if one is switched off, the organism can still develop normally.

While scientists have developed a rich database on the genes implicated in craniofacial development, that kind of knowledge about the heart is sorely lacking, making Cotney's work a groundbreaking contribution to the science.

"It's really one of the most comprehensive studies of chromatin and gene expression during human heart development," Cotney says.

The researchers have filed a patent for their findings that can be useful for companies that use genetic screening to diagnose congenital heart defects. Until now, they have been looking at other genes which are less precise indicators of the underlying problems. Furthermore, the industry lacks agreement on which genes are most relevant.

"What we found is quite novel," Cotney says. "We think the combination of these genes will be important in the future for the diagnosis of congenital heart defects."

The next step for this research is to look at the affected population to see if these genes are mutated as the researchers predict they will be. The team will also conduct experiments mutating certain parts of the genome to determine the influence they have on development.

"I think we're just scratching the surface," Cotney says.

These findings also have implications for evolutionary research looking at the hearts of other organisms, as the heart is one of the most rapidly evolving organs.

"We knew the power of our method to pull out the relevant biological information," Cotney says. "All that information was missing."

LOGAN, UTAH, USA -- Plastic has become ubiquitous in modern life and its accumulation as waste in the environment is sounding warning bells for the health of humans and wildlife. In a recent study, Utah State University scientist Janice Brahney cited alarming amounts of microplastics in the nation's national parks and wilderness areas.

Bioengineers around the world are working to develop plastic-eating "super" enzymes that can break down the man-made material's molecular structure faster to aid recycling efforts. In another research effort published in 2019, entomologists noted leaf-cutter bees were using plastic waste to construct their nests. The researchers suggested such behavior could be an "ecologically adaptive trait" and a beneficial recycling effort.

Not so fast, says USU evolutionary ecologist Joseph Wilson. Just because bees can use plastic, doesn't mean they should.

Wilson and undergraduate researcher Sussy Jones, along with colleagues Scott McCleve, a naturalist and retired math teacher in Douglas, Arizona, and USU alum and New Mexico-based independent scientist Olivia Carril '00, MS'06, jointly authored an observational paper in the Oct. 9, 2020 issue of 'Science Matters', exploring the nest building behavior of bees in the genus Megachile.

"Leaf-cutter bees are among the most recognizable of solitary bees, because of their habit of cutting circles out of leaves to build their cylindrical nests," says Wilson, associate professor of biology at USU-Tooele. "We've heard reports of these bees using plastic, especially plastic flagging primarily in construction and agriculture, and we decided to investigate."

The researchers don't yet know how widespread the use of plastic by leaf-cutter bees is and they also know little about plastic's effects on the insects.

"Building from plastic could change the dynamics and environment of the bee's nest cells, because plastic doesn't breathe like natural materials," says Wilson, who produced a video about the phenomenon. "In the 1970s, some researcher let leaf-cutter bees nest in plastic straws and found ninety percent of the bees' offspring died because of fungal growth. The plastic sealed in the moisture and didn't allow gas exchange."

To deter bees' use of flagging, Wilson suggests use of fabric ribbons made from natural fibers.

"These materials are biodegradable and, if used by bees, will likely avoid the harmful moisture-capturing effects of plastic," he says.