Culture

LA JOLLA--Your lungs and airways need to be stretchy, sort of like balloons. Take a big breath, and they'll open right up.

Damaged lungs can't open properly. Patients with asthma, idiopathic pulmonary fibrosis and systemic sclerosis suffer from fibrosis and tissue remodeling, where a build-up of tissue and immune cells, and proteins that form a glue-like substance, keep the airways from expanding. As fibrosis gets worse, taking a breath feels like blowing up a balloon filled with concrete.

In a new study, researchers at La Jolla Institute for Immunology (LJI) report that a protein called TL1A drives fibrosis in several mouse models, triggering tissue remodeling, and making it harder for lungs and airways to function normally.

"Our new study suggests that TL1A and its receptor on cells could be targets for therapeutics aimed at reducing fibrosis and tissue remodeling in patients with severe lung disease," says LJI Professor Michael Croft, Ph.D., director of scientific affairs at LJI and senior author of the new study in The Journal of Immunology.

Croft's laboratory is focused on understanding the importance of a family of proteins, called tumor necrosis factors (TNF) and tumor necrosis factor receptors (TNFR), in inflammatory and autoimmune diseases. By investigating these molecules, researchers hope to track down the root causes of inflammation and stop tissue damage before it's too late.

Previous research had shown that a TNF protein called TL1A can act on immune cells involved in allergic reactions and drive those immune cells to make inflammatory molecules. The Croft Lab wondered--if TL1A leads to inflammation, could it contribute to fibrosis in the lungs?

For the new study, Croft and his colleagues used genetic and therapeutic interventions, tissue staining, and fluorescence imaging techniques to study protein interactions in mouse models of severe asthma, idiopathic pulmonary fibrosis and systemic sclerosis. They first discovered that TL1A acts directly on a receptor on cells in the lungs and bronchial tubes, which leads to fibrosis and tissue remodeling.

We're all familiar with the idea of tissue remodeling. When a wound on the skin heals, the new area of skin is sometimes shiner, darker or tougher than the skin around it. The tissue has been remodeled. When lungs and airways try to heal--in response to an asthma attack, for example-- the cells in the area also change. The damaged area accumulates cells called fibroblasts, which make several glue-like proteins, including collagen. Too much collagen makes the lungs and airways less elastic--and less functional.

As Croft describes it, tissue remodeling is like wound healing, "but wound healing that goes wrong and becomes so exaggerated that it blocks tissue from behaving in its normal way." With the new study, scientists now know that TL1A is driving this harmful remodeling in the lungs.

In addition to causing fibroblasts to make collagen, the researchers found that TL1A also helps fibroblasts to behave like smooth muscle cells. A thin layer of smooth muscle cells naturally lines the bronchial tubes allowing them to dilate and constrict, but a thick layer of these smooth muscle cells--that includes fibroblasts--will keep the airways from expanding and contracting normally, making it even hard for a patient to breathe.

The scientists then studied lung tissue remodeling in mice that lacked the receptor for TL1A, called DR3, or were given a reagent that blocked TL1A activity. These mice showed less lung remodeling, less collagen deposition and reduced smooth muscle mass in the lungs.

These animal model data may support recent research in humans. Researchers have found that patients with severe asthma have excessive production of TL1A. This could explain why these patients are more vulnerable to lung fibrosis and remodeling.

"This type of research needs to be expanded to really understand if there are subsets of patients with asthma or other inflammatory lung diseases who might express TL1A at higher levels than other patients--which could potentially guide future therapies for targeting TL1A to reduce remodeling and fibrosis," says Croft.

Going forward, Croft and his team plan to investigate how the DR3 receptor is expressed on tissue cells and whether it is affected by other inflammatory factors. They also want to know how active TL1A is in human patients and how many inflammatory activities the protein might be responsible for.

In the United States, individual state laws barring 18- to 20-year-olds from buying or possessing a handgun make little difference in the rate of homicides involving a gun by people in that age group, a new University of Washington study has found.

"The central issue is that there's a very high degree of informal access to firearms, such as through family members or illicit channels," said Caitlin Moe, the study's lead author and a PhD student in epidemiology in the UW School of Public Health. "And we can't address that kind of availability with age limits."

The UW study compared homicide rates involving firearms in this age group between five states that increased the minimum age to buy or possess a firearm higher than the nationwide limits set by the 1994 federal law and the 32 states that did not.

The five states were Massachusetts, Maryland, New Jersey, New York and Wyoming. With the exception of Wyoming, these states also increased the minimum age for possession of a handgun. (States that raised age limits before 1994 were not included. Washington was not included for this reason, and the initiative passed in 2018 increasing age limits became law after the study period, which was 1995 to 2017.)

In the study, published in JAMA Pediatrics, UW researchers found that rates of firearm homicides perpetrated by young adults aged 18 to 20 years old were not significantly different in the two groups of states.

Determining what laws do have an effect on homicide rates is paramount, she added, because of the roughly 275,000 homicides involving a firearm during the years studied nearly 36,000 were perpetrated by people in the study's age range. Because most handguns used in crimes by young adults are acquired from sources unlikely to be affected by age restrictions, "it is not surprising that we found no association" between state laws and homicides, the study said.

Also, Moe emphasized, firearms are the second leading cause of death of American youth, after motor vehicle crashes.

"It's incredibly important that we address this major cause of death in young people," said Moe, who is also affiliated with the Harborview Injury Prevention & Research Center. And that solution will need to be a country-wide, unified effort to address the "de facto availability" of firearms, especially among youth.

As Natsumi Hookabe snorkeled around Panama's Bocas del Toro archipelago, during the Smithsonian Tropical Research Institute's Training in Tropical Taxonomy program, she encountered an unusual ribbon worm or nemertean: large and dark colored, with numerous pale spots. It was her first field trip outside of Japan, so she wondered if it was a rare species or just one that she had never seen before.

Natsumi had been interested in worms since childhood, but when nemerteans were introduced during a university course, she was hooked.

"I was mesmerized by their body movement while crawling, which involves beautiful muscular waves," she recalled. "This led me to pursue nemertean biology for my bachelor's and master's degrees."

She then found out about the Training in Tropical Taxonomy workshop offered by the Smithsonian Tropical Research Institute (STRI) in Panama, and did not have to think for long before flying from Tokyo and plunging into the warm waters of the Caribbean in the Bocas del Toro archipelago.

The two-week course, supported by the U.S. National Science Foundation, teaches skills for the identification of understudied marine organisms, including nemerteans. It also offers an opportunity for students to make connections with other researchers from around the world.

"Hosting the courses has been a really fantastic way, not just to train the next generation of biodiversity researchers, but to also have the Bocas fauna carefully surveyed and identified by experts," said Rachel Collin, STRI staff scientist and director of the Bocas del Toro Research Station. "Over the years this has led to the discovery and description of many new species in Bocas del Toro. For some groups, Bocas has the most documented species for anywhere in the Caribbean."

During her stay in Bocas del Toro, Natsumi met Maycol Madrid, a biologist and assistant in Dr. Collin's lab. She quickly noted Maycol's deep knowledge about Japanese culture. In their spare time, they talked about Japanese manga, anime, and games and taught each other Japanese and Spanish words, respectively.

When Natsumi collected the unusual-looking nemertean, she knew she wanted to study it further in her lab in Japan, but this required sorting out a few bureaucratic processes. Maycol jumped in and lent his hand in getting the permissions to collect specimens, transportation to Japan, among other tasks.

All these efforts paid off: what seemed at first sight like a rare worm to Natsumi, turned out to be a new species of nemertean.

"Without Maycol's help, my trip would not have been as successful as it actually was," said Natsumi. "I really appreciate his sincere assistance throughout the period of my stay in Bocas."

She recently described the new species in the journal Marine Biodiversity, and named it Euborlasia maycoli sp. nov. after Maycol Madrid, as a token of appreciation for all his help. This new Panamanian species became the first Caribbean representative of the genus.

"For me it was a great surprise that Natsumi decided to name the new species of Euborlasia in my honor," said Maycol. "It fills me with great pleasure, knowing that I was somehow able to help Natsumi in the discovery of this new species."

Researchers have sequenced the genome of Alexander Fleming's penicillin mould for the first time and compared it to later versions.

Alexander Fleming famously discovered the first antibiotic, penicillin, in 1928 while working at St Mary's Hospital Medical School, which is now part of Imperial College London. The antibiotic was produced by a mould in the genus Penicillium that accidentally started growing in a Petri dish.

Now, researchers from Imperial College London, CABI and the University of Oxford have sequenced the genome of Fleming's original Penicillium strain using samples that were frozen alive more than fifty years ago.

The team also used the new genome to compare Fleming's mould with two strains of Penicillium from the US that are used to produce the antibiotic on an industrial scale. The results, published today in Scientific Reports, reveal that the UK and US strains use slightly different methods to produce penicillin, potentially suggesting new routes for industrial production.

Lead researcher Professor Timothy Barraclough, from the Department of Life Sciences at Imperial and the Department of Zoology at Oxford, said: "We originally set out to use Alexander Fleming's fungus for some different experiments, but we realised, to our surprise, that no-one had sequenced the genome of this original Penicillium, despite its historical significance to the field."

Although Fleming's mould is famous as the original source of penicillin, industrial production quickly moved to using fungus from mouldy cantaloupes in the US. From these natural beginnings, the Penicillium samples were artificially selected for strains that produce higher volumes of penicillin.

The team re-grew Fleming's original Penicillium from a frozen sample kept at the culture collection at CABI and extracted the DNA for sequencing. The resulting genome was compared to the previously published genomes of two industrial strains of Penicillium used later in the US.

The researchers looked in particular at two kinds of genes: those encoding the enzymes that the fungus uses to produce penicillin; and those that regulate the enzymes, for example by controlling how many enzymes are made.

In both the UK and US strains, the regulatory genes had the same genetic code, but the US strains had more copies of the regulatory genes, helping those strains produce more penicillin.

However, the genes coding for penicillin-producing enzymes differed between the strains isolated in the UK and US. The researchers say this shows that wild Penicillium in the UK and US evolved naturally to produce slightly different versions of these enzymes.

Moulds like Penicillium produce antibiotics to fight off microbes, and are in a constant arms race as microbes evolve ways to evade these defences. The UK and US strains likely evolved differently to adapt to their local microbes.

Microbial evolution is a big problem today, as many are becoming resistant to our antibiotics. Although the researchers say they don't yet know the consequences of the different enzyme sequences in the UK and US strains for the eventual antibiotic, they say it does raise the intriguing prospect of new ways to modify penicillin production.

First author Ayush Pathak, from the Department of Life Sciences at Imperial, said: "Our research could help inspire novel solutions to combatting antibiotic resistance. Industrial production of penicillin concentrated on the amount produced, and the steps used to artificially improve production led to changes in numbers of genes.

"But it is possible that industrial methods might have missed some solutions for optimising penicillin design, and we can learn from natural responses to the evolution of antibiotic resistance."

The COVID-19 pandemic has fired up interest in outdoor activities in our parks and forests. Now a new UBC study highlights the need to be mindful of how these activities may affect wildlife living in protected areas.

Researchers placed motion-activated cameras on the trails in and around the South Chilcotin Mountains Provincial Park in southwestern B.C., a region popular for its wildlife and recreational activities such as hiking, horseback riding, ATV riding and mountain biking. Overall, they found that environmental factors—like the elevation or the condition of the forest around a camera location—were generally more important than human activity in determining how often wildlife used the trails.

However, there were still significant impacts. Deeper analysis of trail use captured by the cameras showed that all wildlife tended to avoid places that were recently visited by recreational users. And they avoided mountain bikers and motorized vehicles significantly more than they did hikers and horseback riders.

The researchers focused on 13 species including grizzly bear, black bear, moose, mule deer and wolf.

“We wanted to better understand the relative impacts of human recreation in this region, given its increasing popularity. We already know that motorized vehicle access can disrupt wildlife; our initial findings suggest that other types of recreation may also be having impacts,” said study author Robin Naidoo, a UBC adjunct professor at the Institute for Resources, Environment and Sustainability.

Like many parks, the South Chilcotin Mountains provincial park and nearby regions are experiencing growing pressure from human activities—both recreational and industrial. According to Naidoo, the study confirms that camera traps can effectively monitor both wildlife and human trail use in these and other remote regions. “We’ll be able to collect more information over time and build a solid basis for research findings that can ultimately inform public policy,” he added

"Study co-author Cole Burton, a professor of forestry at UBC and the Canada Research Chair in terrestrial mammal conservation, says further research will be needed before any firm conclusions can be drawn.

“This is the first year of our multiyear study of the region. We’ll continue to observe and to analyze, so that we can better understand and mitigate the effects of these different human activities on wildlife,” said Burton. “Outdoor recreation and sustainable use of forest landscapes are important, but we need to balance them with potential disruption of the ecosystem and the loss of important species.”

Why are some tarantulas so vividly coloured? Scientists have puzzled over why these large, hairy spiders, active primarily during the evening and at night-time, would sport such vibrant blue and green colouration - especially as they were long thought to be unable to differentiate between colours, let alone possess true colour vision.

In a recent study, researchers from Yale-NUS College and Carnegie Mellon University (CMU) find support for new hypotheses: that these vibrant blue colours may be used to communicate between potential mates, while green colouration confers the ability to conceal among foliage. Their research also suggests that tarantulas are not as colour-blind as previously believed, and that these arachnids may be able to perceive the bright blue tones on their bodies. The study was published in Proceedings of the Royal Society B on 23 September, and is featured on the front cover of the current (30 September 2020) issue.

The research was jointly led by Dr Saoirse Foley from CMU, and Dr Vinod Kumar Saranathan, in collaboration with Dr William Piel, both from the Division of Science at Yale-NUS College. To understand the evolutionary basis of tarantula colouration, they surveyed the bodily expression of various opsins (light-sensitive proteins usually found in animal eyes) in tarantulas. They found, contrary to current assumptions, that most tarantulas have nearly an entire complement of opsins that are normally expressed in day-active spiders with good colour vision, such as the Peacock Spider.

These findings suggest that tarantulas, long thought to be colour-blind, can perceive the bright blue colours of other tarantulas. Using comparative phylogenetic analyses, the team reconstructed the colours of 110 million-year-old tarantula ancestors and found that they were most likely blue. They further found that blue colouration does not correlate with the ability to urticate or stridulate - both common defence mechanisms -- suggesting that it did not evolve as a means of deterring predators, but might instead be a means of attracting potential mates.

The team also found that the evolution of green colouration appears to depend on whether the species in question is arboreal (tree-dwelling), suggesting that this colour likely functions in camouflage.

"While the precise function of blueness remains unclear, our results suggest that tarantulas may be able to see these blue displays, so mate choice is a likely potential explanation. We have set an impetus for future projects to include a behavioural element to fully explore these hypotheses, and it is very exciting to consider how further studies will build upon our results," said Dr Foley.

The team's survey of the presence of blue and green colouration across tarantulas turned up more interesting results. They found that the blue colouration has been lost more frequently than it is gained across tarantulas. The losses are mainly in species living in the Americas and Oceania, while many of the gains are in the Old World (European, Asian, and African) species. They also found that green colouration has evolved only a few times, but never lost.

"Our finding that blueness was lost multiple times in the New World, while regained in the Old, is very intriguing. This leaves several fascinating avenues for future research, when considering how the ecological pressures in the New and the Old Worlds vary," said Dr Saranathan. "For instance, one hypothesis would be differences in the light environments of the habitats between the New and the Old World, which can affect how these colours might be perceived, if indeed they can be, as our results suggest."

A comprehensive search of genetic variation databases has revealed no significant differences across populations and ethnic groups in seven genes associated with viral entry of SARS-CoV-2.

African Americans and Latinos in the United States and ethnic minorities in the United Kingdom are disproportionately affected by COVID-19. They are more likely to develop severe symptoms and also show significantly higher mortality compared with other regional and ethnic groups.

To investigate if this disparity could be caused by genetic variation, a team of three researchers - including Assistant Professor Ji-Won Lee of Hokkaido University's Graduate School of Dental Medicine - surveyed publicly available databases of genomic variants, including gnomAD, the Korean Reference Genome Database, TogoVar (a Japanese genetic variation database) and the 1000 Genomes Project. They studied variants across multiple regional and ethnic groups in seven genes known to play roles in viral entry into host cells and recognition of viral RNA in host cells.

SARS-CoV-2 has spiked protein (S protein) on its envelope, which encloses the virus. Before the virus can enter host cells, the S protein has to bind with the ACE2 receptor on the cell surface. It is then broken into two pieces by the enzymes TMPRSS2 and cathepsin B and L. After the virus enters the cells, the viral RNA binds with proteins such as TLR3, TLR7 and TLR8, triggering an innate immune response.

According to the results, there were genetic variants in these seven proteins, with the largest number of variants in ACE2. However, very few of these variations alter the functions of these proteins. Since the overall variation frequency was extremely low (less than 0.01 percent), the scientists determined there is no significant difference across populations or ethnic groups in the functions of the seven proteins involved in infection.

The team's findings suggest that differences in morbidity and mortality are not the result of genetic variations in genes for viral entry across populations. Rather, it is more likely that preexisting medical conditions, individual medical histories, environmental factors and healthcare disparities play a significant role in affecting the morbidity and mortality of COVID-19. However, due to the limited size of the population databases used in this study, additional research using more diverse human genome databases is required. Additionally, other studies have shown that genetic factors may contribute to serious cases.

Philadelphia, September 24, 2020 - According to a new study in the Journal of the Academy of Nutrition and Dietetics, published by Elsevier, the percentage of heavy sugar-sweetened beverage (SSB) consumers - those who drink more than 500 calories of SSBs daily - trended downwards in the United States between 2003 and 2016. Among children, the percentage of heavy SSB consumers declined from 11 percent to 3 percent consistently across age group, sex, family income level, and most race/ethnicities. For adults, the percentage of heavy SSB consumers declined from about 13 percent to 9 percent overall, but there was variation among different age, sex, and racial/ethnic groups.

"Our study contributes important new evidence and insights to research on SSB consumption, and it tells a public health success story. The percentage of children and adults who are heavy sugary beverage drinkers has declined significantly, which is similar to trends in overall SSB consumption. Public health strategies to reduce excessive intake of sugary beverages appear to be working," said senior investigator Sara N. Bleich, PhD, Professor, Department of Health Policy and Management, Harvard T.H. Chan School of Public Health, Boston, MA, USA.

SSBs are widely consumed in the US, by about 60 percent of children and 50 percent of adults on a typical day, and they represent one of the largest sources of added sugar in the diet. Heavy sugary beverage drinkers are an important group to monitor since excessive intake is linked to chronic conditions like obesity and diabetes as well as cavities. In recent years, concern about excessive SSB consumption has been addressed through various strategies. For example, a number of cities and counties have imposed beverage taxes and passed several healthy beverage ordinances requiring restaurants to offer only healthy beverages with children's meals.

Studies looking at the changing consumption of sugary beverages have generally shown declines over the past decade. Unlike this study, however, little of the prior research has concentrated on heavy SSB drinkers, people who consume more than the equivalent of about 3.5 cans of soda daily.

The investigators used data from 2003 to 2016 for a sample of more than 20,000 children and 30,000 adults from the National Health Examination and Nutrition survey (NHANES), which provided a nationally representative look at beverage consumption for adults and children. In addition to looking at changes in consumption over time by heavy SSB consumers overall, the investigators looked at trends by age, sex, race/ethnicity, and family income level, as well as purchase and consumption locations.

The results showed that the percentage of heavy SSB drinkers has increased among people 60 years old and older, although the absolute percentage of heavy SSB consumers in this group was low. There was no significant change in the percentage of heavy SSB drinkers (no improvement) over the period among the 40-59-year old group and among non-Mexican Hispanic adults, while most other race/ethnicities experienced a decline (improvement). Finally, the investigators looked at the most recent years of data (2015-2016) and found that the majority of SSB calories consumed by heavy SSB drinkers were from stores and about half of the SSB calories were consumed at home.

First author Kelsey A. Vercammen, MSc, Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA, commented, "The insights gleaned from our study can help reduce consumption even further. Because the results zeroed in on several groups who showed no improvement or actually increased their intake, these can be used to better target interventions. Ongoing surveillance is also important to keeping these trends moving in the right direction."

Researchers at the Institut national de la recherche scientifique (INRS), in collaboration with American scientists, have uncovered a new parvovirus strategy for reaching the cell nucleus which is their site of replication.

This new method of entry is a good example of host-driven evolution. Their results were published in the journal Proceedings of the National Academy of Sciences of the United States of America. The parvoviruses are extremely contagious and persistent in the environment. They are transmitted mainly through the feces of a contaminated animal. They can infect invertebrates, vertebrates, mammals and humans. To reach the nucleus of host cells, parvoviruses use mostly enzymatic reactions. They are first absorbed by the cell inside a vesicle, a membrane compartment. To escape, parvoviruses activate a viral enzyme domain called phospholipase A2 (PLA2), a key mechanism discovered in 2001 by the same INRS laboratory.

However, some types of parvoviruses, as well as other nonenveloped viruses, do not have this enzyme domain and must therefore escape from the vesicle by some other means. Using molecular biology and structural studies, INRS researchers have discovered that a new virus targeting the giant tiger shrimp uses a more mechanical response. This type of parvovirus contains an inner pentamer helix bundle held together by calcium ions. When the microorganism is in the vesicle, where the calcium concentration is decreased by the elimination of toxic substances, the bundle is released and opens-up the protein shell (capsid) enclosing its genetic material and the membrane, allowing viral DNA to escape into the nucleus for replication.

“It turns out the incorporation of a PLA2 enzymatic domain is only one strategy, even as far as the family of parvoviruses is concerned. Here, we show yet a new strategy that may not be limited to one parvovirus lineage, but to other economically very important parvoviruses, such as parvoviruses of domestic fowl and farmed mink,” says Judit Pénzes, a former postdoctoral fellow at INRS and first author of the paper published on August 18, 2020.

A Host-Driven Evolution

INRS Professor Emeritus Peter Tijssen, lead author of the publication, raises another interesting point: the host-driven convergent evolution of this method of entry into the cell. “Two parvoviruses with different DNA sequences, which both targeting shrimps, have adopted similar strategies for reaching the nucleus,” he says.

Using a microscope nearly two floors high, the FEI Titan Krios, Judit Pénzes was able to solve the complete structure of the virus on a near-atomic scale. “You could already feel the energy rumbling through the enormous machine upon entering the facility. I think that it’s probably the same to what scientists involved in space exploration must have felt when they saw a rocket ready to lift off for the first time,” says the postdoctoral student.

Eventually, the discovery of this mechanism could lead to a better understanding of how viruses enter cells and even to a cure. “If we know how the parvovirus manages to release its DNA into the nucleus of the host cell, we can try to find a molecule to block this action,” concludes Professor Tijssen. The collaboration with the Florida-based research team will allow them to deepen the knowledge on this subject and possibly find other methods of entry that are yet unknown.

Researchers have shaken up a once accepted timeline for cataclysmic events in the early solar system. About 4.5 Ga (giga-anum, or billion years ago), as a large disc of dust and ice collapsed around our newly formed star, planets and smaller celestial bodies were formed. What followed was a chaotic and violent period of collisions and impacts as the familiar eight planets carved out their orbits to resemble the balanced system we observe today. Geological and geochemical records indicate that after about 600-700 million years after formation - but still early in the solar system's existence - the Earth-Moon system experienced a period of frequent and cataclysmic impacts from asteroids and other bodies. This period is dubbed the late heavy bombardment (LHB) period.

It was once thought that this period had a relatively sudden onset, but a research team at Hiroshima University and The University of Tokyo in Japan have found evidence that this bombardment period may have started much earlier, and decreased in intensity over time.

The team published their findings on August 26 in Earth and Planetary Science Letters.

"According to Apollo's lunar rock studies from the 1970s, the Earth, Moon, and the entire inner solar system are thought to have suffered from numerous meteoritical impacts at around 3.9 Ga. This event is regarded as a key process during the early evolution of our planet, said Mizuho Koike, an author of the study and an assistant professor from The Graduate School of Advanced Science and Engineering at Hiroshima University. "However, the validity of the LHB idea is being questioned recently. To settle this debate, a solid database of the 'impact ages' is required."

The team started building this database using rocks found on Earth that originated from a large, ancient asteroid, called Vesta, to see if they could corroborate the timeframe of the LHB period. If the solar system indeed experienced the LHB period roughly 3.9 Ga, Vesta, like Moon, would likely hold similar evidence of such an event around the same time period. What the team found was a record of impacts 300 to 500 million years earlier than expected.

"We found that the rocks from Vesta recorded the multiple impacts that occurred between 4.4 to 4.15 Ga, clearly earlier than the predicted peak of LHB at ~3.9 Ga. In contrast, no impact evidence was identified at 3.9 Ga or later. These findings suggest that Vesta (and probably other asteroids as well) did not record the LHB. Instead, they experienced massive impacts at the earlier stage," said Koike.

It is still unclear what this means for the LHB period as a whole, but Koike and her colleagues plan to further investigate the chronology of the early solar system.

"Our study reveals that the previously expected impact model was not correct, at least on Vesta," Koike said. "Extrapolating this to the wider solar system, the concept of LHB may not be appropriate to the planets' evolutions, including to the Earth and Moon. To verify such an examination, we are planning to investigate the impact histories on other asteroids and planetary materials by applying our present analytical techniques."

By doing so, the team may be able to add to their database and, ideally, peer with more clarity into our solar systems distant past.

Wolves today live and hunt in packs, which helps them take down large prey. But when did this group behavior evolve? An international research team has reported specimens of an ancestral wolf, Canis chihliensis, from the Ice Age of north China (~1.3 million years ago), with debilitating injuries to the jaws and leg. The wolf survived these injuries long enough to heal, supporting the likelihood of food-sharing and family care in this early canine.

"Top predators are rare in the fossil record because of their position in the food pyramid. Devastating injuries that are healed are even rarer. Fossils preserving grotesque injuries from the distant past have long fascinated paleontologists, and they tell stories rarely told," noted Dr. Xiaoming Wang, curator of vertebrate paleontology at the Natural History Museum of Los Angeles County, who co-led the study.

Dr. Haowen Tong, professor at the Institute of Vertebrate Paleontology and Paleoanthropology of the Chinese Academy of Sciences in Beijing, led the excavations that discovered the fossils in the Nihewan Basin, a well-known Ice Age site in northern China.

Based on its skeleton, C. chihliensis was a large canine with strongly built jaws and teeth specialized for eating meat and cracking bone. Injuries in the skeleton provide additional evidence for how the animal used to move and behave. The study represents the first known record of dental infection in C. chihliensis, likely incurred while crushing bone to reach the marrow inside, which modern wolves do when hunting prey larger than themselves.

One C. chihliensis also badly fractured its shin (tibia), splintering it into three parts. The injury must have incapacitated the wolf, an active predator that hunted by chasing prey--yet it survived, as evidenced by healing of the bone. Survival suggests that, while recovering, it procured food in some way other than by hunting--likely with the support of a pack.

To help interpret the injuries, the study also examined specimens of another extinct large canine: the dire wolf, Canis dirus, which has abundant fossils at the world-famous Rancho La Brea asphalt seeps in Los Angeles, California. The dire wolf was geologically younger than C. chihliensis, having lived at Rancho La Brea approximately 55,000 to 11,000 years ago. Despite the age difference, the dire wolf--which previous studies had established to have been a pursuit predator of large prey, with a social structure likely similar to grey wolves today--sustained injuries to the teeth, jaws, and legs similar to C. chihliensis.

"It is incredible to see these dental infections and fractured tibia from this early Chinese wolf--and find similar injuries in our dire wolves at Rancho La Brea," said Dr. Mairin Balisi, National Science Foundation postdoctoral research fellow at the La Brea Tar Pits and Museum, and co-author of the study. "Museum collections are valuable for many reasons. In this case, they've enabled us to observe shared behavior across species, across continents, across time."

The cell membrane, the wall-like boundary between the cell interior and its outside environment, is primarily made up of two kinds of biomolecules: lipids and proteins. Different lipid species closely pack together to form a double layer, or "bilayer," the membrane's fundamental structure, while proteins are embedded within or attached to the bilayer.

Membrane proteins are responsible for various important cellular activities, and their dysfunction can lead to serious health issues. Studying membrane protein structures and how they behave will help scientists better understand their connection to diseases and aid in developing therapeutics.

A team of researchers led by Vanderbilt University has recently shed light on how membrane proteins could be influenced by the lipids around them. By developing a novel type of membrane model, the scientists were able to show that the shape and behavior of a protein can be altered by exposure to different lipid compositions.

The researchers confirmed the artificial membrane's structure using x-ray and neutron scattering at the Department of Energy's (DOE's) Brookhaven (BNL) and Oak Ridge National Laboratories (ORNL). Their findings were published in the Journal of the American Chemical Society.

"This work showed that a protein can change quite profoundly in different membrane lipid environments, and we think this opens up a whole new area of research," said Charles Sanders, professor of biochemistry at Vanderbilt University and corresponding author of the new study.

Lipid layouts and cell membrane models

Cell membranes are composed of a variety of lipid molecules. Recently, studies have shown that certain lipids in cell membranes can come together to form clusters, also known as rafts. Some scientists suggest that rafts may move throughout the membrane and co-exist with ungrouped molecules. "A lipid raft is like a clique at a party," said Sanders. "They may move around the party, but it's always the same people talking to each other."

His lab is exploring how rafts might impact membrane proteins and cellular activities associated with them. In the new work, Sanders and a team of researchers have created a synthetic membrane capable of incorporating abundant quantities of two lipid molecules thought to make up rafts in cell membranes: cholesterol and sphingomyelin. Their approach involved developing disc-shaped biological structures, known as bicelles, that can produce a simplified model of a cell membrane's lipid bilayer.

"Cholesterol and sphingomyelin are ubiquitous in cell membranes but have not been present together in previous versions of bicelles," said John Katsaras, a biophysicist and neutron scattering scientist at ORNL and study co-author. "This new class of bicelles has a lipid composition that we believe is more biologically relevant."

Complementary techniques give comprehensive analysis

After developing the bicelles, the researchers used small-angle neutron and x-ray scattering techniques to precisely determine the material's shape and structural organization.

"It's really hard to confirm the actual morphology of bicelles. Small-angle neutron and small-angle x-ray scattering are the only ways to get a good overall characterization of these particles," said James Hutchison, a Vanderbilt University researcher and study co-author.

The team used a joint-access program for small-angle neutron and x-ray scattering that allows researchers to more conveniently request beam time at the Bio-SANS instrument at ORNL's High Flux Isotope Reactor (HFIR) and the Bio-SAXS instrument (LiX) at BNL's National Synchrotron Light Source II (NSLS-II).

Neutrons can detect light elements like hydrogen, whereas x-rays are more sensitive to heavier elements, which means each scattering technique can reveal unique information about the same material. By using both methods, the researchers built a more accurate model of the membrane system.

"Neutron and x-ray scattering are very complementary to each other," said Shuo Qian, a neutron scattering scientist at ORNL and study co-author. "Together, those techniques were able to provide a full picture of the bicelle structure."

Complementary bicelle measurements were also performed using transmission cryo-electron microscopy at Vanderbilt University.

Uncovering new protein properties

To assess how the new model membrane could be used to understand lipid composition and membrane protein relationships, the scientists introduced their bicelles to a well-studied protein fragment, referred to as C99. This fragment makes up one region of a membrane protein called amyloid precursor protein, which experts believe is connected to Alzheimer's disease.

Using various characterization methods, the team pinpointed differences in the protein fragment's structure and dynamics when embedded in the new membrane model. Notably, they observed the C99 fragments self-associate with one another in regions that had not previously been reported in other model membranes. The researchers hypothesize these newly uncovered binding sites could play a role in regulating other protein interactions with this fragment.

The team aims to run additional experiments to confirm whether the new bicelle system possesses a lipid raft environment. Scientists have already identified lipid raft properties in artificial vesicles, a spherical hollow biological structure that is enveloped by a lipid bilayer, but not in other small particles, such as bicelles

"There is no known non-vesicle small particle that has lipid raft-like properties," said Hutchison. "It would be a slam dunk to prove it."

At the south pole of Jupiter lurks a striking sight--even for a gas giant planet covered in colorful bands that sports a red spot larger than the earth. Down near the south pole of the planet, mostly hidden from the prying eyes of humans, is a collection of swirling storms arranged in an unusually geometric pattern.

Since they were first spotted by NASA's Juno space probe in 2019, the storms have presented something of a mystery to scientists. The storms are analogous to hurricanes on Earth. However, on our planet, hurricanes do not gather themselves at the poles and twirl around each other in the shape of a pentagon or hexagon, as do Jupiter's curious storms.

Now, a research team working in the lab of Andy Ingersoll, Caltech professor of planetary science, has discovered why Jupiter's storms behave so strangely. They did so using math derived from a proof written by Lord Kelvin, a British mathematical physicist and engineer, nearly 150 years ago.

Ingersoll, who was a member of the Juno team, says Jupiter's storms are remarkably similar to the ones that lash the East Coast of the United States every summer and fall, just on a much larger scale.

"If you went below the cloud tops, you would probably find liquid water rain drops, hail, and snow," he says. "The winds would be hurricane-force winds. Hurricanes on Earth are a good analog of the individual vortices within these arrangements we see on Jupiter, but there is nothing so stunningly beautiful here."

As on Earth, Jupiter's storms tend to form closer to the equator and then drift toward the poles. However, Earth's hurricanes and typhoons dissipate before they venture too far from the equator. Jupiter's just keep going until they reach the poles.

"The difference is that on the earth hurricanes run out of warm water and they run into continents," Ingersoll says. Jupiter has no land, "so there's much less friction because there's nothing to rub against. There's just more gas under the clouds. Jupiter also has heat left over from its formation that is comparable to the heat it gets from the sun, so the temperature difference between its equator and its poles is not as great as it is on Earth."

However, Ingersoll says, this explanation still does not account for the behavior of the storms once they reach Jupiter's south pole, which is unusual even compared to other gas giants. Saturn, which is also a gas giant, has one enormous storm at each of its poles, rather than a geometrically arranged collection of storms.

The answer to the mystery of why Jupiter has these geometric formations and other planets do not, Ingersoll and his colleagues discovered, could be found in the past, specifically in work conducted in 1878 by Alfred Mayer, an American physicist and Lord Kelvin. Mayer had placed floating circular magnets in a pool of water and observed that they would spontaneously arrange themselves into geometric configurations, similar to those seen on Jupiter, with shapes that depended on the number of magnets. Kelvin used Mayer's observations to develop a mathematical model to explain the magnets' behavior.

"Back in the 19th century, people were thinking about how spinning pieces of fluid would arrange themselves into polygons," Ingersoll says. "Although there were lots of laboratory studies of these fluid polygons, no one had thought of applying that to a planetary surface."

To do so, the research team used a set of equations known as the shallow-water equations to build a computer model of what might be happening on Jupiter, and began to run simulations.

"We wanted to explore the combination of parameters that makes these cyclones stable," says Cheng Li (Phd '17), lead author and 51 Pegasi b postdoctoral fellow at UC Berkeley. "There are established theories that predict that cyclones tend to merge at the pole due to the rotation of the planet and so we found in the initial trial runs."

Eventually, however, the team found that a Jupiter-like stable geometric arrangement of storms would form if the storms were each surrounded by a ring of winds that turned in the opposite direction from the spinning storms, or a so-called anticyclonic ring. The presence of anticyclonic rings causes the storms to repel each other, rather than merge.

Ingersoll says the research could help scientists better understand how weather on Earth behaves.

"Other planets provide a much wider range of behaviors than what you see on Earth," he says, "so you study the weather on other planets in order to stress-test your theories."

Paradox-free time travel is theoretically possible, according to the mathematical modelling of a prodigious University of Queensland undergraduate student.

Fourth-year Bachelor of Advanced Science (Honours) student Germain Tobar has been investigating the possibility of time travel, under the supervision of UQ physicist Dr Fabio Costa.

"Classical dynamics says if you know the state of a system at a particular time, this can tell us the entire history of the system," Mr Tobar said.

"This has a wide range of applications, from allowing us to send rockets to other planets and modelling how fluids flow.

"For example, if I know the current position and velocity of an object falling under the force of gravity, I can calculate where it will be at any time.

"However, Einstein's theory of general relativity predicts the existence of time loops or time travel - where an event can be both in the past and future of itself - theoretically turning the study of dynamics on its head."

Mr Tobar said a unified theory that could reconcile both traditional dynamics and Einstein's Theory of Relativity was the holy grail of physics.

"But the current science says both theories cannot both be true," he said.

"As physicists, we want to understand the Universe's most basic, underlying laws and for years I've puzzled on how the science of dynamics can square with Einstein's predictions.

"I wondered: "is time travel mathematically possible?"

Mr Tobar and Dr Costa say they have found a way to "square the numbers" and Dr Costa said the calculations could have fascinating consequences for science.

"The maths checks out - and the results are the stuff of science fiction," Dr Costa said.

"Say you travelled in time, in an attempt to stop COVID-19's patient zero from being exposed to the virus.

"However if you stopped that individual from becoming infected - that would eliminate the motivation for you to go back and stop the pandemic in the first place.

"This is a paradox - an inconsistency that often leads people to think that time travel cannot occur in our universe.

"Some physicists say it is possible, but logically it's hard to accept because that would affect our freedom to make any arbitrary action.

"It would mean you can time travel, but you cannot do anything that would cause a paradox to occur."

However the researchers say their work shows that neither of these conditions have to be the case, and it is possible for events to adjust themselves to be logically consistent with any action that the time traveller makes.

"In the coronavirus patient zero example, you might try and stop patient zero from becoming infected, but in doing so you would catch the virus and become patient zero, or someone else would," Mr Tobar said.

"No matter what you did, the salient events would just recalibrate around you.

"This would mean that - no matter your actions - the pandemic would occur, giving your younger self the motivation to go back and stop it.

"Try as you might to create a paradox, the events will always adjust themselves, to avoid any inconsistency.

"The range of mathematical processes we discovered show that time travel with free will is logically possible in our universe without any paradox."

New research presented at this year's annual meeting of the European Association for the Study of Diabetes (EASD), held online this year, shows the importance of good cardiovascular health in preventing type 2 diabetes (T2D) among middle-aged individuals, regardless of any genetic predisposition they may have towards developing the disease. The study was conducted by Kan Wang, Dr. Fariba Ahmadizar, and colleagues at the Department of Epidemiology, Erasmus University Medical Centre, Rotterdam, the Netherlands.

Data on the association between different CVH categories and lifetime risk of T2D are scarce. Besides, it remains unclear whether being genetically predisposed to T2D has a modifying effect on how CVH affects a person's odds of developing diabetes during their life.

The team used data from the prospective population-based Rotterdam Study to produce a CVH 'score' for each participant with 0 having the worst health status, and 12 having the best. Scores were calculated from measurements taken of body mass index, blood pressure, total cholesterol, smoking status, diet, and physical activity at the start of the study. Individuals were then placed into one of three categories according to their CVH score: poor (CVH score 0-5), intermediate (CVH score 6-7), and ideal (CVH score 8-12).

Genetic predisposition to T2D was quantified in the form of a Genetic Risk Score (GRS) derived from the 403 common genetic variants identified so far as being involved in determining susceptibility to T2D. The sample population was then divided into three equal-sized groups (tertiles) according to each participant's GRS, resulting in them being classed as low, medium, or high genetic risk. Incidence of T2D among the study population during the 17.8 years follow-up period was used by the researchers to estimate the remaining lifetime risk of developing T2D at 55, 65, and 75 years of age for each CVH category. Further analysis was undertaken to estimate lifetime T2D risk for each CVH category based on GRS status.

The sample population contained 5993 people free of T2D at baseline (average age 69.1 years, and 58% female). There were 2020 (33.7%) as ideal CVH, 2605 (43.5%) as intermediate CVH, and 1368 (22.8%) as poor CVH. A total of 869 participants went on to develop T2D in the 17.8 years follow-up period of the study.

The authors found that at age 55, the remaining lifetime risk of T2D was 22.6% for individuals classed as having ideal CVH, 28.3% for intermediate CVH, and 32.6% for poor CVH.

For individuals in each of the three GRS tertiles, the researchers then calculated the remaining lifetime risk of T2D at age 55 based on their CVH category. Those with the highest genetic risk had a likelihood of developing T2D of 23.5% if their CVH was ideal, 33.7% if they had intermediate CVH, and 38.7% when CVH was classed as poor.
The team found: "At age 55 years, more favourable CVH was associated with a lower lifetime risk for type 2 diabetes and was not counterbalanced by the genetic susceptibility for T2D."

They conclude: "Our results highlight the importance of favourable cardiovascular health in preventing T2D among middle-aged individuals regardless of their genetic predisposition."