Culture

More than a year into the pandemic, the disproportionate burden of COVID-19 among racial and ethnic minorities in the US has been well documented. But a new study by Boston University School of Public Health (BUSPH) reveals that previous research has underestimated the true extent of racial disparities in COVID-19 deaths--as well as the extent to which structural racism contributes to these deaths.

Published in the Journal of Racial and Ethnic Health Disparities, the paper is the first to quantify the state-level differences in racial disparities in COVID-19 mortality among Black and White populations, using directly standardized, age-adjusted death rates. When comparing these age-adjusted rates, the study found that the Black-White disparity in COVID-19 mortality rates across states was substantially greater than what has previously been reported.

Until now, few studies on COVID-19 deaths have taken the age distribution of different populations into account, or explicitly compared race-specific mortality rates at the state level. But age is perhaps the single most important predictor of COVID-19 mortality, says study lead author Dr. Michael Siegel, professor of community health sciences at BUSPH. Different racial and ethnic groups have different age distributions, and comparing crude COVID death rates instead of age-adjusted rates can be misleading, he says.

"Because of structural racism, chronic diseases are much more common among the Black population compared to the White population, and for this reason, life expectancy for Black people is substantially less than that for White people," says Siegel. The shorter life expectancy means that the Black population of a state is going to be considerably younger than the White population for that state, he says.

"If you ignore this fact, then it is going to appear that the COVID death rate is much higher among the White population because there are so many more older people," Siegel says. "To get an accurate idea of the true disparity in death rates, you need to compare the COVID death risk of Black people and White people in a state at the same age."

The study is also the first paper to measure structural racism at the state level, and model this racism as a direct, quantifiable predictor of racial disparities in COVID-19 deaths across states.

Siegel and a team of researchers used data from the Centers for Disease Control and Prevention to calculate both crude and age-adjusted COVID-19 mortality rates for non-Hispanic White and non-Hispanic Black populations in 35 states. Then they compared these age-adjusted rates in order to quantify the racial disparity in mortality rates. Using linear regression analyses, they examined the potential relationship between a previously defined structural racism index and the racial disparity in COVID-19 mortality. The team also utilized linear regression analysis to explore potential mediating effects of exposure based on occupation, prevalence of underlying conditions, and disparities in healthcare access. This analysis yielded the following key findings:

For all 35 states, the Black-White disparity in COVID-19 mortality rates was substantially greater when examining age-adjusted rates compared to crude rates. Thus, relying on crude death rates severely underestimates the true magnitude of the Black-White disparity in COVID-19 mortality rates.

A high level of structural racism was a robust predictor of increased racial disparities in COVID deaths. All 35 states showed a pattern of increasing racial disparities as the state structural racism index increased.

The five states with the highest structural racism indices had an average disparity ratio of 2.7, compared to 2.1 for the five states with the lowest racism indices.

Structural racism appears to be a root cause of the Black-White disparity in COVID-19 mortality.

"Even if we could somehow equalize comorbidities between the White and Black populations, our results suggest that the racial disparity in COVID-19 death rates would still persist," says Siegel. "These findings suggest that the only way to fully address the consequences of structural racism is to dismantle structural racism itself."

(Boston)--Researchers from Boston University School of Medicine (BUSM) report the formation of human cells containing a green fluorescent protein or GFP (one of the most important proteins in biology and fluorescence imaging) genetically fused with two interferon stimulated genes (ISGs), namely Viperin and ISG15. This new creation makes these cells highly valuable reagents for reporting innate immune responses to viral infections, including those caused by coronaviruses.

These engineered cells, which turn green when treated with interferon, are highly novel because this is the first time a reporter gene (a gene that enables the detection or measurement of gene expression), such as GFP, has been inserted into endogenous loci of ISGs.

Viral infections cause human cells to sound a biochemical alarm via interferon signaling, leading to a high-level expression of ISGs. However, ISGs are very tightly regulated genes, because too much expression and an inability to later tamp down ISG levels can be just as detrimental to cellular health.

This overactive innate immune signaling leads to a 'cytokine storm' (when an infection triggers the immune system to flood your bloodstream with inflammatory proteins called cytokines) that distinguishes a mild case of virus infection from fully debilitating symptoms, an outcome all too prevalent in the COVID19 pandemic. "Better research tools for studying ISG regulation are still needed, not just now for coronavirus research but for many other viruses that our society will contend with," explained co-corresponding author Nelson Lau, PhD, associate professor of biochemistry at BUSM.

In order to successfully tag human antiviral genes with GFP, the researchers first needed to produce a new methodology for creating a long DNA repair template for more efficient and authentic CRISPR-Cas9 genome editing in animal cells. They named his template methodology the BL3SSO (sounds like "blasso") because it sets up the DNA for more accurate repair and for introduction of a fluorescent transgene like GFP into the site cut by Cas-9 during genome editing.

These findings are the result of a collaboration between the Lau lab and the lab of Mohsan Saeed, PhD, both faculty members in BUSM's department of biochemistry and investigators at the BU National Emerging Infectious Diseases Laboratories (NEIDL).

These findings appear online in the journal G3: Genes | Genomes | Genetics.

A filter made from polymer nanothreads blew three kinds of commercial masks out of the water by capturing 99.9% of coronavirus aerosols in an experiment.

"Our work is the first study to use coronavirus aerosols for evaluating filtration efficiency of face masks and air filters," said corresponding author Yun Shen, a UC Riverside assistant professor of chemical and environmental engineering. "Previous studies have used surrogates of saline solution, polystyrene beads, and bacteriophages -- a group of viruses that infect bacteria."

The study, led by engineers at UC Riverside and The George Washington University, compared the effectiveness of surgical and cotton masks, a neck gaiter, and electrospun nanofiber membranes at removing coronavirus aerosols to prevent airborne transmission. The cotton mask and neck gaiter only removed about 45%-73% of the aerosols. The surgical mask did much better, removing 98% of coronavirus aerosols. But the nanofiber filter removed almost all of the coronavirus aerosols.

The World Health Organization and Centers for Disease Control have both recognized aerosols as a major mechanism of COVID-19 virus transmission. Aerosols are tiny particles of water or other matter that can remain suspended in air for long periods of time and are small enough to penetrate the respiratory system.

People release aerosols whenever they breathe, cough, talk, shout, or sing. If they are infected with COVID-19, these aerosols can also contain the virus. Inhaling a sufficient quantity of coronavirus-laden aerosols can make people sick. Efforts to curb aerosol spread of COVID-19 focus on minimizing individual exposure and reducing the overall quantity of aerosols in an environment by asking people to wear masks and by improving indoor ventilation and air filtration systems.

Studying a contagious new virus is dangerous and done in labs with the highest biosecurity ratings, which are relatively rare. To date, all studies during the pandemic on mask or filter efficiency have used other materials thought to mimic the size and behavior of coronavirus aerosols. The new study improved on this by testing both aerosolized saline solution and an aerosol that contained a coronavirus in the same family as the virus that causes COVID-19, but only infects mice.

Shen and George Washington University colleague Danmeng Shuai produced a nanofiber filter by sending a high electrical voltage through a drop of liquid polyvinylidene fluoride to spin threads about 300 nanometers in diameter -- about 167 times thinner than a human hair. The process created pores only a couple of micrometers in diameter on the nanofiber's surfaces, which helped them capture 99.9% of coronavirus aerosols.

The production technique, known as electrospinning, is cost effective and could be used to mass produce nanofiber filters for personal protective equipment and air filtration systems. Electrospinning also leaves the nanofibers with an electrostatic charge that enhances their ability to capture aerosols, and their high porosity makes it easier to breathe wearing electrospun nanofiber filters.

"Electrospinning can advance the design and fabrication of face masks and air filters," said Shen. "Developing new masks and air filters by electrospinning is promising because of its high performance in filtration, economic feasibility, and scalability, and it can meet on-site needs of the masks and air filters."

Nearly 15 percent of the U.S. population experiences migraine. One subtype of migraine that is not well understood is migraine with aura (MA). Individuals who experience MA often see flashing lights, blind spots, or jagged lines in their visual field prior to onset of their migraine headaches. Individuals who experience MA also face a heightened risk of stroke and cardiovascular disease, although scientists continue to explore why this correlation exists. In a new study from Brigham and Women's Hospital, researchers used a technique in genetic analysis termed Mendelian randomization to examine 12 coagulation measures, uncovering four that are associated with migraine susceptibility. Interestingly, scientists only observed these associations in individuals who experience MA and did not observe such associations among individuals who experience migraine without aura (MO). Their research suggests that these hemostatic factors could potentially have a causal role in MA. Their results are published in Neurology.

"We've always wanted to know why people with MA have this higher risk of stroke and other cardiovascular diseases," said corresponding author Daniel Chasman, PhD, of the Division of Preventive Medicine at the Brigham. "This study offers promising leads specific to MA. Finding a possible cause for migraine with aura has been an outstanding question in the field for a long time."

There has been speculation in the field about relationships between coagulation and migraine susceptibility for some time, but previous research has been largely inconclusive. Most individuals first experience migraine at a young age for example, during childhood or young adulthood. Because previous study designs included only middle-aged and older adults, investigators have questioned whether coagulation causes migraine or if causality exists between these two elements at all. In this study, leveraging Mendelian randomization, which can support or refute potential causal effects on a health outcome, scientists for the first time found evidence that hemostatic factors may contribute to risk of MA.

"Even if we see an association between migraine and these coagulation factors when we measure both factors in a population at the same time, we still wonder: Which one came first?" said co-author Pamela Rist, ScD, of the Division of Preventive Medicine at the Brigham. "One of the interesting parts of Mendelian randomization is that it allows you to examine potential causality."

Researchers used summary statistics from decades of previously collected data from individuals who experience migraine and individuals who do not experience migraine. Because the diagnostic criteria are different for MA versus MO, they could examine these two conditions separately.

Investigators found a strong association between four coagulation factors and migraine susceptibility. They observed that genetically increased levels of three blood clotting factors: coagulation factor VIII, von Willebrand factor, and phosphorylated fibrinopeptide A, and genetically decreased levels of fibrinogen (a protein important in the late stages of the blood clotting process) were all associated, in part, with migraine susceptibility. Interestingly, scientists did not find this association among individuals who experience migraine without aura (MO), indicating a specific relationship between these hemostatic factors and MA.

Scientists note that Mendelian randomization has its limitations. In the future, researchers could examine if the causal associations implied by genetics can be observed in clinical practice.

"It is very exciting that by using Mendelian randomization we were able to show that hemostatic factors are associated with MA," said first author Yanjun Guo, MD, PhD of the Division of Preventative Medicine at the Brigham. "And because in the observational studies we saw that MA patients have a higher risk of stroke, these findings may reveal a potential connection between MA and stroke."

ITHACA, N.Y. - While examining the prevalence of listeria in agricultural soil throughout the U.S., Cornell University food scientists have stumbled upon five previously unknown and novel relatives of the bacteria.

The discovery, researchers said, will help food facilities identify potential growth niches that until now, may have been overlooked - thus improving food safety.

"This research increases the set of listeria species monitored in food production environments," said lead author Catharine R. Carlin, a doctoral student in food science. "Expanding the knowledge base to understand the diversity of listeria will save the commercial food world confusion and errors, as well as prevent contamination, explain false positives and thwart foodborne outbreaks."

One of the novel species, L. immobilis, lacked motility, or the ability to move. Listeria move a lot. Among scientists, motility was thought to be common among listeria closely related to L. monocytogenes, a well-known foodborne pathogen - and used as a key test in listeria detection methods. This discovery effectively calls for a rewrite of the standard identification protocols issued by food safety regulators, Carlin said.

As listeria species are often found co-existing in environments that support the growth of L. monocytogenes, food facilities will monitor for all listeria species to verify their sanitation practices.

Listeria monocytogenes can have profound pathogenic influence on food processing plants and those plants must be kept clean. Listeriosis has a mortality rate of 20% to 30% - even with a patient taking antibiotics, according to the U.S. Food and Drug Administration.

The Centers for Disease Control and Prevention estimate that 1,600 people in the U.S. get listeriosis annually and nearly 260 die.

"This paper describes some unique characteristics of listeria species that are closely related to listeria monocytogenes, which will be important from an evolutionary perspective and from a practical standpoint for the food industry," said co-author Martin Wiedmann, the professor in food safety and food science. "Likely, some tests will need to be re-evaluated."

Understanding the different listeria species is key to comprehending their similarities. "This will help us to get better about identifying listeria monocytogenes," Wiedmann said, "and not misidentifying it as something else."

Since 2010, Wiedmann's research group has discovered 13 of the 26 species classified in the genus listeria.

"When you're inspecting the environments of food processing plants or restaurants, you need to know the pathogenic listeria from the non-pathogenic species," Wiedmann said. "You need to tell the good guys from the bad guys."

In quiet moments, the brain likes to wander—to the events of tomorrow, an unpaid bill, an upcoming vacation.

Despite little external stimulation in these instances, a part of the brain called the default mode network (DMN) is hard at work. "These regions seem to be active when people aren't asked to do anything in particular, as opposed to being asked to do something cognitively," says Penn neuroscientist Joseph Kable.

Though the field has long suspected that this neural network plays a role in imagining the future, precisely how it works hadn't been fully understood. Now, research from Kable and two former graduate students in his lab, Trishala Parthasarathi, associate director of scientific services at OrtleyBio, and Sangil Lee, a postdoc at University of California, Berkeley, sheds light on the matter.

In a paper published in the Journal of Neuroscience, the research team discovered that, when it comes to imagining the future, the default mode network actually splits into two complementary parts. One helps create and predict the imagined event, what the researchers call the "constructive" function. The other assesses whether that newly constructed event is positive or negative, what they call the "evaluative" function.

"It's a neat division," says Kable. "When psychologists talk about why humans have the ability to imagine the future, usually it's so we can decide what to do, plan, make decisions. But a critical function is the evaluative function; it's not just about coming up with a possibility but also evaluating it as good or bad."

Building on previous work

The DMN itself includes the ventromedial prefrontal cortex, posterior cingulate cortex, and regions in the medial temporal and parietal lobes, such as the hippocampus. It's aptly named, Kable says. "When you put people into a brain scanner and ask them to not do anything, to just sit there, these are the brain regions that seem to be active," he says.

Previous research had revealed which areas make up the DMN and that constructing and evaluating imagined events activates different components. Kable wanted to test that idea further, to better pinpoint the implicated regions and what's happening in each.

To do so, he and his team created a study in which 13 females and 11 males received prompts while in a functional magnetic resonance imaging (fMRI) machine. Participants had seven seconds to read one of 32 cues such as, "Imagine you're sitting on a warm beach on a tropical island," or "Imagine you win the lottery next year." They then had 12 seconds to think about the scenario, followed by 14 seconds to rate vividness and valence.

"Vividness is the degree to which the image that comes to mind has a lot of details and how much those details subjectively pop as opposed to being vague," Kable says. "Valence is an emotional evaluation. How positive or negative is the event? Is this something you want to have happen or not?"

Participants went through the process four times. Each time, the Penn researchers watched brain activity from the fMRI. The work confirmed two sub-networks at play.

"One network, which we'll call the dorsal default mode network, was influenced by valence. In other words, it was more active for positive events than for negative events, but it was not influenced at all by vividness. It seems to be involved in the evaluative function," Kable says.

The other sub-network, the ventral default mode network, was more active for highly vivid events than for events with no detail. "But it wasn't influenced by valence," he says. "It was equally active for both positive and negative events, showing that network really is involved in the construction piece of imagination."

Next steps

According to Kable, the findings offer a first step toward understanding the basis of imaginative abilities. This research asked participants to evaluate the positivity or negativity of an imagined event, but more complex assessments—moving beyond the simple good-versus-bad dimension, for instance—might offer further clues about this neural process.

That kind of analysis will likely comprise future work for the Kable lab, which has already begun using these findings to parse why people don't value future outcomes as much as immediate outcomes.

"One theory is that the future isn't as vivid, isn't as tangible and detailed and concrete as something right in front of your face," he says. "We've started to use our identification of the sub-network involved in construction to ask the question, how active is this network when people are thinking about future outcomes compared to the same outcome in the present."

And although the research was completed before COVID-19, Kable sees pandemic-related implications for these findings. "If you described what someone's life was going to be like to them before the pandemic hit—you're going to work from home and wear a mask every time you go outside and not engage in any social contact—it would blow their mind. And yet, once we have the actual experiences, it's no longer so strange. For me, this demonstrates that we still have far to go in understanding our imaginative capabilities."

[Outline]

A research group led by Specially appointed professor, Dr. Tatsuo Suzuki of Shinshu University School of Medicine developed a new purification protocol for Postsynaptic density (PSD) lattice, a core structure of the PSD of excitatory synapses in the central nervous system. The components of the PSD lattice were identified by comprehensive shotgun mass spectrometry and categorized as either minimum essential component (MEC) or non-MEC proteins. Tubulin was found to be a major component of the MEC, with non-microtubule tubulin widely distributed on the purified PSD lattice. The presence of tubulin in and around PSDs was verified by post-embedding immuno-gold labeling EM of cerebral cortex. This study newly identified the PSD lattice backbone structure and provides a new PSD architecture model comprising a non-microtubule tubulin-based backbone structure and its associated proteins, including various PSD scaffold/adaptor proteins and other PSD proteins.

[Background]

Structural changes in postsynaptic density (PSD) (Fig.1A) are important mechanisms for maintaining synaptic plasticity, the basis for memory and learning. The molecular mechanism underlying changes in PSD structure (PSD remodeling) is currently unknown. A complete understanding of the structure of PSD is indispensable to fully elucidate the molecular mechanisms of spine and PSD dynamics during the expression of synaptic plasticity. Currently, it is tacitly believed that PSD is formed as an assembly of various kinds of scaffold/adaptor proteins (Scaffold/adaptor assembly model) (Fig. 1B right). On the contrary, the PSD lattice meshwork structure was found to be buried in the PSD by EM observation as early as the 1970's. However, major constituents of the PSD lattice and the relationship between the PSD lattice and the scaffold protein assembly model, remain unknown (Fig. 1B). In a previous study, the same research group purified a PSD lattice and proposed "PSD lattice-based dynamic nanocolumn" model (Fig. 3A) for the molecular architecture of PSD, in which the scaffold protein model and the PSD lattice model are combined (Suzuki et al., 2018). However, the group was unable to elucidate the molecular components of the PSD lattice due to the insolubility of the protein components.

[The key results of this research]

1) New purification protocol of PSD lattice was established.

2) PSD lattice backbone structure was newly identified (Fig. 3B).

3) Tubulin was by far the most common component of the PSD lattice backbone structure and widely distributed on the purified PSD lattice structure (Fig. 2A).

4) Tubulin associated with the PSD lattice backbone structure is in a non-microtubule form (Fig. 2A).

5) Postembedding immuno-gold EM observation using anti-tubulin antibody confirmed the presence of tubulin-immunoreactivity in and around PSD in the mouse brain (Fig. 2B).

6) Only a minimum amount of typical PSD scaffold/adaptor proteins are associated with PSD lattice backbone structure.

[Conclusion from the results and significance of this study]

This study proposes a PSD lattice model comprising a non-microtubule tubulin-based backbone structure and its associated proteins, including various PSD scaffold/adaptor proteins and other PSD proteins. (Fig. 3B) (This is the 2nd version of our PSD architecture model proposed in 2018.)

PSD lattice backbone structure is different from the three-dimensional assembly constructed by postsynaptic scaffold/adaptor proteins (Fig. 3B).

In the new model, non-microtubule tubulin may play an important role as a platform to which PSD scaffold/adaptor proteins and various PSD-functioning molecules become associated while synapses mature and reorganize (Fig. 3B).

[Future research prospects]

1) Elucidation of the mechanism of how non-microtubule type tubulin is related with PSD lattice backbone is important.

2) Role of PSD lattice other than essential cytoskeleton for the PSD should be searched.

3) Mechanisms of synaptogenesis and synaptic plasticity involving PSD lattice are important research targets.

CHAMPAIGN, Ill. -- A new coronavirus test can get accurate results from a saliva sample in less than 30 minutes, researchers report in the journal Nature Communications. Many of the components of the hand-held device used in this technology can be 3D-printed, and the test can detect as little as one viral particle per 1-microliter drop of fluid.

"We developed a rapid, highly sensitive and accurate assay, and a portable, battery-powered device for COVID-19 testing that can be used anywhere at any time," said University of Illinois Urbana-Champaign chemical and biomolecular engineering professor Huimin Zhao, who led the research. Though it is still in the prototype stage, the device is estimated to cost less than $78 and the reagents and other materials needed for testing would amount to $6-$7 per test, the researchers found.

Current coronavirus testing technologies are complex, expensive, time-consuming and require bulky equipment and expert analysts, whereas the new device can be operated by anyone with minimal training who is careful when loading samples, Zhao said.

The innovation was made possible by the recent discovery in Zhao's laboratory of a system for making artificial restriction enzymes that can be programmed to recognize and cleave specific genes in an organism's genome. In the new device, these enzymes carry DNA guides that tag the viral genes of interest. The enzyme cleaves the genes, which have been tagged with a dye that fluoresces only after the genes are cut. The resulting fluorescence signals that those genes are present - a positive test result.

The new technology, called Scalable and Portable Testing, does away with the complicated process of heating and cooling each sample to get results, as many current testing protocols require. SPOT also can detect multiple genes per sample, making it more accurate than single-gene tests, which can yield incorrect or inconclusive results. Another advantage is that it utilizes saliva, which is easier to collect and less invasive than a nasal swab.

The research team tested SPOT using 104 clinical saliva samples. They found that it accurately identified 28 out of 30 SARS-CoV-2-positive samples and 73 of 74 SARS-CoV-2-negative samples.

"Based on the data reported in the literature, the accuracy of our test is comparable to or better than other SARS-CoV-2 tests," Zhao said.

The researchers also tested SPOT with samples containing - or lacking - the influenza virus, the new coronavirus and three other human coronaviruses. It accurately identified samples containing the new coronavirus, whether or not other viruses were present in the sample.

"We are interested in exploring this technology for detection of other diseases as well," Zhao said. "One key advantage to this technology is its multiplexing capability, so in principle, we can detect many viruses simultaneously using the same device."

A new study published in Nature Communications provides an important new basis for comparing the effectiveness of different tuberculosis treatments.

Tuberculosis, a disease caused by the bacterium Mycobacterium tuberculosis (Mtb), is typically the leading infectious cause of death globally, killing 1.2 million people each year. The availability of a new way to evaluate treatments can save lives.

In the study, faculty at the University of Colorado School of Medicine at the University of Colorado Anschutz Medical Campus partnered with the University of California San Francisco (UCSF) Center for Tuberculosis and the Mycobacteria Research Laboratories at Colorado State University to provide a new perspective on assessing the effectiveness of tuberculosis drugs.

"A key roadblock that holds back new tuberculosis treatments is our current inability to accurately measure how effectively different treatments shorten the time needed to cure tuberculosis," said lead author Nicholas Walter, MD, PhD, associate professor at the University of Colorado Anschutz Medical Campus. "Without improved tools to measure and compare the effectiveness of drug treatments, the evaluation and roll-out of new combination drug treatments will continue to proceed slowly."

"In the past, the effectiveness of tuberculosis treatment has been judged by estimating the burden of the pathogen M. tuberculosis as enumerated via culture based approaches. This historical method correlates poorly with what we care about most, which is whether tuberculosis patients are durably cured," adds co-first author Gregory Robertson, PhD, assistant professor at Colorado State University.

In this study, the researchers measured the degree to which drugs interrupt the synthesis of ribosomal RNA, required for the protein-making machinery of the bacterium. The researchers discovered that drugs and drug regimens that shorten tuberculosis treatment duration inhibit Mtb rRNA synthesis more than less potent drugs and regimens. Their new measure, called the rRNA synthesis (RS) Ratio provides an urgently needed molecular metric of drug activity based on a key microbial physiologic property rather than recapitulation of bacterial burden.

"The RS Ratio gives us a readout of drug effect that opens a new era in understanding antibiotics. Measuring a key physiologic property of pathogens provides an innovative way of thinking beyond conventional measures of bacterial burden," said senior author Martin Voskuil, PhD, associate professor at the University of Colorado Anschutz Medical Campus.

"The RS Ratio can enable more intelligent design and evaluation of candidate drug combination regimens, accelerating the development of treatments that can cure tuberculosis faster. This has crucial implications for combatting the global tuberculosis epidemic," adds co-author Payam Nahid, MD, MPH, professor and director of the UCSF Center for Tuberculosis.

Ants are renowned in the insect world for their complex social structure and behaviors. Workers and foragers support the queen, faithfully carrying out their social roles for the overall health of the colony. This complex "superorganism" ---as scientists have dubbed it --- has become a prime model to explore the genetic and behavioral roots of social organisms.

Remarkably, there are also rare instances of ants not playing well with others and shrugging off their societal duties to become free-loading parasites amongst their free-living relatives.

Now, in a new study published in Nature Communications, an international collaboration of researchers from Europe (the Universities of Münster and Copenhagen), South America (University of the Republic in Montevideo, Uruguay), and the U.S., (led by Arizona State University), teamed up to discover and collect these rare ant social parasites. Together, they have obtained and analyzed the full DNA genome sequences of three rare "social parasite" leaf-cutting ant species (called Acromyrmex inquilines) to better understand the differences between them and their respective host species.

It's the first time several species of socially parasitic ants could have their genomes sequenced.

"Our findings advance our understanding of the genomic consequences of transitioning to a novel, highly specialized life history and provide detailed insights into the molecular evolution of social parasitism in ants," said Christian Rabeling, an associate professor in ASU's School of Life Sciences and a corresponding author of the study.

From social to social parasite

The unusual social parasite transition is important to understand because the genomes of ants have evolved for more than 100 million years. A single major transition occurred to introduce the novel "superorganism" level of social organizational structure with queen-worker caste segregation and unconditional altruism. This superorganism was so successful, it produced a biodiversity of 17 subfamilies, 338 genera and more than 13,900 living species.

"It is therefore no surprise that parallel shifts to a highly specialized socially parasitic behavior and lifestyle abandoning this fundamental ancestral condition, usually based on outbreeding and larger effective populations, leave significant genomic footprints," said Rabeling. "The results of our analyses of just three of these species confirm that ant social parasites offer important study systems for identifying hallmarks of cooperative social colony life.

And in doing so, their analyses have confirmed that over a time span of about a million and a half years, these ant species have each found independent, separate ways to evolve and become social parasites. The signatures of genome-wide and trait-specific genetic erosion were found to be most extreme in social parasite ants.

Think of how it would start. A group of queen ants wants to just live in a colony without doing the work. And not work on the nest anymore. Next, the queen ants focus on solely producing new queens and males, and this small population size of social parasites would start frequent inbreeding to survive. This immediately reduces their genomic diversity over time. Then, over a blink in evolutionary time, due to natural selection and an increase in the prevalence of genetic drift, it would enhance the rates by which ancestral traits were lost while also slowing down the rates by which new, more adaptive traits could emerge.

It's almost like a 'snooze and lose it' phenomena occurred within the parasitic ant DNA to trigger the genome erosion.

To prove this effect within the ant genome, the research team investigated the overall genomic structure and the individual genes that may be affected by this genomic decay. First, they found widespread evidence of genomic rearrangements and inversions that are hallmarks of instability and decay. Then, within gene networks, they identified 233 genes that showed evidence of relaxed selection in at least one of the social parasite branches and signatures of intensified selection in 102 genes. "Our analysis showed that gene family evolution at three of the four social parasite nodes is indeed largely characterized by gene losses," said Rabeling.

The genome losses and reductions most affected were in the social parasite ants' sense of smell and to a lesser degree taste.

Failing the sniff test

Not only did some of the genes responsible for ant smell become lost over time, but as a result, the ants also showed a reduced size in the olfactory lobes in their brains when microCT scans were performed.

"This is no surprise because ants predominantly communicate via chemical cues and have once been described as chemical factories," explains Rabeling. "So, the loss of olfactory genes is correlated with an extreme transition of extensive morphological and behavioral changes."

This includes the reduction or complete loss of the worker caste system, simplified mouthparts, antennae and integuments, loss of certain hormonal glands, and a nervous system of reduced complexity likely associated with a drastically narrowed behavioral repertoire.

From their comparative analysis, they could also put these changes into the larger perspective of evolutionary time. They were also able to date the origins of social parasitism within the leaf-cutting ant family tree.

Two independent origins of social parasitism occurred in the ant genus Acromyrmex. Within this genus, A. heyeri, a social ant, is the host species of both A. charruanus and P. argentina parasitic species.

First, a South American lineage of social ants (A. heyeri) separated from the last common (thought to be socially parasitic) ancestor of A. charruanus and P. argentina before the two social parasites diverged. Second, a Central American speciation event occurred when A. insinuator diverged from its host A. echinatior.

Both origins of social parasitism are evolutionarily recent, estimated to be about 2.5 million years ago for the divergence between A. heyeri and the last common ancestor of A. charruanus and P. argentina, and about 1 million years ago for the divergence between A. insinuator and A. echinatior.

"We infer that relaxed natural selection accelerated general genome erosion in social parasites and alleviated evolutionary constraints, which facilitated rapid adaptive evolution of specific traits associated with a socially parasitic lifestyle," said Rabeling.

Joy of discovery

Why did it take so long to do the genome analysis? It turns out that the easiest part of the study may have been the comparative genome analysis. Finding the ants in the first place proved to be the greatest major hurdle. Why?

Populations of ant social parasites are almost invariably small and patchily distributed. How patchy?

Well, the last time that one of the species, P. argentina was seen in the wild was 1924, a time well before the discovery of DNA as the hereditary chemical unit of life.

Rabeling remembers prior trips to South America that were in vain because they could not find P. argentina. Then, about a decade ago, a phone call from colleague Martin Bollazzi and study co-author changed his life.

"Martin Bollazzi said his wife Leticia just re-discovered P. argentina!!!"

Rabeling hopped on a plane as fast as he could. When he saw P. argentina up close, it was a moment of discovery he'll never forget.

"Leticia's rediscovery of P. argentina was the find of a lifetime. What I especially love is to connect the ant field work and natural history observations with the new technologies like whole genome sequencing, and to have the opportunity to do so was such a joy."

Now, they could make their research dreams a reality by collecting P. argentina and put their field work-based hypotheses to the test by doing the first modern whole genome sequencing of social parasitic ants.

Next steps

Their results are not only important to understanding ants, but offer insights into the role of these genomic 'loss-of-function' study systems in other parasites and for identifying hallmarks of cooperative social colony life at both the phenotypic and the genomic levels.

"Social parasites came to exploit the foraging efforts, nursing behavior and colony infrastructure of their hosts," said Rabeling.

Rabeling also points to other species, such as the Mexican blind cave-dwelling fish or other parasites such as tapeworms as examples of organisms that lost important traits over time. In each case, they have developed and exploited novel ecological niches. for their species survival.

From these first 3 social parasite ant species, they have learned a lot. Next, they plan on future genomics studies of these ant social parasites to generate exciting further insights, particularly with long-read sequencing technologies allowing analyses in even greater detail.

But Rabeling and his colleagues are now involved in another race against time----as every year, more and more natural ant habitats are lost to deforestation and development. Now, our understanding of ant evolution depends on people to cooperate to save biodiversity---while we still can.

"We hope such future studies can expand our knowledge on the signatures of the evolution of social behavior in ants, for which few other model systems can offer such species-level sample sizes of several dozens."

Optimistic predictions expect reliable autonomous vehicles to be commercially available by 2030, at a time when mobility is undergoing a profound shift away from traditional modes of transportation and towards door-to-door services. Previous analysis suggested that public transport will lose market share to autonomous vehicles, but the environmental impact of changing transport use has hardly been considered. New research shows that the convenience of autonomous vehicles would likely come at an environmental cost.

A recent paper by researchers from the University of Wisconsin-Madison addresses the use-phase implications of autonomous vehicles using a stated preference survey to reveal the potential users of autonomous vehicles and the resulting level of competition with traditional modes of transport. The results show an expected increase in environmental impacts across all the categories studied, due to a shift from less carbon intensive transportation options. The authors also confirm that the use of electric autonomous vehicles could change this environmental outcome. Their research is published today in the IOP Publishing journal Environmental Research Letters.

Autonomous vehicles are expected to offer significant benefits in terms of transport operations, safety and accessibility; however, these benefits may mask potential environmental impacts. Clearly, the adoption of autonomous vehicles will be accompanied by travel behavior changes, however research to date has mostly focused on autonomous vehicle technology and not on the environmental impacts that will result from transport mode shifts. This new research therefore examines these impacts based on four categories: energy consumption, greenhouse gas emissions, particulates, and pollutants.

A survey conducted in Madison, Wisconsin, examined attitudes to transport modes and found that in choice experiments between private vehicles, autonomous taxis, buses, and bicycles, respondents would use autonomous vehicle taxis 31% of the time due to their desirable operational and modal attributes. By contrast, buses had a significantly longer access time due to walking and waiting, and personal vehicles were the midway choice. However, commuters who owned a personal vehicle were less likely to choose an autonomous vehicle, implying that autonomous vehicles primarily compete with public transport; therefore, policies aiming to reduce commuting in personal vehicles might not be fully successful in reducing environmental impacts.

The researchers then examined the impacts of policy and service changes via a series of simulations, which confirmed that autonomous vehicles primarily compete with the environmentally preferred transport mode, buses. They also showed that a decrease in bus travel times would result in a significant increase in bus usage. The environmental predictions showed increases of between 5.7% and 6.85% in the energy and pollution categories, a significant impact, given that transport accounts for 28% of the greenhouse gas emissions in the U.S.

To offset the environmental impacts of autonomous vehicles, the researchers considered the use of electric autonomous vehicles, considering the use phase only. The results showed that electric autonomous vehicles can offset the environmental impact of autonomous vehicles, subject to a suitable mix of electricity generation methods, and if the adoption rate of electric autonomous vehicles is over about 40%.

This new research into the use-phase environmental impacts of autonomous vehicles will help researchers and policy makers to exploit the full potential of autonomous vehicles while taking any potential environmental implications into account. Cities seeking to deploy autonomous vehicles will need to steer their deployment in ways that both match consumer adoption patterns and are environmentally beneficial.

Author Wissam Kontar said: "The transportation system is on the verge of a major paradigm shift. Emerging technologies as autonomous and electric vehicles, along with change in commuting behavior will have significant operational and environmental impacts. It is of crucial importance that we consider those impacts conjointly, if we are to forge an efficient and sustainable mobility of the future."

Information flows in a well-defined direction in the brain: Chemical and electrical signals are passed from one neuron to the other across the synapse, from the pre-synaptic to the post-synaptic neuron. Now, Peter Jonas and his group at the Institute of Science and Technology Austria (IST Austria) show that information also travels in the opposite direction at a key synapse in the hippocampus, the brain region responsible for learning and memory. At the so-called mossy fiber synapse, the post-synaptic CA3 neuron influences how the pre-synaptic neuron, the so-called mossy fiber neuron, fires. "We have shown, for the first time, that a retrograde information flow is physiologically relevant for pre-synaptic plasticity," says Yuji Okamoto, a postdoc in the group of Peter Jonas at IST Austria and co-first author of the paper published in Nature Communications.

The mossy fiber synapse is crucial for information storage in the neuronal network. Synaptic transmission is plastic meaning that a variable amount of chemical signal, the so-called neurotransmitter, is released into the synapse. To understand the mechanism of plasticity at work in this synapse, Okamoto precisely stimulated the pre-synaptic terminal of the mossy fiber synapse in rats and at the same time recorded from the post-synaptic neuron. "We need to know the synapse's exact properties - with the numerical values, e.g., for its conductance - to create an exact model of this synapse. With his exact measurements, Yuji managed to obtain these numbers," adds Peter Jonas, co-corresponding author with postdoc David Vandael.

Smart teacher reacts to overloaded student

Unexpectedly, the researchers found that the post-synaptic neuron influences plasticity in the pre-synaptic neuron. Previously, the mossy fiber synapse was assumed to be a "teacher synapse" that induces firing in the post-synaptic neuron. "Instead, we find that this synapse acts like a 'smart teacher', who adapts the lessons when students are overloaded with information. Similarly, the pre-synaptic mossy fiber detects when the post-synaptic neuron can't take more information: When activity increases in the post-synaptic neuron, the pre-synaptic neuron reduces the extent of plasticity," explains Jonas.

This finding raises the question of how the post-synaptic neuron sends information about its activity status to the pre-synaptic neuron. Pharmacological evidence points to a role for glutamate, one of the key chemicals or neurotransmitters used by neurons to send signals to other cells. Glutamate is also the transmitter that is released from pre-synaptic mossy fiber terminals. When calcium levels increase in the post-synaptic neuron - a sign that the neuron is active - the post-synaptic neuron may release vesicles with glutamate into the synapse. The glutamate travels back to the pre-synaptic neuron against the usual flow of neuronal information. "This retrograde modulation of plasticity likely helps to improve information storage in the downstream hippocampal network," says Jonas, and he adds: "Once again, exact measurements have shown that reality is more complex than a simplified model would suggest."

PULLMAN, Wash. - Alterations in the epigenetic programming of hatchery-raised steelhead trout could account for their reduced fertility, abnormal health and lower survival rates compared to wild fish, according to a new Washington State University study.

The study, published May 18 in Environmental Epigenetics, establishes a link between feeding practices that promote faster growth, as well as other environmental factors in fish hatcheries, and epigenetic changes found in the sperm and red blood cells of of steelhead trout.

The research was done at a national fish hatchery on the Methow River in Winthrop, Washington and at another hatchery close by on the Colombia River. It could have broader implications as hatchery-raised steelhead reproduce with wild steelhead after being released.

"Despite being genetically very similar, steelhead trout raised under hatchery conditions don't have the same level of health and survivability of wild-raised fish," said Michael Skinner, study co-author and professor in the WSU School of Biological Sciences.  "This research provides a molecular explanation for why we are seeing these differences."

Skinner is an expert in the field of epigenetics, which is the study of molecular factors and processes around DNA that regulate genome activity independent of the DNA sequence.

While exposure to environmental conditions doesn't typically affect an organism's genetic code, previous research has shown that a range of factors including toxicants, stress and nutrition can developmentally alter the phenotype of a variety of species through epigenetics.

In the current study, Skinner and colleagues performed a molecular analysis of sperm and red blood cells taken both from steelhead trout raised in two Washington fish hatcheries and trout that spent their entire life in the wild.

While there were negligible genetic differences between the two fish populations, the researchers identified a set of epigenetic features, called DNA methylation regions, in the sperm and red blood cells of the hatchery-raised steelhead that weren't present in their wild-raised counterparts.

Skinner's study connects the dots to identify a molecular mechanism that can help explain many of the physiological differences scientists have noted between hatchery-raised and wild fish.

For instance, it has been shown that the offspring of fish experiencing even a single generation of hatchery-rearing can have decreased fitness, changes in age at spawning, altered morphologies, and mal-adapted anti-predator behavior.

In fact, hatchery rearing has been shown to decrease reproductive success in steelhead trout by as much as 40% in the first two generations after fish are moved back to their natural environment.

Another important aspect of the epigenetic alterations Skinner identified is that they can be passed via the sperm to subsequent generations.

In places like the Methow and Columbia rivers where hatchery-raised trout are frequently released and bred with wild trout, epigenetic inheritance could have already had a substantial impact on the overall health and fitness of the fish population, Skinner said.

"We think that the large number of hatchery fish that have been released and bred with the wild fish population on the Methow River over the past 60 years has had a significant influence on the health of the overall population," he said. "Moving forward, our research suggests hatchery operations should consider not allowing interbreeding with wild fish populations. If not, impacts on wild-raised steelhead trout and the environment could be dramatic and alter the future trajectory of the overall population."

A study using a mouse model of eccentric contraction (*1) has revealed that icing injured muscles delays muscle regeneration. The discovery was made by a research group including Associate Professor ARAKAWA Takamitsu and then PhD. Student KAWASHIMA Masato from Kobe University's Graduate School of Health Sciences, and Chiba Institute of Technology's Associate Professor KAWANISHI Noriaki et al. In addition, the researchers illuminated that this phenomenon may be related to pro-inflammatory macrophages' (*2, 3, 4) ability to infiltrate damaged cells. This research raises questions as to whether or not severe muscle injuries (such as torn muscles) should be iced.

These research results were published online as one of the Journal of Applied Physiology's Articles in Press on March 25, 2021.

Main points

The research results revealed that applying an ice pack to a severe muscle injury resulting from eccentric contraction may prolong the time it takes to heal.

The cause of this phenomenon is that icing delays the arrival of pro-inflammatory macrophages, which are responsible for the phagocytosis (*5), or removal, of damaged tissue. Furthermore, this makes difficult for the macrophages to sufficiently infiltrate the damaged muscle cells.

Research Background

Skeletal muscle injuries encompass a range of damage to muscles; from a microcellular level to a severe level. These injuries include not only those that happen during sports or schools' physical education lessons but also external injuries that occur as a result of accidents and disasters.

'RICE treatment' is a common approach for skeletal muscle injuries, regardless of the extent of the injury. This acronym stands for Rest, Ice, Compression and Elevation and is often used in physical education, sports and even medicine. Ice is commonly applied regardless of the type of muscle injury, yet little is known about the long-term effects of icing.

Ice is used to suppress inflammation, however, inflammation in response to tissue injury is one of the body's healing mechanisms. This has come to be understood as a vital response for tissue regeneration. In other words, suppressing inflammation with ice may also inhibit the body's attempt to repair itself.

Experiments investigating the effect of icing muscles after injury have produced conflicting results. Some have reported that it delays muscle regeneration while others have stated that it doesn't inhibit this process. However, none of the research up until now has investigated the effects of icing using an injury model that mimics common sports injuries caused by muscle contraction.

Using a mouse model of eccentric contraction injury, the current research team decided to observe the effects of post-injury icing. In this mouse model, injuries were induced to resemble severe torn muscles.

Research Methodology and Results

Eccentric contraction was induced by electrically stimulating the leg muscles of the mice and then exerting a stronger force during this stimulation to make the leg muscles move in the opposite direction. After this, the muscles were harvested. Icing was performed by placing polyurethane bags of ice on top of the skin over three 30 minute sessions per day, with each session being 2 hours apart. This was continued until two days after the injury. The icing was based on the usual clinically recommended method.

The researchers investigated the regenerated skeletal muscle two weeks after injury, comparing the icing group with the non-icing group. A significantly higher percentage of smaller regenerated muscle fibers were found in cross-sections from the icing group, with a greater number of medium to large fibers in the non-icing group (Figure 1). In other words, this revealed that skeletal muscle regeneration may be delayed as a result of icing.

Next, the researchers periodically took samples of muscle from the icing and non-icing groups of animals in order to investigate what was happening in the regeneration process up until this point.

In the regeneration process, inflammatory cells gather at the site of the injury, remove the debris from the damaged muscle and then begin to build new muscle. However, the results revealed that it is harder for inflammatory cells to enter the injured muscle cells if ice is applied (Figure 2).

Macrophages are typical of the inflammatory cells that enter the injured muscle. These consist of pro-inflammatory macrophages, which phagocyte damaged tissue thus causing inflammation, and anti-inflammatory macrophages (*6), which suppress the inflammatory reaction and promote repair. It is thought that pro-inflammatory macrophages change their characteristics, becoming anti-inflammatory. The results of this research team's experiments showed that icing delays the arrival of pro-inflammatory macrophages at the site of the injury (Figure 3).

These results indicate the possibility that macrophages are unable to sufficiently phagocyte the damaged muscle when ice is applied after severe muscle injuries caused by eccentric contraction, consequently delaying the formation of new muscle cells.

Comment from Associate Professor Arakawa

In sports, the mantra of immediately applying ice to an injury is commonplace, regardless of the injury's severity. However, the mechanism that we illuminated through this research suggests that not icing a severe muscle injury may lead to faster recovery. The idea of immediately cooling any type of injury is also entrenched in schools' physical education classes. I hope that in the future, the alternative option of speeding up recovery by not cooling severe muscle injuries will become known.

However, even though icing may disrupt the recovery process for severe muscle injuries, there is no denying the possibility that there are degrees of mild muscle injuries that can be iced. The next issue is to work out where to draw the line. We are now in the middle of investigating what effect icing has on slight muscle injuries.

Next, we will continue to investigate how icing should be carried out according to the extent of the muscle injury. We aim to contribute guidelines that will enable people in sports and clinical rehabilitation to make accurate judgements about whether or not to ice an injury.

Robust data and genetic research are providing important evidence on a colony of wild African vervet monkeys that landed in Dania Beach more than 70 years ago and settled in a thick mangrove forest near the Fort Lauderdale-Hollywood International Airport in South Florida.

The non-native vervet monkey (Chlorocebus sabaeus) population living in this urban coastal region is well known and beloved among local residents and city officials; however, it is relatively unknown to primatologists. Despite wide public interest, there has been only one scientific study (early 1990s), suggesting that the monkeys escaped from a failed roadside zoo in the 1950s and 1970s. Until now, there was no confirmation about the species' identification, geographic origins, or introduction history.

A Florida Atlantic University team of scientists combined multiple methodological approaches to determine the species of Chlorocebus monkey in Dania Beach, where they came from, and their pathway of introduction. Results of the study, published in the journal Primates, provide critical baseline information to the scientific community about a little-known population of Chlorocebus monkeys that have survived for decades in a novel environment.

Through interviews, historical archives and popular media, FAU scientists traced the monkeys to an escape from the Dania Chimpanzee Farm in 1948. The facility acted as a zoo and also provided primates imported from Africa as research subjects in the development of the polio vaccine and other medical research. Historical archives suggest that the monkeys were caught in Sierra Leone. Scientists tested the hypothesis of West African origins using three genetic markers: one mitochondrial DNA gene (cytochrome b) and two fragments from the Y-chromosome, the sex-determining gene and the zinc-finger gene. Phylogenetic analyses confirmed that the Dania Beach monkeys are in fact Chlorocebus sabaeus (green monkey) and have West African origins.

The monkeys of Dania Beach were photographed to create a database of all individuals (36). Scientists recorded the following traits to help identify species of monkey: color of their fur; presence or absence of brow band; color of tail tip; and scrotum color of adult males. These attributes were then compared to all species qualitatively within the genus Chlorocebus to estimate study species using these traits.

"Our monkeys in Dania Beach have a golden-tipped tail and greenish-brown hair, lack a pronounced brow band around the face, and males have a pale blue scrotum. These phenotypic traits are characteristic of Chlorocebus sabaeus," said Deborah "Missy" Williams, Ph.D., lead author, Biological Sciences Department in FAU's Charles E. Schmidt College of Science, who leads the Dania Beach Vervet Project to conserve this population of monkeys and has been studying them for almost a decade. Williams conducted the study with Kate Detwiler, Ph.D., senior author and an associate professor in the Department of Anthropology in FAU's Dorothy F. Schmidt College of Arts and Letters.

This species is commonly referred to as a green monkey because of the color of its fur. Species within Chlorocebus have hair color ranging from greenish-brown to grayish olive with black faces, hands and feet. Males have a blue scrotum and red penis and perianus surrounded by white hair.

Green monkeys are endemic to West Africa, with a range from Senegal and west Guinea-Bissau into Ghana. They are the most widespread of the African monkeys and are habitat generalists, limited only by the availability of water and sleeping trees.

"Data from our study lays the groundwork for future studies to address new questions about the status of the population and how the monkeys have adapted to the urban and industrial environment of South Florida," said Detwiler. "The correct taxonomic identification and history of the introduced Dania Beach monkeys is important for community outreach and wildlife management, given the remarkable ability for Chlorocebus to thrive in most environments."

In the southeastern United States, Florida is home to three introduced, free ranging primates: Saimiri sciureus (squirrel monkey), Chlorocebus sabaeus (green monkey), and Macaca mulatta (rhesus macaque). All three primate species were introduced through various zoos, research facilities, private collections, and entertainment businesses.