Precisely howbutterflies are able to generate the vibrant patterns and colors on their wings has fascinated biologists for centuries. The genetic code contained within the cells of developing butterfly wings dictates the specific arrangement of the color on the wing’s scales — the microscopic tiles that form wing patterns — similar to the arrangement of colored pixels to form a digital image. Cracking this code is fundamental to understanding how our own genes build our anatomy. In the lab, researchers can manipulate that code in butterflies with gene-editing tools and observe the effect on visible traits, such as coloration on a wing.

Scientists have long known that protein-coding genes are crucial to these processes. These types of genes create proteins that can dictate when and where a specific scale should generate a particular pigment. When it comes to black pigments, researchers thought this process would be no different, and initially implicated a protein-coding gene. The new research, however, paints a different picture.

The team discovered a gene that produces an RNA molecule — not a protein — controls where dark pigments are made during butterfly metamorphosis. Using the genome-editing technique CRISPR, the researchers demonstrated that when you remove the gene that produces the RNA molecule, butterflies completely lose their black pigmented scales, showing a clear link between RNA activity and dark pigment development.

“What we found was astonishing,” said Livraghi, a postdoctoral scientist at GW. “This RNA molecule directly influences where the black pigment appears on the wings, shaping the butterfly’s color patterns in a way we hadn’t anticipated.”

The researchers further explored how the RNA molecule functions during wing development. By examining its activity, they observed a perfect correlation between where the RNA is expressed and where black scales form.

“We were amazed that this gene is turned on where the black scales will eventually develop on the wing, with exquisite precision” said Arnaud Martin, associate professor of biology at GW. “It is truly an evolutionary paintbrush in this sense, and a creative one, judging by its effects in several species.”

The researchers examined the newly discovered RNA in several other butterflies whose evolutionary history diverged around 80 million years ago. They found that in each of these species, the RNA had evolved to control new placements in the patterns of dark pigments.

“The consistent result obtained from CRISPR mutants in several species really demonstrate that this RNA gene is not a recent invention, but a key ancestral mechanism to control wing pattern diversity,” said Riccardo Papa, professor of biology at the University of Puerto Rico — Río Piedras.

“We and others have now looked at this genetic trait in many different butterfly species, and remarkably we are finding that this same RNA is used again and again, from longwing butterflies, to monarchs and painted lady butterflies,” said Joe Hanly, a postdoctoral scientist and visiting fellow at GW. “It’s clearly a crucial gene for the evolution of wing patterns. I wonder what other, similar phenomena biologists might have been missing because they weren’t paying attention to the dark matter of the genome.”

The findings not only challenge long-standing assumptions about genetic regulation but also open up new avenues for studying how visible traits evolve in animals.

“Improvements in MI management and data from observational studies have led physicians to question whether continuing beta-blockers after 1 year post-MI is needed since unnecessary treatment may result in side effects.^2-5 We conducted the ABYSS trial to provide conclusive randomised data on the effects of beta-blocker interruption vs. continuation on cardiovascular events and quality of life, but we were unable to show safety preservation in terms of clinical events nor any benefit on quality of life with beta-blocker interruption,” said Principal Investigator, Professor Johanne Silvain of the Sorbonne University, Paris, France.

The open-label, non-inferiority, randomised ABYSS trial, conducted by the ACTION Group, included patients with a prior MI taking long-term beta-blockers, with a left ventricular ejection fraction of at least 40% and no cardiovascular events in the previous 6 months. Participants were randomised (1:1) to interrupting or continuing their β-blocker medication.

The primary endpoint was a composite of death, non-fatal MI, non-fatal stroke or hospitalisation for cardiovascular reasons at the longest follow-up (minimum, 1 year), according to an analysis of non-inferiority (defined as a between-group absolute difference of <3 percentage points for the upper boundary of the two-sided 95% confidence interval [CI]). The main secondary endpoint was the change in quality of life as measured by the European Quality of Life-5 Dimensions questionnaire.

In total 3,698 patients were randomised from 49 sites in France. The mean age was 64 years and 17% were female. The median time between last MI and randomisation was 2.9 years (interquartile range 1.2-6.4 years).

Over median follow-up of 3 years, interruption of long-term beta-blocker treatment was not shown to be non-inferior to beta-blocker continuation. A primary-outcome event occurred in 23.8% of patients in the interruption group and in 21.1% in the continuation group (risk difference 2.8 percentage points; 95% CI <0.1-5.5), with a hazard ratio of 1.16 (95% CI 1.01-1.33; p=0.44 for non-inferiority).

Death occurred in 4.1% in the interruption group and 4.0% in the continuation group, while MI occurred in 2.5% and 2.4%, respectively. Of note, hospitalisation for cardiovascular causes occurred in 18.9% in the interruption group and 16.6% in the continuation group. Beta-blocker interruption was also associated with increases in systolic and diastolic blood pressure and heart rate at 6 months (all p<0.001 vs. beta-blocker continuation) and during the study follow up. Beta-blocker interruption did not improve the patients’ quality of life.

Summing up the evidence from the ABYSS trial, Professor Silvain concluded: “Differences between the groups with respect to hospitalisation for cardiovascular reasons and the negative effect on blood pressure levels, together with the absence of quality-of-life improvement do not support interruption of a chronic beta-blocker treatment in post-MI patients. These results must be put into context with recent findings from the open-label REDUCE-MI⁶ trial and ongoing trials to provide additional evidence on the optimal use of beta-blockers after MI.”

1 ‘Beta blocker interruption in patients with prior myocardial infarction: results of the ABYSS trial and effect on blood pressure and heart rate control’ will be discussed during Hot Line 1 on Friday 30 August in room London.

2 Holt A, Blanche P, Zareini B, et al. Effect of long-term beta-blocker treatment following myocardial infarction among stable, optimally treated patients without heart failure in the reperfusion era: a Danish, nationwide cohort study. Eur Heart J. 2021;42:907-914.

3 Park CS, Yang H-M, Ki Y-J, et al. Left ventricular ejection fraction 1 year after acute myocardial infarction identifies the benefits of the long-term use of beta-blockers: analysis of data from the KAMIR-NIH Registry. Circ Cardiovasc Interv. 2021;14:e010159.

4 Puymirat E, Riant E, Aissaoui N, et al. β Blockers and mortality after myocardial infarction in patients without heart failure: multicentre prospective cohort study. BMJ. 2016;354:i4801.

5 Kim J, Kang D, Park H, et al. Long-term β-blocker therapy and clinical outcomes after acute myocardial infarction in patients without heart failure: nationwide cohort study. Eur Heart J. 2020;41:3521-3529.

6 Yndigegn T, Lindahl B, Mars K, et al. Beta-blockers after myocardial infarction and preserved ejection fraction. N Engl J Med. 2024;390:1372-1381.

Mindfulness refers to the ability of an individual to focus attention on the present, in a way that is open, curious and not judgmental. Essentially, the ability to be fully in the moment.

“There’s a lot of discussion about the benefits of mindfulness, but it poses two challenges when you’re going through periods of stress,” says Tom Zagenczyk, co-author of a paper on the work and a professor of management in North Carolina State University’s Poole College of Management. “First, it’s hard to be mindful when you’re experiencing stress. Second, if it’s a truly difficult time, you don’t necessarily want to dwell too much on the experience you’re going through.

“Because hope is inherently forward looking, while mindfulness is about appreciating your current circumstances, we wanted to see how each of these two mindsets influenced people’s well-being and professional attitudes during difficult times,” Zagenczyk says. “The COVID pandemic presented us with an unfortunate, but useful, opportunity to explore this topic. And we chose to focus on the performing arts since that sector was particularly hard hit by the pandemic.”

For the study, researchers recruited 247 professional musicians from the organization MusiCares to take two surveys, one month apart. The first survey was given in September 2021. In addition to collecting broad demographic data, study participants were asked about their thoughts and experiences at the beginning of the pandemic — March to August 2020. They were also asked questions aimed at capturing how hopeful and mindful they were from September 2020 through March 2021.

The second survey was given in October 2021 and asked study participants questions aimed at capturing work engagement, work tensions, how positive their emotions were, and the extent to which they were experiencing distress.

The researchers then used statistical techniques to identify relationships between hope, mindfulness, and outcomes related to their personal well-being and attitudes toward work.

“Fundamentally, our findings tell us that hope was associated with people being happy, and mindfulness was not,” says Kristin Scott, study co-author and a professor of management at Clemson University. “And when people are hopeful — and happy — they experience less distress, are more engaged with their work, and feel less tension related to their professional lives.”

“Being mindful can be tremendously valuable — there are certainly advantages to living in the moment,” says Sharon Sheridan, study co-author and an assistant professor of management at Clemson. “But it’s important to maintain a hopeful outlook — particularly during periods of prolonged stress. People should be hopeful while being mindful — hold on to the idea that there’s a light at the end of the tunnel.”

While the study focused on musicians during an extreme set of circumstances, the researchers think there is a takeaway message that is relevant across industry sectors.

“Whenever we have high levels of job stress, it’s important to be hopeful and forward looking,” says Emily Ferrise, study co-author and a Ph.D. student at Clemson. “And to the extent possible, there is real value for any organization to incorporate hope and forward thinking into their corporate culture — through job conditions, organizational communications, etc.”

“Every work sector experiences periods of high stress,” says Zagenczyk. “And every company should be invested in having happy employees who are engaged with their work.”

Now researchers from The Rockefeller University have found another rare mutation that leaves its carriers much more likely to become ill with TB — but, curiously, not with other infectious diseases. This finding, recently published in Nature, may upend long held assumptions about the immune system.

It’s long been known that an acquired deficiency of a pro-inflammatory cytokine called TNF is linked to an increased risk of developing TB. The current study, led by Rockefeller’s Stéphanie Boisson-Dupuis and Jean-Laurent Casanova, revealed a genetic cause of TNF deficiency, as well as the underlying mechanism: a lack of TNF incapacitates a specific immune process in the lungs, leading to severe — but surprisingly targeted — illness.

The findings suggest that TNF, long considered a key galvanizer of the immune response, might actually play a much narrower role — a discovery with far-reaching clinical implications.

“The past 40 years of scientific literature have attributed a wide variety of pro-inflammatory functions to TNF,” says Casanova, head of the St. Giles Laboratory of Human Genetics of Infectious Diseases. “But beyond protecting the lungs against TB, it may have a limited role in inflammation and immunity.”

Rare risk

Casanova’s lab has been studying the genetic causes of TB for more than two decades through field work in several countries and a wide network of collaborating physicians across the world. They maintain an ever-growing database of whole-exome sequences from a global pool of patients — more than 25,000 people to date. Of those, some 2,000 have had TB.

Over the years they’ve identified several rare genetic mutations that render some people vulnerable to TB. For example, mutations in a gene called CYBB can disable an immune mechanism called the respiratory burst, which produces chemicals called reactive oxygen species (ROS). Despite its pulmonary-sounding name, the respiratory burst takes place in immune cells throughout the body.

ROS help pathogen-consuming white blood cells called phagocytes (from the Greek for “eating”) to destroy the invaders they’ve devoured. If ROS aren’t produced, those pathogens can thrive unchecked, leading to debilitating complications. As a result, carriers of this CYBB mutation become vulnerable to not just TB but to a wide variety of infectious diseases.

For the current study, the team suspected that a similar inborn error of immunity may lay behind the severe, recurring TB infections experienced by two people in Colombia — a 28-year-old woman and her 32-year-old cousin — who had been repeatedly hospitalized with significant lung conditions. In each cycle, they initially responded well to anti-TB antibiotics, but within a year, they were sick again.

Puzzlingly, however, their long-term health records showed that their immune systems functioned normally, and that they were otherwise healthy.

A telling deficiency

To find out why they were particularly prone to getting TB, the researchers performed whole-exome sequencing on the two, as well as a genetic analysis of their respective parents and relatives.

The two were the only members of their extended family with a mutation in the TNF gene, which encodes for proteins linked to the regulation of a variety of biological processes. Short for “tumor necrosis factor,” increased TNF production is also associated with a variety of conditions, including septic shock, cancer, rheumatoid arthritis, and cachexia, which causes dangerous weight loss.

The protein is largely secreted by a type of phagocyte called a macrophage, which relies on the ROS molecules generated by the respiratory burst to finish off pathogens they’ve consumed.

In these two patients, the TNF gene failed to function, preventing the respiratory burst from occurring, and thus the creation of ROS molecules. As a result, the patients’ alveolar macrophages, located in their lungs, were overrun with Mtb.

“We knew that the respiratory burst was important for protecting people against various types of mycobacteria, but now we know that TNF is actually regulating the process,” says Boisson-Dupuis. “And when it’s missing in alveolar macrophages, people will be susceptible to airborne TB.”

She adds, “It’s very surprising that the people we studied are adults who have never been sick with other infectious diseases, despite being repeatedly exposed to their microbes. They are apparently selectively at risk for TB.”

Treatment potential

The discovery also solves a long-standing mystery about why TNF inhibitors, which are used to treat autoimmune and inflammatory diseases, raise the chances of contracting TB. Without TNF, a key part of the defense against it is defunct.

The findings may lead to a radical reassessment of TNF’s role in immune function — and new treatment possibilities. “TNF is required for immunity against Mtb, but it seems to be redundant for immunity against many other pathogens,” Casanova says. “So the question is, what other pro-inflammatory cytokines are doing the jobs we thought TNF was doing? If we can discover that, we may be able to block these cytokines rather than TNF to treat diseases where inflammation plays a role.”

The structure within Earth’s liquid core is found only at low latitudes and sits parallel to the equator. According to ANU seismologists, it has remained undetected until now.

The Earth has two core layers: the inner core, a solid layer, and the outer core, a liquid layer. Surrounding the Earth’s core is the mantle. The newly discovered doughnut-shaped region is at the top of Earth’s outer core, where the liquid core meets the mantle.

Study co-author and ANU geophysicist, Professor Hrvoje Tkalčić, said the seismic waves detected are slower in the newly discovered region than in the rest of the liquid outer core.

“The region sits parallel to the equatorial plane, is confined to the low latitudes and has a doughnut shape,” he said.

“We don’t know the exact thickness of the doughnut, but we inferred that it reaches a few hundred kilometres beneath the core-mantle boundary.”

Rather than using traditional seismic wave observation techniques and observing signals generated by earthquakes within the first hour, the ANU scientists analysed the similarities between waveforms many hours after the earthquake origin times, leading them to make the unique discovery.

“By understanding the geometry of the paths of the waves and how they traverse the outer core’s volume, we reconstructed their travel times through the Earth, demonstrating that the newly discovered region has low seismic speeds,” Professor Tkal?i? said.

“The peculiar structure remained hidden until now as previous studies collected data with less volumetric coverage of the outer core by observing waves that were typically confined within one hour after the origin times of large earthquakes.

“We were able to achieve much better volumetric coverage because we studied the reverberating waves for many hours after large earthquakes.”

Study co-author, Dr Xiaolong Ma, said that the discovery uncovers some mysteries of the dynamics of Earth’s magnetic field.

“There are still mysteries about the Earth’s outer core that are yet to be solved, which requires multidisciplinary efforts from seismology, mineral physics, geomagnetism and geodynamics,” Dr Ma said.

The outer core is predominantly made of liquid iron and nickel, and the vigorous movement of the electrically conductive liquid creates Earth’s magnetic field, which shields around Earth and helps to sustain all life, protecting it from damaging solar winds and harmful radiation.

The scientists believe that knowing more about the Earth’s outer core’s composition, including light chemical elements, is fundamental to understanding the magnetic field and predicting when it could potentially cease or weaken.

“Our findings are interesting because this low velocity within the liquid core implies that we have a high concentration of light chemical elements in these regions that would cause the seismic waves to slow down. These light elements, alongside temperature differences, help stir liquid in the outer core,” Professor Tkalčić said.

“The magnetic field is a fundamental ingredient that we need for life to be sustained on the surface of our planet.

“The dynamics of Earth’s magnetic field is an area of strong interest in the scientific community, so our results could promote more research about the magnetic field on both Earth and other planets.”

The research is published in Science Advances.

The study, published Aug. 30 in the journal Science Advances, offers renewed promise when it comes to discovering new drugs.

“The hope is we can speed up the timeline of drug discovery from years to months,” said Alex Thorman, PhD, co-first author and a postdoctoral fellow in the Department of Environmental and Public Health Sciences in the College of Medicine.

Researchers combined two approaches for screening potential new drugs. First, they used a database from the Library of Integrated Network-based Cellular Signatures (LINCS) to screen tens of thousands of small molecules with potential therapeutic effects simultaneously. Then they combined the search with targeted docking simulations used to model the interaction between small molecules and their protein targets to find compounds of interest. That sped up the timing of the work from months to minutes — taking weeks of work required for initial screening down to an afternoon.

Thorman said this faster screening method for compounds that could become drugs accelerates the drug research process. But it’s not only speed that is crucial.

He added that this newer approach is more efficient at identifying potentially effective compounds.

“And the accuracy will only improve, hopefully offering new hope to many people who have diseases with no known cure, including those with cancer,” Thorman said.

It can also create more targeted treatment options in precision medicine, an innovative approach to tailoring disease prevention and treatment that takes into account differences in people’s genes, environments and lifestyles.

“An accelerated drug discovery process also could be a game changer in the ability to respond to public health crises, such as the COVID-19 pandemic,” said Thorman. “The timeline for developing effective drugs could be expedited.”

The other co-first authors were Jim Reigle, PhD, a postdoctoral fellow at Cincinnati Children’s Hospital, and Somchai Chutipongtanate, PhD, an associate professor in the Department of Environmental and Public Health Sciences in the College of Medicine.

The corresponding authors of the study were Jarek Meller, PhD, a professor of biostatistics, health informatics and data sciences in the College of Medicine, and Andrew Herr, PhD, a professor of immunobiology in the Department of Pediatrics in the College of Medicine.

Other co-investigators included Mario Medvedovic, PhD, professor and director of the Center for Biostatistics and Bioinformatics Services in the College of Medicine, and David Hildeman, PhD, professor of immunobiology in the College of Medicine. Both Herr and Hildeman have faculty research labs at Cincinnati Children’s Hospital.

This research was funded in part by grants from the National Institutes of Health, a Department of Veterans Affairs merit award, a UC Cancer Center Pilot Project Award and a Cincinnati Children’s Hospital Innovation Fund award.

Those involved in the research are also co-inventors on three U.S. patents that are related to their work and have been filed by Cincinnati Children’s Hospital.

Younger vultures shy away from the most popular roosts, suggesting they might be intimidated by the older ones or that there’s a vulture equivalent of “Hey you kids, get off my lawn.”

The research, published in Proceedings of the National Academy of Sciences, shows that like many people, older vultures tend to have fewer, more selective friendships with stronger bonds. They may also have a more thorough knowledge of where to find food resources.

Eurasian griffon vultures, or Gyps fulvus, are large vultures that live in the Mediterranean, the Middle East and India. With wingspans up to 9 feet, they’re much larger than North American turkey vultures and bigger than bald eagles.

Finding food can be tricky for vultures because it depends on locating animal carcasses — an unpredictable and ephemeral source. When griffon vultures find a carcass, they tend to sleep or roost nearby and feed on it over a period of days. Roosting sites can thus be ‘information hubs,’ where vultures that recently fed signal to others about food sources; they then follow each other to carcasses and form friendships that help them stay in the loop about food.

The researchers wanted to know if an individual griffon vulture’s movement patterns and social behavior changed over the course of its life. They used GPS data from 142 individually tagged birds in Israel gathered over a period of 15 years to cross-reference the vultures’ ages with their movement and social interactions at roost sites.

“What we found was as they age, their loyalty to certain roost sites increases,” said co-author Noa Pinter-Wollman, a UCLA professor of ecology and evolutionary biology. “Young vultures check out many different roosts but in middle age, they start going repeatedly to the same places.”

The study showed young vultures sometimes returned to the same roost but usually chose different ones, rarely spending two nights in the same place. From young adulthood at around 5 years old through middle age, they spent about half their nights at the same “home” site and half elsewhere. In old age, they became true homebodies.

“When they are old, from the age of 10 onward, they no longer have the energy to be ‘out and about’ and return consistently to the same site,” said corresponding author Orr Spiegel of Tel Aviv University. “Those who were adventurous at the age of 5 became more sedentary by age 10.”

As the vultures grew older, the strength of their social bonds decreased as well for at least part of the year. The number of individuals they interacted with didn’t change with age — if they had five friends when young, they still had five when older. But the amount of time they spent with vultures outside of their close friend group plummeted. Older vultures spent most of their time with and roosted mostly with these close friends. Their movements also became more routine, eventually following a predictable pattern.

The study is unique because the researchers were able to track the movements and social behaviors of the same vultures for up to 12 nearly consecutive years over a 15-year period.

“We are able to show that the trends of individuals becoming more loyal to the same sites with age is not because the more exploratory individuals die earlier and live shorter lives, and the older, more sedentary individuals live longer lives,” said first author and Tel Aviv University postdoctoral fellow Marta Acácio. “Individuals actually change their behavior with age, and this has rarely been shown in nature for long-lived birds due to the difficulty of tracking individuals for such a long time.”

The research backs up findings from studies in other species that, with age, animals become more faithful to their known sites and routines — and potentially become more selective in their social relationships. These behaviors are commonly attributed to aging in humans and can help improve understanding of how animal populations move about in their environments and relate to other members of their species, as well as identify better ways to protect them from threats. For griffon vultures, this could mean better protection of important roosting sites and using knowledge about their social interactions to reduce the risk of poisoning.

“It looks like they just get set in their ways,” Pinter-Wollman said. “They’ve gathered information over the years, and they might as well use it. Carcasses are hard to come by and roosts are information hubs. Some roosts become popular for a reason; for example, they tend to be closer to reliable food sources and older vultures potentially monopolize these roosts.”