WASP-76b is an ultra-hot giant planet. Orbiting its host star twelve times closer than Mercury orbits our Sun, it receives more than 4,000 times the Sun’s radiation on Earth. ”The exoplanet is ‘inflated’ by the intense radiation from its star. So, although it is 10% less massive than our cousin Jupiter, it is almost twice as big,” explains Monika Lendl, assistant professor in the Department of Astronomy of the UNIGE Faculty of Science, and co-author of the study.

Since its discovery in 2013, WASP-76b has been the subject of intense scrutiny by astronomers. A strangely hellish picture has emerged. One side of the planet is always facing its star, reaching temperatures of 2,400 degrees Celsius. Elements that would form rocks on Earth melt and evaporate here, before condensing on the slightly cooler night side, creating clouds of iron that drip molten iron rain.

The crucial contribution of CHEOPS

One of the most disturbing observations for astronomers is the asymmetry between the planet’s two terminators. The terminator is the imaginary line that separates the day and night sides of a planet. In the case of WASP-76b, the observations show an increase in the amount of light from the terminator to the east of the planet compared with the one to the west.

To solve this mystery, astronomers used no fewer than twenty-three observations with the CHEOPS space telescope, spread over three years. The ESA satellite, which is piloted by Switzerland and has its scientific operations centre at the UNIGE Department of Astronomy, observed numerous secondary eclipses of the planet (when it passes behind its star) and several phase curves (continuous observation during a complete revolution of the planet).

Combining these new data with those from other telescopes (TESS, Hubble and Spitzer), the astronomers were able to put forward a surprising hypothesis to explain the excess luminous flux on the eastern side of the planet: ”This unexpected glow could be caused by a strong, localised and anisotropic reflection — i.e. one that depends on direction — what we call a glory,” explains Olivier Demangeon, researcher at the Instituto de Astrofísica e Ciências do Espaço in Portugal and lead author of the study.

A first outside our solar system

Glories are common phenomena on Earth. They have also been observed on Venus. The effect, similar to a rainbow, occurs when light is reflected by clouds made up of perfectly uniform droplets. In the case of Earth, the droplets are made out of water, but the nature of these droplets on WASP-76b remains mysterious. It could be iron, as this has already been detected in the planet’s extremely hot atmosphere. The detection of this phenomenon on WASP-76b is the first of its kind outside our solar system.

”The reason why no such glory has ever been observed outside our solar system is that this phenomenon requires very specific conditions. First of all, the atmospheric particles must be almost perfectly spherical, completely uniform and sufficiently stable to be observed throughout a long time. These droplets have to be directly illuminated by the planet’s host star, and the observer — in this case CHEOPS — must be in the right position,” explains Olivier Demangeon.

Results to be confirmed

Further data will be needed to confirm with certainty that this intriguing excess of light on the eastern terminator of WASP-76b is a glory. This confirmation would attest to the presence of clouds made up of perfectly spherical droplets that have existed for at least three years, or that are constantly renewing themselves. For such clouds to persist, the temperature of the atmosphere would also have to be stable over time — a fascinating and detailed insight into what could be happening on WASP-76b.

Detecting such tiny phenomena at such a great distance will enable scientists and engineers to identify others that are just as crucial. For example, the reflection of starlight off liquid lakes and oceans — a necessary condition for habitability.

Every minute, a garbage truck’s worth of plastic enters the ocean. With plastic use expected to double by 2040, understanding how and where it travels is crucial to protecting marine ecosystems and wildlife.

Dr Denise Hardesty, Senior Research Scientist with CSIRO, said this is the first estimate of how much plastic waste ends up on the ocean floor, where it accumulates before being broken down into smaller pieces and mixed into ocean sediment.

“We know that millions of tonnes of plastic waste enter our oceans every year but what we didn’t know is how much of this pollution ends up on our ocean floor,” Dr Hardesty said.

“We discovered that the ocean floor has become a resting place, or reservoir, for most plastic pollution, with between 3 to 11 million tonnes of plastic estimated to be sinking to the ocean floor.

“While there has been a previous estimate of microplastics on the seafloor, this research looks at larger items, from nets and cups to plastic bags and everything in between.”

Ms Alice Zhu, a PhD Candidate from the University of Toronto who led the study, said the estimate of plastic pollution on the ocean floor could be up to 100 times more than the amount of plastic floating on the ocean’s surface based on recent estimates.

“The ocean surface is a temporary resting place of plastic so it is expected that if we can stop plastic entering our oceans, the amount would be reduced,” Ms Zhu said.

“However, our research found that plastic will continue to end up in the deep ocean, which becomes a permanent resting place or sink for marine plastic pollution,”

Scientific data was used to build two predictive models to estimate the amount and distribution of plastic on the ocean floor — one based on data from remote operated vehicles (ROVs) and the other from bottom trawls.

Using ROV data, 3 to 11 million metric tonnes of plastic pollution is estimated to reside on the ocean floor.

The ROV results also reveal that plastic mass clusters around continents — approximately half (46 per cent) of the predicted plastic mass on the global ocean floor resides above 200 m depth. The ocean depths, from 200 m to as deep as 11,000 m contains the remainder of predicted plastic mass (54 per cent).

Although inland and coastal seas cover much less surface area than oceans (11 per cent vs 56 per cent out of the entire Earth’s area), these areas are predicted to hold as much plastic mass as does the rest of the ocean floor.

“These findings help to fill a longstanding knowledge gap on the behaviour of plastic in the marine environment,” Ms Zhu said.

“Understanding the driving forces behind the transport and accumulation of plastic in the deep ocean will help to inform source reduction and environmental remediation efforts, thereby reducing the risks that plastic pollution may pose to marine life.”

The article, Plastics in the deep sea — A global estimate of the ocean floor reservoir, was published in Deep Sea Research Part I: Oceanographic Research Papers.

This research is part of CSIRO’s Ending Plastic Waste Mission, which aims to change the way we make, use, recycle and dispose of plastic.

They ate their neighbors.

This is just one of the more peculiar findings from new Northwestern University research. Using a new model, astrophysicists traced the violent journeys of 1,000 simulated stars orbiting our galaxy’s central supermassive black hole, Sagittarius A* (Sgr A*).

So densely packed with stars, the region commonly experiences brutal stellar collisions. By simulating the effects of these intense collisions, the new work finds that collision survivors can lose mass to become stripped down, low-mass stars or can merge with other stars to become massive and rejuvenated in appearance.

“The region around the central black hole is dense with stars moving at extremely high speeds,” said Northwestern’s Sanaea C. Rose, who led the research. “It’s a bit like running through an incredibly crowded subway station in New York City during rush hour. If you aren’t colliding into other people, then you are passing very closely by them. For stars, these near collisions still cause them to interact gravitationally. We wanted to explore what these collisions and interactions mean for the stellar population and characterize their outcomes.”

Rose will present this research at the American Physical Society’s (APS) April meeting in Sacramento, California. “Stellar Collisions in the Galactic Center” will take place on Thursday (April 4) as part of the session “Particle Astrophysics and the Galactic Center.”

Rose is the Lindheimer Postdoctoral Fellow at Northwestern’s Center for Interdisciplinary Exploration and Research in Astrophysics (CIERA). She began this work as a Ph.D. candidate at UCLA.

Destined to collide

The center of our Milky Way is a strange and wild place. The gravitational pull of Sgr A* accelerates stars to whip around their orbits at terrifying speeds. And the sheer number of stars packed into the galaxy’s center is upwards of a million. The densely packed cluster plus the lightning-fast speeds equal a high-speed demolition derby. In the innermost region — within 0.1 parsecs of the black hole — few stars escape unscathed.

“The closest star to our sun is about four light-years away,” Rose explained. “Within that same distance near the supermassive black hole, there are more than a million stars. It’s an incredibly crowded neighborhood. On top of that, the supermassive black hole has a really strong gravitational pull. As they orbit the black hole, stars can move at thousands of kilometers per second.”

Within this tight, hectic neighborhood, stars can collide with other stars. And the closer stars live to the supermassive black hole, the likelihood of collision increases. Curious of the outcomes of these collisions, Rose and her collaborators developed a simulation to trace the fates of stellar populations in the galactic center. The simulation takes several factors into account: density of the stellar cluster, mass of the stars, orbit speed, gravity and distances from the Sgr A*.

From ‘violent high fives’ to total mergers

In her research, Rose pinpointed one factor that is most likely to determine a star’s fate: its distance from the supermassive black hole.

Within 0.01 parsecs from the black hole, stars — moving at speeds reaching thousands of kilometers per second — constantly bump into one another. It’s rarely a head-on collision and more like a “violent high five,” as Rose describes it. The impacts are not strong enough to smash the stars completely. Instead, they shed their outer layers and continue speeding along the collision course.

“They whack into each other and keep going,” Rose said. “They just graze each other as though they are exchanging a very violent high five. This causes the stars to eject some material and lose their outer layers. Depending on how fast they are moving and how much they overlap when they collide, they might lose quite a bit of their outer layers. These destructive collisions result in a population of strange, stripped down, low-mass stars.”

Outside of 0.01 parsecs, stars move at a more relaxed pace — hundreds of kilometers per second as opposed to thousands. Because of the slower speeds, these stars collide with one another but then don’t have enough energy to escape. Instead, they merge to become more massive. In some cases, they might even merge multiple times to become 10 times more massive than our sun.

“A few stars win the collision lottery,” Rose said. “Through collisions and mergers, these stars collect more hydrogen. Although they were formed from an older population, they masquerade as rejuvenated, young-looking stars. They are like zombie stars; they eat their neighbors.”

But the youthful appearance comes at the cost of a shorter life expectancy.

“They die very quickly,” Rose said. “Massive stars are sort of like giant, gas-guzzling cars. They start with a lot of hydrogen, but they burn through it very, very fast.”

Extreme environment ‘unlike any other’

Although Rose finds simple joy in studying the bizarre, extreme region near our galactic center, her work also can reveal information about the history of the Milky Way. And because the central cluster is extremely difficult to observe, her team’s simulations can illuminate otherwise hidden processes.

“It’s an environment unlike any other,” Rose said. “Stars, which are under the influence of a supermassive black hole in a very crowded region, are unlike anything we will ever see in our own solar neighborhood. But if we can learn about these stellar populations, then we might be able to learn something new about how the galactic center was assembled. At the very least, it certainly provides a point of contrast for the neighborhood where we live.”

Rose’s APS presentation will include research published by The Astrophysical Journal Letters in March 2024and by The Astrophysical Journal in September 2023.

This work was supported by the National Science Foundation (grant number AST 2206428) and NASA (grant number 80NSSC20K050) as well as by the Charles E. Young Fellowship, the Dissertation Year Fellowship at UCLA, the Thacher Fellowship, the Bhaumik Institute and the CIERA Lindheimer Fellowship.

Patients with acute heart attacks (ST elevation myocardial infarction, or STEMI) are very likely to survive if they undergo timely reopening of the occluded coronary artery (coronary reperfusion) in specialized clinical centers. Despite the given survival rates and major improvements in treatment, progression to heart failure still represents a major clinical problem. The patients’ longer-term outcomes depend on the extent of the damage to their heart tissue.

Lead investigator Helen M. Arthur, PhD, Biosciences Institute, Faculty of Medical Sciences, Newcastle University, explains: “Coronary reperfusion after STEMI is standard therapy to salvage ischemic heart muscle. However, evidence suggests that the subsequent inflammatory response that the body initiates to repair the damaged heart tissue can also cause further loss of viable heart muscle. The more muscle that is lost, the greater the risk of subsequent progression to heart failure. The reason for this study was to investigate the potential protective effects of TGFβ1as a possible intervention to minimize this additional damage to the heart beyond the ischemic damage caused by the heart attack itself.”

The research team found that levels of an important anti-inflammatory protein TGFβ1 in the blood of STEMI patients 24 hours after reperfusion correlated with a reduction in infarct size after three months. To investigate this further they used an established mouse model of a heart attack to test the protective effects of TGFβ1, a protein known to be released in the body in response to tissue injury. They also studied its mimic HpTGM, a protein produced by a parasitic worm to help evade the immune response and thereby enable the worm to live within the tissue lining the gut. Intravascular delivery of either of these naturally occurring anti-inflammatory proteins reduced the injurious inflammatory response within the heart and importantly, the extent of heart injury as evidenced by reduced mature scar size.

The investigators were surprised to find almost identical beneficial effects of TGFβ1 and HpTGM treatment. Although TGFβ1 and HpTGM are evolutionarily unrelated, both these molecules interact with cells in a similar manner by activating the same signalling pathway. The dose of anti-inflammatory therapy was given at the time of reperfusion, which corresponds to a clinically useful time for a therapeutic intervention in humans.

Investigators could attribute the beneficial outcomes to the protective effect of these molecules on endothelial cells — the cells lining the blood vessels that help to regulate the exit of proinflammatory white blood cells from the circulation and enter the injured tissue. TGFβ1 has well-established anti-inflammatory properties, whereas HpTGM is a parasitomimetic with great clinical potential. Recent work in the Maizels laboratory at the University of Glasgow has also shown that delivery of HpTGM has a major anti-inflammatory effect in mouse models of colitis or airway inflammation, taking advantage of the product evolved by a parasite to quell the immune response to its presence.

Dr. Arthur concluded: “The current study shows that exogenous delivery of HpTGM at the time of coronary artery reperfusion dampens the proinflammatory response of coronary endothelial cells and reduces cardiac injury, leading to increased myocardial salvage and reduced scar size with the corollary of improved prospects for long-term cardiac function. The use of HpTGM as an anti-inflammatory therapy in treating heart attack patients is clearly an exciting prospect that requires further translational studies.”

Most current asthma treatments stem from the idea that it is an inflammatory disease. Yet, the life-threatening feature of asthma is the attack or the constriction of airways, making breathing difficult. The new study, published today in Science, shows for the first time that many features of an asthma attack — inflammation, mucus secretion, and damage to the airway barrier that prevents infections — result from this mechanical constriction in a mouse model.

The findings suggest that blocking a process that normally causes epithelial cell death could prevent the damage, inflammation, and mucus that result from an asthma attack.

Professor Jody Rosenblatt from King’s College London said: “Our discovery is the culmination of more than ten years work. As cell biologists who watch processes, we could see that the physical constriction of an asthma attack causes widespread destruction of the airway barrier. Without this barrier, asthma sufferers are far more likely to get long-term inflammation, wound healing, and infections that cause more attacks. By understanding this fundamental mechanism, we are now in a better position to prevent all these events.”

In the UK, 5.4 million people have asthma and can suffer from symptoms such as wheezing, coughing, feeling breathlessness and a tight chest. Triggers such as pollen or dust can make asthma symptoms worse and can lead to a life-threatening asthma attack.

Despite the disease commonality, the causes of asthma are still not understood. Current medications treat the consequences of an asthma attack by opening the airways, calming inflammation, and breaking up the sticky mucus which clogs the airway, which help control asthma, but do not prevent it.

The answer to stopping asthma symptoms may lie in cell extrusion, a process the researchers discovered that drives most epithelial cell death. Scientists used mouse lung models and human airway tissue to discover that when the airways contract, known as bronchoconstriction, the epithelial cells that line the airway get squeezed out to later die.

Because bronchoconstriction causes so many cell extrusions, it damages the airway barrier which causes inflammation and excess mucus.

In previous studies, the scientists found that the chemical compound gadolinium can block extrusion. In this study, they found it could work in mice to prevent the excess extrusion that causes damage and inflammation after an asthma attack. The authors note that gadolinium has not been tested in humans and has not been deemed to be safe or efficacious.

Professor Rosenblatt said: “This constriction and destruction of the airways causes the post-attack inflammation and excess mucus secretion that makes it difficult for people with asthma to breathe.

“Current therapies do not prevent this destruction — an inhaler such as Albuterol opens the airways, which is critical to breathing but, dishearteningly, we found it does not prevent the damage and the symptoms that follow an attack. Fortunately, we found that we can use an inexpensive compound, gadolinium which is frequently used for MRI imaging, to stop the airway damage in mice models as well as the ensuing inflammation and mucus secretion. Preventing this damage could then prevent the build-up of musculature that cause future attacks.”

Professor Chris Brightling from the University of Leicester and one of the co-authors of the study said: “In the last decade there has been tremendous progress in therapies for asthma particularly directed towards airway inflammation. However, there remains ongoing symptoms and attacks in many people with asthma. This study identifies a new process known as epithelial extrusion whereby damage to the lining of the airway occurs as a consequence of mechanical constriction and can drive many of the key features of asthma. Better understanding of this process is likely to lead to new therapies for asthma.”

Dr Samantha Walker, Director of Research and Innovation at Asthma + Lung UK, said: “Only two per cent of public health funding is allocated to developing new treatments for the 12 million people living with lung conditions in the UK so new research that can help in the treatment or prevention of asthma is good news.

“This research using an experimental mouse model shows that constricting the airways leads to damage to the lung lining and inflammation, like that seen in asthma. It is this constriction and resulting damage that makes it difficult for people with asthma to breathe.

“Current medications for asthma work by treating the inflammation, but this isn’t effective for everyone. Treatments aim to prevent future asthma attacks and improve asthma control by taking inhalers every day, but we know that ~31 per cent of people with asthma don’t have treatment options that work for them, putting them at risk of potentially life-threatening asthma attacks.

“This discovery opens important new doors to explore possible new treatment options desperately needed for people with asthma rather than focusing solely on inflammation.”

The discovery of the mechanics behind cell extrusion could underlie other inflammatory diseases that also feature constriction such as cramping of the gut and inflammatory bowel disease.

The paper is in collaboration with the University of Leicester and funded by Wellcome, Howard Hughes Medical Institute and the American Asthma Foundation.