NASA Model Describes Nearby Star which Resembles Ours in its Youth (Planetary Science)

New research led by NASA provides a closer look at a nearby star thought to resemble our young Sun. The work allows scientists to better understand what our Sun may have been like when it was young, and how it may have shaped the atmosphere of our planet and the development of life on Earth. 

Many people dream of meeting with a younger version of themselves to exchange advice, identify the origins of their defining traits, and share hopes for the future. At 4.65 billion years old, our Sun is a middle-aged star. Scientists are often curious to learn exactly what properties enabled our Sun, in its younger years, to support life on nearby Earth.

An artist's concept of what the Sun may have looked like 4 billion years ago.
Illustration of what the Sun may have been like 4 billion years ago, around the time life developed on Earth.Credits: NASA’s Goddard Space Flight Center/Conceptual Image Lab

Without a time machine to transport scientists back billions of years, retracing our star’s early activity may seem an impossible feat. Luckily, in the Milky Way galaxy – the glimmering, spiraling segment of the universe where our solar system is located – there are more than 100 billion stars. One in ten share characteristics with our Sun, and many are in the early stages of development.

“Imagine I want to reproduce a baby picture of an adult when they were one or two years old, and all of their pictures were erased or lost. I would look at a photo of them now, and their close relatives’ photos from around that age, and from there, reconstruct their baby photos,” said Vladimir Airapetian, senior astrophysicist in the Heliophysics Division at NASA’s Goddard Space Flight Center in Greenbelt, Maryland, and first author on the new study. “That’s the sort of process we are following here – looking at characteristics of a young star similar to ours, to better understand what our own star was like in its youth, and what allowed it to foster life on one of its nearby planets.”

Kappa 1 Ceti is one such solar analogue. The star is located about 30 light-years away (in space terms, that’s like a neighbor who lives on the next street over) and is estimated to be between 600 to 750 million years old, around the same age our Sun was when life developed on Earth. It also has a similar mass and surface temperature to our Sun, said the study’s second author, Meng Jin, a heliophysicist with the SETI Institute and the Lockheed Martin Solar and Astrophysics Laboratory in California. All of those factors make Kappa 1 Ceti a “twin” of our young Sun at the time when life arose on Earth, and an important target for study.

Airapetian, Jin, and several colleagues have adapted an existing solar model to predict some of Kappa 1 Ceti’s most important, yet difficult to measure, characteristics. The model relies on data input from a variety of space missions including the NASA/ESA Hubble Space Telescope, NASA’s Transiting Exoplanet Survey Satellite and NICER missions, and ESA’s XMM-Newton. The team published their study today in The Astrophysical Journal.

Star Power

Like human toddlers, toddler stars are known for their high bursts of energy and activity. For stars, one way this pent-up energy is released is in the form of a stellar wind.

Stellar winds, like stars themselves, are mostly made up of a superhot gas known as plasma, created when particles in a gas have split into positively charged ions and negatively charged electrons. The most energetic plasma, with the help of a star’s magnetic field, can shoot off away from the outermost and hottest part of a star’s atmosphere, the corona, in an eruption, or stream more steadily toward nearby planets as stellar wind. “Stellar wind is continuously flowing out from a star toward its nearby planets, influencing those planets’ environments,” Jin said.

Younger stars tend to generate hotter, more vigorous stellar winds and more powerful plasma eruptions than older stars do. Such outbursts can affect the atmosphere and chemistry of planets nearby, and possibly even catalyze the development of organic material – the building blocks for life – on those planets.

Stellar wind can have a significant impact on planets at any stage of life. But the strong, highly dense stellar winds of young stars can compress the protective magnetic shields of surrounding planets, making them even more susceptible to the effects of the charged particles.

An artist concept of a coronal mass ejection hitting young Earth's weak magnetosphere.
An artist concept of a coronal mass ejection hitting young Earth’s weak magnetosphere.Credits: NASA/GSFC/CIL

Our Sun is a perfect example. Compared to now, in its toddlerhood, our Sun likely rotated three times faster, had a stronger magnetic field, and shot out more intense high-energy radiation and particles. These days, for lucky spectators, the impact of these particles is sometimes visible near the planet’s poles as aurora, or the Northern and Southern Lights. Airapetian says 4 billion years ago, considering the impact of our Sun’s wind at that time, these tremendous lights were likely often visible from many more places around the globe.

That high level of activity in our Sun’s nascence may have pushed back Earth’s protective magnetosphere, and provided the planet – not close enough to be torched like Venus, nor distant enough to be neglected like Mars – with the right atmospheric chemistry for the formation of biological molecules.

Similar processes could be unfolding in stellar systems across our galaxy and universe.

“It’s my dream to find a rocky exoplanet in the stage that our planet was in more than 4 billion years ago, being shaped by its young, active star and nearly ready to host life,” Airapetian said. “Understanding what our Sun was like just as life was beginning to develop on Earth will help us to refine our search for stars with exoplanets that may eventually host life.”

A Solar Twin

Though solar analogues can help solve one of the challenges of peeking into the Sun’s past, time isn’t the only complicating factor in studying our young Sun. There’s also distance.

We have instruments capable of accurately measuring the stellar wind from our own Sun, called the solar wind. However, it’s not yet possible to directly observe the stellar wind of other stars in our galaxy, like Kappa 1 Ceti, because they are too far away.

When scientists wish to study an event or phenomenon that they cannot directly observe, scientific modeling can help fill in the gaps. Models are representations or predictions of an object of study, built on existing scientific data. While scientists have previously modeled the stellar wind from this star, Airapetian said, they used more simplified assumptions.

The basis for the new model of Kappa 1 Ceti by Airapetian, Jin, and colleagues is the Alfvén Wave Solar Model, which is within the Space Weather Modeling Framework developed by the University of Michigan. The model works by inputting known information about a star, including its magnetic field and ultraviolet emission line data, to predict stellar wind activity. When the model has been tested on our Sun, it has been validated and checked against observed data to verify that its predictions are accurate.

“It’s capable of modeling our star’s winds and corona with high fidelity,” Jin said. “And it’s a model we can use on other stars, too, to predict their stellar wind and thereby investigate habitability. That’s what we did here.”

Previous studies have drawn on data gathered by the Transiting Exoplanet Survey Satellite (TESS) and Hubble Space Telescope (HST) to identify Kappa 1 Ceti as a young solar proxy, and to gather the necessary inputs for the model, such as magnetic field and ultraviolet emission line data.

The hot stellar corona, the outermost layer in a star’s atmosphere, expands into the stellar wind, driven by heating from the star’s magnetic field and magnetic waves. The researchers modeled the stellar magnetic corona of Kappa 1 Ceti in 3D, based on data from 2012 and 2013.Credits: NASA

“Every model needs input to get output,” Airapetian said. “To get useful, accurate output, the input needs to be solid data, ideally from multiple sources across time. We have all that data from Kappa 1 Ceti, but we really synthesized it in this predictive model to move past previous purely observational studies of the star.”

Airapetian likens his team’s model to a doctor’s report. To get a full picture of how a patient is doing, a doctor is likely to talk to the patient, gather markers like heart rate and temperature, and if needed, conduct several more specialized tests, like a blood test or ultrasound. They are likely to formulate an accurate assessment of patient well-being with a combination of these metrics, not just one.

Similarly, by using many pieces of information about Kappa 1 Ceti gathered from different space missions, scientists are better able to predict its corona and the stellar wind. Because stellar wind can affect a nearby planet’s magnetic shield, it plays an important role in habitability. The team is also working on another project, looking more closely at the particles that may have emerged from early solar flares, as well as prebiotic chemistry on Earth.

Our Sun’s Past, Written in the Stars

The researchers hope to use their model to map the environments of other Sun-like stars at various life stages.

Specifically, they have eyes on the infant star EK Dra – 111 light-years away and only 100 million years old – which is likely rotating three times faster and shooting off more flares and plasma than Kappa 1 Ceti. Documenting how these similar stars of various ages differ from one another will help characterize the typical trajectory of a star’s life.

Their work, Airapetian said, is all about “looking at our own Sun, its past and its possible future, through the lens of other stars.”

To learn more about our Sun’s stormy youth, watch this video and see how energy from our young Sun — 4 billion years ago — aided in creating molecules in Earth’s atmosphere, allowing it to warm up enough to incubate life.

Banner image: A view of the Sun from the Extreme ultraviolet Imaging Telescope on ESA/NASA’s Solar and Heliospheric Observatory, or SOHO.  Credits: ESA/NASA


Reference: Vladimir S. Airapetian et al, One Year in the Life of Young Suns: Data-constrained Corona-wind Model of κ 1 Ceti, The Astrophysical Journal (2021). DOI: 10.3847/1538-4357/ac081e


Provided by NASA

Space Scientists Reveal Secret Behind Jupiter’s ‘Energy Crisis’ (Planetary Science)

New research published in Nature has revealed the solution to Jupiter’s ‘energy crisis’, which has puzzled astronomers for decades.

Space scientists at the University of Leicester worked with colleagues from the Japanese Space Agency (JAXA), Boston University, NASA’s Goddard Space Flight Center and the National Institute of Information and Communications Technology (NICT) to reveal the mechanism behind Jupiter’s atmospheric heating.

Now, using data from the Keck Observatory in Hawai’i, astronomers have created the most-detailed yet global map of the gas giant’s upper atmosphere, confirming for the first time that Jupiter’s powerful aurorae are responsible for delivering planet-wide heating.

Dr James O’Donoghue is a researcher at JAXA and completed his PhD at Leicester, and is lead author for the research paper.

He said: “We first began trying to create a global heat map of Jupiter’s uppermost atmosphere at the University of Leicester. The signal was not bright enough to reveal anything outside of Jupiter’s polar regions at the time, but with the lessons learned from that work we managed to secure time on one of the largest, most competitive telescopes on Earth some years later.

“Using the Keck telescope we produced temperature maps of extraordinary detail. We found that temperatures start very high within the aurora, as expected from previous work, but now we could observe that Jupiter’s aurora, despite taking up less than 10% of the area of the planet, appear to be heating the whole thing.

“This research started in Leicester and carried on at Boston University and NASA before ending at JAXA in Japan. Collaborators from each continent working together made this study successful, combined with data from NASA’s Juno spacecraft in orbit around Jupiter and JAXA’s Hisaki spacecraft, an observatory in space.”

Dr Tom Stallard and Dr Henrik Melin are both part of the School of Physics and Astronomy at the University of Leicester. Dr Stallard added: “There has been a very long-standing puzzle in the thin atmosphere at the top of every Giant Planet within our solar system.

“With every Jupiter space mission, along with ground-based observations, over the past 50 years, we have consistently measured the equatorial temperatures as being much too hot.

“This ‘energy crisis’ has been a long standing issue – do the models fail to properly model how heat flows from the aurora, or is there some other unknown heat source near the equator?

“This paper describes how we have mapped this region in unprecedented detail and have shown that, at Jupiter, the equatorial heating is directly associated with auroral heating.”

Aurorae occur when charged particles are caught in a planet’s magnetic field. These spiral along the field lines towards the planet’s magnetic poles, striking atoms and molecules in the atmosphere to release light and energy.

On Earth, this leads to the characteristic light show that forms the Aurora Borealis and Australis. At Jupiter, the material spewing from its volcanic moon, Io, leads to the most powerful aurora in the Solar System and enormous heating in the polar regions of the planet.

Although the Jovian aurorae have long been a prime candidate for heating the planet’s atmosphere, observations have previously been unable to confirm or deny this until now.

Previous maps of the upper atmospheric temperature were formed using images consisting of only several pixels. This is not enough resolution to see how the temperature might be changed across the planet, providing few clues as to the origin of the extra heat.

Researchers created five maps of the atmospheric temperature at different spatial resolutions, with the highest resolution map showing an average temperature measurement for squares two degrees longitude ‘high’ by two degrees latitude ‘wide’.

The team scoured more than 10,000 individual data points, only mapping points with an uncertainty of less than five per cent.

Models of the atmospheres of gas giants suggest that they work like a giant refrigerator, with heat energy drawn from the equator towards the pole, and deposited in the lower atmosphere in these pole regions.

These new findings suggest that fast-changing aurorae may drive waves of energy against this poleward flow, allowing heat to reach the equator.

Observations also showed a region of localised heating in the sub-auroral region that could be interpreted as a limited wave of heat propagating equatorward, which could be interpreted as evidence of the process driving heat transfer.

Planetary research at the University of Leicester spans the breadth of Jovian system, from the planet’s magnetosphere and atmosphere, out to its diverse collection of satellites.

Leicester researchers are members of the Juno mission made up of a global team astronomers observing the giant planet, and are leading Jupiter observations from the forthcoming James Webb Space Telescope. Leicester also plays a leading role in science and instrumentation on the European Space Agency (ESA)’s Jupiter Icy Moons Explorer (JUICE), due for launch in 2022.

‘Global upper-atmospheric heating on Jupiter by the polar aurorae’ is available in Nature.


Featured image: Jupiter is shown in visible light for context underneath an artistic impression of the Jovian upper atmosphere’s infrared glow. The brightness of this upper atmosphere layer corresponds to temperatures, from hot to cold, in this order: white, yellow, bright red and lastly, dark red. The aurorae are the hottest regions and the image shows how heat may be carried by winds away from the aurora and cause planet-wide heating. Credit: J. O'Donoghue (JAXA)/Hubble/NASA/ESA/A. Simon/J. Schmidt


Reference: O’Donoghue, J. et al, Global upper-atmospheric heating on Jupiter by the polar aurorae, Nature (2021). DOI: 10.1038/s41586-021-03706-w


Provided by University of Leicester

CHOP Researchers Develop Coating for Endotracheal Tubes that Releases Antimicrobial Peptides (Biology)

Proof-of-concept study demonstrates the coating can release peptides consistently over a two-week period, targeting specific infectious bacteria

In a proof-of-concept study, researchers at Children’s Hospital of Philadelphia (CHOP) have created a coating that can be applied to endotracheal tubes and release antimicrobial peptides that target infectious bacteria with specificity. The innovation could reduce upper-airway bacterial inflammation during intubation, a situation that can lead to chronic inflammation and a condition called subglottic stenosis, the narrowing of the airway by an accumulation of scar tissue. The findings were published recently in the journal The Laryngoscope.

“We have created a novel device to modulate the upper-airway microbiome, which could be used to prevent bacterial infections during intubation and help prevent subglottic stenosis and other airway diseases,” said senior study author Riccardo Gottardi, PhD, Assistant Professor of Pediatrics and head of the Bioengineering and Biomaterials Laboratory at CHOP. “Not only does this technology work predictably and continuously over the normal duration of chronically intubated patients, but it is also fast and easy to produce and could easily be modulated to target any bacteria of interest.”

Recent studies have shown that the endotracheal microbiome of intubated patients with subglottic stenosis is unbalanced. However, addressing the overgrowth of certain bacteria with conventional antibiotics is not ideal, as their use can disrupt the balance of both “good” and “bad” bacteria, while also causing antimicrobial resistance.

Instead, the investigators explored the use of antimicrobial peptides (AMPs), which are small proteins that destabilize bacterial membranes, causing bacterial cells to fall apart and die. This mechanism of action allows them to target specific bacteria and makes them unlikely to promote antimicrobial resistance. Prior studies have shown that it is possible to coat endotracheal tubes with conventional antibiotics, so the research team investigated the possibility of incorporating AMPs into polymer-coated tubes to inhibit bacterial growth and modulate the upper-airway microbiome.

The researchers, led by Matthew Aronson, a graduate student in Penn Engineering’s Department of Bioengineering, tested their theory by creating a polymer coating that would release Lasioglossin-III, an AMP with broad-spectrum antibacterial activity. They found that Lasio released from coated endotracheal tubes, reached the expected effective concentration rapidly and continued to release at the same concentration for a week, which is the typical timeframe that an endotracheal is used before being changed. The investigators also tested their drug-eluting tube against airway microbes, including S. epidermidis, S. pneumoniae, and human microbiome samples and observed significant antibacterial activity, as well as prevention of bacterial adherence to the tube.

“This study shows that it is possible to create a drug-eluting endotracheal tube to prevent airway complications, which opens the door to future research on targeting specific pathogens that are responsible for laryngotracheal stenosis,” said study co-author Ian N. Jacobs, MD, Medical Director of the Center for Pediatric Airway Disorders in the Division of Otolaryngology and Endowed Chair in Pediatric Otolaryngology and Pediatric Airway Disorders at Children’s Hospital of Philadelphia. “Moreover, the ability to purposefully select AMPs against certain microbes in the trachea and other organs could have significant implications in the prevention of specific diseases, even beyond airway disorders.”

The study was supported in part by the Ri.MED Foundation, the Children’s Hospital of Philadelphia Research Institute, the Frontier Program in Airway Disorders of the Children’s Hospital of Philadelphia, and the National Science Foundation Graduate Research Fellowship No. DGE 1845298.

Featured image: Schematics of endotracheal tube and electron microscopy images of coated and uncoated tubes © CHOP


Reference: Aronson et al. “Drug-eluting Endotracheal Tubes for Preventing Bacterial Inflammation in Subglottic Stenosis,” The Laryngoscope, online July 28, 2021, DOI: 10.1002/lary.29769


Provided by CHOP

Common Weight-loss Drug Successfully Targets Fat That Can Endanger Heart Health (Medicine)

Researchers at UT Southwestern announced successful results of a clinical trial for a commonly prescribed weight-loss drug called liraglutide. In adults who are overweight or have obesity combined with high cardiovascular risk, once-daily liraglutide combined with lifestyle interventions significantly lowered two types of fat that have been associated with risk to heart health: visceral fat and ectopic fat.

“Our study used the latest imaging technology to evaluate different fat components in the body. The main finding was a significant decrease in visceral fat in patients without diabetes but who were overweight or had obesity. These results show the potential of liraglutide treatment for significantly lowering the risk of chronic disease in this population,” said Parag Joshi, M.D., preventive cardiologist, Assistant Professor of Cardiology, and senior author of the study published in The Lancet Diabetes & Endocrinology.

Visceral fat is stored within the abdominal cavity around important internal organs, such as the liver, pancreas, and intestines. Ectopic fat is stored in tissues that normally contain small amounts of fat, such as the liver, skeletal muscle, heart, and pancreas.

The 185 study participants were given a once-daily injection of liraglutide over 40 weeks of treatment. The relative effects of liraglutide on fat reduction were two-fold greater in the abdominal tissues and six-fold greater in the liver than seen on overall body weight. The treatment effect was consistent across race/ethnicity and BMI categories, and among those with or without baseline prediabetes. Liraglutide also reduced fasting blood glucose and inflammation in this trial population without diabetes, the majority of whom had normal blood sugar levels at baseline.

In a 2016 study led by UTSW investigators called the Leader trial, the rate of the first occurrence of death from cardiovascular causes, nonfatal myocardial infarction, or nonfatal stroke among patients with type 2 diabetes was lower in those treated with liraglutide than with placebo. “Our findings help add a possible mechanism for why there is a benefit of liraglutide on cardiovascular outcomes while also showing its benefits in people without diabetes,” said Dr. Joshi.

According to the researchers, obesity affects an estimated 1 in every 4 adults and 1 in every 5 youths, leading to substantial risk of cardiovascular disease and mortality. “Excess visceral fat and ectopic (e.g., liver) fat are central to the development of type 2 diabetes and cardiovascular disease,” said Dr. Joshi. “It remains challenging to identify those at highest risk, in order to offer them treatment in addition to lifestyle changes such as diet and exercise.”

The study was funded by an investigator-initiated grant from Novo Nordisk.

Other UT Southwestern researchers who contributed to the study include Colby R. Ayers, Bienka Lewis, Robert Oslica, Susan Rodder, and Ambarish Pandey.

UT Southwestern is nationally ranked No. 11 in Cardiology and Heart Surgery and No. 24 in Diabetes and Endocrinology in U.S. News & World Report’s 2021-22 Best Hospitals survey.

Featured image: Parag Joshi, M.D., preventive cardiologist © UT Southwestern Medical Center


Reference: Ian J Neeland et al, Effects of liraglutide on visceral and ectopic fat in adults with overweight and obesity at high cardiovascular risk: a randomised, double-blind, placebo-controlled, clinical trial, The Lancet Diabetes & Endocrinology (2021). DOI: 10.1016/S2213-8587(21)00179-0


Provided by UT Southwestern Medical Center

Study Identifies DNA Signatures Linked to Heart Disease (Biology)

A new study identifies DNA signatures associated with risk for cardiovascular disease, a discovery that could lead to opportunities for clinical intervention years before symptoms manifest. Based on analyses of data from five large heart cohort studies of diverse populations, the findings are published in the journal JAMA Cardiology.

“The science is rapidly advancing in the area of epigenetics—modifications to our DNA that are often environmentally driven and have the potential to serve as early warning sign for disease,” says Ana Navas-Acien, MD, Ph.D., the study’s first author and professor of environmental health sciences at Columbia University Mailman School of Public Health. “In this study, we harness the country’s best clinical data on heart disease from diverse populations to begin to unlock the specific epigenetic changes involved the complex biology that leads to disease. Ultimately, we hope the research will allow us to identify and prevent disease before the worst damage takes place, although developing appropriate DNA methylation tests is still years away.”

The researchers began their analysis with data from the Strong Heart Study, the largest study of cardiovascular disease in American Indians, conducted in partnership with communities across the Great Plains and the Southwest since 1988. They analyzed blood samples to identify specific locations on DNA where methylation activity was associated with incidents of coronary heart disease, including heart attack and coronary deaths (methylation can change the activity of a DNA segment without changing the genetic sequence).

“The use of high-dimensional statistical methods allowed us to study methylation in hundreds of thousands specific locations in the DNA at the same time” says Arce Domingo-Relloso, MSc, data scientist and study co-author leading the statistical analyses for this project. 

The researchers then took the same approach with four other major heart disease cohorts: Atherosclerosis Risk in Communities (divided into Black and white cohorts due to differences in timing and laboratory methods), Framingham Heart Study, and Women’s Health Initiative. In all, they examined more than 400,000 DNA locations and 1,894 coronary heart disease events.

In the initial analysis of Strong Heart data, they identified 506 epigenetic marks linked to cardiovascular risk. Of these, 33 were also linked to cardiovascular risk in three or more of the other cohorts, although some of these sites were associated with higher risk of disease in one cohort but with lower risk of disease in other cohorts. Among the 33 methylation sites are those previously linked to cardiovascular risk and smoking, as well as novel sites that the researchers say are worthy of future investigation. Further analysis of the commonalities between the 33 marks found that many of them are connected with EGFR gene, which is involved in cell growth and cell survival.

“The overlap of these methylation sites across diverse cohorts supports the idea of interconnected biological pathways for cardiovascular risk,” says Yuling Hong, MD, Ph.D., chief of the epidemiology branch within the Division of Cardiovascular Sciences at the National Heart, Lung, and Blood Institute. “The more we understand about early risk for cardiovascular disease the better we may be able to prevent illness, particularly in populations such as American Indians with relatively high risk for heart disease.”


Reference: Ana Navas-Acien et al, Blood DNA Methylation and Incident Coronary Heart Disease, JAMA Cardiology (2021). DOI: 10.1001/jamacardio.2021.2704


Provided by Columbia University’s Mailman School of Public Health

How Sleep Loss Sabotages New Memory Storage in the Hippocampus (Neuroscience)

While some students may think it’s a good idea to pull an all-nighter before an exam, conventional wisdom may be correct: A good night’s sleep may actually be more helpful, according to University of Michigan research.

U-M scientists Sara Aton and James Delorme found when mice are sleep-deprived, there is an increase in activity in inhibitory neurons in the hippocampus, an area of the brain essential for navigation, as well as for processing and storing new memories.

“Because these neurons limit activity in their neighbors, this physiological response makes it impossible to muster normal neuronal activity in the hippocampal structure,” said Aton, an associate professor in the U-M Department of Molecular, Cellular and Developmental Biology and a member of the U-M Center for RNA Biomedicine executive committee. “I always tell my students that an overnighter is not helping them prepare for an exam.”

The researchers’ results are published in the Proceedings of the National Academy of Sciences, and their findings could have implications for human performance and learning strategies.

Previous research has shown there is a sensitive window of time—a few hours following learning—during which mice have to sleep in order to fully consolidate a memory. During this period, neuronal activity must remain undisturbed in the hippocampus, and RNA transcription and translation within the neurons must occur normally. Aton and Delorme, formerly a U-M neuroscience graduate student, studied the possible links between changes in neurons’ activity after learning and changes in their protein translation.

First, Delorme investigated the interaction between sleeping and waking, hippocampal neuron activity, and activity-driven phosphorylation of S6, a component of ribosomes—tiny organelles which translate mRNA into protein. This phosphorylation event is thought to affect which mRNAs that are being translated into protein as neurons become more active. This regulation may be important for adapting to neurons’ ever-changing metabolic demands.

To do this, Delorme gave mice a fear stimulus. When mice were allowed to freely sleep following the stimulus, he saw that S6 phosphorylation increased in a part of the hippocampus called the dentate gyrus, the first region where memories begin to form.

But when the mice were deprived of sleep, Delorme found that phosphorylation decreased throughout the hippocampus. This disrupted the mice’s memories that otherwise would have been formed in response to the fear stimulus.

Delorme’s next question was whether this reduction in activity-driven S6 phosphorylation affected all neurons similarly after sleep loss. Using bioinformatics, he compared the abundance of mRNAs associated with phosphorylated S6-containing ribosomes. He also examined mRNA profiles under conditions of prior sleep or no sleep.

Delorme then collaborated with U-M Advanced Genomics core for the RNA sequencing. He observed that, after sleep deprivation, there was a significant increase in abundance of a type of RNA transcripts known to be present specifically in interneurons that express the neuropeptide somatostatin as well as the inhibitory neurotransmitter GABA.

This relative increase suggested that greater activity among somatostatin-containing interneurons inhibits surrounding neurons, and thus overall S6 phosphorylation in the hippocampus, acting as a gate that slows down their firing.

When they mimicked this inhibitory gating mechanism in freely sleeping mice, they were able to disrupt hippocampal activity and memory consolidation. In contrast, suppressing the activity of somatostatin-expressing interneurons after learning increased activity among dentate gyrus neurons and was beneficial to memory consolidation.

In disorders such as Alzheimer’s disease, where sleep difficulties are common, there could be a relation between the physiological mechanism described in this study and memory loss. But there could be a neuron protection function, or an adaptive psychological reaction against stressful memories, says Aton.

“Sleep loss could at times be therapeutic. For example, using sleep deprivation after a traumatic event could be a way to prevent post-traumatic stress syndrome,” she said.

This study opens the door to further investigate how manipulating the relative balance between the activity of excitatory and inhibitory neurons affects memory, as well as comparing how these mechanisms are affected between REM and non-REM sleep.

Featured image: Somatostatin-expressing interneurons in the mouse dentate gyrus, labeled with Brainbow 3.0, which labels each neuron a distinct color. cFos, labeled green, is present in the nuclei of surrounding pyramidal cells which are active during sleep. Image credit: Frank Raven


Reference: James Delorme et al, Sleep loss drives acetylcholine- and somatostatin interneuron–mediated gating of hippocampal activity to inhibit memory consolidation, Proceedings of the National Academy of Sciences (2021). DOI: 10.1073/pnas.2019318118


Provided by University of Michigan

Steroid Could Reduce Heavy Menstrual Bleeding (Medicine)

Women who experience heavy menstrual bleeding could have their blood loss reduced by treatment with a common anti-inflammatory steroid, research suggests.

The study could pave the way for dexamethasone to be used as a safe, effective therapy – the first new class of treatment for heavy menstrual bleeding in nearly 20 years.

It is the first time an anti-inflammatory steroid has been trialed to treat this common health problem, which affects around one in four women in the UK and can persist for years.

The most commonly used treatment for reducing menstrual bleeding – a hormone-releasing device that is inserted into the womb cavity – is highly effective. However, nearly one fifth of new users are dissatisfied with the side effects, which include unpredictable bleeding. It is also unsuitable for women who are trying to get pregnant.

Treatment option

The trial – undertaken by a team from the University of Edinburgh – involved 107 women aged between 21 and 54 years old who had experienced heavy menstrual bleeding for time spans ranging from six months to 37 years.

The study found that women who were given a 0.9 mg dose of dexamethasone twice daily for five days showed an average reduction in menstrual blood loss volume of 19 per cent.

Researchers say the findings mean dexamethasone could be a future treatment option for women whose heavy menstrual bleeding harms their quality of life or health. It could also be used by women who experience unacceptable side-effects with hormonal treatment but do not want surgical treatment, and those who wish to try for pregnancy.

Taboo topics

Menstruation and heavy menstrual bleeding are still taboo topics and the debilitating impact of the latter is under-reported by patients. Our findings open the way for further study of dexamethasone as a possible safe and effective therapy.Hilary CritchleyProfessor of Reproductive Medicine at the University’s MRC Centre for Reproductive Health

This trial evolved from groundbreaking laboratory research and years of multi-disciplinary collaboration between clinicians and methodologists, combined with specialist expertise in new efficient and ethical approaches to trial design. It has been an exciting and gratifying journey.Dr Pamela WarnerReader in Medical Statistics at the University’s Usher Institute

This research was funded by the UK Medical Research Council and is published in the medical journal EBioMedicine.

Related links

Article published in EBioMedicine

Study medicine at the University of Edinburgh

[Satjawat Boontanataweepol via Getty Images]


Provided by Edinburgh University

Researchers Find Possible Culprit of Inflammation That Causes Death in COVID-19 Patients (Biology)

Blood plasma protein galectin-9 linked to ‘cytokine storms’ that damage organs and tissue, U of A team study finds.

As clinical evidence mounts that the leading cause of death in COVID-19 patients is the dangerous condition known as a cytokine storm, University of Alberta researchers have identified a protein in the blood that could be responsible. 

The team found that COVID-19 patients have significantly elevated levels of a protein called galectin-9 in their blood plasma. Perhaps more importantly, they also found a positive correlation between the levels of galectin-9 and pro-inflammatory cytokines released in the blood, which can lead to a cytokine storm. 

The research was led by Shokrollah Elahi, associate professor in the School of Dentistry’s Division of Foundational Sciences. 

Expanding on his prior work with HIV, AIDS and cancer patients, Elahi and his team analyzed the blood plasma of 120 patients with COVID-19. They found that levels of galectin-9 were substantially higher in those patients than in individuals with HIV and cancer. 

“We have reported in the past that galectin-9 levels go up in HIV infection and with some cancers,” said Elahi, who is also a member of the Women and Children’s Health Research Institute and Cancer Research Institute of Northern Alberta

“However, when we compared the levels of galectin-9 in the COVID-19 patients to HIV and cancer patients, we could easily distinguish the COVID patients based on the galectin-9 levels.” 

The findings suggest that galectin-9 levels in the body could be used as a biomarker to diagnose COVID-19 using a patient’s blood, potentially providing another non-invasive tool for COVID-19 testing. The levels could also be used to indicate the severity of the disease, though further study on that aspect is required, Elahi said.

Eye of the storm

The discovery of elevated galectin-9 levels in COVID-19 patients is important because of the positive correlation between the protein and a wide range of pro-inflammatory cytokines. 

“Cytokines as small cell-signalling proteins are involved in checks and balances in the immune system; they can turn on or turn off some cells to regulate the immune system,” said Elahi. 

“In the context of COVID, the problem is that there is a dysregulation of cytokine production—they are released very quickly in elevated levels. That’s what we call a ‘cytokine storm.’”

Elahi found that galectin-9 is responsible for instructing immune cells to release the pro-inflammatory cytokines quickly in response to COVID-19 infection by binding to immune cells and forcing them to produce the cytokines. Further, as tissues are damaged as a result of inflammation, more galectin-9 is released from the cells—which activates more immune cells and releases more cytokines in a vicious cycle. The resulting cytokine storm damages tissue and organs, causes severe inflammation and can lead to death, Elahi said. Even if patients survive the storm, the dysregulation of the immune system can have ongoing consequences and could be associated with the condition known as post-COVID-19 syndrome or long COVID..

The next step is to develop treatments that block or inhibit the protein, Elahi said. While there are compounds available that could potentially be used, such as lactose or anti-galectin-9 antibodies, currently there are no treatments on the market specifically for blocking galectin-9 in humans. 

“We are now looking at expanding our study to a larger cohort of patients, and then working on a proof of concept in animal models,” Elahi said. “What is killing COVID patients is not the virus; it’s the cytokine storm. Therefore, if we can reduce the cytokine storm damage by inhibiting galectin-9, then we can reduce complications, reduce hospitalizations and prevent mortality.”

The work was shared in a study published in the American Society for Microbiology journal, mBio

Elahi’s study was supported by the Canadian Institutes of Health Research through COVID-19 Research Gaps and Priorities and in part by a Fast grant.

Featured image: A research team led by Shokrollah Elahi, associate professor in the School of Dentistry’s Division of Foundational Sciences, found a positive correlation between levels of galectin-9 and pro-inflammatory cytokines released in the blood. (Photo: Faculty of Medicine & Dentistry)


Reference: Najmeh Bozorgmehr et al, Galectin-9, a Player in Cytokine Release Syndrome and a Surrogate Diagnostic Biomarker in SARS-CoV-2 Infection, mBio (2021). DOI: 10.1128/mBio.00384-21


Provided by University of Alberta

Pioneering Therapy Provides Long-term Survival For Babies Lacking Thymus (Medicine)

An investigational treatment pioneered by a Duke Health pediatrician resulted in a one-year survival rate of 77% among children born with a rare condition in which they lack an immune system.null

The treatment, using cultured thymus tissue (CTT), has been studied at Duke since 1993 for babies born without a thymus gland, which produces the all-important T cells that are key to fighting infections.

Without treatment, babies born with the rare condition, called congenital athymia, are vulnerable to fatal infections and do not survive beyond early childhood.

“The survival rates for CTT are encouraging and give families hope that their children could live full lives,” said Louise Markert, M.D., professor in the Department of Pediatrics at Duke and lead author of a study published in the Journal of Allergy and Clinical Immunology.

Markert, a pediatric immunologist, launched the therapy in 1993 using donated thymus tissue that was otherwise routinely discarded as a byproduct of other procedures. Her initial approach involved implanting pieces of the tissue in the thigh—seeding it in well-vascularized muscle in a manner she likened to planting tulip bulbs.

Early successes demonstrated the potential for the therapy, as bone marrow stem cells navigated to the implanted thymus tissue to develop into T cells. Markert further honed the procedure over the years and the treatment now uses engineered human tissue, which is under FDA review. Enzyvant Therapeutics has licensed the technology and is seeking FDA approval; Markert and Duke have financial ties to the company.

The published analysis includes 105 patients who received the therapy over a span of more than 25 years. Ninety-five patients diagnosed with congenital athymia were included in the efficacy analysis. Of the patients who survived past one year, the survival rate was 93% at a median follow-up of 10.9 years.

Some of the surviving patients developed alopecia, autoimmune hepatitis, psoriasis, and psoriatic arthritis after the first year.

“We have demonstrated that CTT can act similarly to normal thymus tissue to produce naïve T cells that can then fight infection,” Markert said. “Our data show that cultured thymus tissue has been lifesaving for these children.”


Reference: M. Louise Markert et al, Experience with cultured thymus tissue in 105 children, Journal of Allergy and Clinical Immunology (2021). DOI: 10.1016/j.jaci.2021.06.028


Provided by Duke University School of Nursing