Astronomers Discover Most Energetic Cosmic Explosions Ever Observed
Astronomers in Hawaii have discovered a new kind of explosion, and they're the most energetic stellar explosions ever recorded.
Meet 'extreme nuclear transients' (ENTs): when supermassive black holes tear apart stars at least three times heavier than the Sun, triggering an immense release of energy. An international team of researchers describes the discovery of this newly observed phenomenon in a study published Wednesday in the journal Science Advances, shedding light on events that will help astronomers study the distant universe.
'We've observed stars getting ripped apart as tidal disruption events for over a decade, but these ENTs are different beasts, reaching brightnesses nearly ten times more than what we typically see,' Jason Hinkle, lead author of the study and PhD student at the Institute for Astronomy at the University of Hawaii, said in a W. M. Keck Observatory statement. Tidal disruptions consist of supermassive black holes tearing apart any star that wanders too close, so ENTs are a kind of tidal disruption.
'Not only are ENTs far brighter than normal tidal disruption events, but they remain luminous for years, far surpassing the energy output of even the brightest known supernova explosions,' he added.
Their discovery took place almost by accident. While searching for enduring flares projecting from the center of galaxies in data from the European Space Agency's Gaia mission, Hinkle came across two strange signals from 2016 and 2018, which started a multi-year investigation. At the same time, two separate teams found a comparable flare from 2020 in an astronomical survey called the Zwicky Transient Facility (ZTF). More data from the W. M. Keck Observatory in Hawaii confirmed the 2020 event's similarity to the two Gaia events.
Given that these events unleashed more energy than any supernova known to science, Hinkle and his colleagues concluded that they weren't your average stellar explosions. The enormous energy release and the shape of the event's light curves indicated the presence of a supermassive black hole actively absorbing material, a process called accretion. Unlike regular black hole accretion, however—which sees nearby matter heat up and project irregular light—the astronomers discovered that these astrophysical events clearly involve a supermassive black hole systematically shredding and eating a giant star.
ENTs represent the most energetic known explosions in the universe. Gaia18cdj, the team's strongest documented ENT, released 25 times more energy than the most energetic supernovae known to science. More broadly, each ENT releases as much energy as 100 Suns would emit over their entire 10-billion-year lifespans. For comparison, a regular supernova usually unleashes similar amounts of energy to a single Sun.
'These ENTs don't just mark the dramatic end of a massive star's life,' Hinkle explained. 'They illuminate the processes responsible for growing the largest black holes in the universe.' ENTs are also at least 10 million times rarer than supernovae. Nevertheless, their massive energy outputs will prove to be extremely useful for astronomers studying far-away massive black holes.
'Because they're so bright, we can see them across vast cosmic distances—and in astronomy, looking far away means looking back in time,' said Benjamin Shappee, study co-author and Associate Professor at the University of Hawaii's Institute for Astronomy. 'By observing these prolonged flares, we gain insights into black hole growth during a key era known as cosmic noon, when the universe was half its current age when galaxies were happening places—forming stars and feeding their supermassive black holes 10 times more vigorously than they do today.'
From theories of black holes leading to white holes to the suggestion that the universe might exist in a black hole and that supermassive black holes could replace particle colliders, the recent study joins a host of research shedding light on one of the most mysterious components of our universe.
Hashtags
Try Our AI Features
Explore what Daily8 AI can do for you:
Comments
No comments yet...
Related Articles
Yahoo
3 hours ago
- Yahoo
If Your Baby Seems Kinda Dumb at Seven Months, Scientists Have Terrible News About What'll Happen When It Grows Into an Adult
Next time you see your baby trying to play or talk, pay close attention — because it may give you a strong clue about how intelligent the kiddo will turn out as an adult, according to a new paper in the journal PNAS. A team of scientists led by the University of Colorado Boulder have found that cognitive tests on babies as young as seven months can anticipate their future performance as 30-year-old adults on intelligence tests. "We certainly do not want to imply that cognition is somehow fixed by seven months old," said first author Daniel Gustavson, an assistant research professor at the university's Institute for Behavioral Genetics, in a statement. "But the idea that a very simple test in infancy can help predict the results of a very complicated cognitive test taken 30 years later is exciting." But all isn't lost if your baby seems slow on the uptake right now: the scientists also determined that environmental factors have an impact on childhood development. The researchers examined data from the Colorado Longitudinal Twin Study, which was started in 1985 and involved more than 1,000 twins who were followed since they were babies in order to study the impact of genes and environment. Previous research has already found that general cognitive ability doesn't shift much after a kid is eight years old or so, but this team wanted to investigate if this was also true starting from when children are very young. The researchers looked at several metrics to assess cognitive ability in babies, such as the focus and vocalization found in baby babbles. From these yardsticks, they determined that two metrics — object novelty and task orientation — strongly predicted the cognitive abilities of the tykes once they hit adulthood. They also compared identical and fraternal twins, from which they determined that 22 percent of the variance in adult cognitive ability was connected with genetic influences present in children three years of age or younger. However, they also found out that environmental influences when a child was one or two years old could explain 10 percent of variability in adult cognitive tests. Perhaps this finding will dispel the notion that genes have a total monopoly on intelligence, especially in light of right wing activists recently glomming onto race science and IQ. After all, the human brain is complex; if you feel dumb, maybe you just haven't found the right type of task yet. More on babies: The World Birth Rate Is Now Dropping Precipitously
Bloomberg
3 hours ago
- Bloomberg
Senate Can Keep Ban on State AI Rules in Trump Tax Bill
A Republican effort to block US states from enforcing new artificial intelligence regulations will remain in President Donald Trump's massive tax and spending package for now, marking a win for tech companies pushing to stall and override dozens of AI safety laws across the country. In a surprise decision, Democrats said the Senate parliamentarian ruled the provision aligns with the special budgetary process Republicans are using to consider the tax package. That process allows the GOP to avoid making concessions to Democrats, who otherwise could filibuster legislation.
Yahoo
3 hours ago
- Yahoo
Parkinson's Discovery Suggests We Could Have an FDA-Approved Treatment Already
Researchers have discovered how a surface protein on brain cells, called Aplp1, can play a role in spreading material responsible for Parkinson's disease from cell to cell in the brain. Promisingly, an FDA-approved cancer drug that targets another protein – Lag3 – which interacts with Aplp1 – was found to block this process in mice. This suggests a potential treatment for Parkinson's may already exist. In a paper published last year, an international team of scientists detailed how the two proteins work together to help toxic clumps of alpha-synuclein protein get into brain cells. "Now that we know how Aplp1 and Lag3 interact, we have a new way of understanding how alpha-synuclein contributes to the disease progression of Parkinson's disease," neuroscientist Xiaobo Mao from Johns Hopkins University said in June 2024. "Our findings also suggest that targeting this interaction with drugs could significantly slow the progression of Parkinson's disease and other neurodegenerative diseases." More than 8.5 million people globally have Parkinson's, the second most common neurodegenerative disease after Alzheimer's. The disease is progressive and currently incurable, and it's usually only diagnosed when symptoms show. These include tremors, stiffness, balance issues, speech difficulties, disturbed sleep patterns, and mental health issues. In advanced stages, patients may eventually struggle to walk or speak. Most Parkinson's symptoms stem from the loss or dysfunction of dopamine-producing neurons in a brain region involved in fine motor control, called the substantia nigra. This is thought to be caused by Lewy bodies – abnormal clumps of protein, primarily made up of misfolded alpha-synuclein, that move from neuron to neuron. Although alpha-synuclein normally helps neurons communicate, when it misfolds and becomes insoluble, it can cause serious damage. That said, identifying whether this is a cause of Parkinson's or a symptom is difficult. Past studies on mice found Lag3 binds to alpha-synuclein proteins and spreads Parkinson's disease pathology in neurons. While deleting Lag3 significantly impedes this process, it does not completely prevent it, indicating another protein was also implicated in neurons taking in misfolded alpha-synuclein. "Our work previously demonstrated that Lag3 wasn't the only cell surface protein that helped neurons absorb alpha-synuclein, so we turned to Aplp1 in our most recent experiments," said Johns Hopkins neuroscientist Valina Dawson. The scientists conducted tests with genetically modified mice that were missing either Aplp1 or Lag3, or both. They found Aplp1 and Lag3 can each independently help brain cells absorb harmful alpha-synuclein, but together they significantly increase the uptake. When mice were missing both Aplp1 and Lag3, 90 percent less of the harmful alpha-synuclein entered healthy brain cells, meaning a greater amount of the harmful protein clumps was blocked with both proteins missing compared with a deletion of just one. The researchers gave normal mice the drug nivolumab/relatlimab, a melanoma medication that contains a Lag3 antibody, and found that it also stopped Aplp1 and Lag3 from interacting, again almost completely blocking the formation of disease-causing alpha-synuclein clumps in neurons. "The anti-Lag3 antibody was successful in preventing further spread of alpha-synuclein seeds in the mouse models and exhibited better efficacy than Lag3-depletion because of Aplp1's close association with Lag3," said Ted Dawson, a neuroscientist at Johns Hopkins University. The next step will be to test the Lag3 antibody on mouse models of Parkinson's disease and Alzheimer's – where research has pointed to Lag3 as a target too. The research has been published in Nature Communications. An earlier version of this article was published in June 2024. Microplastics Have a Concerning Effect on The Microbes in Our Gut Something in Your Poop May Predict an Imminent Death Long-Term Contraceptive Pill Use Linked With Brain Tumor Risk
