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After reinventing Predator, Dan Trachtenberg is reimagining an unexpected Disney classic

Prey and Predator: Badlands director is tackling a new reboot for Disney

Image: 20th Century Studios

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Dan Trachtenberg has spent the past few years proving he can put a fresh spin on some of Hollywood’s most recognizable franchises. After making his feature debut with the tense 2016 thriller 10 Cloverfield Lane, Trachtenberg moved into the Predator universe with 2022’s Prey, followed by Predator: Badlands and the animated Predator: Killer of Killers. Now, he’s turning his attention to another iconic piece of pop culture — but this time, it’s coming from Disney.

According to Deadline, Trachtenberg is developing an original film inspired by one of Disney’s most famous stories: Sleeping Beauty.

The untitled project is still in the early stages of development, with Trachtenberg and Rayna McClendon developing the story and Alex Anfanger and Dan Schimpf writing the screenplay. Plot details are being kept under wraps, though Deadline reports that the film will take the classic tale in an entirely new direction.

And despite the obvious connection, this isn't another Maleficent. The new movie reportedly has no connection to Disney's two Maleficent films starring Angelina Jolie.

What Could Trachtenberg Do With Sleeping Beauty?

Image: Disney

It's difficult to say exactly what Trachtenberg's version of Sleeping Beauty will look like right now. Disney has plenty of precedent for reworking its animated classics, whether that's through traditional live-action remakes or films that completely rethink familiar characters and stories.

Maleficent famously turned the villain of Sleeping Beauty into the central character, while Mufasa: The Lion King explored the backstory of another familiar Disney figure. That could leave plenty of room for Trachtenberg to find an unexpected angle, particularly with Maleficent now more than a decade old.

Of course, anyone familiar with Trachtenberg's work might be wondering just how far he'll push things. Disney isn't exactly in the business of making Predator-level bloodbaths, but that doesn't mean it can't experiment with its established worlds. The success of projects like Andor has shown that Disney can find room for more mature storytelling within its biggest franchises.

That's also part of what made Trachtenberg's Predator movies stand out. Rather than simply returning to the formula established by Arnold Schwarzenegger's original 1987 film, Prey, Badlands, and Killer of Killers expanded what a Predator story could be.

Whether he'll do something similarly radical with Sleeping Beauty remains to be seen. For now, the project is still early enough that even its basic premise is being kept secret. %!s()

This as-told-to essay is based on a conversation with David Rabie, founder of Tovala. It has been edited for length and clarity.

When I was in business school, I was cooking dinner for myself one day, prepping meals for the week. I was using my oven, the stovetop, and a countertop steam machine, spending hours turning dials and pushing buttons. I thought, couldn't this be automated?

That was the seed of the idea for my company, Tovala, which launched in 2015. Tovala is a meal service that allows users to cook at home, simply. Once you purchase a Tovala oven, you get fresh meals delivered weekly. You scan a code, and have a home-cooked meal in 20 minutes.

I wanted to provide a solution that lets busy people like me create a home-cooked meal without spending hours in the kitchen. The product evolved over time, but we stuck to that core tenet: a meal made with raw ingredients, but without the fuss.

My family's immigration story shaped my outlook

Before I created Tovala, I was looking for business opportunities. I knew I wanted to be an entrepreneur; I just didn't know what my business would be.

My family immigrated from Iran, and almost all of them became entrepreneurs, including my dad, who developed properties. My family — like many immigrants who find success in the US — is a big believer in the American dream.

I was raised on the idea that if you have an idea in this country and the resilience and grit to pursue it, you can achieve success. Since that was instilled in me from a very young age, I always thought I would achieve my goal of being an entrepreneur.

My family's experience also gave me a higher tolerance for risk. I was colored by the stories I heard growing up. Compared to what my extended family had to go through leaving Iran, figuring out life and business in this country felt easy.

Creating the product with a small team was difficult

I would need that risk tolerance more than I realized. Tovala had early successes, including winning a $70,000 prize in a new venture challenge at the University of Chicago. And yet, even with that funding, launching the company was difficult.

I needed money to hire a team and develop the product. And yet, without that team, I didn't have the tech I needed to prove the concept to investors. I needed one to get the other, and balancing that was difficult and lonely.

I managed to make it work with a small team that took very modest salaries. When we launched a Kickstarter and reached $100,000 in sales, we celebrated wildly. The immediate feedback was that this was a product people wanted to buy.

Overcoming challenges became part of our company lore

That wasn't the end of the challenges — not even close. In March of 2020, we were slated to close on our Series B fundraise. The deal came apart at the 11th hour, after a conflict of interest surfaced.

I had a newborn at the time, and the pandemic was starting to shut down the global economy. It felt like a confluence of really horrible things. It was a pretty dark time.

However, once we survived, that story became part of company lore. That helped in 2023, when Silicon Valley Bank collapsed. We had almost all our cash tied up there, and we weren't yet profitable. For a very stressful three days, we weren't sure we would get our money back. Still, we were fairly assured that we'd take it through, just like we did when the series B collapsed.

The company is successful, and I've learned to live with worry

Today, Tovala has done more than $100 million in revenue during the past six months. The business has matured, and the team has grown. We've been profitable since 2024, which has taken a huge stressor off me.

And yet, a little part of me is still worried that it will all go back to zero. I think I've lived with that risk for so long that it won't ever fully leave me. Over ten years in business, I've learned to continue to grow in spite of it.

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Kelly Burch

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Kelly Burch has been writing about personal finance for more than a decade.She's particularly interested in how finances impact the most intimate parts of a person’s life, from educational and reproductive choices to love, immigration, or estate planning. Kelly has written about these topics personally and explored them with experts, including entrepreneurs, multi-millionaires, financial planners, and more.Kelly is a first-generation college graduate and homeowner who integrates her personal experience creating financial stability into her reporting. She’s a career journalist, with work appearing in “The Washington Post,” “The Chicago Tribune,” “Boston Magazine” and more.Kelly lives in rural New Hampshire with her husband, two children, and two dogs. When she’s not behind her desk, she can be found getting lost in the mountains and lakes around her home.Follow her on Facebook or Twitter, or learn more here.   

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Researchers at King's College London found that urolithin A, which is produced in the body after eating foods including pomegranates, walnuts and some berries, can help the heart relax more effectively. The compound also reduced scarring and limited harmful enlargement of the heart.

A Difficult Form of Heart Failure to Treat

The findings could eventually benefit nearly half a million people in the UK who have a form of heart failure in which the heart can still pump blood effectively but becomes too stiff to relax properly between beats. As a result, the heart has more difficulty filling with blood.

This condition, known as heart failure with preserved ejection fraction, accounts for roughly half of all heart failure cases. It can cause shortness of breath, fatigue, reduced ability to exercise and a poorer overall quality of life.

Treatment options remain relatively limited. The condition is difficult to manage because many different factors can contribute to it, including aging, high blood pressure, and diabetes. Because the heart continues to pump normally but does not relax and fill properly, many traditional heart failure treatments are less effective. Clinicians therefore tend to focus on treating underlying conditions and recommending lifestyle changes, including weight loss and better blood sugar control.

Dr. Joseph Burgoyne, senior author of the study, King's College London, said: "This type of heart failure is becoming increasingly common as populations age and rates of obesity and diabetes rise. Despite its growing burden, treatment options remain limited because the disease is complex and varies considerably between patients."

How Urolithin A Affects the Heart

Scientists have become increasingly interested in urolithin A because of its associations with healthy aging and mitochondrial function, a process in the body which generates energy.

For the first time, the researchers found that urolithin A activates a protein called PKGlα, which plays an important role in blood vessel function and the relaxation of heart muscle. The compound acts on a specific amino acid within the protein, triggering a pathway associated with cardiovascular benefits.

In animal models, treatment with urolithin A improved measures of heart function by as much as 80% compared with models that did not receive the compound. Laboratory experiments also showed that urolithin A helped heart tissue relax more effectively and reduced fibrosis, the harmful scarring that can interfere with normal heart function.

The compound also limited enlargement of heart muscle cells compared with controls, helping the cells maintain more normal function.

Results in Engineered Human Heart Tissue

The team also tested urolithin A in engineered human heart tissue created from human stem cells. This is a cutting-edge laboratory model that closely mimics the structure and function of human heart muscle.

Urolithin A significantly improved relaxation in the engineered tissue, suggesting that the effects seen in animal models could potentially translate to human heart function.

Unlike many compounds being explored as experimental treatments, urolithin A has already been studied in humans and has shown a favorable safety profile.

More research will still be required before the findings can lead to treatments for patients. However, the results point to both a promising therapeutic target and a naturally derived compound that could help researchers address an important unmet need in cardiovascular medicine.

A Potential New Therapeutic Target

Dr. Joseph Burgoyne, senior author of the study, said: "This type of heart failure remains one of the most challenging forms of heart disease to treat. Our findings identify a completely new therapeutic target and show that urolithin A can activate this pathway to improve heart relaxation and reduce disease severity. This raises the exciting possibility of developing new treatments that improve clinical outcomes and quality of life for people living with the condition.

"While there isn't enough evidence to suggest that people should eat pomegranates to treat heart failure, these findings raise the possibility that dietary approaches that enhance urolithin A production may help alleviate this condition."

Dr. Joseph Burgoyne is a cardiovascular scientist at King's College London whose work focuses on the molecular processes that regulate the health of the heart and blood vessels. His research examines how cells respond to oxidative stress and is helping reveal new mechanisms involved in blood pressure, heart function and vascular health. By identifying these fundamental biological processes, his work aims to support the development of new treatments for cardiovascular diseases such as hypertension and heart failure, with the ultimate goal of improving patient outcomes.

Clinical Trials Are Still Needed

Professor James Leiper, Director of Research at the British Heart Foundation, said: "Heart failure with preserved ejection fraction (HFpEF) makes up roughly half of all heart failure cases in the UK, and can be debilitating. This early-stage study in experimental models suggests that urolithin A may help to improve the heart tissue's ability to relax and fill with blood between beats, reducing the harmful changes to the heart muscle seen in HFpEF.

"While these findings are promising, the benefits have so far been seen in animals and engineered human tissue, so clinical trials involving people are needed to test if this approach is effective for patients. In the meantime, a healthy, balanced diet remains one of the best ways to look after your heart. Eating plenty of fruit and vegetables is linked to better heart health, but it's important to remember that no single food can prevent or treat heart disease on its own."

The study was published in Science Advances and funded by the British Heart Foundation.

A compound produced in the body after eating pomegranates improves heart function by up to 80% in a type of heart failure with limited treatment options.

Scientists at King's College London have discovered that urolithin A - a natural compound produced in the body after consuming foods such as pomegranates, walnuts and some berries - improves the heart's ability to relax, reduces scarring and prevents harmful enlargement of the heart.

The finding could give hope to nearly half a million people in the UK who have a type of heart failure where the heart retains its ability to pump blood but becomes stiff and less able to relax between beats, making it harder to fill with blood. This is known as heart failure with preserved ejection fraction and accounts for around half of all heart failure cases. The condition can lead to breathlessness, fatigue, reduced ability to exercise and an overall poor quality of life.

Despite its growing prevalence, effective treatments remain relatively limited. The condition is hard to treat because it is driven by many different factors - including aging, high blood pressure, and diabetes. As the heart can still pump normally, but becomes stiff and does not fill properly, heart failure treatments are less effective. Instead, clinicians focus on managing the underlying conditions and advise lifestyle modifications, such as weight loss and controlling blood sugar.

Dr. Joseph Burgoyne, senior author of the study, King's College London, said: "This type of heart failure is becoming increasingly common as populations age and rates of obesity and diabetes rise. Despite its growing burden, treatment options remain limited because the disease is complex and varies considerably between patients."

Urolithin A has attracted growing interest in recent years because of its links to healthy aging and mitochondrial function, a process in the body which generates energy.

In a research first, the scientists discovered that urolithin A activates a protein called PKGlα, which plays an important role in both blood vessel function and heart muscle relaxation. Urolithin A targets a specific amino acid on the protein, activating a pathway resulting in cardiovascular benefits.

Animal models treated with urolithin A had improved measures of heart function by up to 80% compared to models which were not treated with urolithin A. The laboratory experiment revealed that urolithin A increased the heart tissue's ability to relax and reduced harmful scarring, also known as fibrosis, compared to controls. The compound also reduced enlargement of heart muscle cells compared to controls, helping to preserve normal cell function.

The researchers also tested urolithin A in engineered human heart tissue created from human stem cells. This is a cutting-edge laboratory model that closely mimics the structure and function of human heart muscle. Urolithin A significantly improved tissue relaxation in these cells, suggesting the findings could translate to human cardiac function.

Unlike many experimental compounds, urolithin A has already been evaluated in human studies and shows to have a favourable safety profile.

While more research is needed before the findings can be translated into treatments for patients, the study identifies both a promising new drug target and a naturally derived compound that could help address a significant challenge in cardiovascular medicine.

Dr. Joseph Burgoyne, senior author of the study, said: "This type of heart failure remains one of the most challenging forms of heart disease to treat. Our findings identify a completely new therapeutic target and show that urolithin A can activate this pathway to improve heart relaxation and reduce disease severity. This raises the exciting possibility of developing new treatments that improve clinical outcomes and quality of life for people living with the condition.

"While there isn't enough evidence to suggest that people should eat pomegranates to treat heart failure, these findings raise the possibility that dietary approaches that enhance urolithin A production may help alleviate this condition."

Dr. Joseph Burgoyne is a cardiovascular scientist at King's College London whose research is uncovering the molecular mechanisms that control the health of the heart and blood vessels. His work focuses on how cells respond to oxidative stress, revealing new ways that blood pressure, heart function and vascular health are regulated. By identifying these fundamental biological processes, his research aims to develop new treatments for cardiovascular diseases such as hypertension and heart failure, with the ultimate aim of improving outcomes for patients.

This study was funded by the British Heart Foundation.

Professor James Leiper, Director of Research at the British Heart Foundation, said: "Heart failure with preserved ejection fraction (HFpEF) makes up roughly half of all heart failure cases in the UK, and can be debilitating. This early-stage study in experimental models suggests that urolithin A may help to improve the heart tissue's ability to relax and fill with blood between beats, reducing the harmful changes to the heart muscle seen in HFpEF.

"While these findings are promising, the benefits have so far been seen in animals and engineered human tissue, so clinical trials involving people are needed to test if this approach is effective for patients. In the meantime, a healthy, balanced diet remains one of the best ways to look after your heart. Eating plenty of fruit and vegetables is linked to better heart health, but it's important to remember that no single food can prevent or treat heart disease on its own."

The study was published in Science Advances. %!s()

Half-back Cleary - who helped Australia win the World Cup in Manchester four years ago - needed emergency surgery in hospital after being injured in a tackle by Phoenix Crossland.

Knights hooker Crossland was sent off for a 'hip-drop' tackle - which the NRL outlawed in 2020.

A hip-drop tackle is committed when a defender grabs the runner with both hands or wraps them with both arms, and then swivels or drops the hips or lower body, landing on and trapping the opponent's leg below the knees.

"Surgery done... Thank you so much to everyone that has reached out, the support has been unbelievable," Cleary posted on Instagram.

"Yesterday sucked but it's all part of the journey and it's made me even more grateful for the people I have around me. I'll be back."

Cleary had started Sunday's match on the bench because he was already carrying an injury to his right foot, which had a broken bone.

His father Ivan, the Panthers' head coach, said afterwards that his son would have surgery on both feet.

"I think that's why I was even more emotional on what happened to him, how hard he worked and what he put himself through to get himself to play today," the coach said.

Crossland was referred to the NRL Judiciary over the tackle, and is likely to receive a lengthy ban which would not only rule him out of Sunday's NRL Grand Final, in which Newcastle face Sydney Roosters, but may also affect his availability for New Zealand during the World Cup.

Australia will face New Zealand in the opening match of the World Cup in Sydney on 15 October (10:05 BST). The two teams are also favourites to face each other in the final, in Brisbane on 15 November (08:35 GMT). %!s()

The work, described in a paper published in PLOS Biology on Aug. 25, traced the evolutionary history of peptides, short fragments of proteins, back to the earliest placental mammals. This broad group includes humans and nearly all mammals living today. Laboratory experiments showed that some reconstructed peptides from extinct ancestors were more effective against drug resistant bacteria than some versions found in modern species.

These long lost biological defenses could give researchers useful starting points for developing treatments that complement or replace antibiotics that no longer work, according to Matt Barber, senior author of the study and an evolutionary biologist at the UO College of Arts and Sciences.

"For anybody who studies pathogenic bacteria, it's always in the back of our minds that antibiotics are one of the most important breakthroughs in medicine in the 20th century," Barber said. "But bacteria are, and have been for a long time, evolving resistance to them."

He continued: "We're definitely interested in whether by resurrecting or engineering some enhanced antimicrobial peptides, we could use these as therapeutics down the road."

Tracing an Ancient Antimicrobial Defense

About 160 million years ago, near the end of the Jurassic Period, the common ancestor of all placental mammals, whose young develop in the womb, appeared. Around that same time, lactoferrin, the protein at the center of Barber's research, also emerged.

Lactoferrin is an immune protein present in almost every body fluid except blood, including breast milk, tears, saliva, snot, and intestinal mucus. One of its primary jobs is to keep iron away from pathogens. Bacteria inside the body depend on iron, but lactoferrin binds tightly to the element, making it much harder for microbes to access.

Lactoferrin also carries its own direct defense against pathogens. It contains an antimicrobial peptide capable of damaging bacterial membranes, creating holes that can rupture the cells.

"Antimicrobial peptides are a key part of the body's first line of defense," said Titas Sil, lead author of the paper and a doctoral student in Barber's lab. "They can target a broad range of pathogens, and due to their potency, scientists have been trying to synthesize a variety for therapeutic uses."

Close relatives of lactoferrin do not share this bacteria killing ability. That suggests the trait appeared sometime after lactoferrin emerged during mammalian evolution. To determine when the ability developed and how it changed over time, the team retraced lactoferrin's evolutionary history and reconstructed versions belonging to its extinct ancestors.

For Barber, that evolutionary record offers a natural archive of biological experiments that could help researchers develop new medical tools.

"Evolution is essentially a billions-year-old science experiment, right?" he said.

"We're seeing the results of what worked and what didn't work. Looking at how traits are naturally produced and selected through evolution, you can get information that could be useful for designing new antimicrobial tools."

Rebuilding Proteins From 160 Million Years Ago

To recreate the extinct antimicrobial peptide, Sil began by comparing lactoferrin gene sequences from living species such as humans and cows. She then mapped the evolutionary relationships among those sequences and used statistical methods to estimate the most likely genetic sequences carried by their common ancestors, extending the reconstruction back roughly 160 million years.

The advanced method is known as ancestral sequence reconstruction, which was pioneered by Joseph Thornton, a former UO scientist whose old laboratory space is now occupied by Barber's group.

Sil synthesized the predicted genes and used cells to produce the reconstructed ancient proteins. She then tested them against several pathogens linked to human disease, including Pseudomonas aeruginosa, Staphylococcus aureus, Escherichia coli, and Streptococcus.

The oldest resurrected antimicrobial peptides were able to disrupt bacterial membranes, but the bacteria apparently repaired the damage and survived exposure to the peptides. Versions reconstructed from more recent mammalian ancestors, dating back a few million years, became progressively more effective. In some cases, they performed better than the corresponding modern human peptides.

One Mutation Produced a Major Change

Researchers traced much of that increased potency to a remarkably small structural difference. A single mutation in the chain of amino acids, the protein "building blocks," was enough to make the antimicrobial peptide substantially more effective.

"What was surprising and unexpected was how small changes in these domains could have such large effects," Barber said. "There have been clinical trials using derivatives of human lactoferrin peptides to treat infections. But there were several instances where (Sil) showed that you don't need a lot of changes for evolution to enhance the activity of these peptides beyond the human versions."

Barber and Sil caution that resurrected antimicrobial peptides are unlikely to become new medicines anytime soon. Unlike conventional antibiotics, these peptides are less structurally stable and are rapidly broken down inside the body.

Even so, reconstructing their evolutionary history could reveal useful strategies for designing future treatments. By learning how antimicrobial peptides changed over millions of years, researchers may be able to create new approaches that make it harder for pathogens to develop resistance.

"Similar to antibiotics, pathogens are going to be able to evolve against antimicrobial peptides," he said. "But if we understand and can anticipate how they become resistant to these molecules, we can hopefully find better ways to target them or develop combination treatments that better avoid resistance."

This research was funded by the National Institutes of Health. %!s()