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Orlando Magic's Offseason a Slam Dunk – NBA
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‘Chimpfluencers’ Are Sticking Grass in Their Ears And Butts in Latest Viral Trend : ScienceAlert
If chimpanzees had access to TikTok, the platform might soon be flooded with videos of ‘chimpfluencers’ wearing grass in their ears and butts – the latest trend going around a chimp sanctuary in Africa.
In August 2023, at the Chimfunshi Wildlife Orphanage Trust sanctuary in Zambia, a trendsetting chimp named Juma was seen sticking a piece of grass into his ear, deep enough to stay there on its own. Within a week the fad went viral, as four other chimps in the group started copying his unusual accessory.
Not to be outdone, later that month Juma debuted a risqué variation: he inserted a blade of grass into his rectum, and left it dangling. This unorthodox trend also caught on, with five other chimps adopting the strange new fashion.
Related: Bored Capuchin Monkeys Are Kidnapping Howler Babies in Weird New ‘Trend’
The behavior fascinated researchers observing the captive chimpanzees (Pan troglodytes) . The grass didn’t seem to serve a biological purpose – they weren’t scratching itchy ears or butts, for example. Instead, the team hypothesizes that it might serve a social purpose.
“By copying someone else’s behavior, you show that you notice and maybe even like that individual. So, it might help strengthen social bonds and create a sense of belonging within the group, just like it does in humans,” says Edwin van Leeuwen, biologist at Utrecht University in the Netherlands.
A chimp showing off its trendy new ear grass. (Jake Brooker/Chimfunshi Wildlife Orphanage Trust) Intriguingly, the event wasn’t the first time Chimfunshi chimps had decorated their orifices with grass. An original trendsetter named Julie started the whole grass-in-ear thing way back in 2010, which caught on with seven other chimps. The behavior continues to this day among the group, even after Julie’s death.
This seems to be a case of social learning and cultural transmission – after all, only one of the four groups observed back then exhibited the behavior, even though all lived in similar conditions. Weirdest of all is that more than a decade after Julie, Juma seems to have come up with the idea independently, since his group never had contact with hers.
The researchers suggest that fads with no clear purpose could be a holdover from the important ability to learn new survival skills. It’s telling that wild chimps haven’t been observed following ‘useless’ trends – only captive ones seem to have enough time on their hands.
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“Chimpanzees can socially learn novel skills and primarily use them in contexts of personal interest, like nut-cracking and termite fishing,” the researchers write in a paper about their observations.
“Yet, when selection pressures relax (e.g., due to systematic provisioning in captive care), chimpanzees may extend their social learning occasionally to behaviors without direct instrumental utility.”
Non-functional cultural trends aren’t unique to chimps either. In recent years, orcas have been seen wearing dead salmon on their heads like hats, and sinking boats in European waters – both of which seem to be fads.
A group of wild Indo-Pacific bottlenose dolphins (Tursiops aduncus) in South Australia started ‘tail-walking’ along the surface of the water after one of them observed captive dolphins that had been trained to do the trick. Wild dolphins continued to perform the feat for decades afterwards, indicating the trend had been passed down culturally.
Studying animal cultures could help teach us more about our own. After all, is sticking grass in your butt really that different from planking or eating laundry detergent pods?
The research was published in the journal Behaviour.
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Tomato genes point to new medicines
COLD SPRING HARBOR, N.Y., July 9, 2025 /PRNewswire/ — Picture juicy red tomatoes on the vine. What do you see? Some tomato varieties have straight vines. Others are branched. The question is why. New research from Cold Spring Harbor Laboratory (CSHL) provides the strongest evidence to date that the answer lies in what are called cryptic mutations. The findings have implications for agriculture and medicine, as they could help scientists fine-tune plant breeding techniques and clinical therapeutics.
Tomatoes grow on the vine at Uplands Farm, about a mile east of Cold Spring Harbor Laboratory’s main campus on Long Island. The agricultural research station offers a shared resource for CSHL scientists studying various topics, from plant genetics to quantitative biology and cancer.
Cryptic mutations are differences in DNA that don’t affect physical traits unless certain other genetic changes occur at the same time. CSHL Professor & HHMI Investigator Zachary Lippman has been researching cryptic mutations’ effects on plant traits alongside CSHL Associate Professor David McCandlish and Weizmann Institute Professor Yuval Eshed. Their latest study, published in Nature, reveals how interactions between cryptic mutations can increase or decrease the number of reproductive branches on tomato plants. Such changes result in more or fewer fruits, seeds, and flowers. The interactions in question involve genes known as paralogs.
“Paralogs emerge across evolution through gene duplication and are major features of genetic networks,” Lippman explains. “We know paralogs can buffer against each other to prevent gene mutations from affecting traits. Here, we found that collections of natural and engineered cryptic mutations in two pairs of paralogs can impact tomato branching in myriad ways.”
One crucial component of the project was the pan-genome Lippman and colleagues completed for Solanum plants around the globe, including cultivated and wild tomato species. Where genomes typically encompass one species, pan-genomes capture DNA sequences and traits across many species. The pan-genome pointed Lippman’s lab toward natural cryptic mutations in key genes controlling branching. Lippman lab postdoc Sophia Zebell then engineered other cryptic mutations using CRISPR. That enabled Lippman’s lab to count the branches on more than 35,000 flower clusters with 216 combinations of gene mutations. From there, McCandlish lab postdoc Carlos Martí-Gómez used computer models to predict how interactions between specific combinations of mutations in the plants would change the number of branches.
“We can now engineer cryptic mutations in tomatoes and other crops to modify important agricultural traits, like yield,” Lippman says.
Additionally, the kind of modeling done here could have many other applications. McCandlish explains: “When making mutations or using a drug that mimics the effects of a mutation, you often see side effects. By being able to map them out, you can choose the manner of controlling your trait of interest that has the least undesirable side effects.”
In other words, this research points not only to better crops but also better medicines. So, you see tomatoes? Science sees tomorrow.
About Cold Spring Harbor Laboratory
Founded in 1890, Cold Spring Harbor Laboratory has shaped contemporary biomedical research and education with programs in cancer, neuroscience, plant biology and quantitative biology. Home to eight Nobel Prize winners, the private, not-for-profit Laboratory employs 1,000 people including 600 scientists, students and technicians. For more information, visit www.cshl.edu.SOURCE Cold Spring Harbor Laboratory
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Owen signs new Brentford deal | Brentford FC
Brentford B midfielder Riley Owen has put pen to paper on a new deal with the club, signing on until at least the summer of 2026.
Across 40 matches last season, he played 90 minutes in 28 of them, becoming a reliable presence in the heart of the midfield. Often operating in a deeper role, his calmness in possession and ability to progress play under pressure stood out.
And it’s been a steady rise for Owen since signing with the club after a successful trial period in August 2023, with the midfielder enjoying back-to-back strong seasons under former Brentford B head coach Neil MacFarlane’s leadership.
Brentford technical director Lee Dykes said: “Riley is a player with a high technical level and has the ability to influence games from midfield.
“He has excelled in the B team, and we believe we can help him develop to another level over the next few years.”
Having signed a contract extension, Owen sees the decision as a reflection of his development so far and a platform for what’s to come.
“I’ve grown a lot since I joined the club,” he said. “I want that to continue, wherever and whatever that looks like. I’m just focused on giving my all and making the most of whatever comes next.
“I played most of the games and was one of the main players in midfield.
“We had hoped to win the Premier League Cup as well as the U21 PDL title, but overall, it was a good season, for the team and for me personally, so I’m very happy about it.”
Trusted with responsibility in the centre of the pitch, he formed a solid partnership with team-mate Ethan Brierley, who completed a season-long loan deal to Exeter City in June, with both players taking on key roles across the campaign.
“We worked well together, me and Ethan,” he added. “I’m really pleased for him that he’s out on loan now and getting the chance to show what he can do. We both took on a lot in midfield and had real trust in each other.
“I’m happy for all the boys who’ve gone out on loan – these are good opportunities and I know they’ll take them.
“For me, I’m just focused on continuing to grow, whether that’s training more with the first team, going on loan, or developing further here with the B team.”
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New Research Questions Severity of Withdrawal From Antidepressants – The New York Times
- New Research Questions Severity of Withdrawal From Antidepressants The New York Times
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Research finds 18-million-year-old enamel proteins in mammal fossils — Harvard Gazette
Proteins degrade over time, making their history hard to study. But new research has uncovered ancient proteins in the enamel of the teeth of 18-million-year-old fossilized mammals from Kenya’s Rift Valley, opening a window into how these animals lived and evolved.
In their new paper in Nature, researchers from Harvard and the Smithsonian Museum Conservation Institute discuss their findings.
“Teeth are rocks in our mouths,” explained Daniel Green, field program director in the Department of Human Evolutionary Biology and the paper’s lead author. “They’re the hardest structures that any animals make, so you can find a tooth that is a hundred or a hundred million years old, and it will contain a geochemical record of the life of the animal.”
That includes what the animal ate and drank, as well as its environment.
“In the past, we thought that mature enamel, the hardest part of teeth, should really have very few proteins in it at all,” said Green. However, utilizing a newer proteomics technique called liquid chromatography tandem mass spectrometry, the team was able to detect “a great diversity of proteins … in different biological tissues.”
“The technique involves several stages where peptides are separated based on their size or chemistry so that they can be sequentially analyzed at higher resolutions than was possible with previous methods,” explained Kevin T. Uno, associate professor in HEB and one of the paper’s corresponding authors.
“We and other scholars recently found that there are dozens — if not even hundreds — of different kinds of proteins present inside tooth enamel,” said Green.
With the realization that many proteins are found in contemporary teeth, the researchers turned to fossils, collaborating with the Smithsonian and the National Museum of Kenya for access to fossilized teeth, particularly those of early elephants and rhinos.
Formed approximately 16 million years ago, the Buluk site in Kenya is found in one of the most remote and inhospitable places in the rift, but has yielded an extraordinary diversity of fossil fauna.
Photo by Ellen Miller
As herbivores, they had large teeth to grind the plants that made up their diets. These mammals, Green said, “can have enamel two to three millimeters thick. It was a lot of material to work with.”
What they found — peptide fragments, chains of amino acids, that together form proteins as old as 18 million years — was “field-changing,” according to Green.
“Nobody’s ever found peptide fragments that are this old before,” he said, calling the findings “kind of shocking.”
Until now, the oldest prior findings were put at about 3.5 million years old, he said.
“With the help of our colleague Tim Cleland, a superb paleoproteomicist at the Smithsonian, we’re pushing back the age of peptide fragments by five or six times what was known before.”
The newly discovered peptides cover a range of proteins that perform different functions, altogether known as the proteome, Green said.
“One of the reasons that we’re excited about these ancient teeth is that we don’t have the full proteome of all proteins that could have been found inside the bodies of these ancient elephants or rhinoceros, but we do have a group of them.”
With such a collection, “There might be more information available from a group of them than just one protein by itself.”
This research “opens new frontiers in paleobiology, allowing scientists to go beyond bones and morphology to reconstruct the molecular and physiological traits of extinct animals and hominins,” said Emmanuel K. Ndiema, senior research scientist at the National Museum of Kenya and paper co-author. “This provides direct evidence of evolutionary relationships. Combined with other characteristics of teeth, we can infer dietary adaptations, disease profiles, and even age at death — insights that were previously inaccessible.”
In addition to shedding light on the lives of these creatures, it helps place them in history.
“We can use these peptide fragments to explore the relationships between ancient animals, similar to how modern DNA in humans is used to identify how people are related to one another,” Uno said.
“Even if an animal is completely extinct — and we have some animals that we analyze in our study who have no living descendants — you can still, in theory, extract proteins from their teeth and try to place them on a phylogenetic tree,” said Green.
Such information “might be able to resolve longstanding debates between paleontologists about what other mammalian lineages these animals are related to using molecular evidence.”
Although this research began as “a small side project” of a much larger project involving dozens of institutions and researchers from around the world, said Green, “We were surprised at just how much we found. There really are a lot of proteins preserved in these teeth.”
This research was partially funded by the National Science Foundation and Smithsonian’s Museum Conservation Institute.
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8-year-old with rare, fatal disease shows dramatic improvement on experimental treatment
The 8-year-old boy declined rapidly over only a few months. In August 2023, he was running and playing soccer, but by September, involuntary muscle contractions took hold of both his ankles. By October, he’d lost the ability to run and play sports, and by late November, he fell down frequently enough that physical therapists advised his family to get him a wheelchair.
Genetic testing confirmed the cause of the child’s sudden deterioration: He carried two mutant copies of a gene called HPDL. The HPDL protein helps make an antioxidant, called coenzyme Q10, that is critical to the functioning of mitochondria, the powerhouses of cells.
HDPL deficiencies are rare and can vary in severity depending on which mutations a person carries. In the boy’s case, the telltale symptoms of muscle spasticity and paralysis didn’t emerge until after his eighth birthday — but two of his siblings had died in infancy of a more severe form of the condition, marked by brain damage and seizures.
The child’s parents feared he might meet the same fate, given that there were no available treatments.
“They were so scared when we met,” said Dr. Claire Miller, a pediatric neurologist who specializes in movement disorders at NYU Langone Health. At that time, in November 2023, the child couldn’t cross the hospital lobby without falling, and his condition grew noticeably worse from one week to the next.
But with the help of Miller, other NYU specialists and special permission from the Food and Drug Administration, the child started an experimental treatment for his condition that had never been tested in humans before. The treatment includes a molecule that likely works by helping the body bypass the lack of HDPL in order to make CoQ10, the researchers think.
Related: Scientists just discovered a single molecule that may treat rare, devastating mitochondrial diseases
Within a month, the boy could walk more than half a mile (1 kilometer) through Central Park with his family. Fast-forward to today, and he’s joined them on a 4-mile (6 km) hike and also operates the pedals of a go-kart by himself. His strength is returning, along with his energy and stamina.
“Even small improvements — like walking more easily or having more energy — mean a lot,” his family, who wish to remain anonymous, told Live Science in an email. “It’s reassuring to know the treatment is making a difference.”
For now, the plan is to keep the child taking the oral medication daily, and so far, the regimen has not had any concerning side effects. The child’s medical team hopes to test the treatment in more patients with these HPDL deficiencies and then in a broader group of patients with related conditions that affect CoQ10.
“For us, trying an experimental treatment gave our child a chance at a better life,” the family told Live Science. “And we’re grateful we took that chance.”
From mouse to human
This first-in-human clinical trial was enabled by promising experiments in lab mice, conducted in the lab of Dr. Michael Pacold, an assistant professor in the Department of Radiation Oncology at the NYU Grossman School of Medicine and the Perlmutter Cancer Center. Some of these mouse experiments were described in a new paper published Wednesday (July 9) in the journal Nature, along with details of the one-patient trial.
Prior to their latest work, the Pacold lab had published a study helping to unpack one of the roles of HPDL in mitochondria. They found that protein fulfills the first step in a chain reaction that ends with the creation of the antioxidant CoQ10. In summary, HPDL turns a compound called 4-HMA into another called 4-HB, which is then used to build the “head” of CoQ10.
It’s thought that CoQ10 helps mitochondria diffuse reactive molecules that would otherwise damage them, and it may also be crucial to the processes by which mitochondria make fuel, Pacold told Live Science. It also performs other functions in the body, particularly in cell membranes, and when people don’t make enough, that deficiency can cause widespread issues, especially in energy-hungry organs like the brain, kidneys and muscles.
HPDL deficiencies also fall under the broader umbrella of CoQ10 deficiencies, because the protein helps to make the head of this antioxidant.
Pictured above is the mouse cerebellum, part of the brain critical for balance and muscle control. Mice with a condition similar to that of the child described in the current study, HPDL encephalopathy, have an underdeveloped cerebellum (as seen on the left). The study treatment restored cerebellar size and development (as seen on the right). (Image credit: Nature) CoQ10 is available as a supplement, but very little makes it into the brain when patients take it this way. The reason is not fully understood, but it’s known that the antioxidant is poorly absorbed in the gut, so little makes it to the bloodstream, and even less makes it across the brain’s protective barrier because the molecule is large, Pacold said. It’s also hydrophobic, or greasy, which likely impedes its movement through the body, he added.
For these reasons, scientists have been searching for other ways to boost the antioxidant’s levels in the central nervous system and thus treat these patients. The pathway defined by Pacold and colleagues offered a clue as to how to do that.
They tested their idea in genetically engineered lab mice that do not make HPDL. At baseline, these mice develop severe seizures and die within 15 days of birth. Treating the mice orally with CoQ10 does not save them.
So instead, the team tried giving the mice 4-HMA and 4-HB, so they essentially bypassed the missing domino in the chain. If treated early enough after birth, 90% of the mice given this treatment survived as long as normal lab mice — upward of 18 months — and they showed only limited neurological symptoms, such as paw weakness.
“His data was incredibly convincing to me,” Miller said of Pacold’s findings. Seeing the benefits of the treatment and the lack of side effects in mice, Miller agreed there was a chance that the same molecule could work in a person with HPDL deficiency — namely, the 8-year-old patient referred to their clinic.
“It seemed that the risk of trying this, although in a way unquantifiable, was also low,” she said. “And the benefit was possibly huge, with the caveat that sometimes animal models don’t necessarily translate well into humans.”
More to learn
Like the lab mice, the 8-year-old child took a daily treatment orally in a solution dissolved in water. The patient was treated with only 4-HB, in part because the compound was already available in a “highly pure form,” the researchers noted in their report.
The child says the medicine is sour and tastes better cold, Miller noted, but on the whole, it’s fairly palatable. Having started the treatment in December 2023, now, “he practically is able to do all daily functional activities by himself except sports,” his family told Live Science.
Taken together, the study and trial findings suggest that the treatment can restore function and boost survival in both mice and humans that lack HDPL, Siegfried Hekimi, a professor in the Department of Biology at McGill University who was not involved in the research, told Live Science in an email.
However, based on the available data, Hekimi questions whether the improvements seen in the lab mice and the 8-year-old boy are directly related to restored CoQ10 levels or to some other mechanism. It may be that the increases in 4-HMA and 4-HB have their own effects, independent of CoQ10, that are not yet fully understood and actually explain the medicine’s therapeutic effect. At this point, it would be speculative to suggest that this same treatment might treat other types of CoQ10 deficiencies, Hekimi argued.
The study authors agreed that more research is needed to understand exactly how the experimental treatment works.
Pacold emphasized that this experimental treatment has so far been tried in only one patient. “The immediate next step is to try to get this into more patients with this disease … and establish whether or not the response that we saw in this child is typical,” he said.
For now, though, Miller sees reason for hope.
“We all know that research does not always turn out as one hopes, and life does not turn out as one hopes,” Miller said. But “this is a really happy story. This is a heartwarming story. This is a child who appeared to become very, very sick with symptoms in a very short amount of time, and he’s doing so much better.”
This article is for informational purposes only and is not meant to offer medical advice.
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Black holes could act as cosmic supercolliders – Physics World
Black holes could act as cosmic supercolliders – Physics World
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Copyright © 2025 by IOP Publishing Ltd and individual contributors
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Thierno Barry: Everton sign Villarreal striker for £27m
Everton have completed the signing of Thierno Barry from Villarreal for £27m.
The France Under-21 striker has signed a four-year contract with the Toffees until the end of June 2029.
Barry had a £34.5m release clause in his Villarreal contract, but Everton negotiated a lower fee for the 22-year-old, who scored 11 goals and provided four assists in 38 games last season as the Spanish club finished fifth in La Liga to qualify for the Champions League.
He will add to Everton’s attacking resources after Dominic Calvert-Lewin left at the end of his contract.
“I’m very happy,” Barry told Evertontv. “It’s very exciting to be here.
“Everton is a big club in the Premier League. They have a good history and good players have played here, like Wayne Rooney and Romelu Lukaku.
“When I was young, I liked to watch these players, now I want to do like these players who have gone before.”
Forward Armando Broja also exited when his loan ended, returning to Chelsea without the deal being made permanent.
Barry was born in Lyon and left French club Sochaux aged 19 to play in the Belgian second division with Beveren.
The following season, he moved to Swiss Super League club Basel, before joining Villarreal in August 2024 in a deal worth about £13m.
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Perplexity launches Comet, an AI-powered web browser
Perplexity on Wednesday launched its first AI-powered web browser, called Comet, marking the startup’s latest effort to challenge Google Search as the primary avenue people use to find information online.
At launch, Comet will be available first to subscribers of Perplexity’s $200-per-month Max plan, as well as a small group of invitees that signed up to a waitlist.
Here’s what a New tab looks like for me on CometImage Credits:Screengrab/Maxwell Zeff / Perplexity Comet’s headline feature is Perplexity’s AI search engine, which is pre-installed and set as the default, putting the company’s core product — AI generated summaries of search results — front and center.
Users can also access Comet Assistant, a new AI agent from Perplexity that lives in the web browser and aims to automate routine tasks. Perplexity says the assistant can summarize emails and calendar events, manage tabs, and navigate web pages on behalf of users. Users can access Comet Assistant by opening a sidecar on any web page, which lets the AI agent see what’s on the web page and answer questions about it.
Comet Assistant in your email inboxImage Credits:Perplexity Perplexity has released several products and initiatives in recent months, but none feel quite as consequential as Comet. The company’s CEO, Aravind Srinivas, has significantly hyped Comet’s launch in particular, perhaps because he sees it as vital in Perplexity’s battle against Google.
With Comet, Perplexity is aiming to reach users directly without having to go through Google Chrome, the most popular browser currently. While AI-powered browsers present uncharted territory for many users, Google itself seems convinced this is the direction browsers are headed: The Search giant has deployed several AI integrations into Chrome in recent months, not to mention AI mode, an AI search product with a striking resemblance to Perplexity.
Srinivas said in March that his goal with Comet was to “develop an operating system with which you can do almost everything,” enabling Perplexity’s AI to help users across apps and websites. Becoming the default browser for users can translate to “infinite retention,” Srinivas said in June, which would ostensibly lead to more requests on Perplexity.
Perplexity’s Comet Assistant can open new tabs for youImage Credits:Perplexity That said, Comet is entering a crowded arena. While Google Chrome and Apple’s Safari hold most of the market, The Browser Company launched an AI-powered browser, Dia, in June that seems to offer many of the same features as Comet. OpenAI has also reportedly considered launching its own browser to compete with Google, and has even hired some key members from the original Google Chrome team in the last year.
Comet could get an initial leg up in the browser wars if a meaningful chunk of Perplexity users sign up for the product. Srinivas recently said that Perplexity saw 780 million queries in May 2025, and that the company’s search products are seeing more than 20% growth month-over-month.
Taking on Google Search is no small task, but Perplexity seems to have the right idea by launching a browser of its own. But the startup’s team may find it even harder to convince users to switch browsers than weaning them off Google Search.
Hands on with Comet
The most unique aspect of this browser seems to be Comet Assistant. During our testing, we found Comet’s AI agent to be surprisingly helpful for simple tasks, but it quickly falls apart when given more complex requests. Using Comet Assistant to its fullest potential also requires you to hand over an uncomfortable level of access to Perplexity.
My favorite way to use Comet Assistant, so far, is loading it in the sidecar while I’m browsing the web. Perplexity’s on-browser AI agent can automatically see what I’m looking at, so I can simply ask it questions without needing to open a new window or copy and paste text or links. It’s right there, and it always has the context for what I’m looking at.
Comet Assistant can see your web pageImage Credits:Perplexity Comet Assistant was able to answer questions about posts on social media, YouTube videos, and even sentences I just wrote in a Google Doc. I imagine this will streamline workflows for millions of people that are sending screenshots, files, and links to ChatGPT all day.
Next, I tried getting Comet Assistant to look through my Google Calendar. But before I could do so, I had to give Perplexity significant access to my Google Account — a lot of access. Just look at how long this list is.
Image Credits:Screengrab/Maxwell Zeff / Perplexity I have to say, giving Perplexity permission to view my screen, send emails, look at my contacts, and add events to my Calendar made me a little uneasy. But it seems AI agents need this kind of access to be useful.
Nevertheless, Comet Assistant did a reasonably good job looking through my Calendar. It notified me about some upcoming events, and offered me some advice on when to leave my home, and how to navigate public transit, to get to those events.
The assistant was also able to summarize emails I received that morning from noteworthy senders — in my case, important startups and tech companies with upcoming news. I’ve found that AI agents have a very difficult time parsing through what’s important in an email inbox, but Comet Assistant fared pretty well.
But Comet Assistant fails at more complicated tasks. For example, I tried asking it to help me find a long-term parking spot at San Francisco’s airport for an upcoming trip, specifically places with good reviews that cost less than $15 a day.
The assistant offered up several options that seemed to fit the criteria, so I asked it to book me a spot at one of the locations for the dates I’d be away. The agent navigated the parking lot’s website for me, entered in dates, and even some of my information, then asked me to review what it did and check out.
Turns out, Comet Assistant hallucinated and entered completely wrong dates, later telling me that the dates I wanted were booked, but still wanted to have me complete the check-out anyways. I had to tell the AI agent that the dates were non-negotiable, and asked it to find another location. It ran into the same problem again.
AI agents that mess up key details like this are not new. My experience with OpenAI’s agent, Operator, and Perplexity’s previous shopping agent yielded similar results. Clearly, hallucinations stand in the way of these products becoming real tools. Until AI companies can solve them, AI agents will still be a novelty for complex tasks.
Nevertheless, Comet does seem to offer some new capabilities that may just give Perplexity a leg up over the competition in the modern browser wars.
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