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Comment by Dr. Krishna Kumari Challa on June 24, 2025 at 10:02am

Earth's satellites at risk if asteroid smashes into moon

If a huge asteroid smashes into the moon in 2032, the gigantic explosion would send debris streaming toward Earth that would threaten satellites and create a spectacular meteor shower, according to researchers.

It was given the highest chance—3.1%—of hitting our home planet that scientists have ever measured for such a giant space rock.

Subsequent observations from telescopes definitively ruled out a direct hit on Earth.

However, the odds that it will crash into the moon have risen to 4.3%, according to data from the James Webb Space Telescope in May.

A new preprint study, which has not been peer-reviewed, is the first to estimate how such a collision could affect Earth.

It would be the largest asteroid to hit the moon in around 5,000 years. The impact would be comparable to a large nuclear explosion in terms of the amount of energy released.

Up to 100 million kilograms (220 million pounds) of material would shoot out from the moon's surface, according to a series of simulations run by the researchers.

If the asteroid hit the side of the moon facing Earth—which is roughly a 50% chance—up to 10% of this debris could be pulled in by Earth's gravity over the following days, they said.

 These meteors could be capable of destroying some satellites—and there are expected to be a lot more of those orbiting the planet by 2032.

A centimeter-sized rock traveling at tens of thousands of meters per second is a lot like a bullet.

In the days after the impact, there could be more than 1,000 times the normal number of meteors threatening Earth's satellites.

Meanwhile, those of us on the ground would be treated to a "spectacular" meteor shower lighting up the night sky, the study said.

But the current odds of a direct hit on the near side of the moon remain at just two percent

The asteroid is not expected to be visible again until 2028, so the world will have to wait to find out more.

If a direct hit is eventually found to be likely, humanity probably has enough time to plan a mission to spare the moon.

The preprint study, which was published on the arXiv database last week, has been submitted to the Astrophysical Journal Letters.

 Paul Wiegert et al, The Potential Danger to Satellites due to Ejecta from a 2032 Lunar Impact by Asteroid 2024 YR4, arXiv (2025). DOI: 10.48550/arxiv.2506.11217

Comment by Dr. Krishna Kumari Challa on June 24, 2025 at 8:59am

While thousands of RiPPs have been identified in bacteria, only a handful have been found in fungi. In part, this is because past researchers misidentified fungal RiPPs as non-ribosomal peptides and had little understanding of how fungi created the molecules.

The synthesis of these compounds is complicated. But that's also what gives them this remarkable bioactivity.
To find more fungal RiPPs, the researchers first scanned a dozen strains of Aspergillus, which previous research suggested might contain more of the chemicals.

By comparing chemicals produced by these strains with known RiPP building blocks, the researchers identified A. flavus as a promising candidate for further study.

Genetic analysis pointed to a particular protein in A. flavus as a source of fungal RiPPs. When the researchers turned the genes that create that protein off, the chemical markers indicating the presence of RiPPs also disappeared.

This novel approach—combining metabolic and genetic information—not only pinpointed the source of fungal RiPPs in A. flavus, but could be used to find more fungal RiPPs in the future.After purifying four different RiPPs, the researchers found the molecules shared a unique structure of interlocking rings. The researchers named these molecules, which have never been previously described, after the fungus in which they were found: asperigimycins.

Even with no modification, when mixed with human cancer cells, asperigimycins demonstrated medical potential: two of the four variants had potent effects against leukemia cells.
Another variant, to which the researchers added a lipid, or fatty molecule, that is also found in the royal jelly that nourishes developing bees, performed as well as cytarabine and daunorubicin, two FDA-approved drugs that have been used for decades to treat leukemia.
Through further experimentation, the researchers found that asperigimycins likely disrupt the process of cell division. Cancer cells divide uncontrollably. These compounds block the formation of microtubules, which are essential for cell division.
Notably, the compounds had little to no effect on breast, liver or lung cancer cells—or a range of bacteria and fungi—suggesting that asperigimycins' disruptive effects are specific to certain types of cells, a critical feature for any future medication.
In addition to demonstrating the medical potential of asperigimycins, the researchers identified similar clusters of genes in other fungi, suggesting that more fungal RiPPS remain to be discovered.

 A class of benzofuranoindoline-bearing heptacyclic fungal RiPPs with anticancer activities, Nature Chemical Biology (2025). DOI: 10.1038/s41589-025-01946-9

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Comment by Dr. Krishna Kumari Challa on June 24, 2025 at 8:55am

Researchers turn toxic ancient tomb fungus into anti-cancer drug

Researchers have turned a deadly fungus into a potent cancer-fighting compound. After isolating a new class of molecules from Aspergillus flavus, a toxic crop fungus linked to deaths in the excavations of ancient tombs, the researchers modified the chemicals and tested them against leukemia cells. The result? A promising cancer-killing compound that rivals FDA-approved drugs and opens up new frontiers in the discovery of more fungal medicines.

Aspergillus flavus, named for its yellow spores, has long been a microbial villain. After archaeologists opened King Tutankhamun's tomb in the 1920s, a series of untimely deaths among the excavation team fueled rumors of a pharaoh's curse. Decades later, doctors theorized that fungal spores,

 dormant for millennia, could have played a role.

In the 1970s, a dozen scientists entered the tomb of Casimir IV in Poland. Within weeks, 10 of them died. Later investigations revealed the tomb contained A. flavus, whose toxins can lead to lung infections, especially in people with compromised immune systems.

Now, that same fungus is the unlikely source of a promising new cancer therapy.

The therapy in question is a class of ribosomally synthesized and post-translationally modified peptides, or RiPPs, pronounced like the "rip" in a piece of fabric. The name refers to how the compound is produced—by the ribosome, a tiny cellular structure that makes proteins—and the fact that it is modified later, in this case, to enhance its cancer-killing properties.

Part1

Comment by Dr. Krishna Kumari Challa on June 23, 2025 at 11:15am

Using ChatGPT to write essays may be eroding critical thinking skills

A team of neurologists and AI specialists at MIT's Media Lab has led a study looking into the brain impacts of large language model (LLM) use among people who engage with them for study or work. They report evidence that the use of LLMs may lead to an erosion of critical thinking skills. In their study, posted on the arXiv preprint server, the researchers asked groups of volunteers to write essays while connected to EEG monitors.

Researchers recruited 54 volunteers. The initial group was then split into three small groups, all of whom were asked to write a 20-minute esay on the topic of philanthropy—one group was asked to use ChatGPT for help, the second was asked to use Google Search, and the third "Brain-only" group was given no tools or resources at all. The participants remained in these same groups for three writing sessions.

Each of the volunteers was fitted with an EEG device to monitor brain activity, such as cognitive engagement and mental workload, while they wrote. The researchers also performed natural language processing analysis and interviewed participants after each session. Essays were scored by human teachers as well as an AI agent.

For these first three sessions, the EEG analysis showed clear differences in brain connectivity between the groups. The Brain-only group showed the strongest and most widespread brain network activity, the search engine group showed intermediate levels of engagement, and the ChatGPT group showed the weakest overall brain connectivity.

Out of the 54 volunteers, 18 also returned months later to complete a fourth session. Those who had used ChatGPT now went the Brain-only route, and vice versa. In this session, those who had originally used ChatGPT in the first three sessions showed weaker neural connectivity, while those from the previous Brain-only group demonstrated higher memory recall.

Overall, the interviews also revealed that volunteers who used the LLM felt less ownership over their essays compared to the other groups. ChatGPT users also struggled to recall or quote from their own essays shortly after writing them. Across all measures—brain activity, language analysis, and essay scoring—participants who relied on ChatGPT performed worse than the Brain-only group.

These findings highlight the potential educational impact of relying on LLMs for writing tasks. While they can provide immediate benefits, they run the risk of reduced learning outcomes over time and frequent use may hinder the development of critical thinking skills.

Nataliya Kosmyna et al, Your Brain on ChatGPT: Accumulation of Cognitive Debt when Using an AI Assistant for Essay Writing Task, arXiv (2025). DOI: 10.48550/arxiv.2506.08872

Comment by Dr. Krishna Kumari Challa on June 23, 2025 at 11:10am

 But what makes our brains decide a smell is bad?

A new study from UF Health researchers reveals the mechanisms behind how your brain decides you dislike—even loathe—a smell. The findings are published in the journal Molecular Psychiatry.

Odors are powerful at driving emotions, and it's long been thought that the sense of smell is just as powerful, if not more powerful, at driving an emotional response as a picture, a song or any other sensory stimulus.

Researchers wanted to answer these questions. 

They  started off with the amygdala, a brain region that curates your emotional responses to sensory stimuli. Although all our senses (sound, sight, taste, touch and smell) interact with this small part of your brain, the olfactory system takes a more direct route to it.

Smells evoke strong, emotional memories, but the brain's smell centers are more closely connected with emotional centers like the amygdala.

In the study, researchers looked at mice, who share neurochemical similarities with people. They can learn about odors and categorize them as good or bad. After observing their behavior and analyzing brain activity, the team found two genetically unique brain cell types that allow odors to be assigned into a bucket of good feelings or bad feelings.

Initially, the team expected that one cell type would generate a positive emotion to an odor, and another would generate a negative emotion. Instead, the brain's cellular organization gives the cells the capability of doing either.

It can make an odor positive or negative to you. And it all depends upon where that cell type projects in your brain and how it engages with structures in your brain.

 Sarah E. Sniffen et al, Directing negative emotional states through parallel genetically-distinct basolateral amygdala pathways to ventral striatum subregions, Molecular Psychiatry (2025). DOI: 10.1038/s41380-025-03075-0

Comment by Dr. Krishna Kumari Challa on June 22, 2025 at 7:12am

Using psychology  to cheat you: Casino Lights Could Be Warping Your Brain to Take Risks, Scientists Warn

Casino lighting could be nudging gamblers to be more reckless with their money, according to a new study, which found a link between blue-enriched light and riskier gambling behaviour.

The extra blue light emitted by casino decor and LED screens seems to trigger certain switches in our brains, making us less sensitive to financial losses compared to gains of equal magnitude, researchers found.

 As gambling addiction continues to be a growing global problem – with 1.2 percent of the world's population thought to have a gambling disorder – the study offers some important insight into how risky behaviors might be encouraged or discouraged.

Researchers found that light with more blue wavelengths in it, which is frequently emitted by LED screens and casino lighting, could subtly influence how people perceive losses and gains. This raises questions about the role of lighting in environments like casinos or online gambling platforms.

In the research conducted, on average, the participants were significantly less loss-averse under blue-enriched light. Men were more likely to take risky bets than women, which fits in with previous research into how gambling differs between the sexes.

The researchers think circadian photoreception, which is our non-visual response to light, is playing a part here. The level of blue spectrum light may be activating specific eye cells connected to brain regions in charge of decision-making, emotional regulation, and processing risk versus reward scenarios.

Under bright, blue-heavy light such as that seen in casino machines, the $100 loss didn't appear to feel as bad, so people were more willing to take the risk.

If you open up a gambling website or head into a casino, you'll notice there's a lot of blue light going on – the opposite of the warmer light that you'll often find in bedroom lighting and sleep aids such as lamps. Under light with more blue wavelengths, people may be less able to accurately judge risk and reward due to a decreased cognitive sensitivity to loss.

That raises some questions around ethics and responsibility, according to the researchers. While encouraging risk taking might be good for the gambling business, it's not good for the patrons spending their cash.

https://www.nature.com/articles/s41598-025-97370-z

Comment by Dr. Krishna Kumari Challa on June 21, 2025 at 9:34am

Acute and chronic pain are different

A new study reveals that when we experience short-term (acute) pain, the brain has a built‑in way to dial down pain signals—like pressing the brakes—to keep them from going into overdrive. But in long‑term (chronic) pain, this braking system fails, and the pain signals just keep firing. This discovery helps explain why some pain goes away while other pain lingers, and it opens the door to new treatments that could stop pain from becoming chronic in the first place.

In a study published in Science Advances, researchers reveal that our bodies respond to acute (short‑term) and chronic (long‑lasting) pain in surprisingly different ways at the cellular level. Their discovery sheds new light on how pain becomes chronic—and opens the door to better‑targeted treatments.

The team studied a small but crucial region in the brainstem called the medullary dorsal horn, home to neurons that act as a relay station for pain signals. These projection neurons help send pain messages from the body to the brain.

The scientists found that during acute inflammatory pain, these neurons actually dial down their own activity. This built‑in "braking system" helps limit the amount of pain‑related signals sent to the brain. Once the inflammation and pain subside, the neurons return to their normal state.

However, in chronic pain, this braking system fails. The neurons don't reduce their activity—in fact, they become more excitable and fire more signals, potentially contributing to the persistence of pain.

Using a combination of electrophysiology and computer modeling, the researchers identified a key mechanism: a specific potassium current known as the A‑type potassium current (IA). This current helps regulate the excitability of neurons.

In acute pain, IA increases—acting like a natural sedative for the pain pathways. But in chronic pain, this current doesn't ramp up, and the neurons become hyperactive. The absence of this regulation may be one of the biological switches that turns temporary pain into a long‑lasting condition.

This is the first time  the researchers have seen how the same neurons behave so differently in acute versus chronic pain. The fact that this natural 'calming' mechanism is missing in chronic pain suggests a new target for therapy. If we can find a way to restore or mimic that braking system, we might be able to prevent pain from becoming chronic.

Ben Title et al, Opposite regulation of medullary pain-related projection neuron excitability in acute and chronic pain, Science Advances (2025). DOI: 10.1126/sciadv.adr3467. www.science.org/doi/10.1126/sciadv.adr3467

Comment by Dr. Krishna Kumari Challa on June 20, 2025 at 12:14pm

Chemical profile of fecal samples can help predict mortality in critically ill patients

The gut microbiome and the metabolites it produces offer promising insight into disease severity in critically ill patients. In a collaborative effort, researchers developed the metabolic dysbiosis score (MDS), a novel biomarker index based on the levels of 13 key fecal metabolites—the chemical byproducts of digestion. The designed index can identify high-risk patients early and guide timely interventions that could save the lives of critically ill hospitalized patients.

According to the research article published in Science Advances, the team collected fecal specimens from 196 critically ill patients admitted to the medical intensive care unit (MICU) for non-COVID-19 respiratory shock or failure. They analyzed the samples by mapping the microbiome's composition using shotgun metagenomic sequencing and measuring the gut-derived metabolites with high-precision mass spectrometry. The MDS assigned based on the results helped identify MICU patients who are at a higher risk of 30-day mortality.

Experts have long observed that the complex ecosystem of microorganisms residing in our digestive tract plays a crucial role in maintaining overall health, and its dysbiosis or imbalance in this microbiota has been linked to a range of metabolic and chronic illnesses.

Several studies have investigated possible links between fecal microbiome diversity profiles and mortality in critically ill patients in search of a potentially treatable trait. They found that ICU stays can reduce microbiome diversity, allowing harmful species such as Enterococcus and Enterobacterales to dominate over beneficial bacteria that support healthy gut function. These imbalances are often associated with serious outcomes, including an increased risk of infection and death.

Short-chain fatty acids (SCFAs), bile acids, and tryptophan metabolites are key groups of metabolites produced by the gut microbiota. Admission to the ICU, particularly following antibiotic treatment, can cause significant disruptions in these metabolites, leading to fecal metabolic dysbiosis—a condition that may contribute to increased susceptibility to various diseases.

Upon scoring the fecal samples based on the MDS, researchers found that a high MDS (>7.5) increased the risk of 30-day mortality by a factor of 8.66 in critically ill patients. The researchers, however, found no independent association between traditional microbiome diversity profile (or Enterococcus abundance) and 30-day mortality.

The researchers noted that fecal metabolic dysbiosis may represent a treatable trait in critically ill patients, with the MDS serving as a potential biomarker to identify those who could benefit from targeted interventions to correct this imbalance and improve outcomes.

 Alexander P. de Porto et al, Fecal metabolite profiling identifies critically ill patients with increased 30-day mortality, Science Advances (2025). DOI: 10.1126/sciadv.adt1466

Comment by Dr. Krishna Kumari Challa on June 19, 2025 at 11:21am

The researchers showed that humans greatly increased the breadth of habitats they were able to exploit within Africa before the expansion out of the continent. This increase in the human niche may have been a result of positive feedback of greater contact and cultural exchange, allowing larger ranges and the breakdown of geographic barriers.

Unlike previous humans dispersing out of Africa, those human groups moving into Eurasia after approximately 60–50,000 years ago were equipped with a distinctive ecological flexibility as a result of coping with climatically challenging habitats. This likely provided a key mechanism for the adaptive success of our species beyond their African homeland.

 Emily Hallett, Major expansion in the human niche preceded out of Africa dispersal, Nature (2025). DOI: 10.1038/s41586-025-09154-0. www.nature.com/articles/s41586-025-09154-0

Part 2

Comment by Dr. Krishna Kumari Challa on June 19, 2025 at 11:20am

Before dispersing out of Africa, humans likely had to learn to thrive in diverse habitats

All non-Africans are known to have descended from a small group of people that ventured into Eurasia around 50,000 years ago. However, fossil evidence shows that there were numerous failed dispersals before this time that left no detectable traces in living people.

In a paper published in Nature, new evidence explains for the first time why those earlier migrations didn't succeed.

It was found that before expanding into Eurasia 50,000 years ago, humans began to exploit different habitat types in Africa in ways not seen before.

The results showed that the human niche began to expand significantly from 70,000 years ago, and that this expansion was driven by humans increasing their use of diverse habitat types, from forests to arid deserts.

Previous dispersals seem to have happened during particularly favorable windows of increased rainfall in the Saharo-Arabian desert belt, thus creating 'green corridors' for people to move into Eurasia. However, around 70,000–50,000 years ago, the easiest route out of Africa would have been more challenging than during previous periods, and yet this expansion was sizable and ultimately successful.

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