Comment

Comment by Dr. Krishna Kumari Challa on March 7, 2025 at 11:43am

High temperatures could affect brain function in preadolescents

Exposure to high ambient temperatures is associated with lower connectivity in three brain networks in preadolescents, suggesting that heat may impact brain function. This is the conclusion of a study whose results have been published in the Journal of the American Academy of Child & Adolescent Psychiatry.

The study involved 2,229 children aged 9 to 12 from the "Generation R" cohort in Rotterdam, Netherlands. Functional connectivity data from brain networks, i.e., how different regions of the brain communicate and collaborate, were assessed using resting-state magnetic resonance imaging, when the children were not performing any active tasks.

Higher ambient temperatures during the week preceding the MRI assessment were associated with lower functional connectivity within the medial parietal, salience, and hippocampal networks, which are essential for proper brain functioning.

This implies that brain areas may work less synchronously, affecting processes such as attention, memory, and decision-making. The medial parietal network is related to introspection and self-perception; the salience network detects environmental stimuli and prioritizes what deserves our attention; and the hippocampal network is critical for memory and learning.

The research shows that the association between high temperatures and lower functional connectivity was strongest on the day before the brain scan and progressively decreased on subsequent days. In contrast, low average daily temperatures were not associated with functional connectivity.

 Researchers hypothesized that dehydration could explain their findings, as children are particularly vulnerable to fluid loss when exposed to heat, which can affect the functional connectivity of brain networks.

 In the current climate emergency, public health policies aimed at protecting children and adolescents from high temperatures could help mitigate potential effects on brain function, say the researchers.

The same research team found that exposure to cold and heat can affect psychiatric symptoms such as anxiety, depression and attention problems. In addition, other studies have linked lower connectivity within the brain's salience network to suicidal ideation and self-harming behaviors in adolescents with depression, as well as to anxiety disorders.

A new hypothesis: high temperatures could decrease the functional connectivity of brain network, indirectly contributing to a higher risk of suicide in individuals with pre-existing mental health conditions.

The researchers, however, do not propose that these connectivity changes, triggered by heat exposure, directly induce suicidal behaviors, they could act as a trigger in vulnerable individuals.

 Laura Granés et al, Exposure to Ambient Temperature and Functional Connectivity of Brain Resting-State Networks in Preadolescents, Journal of the American Academy of Child & Adolescent Psychiatry (2025). DOI: 10.1016/j.jaac.2024.11.023

Comment by Dr. Krishna Kumari Challa on March 7, 2025 at 11:27am

Diet-related brain inflammation: Three days of high-fat eating impair memory in aged rats

Just a few days of eating a diet high in saturated fat could be enough to cause memory problems and related brain inflammation in older adults, a new study in rats suggests.

Researchers fed separate groups of young and old rats the high-fat diet for three days or for three months to compare how quickly changes happen in the brain versus the rest of the body when eating an unhealthy diet.

As expected based on previous diabetes and obesity research, eating fatty foods for three months led to metabolic problems, gut inflammation and dramatic shifts in gut bacteria in all rats compared to those that ate normal chow, while just three days of high fat caused no major metabolic or gut changes.

When it came to changes in the brain, however, researchers found that only older rats—whether they were on the high-fat diet for three months or only three days—performed poorly on memory tests and showed negative inflammatory changes in the brain.

The results dispel the idea that diet-related inflammation in the aging brain is driven by obesity. Unhealthy diets and obesity are linked, but they are not inseparable. 

The researchers now showed that within three days, long before obesity sets in, tremendous neuroinflammatory shifts are occurring.

Changes in the body in all animals are happening more slowly and aren't actually necessary to cause the memory impairments and changes in the brain. We never would have known that brain inflammation is the primary cause of high-fat diet-induced memory impairments without comparing the two timelines.

The research was published recently in the journal Immunity & Ageing.

Michael J. Butler et al, Obesity-associated memory impairment and neuroinflammation precede widespread peripheral perturbations in aged rats, Immunity & Ageing (2025). DOI: 10.1186/s12979-024-00496-3

Comment by Dr. Krishna Kumari Challa on March 7, 2025 at 10:29am

Wireless pacifier could monitor babies' vitals in the NICU, eliminating the need for painful blood draws

A small but powerful invention could soon make life in the NICU easier for the tiniest patients. Newborns must have their vitals checked frequently, and one of the most critical measures of newborn health is electrolyte levels. Right now, the only way to monitor electrolytes is to draw their blood multiple times a day. This can be painful and frightening for babies, and challenging to perform for medical staff, who can have trouble drawing blood from tiny, underdeveloped blood vessels.

Now, researchers have developed a pacifier that can constantly monitor a baby's electrolyte levels in real time, eliminating the need for repeated invasive blood draws.

https://research.gatech.edu/feature/pacifier

Comment by Dr. Krishna Kumari Challa on March 7, 2025 at 10:25am

Alzheimer's treatment may lie in the brain's own cleanup crew: Harnessing microglia to clear plaques

For more than three decades, scientists have been racing to stop Alzheimer's disease by removing amyloid beta plaques—sticky clumps of toxic protein that accumulate in the brain.

Now, a new Northwestern Medicine study suggests a promising alternative: enhancing the brain's own immune cells to clear these plaques more effectively. The paper was published in Nature Medicine.

The findings could reshape the future of Alzheimer's treatments, shifting the focus from simply removing plaques to harnessing the brain's natural defenses.

The study is the first to use a cutting-edge technique called spatial transcriptomics on human clinical-trial brains with Alzheimer's disease. The technique allows scientists to pinpoint the specific spatial location of gene activity inside a tissue sample.

By analyzing donated brain tissue from deceased people with Alzheimer's disease who received amyloid-beta immunization and comparing it to those who did not, the scientists found that when these treatments work, the brain's immune cells (called microglia) don't just clear plaques—they also help restore a healthier brain environment.

But not all microglia are created equal. Some are quite effective at removing plaques, while others struggle, the study found. Also, microglia in treated brains adopt distinct states depending on the brain region and type of immunization. Lastly, certain genes, like TREM2 and APOE, are more active in microglia in response to treatment, helping these cells remove amyloid beta plaques, according to the findings.

Microglial mechanisms drive amyloid-β clearance in immunized Alzheimer's disease patients, Nature Medicine (2025). DOI: 10.1038/s41591-025-03574-1. www.nature.com/articles/s41591-025-03574-1

Comment by Dr. Krishna Kumari Challa on March 7, 2025 at 10:04am

Antimicrobial resistance in soil bacteria without the use of antibiotics: Predatory interactions drive development

Overuse of antibiotics is currently the primary reason for the rise of antimicrobial resistance (AMR). Researchers,  however, have shown that AMR can surprisingly be found in soil bacterial communities due to microbial interactions too, driven by a species of predatory bacteria.

Published in Current Biology, the study looked at how the presence of the bacterium Myxococcus xanthus affects the number of antimicrobial-resistant bacteria in soil samples. M. xanthus is a predatory species which is known to release antimicrobials and other molecules to kill its prey.

The researchers found that the death of M. xanthus in soil bacterial communities increased the frequency of resistant isolates—bacterial cells resistant to antibiotics—in many different species of soil bacteria. These cells also showed resistance to certain antibiotics even without exposure to these drugs. 

When faced with starvation, populations of M. xanthus die en masse. In famine-like conditions, which are very common in soil environments, these bacterial cells form stress-resistant structures called fruiting bodies that are filled with spores.

During the development of fruiting bodies, only a minority of cells succeed in becoming spores, whereas the majority of the bacterial cells undergo lysis (rupture) and release growth-inhibitory substances into the environment.

The researchers think that exposure to these growth inhibitory molecules is the reason behind the increased frequency of resistant isolates in the soil bacterial community. Interestingly, not all strains of M. xanthus triggered enrichment of resistance; it was the ones with higher diversity of biosynthetic clusters that seem to drive it.

When analyzing these inhibitory molecules, the researchers found something even more interesting. They identified multiple different molecules and did a very crude classification. Individually, these molecules might not do anything, but when you put them together, they suddenly do this strange thing where they can enrich other resistant isolates.

The researchers found that resistance was enriched against several antibiotics, which include commonly used drugs such as tetracycline and rifampicin.

It is important to test whether the observations derived from culturable bacteria are also applicable for unculturable microbes, say the researchers.

They found that AMR enriched through this phenomenon could be extended to unculturable bacterial species via similar exposure to growth inhibitory molecules.

The fact that AMR can be maintained by microbial antagonism even in the absence of human-driven contamination of antibiotics is a new and unexpected discovery, the researchers say.

Saheli Saha et al, Mass lysis of predatory bacteria drives the enrichment of antibiotic resistance in soil microbial communities, Current Biology (2025). DOI: 10.1016/j.cub.2025.01.068

Comment by Dr. Krishna Kumari Challa on March 7, 2025 at 9:56am

Bacterial 'jumping genes' can target and control chromosome ends

Transposons, or "jumping genes"—DNA segments that can move from one part of the genome to another—are key to bacterial evolution and the development of antibiotic resistance.

Researchers have discovered a new mechanism these genes use to survive and propagate in bacteria with linear DNA, with applications in biotechnology and drug development.

In a paper published in Science, researchers show that transposons can target and insert themselves at the ends of linear chromosomes, called telomeres, within their bacterial host. In Streptomyces—historically one of the most significant bacteria for antibiotic development—they found that transposons controlled the telomeres in nearly a third of the chromosomes. 

Bacteria are like these little tinkerers. They're always collecting these mobile DNA pieces, and they're making new functions all the time—everything in antibiotic resistance is really about mobile genetic elements and almost always transposons that can move between bacteria.

The researchers identified several families of transposons in cyanobacteria and Streptomyces that, using different mechanisms, can find and insert themselves at the telomere, with benefits for the transposon and their bacterial host.

For one, inserting at the end of the chromosome helps the transposon avoid genes for the cell's core functioning, which reside in the middle of the chromosomes; transposons that can target the ends are less likely to disrupt an essential function or cause cell death.

For any element to survive—a transposon, bacteria—they really need to be able to do those two things: they need to not cause too much damage, and they need a way to move to new hosts. By inserting into the telomeres, they're able to do both.

Transposons have been found clustered at the chromosome ends in eukaryotic cells, but this is the first time it's been documented in bacteria with linear chromosomes, and the researchers found that bacterial transposons (versus eukaryotes) use unique mechanisms to control the telomeres.

Shan-Chi Hsieh et al, Telomeric transposons are pervasive in linear bacterial genomes, Science (2025). DOI: 10.1126/science.adp1973. www.science.org/doi/10.1126/science.adp1973

Comment by Dr. Krishna Kumari Challa on March 7, 2025 at 9:31am

When outplayed, AI models resort to cheating to win chess matches

A team of AI researchers  has found that several leading AI models will resort to cheating at chess to win when playing against a superior opponent. They have published a paper on the arXiv preprint server describing experiments they conducted with several well-known AI models playing against an open-source chess engine.

As AI models continue to mature, researchers and users have begun considering risks. For example, chatbots not only accept wrong answers as fact, but fabricate false responses when they are incapable of finding a reasonable reply. Also, as AI models have been put to use in real-world business applications such as filtering resumes and estimating stock trends, users have begun to wonder what sorts of actions they will take when they become uncertain, or confused.

In this new study, the team in California found that many of the most recognized AI models will intentionally cheat to give themselves an advantage if they determine they are not winning.

The work involved pitting OpenAI's o1-preview model, DeepSeek's current R1 model and several other well-known AI models against the open-source chess engine Stockfish. Each of the models played hundreds of matches with Stockfish as the researchers monitored the action.

The research team found that when being outplayed, the AI models resorted to obvious cheating strategies, such as running a separate copy of Stockfish to learn how it made its moves, replacing its engine or simply overwriting the chessboard with pieces removed or in more favorable positions.

Those models with the most recent updates tended to be more likely to cheat when cornered. This, they reason, was because of programming trends that have pushed AI models to try harder to find solutions to problems they encounter.

It also introduces a worrying aspect of AI engines in general, they claim. If they cheat at chess, will they cheat in other ways when asked to carry out other tasks? 

Alexander Bondarenko et al, Demonstrating specification gaming in reasoning models, arXiv (2025). DOI: 10.48550/arxiv.2502.13295

Comment by Dr. Krishna Kumari Challa on March 6, 2025 at 12:24pm

When you get hurt matters: Circadian rhythms shown to play a role in muscle repair

The body's internal clock doesn't just dictate when we sleep—it also determines how quickly our muscles heal. A new study in mice, published today in Science Advances, suggests that muscle injuries heal faster when they occur during the body's natural waking hours.

The findings could have implications for shift workers and may also prove useful in understanding the effects of aging and obesity. 

The study also may help explain how disruptions like jetlag and daylight saving time changes impact circadian rhythms and muscle recovery.

"In each of our cells, we have genes that form the molecular circadian clock. These clock genes encode a set of transcription factors that regulate many processes throughout the body and align them with the appropriate time of day. Things like sleep/wake behaviour, metabolism, body temperature and hormones—all these are circadian.

Earlier it was found that mice regenerated muscle tissues faster when the damage occurred during their normal waking hours. When mice experienced muscle damage during their usual sleeping hours, healing was slowed.

In the current study, the researchers sought to better understand how circadian clocks within muscle stem cells govern regeneration depending on the time of day.

They found that the time of day influenced inflammatory response levels in stem cells, which signal to neutrophils—the "first responder" innate immune cells in muscle regeneration.

They  discovered that the cells' signaling to each other was much stronger right after injury when mice were injured during their wake period. This finding  is further evidence that the circadian regulation of muscle regeneration is dictated by this stem cell-immune cell crosstalk.

The scientists found that the muscle stem cell clock also affected the post-injury production of NAD+, a coenzyme found in all cells that is essential to creating energy in the body and is involved in hundreds of metabolic processes.

Next, using a genetically manipulated mouse model, which boosted NAD+ production specifically in muscle stem cells, the team of scientists found that NAD+ induces inflammatory responses and neutrophil recruitment, promoting muscle regeneration.

The findings may be especially relevant to understanding the circadian rhythm disruptions that occur in aging and obesity.

Circadian disruptions linked to aging and metabolic syndromes like obesity and diabetes are also associated with diminished muscle regeneration.

 Pei Zhu et al, Immunomodulatory role of the stem cell circadian clock in muscle repair, Science Advances (2025). DOI: 10.1126/sciadv.adq8538

Comment by Dr. Krishna Kumari Challa on March 6, 2025 at 12:10pm

The researchers previously screened 810 genes in mice and found 15 that had an effect on cancer metastasis. In particular, they found that mice lacking a gene which produces a protein called ARHGEF1 had less metastasis of various primary cancers to the lungs and liver.

The researchers determined that ARHGEF1 suppresses a type of immune cell called a T cell, which can recognize and kill metastatic cancer cells.

To develop treatments to take advantage of this discovery, they needed to find a way for drugs to target it. The scientists traced signals in the cell to determine that ARHGEF1 is switched on when T cells are exposed to a clotting factor called thromboxane A2 (TXA2).

This was an unexpected revelation for the scientists, because TXA2 is already well-known and linked to how aspirin works.

TXA2 is produced by platelets—a cell in the blood stream that helps blood clot, preventing wounds from bleeding, but occasionally causing heart attacks and strokes. Aspirin reduces the production of TXA2, leading to the anti-clotting effects which underlie its ability to prevent heart attacks and strokes.

This new research found that aspirin prevents cancers from spreading by decreasing TXA2 and releasing T cells from suppression. They used a mouse model of melanoma to show that in mice given aspirin, the frequency of metastases was reduced compared to control mice, and this was dependent on releasing T cells from suppression by TXA2.
Aspirin, or other drugs that could target this pathway, have the potential to be less expensive than antibody-based therapies, and therefore more accessible globally.
In a small proportion of people, aspirin can cause serious side effects, including bleeding or stomach ulcers. Therefore, it is important to understand which people with cancer are likely to benefit and always talk to your doctor before starting aspirin, the researchers say.

Rahul Roychoudhuri, Aspirin prevents metastasis by limiting platelet TXA2 suppression of T cell immunity, Nature (2025). DOI: 10.1038/s41586-025-08626-7. www.nature.com/articles/s41586-025-08626-7

Part 2

Comment by Dr. Krishna Kumari Challa on March 6, 2025 at 12:08pm

Scientists discover how aspirin could prevent some cancers from spreading

Scientists have uncovered the mechanism behind how aspirin could reduce the metastasis of some cancers by stimulating the immune system. In the study, published in Nature, the scientists say that discovering the mechanism will support ongoing clinical trials, and could lead to the targeted use of aspirin to prevent the spread of susceptible types of cancer, and to the development of more effective drugs to prevent cancer metastasis.

The scientists caution that, in some people, aspirin can have serious side effects and clinical trials are underway to determine how to use it safely and effectively to prevent cancer spread, so people should consult their doctor before starting to take it.

Studies of people with cancer have previously observed that those taking daily low-dose aspirin have a reduction in the spread of some cancers, such as breast, bowel, and prostate cancers, leading to ongoing clinical trials. However, until now it wasn't known exactly how aspirin could prevent metastases.

Scientists  were investigating the process of metastasis, because, while cancer starts out in one location, 90% of cancer deaths occur when cancer spreads to other parts of the body.

The scientists wanted to better understand how the immune system responds to metastasis, because when individual cancer cells break away from their originating tumor and spread to another part of the body they are particularly vulnerable to immune attack.

The immune system can recognize and kill these lone cancer cells more effectively than cancer cells within larger originating tumors, which have often developed an environment that suppresses the immune system.

Part 1

• ‹ Previous
• 1
• …
• 50
• 51
• 52
• 53
• 54
• …
• 1081
• Next ›
• Page