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Comment by Dr. Krishna Kumari Challa 5 minutes ago

Chemotherapy rewires gut bacteria to curb metastasis, research reveals

Chemotherapy commonly damages the intestinal lining, a well-known side effect. But this injury does not remain confined to the gut. It reshapes nutrient availability for intestinal bacteria, forcing the microbiota to adapt.

In Nature Communications, researchers report that chemotherapy-induced damage to the intestinal lining alters nutrient availability for gut bacteria, reshaping the microbiota and increasing the production of indole-3-propionic acid (IPA), a tryptophan-derived microbial metabolite.

Rather than acting locally, IPA functions as a systemic messenger. It travels from the gut to the bone marrow, where it rewires immune cell production. Elevated IPA levels reprogram myelopoiesis, reducing the generation of immunosuppressive monocytes that facilitate immune evasion and metastatic growth.

By reshaping the gut microbiota, chemotherapy sets off a cascade of events that rewires immunity and makes the body less permissive to metastasis.

Ludivine Bersier et al, Chemotherapy-driven intestinal dysbiosis and indole-3-propionic acid rewire myelopoiesis to promote a metastasis-refractory state, Nature Communications (2025). DOI: 10.1038/s41467-025-67169-7

Comment by Dr. Krishna Kumari Challa 8 minutes ago

The researchers then transplanted skin from the face, scalp, back and abdomen of mice onto the backs of control mice. After the transplants had engrafted, they repeated the experiment on the transplanted skin. As before, wounds in the skin transplanted from the faces of the donor mice expressed lower levels of scarring-associated proteins.
They isolated fibroblasts from skin samples from the four body sites in the donor mice and injected them into the backs of control mice. They observed reduced levels of scarring-associated proteins on the recipient animals' backs injected with fibroblasts from the donor animals' faces as compared with fibroblasts from the scalp, back or abdomen.
The researchers identified changes in gene expression between facial fibroblasts and those from other parts of the body and followed these clues to identify a signaling pathway involving a protein called ROBO2 that maintains facial fibroblasts in a less-fibrotic state. They also saw something interesting in the genomes of fibroblasts making ROBO2.
In general, the DNA of the ROBO2-positive cells is less transcriptionally active, or less available for binding by proteins required for gene expression, These fibroblasts more closely resemble their progenitors, the neural crest cells, and they might be more able to become the many cell types required for skin regeneration."
In contrast, the DNA in fibroblasts from other sites of the body allows free access to genes like collagen that are involved in the creation of scar tissue.

"It seems that, in order to scar, the cells must be able to express these pro-fibrotic genes.
"And this is the default pathway for much of the body."

ROBO2 doesn't act alone. It triggers a signaling pathway that results in the inhibition of another protein called EP300 that facilitates gene expression. EP300 plays an important role in some cancers, and clinical trials of a small drug molecule that can inhibit its activity are underway. Li and his colleagues found that using this pre-existing small molecule to block EP300 activity in fibroblasts prone to scarring caused back wounds to heal like facial wounds.

Now that we understand this pathway and the implications of the differences among fibroblasts that arise from different types of stem cells, we may be able to improve wound healing after surgeries or trauma, say the researchers.

Fibroblasts of disparate developmental origins harbor anatomically variant scarring potential, Cell (2026). DOI: 10.1016/j.cell.2025.12.014. www.cell.com/cell/fulltext/S0092-8674(25)01427-8

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Comment by Dr. Krishna Kumari Challa 12 minutes ago

Why the face scars less than the body

Tweaking a pattern of wound healing established millions of years ago may enable scar-free injury repair after surgery or trauma, researchers have found. If results from their study, which was conducted in mice, translate to humans, it may be possible to avoid or even treat the formation of scars anywhere on or within the body.

Scarring is more than a cosmetic problem. Scars can interfere with normal tissue function and cause chronic pain, disease and even death.

Scars on the skin's surface, while rarely fatal, are stiffer and weaker than normal skin and they lack sweat glands or hair follicles, making it difficult to compensate for temperature changes.

Surgeons have known for decades that facial wounds heal with less scarring than injuries on other parts of the body. This phenomenon makes evolutionary sense: Rapid healing of body wounds prevents death from blood loss, infection or impaired mobility, but healing of the face requires that the skin maintain its ability to function well.

The face is very important. We need to see and hear and breathe and eat. In contrast, injuries on the body must heal quickly. The resulting scar may not look or function like normal tissue, but you will likely still survive to procreate.

Exactly how this discrepancy happens has remained a mystery, although there were some clues.

The face and scalp are developmentally unique. Tissue from the neck up is derived from a type of cell in the early embryo called a neural crest cell. In the study researchers identified specific healing pathways in scar-forming cells called fibroblasts that originate from the neural crest and found that they drive a more regenerative type of healing.

Activating this pathway in even a subset of fibroblasts around small wounds on the abdomen or backs of mice caused them to heal with much less scarring—similar to untreated facial or scalp wounds.

The researchers in their experiments found that after 14 days, the wounds on the face and scalp expressed lower levels of proteins known to be involved in scar formation as compared with those on the abdomen or back of the animals. The sizes of the scars were also smaller.

Part 1

Comment by Dr. Krishna Kumari Challa 21 minutes ago

AI models mirror human 'us vs. them' social biases

Large language models (LLMs), the computational models underpinning the functioning of ChatGPT, Gemini and other widely used artificial intelligence (AI) platforms, can rapidly source information and generate texts tailored for specific purposes. As these models are trained on large amounts of texts written by humans, they could exhibit some human-like biases, which are inclinations to prefer specific stimuli, ideas or groups that deviate from objectivity.

One of these biases, known as the "us vs. them" bias, is the tendency of people to prefer groups they belong to, viewing other groups less favorably. This effect is well-documented in humans.

Researchers at University of Vermont's Computational Story Lab and Computational Ethics Lab recently carried out a study investigating the possibility that LLMs "absorb" the "us vs. them" bias from the texts that they are trained on, exhibiting a similar tendency to prefer some groups over others. Their paper, posted to the arXiv preprint server, suggests that many widely used models tend to express a preference for groups that are referred to favorably in training texts, including GPT-4.1, DeepSeek-3.1, Gemma-2.0, Grok-3.0 and LLaMA-3.1.

The results of this recent study highlight the tendency of AI models to pick up the biases and views expressed in the data used to train them. In their paper, the researchers introduced a strategy that could help to reduce this bias in LLMs, which they dubbed ION.

 Tabia Tanzin Prama et al, Us-vs-Them bias in Large Language Models, arXiv (2025). DOI: 10.48550/arxiv.2512.13699

Comment by Dr. Krishna Kumari Challa 34 minutes ago

This effectively locked it away from the ocean and atmosphere by storing it in sediments on the seafloor.

As dissolved calcium levels decreased across millions of years, it altered how these organisms produced and buried calcium carbonate on the seafloor.
The process effectively pulls carbon dioxide out of the atmosphere and locks it away.

This shift could have changed the composition of the atmosphere, effectively turning down the planet's thermostat.

David Evans et al, The major ion chemistry of seawater was closely coupled to the long-term carbon cycle during the Cenozoic, Proceedings of the National Academy of Sciences (2026). DOI: 10.1073/pnas.2511781122

Part 2

Comment by Dr. Krishna Kumari Challa 35 minutes ago

Scientists solve 66 million-year-old mystery of how Earth's greenhouse age ended

A 66 million-year-old mystery behind how our planet transformed from a tropical greenhouse to the ice-capped world of today has been unraveled by scientists. Their new study has revealed that Earth's massive drop in temperature after the dinosaurs went extinct could have been caused by a large decrease in calcium levels in the ocean.

An international team of experts  discovered that concentrations of calcium in the sea dropped by more than half across the last 66 million years.

The study, published in Proceedings of the National Academy of Sciences, showed that the dramatic calcium shift may have sucked carbon dioxide—a major greenhouse gas—out of the atmosphere, driving global cooling.

Large changes in the composition of seawater chemistry may have been a key driver for climate change.

Their results show that dissolved calcium levels were twice as high at the start of the Cenozoic Era, shortly after dinosaurs roamed the planet, compared to today.

When these levels were high, the oceans worked differently, acting to store less carbon in seawater and releasing carbon dioxide into the air.

As those levels decreased, CO₂ was sucked out of the atmosphere, and Earth's temperature followed, dropping our climate by as much as 15 to 20 degrees Celsius.

They used fossilized remains of tiny sea creatures dug up from sediments at the seafloor to construct the most detailed record of ocean chemistry to date. The chemical composition of the fossils, called foraminifera, showed a close link between the amount of calcium in seawater and the level of carbon dioxide in the air.

Using computer-made models, the team showed that high levels of calcium change how much carbon is "fixed" by marine life, such as corals and plankton.

Part1

Comment by Dr. Krishna Kumari Challa 47 minutes ago

Scientists may have discovered a new extinct form of life

Prototaxites are something of a prehistoric mystery. They were the first giant organisms on land, towering over ancient landscapes at heights of up to 8 meters. They had smooth trunk-like pillars and no branches, leaves or flowers. And unlike trees, they had no true root system. Instead, they may have been anchored to the ground by a simple bulbous base.

Since their first fossils were discovered in the mid-19th century, scientists have argued over their place in the tree of life. Are they giant fungi, massive algae or some kind of plant? But new evidence has emerged that may help settle the matter.

According to a new study published in the journal Science Advances, Prototaxites belonged to a previously unknown, now-extinct branch of life.

The researchers studied a specimen of Prototaxites taiti recovered from the Rhynie Chert in northeastern Scotland. This paleontological site is well-known for its exceptionally well-preserved plant, fungal and animal material.

The team used lasers and 3D imaging to look inside the fossils and compared their chemical compositions with those of other fossils found in the same rock. They discovered two significant differences.

While fungi have simple networks of long, tubular structures called hyphae, the Prototaxite specimen had a much more complex internal structure. It comprised three different types of tubes and dense hubs where they branch and connect.

To study its chemical fingerprint (the chemical signature organisms leave behind based on the cells they are made of), the team used artificial intelligence. The protein chitin is often detected in fossilized fungi and insects, but it was completely missing from the Prototaxites sample. They also used artificial intelligence to see if its chemistry matched that of any living organism. It didn't.

The researchers ruled out the giant fossils being fungi or plants, and instead, they conclude that Prototaxites were members of an extinct lineage of eukaryotes (complex-celled organisms).

The findings may have finally solved the long-standing mystery about the true nature of Prototaxites. However, further analysis and fossil discoveries may well be needed before the results are considered conclusive.

Corentin Loron et al, Prototaxites fossils are structurally and chemically distinct from extinct and extant Fungi, Science Advances (2026). DOI: 10.1126/sciadv.aec6277. www.science.org/doi/10.1126/sciadv.aec6277

Comment by Dr. Krishna Kumari Challa 23 hours ago

What should you do with unused or expired prescription medications?

Unused or expired prescription medications should be disposed of promptly to prevent accidental ingestion, especially by children. Preferred disposal methods include take-back programs at pharmacies, police stations, or DEA events. If these are unavailable, mix medications with unpalatable substances before discarding in the trash. Some drugs, mainly opioids, may be flushed per FDA guidance. Sharps require separate disposal.

If you have unused or expired medication, the best thing is to dispose of it. Many people hang on to them, and this just creates opportunity for things to go wrong.

https://medicalxpress.com/news/2026-01-unused-expired-prescription-...

Comment by Dr. Krishna Kumari Challa 23 hours ago

Small number of 'highly plastic' cancer cells drive disease progression and treatment resistance
A small subset of highly plastic cancer cells, capable of shifting identity and behavior, drives tumor progression and treatment resistance. These cells, which increase in prevalence as tumors advance, exploit injury-repair programs and can survive therapies by adapting rapidly. Targeting them, for example via uPAR-directed CAR T cells, significantly impairs tumor growth and may enhance treatment efficacy.

In healthy tissues, stem cells make new cells to replace those that are lost or damaged through normal wear and tear.

Most organs maintain themselves with resident stem cells tailored to that type of tissue—alveoli or bronchial cells in the lung, skin cells, intestinal cells, and so on.

But when an injury occurs, special injury repair programs get triggered that put stem cells in an even more flexible state—"like a super stem cell." This allows the cell to expand its capabilities and produce a much wider variety of new cells.

The problem is when cancer cells borrow these programs that are normally only available to stem cells.

Indeed, it's these highly flexible—highly plastic—cell states related to injury repair that cancer hijacks. Highly plastic cells become more abundant as these tumors grow,  researchers found. 

These highly plastic cells aren't necessary to initiate a tumor. But they're critical to cancer's progression, the team found—including its ability to give rise to fast-growing cells, to evolve resistance to treatment, and to potentially help the cancer spread to other parts of the body.

If we kill off these plastic cells very early in the initiation of a tumor, you can basically prevent mutated cells from ever becoming cancers, say teh researchers.

Tuomas Tammela, Critical role for a high-plasticity cell state in lung cancer, Nature (2026). DOI: 10.1038/s41586-025-09985-x. www.nature.com/articles/s41586-025-09985-x

Comment by Dr. Krishna Kumari Challa yesterday

Strikingly, these same genetic variants that influence the risk of pregnancy loss are also associated with recombination, the genetic shuffling process that generates diversity when eggs and sperm are made, they found.

Female meiosis, or the cell division necessary for reproduction, begins during fetal development, when chromosomes pair and recombine. The process then pauses for decades, until ovulation and fertilization. During this long pause, problems in the machinery that keeps chromosomes together can cause them to separate too soon, leading to an abnormal chromosome count when meiosis resumes.
The results demonstrate that inherited differences in these meiotic processes contribute to natural variation in risk of aneuploidy and pregnancy loss between individuals.

Rajiv McCoy, Common variation in meiosis genes shapes human recombination and aneuploidy, Nature (2026). DOI: 10.1038/s41586-025-09964-2. www.nature.com/articles/s41586-025-09964-2

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