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Comment by Dr. Krishna Kumari Challa 7 hours ago

Why you wake up so tired after vivid dreams
Feeling tired after vivid dreams is typically due to waking during REM sleep, which disrupts deep, restorative sleep stages. Remembering dreams often indicates sleep fragmentation, reducing the brain's ability to clear adenosine and leading to fatigue. Dreaming itself does not cause tiredness; rather, it is the timing and frequency of awakenings that impact sleep quality.

original article.

Comment by Dr. Krishna Kumari Challa 7 hours ago

For more than a century, scientists have relied on Atwater parameters to estimate the energy people get from food, measured in calories. The method multiplies the amount of protein, carbohydrates and fat in the food by the average metabolizable calories per gram of each.

The system is simple and useful, but it does not capture the microbial side of digestion, including how different diets feed gut microbes or how those microbes produce compounds such as short-chain fatty acids from fiber and other undigested food in the colon.

The new research builds on a controlled diet study that examined how the gut microbiome affects human energy balance. The gut microbiome is the vast community of bacteria and other microbes living in the digestive tract.
What is truly unique about the DAMM model is that it quantitatively links human metabolism to the metabolism of the microorganisms in the colon in a way that matches the results from the clinical study and provides fundamental insight into how the microbial community works in partnership with the human host.
DAMM starts by splitting a diet into the nutrients that make up the protein, carbohydrates and fat; then, it estimates how much usable energy of those components is absorbed in the upper digestive tract.

Next, it follows the material into the colon, where gut microbes break down the remaining food components that escaped earlier digestion. In the process, they produce short-chain fatty acids, which can be absorbed through the colon and used by the body as additional calories. The model also accounts for methane production by certain microbes known as methanogens.

That microbial contribution is meaningful. The model estimated that short-chain fatty acids absorbed from the colon contributed an average of about 140 calories per day, or roughly 7.4% of total usable energy. About 85% of usable energy came from the upper gastrointestinal tract, while about 15% came from the lower gastrointestinal tract, where microbial activity plays a central role.

When researchers tested DAMM against results from the controlled diet study, it came closer than the standard Atwater approach to estimating how many calories people actually absorbed from food. The standard method tended to underestimate absorbed calories, while DAMM produced estimates that more closely matched the study measurements.
The model also captured meaningful differences between the high- and low-fiber diets. The microbiome-enhancer diet delivered more fermentable material to the colon, where microbes could convert it into short-chain fatty acids.

Taylor L. Davis et al, Modeling the microbial contribution to human energy balance using the Digestion, Absorption, and Microbial Metabolism (DAMM) model, PLOS One (2026). DOI: 10.1371/journal.pone.0347668

Part 2

Comment by Dr. Krishna Kumari Challa 7 hours ago

Gut microbes help shape how many calories you absorb from food

Food labels make calories seem simple. They show the number of calories per serving, which is calculated based on how much fat, carbohydrates and protein the food contains. But inside the body, digestion is far more complicated. Food passes through a living microbial ecosystem that can influence how many of those calories people actually absorb.

Digestion is not just a human process—it is a collaboration between our bodies and trillions of microbes living in the gut.
Gut microbes significantly influence the number of calories absorbed from food by fermenting undigested components in the colon, producing short-chain fatty acids that contribute to total energy intake. A new model, DAMM, more accurately estimates calorie absorption by accounting for both human and microbial metabolism, revealing that high-fiber diets result in fewer net absorbed calories despite increased microbial activity.
A new mathematical model developed by researchers takes a closer look at that hidden part of digestion. The model, called DAMM—for digestion, absorption and microbial metabolism—follows food through the digestive tract, estimating what the body absorbs directly, what reaches the colon and how gut microbes help process the remaining material into products that are either absorbed or excreted.
DAMM gives us a powerful new way to quantify how those microbial partners contribute to human health and energy balance, and also point at the importance of properly feeding our gut microbes.
The model could eventually help researchers better understand obesity, diabetes and other metabolic disorders by showing how different diets affect both the human body and the microbial community inside the colon.
part 1

Comment by Dr. Krishna Kumari Challa 8 hours ago

Dying cells don't all release key inflammatory cytokine in the same way, research reveals

Researchers have uncovered a previously unrecognized mechanism controlling how dying cells release the inflammatory cytokine IL-33, a key driver of allergy, asthma, tissue inflammation, and cancer progression. The findings reveal that cells do not release IL-33 uniformly; instead, individual cells exhibit striking differences in release timing controlled by the membrane rupture protein NINJ1.

The research team discovered that IL-33 release frequently occurs only after catastrophic plasma membrane rupture mediated by NINJ1, rather than directly through Gasdermin pores as previously thought.

The study further demonstrated that the timing of IL-33 release differs dramatically depending on the type of cell death. During necroptosis, IL-33 is released almost instantaneously when membrane integrity collapses. In contrast, during apoptosis and pyroptosis, some cells released IL-33 immediately, whereas others waited tens of minutes before release.

This study reveals that inflammatory signal release is not a simple on/off event.

Even cells dying under the same conditions can release IL-33 with very different timing. They found that temporal regulation of NINJ1 activation is a key determinant of this heterogeneity.

The researchers also showed that deleting NINJ1 strongly suppressed IL-33 release across multiple cell types and cell death pathways. This highlights NINJ1 as a central executor of the release of damage-associated molecular patterns (DAMPs)—molecules released from dying cells that alert the immune system.

Because IL-33 plays critical roles in allergic disease, fibrosis, cancer, and immune activation, the findings may open new therapeutic avenues for controlling excessive inflammation by targeting membrane rupture mechanisms rather than upstream cytokine production alone.

Takumi Kanokogi et al, Temporal control of Ninj1 activation determines cell-to-cell heterogeneity in IL-33 release, Communications Biology (2026). DOI: 10.1038/s42003-026-10300-1

Comment by Dr. Krishna Kumari Challa 8 hours ago

Reconstructed 1.5‑billion‑year‑old protein network reveals hundreds of hidden disease‑linked genes

The cells inside every living thing are like microscopic cities with molecular machines that make energy, transport supplies from place to place, build structures and get rid of trash. Because these machines are so critical for the survival of an organism, versions of them have been passed down over more than a billion years of evolution. Molecular machines are made of proteins, which are produced with instructions stored in genes. And because these ancient molecular machines are so important for life, when one of the genes that helps build them breaks, it can lead to serious diseases in humans.
There was a huge range of diseases that we could predict pretty well, just using ancient protein complexes
Reconstruction of a 1.5-billion-year-old protein interactome identified hundreds of previously unrecognized human disease-associated genes, with about half of all human genes traceable to the Last Eukaryotic Common Ancestor (LECA). Experimental validation in animal models confirmed associations with three rare disorders, suggesting that ancient protein complexes can predict gene-disease links across eukaryotes.
This representation of protein networks, known as the protein interactome and published in Cell Genomics, is like a treasure map the researchers have used to dig up hundreds of genes that weren't previously known to be associated with human diseases. Using animal models and human patient data, they have already confirmed for the first time that three of these genes are connected to rare disorders. The work could potentially lead to new targets for treating a host of other diseases.

A protein interactome for the last eukaryotic common ancestor illuminates the biochemical basis of modern genetic diseases, Cell Genomics (2026). DOI: 10.1016/j.xgen.2026.101254. www.cell.com/cell-genomics/ful … 2666-979X(26)00116-3

Comment by Dr. Krishna Kumari Challa 14 hours ago

The researchers ran a number of experiments in flowing seawater with tissue removed from the feet, main body, and tentacles of three individuals of Psolus fabricii, a cold-water species of sea cucumber.

They found evidence of diversifying cells, immune activity, and tissue reorganization in the explanted tissue. And in the absence of a mouth, the cells appeared to be getting nutrients by absorbing amino acids dissolved in the seawater. Even after three years, when the researchers stopped the experiments in order to publish, the tissue was still active. This ability to survive in a complex, stressful environment makes this cell line unique compared to other tissue cultures.
and the rich environment full of bacteria and all this organic matter was actually feeding them and allowing this tissue to heal and grow.
The implications for biomedical sciences and engineering are profound, with potential applications in everything from tissue regrowth to antimicrobial healing.

It also opens up new opportunities for biological research and education more broadly. The tissue they've preserved shows an unprecedented ability to maintain its structural integrity and complexity in culture. It can be grown more easily in the lab.

Sara Jobson, Natural tissue immortality: Indefinite survival of sea cucumber explants, Science Advances (2026). DOI: 10.1126/sciadv.aeb1394. www.science.org/doi/10.1126/sciadv.aeb1394

Part 2

Comment by Dr. Krishna Kumari Challa 14 hours ago

A severed piece of sea cucumber refused to die, and what happened next could transform medicine

In a new study, researchers documented the continued viability of amputated tissue from a sea cucumber for over three years in natural seawater. It's the first known report of the long-term survival—and continued growth—of discarded tissue outside of a highly controlled, sterilized environment.

The finding challenges assumptions of what's possible for tissue immortality and opens up exciting possibilities in the biomedical field. It could also be used as an experimental model for biological research that is more widely accessible, without the ethical and logistical challenges of many existing cell lines.

Since the mid-20th century, scientists have made significant breakthroughs with "immortal" cell lines, like the famous HeLa cells, that can be grown in a lab and proliferate indefinitely for long-term research.
In earlier studies, though, tissue cultures have only been maintained under "axenic" conditions that are tightly controlled, rigorously maintained, and lack any bacteria or other organisms. Even then, they have not demonstrated signs of actual healing and growth, nor retained the ability to move independently.

Many echinoderms, the phylum that includes sea cucumbers, are known to display impressive regeneration capacity and negligible cell aging. Lost tissue, though, was always assumed to eventually decay or die. Yet the researchers noticed that some discarded tissue from a tube foot of a sea cucumber hadn't decayed after a number of weeks. In fact, it seemed to be growing.

Part 1

Comment by Dr. Krishna Kumari Challa yesterday

AI uncovers why squeezed tumors grow slower under physical pressure

Researchers have solved a long-standing mystery about why physical forces slow cancer growth—and the answer could reshape how the disease is treated.
Cancer cells are known to bypass many of the body's normal growth controls, but tumors still respond to mechanical pressure.

Mechanical pressure on tumors increases hydrostatic pressure, counteracting osmotic swelling required for cell growth and division, thereby inhibiting tumor expansion. AI-accelerated computational modeling and experimental validation with breast cancer spheroids confirm that physical confinement prevents cells from reaching the critical size needed for division, highlighting the tumor microenvironment's active role in growth regulation and implications for mechanotherapy and drug efficacy.
The research findings suggest that learning to harness the pressure of physical force on a tumor could open an entirely new role for treatments known as mechanotherapies in the fight against cancer.
The research highlighted how, for decades, scientists have noticed that tumor cells seem to respond to one thing that chemicals cannot easily override: physical pressure—put enough physical pressure on a tumor, and its growth slows down.
The key lies in how cells grow in the first place. Before a cell can divide, it has to get bigger. It does this by manufacturing complex biological molecules (proteins, lipids, and other building blocks) which draws water into the cell through osmosis, inflating it like a tiny balloon. Once the cell reaches a critical size, it can split in two. Under normal circumstances, this swelling process works smoothly.

But when a tumor becomes physically confined by the surrounding tissue pressing in on it, something disrupts that process. The external mechanical load creates high hydrostatic pressure that fights against the osmotic swelling from the inside. The result? Cells can no longer reach the size needed to trigger division. Growth stalls. In other words, the physical architecture of a tumor is not just a passive backdrop, it's an active participant in the disease.
The implications stretch well beyond explaining an interesting biological process. Many cancer drugs work by targeting cell division. If a tumor's mechanical environment is already suppressing growth, understanding that interaction could reveal why some drugs work better in certain tumor types or locations, and why others fail.

Irish Senthilkumar et al, Stress-dependent growth in breast cancer arises from a mechano-osmotic coupling and cell-sizing checkpoint, Proceedings of the National Academy of Sciences (2026). DOI: 10.1073/pnas.2523159123

Comment by Dr. Krishna Kumari Challa yesterday

Magnet-guided soft robots could lead to safer treatment of life-threatening blood clots

Researchers have developed an AI-assisted technique and a robotic platform that may one day help surgeons perform safer, faster and less invasive procedures to treat conditions such as blood clots located deep inside a patient's neurovascular pathways.

The method relies on small, soft, flexible robots that can maneuver through the delicate and complicated pathways of the human body to find and remove potentially dangerous obstacles to blood flow. The robots are made of a biocompatible rubber-like composite that contains microparticles that allow them to be wirelessly guided by external magnets.
A magnetically guided, soft robotic platform using AI-assisted closed-loop control enables precise navigation and manipulation within simulated vascular environments, outperforming conventional catheter-based methods in accuracy, stability, and resistance to fluid disturbances. The system reduces tracking errors by up to 77% and minimizes control effort, indicating potential for safer, less invasive treatment of deep-seated blood clots.

Alireza Moezi et al, Robotic-assisted tracking control of magnetoactive soft continuum robots in magnetic gradients, Smart Materials and Structures (2026). DOI: 10.1088/1361-665x/ae2708

Comment by Dr. Krishna Kumari Challa yesterday

How did we learn which plants are safe to eat? Food scientists explain
Humans identified edible and toxic plants through generations of observation, experimentation, and cultural knowledge, later enhanced by scientific analysis. Many plants contain natural toxins, but preparation methods such as soaking, cooking, and fermentation can reduce or eliminate harmful compounds. Modern science has further improved safety by breeding plant varieties with lower toxin levels. Toxicity often depends on dose and preparation, not just the presence of specific compounds.
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Memory decline after menopause linked to loss of estrogen production in brain tissue
Loss of brain-derived estrogen in aging female mice disrupts the extracellular matrix (ECM) in the hippocampus, impairing memory and social function, while males are unaffected. These findings suggest that postmenopausal estrogen decline uniquely increases Alzheimer's disease risk in women by altering ECM biology, highlighting a potential therapeutic target beyond amyloid-focused treatments.

Loss of brain-derived estrogen is associated with sex- and age-dependent alterations in memory, affective behavior, and hippocampal extracellular matrix gene expression, Aging Cell (2026).

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