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Comment by Dr. Krishna Kumari Challa on May 29, 2026 at 9:53am

Lab-grown brain-spinal cord model shows 'irreversible' nerve damage may be reversed
Lab-grown human brain-spinal cord organoid models revealed that axon regrowth capacity is lost during neuronal maturation but can be restored by blocking specific gene networks. The hormone drug lynestrenol significantly enhanced axon regeneration in damaged mature neurons, indicating that neuron-intrinsic barriers to repair are reversible and suggesting new therapeutic avenues for central nervous system injuries.

George M. Gibbons et al, A human corticospinal organoid-slice connectoid model informs enhancer strategies for post-injury axon regrowth, Cell Reports (2026). DOI: 10.1016/j.celrep.2026.117399

Comment by Dr. Krishna Kumari Challa on May 29, 2026 at 9:51am

Depression may not only be a consequence, but also a cause of rheumatoid arthritis

According to researchers not only inflammation, but also sleep disorders, depression, obesity, and smoking may sustain persistent rheumatic symptoms. In their publications in the journals Nature Reviews Rheumatology and The Lancet Rheumatology, they also proposed a model that can help identify and treat the true causes of symptoms in time.
Rheumatoid arthritis is a chronic autoimmune disease in which the immune system attacks the joints, causing pain, swelling, and stiffness. It affects tens of thousands of people in Hungary only. Most patients respond well to treatment, but 6%–28% belong to the so-called "difficult-to-treat" group because they do not achieve lasting remission despite therapy.
According to the publications in Nature Reviews Rheumatology and The Lancet Rheumatology, these factors may not only coexist with the disease but may also help maintain it.

For example, pain and depression may reduce physical activity, increase body weight, worsen sleep and mood—all of which can feed back into pain and everyday functioning, creating a difficult-to-break "vicious cycle."

The researchers not only identified these patterns but also developed a new model that could improve the treatment of such difficult-to-treat patients.

Depression, sleep disorders, obesity, and smoking can contribute to the persistence of difficult-to-treat rheumatoid arthritis, not merely coexist with it. These factors may sustain symptoms independently of inflammation, creating a self-perpetuating cycle. A new model emphasizes identifying and addressing these non-inflammatory contributors to improve patient outcomes and guide more effective, individualized treatment.

Lilla Gunkl-Tóth et al, Bridging the gap: combining treat-to-target and difficult-to-treat strategies in the management of rheumatoid arthritis, Nature Reviews Rheumatology (2026). DOI: 10.1038/s41584-026-01354-w

Wenhui Xie et al, Associated lifestyle factors and comorbidities of difficult-to-treat rheumatoid arthritis: a systematic review and meta-analysis, The Lancet Rheumatology (2026). DOI: 10.1016/s2665-9913(26)00041-x

Lilla Gunkl-Tóth et al, Lifestyle factors in difficult-to-treat rheumatoid arthritis, The Lancet Rheumatology (2026). DOI: 10.1016/s2665-9913(26)00108-6

Comment by Dr. Krishna Kumari Challa on May 29, 2026 at 9:36am

Gut microbe found to worsen sepsis by triggering hyperinflammatory immune responses

Why do some people recover easily from bacterial infections while others rapidly deteriorate into life-threatening sepsis? According to a new study published in Nature Communications, the answer may lie not only in the invading pathogen itself, but also in the microorganisms already living inside the gut.
Sepsis is a severe condition in which the body's immune system overreacts to infection, causing widespread inflammation and organ damage. In many cases, the excessive immune response itself becomes more dangerous than the bacteria causing the infection.

Recent studies have suggested that gut microbiota play an important role in regulating baseline immune status and may influence susceptibility to infectious diseases.
Researchers has now identified a specific gut microbial group that can dramatically worsen sepsis by excessively sensitizing immune cells.
The researchers observed that even genetically identical mice showed strikingly different infection outcomes depending on the composition of their gut microbiota. When exposed to the same amount of pathogenic bacteria, some mice survived with relatively mild symptoms, whereas others rapidly deteriorated and showed significantly lower survival rates due to overwhelming immune activation.

Further analysis revealed that one key factor associated with severe disease was the enrichment of a gut bacterial family known as Muribaculaceae. Among these microbes, a bacterium called Sangeribacter muris KT1-3 was found to produce metabolites that placed immune cells into an excessively hypersensitive state.
As a result, when pathogens invaded the body, the immune system reacted far more aggressively than necessary, leading to uncontrolled inflammation and fatal sepsis.
To confirm that the gut microbiota itself was responsible for these effects, the team also performed fecal microbiota transplantation experiments. When gut microbes associated with severe infection were transferred into otherwise resistant mice, survival rates declined sharply. Conversely, transferring healthier microbial communities improved survival outcomes.

The study further demonstrated that tiny metabolites produced by specific gut microbes can prime immune cells beyond their normal activation threshold. This exaggerated immune sensitivity caused even relatively small external stimuli to trigger explosive inflammatory reactions, ultimately resulting in life-threatening sepsis.
These findings suggest that sepsis severity is determined not only by the virulence of invading pathogens but also by the composition of the gut microbial environment.
This study demonstrates that gut microbiota can fundamentally alter the intensity of immune responses and thereby determine infection outcomes.

Enrichment of specific gut microbes, particularly Muribaculaceae and Sangeribacter muris KT1-3, increases sepsis severity by producing metabolites that excessively sensitize immune cells, leading to hyperinflammatory responses and reduced survival. Fecal microbiota transplantation confirmed that gut microbial composition directly influences susceptibility to severe sepsis.

Seonghan Jang et al, A Muribaculaceae-enriched microbiota exacerbates TLR4-dependent Acinetobacter baumannii-induced hyperinflammatory sepsis, Nature Communications (2026). DOI: 10.1038/s41467-026-72435-3

Comment by Dr. Krishna Kumari Challa on May 29, 2026 at 9:03am

Pigeons navigate using magnetic sensors in their livers, say researchers

How pigeons fly hundreds of kilometers and still find their way home has long fascinated people. Now, researchers say a surprising answer may be hidden, not in the brain or eyes of birds, but in the liver.

Pigeons possess iron-rich macrophages in their livers that act as magnetic sensors, enabling detection of Earth's magnetic field for navigation. Removal of these cells disrupts magnetic-based homing, especially under overcast conditions, indicating their essential role. These macrophages are positioned near nerve fibers, suggesting a pathway for transmitting magnetic information to the brain.

A study published in Science suggests that special cells in the liver of pigeons can sense Earth's magnetic field, giving the birds an internal compass.

The special cells, known as "macrophages," are immune cells that break down old red blood cells. As part of this process, they accumulate iron, giving them quantum properties that may allow them to respond to magnetic fields. Without these cells intact, pigeons could not navigate home, the study shows.

To identify where magnetic cells are found in pigeons, the researchers used techniques known as "vibrating sample magnetometry" and "magnetic cell separation" to screen organs thought to be involved in magnetic sensing, including the eyes, beak, and brain. They also examined the liver and spleen.

They had some clues that the liver and spleen have magnetic properties, because they break down red blood cells and so store much iron in the body.
The results supported that idea. Of all the tissues examined, the liver showed the highest concentration of iron.

Iron is crystallized in oxide nanoparticles, making the cells superparamagnetic and reactive to magnetic fields. They found by far the strongest magnetic response in liver tissue.
Further analysis identified macrophages in the liver as the cells responsible.
To test if liver macrophages played a role in navigation, the ornithological team conducted experiments on pigeons that were trained to return from distances over twenty kilometers back to their aviary.
After the macrophages were removed, pigeons lost their sense of direction on overcast days when the sun was obscured. When the sun was visible, however, the pigeons successfully navigated home, likely using solar cues. Together, these results illustrate the mechanism behind how birds use magnetic sensing, in addition to the sun's orientation, for navigation.

With evidence that these cells influence navigation, the researchers then looked for how signals from the liver might be relayed. Electron microscopy showed that the iron-rich macrophages sit close to nerve fibers, suggesting a pathway for magnetic information to reach the brain.
These findings provide the first concrete evidence of how Earth's magnetic field can be perceived within the body and passed on to the brain to guide movement.
The study brings together known biological processes, including iron metabolism and how the immune and nervous systems communicate, into a clear answer to the fundamental question of how animals navigate.

Clivia Lisowski et al, Homing pigeon navigation relies on superparamagnetic macrophages under overcast conditions, Science (2026). DOI: 10.1126/science.ady2486. www.science.org/doi/10.1126/science.ady2486

Comment by Dr. Krishna Kumari Challa on May 29, 2026 at 8:31am

Unprecedented view inside live stem cells reveals aging process and loss of regenerative capacity

Scientists have developed a powerful new technique that allows them to observe how individual cells manufacture proteins during aging, offering an unprecedented glimpse into the hidden molecular activity of stem cells in living tissue. As a result of the research, conducted at the Institute for Regenerative Medicine in Switzerland, scientists were able to observe aging unfold inside individual epidermal stem cells.

What scientists saw was the intricate choreography within stem cells and how those molecular dance steps slow and change with age. The team of  scientists has concluded that the process of aging reshapes how skin stem cells manufacture proteins. The findings are published in the journal Molecular Cell.

The study revealed that aging epidermal stem cells undergo distinct shifts in their protein-production capabilities, changes that could help explain declining regenerative capacity of these cells in older tissue.

Stem cells are characterized by two features: their ability to self-renew throughout life and to differentiate into other cell types. 

Because stem cells are essentially blank slates capable of morphing into any cell type, their biological role and fate differ significantly from other cell types. By tracking them through stages of life, it's possible to see how they impact processes such as inflammation and immunity, the team found.

Paradoxically, even during youth, stem cells are not high-energy cells that keep their ribosomes busy with the production of proteins. Instead, these workbenches in stem cells where proteins are constructed exist as relatively quiescent structures.

"Somatic stem cells are characterized by their low overall protein-synthesis rates, a feature implicated in driving their stemness. 

The term "stemness," refers to the cells' capacities for self-renewal and remaining unspecialized until needed.

Both of these functions are closely linked to their precise regulation of gene expression. Somatic stem cells exhibit a unique signature marked by high ribosome biogenesis and a low protein synthesis rate.

Clara Duré et al, In vivo single-cell ribosome profiling reveals cell-type-specific translational programs during aging, Molecular Cell (2026). DOI: 10.1016/j.molcel.2026.04.017

Comment by Dr. Krishna Kumari Challa on May 28, 2026 at 3:16pm

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 on May 28, 2026 at 3:13pm

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 on May 28, 2026 at 3:11pm

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 on May 28, 2026 at 3:02pm

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 on May 28, 2026 at 2:56pm

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

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