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Comment by Dr. Krishna Kumari Challa 1 hour ago

How much protein you really need

Most official guidelines recommend a bare minimum of close to one gram of protein per kilogram of body weight per day. But many scientists object to suggestions flying around social media that people need m.... Here’s what experts advise:

• Protein needs can vary from person to person and can change throughout a lifetime. “For older adults, 1.2 grams per kilogram is just giving them a little extra protection,” says nutrition and exercise researcher Nicholas Burd.
• Meeting your protein needs with plants rather than meat is better for your heart and the planet, but it might require a greater variety of foods (and maybe supplements).
• If you’re getting enough calories and eating a varied diet, you’re probably getting enough protein.
• For most people, unless you have kidney disease, too much protein won’t hurt you.

https://www.nature.com/articles/d41586-025-03632-1?utm_source=Live+...

Comment by Dr. Krishna Kumari Challa 1 hour ago

How Lung and Breast Cells Fight Cancer Differently

The study findings can help develop early-stage cancer prevention strategies.

Researchers have discovered why a specific mutation leads to tumorous growth in human lungs. The same mutation, however, fails to develop a tumor in human breasts, reducing the chances of a cancer.

They focused on the human epithelial tissues, the thin sheets of cells that line our vital organs. That’s because eighty percent of all human cancers begin in epithelial tissues. 

epithelial cells act as the body’s first barrier and are constantly exposed to stress, damage, and mutations. In fact, both the lung and the breast epithelial tissues display ‘epithelial defense against cancer’ — the epithelium’s natural act against tumorous cells. That’s why the group tested a specific cancerous mutation that occurs in both breast and lung epithelial tissues.

Researchers have long recognized that breast and lung epithelial tissues exhibit distinct differences. Breast epithelium is relatively stable and compact — the cells are tightly packed with stronger junctions. On the other hand, lung epithelium expands and relaxes with each breath, which is why its cells are more flexible, elongated, and loosely connected.

The group, through a combination of live imaging and computer models, has determined how these differences directly lead to the lung epithelium being more prone to growing tumors compared to the breast.

Once a cancerous mutation sets in the breast tissue, single mutant cells are pushed out, and groups of cells get stuck together. In lung tissue, the same mutant cells spread easily and make finger-like shapes.

The team found that the “tug-of-war” forces between normal and mutant cells decide whether cancerous cells are removed, trapped, or allowed to grow. Thus, cell mechanics help explain tissue-specific cancer risk. The surprise was how directly those mechanics determine whether mutant cells are restrained or allowed to spread.

A belt forms around the tumor in the breast epithelia, raises tension, jams the mutant cluster, and often forces out single mutants. Thus, this belt restrains the tumor.

In the lung epithelia, the cells are more elongated, motile, and weakly connected. So, no such belt forms, allowing the mutant cells to survive, grow longer, and spread into the tissue.

The group’s work demonstrates a pathway to resisting the growth of mutations into tumors, and eventually, into cancers. 

https://elifesciences.org/reviewed-preprints/106893v1

Comment by Dr. Krishna Kumari Challa 1 hour ago

The internal clock of immune cells: Is the immune system younger in the morning?

As the immune system ages, it reacts more slowly to pathogens, vaccines become less effective, and the risk of cancer increases. At the same time, the immune system follows a 24-hour rhythm, as the number and activity of many immune cells fluctuate throughout the day.

Researchers  have now investigated whether this daily rhythm influences the aging of the immune system and whether the immune system behaves "younger" or "older" at certain times of the day.

For the new study published in Frontiers in Aging, researchers took blood samples from participants in the morning, at noon, and in the evening. Using the so-called "IMMune Age indeX (IMMAX)," they determined each individual's immune age and analyzed how it changed throughout the day.

The IMMAX is a biomarker determined by the ratio of certain immune cells in the blood. As part of biological age, it correlates with actual chronological age.

Individual immune cells that are relevant for calculating the IMMAX fluctuate throughout the day. For example, in the morning, researchers observed an increased frequency of natural killer cells (NK cells)—key protective cells that defend the body against infections and cancer. In contrast, other immune cell types showed the opposite pattern.

The circadian rhythm regulates immune system activity. Hormones, body temperature, nerve signals, and messenger molecules tell immune cells when to move or become active. This leads to daily fluctuations in the number of immune cells in the blood. However, these fluctuations do not appear to influence immune age over the course of the day, as the researchers discovered. Despite measurable daily differences, the IMMAX remained largely stable, as individual immune cell types apparently balance each other out.

The IMMAX is a biomarker for immune age that is largely independent of the time of day. Nevertheless, slight differences were observed depending on a person's chronotype—that is, whether they are more active early in the day ("larks") or late in the day ("owls"). For early risers ("larks"), the IMMAX value decreased slightly from morning to noon. This suggests that the time of blood sampling in relation to waking up is important.
"When we wake up in the morning and become active, this apparently influences the movement of our immune cells and thus has a slight effect on the IMMAX value.

In large cohort studies, the timing of sampling is less critical, as fluctuations are balanced out.

Sina Trebing et al, Influence of circadian rhythm on the determination of the IMMune age indeX (IMMAX), Frontiers in Aging (2025). DOI: 10.3389/fragi.2025.1716985

Comment by Dr. Krishna Kumari Challa 1 hour ago

Indeed, a more diverse microbiome is generally correlated with increased sleep efficiency and total sleep time. Better sleep is also associated with a higher abundance of bacteria with health-promoting metabolic functions, like production of short-chain fatty acids (SCFAs), whereas conditions like insomnia are linked with lower abundances of these microbes. Whether insomnia causes these alterations, or vice versa, is still unclear—likely, they feed into one another.

Like many of the chemicals and processes powering our bodies, the composition of the microbiome naturally fluctuates throughout the day. These changes are linked to host circadian processes, and alterations in sleep (e.g., jet lag) can disrupt microbiota rhythms, resulting in important health implications.

"[What] we find in stress-related disorders, [and] in many mental health disorders in general, is that they're often associated with disordered sleep and dysregulation of sleep and circadian rhythms.
Researchers recently showed in animal models that daily fluctuations in stress pathways closely linked to sleep (e.g., cortisol levels) are modulated by the microbiome. 

They found  that there are circuits in the brain that are sensitive to microbial signals. Now, they  are seeking to identify the mechanisms that underlie those sensitivities.

https://asm.org/articles/2025/november/cant-sleep-your-microbiome-m...

Part 2

Comment by Dr. Krishna Kumari Challa 1 hour ago

Can't sleep? Your microbiome may play a role

Sleep is an absolute necessity but most of us aren't getting enough of it.

Sleep is required to consolidate memories, regenerate tissue and build up energy for emotional regulation and alertness during the day. Sleep deprivation disrupts these processes, increases stress and predisposes people to heart, psychiatric and neurological problems.

Factors like stress, jet lag, work, diet and screen time all interfere with our ability to get the 7–9 hours of solid slumber needed to recover from the physiological pummels of the day.

But there's more to this story than travel and cellphones. How much sleep we get, and its quality, may have ties to the microbial variety your body harbours!

We may have some control over how our sleep plays out, but many pieces of the puzzle—particularly those at the cellular level—are out of our hands. Some of them, in fact, are in our guts.
Studies in animal models and humans suggest there is a bidirectional relationship between the composition of the gut microbiota and sleep quality and duration. In mice, altering the gut microbial community, such as through antibiotic treatment, can lead to poorer, more fragmented sleep.

Comment by Dr. Krishna Kumari Challa 1 hour ago

Suspecting that what was changing was not the mosquitoes' ability to sense us at these times of day, but the persistence, or aggressiveness, of their response, the research team used CRISPR-Cas9, a gene editing tool, to mutate a gene that controls mosquitoes' internal clocks..
They found that mutating the gene changed their behavioral timing, making the mosquitoes less persistently responsive to carbon dioxide in the morning. Normally, biting rates are high in the mornings, but when they disrupted the clock gene, the mutant mosquitoes were less successful at feeding during that time.
This is the first time we've found that there's an internal rhythm in the mosquito's behavior that could be driving these bites at dawn and dusk. Their internal clocks make them more persistent and predatory in their response to humans at these times of day.
Scientists could, in theory, find ways to lock mosquitoes in a state that prevents them from effectively seeking out humans. This could mean fewer uncomfortable bites and less disease.
But the mosquitoes in our place bite us all the time, not only during dawn and dusk.
When we try to protect ourselves at dawn and dusk, they evolve to bite us all through the day!
Hmmm! Researchers are you listening?

Linhan Dong et al, Time-of-day modulation in mosquito response persistence to carbon dioxide is controlled by Pigment-Dispersing Factor, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2520826122

Part 2

Comment by Dr. Krishna Kumari Challa 1 hour ago

Could altering mosquitoes' internal clocks stop them from biting?

People who live in the tropical areas where Aedes aegypti mosquitoes reside have probably known for centuries, or even millennia—thanks to their itchy bites—that the mosquitoes hunt most often at dawn and dusk.

A new study offers scientific proof of that hunting behavior, and new insight into the biological mechanism behind it. It also offers a potential path to reducing bites and helping stop the spread of deadly, mosquito-borne disease.

The research focuses on Aedes aegypti, a type of mosquito that lives primarily in tropical areas, and that can carry diseases like dengue, chikungunya, and Zika. Although this mosquito species cannot survive harsh winters, in recent years they have made their habitats in new areas as climate change enables them to thrive in more temperate climates.

There are many reasons people could, in theory, get more bites from these mosquitoes at dawn and dusk. It could be that they're just outside more, or that humans are more attractive to them at these times. This study focused on understanding if this biting pattern is also influenced by mosquitoes' own daily rhythm.

The research team began by video recording mosquitoes, and watching how they responded to carbon dioxide, a signal mosquitoes use to locate humans. The team used machine learning to quantify the mosquitoes' movements.
They found that the mosquitoes had a more persistent response to the same amount of carbon dioxide at dawn and dusk, exactly the times of day that many people (both mosquito researchers and not) have reported getting more bites.

This is consistent with the idea that they're actually better predators at that time of day.
Part 1

Comment by Dr. Krishna Kumari Challa 2 hours ago

Bacteria spin rainbow-colored, sustainable textiles

In the future, clothes might come from vats of living microbes. Reporting in the journal Trends in Biotechnology, researchers demonstrate that bacteria can both create fabric and dye it in every color of the rainbow—all in one pot. The approach offers a sustainable alternative to the chemical-heavy practices used in today's textile industry.

The industry relies on petroleum-based synthetic fibers and chemicals for dyeing, which include carcinogens, heavy metals, and endocrine disruptors.

These processes generate lots of greenhouse gases, degrade water quality, and contaminate the soil, so researchers wanted to find a better solution.

Known as bacterial cellulose, fibrous networks produced by microbes during fermentation have emerged as a potential alternative to petroleum-based fibers such as polyester and nylon.

Researchers set out to create fibers with vivid natural pigment by growing cellulose-spinning bacteria alongside color-producing microbes. The microbial colors stemmed from two molecular families: violaceins—which range from green to purple—and carotenoids, which span from red to yellow.

But the first experiments failed. The team learned that the cellulose-spinning bacteria Komagataeibacter xylinus and the color-producing bacteria Escherichia coli interfered with each other's growth.

Tweaking their recipe, the researchers found a way to make peace between the microbes. For the cool-toned violaceins, they developed a delayed co-culture approach by adding in the color-producing bacteria after the cellulose bacteria had already begun growing, allowing each to do its job without thwarting the other.

For the warm-toned carotenoids, the team devised a sequential culture method, where the cellulose is first harvested and purified, then soaked in the pigment-producing cultures. Together, the two strategies yielded a vibrant palette of bacterial cellulose sheets in purple, navy, blue, green, yellow, orange, and red.

To see if the colors could survive the rigors of daily life, the team tested the materials by washing, bleaching, and heating them, as well as soaking them in acid and alkali. Most held their hues, and the violacein-based textile even outperformed synthetic dye in washing tests.

Researchers are  proposing an environmentally friendly direction toward sustainable textile dyeing while producing cellulose at the same time.

Accepting it is in your hands!

Scaling up production and competing with low-cost petroleum products are among the remaining hurdles. Real progress will also require a shift in the consumer mindset toward prioritizing sustainability over price.

But the bacteria-based fabrics are at least five years from store shelves.  

One-pot production of colored bacterial cellulose, Trends in Biotechnology (2025). DOI: 10.1016/j.tibtech.2025.09.019

Comment by Dr. Krishna Kumari Challa 3 hours ago

Scientists suspect that this cascade of EBV-generated self-targeting B-cell activation might extend beyond lupus to other autoimmune diseases such as multiple sclerosis, rheumatoid arthritis and Crohn's disease, where hints of EBV-initiated EBNA2 activity have been observed.
The million-dollar question: If about 95% of us are walking around with latent EBV in our B cells, why do some of us—but not all of us—get autoimmunity? The researchers speculate that perhaps only certain EBV strains spur the transformation of infected B cells into antigen-presenting "driver" cells that broadly activate huge numbers of antinuclear B cells.
Many companies are working on an EBV vaccine, and clinical trials of such a vaccine are underway. But that vaccine would have to be given soon after birth, they noted, as such vaccines are unable to rid an already-infected person of the virus.

Shady Younis et al, Epstein-Barr virus reprograms autoreactive B cells as antigen presenting cells in systemic lupus erythematosus, Science Translational Medicine (2025). DOI: 10.1126/scitranslmed.ady0210

Part 4

Comment by Dr. Krishna Kumari Challa 3 hours ago

But at times, somnolent autoreactive B cells become activated, take aim at our own tissues and instigate one of the disorders collectively called autoimmunity. Some awakened autoreactive B cells crank out antibodies that bind to proteins and DNA inside the nuclei of our cells. Such activated "antinuclear antibodies"—the hallmark of lupus—trigger damage to tissues randomly distributed throughout the body, because virtually all our body's cells have nuclei.

The vast majority of EBV-infected people (most of us, that is) have no idea they're still sheltering a virus and never get lupus. But essentially everyone with lupus is EBV-infected, studies have shown. An EBV-lupus connection has long been suspected but never nailed down until now.
Although latent EBV is ubiquitous in the sense that almost everybody carries it, it resides in only a tiny fraction of any given person's B cells. As a result, until the new study, it was virtually impossible for existing methods to identify infected B cells and distinguish them from uninfected ones.
But researchers now developed an extremely high-precision sequencing system that enabled them to do this. They found that fewer than 1 in 10,000 of a typical EBV-infected but otherwise healthy individual's B cells are hosting a dormant EBV viral genome.

Employing their new EBV-infected-B-cell-identifying technology along with bioinformatics and cell-culture experimentation, the researchers found out how such small numbers of infected cells can cause a powerful immune attack on one's own tissues. In lupus patients, the fraction of EBV-infected B cells rises to about 1 in 400—a 25-fold difference.
It's known that the latent EBV, despite its near-total inactivity, nonetheless occasionally nudges the B cell in which it's been snoozing to produce a single viral protein, EBNA2. The researchers showed that this protein acts as a molecular switch—in geneticists' language, a transcription factor—activating a battery of genes in the B cell's genome that had previously been at rest. At least two of the human genes switched on by EBNA2 are recipes for proteins that are, themselves, transcription factors that turn on a variety of other pro-inflammatory human genes.

The net effect of all these genetic fireworks is that the B cell becomes highly inflammatory: It dons its "professional antigen-presenting cell" uniform and starts stimulating other immune cells (called helper T cells) that happen to share a predilection for targeting cell-nuclear components. These helper T cells enlist multitudes of other antinuclear B cells as well as antinuclear killer T cells, vicious attack dogs of the immune system.

When that militia bulks up, it doesn't matter whether any of the newly recruited antinuclear B cells are EBV-infected or not. (The vast majority of them aren't.) If there are enough of them, the result is a bout of lupus.
Part 3

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