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Comment by Dr. Krishna Kumari Challa 5 hours ago

Faecal transplant soothes peanut allergy
Six people with a severe peanut allergy can tolerate the nut after a transplant of gut bacteria from the stool of people without the allergy. Four months after the transplant, five participants could eat 600 milligrams or more of peanut protein — the equivalent of about two and a half peanuts — without triggering a severe immune response. The potential of this type of therapy to have a lasting benefit is really, really exciting, because available treatments for food allergies are limited and short-lived.

https://www.science.org/doi/10.1126/scitranslmed.aee3263

Comment by Dr. Krishna Kumari Challa 6 hours ago

Levels of ALT, an enzyme indicative of poor liver health, and liver triglycerides were higher in both groups of mice in the experiments whose diets were laced with microplastics than in animals fed the same corresponding diet without polyethylene.

The same went for liver cell inflammation and ballooning, and steatosis (fat buildup in the liver).
Genes encoding proteins PPAR-alpha (which regulates liver fat production) and Annexin A2 (which, in the liver, is involved with tissue repair) were both in overdrive in the microplastics-affected livers.

https://www.science.org/doi/10.1126/sciadv.aec8681

Part 2

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Comment by Dr. Krishna Kumari Challa 6 hours ago

A Common Plastic Increases Risk of Fatty Liver Disease

One of the world's most common plastics – used in food packaging, plastic wraps, storage containers, and takeaway cups – may be partially responsible for your risk of fatty liver disease.

The disease, as we know it today, was first described in 1980.

But physicians have known since the 19th century that fatty infiltration of the liver is somehow related to diet, long before formal studies began.

A new study in mice suggests modern food conveniences might be adding to the problem.
People often aren't aware they have fatty liver disease (the non-alcoholic kind) until it is detected incidentally when they get a scan for some other condition.

When people do experience symptoms, they may present with fatigue, feeling generally unwell, and discomfort under the right side of their ribs.

Excess fat builds up in the liver cells, which can eventually lead to inflammation, then fibrosis (an accumulation of scar tissue), and even cirrhosis (serious damage), if untreated.
You're more at risk for fatty liver disease if you're carrying extra weight, especially around the middle.

Other risk factors include high blood fat levels (LDL cholesterol or triglycerides), type 2 diabetes or prediabetes, and high blood pressure.
All of these risk factors involve food and metabolism, but a new study in mice shows there may be an important aspect of people's diets that has been overlooked: exposure to microplastics, specifically polyethylene.

It's one of the most important plastics for food convenience: it packages takeaways, cling-wraps leftovers, stops your single-use cup from dissolving in your hand.

And, compared to many other polymers, polyethylene has kind of been considered a lesser concern.
Studies suggest that microscopic polyethylene can trigger signs of fatty liver disease, even with a standard diet. Regardless of diet, the addition of microplastics appeared to exacerbate the condition – even among the mice who ate a relatively healthy diet.
Part 1

Comment by Dr. Krishna Kumari Challa 6 hours ago

Essentially, the lingering bubbles begin to link together, dry out the surface faster, and cause the cooling mechanism to collapse. Reduced gravity is an advantage for heat transfer, right up until it isn't.

There are limitations to consider here: only nitrogen was tested, and on short parabolic flights.

However, the data gathered will be useful for future modeling as researchers devise equipment for more efficient, safer space travel.

https://www.nature.com/articles/s41526-026-00631-y

Part 2

Comment by Dr. Krishna Kumari Challa 6 hours ago

Boiling Liquid Does Something in Near-Zero Gravity
Out in deep, dark depths of space, electronics and fuel can still get hot – very hot.

As plans are made for longer missions and more advanced tech systems, one of the key areas scientists want to understand better is what happens to ultra-cold, cryogenic liquids when they boil.

These liquids are used as rocket fuel and to cool electronics, for example, but at the moment, we don't know enough about their boiling behavior in microgravity.

A new study investigating just that, in a series of airborne experiments, has turned up some surprising results. The findings are published in npj Microgravity

We know boiling liquids behave strangely in space; we've seen it happen before.
With less gravity, convection doesn't circulate heat through liquids as readily. And bubbles don't detach from surfaces as easily; they are less buoyant, so they don't float up as they do on Earth.
So it might reasonably be assumed that low gravity would also reduce the cooling capacity of those space bubbles because they can't carry heat away as fast.

But the researchers found the opposite: reduced gravity improved heat removal under certain conditions.

That is, until a heat threshold was exceeded and boiling became unstable.
Researcher s found that bubbles started forming sooner, and heat transfer was improved under near-zero-gravity conditions. The researchers think it's because in microgravity, the bubbles stick closer to the heated surface, which improves heat removal efficiency.
Their hypothesis is that bubbles stop floating away, so they linger on the surface.
When bubbles are on the surface, there is a small liquid gap between the bubble and the heater, and that liquid layer is so thin that it can improve heat transfer.
While that sounds beneficial, the cooling systems reached their limit faster in the simulated space conditions.

The maximum amount of heat that the liquid nitrogen coolant could handle dropped by 65 percent in microgravity compared to the lab tests.

Part 1

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Comment by Dr. Krishna Kumari Challa yesterday

What happens when someone's chromosomes, sex hormones and body don't align?
Differences of sex development arise when chromosomes, gonads, hormone production, or hormone responsiveness diverge from typical pathways. Conditions such as congenital adrenal hyperplasia, androgen insensitivity, 5-alpha-reductase deficiency, and sex-chromosome variations can affect anatomy, puberty, fertility, and health. Individualized specialist care, clear information, and psychological support are important.

original article.

Comment by Dr. Krishna Kumari Challa yesterday

What are chalk streams and why are these rare rivers under threat?
Chalk streams are groundwater-fed rivers with clear, cool, mineral-rich water and stable flows; seasonal headwaters called winterbournes support specialised aquatic and terrestrial species. Their biodiversity is threatened by water abstraction, pollution, channel modification, drought and heat. Reducing pollution and restoring natural flows can improve resilience.

Comment by Dr. Krishna Kumari Challa yesterday

Our tissues carry a remarkably detailed record of the aging process.
By combining histology images with artificial intelligence, we can detect patterns of biological aging that are invisible to the human eye and begin to understand how aging unfolds differently across the body.
The analysis revealed that aging does not occur uniformly: Some tissues, such as the lung, kidney, pancreas and adrenal gland, showed signs of accelerated aging between the ages of 20 and 40. Others followed more complex trajectories, with peaks of accelerated aging appearing later in life. The uterus displayed a particularly striking shift around the age of menopause.

The researchers also identified strong links between tissue-specific aging and medical conditions or lifestyle-associated factors. For example, kidney failure was associated with accelerated aging signals in multiple tissues, while diabetes showed pronounced effects in the pancreas.

What stands out is how differently each organ ages, and how that shows up in tissue architecture.
Deep learning lets us read these spatial patterns, capturing aging as architectural remodelling, not just molecular drift. While the tissue clocks captured the normal pace of aging across organs, they also highlighted outliers—individuals whose tissues showed pronounced structural shifts ahead of their chronological age.
However, tissue samples cannot always be collected. By linking blood-based gene expression profiles with the histologically derived tissue age gaps of the same individuals, the researchers built predictors of tissue-specific biological age from blood samples alone.
These blood-based predictors successfully identified aging patterns linked to several diseases, including Alzheimer's disease, Crohn's disease, cystic fibrosis, vasculitis, diabetes and stroke. In Alzheimer's disease, for example, the strongest aging signal was detected specifically in the brain, whereas Crohn's disease showed accelerated aging across the gastrointestinal tract.

Histological aging signatures for monitoring tissue-specific aging and disease, Nature Medicine (2026). DOI: 10.1038/s41591-026-04566-5

Part 2

Comment by Dr. Krishna Kumari Challa yesterday

Organs age at different speeds: A blood test might soon tell which ones

Some people seem to age more slowly than others, looking and acting like 45 at 60. Others appear to have gotten ahead of the calendar. But why is that, and what is actually happening inside the body?
AI-based "tissue clocks" can estimate the biological age of human organs from histological images, researchers showed. By analyzing more than 25,000 tissue samples across 40 tissue types, their study reveals that organs age at different rates throughout life and that these changes can even be detected from blood samples. The findings, published in Nature Medicine, provide a new framework for understanding aging and may open new avenues for disease monitoring and early diagnosis.
the researchers turned to the Genotype-Tissue Expression Project (GTEx), which collected tissue samples from 983 individuals across 40 different tissue types, ranging from the brain and heart to the lung, pancreas, skin and intestine. These were transformed into high-resolution digital images of tissue slices, each revealing the microscopic architecture of the organ in question. The scale is staggering: 25,712 images, representing about 480 million individual image tiles, analyzed with state-of-the-art vision models.

They found that the architecture of organs keeps a silent diary of time: Even without explicitly teaching the AI about it, age turned out to be the single strongest factor shaping tissue appearance across all 40 tissue types. Building on this, the research team developed so-called "tissue clocks"—predictive models that estimate a person's biological age from the appearance of their tissue, for each organ independently.

These clocks achieved a mean prediction error of just 4.9 years and outperformed existing DNA-based aging estimates in capturing tissue-specific pathology. Importantly, the predicted biological age was strongly linked to known hallmarks of aging, including telomere shortening, tissue pathology and the number of chronic diseases an individual had.
Part 1

Comment by Dr. Krishna Kumari Challa yesterday

Cells use a little-known molecule to protect themselves from iron overload

Iron is essential. Our cells need it to produce energy, carry oxygen throughout the body and power countless chemical reactions that sustain life. But this metal has a dark side. When too much of it is left free inside cells, it can trigger destructive reactions that break down DNA, proteins and even cell membranes.
Now researchers have discovered that cells rely on an unexpected protector against this threat: small molecules called polyamines.

The researchers' detailed findings, published in the journal Cell, reveal that polyamines act like storage lockers for iron, safely holding the metal in a nonreactive state until cells need it.
These findings solve a decades-old mystery about why cells maintain such extraordinarily high levels of polyamines and uncover a previously unknown defense mechanism that protects cells from toxic iron overload.

This work could also help scientists develop better cancer treatments by allowing iron overload to trigger cancer cell death. It could also offer new clues about diseases like early-onset Parkinson's disease, in which mutations affect polyamine levels within neurons.

Polyamines buffer labile iron to suppress ferroptosis, Cell (2026). DOI: 10.1016/j.cell.2026.07.040. www.cell.com/cell/fulltext/S0092-8674(26)00872-X

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