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Comment by Dr. Krishna Kumari Challa on Thursday

Ovaries remain active decades after menopause, study reveals

Contrary to popular belief, the postmenopausal ovary is not defunct. In a new study of ovaries from 28 women, scientists found that in the decades well past menopause, the ovary remains biologically active and continues to remodel with age, showing increased inflammation and changes in tissue structure. The study also found a molecular link between ovarian aging and cancer.
In the ovary, we reach a point of no return with respect to fertility in which it's no longer producing eggs, and most people assume those ovaries are just sitting there doing nothing, similar to the appendix.
The findings challenge the notion that the ovary is an innocent bystander after reproduction ends, raising new questions about whether it could play a more active role in aging and chronic disease in women.

The ovary is not just a reproductive organ. It really influences how somebody ages because it speaks to all these other organs, such as the brain, and also to the bone, and women after menopause often experience a lot of bone problems. So, researchers think there is a connection between all these organs.
Women now routinely live for decades after menopause, making it increasingly important to understand what the ovary is doing during this long post-reproductive period.
The new data point to progressive aging features in which the ovary appears to lose its original identity and ends up doing something different.
To find out what was changing, the scientists went beyond ovarian hormones to analyze the composition of the tissue at high resolution.
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Comment by Dr. Krishna Kumari Challa on Thursday

The next puzzle was to untangle how a fatty acid could help clear cholesterol from blood.

Experiments showed that pentadecanoic acid binds to and inhibits HMG-CoA reductase, an enzyme needed to make cholesterol. As cholesterol production fell, liver cells increased their supply of LDL receptors: proteins that capture cholesterol-carrying particles from the bloodstream.

The two effects worked together. The liver made less cholesterol and took in more from circulating blood.

The researchers tested that explanation by disabling LDL receptor production specifically in the mouse liver. Without those receptors, neither the bacterium nor the fatty acid provided its usual protection against plaque buildup.

Changing the bacterium supplied another check. Engineered strains that made less pentadecanoic acid still colonized the gut but offered substantially weaker protection. That finding helped connect the bacterial product to the arterial benefit.
Pentadecanoic acid is a saturated fatty acid found in foods such as dairy fat. The study strengthens the evidence that gut microbes also supply it, but showing a protective mechanism in mice does not establish a treatment for people.

Human findings offer reasons to investigate further, alongside reasons for caution. A small 2024 trial in women with fatty liver disease found that adding pentadecanoic acid to a Mediterranean-style dietary intervention further reduced LDL cholesterol. However, a 2026 analysis of two long-running studies found no association between higher blood levels of the molecule and a lower incidence of cardiovascular disease.

The molecule is already marketed as a heart-health supplement. Yet the clinical evidence supporting a cardiovascular benefit remains limited.
It should be noted that the new experiments used only male mice, and human diets and gut communities could change the response seen in the animal experiments.

Chao Yin et al., A gut microbial odd-chain fatty acid alleviates atherosclerosis in mice, Nature (2026). DOI: 10.1038/s41586-026-11142-x

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Comment by Dr. Krishna Kumari Challa on Thursday

A gut microbe makes a fatty acid that cuts artery plaque in half in mice

A common gut bacterium produces a molecule that slows cholesterol production in the liver. When researchers gave the molecule to mice prone to artery disease, the animals developed roughly half as much fatty plaque as untreated controls.
The molecule acts on the same enzyme targeted by statins, the widely used cholesterol-lowering drugs. That connection offers a concrete explanation for something harder to untangle: how bacteria living in the intestine might influence the health of arteries elsewhere in the body.

Researchers identified the substance as pentadecanoic acid. Their study, published in Nature, followed its effects from bacterial production to cholesterol clearance.
Observational studies over the past two decades have shown that the gut microbiota plays an important role in metabolic health, and disruptions can lead to common disorders including diabetes, liver disease and cardiovascular disease. More recent cause-and-effect studies are trying to pinpoint the molecular mechanisms that drive the development of these conditions.

Investigating this connection, the researchers began with existing gut microbiome data from people with and without atherosclerotic cardiovascular disease, in which fatty deposits accumulate in artery walls. Several bacterial species were more abundant in healthy people, with Bacteroides uniformis standing out.

Was the bacterium helping protect arteries, or is it simply more common in healthier people?

To find out, the researchers gave it to male mice genetically prone to atherosclerosis that were fed a high-fat diet. After 12 weeks, treated mice had less plaque in their aortas and lower blood levels of LDL, often called "bad" cholesterol. Heat-killed bacteria did not produce the same benefits.

The key appeared to be something the living microbes produced. The team separated substances released into the bacterial culture fluid, testing which one helped the laboratory-grown liver cells take up LDL. Repeatedly narrowing the mixture led them to pentadecanoic acid.

Given directly to mice three times a week for eight weeks, the fatty acid lowered cholesterol and reduced plaque buildup by about half.
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Comment by Dr. Krishna Kumari Challa on Wednesday

Candida auris copies its entire genome to survive antifungal treatment, research reveals

New research has revealed an unexpected new mechanism through which the killer fungus Candida auris is resisting antifungal drug treatment.
Researchers discovered that the fungus creates multiple versions of its entire genome, including mutating a gene that plays a role in cell wall integrity, called "Crazy-one" (CRZ1).
In laboratory tests, Candida auris survived high antifungal concentrations by producing multiple copies of its entire genome. Surviving populations grew at different rates; faster-growing cells carried mutations in CRZ1, a regulator of cell wall synthesis, and their cell walls remained unaffected by treatment.
The researchers did not identify any of the DNA mutations that we might have expected. Antifungal drugs target the enzymes that make cell walls, so that fungi die by shriveling, exploding or not being able to grow. Somehow, these fungi had survived antifungal drugs.
Surviving cells had made multiple copies of their entire genome. This is a trick that other fungi have used in the past, but not one that is well known in C. auris. In fact, there were two populations, some growing slowly, others growing more rapidly. Researchers call it 'bet-hedging' when a bug uses multiple tactics to increase its chances of developing resistance and evading treatment."

Study authors say their findings unlock a new mechanism that allows Candida auris to adapt to antifungal treatment and survive, which could lead to new ways to tackle the fungus.
Researchers are now looking at options including the use of antifungal drugs in combination.

FKS1/2-variant independent mechanisms underlying the emergence of resistance in echinocandin-refractory Candida auris infections, Nature Communications (2026). DOI: 10.1038/s41467-026-76954-x. On bioRxiv: www.biorxiv.org/content/10.648 … /2026.01.17.700071v1

Comment by Dr. Krishna Kumari Challa on Wednesday

Link between lithium in drinking water and a rare heart condition

Children living in areas with higher levels of lithium in drinking water were more likely to be diagnosed with Wolff-Parkinson-White syndrome, a rare heart condition that can cause a dangerously fast heartbeat, according to a new study.

The findings, which were published online in The Journal of Clinical Investigation, are based on health and water-quality data for more than 2.3 million children in California and were also observed among nearly 2 million children in New York. Children in California counties with lithium levels in the highest 25% had 71% greater odds of a Wolff-Parkinson-White (WPW) diagnosis than those living in counties with lower levels.

Lithium occurs naturally in groundwater, and concentrations vary widely by location. Although the research focused on California and New York, lithium is found in groundwater used for drinking water across the United States and elsewhere, raising questions about the potential broader public health significance of the findings.

WPW occurs when an extra strand of heart muscle, known as an accessory pathway, creates an abnormal electrical connection in the heart. These pathways form during fetal development, but why they develop has remained largely unknown. Most people with accessory pathways do not have a family history of the condition, suggesting that environmental exposures during fetal development could play a role.

Accessory pathways are among the most common causes of supraventricular tachycardia (SVT), a rapid heart rhythm that can cause palpitations and other symptoms. WPW, which involves a particular type of accessory pathway, is also associated with a small increased risk of sudden death.

The pathways can be treated with catheter ablation, a minimally invasive procedure that eliminates the small area of heart tissue responsible for the abnormal electrical connection.

Medicinal doses of lithium during pregnancy have been associated with an increased risk of congenital heart defects, including Ebstein's anomaly, a rare condition that is frequently accompanied by accessory pathways. That led the UCSF researchers to ask whether lithium in drinking water might also be associated with changes in the developing heart.

In addition to the association with WPW, higher lithium levels in California were associated with SVT, palpitations and fainting. Researchers then retested their main finding in New York, where children living in areas with lithium levels above 10 parts per billion also had greater odds of WPW.

The study does not prove that lithium causes WPW. Researchers did not know how much lithium individual children or their mothers consumed, and they used county of residence to estimate exposure. Other environmental or genetic factors could also help explain the association.

Elevated lithium levels in drinking water are associated with higher prevalence of Wolff-Parkinson-White diagnoses, Journal of Clinical Investigation (2026).

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Comment by Dr. Krishna Kumari Challa on Wednesday

Mushroom-derived peptides boost saltiness by up to 70%, offering a path to low-sodium foods

Cutting down on salt might be good for health but not so good for the taste buds. So, scientists have been looking for alternatives that keep the saltiness while reducing sodium content. The most common sodium chloride (NaCl) alternatives on the market contain potassium. With regular use, these alternatives can increase the risk of excess potassium retention, potentially posing health risks for older adults.

Scientists have found a way to make salt taste saltier without increasing its sodium content, a welcome development in the culinary world. Salt is a powerful flavour enhancer, drawing out the subtle flavours of a dish while balancing sweetness and bitterness. Its appeal comes hand in hand with some drawbacks. Salt activates the brain's reward system, making food more pleasurable, but eating too much salty food can negatively affect cardiovascular health.
In a recent study published in npj Science of Food, researchers turned to Hypsizygus marmoreus, a popular edible mushroom, to see whether its proteins contain natural peptides that can amplify how our taste buds perceive saltiness.

They successfully extracted three mushroom-derived peptides: ASHGEGF, GDDWT and LDDGF. To measure how much saltier the solution tasted, the researchers used an electronic tongue, a device that mimics our sense of taste by translating chemical signals in liquids into electrical readings.

ASHGEGF was the standout performer, delivering the strongest salty kick by increasing the saltiness intensity of a 3 mg/mL NaCl solution by 70.59%. The three peptides boosted saltiness on their own and in combination, reinforcing each other to deliver a saltier taste that lasted longer.
Peptides, short chains of amino acids often extracted from yeast, soy and bovine bone, offer a way to lower sodium in food without a major loss of flavor. They intensify the taste of salt solutions, so you can reduce sodium while the food still tastes salty. Interest in them is growing because they come from food sources, have nutritional value and are readily absorbed by the body.

In this study, researchers focused on the edible mushroom Hypsizygus marmoreus, which is rich in proteins and flavour compounds but whose specific saltiness-enhancing peptides remained poorly studied.
Taken together, these findings point to a promising route for creating new seasonings from Hypsizygus marmoreus mushrooms that enhance saltiness.

Wenping Kong et al., Discovery of saltiness-enhancing peptides from Hypsizygus marmoreus via virtual screening, multisensory evaluation, electronic tongue, and molecular simulation, npj Science of Food (2026). DOI: 10.1038/s41538-026-01088-9

Comment by Dr. Krishna Kumari Challa on Wednesday

The researchers also examined microbes associated with the lining of the ileum, the final part of the small intestine. They observed changes in the relative abundance of several bacterial groups, alongside increases in intestinal inflammatory markers.

Compared with untreated mice, schizophrenia-donor recipients had lower levels of occludin, a protein that helps seal gaps between intestinal lining cells. This suggests a weakened intestinal barrier, although the researchers did not directly measure its permeability.

Blood tests revealed higher levels of two immune signaling proteins, interferon-gamma and interleukin-17, in animals that received gut microbes from people with schizophrenia compared with untreated animals. These increases were not statistically significant relative to healthy-donor recipients.

Immune cells called microglia in the prefrontal cortex, a brain region involved in cognition and social behavior, also exhibited some changes. These cells help maintain brain tissue and remodel connections between neurons.

The branching extensions of these cells were found to be less complex, while molecular measurements indicated a more reactive immune state. Together, the team's findings suggest a possible connection between intestinal microbes, circulating immune signals and brain inflammation, yet they do not establish whether any of these changes caused the others.
The team examined a separate collection of brain tissue obtained after death from four people with schizophrenia and three people without it. These samples showed some overlapping changes in microglial and inflammatory markers, although the patterns did not match completely.

Both the stool-donor sample and human brain comparison were small, which limits how broadly the study's findings can be applied. The experiment also does not establish that gut microbes cause or prompt the development of schizophrenia in humans.
Future experiments could change the microbes or block particular immune signals in mice, then assess whether this prevents the observed brain and behavioural changes. This would help determine whether the proposed gut-brain pathway could eventually be targeted therapeutically.

Ana Raquel Pereira-Santos et al., Unveiling the gut microbiome-immune-brain axis in schizophrenia, Translational Psychiatry (2026). DOI: 10.1038/s41398-026-04497-2

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Comment by Dr. Krishna Kumari Challa on Wednesday

Gut microbes from people with schizophrenia alter mouse behaviour

Schizophrenia is an often debilitating psychiatric disorder that can disrupt people's thinking, perception and behavior. While genetic and environmental factors can contribute to its emergence, researchers are still trying to understand its underlying biological processes.

Previous studies have identified differences in the gut microbiome, the community of microorganisms living in the intestine, of people with schizophrenia. Yet how these differences might influence brain function still needs further investigation.

Researchers  recently investigated whether gut microbes from people with schizophrenia could affect behaviour and immune activity in mice. Their findings, published in Translational Psychiatry, hint at a possible immune connection between the gut and brain.

In their new study, the team collected stool samples from three people with schizophrenia and three healthy donors. They then fed young mice gelatin portions containing material from individual donors repeatedly over a period of five weeks.
The mice already had their own gut microbial communities, so the transferred material entered an already established environment. The researchers then compared animals receiving samples from people with schizophrenia with healthy-donor recipients and untreated mice.

To assess their behavior, the team introduced the mice into a T-shaped maze. Each mouse explored one arm of the maze, took a brief break and then returned. Mice receiving schizophrenia-donor samples were less likely to choose the other arm than animals in either comparison group.

This test probes short-term working memory and the ability to switch between choices, although reduced alternation does not necessarily reflect forgetting alone.

In a separate test, the mice could approach a cage containing an unfamiliar mouse or an empty cage. Those receiving schizophrenia-donor samples showed less preference for investigating the unfamiliar animal.

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Comment by Dr. Krishna Kumari Challa on October 11, 2026 at 12:10pm

The most likely starting site was twin A's facial mass. The cancer diversified into different cell populations and spread within her body before reaching her sister. The pattern in twin B supported a relatively late, single transfer.

The researchers then used accumulated mutations to estimate when this happened. Assuming mutations built up at a constant rate, they placed the tumor's origin near the end of the first trimester and its transfer late in the second trimester.

Those dates are estimates that depend on the assumed mutation rate, rather than direct observations.

There was another surprise: normal cells had moved in the opposite direction. Genetic markers in a spleen sample from twin A suggested around 75 percent of the sampled cells originated in twin B, consistent with blood-cell mixing between the sisters.

The twins' earliest cell lineages also contributed unevenly to their bodies and placenta. One branch contributed almost exclusively to twin A, another to both sisters and the placenta, and a third to twin B and the placenta. The pattern favored an earlier embryonic split than the classical model for this type of identical twinning predicts.

However, this was one pair of twins, and the analysis could recover only lineages that survived in the tissues sampled.

Earlier research on twins with leukemia has also explored cancer's beginnings before birth. This case adds a detailed reconstruction of a soft tissue tumor's journey, without establishing how often such transfers occur.

https://www.nature.com/articles/s41467-026-78178-5

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Comment by Dr. Krishna Kumari Challa on October 11, 2026 at 12:09pm

Embryonic origin of cancer in newborn twins

Cancer Passed Between Twins Before Birth
A facial mass detected before birth prompted the early delivery of identical twin sisters. A fetal MRI at 33 weeks showed the mass on one baby's face. When the sisters were born a week later, tumors were found in both.

Two children had the same cancer, raising a question that their shared beginnings alone could not answer.

Had the disease started separately in each sister, or had cancer cells crossed from one to the other before birth?

Researchers turned to a record hidden within their cells. DNA changes, accumulated as their bodies developed, allowed the team to reconstruct events that had happened months before anyone saw a tumor.

The study in Nature Communications shows that the cancer began in one sister and passed to the other in the womb, most likely through a single transfer late in the second trimester. The same investigation uncovered clues to how the sisters themselves had formed.

The two girls, Amelia and Amaya, died soon after birth. Their family consented to post-mortem examinations for research.
The baby with the facial mass is called twin A in the paper. At birth, she had tumor deposits in several organs. Her sister, twin B, initially had lesions in her skin; disease involving the membranes around the brain and spinal cord was detected later.
The tumors were reported as undifferentiated sarcomas. Soft tissue sarcomas arise in tissues such as muscle, fat and the body's supporting structures. All the twins' tumor samples carried the same fusion of two genes, MN1 and ZNF341.

Matching tumors were only the beginning: the team needed to identify whose cells had started the cancer.

Here, an apparent contradiction proved useful: identical twins are not necessarily genetically identical.

They begin with the same fertilized egg, but DNA changes can arise as their cells multiply. A change acquired by one cell can pass to its descendants, marking a particular branch of the developing body's cellular family tree.

Comparing those marks across tissues reveals shared ancestors and distinguishes one twin's cells from her sister's.

The team sequenced 10 tumor samples, 12 normal tissue samples from the twins and 11 placental samples. They also examined 12 placental samples enriched for cells involved in forming the placenta.

The researchers found that cancer began in twin A, then cancer cells passed to twin B before birth and formed tumors there too. The evidence was in the second baby's tumors: their cells carried genetic markers belonging to her sister.

The study points to spread across the placenta they shared. The genetic analysis establishes which sister the cancer came from, but does not directly show the cells crossing or the route they took.
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