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Comment by Dr. Krishna Kumari Challa 3 hours ago

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 5 hours ago

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 6 hours ago

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 6 hours ago

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

Part 2

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Comment by Dr. Krishna Kumari Challa 6 hours ago

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.

Par t1

Comment by Dr. Krishna Kumari Challa on Sunday

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

Part 2

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Comment by Dr. Krishna Kumari Challa on Sunday

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.
Part 1

Comment by Dr. Krishna Kumari Challa on Saturday

Tiny marine microbe sheds new light on how little genetic machinery a cell needs to survive
The marine archaeon Candidatus Sukunaarchaeum mirabile has 189 protein-coding genes, retaining machinery for DNA replication and protein synthesis. It lacks nearly all genes for nutrient and energy production, suggesting strong dependence on other organisms. It has not been directly observed, and its host and possible parasitic lifestyle remain unknown.

A hidden archaeal lineage with an ultra-reduced genome retaining only its replicative core, Current Biology (2026). DOI: 10.1016/j.cub.2026.09.042. www.cell.com/current-biology/f … 0960-9822(26)01251-0

Comment by Dr. Krishna Kumari Challa on Saturday

Strong magnetic fields could allow white dwarfs to grow beyond the Chandrasekhar limit

When a dying star runs out of fuel and sheds its outer layers, its remaining core can become an approximately Earth-sized, extremely dense stellar remnant called a white dwarf. For a white dwarf that is not strongly rotating or magnetized, there is a well-known upper mass limit of about 1.4 times the mass of the sun, known as the Chandrasekhar limit.
As a carbon-oxygen white dwarf approaches this limit, its core can become dense enough to ignite carbon, potentially triggering a thermonuclear explosion known as a Type Ia supernova.

If the Chandrasekhar limit is fixed, the supernova energy release rate and luminosity should be fixed. Scientists have used this constancy of luminosity to understand the evolution and size of the universe, which is presently thought to be expanding.
Now, simulations by researchers from the Department of Physics at the Indian Institute of Science (IISc) and collaborators show that strong internal magnetic fields could allow some white dwarfs to grow to substantially higher masses than the Chandrasekhar limit allows. In one of their simulations, the researchers found that a magnetized carbon-oxygen white dwarf can reach about 2.4 times the mass of the sun—well above the limit.
Stellar evolution simulations predict that magnetic pressure can support accreting carbon–oxygen white dwarfs up to about 2.4 solar masses, exceeding the usual 1.4-solar-mass Chandrasekhar limit. Accretion-driven contraction strengthens internal magnetic fields, providing additional support against gravity.

Zenia Zuraiq et al, Super-Chandrasekhar White Dwarfs by the Evolution of Magnetized Main-sequence Stars: New Mass Limits from STARS Simulation, The Astrophysical Journal Letters (2026). DOI: 10.3847/2041-8213/aea97e

Comment by Dr. Krishna Kumari Challa on Saturday

Bees struggle to smell flowers when air pollutants combine

Bees, moths and other pollinating insects have a harder time smelling flowers in polluted air, according to new research.
Scientists analyzed 22 experimental studies on how the air pollutants ozone and nitrogen oxides (NOx) affect pollinators. Both pollutants make it harder for pollinators to find flowers by breaking down or altering the scents that flowers give off.
The new research, published in the journal Frontiers in Ecology and the Environment, found that elevated ozone reduced pollinator performance by an average of 42%, while NOx cut performance by 46%. When the two pollutants occurred together, the average reduction was 68%.

Only a few studies tested both pollutants together, and in those the extra harm from combining them was smaller than the averages suggest. This is because the two gases react with each other in the air and partly cancel each other out.
The study also found specialist pollinators reliant on one plant's scent, such as some moths, are more at risk than generalists like many bees. Additionally, day-active pollinators such as bees and butterflies face higher ozone levels, while night-active pollinators (including many moths) encounter higher nitrogen oxides. Both need protection.

Pollinator risks and recovery from air pollutant interactions during the fossil fuel transition, Frontiers in Ecology and the Environment (2026). DOI: 10.1002/fee.70076

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