Comment

Comment by Dr. Krishna Kumari Challa 3 hours ago

Antibiotic resistance can vary depending on where the bacteria live

New research  indicates that the outcome of a resistance measurement may depend on the conditions under which the bacterium is tested. Standard laboratory tests are carried out under fixed, uniform conditions, but if, for example, the test environment is altered, the very same bacterium may in some cases be either more or less susceptible to an antibiotic than the laboratory result indicates.
When doctors or veterinarians receive a laboratory report stating whether a bacterial sample is resistant to an antibiotic, the answer will typically be that the bacterium is susceptible (and can therefore be treated with antibiotics), or that it is not. That answer is correct for the standardized test conditions laboratories use, and it is this standardization that allows results to be compared across laboratories.

However, standard conditions do not necessarily reflect all the environments bacteria encounter in real life. In the body (and across different hosts), factors such as pH level (how acidic or alkaline an environment is) and temperature can vary, and this may influence how effectively particular resistance genes function.

Understanding how antimicrobial resistance develops and spreads is crucial, as antibiotic resistance has become an imminent threat to global public health.
In the study, the researchers investigated two widely prevalent resistance genes to determine how levels of resistance changed when pH and temperature were varied under controlled laboratory conditions. Among other measures, they quantified the amount of antibiotic required to kill the bacterium as pH was altered.

The researchers also examined the significance of temperatures comparable to the body temperatures of different hosts. Here, they observed an effect at temperatures corresponding to birds (around 42°C) compared with humans (around 37°C).

If a resistance gene functions better at 42°C than at 37°C (or vice versa), this may affect how readily bacteria carrying the gene survive and spread in birds, and thus the extent to which birds may act as hosts for bacteria with that type of resistance.
Antibiotic resistance in bacteria can vary significantly depending on environmental factors such as pH and temperature. The resistance genes CTX-M-15 and CMY-2 showed different levels of antibiotic susceptibility under varying conditions, with CTX-M-15 being strongest in acidic environments and weaker in alkaline ones. These findings suggest that standard laboratory tests may not fully reflect resistance in real-world settings.
Findings
CTX-M-15 conferred the strongest resistance in acidic conditions and became weaker as the environment became more alkaline.
CMY-2 performed better at more alkaline pH than CTX-M-15.
At more alkaline pH, bacteria carrying CTX-M-15 could, in the experiment, shift from resistant to susceptible.
Temperature also affected the results, which may be relevant when comparing different hosts and environments.

Mikkel Anbo et al, Contrasting pH optima of β-lactamases CTX-M and CMY influence Escherichia coli fitness and resistance ecology, Applied and Environmental Microbiology (2026). DOI: 10.1128/aem.01775-25

Comment by Dr. Krishna Kumari Challa 3 hours ago

Why lethal mutations persist: Fruit fly study points to newly transferred jumping genes, not small DNA errors
Lethal mutations in wild fruit flies are primarily caused by recently transferred transposable elements, rather than small DNA errors. These jumping genes can rapidly increase mutation rates, temporarily outpacing natural selection until host genomes evolve defenses. This mechanism influences genetic health and persistence of harmful mutations in populations, with implications for conservation and human disease.

Transposable elements contribute substantially to naturally occurring genetic lethality in Drosophila melanogaster, PLOS Biology (2026). DOI: 10.1371/journal.pbio.3003467

Comment by Dr. Krishna Kumari Challa 4 hours ago

Scientists discover how falling cats almost always make perfect landings

When cats fall, they usually land on their feet. This uncanny ability to right themselves before hitting the ground has long puzzled people. Now, a research team has the answer, and it's all down to the thoracic spine being more flexible than the lumbar spine, as they detail in a study published in the journal The Anatomical Record.

The air-righting reflex is a complex maneuver that protects cats from serious injury if they fall. As they tumble, the spine twists, which seems to contradict the laws of physics. That's because an object in midair shouldn't be able to turn without something to push against.

To find out how they do it, the researchers first studied the spines of five cat cadavers. They separated the thoracic spine (upper/middle back) from the lumbar spine (lower back) and mechanically tested them under twisting forces to measure flexibility, strength and resistance to rotation. This revealed the capability of a cat's body.

The team also used high-speed cameras to film two healthy cats as they dropped onto a soft cushion. They placed markers on their shoulders and hips to track the movement of their body parts.

The team discovered that the cat's spine is not uniformly flexible. Different parts move in different ways to help the animal land safely. The thoracic spine is incredibly flexible and has a neutral zone, a range where it can twist almost freely for nearly 50 degrees with very little effort. Meanwhile, the lumbar spine is much stiffer and acts as a stabilizer.

During air-righting, the cat rotates its head and front legs toward the ground first because the thoracic spine is flexible and the front of the body is lighter. Then the back half follows. The stiff lumbar spine acts as a solid anchor, allowing the cat to whip its front around without spinning out of control.

These results suggest that trunk rotation during air-righting in cats occurs sequentially, with the anterior trunk rotating first, followed by the posterior trunk, and that their flexible thoracic spine and rigid lumbar spine in axial torsion are suited for this behaviour," commented the study authors in their paper.

Yasuo Higurashi et al, Torsional flexibility of the thoracic spine is superior to that of the lumbar spine in cats: Implications for the falling cat problem, The Anatomical Record (2026). DOI: 10.1002/ar.70165

Comment by Dr. Krishna Kumari Challa yesterday

Why most foods don't trigger allergies: Three common seed proteins may train gut immune tolerance

Since 6% of young children and 3% to 4% of adults experience food allergies, scientists have been hard at work figuring out exactly what elicits these allergic reactions to foods that should be safe.
Three specific seed protein epitopes from soybean, corn, and wheat have been identified as key in training gut regulatory T cells to promote immune tolerance to foods. These epitopes help explain why most foods do not trigger allergies and suggest a mechanism for cross-tolerance. The findings may inform future therapies to induce tolerance in individuals with food allergies.
When you sip coffee or lick an ice cream cone, it doesn't seem like your body is pulling off a biological miracle. But it is. That cookie is not you—yet when you put it in your mouth, your body is able to tolerate it and process it without any detriment to your health in a process called oral tolerance. How does the human body make that decision between tolerance and rejection?
An investigation by scientists identifies new bits of food proteins that tell gut immune cells when to tolerate certain foods. They found three of these protein segments, called epitopes—one each from soybean, corn, and wheat. These epitopes interact with specialized immune cells called regulatory T cells to inform that tolerance-or-rejection decision. The findings are an enormous step forward in understanding food tolerance, and may inform future immunotherapies for people with food allergies.
The researchers found three proteins—more specifically, they found small, specific bits of those proteins called epitopes—that the regulatory T cells recognized. The epitopes were found in three different food proteins, one from corn, one from wheat, and one from soybean. Notably, all three epitopes are from seed proteins, suggesting that these highly abundant plant proteins are commonly recognized by the immune system's tolerance mechanisms.
Furthermore, the most abundant T cells were those reactive to the corn epitope, which makes sense given that corn is not a common allergy. Soy, on the other hand, is one of the major allergies in humans, so the identification of a soybean epitope is especially exciting.
Additionally, the mammalian receptor that interacts with the identified soybean epitope also interacts with sesame, helping explain cross-tolerance, or when a tolerance to one food infers a tolerance to another.
These seed epitopes are an exciting new addition to our understanding of oral tolerance. Scientists have already considered regulatory T cells as a promising immunotherapy route for people with severe food allergies. It may one day be possible to create regulatory T cells that are pre-programmed to tolerate certain foods and dampen immune responses to common allergens.

Jamie Blum et al, Identification and characterization of dietary antigens in oral tolerance, Science Immunology (2026). DOI: 10.1126/sciimmunol.aeb4684. www.science.org/doi/10.1126/sciimmunol.aeb4684

Comment by Dr. Krishna Kumari Challa yesterday

Daily multivitamins may slow biological aging, two-year trial suggests

A two-year randomized trial in older adults found that daily multivitamin use slowed biological aging, as measured by five epigenetic clocks, by approximately four months compared to placebo. The effect was more pronounced in participants with accelerated biological age at baseline. These findings suggest multivitamins may modestly slow cellular aging, particularly in those aging faster biologically.
An analysis by investigators found slower aging in older adults after two years of a daily multivitamin, with greater benefits for those who began the trial with accelerated biological age.
How quickly our bodies age on a cellular level, our "biological age," can differ from how old we actually are in years. Using data from a large randomized clinical trial of older adults, researchers evaluated the effects of taking a daily multivitamin over the course of two years on five measures of biological aging and found a slowing equivalent to about four months of aging.

The benefits were increased in those who were biologically older than their actual age at the start of the trial. Their results are published in Nature Medicine.
Epigenetic clocks estimate biological aging based on tiny changes in our DNA. These clocks look at specific sites in our DNA that regulate gene expression (known as DNA methylation) and change naturally as we get older, helping track mortality and the pace of aging.

This study, which uses data from the well-established COcoa Supplement Multivitamins Outcomes Study (COSMOS), analyzed DNA methylation data from blood samples of 958 randomly selected healthy participants with an average chronological age of 70.

The study participants were randomized to take a daily cocoa extract and multivitamin; daily cocoa extract and placebo; placebo and multivitamin; or placebos only. Samples were analyzed for changes in five epigenetic clocks from the start of the trial and at the end of the first and second years.
Compared to the placebo-only group, people in the multivitamin group had slowing in all five epigenetic clocks, including statistically significant slowing seen in the two clocks that are predictive of mortality. The changes equated to about four months less biological aging over the course of two years. Additionally, people who were biologically older than their actual age at the start of the trial benefitted the most.

Howard Sesso, Effects of daily multivitamin–multimineral and cocoa extract supplementation on epigenetic aging clocks in the COSMOS randomized clinical trial, Nature Medicine (2026). DOI: 10.1038/s41591-026-04239-3. www.nature.com/articles/s41591-026-04239-3

Comment by Dr. Krishna Kumari Challa yesterday

This doesn't mean lab accidents don't happen. But it does mean that if a virus had been extensively passaged in a lab before an outbreak, we would expect to see it in the evolutionary record. In nearly all pandemics we've studied, that signal simply isn't there.

Looking ahead, the researchers see potential applications in outbreak forensics, viral surveillance and pandemic preparedness.

Jennifer L. Havens et al, Dynamics of natural selection preceding human viral epidemics and pandemics, Cell (2026). DOI: 10.1016/j.cell.2026.02.006

Part 2

Comment by Dr. Krishna Kumari Challa yesterday

Recent pandemic viruses jumped to humans without prior adaptation, study finds

A new  study published in Cell challenges a long-standing assumption about how animal viruses become capable of sparking human epidemics and pandemics. Using a phylogenetic, genome-wide analysis across multiple viral families, researchers report that most zoonotic viruses—infectious pathogens that spread from animals to humans, including the cause of COVID-19—do not show evidence of special evolutionary adaptation before spilling over into humans.

From an evolutionary perspective, researchers find no evidence that SARS-CoV-2 was shaped by selection in a laboratory or prolonged evolution in an intermediate host prior to its emergence. That absence of evidence is exactly what we would expect from a natural zoonotic event—and it represents another nail in the coffin for theories invoking laboratory manipulation.

The prevailing model of zoonotic emergence has often assumed that viruses must first acquire adaptive mutations before they can sustain human-to-human spread. To test that assumption, the research team analyzed viral genomes from outbreaks caused by influenza A virus, Ebola virus, Marburg virus, mpox virus, SARS-CoV and SARS-CoV-2. They focused on the evolutionary period immediately preceding human outbreaks, where any substantial pre-spillover adaptation should leave a detectable imprint.

Across these diverse viruses, the investigators found a strikingly consistent pattern: selection pressures before zoonotic emergence were indistinguishable from those acting during routine circulation in animal reservoirs. In other words, there was no evolutionary signal suggesting that these viruses were being "pre-adapted" for humans prior to their outbreaks. Instead, measurable changes in selection typically appeared only after sustained transmission began in people.

These findings challenge the idea that pandemic viruses are evolutionarily special before they reach humans.

Rather than requiring rare, finely tuned adaptations in animals, many viruses may already possess the basic capacity to infect and transmit between humans. What matters most is human exposure to a diverse array of animal viruses.

The study relies on a sophisticated phylogenetic framework that measures changes in the intensity of natural selection across entire viral genomes. By comparing rates of different types of mutations, the researchers were able to detect whether natural selection was intensified, relaxed or unchanged across key evolutionary transitions. Importantly, the team validated their approach using known examples of artificially selected viruses propagated in cell culture or in laboratory animals, which produced clear and reproducible evolutionary signatures distinct from natural transmission.

Part 1

Comment by Dr. Krishna Kumari Challa on Sunday

Microplastics May Be Fueling Parkinson's Disease, Scientists Warn

Plastic pollution is seeping into the Earth, into wildlife, and into our bodies, and a new research review suggests tiny microplastics and nanoplastics could be disrupting some of the brain processes associated with Parkinson's.

While Parkinson's disease is associated with a wide range of risk factors, the rise we're seeing in the number of people being diagnosed – its prevalence has doubled in the last 25 years – could be at least partly down to a rise in pollutants in the environment.
For this recent review, a team of researchers referenced more than 100 previous studies, including animal studies, laboratory experiments, and computational models, to build a compelling case linking plastics to Parkinson's.
While it's not yet clear that microplastics are directly responsible, the researchers are calling for the association to be investigated further: more data is badly needed on how these ubiquitous particles may accumulate in the body and harm human health.

"With the intensification of global plastic pollution, the potential threats posed by micro- and nanoplastics (MPs/NPs) to human health have become a major concern," write the researchers in their published paper.
MPs/NPs enter the organism through ingestion, inhalation, and skin contact, subsequently accumulating in multiple organs – particularly the brain."
Microplastics are defined as fragments smaller than 5 millimeters, while nanoplastics are smaller than a micrometer – a thousandth of a millimeter. They enter the environment in numerous ways, including dissentegration of plastic waste and the release of water used to wash synthetic clothing.
Connecting findings from previous studies, the review states we ingest plastics through our food and drink, breathe them in through the air, and even absorb them through our skin.
From there, microscopic plastic fragments make their way into our brain by crossing the blood-brain barrier or entering the nerve cells lining of our nasal cavity.
To speculate on what the plastic might do when it's in the brain, the researchers point to studies showing microplastics and nanoplastics encouraging the formation of toxic alpha-synuclein protein clumps typical of brains with Parkinson's.
The review presents evidence that plastic fragments may drive neuroinflammation, disrupt communications between the brain and the gut, and carry damaging metals into the brain – a process known as ferroptosis.
All of these types of damage have been connected to Parkinson's disease in the past.

https://www.nature.com/articles/s41531-026-01272-4

Comment by Dr. Krishna Kumari Challa on Sunday

Tinnitus may be linked to sleep. Here's how.

Comment by Dr. Krishna Kumari Challa on Sunday

Scientists Cut Amyloid Plaques by 50% in Mice With Engineered Cells

A new kind of cellular immunotherapy shows promise in preventing Alzheimer's-associated plaques from forming in the brain – and even removing some when given in advanced cases.
Working with mice, scientists at Washington University developed a specially engineered virus that genetically alters cells into "super cleaners" that remove harmful proteins in the brain.
The study's authors have shown that a single injection of their new gene therapy seemed to prevent amyloid plaque development when administered before plaques had begun to form.
Even in mice with existing amyloid plaques, one injection of the gene therapy was associated with a roughly 50 percent reduction in plaques, the researchers report.
The new method borrows from a type of cancer treatment known as chimeric antigen receptor (CAR) T cell therapy, in which scientists can genetically modify the immune system's T cells to attack cancer cells.
In the new study, researchers focused on star-shaped brain cells called astrocytes, which they engineered to hunt down the amyloid beta proteins associated with cognitive decline in Alzheimer's.
This study marks the first successful attempt at engineering astrocytes to specifically target and remove amyloid beta plaques in the brains of mice with Alzheimer's disease.

https://www.science.org/doi/10.1126/science.ads3972

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