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Comment by Dr. Krishna Kumari Challa 11 hours ago

Scientists studying cockroach milk and nose-blowing win Ig Nobel prizes for quirky science

Ten research teams were honoured this week at a satirical science awards ceremony that was hosted outside the U.S. for the first time due to travel concerns.
Ig Nobel prizes recognized unconventional work on cockroach milk, nose blowing, kissing evolution, and soil decomposition measured using buried underwear. The ceremony moved to Zurich because of travel and visa concerns, with future events planned across Europe.
Researchers who studied milk from cockroaches and analyzed soil health using underwear received Ig Nobel prizes celebrating unusual and imaginative contributions to science.
Another research team buried 1,000 pairs of underwear in more than 25 countries to study how critters in the soil helped them decompose.

Comment by Dr. Krishna Kumari Challa 12 hours ago

Patients diagnosed with lung cancer found to have more microplastic in their lungs

People with lung cancer are more likely to have microplastics in their lungs and to have larger quantities of microplastics in their lungs, according to research that has been presented at the European Respiratory Society (ERS) Congress in Barcelona, Spain.
Among 100 patients undergoing bronchoscopy, microplastics were detected in 70%, with higher detection frequency and burden in those later diagnosed with lung cancer. Polypropylene and polyethylene predominated. The observational results show an association but cannot determine whether microplastics contribute to cancer or are retained differently by diseased lungs.
Researchers say their study adds to evidence that microplastics are entering our bodies via the air we breathe and suggests that there may be a link between microplastics and lung disease.
Across all samples, the researchers identified a total of 232 microplastic particles. Overall, 70% of patients had detectable microplastics in at least one sample (either the lung wash, tissue or both). When the lung wash and tissue samples from each patient were analyzed together, patients with lung cancer were more likely to have detectable microplastics and had a higher overall microplastic burden than those without cancer.

Patients with lung cancer were also more likely to have detectable microplastics in their lung wash samples (66% versus 46%) and had a higher microplastic burden than patients without lung cancer.

When the researchers compared the lung wash and tissue samples from the same individual, they found that patients with more microplastic in their lung wash tended to have less in the corresponding tissue sample, and vice versa. Because lung wash samples collect particles from the airspaces whereas tissue samples capture particles embedded within the lung itself, this finding suggests that microplastics may not be distributed evenly throughout the lung and that different regions may retain particles differently.

Analysis of the microplastics showed that polypropylene and polyethylene were the most common types of plastic. These are widely used in everyday products such as packaging, textiles, household materials and consumer goods.
This adds to the growing evidence that reducing environmental plastic pollution may have benefits that extend beyond ecosystems and into human health.

‘High respiratory microplastic burden across paired airway and tissue samples in patients with lung cancer’ by Ilias E. Dimeas et al. was presented in session at European Respiratory Society Congress 2026 on Thursday 3rd September.

Comment by Dr. Krishna Kumari Challa 14 hours ago

Cancer cells release antioxidants to prevent immune cells from destroying them

Molecules called reactive oxygen species, which include so-called "free radicals," have long been viewed as damaging by-products of our body's metabolism—a reason antioxidant supplements have been considered a potential way to reduce cancer risk.
Now, scientists have discovered that certain immune cells depend on these molecules to activate and destroy cancer cells and that tumours exploit this dependency by releasing natural antioxidants to shut down the immune attack.
Our immune system keeps us healthy by hunting down and destroying harmful material, including invading bacteria and viruses, as well as cancer cells. It does so by deploying a number of different types of immune cells, including specialized cells known as T cells. These T cells hunt down and destroy tumor cells, but they need small amounts of reactive oxygen species to activate and switch on their killing ability.
Researchers analyzed the fluid surrounding cells within tumours grown in mice and found that cancers chemically 'smother' T cells, stopping their activation and preventing them from destroying cancer cells. Tumours do this by releasing large amounts of a protein that is a natural antioxidant, Peroxiredoxin 1 (PRDX1), which mops up reactive oxygen species and deprives T cells of the activating signals they need to kill cancer cells.

Next, the team used CRISPR gene-editing technology to create mouse cancer cells that could no longer make the antioxidant protein. They found that removing the cancer cells' capacity to produce the antioxidant promoted immune-cell activity and limited tumor growth.

Finally, the team looked for the same mechanism in people. They analyzed published data on the proteins released by human cancer cell lines, examined gene activity across thousands of human tumours, and isolated the fluid surrounding tumours removed from patients. All three approaches pointed the same way: Human cancers also release PRDX1 into their surroundings, where it can strip away the reactive oxygen species that T cells depend on.
Now that the researchers found a new way by which cancers shut down the immune system, we can block this process and make tumours that don't respond to some immunotherapies start responding to treatment. That tells us this is a pathway worth targeting therapeutically, and there are several ways we might be able to achieve this.
The findings also carry broader implications. Several large randomized clinical trials have found that antioxidant supplements fail to reduce cancer risk and, in some cases, worsen outcomes.

The discovery that T cells depend on reactive oxygen species to fight tumours may help explain why: Antioxidants could inadvertently blunt the immune system's ability to attack cancer.

Tumor-derived antioxidants suppress immunity by depriving T cells of reactive oxygen species, Science (2026). DOI: 10.1126/science.adz8203

Comment by Dr. Krishna Kumari Challa 14 hours ago

Brain scans reveal new link between progesterone and women's mood

The influence of the hormone progesterone on mood is well known. Now, researchers have shown how higher levels of progesterone during the menstrual cycle are linked to less distinct patterns of activity in areas of the brain involved in controlling emotions.
The study, published in Psychological Medicine, explored how natural levels of the ovarian hormones estradiol and progesterone influence parts of the brain involved in emotion control and whether this could help explain differences in mood.

Emotion control is the ability to regulate behaviour in response to emotional information, particularly when automatic emotional responses need to be overridden. For example, if someone needed to ask an unfriendly person for help, their instinct might be to avoid them—emotion control would help overcome that impulse and approach them anyway.
Analysis of MRI scan data from study participants revealed that when progesterone levels were higher, there was a less clear distinction between "easy" and "difficult" emotional situations in the brain scans. This suggests that the brain would be less able to distinguish between different emotional situations in real life.

In contrast, participants whose brain scans had a clearer distinction between "easy" and "difficult" emotional situations tended to report better mood in the preceding week.

This brain mechanism accounted for roughly 7% of the variation in mood scores.
The researchers found that higher progesterone levels were linked to brain activity patterns that made it harder to tell different emotion control situations apart, which also corresponded with lower mood in participants.

This suggests that if the brain can tell different emotional situations apart more clearly, it may be better at regulating emotion in daily life.

Endogenous progesterone blurs frontostriatal representations of emotion control in healthy young women, Psychological Medicine (2026). DOI: 10.1017/S0033291726105315

Comment by Dr. Krishna Kumari Challa 14 hours ago

Healthy aging shaped by more varied biology than previously thought

Molecular changes in aging are far more unique than previously thought, meaning two healthy individuals of identical age can experience significantly different aging journeys.
A new study is the most comprehensive molecular study of aging to date. It demonstrates for the first time that genetic factors and environmental influences continuously interact across a person's lifespan.

The study, published in Science, observed how multiple genetic variants shape how an individual ages.

Notably, researchers found different courses of change among participants with a gene linked to cardiac aging (CXCL9). They also found that levels of the tumour suppressor gene tumour protein p53 (TP53) declined in certain individuals as they grew older, potentially altering their risk of cancer.

Such biological shifts can indicate distinct environmental exposures or reveal an underlying genetic predisposition to disease. Pinpointing individuals at higher risk offers future opportunities for earlier targeted health care interventions.

Importantly, the research also highlights correlations between environmental exposures, such as shifting blood levels of PFAS, commonly referred to as "forever chemicals," and evolving molecular profiles over time. This highlights how public health measures targeting environmental risks can affect the molecular level.

Molecular aging involves the steady accumulation of cellular damage alongside chemical changes in key molecules like DNA, proteins and lipids. Over time, this progression drives a gradual deterioration of tissue function, heightened physical vulnerability and a higher risk of age-related conditions, including cancer as well as cardiometabolic and neurodegenerative disorders.

Understanding how aging happens at the molecular level is vital to preventing or even reversing a range of age-related diseases—as well as increasing longevity.
Rather than there being a single molecular roadmap of aging, this study shows that people follow distinct biological journeys. Two healthy people of the same age can be aging in surprisingly different ways at the molecular level. That raises the possibility of much more personalized approaches to predicting disease risk and maintaining health as we grow older.
Over eight years, the team repeatedly measured blood RNA levels, the activity levels of around 16,000 genes and hundreds of metabolites in the same 335 individuals from TwinsUK during the study, creating one of the most detailed long-term multi-omic studies of healthy aging to date. They found that some study participants had markedly different, and sometimes opposite, molecular changes.

Aging patterns were not uniform across the immune system, which is key to the aging process—molecular changes over time differed between innate and adaptive immune cells. Innate immune cells are the fast, first line of defense you are born with, while adaptive immunity is a slower immune response that builds memory over time.
These findings suggest that human aging at the molecular level is not a uniform process, but one that is dynamic and environment-dependent.

Longitudinal dynamics of gene expression and metabolomics in an ageing population cohort, Science (2026). DOI: 10.1126/science.aed6452

Comment by Dr. Krishna Kumari Challa 14 hours ago

Instead of treating just one disease, metformin acts on multiple biological root causes of aging at the same time. It can trigger autophagy, the cell's cleanup system, helping clear cellular waste while supporting DNA stability. As we age, the chemical tags on our DNA called methylation begin to shift, affecting how genes are regulated. Metformin slows abnormal changes in DNA by stabilizing an enzyme called TET2, helping preserve a more youthful genetic profile. Its effects also reach the gut and its microbiome, where it can boost beneficial, mucus-protecting bacteria and the production of short-chain fatty acids. This is promising news, as previous studies have found that a healthy gut microbiome can lower age-related inflammation throughout the body.

In microscopic worms called C. elegans, metformin extended lifespan by 36% to 40% by putting the animals into a state similar to calorie restriction. In mice, across different models, metformin increased average lifespan by 5.8% to 20.1% and delayed the onset of certain tumours.

Jarra Manneh et al, Metformin at the convergence of aging and longevity, Aging (2026). DOI: 10.18632/aging.206407

Part 2

Comment by Dr. Krishna Kumari Challa 15 hours ago

Diabetes drug metformin could be repurposed to help slow aging mechanisms

Over the past few years, a new field of science has been gaining momentum: geroscience. Instead of treating age-related diseases one by one, geroscience asks a bigger question: What if we could target the biological drivers of aging itself? Researchers are uncovering the common mechanisms that fuel aging and multiple chronic diseases, hoping to slow these processes and help people stay healthier for longer.

Metformin, a widely prescribed, safe and inexpensive drug for type 2 diabetes, is a first-line treatment that lowers blood sugar and improves the body's response to insulin. The drug appears to trick cells into sensing an energy shortage, similar to what happens during fasting or dieting. This activates a key cellular energy sensor called AMPK, which helps trigger cellular waste cleanup and supports cellular repair. Now, a recent review suggests metformin might also help counter some effects of aging.

Researchers compiled decades of global research, from cellular and molecular studies to animal and human studies, to provide a comprehensive, unified picture of how metformin might affect aging and longevity. The collective data indicated that metformin acts as a geroprotective agent that can target the biological root causes of aging and potentially improve health span.

Metformin's anti-aging effects are evident across species. Male monkeys treated for 40 months saw their tissues become biologically younger, with their brains alone reversing by nearly 6 years—a leap equivalent to 18 years in human terms. A similar pattern was seen in humans, where observational data indicate that people taking metformin had biological ages up to 3.43 years younger, with people with diabetes taking the drug living as much as 15% longer than their peers without diabetes.
A large body of evidence indicates that people prescribed metformin to manage blood sugar levels also had fewer cardiovascular events and showed lower rates of cognitive decline. Because developing new drugs takes years, researchers shifted their focus toward investigating whether metformin could be repurposed to slow the effects of aging.
Part 1

Comment by Dr. Krishna Kumari Challa yesterday

Is this the first glimpse of dark matter?
A single data point from a dark-matter detector in the United States could be the first discovery of the elusive particle we call dark matter. The LUX-ZEPLIN experiment at the Sanford Underground Research Facility in South Dakota contains 10 tonnes of liquid xenon. It seeks evidence of a candidate particle called a WIMP (weakly interacting massive particle) by looking for flashes created when such a particle collides with the nucleus of just one xenon atom. If the finding can be backed up with more data, it could mean that the material that seems to make up most of the mass of the Universe has finally been discovered.

https://lz.lbl.gov/wp-content/uploads/sites/6/2026/08/LZ_Preprint_2...

https://www.nature.com/articles/d41586-026-01985-9?utm_source=Live+...

Comment by Dr. Krishna Kumari Challa yesterday

How cells teach themselves to move together

Scientists have long wondered how cells organized into sheets begin to move together to form organs, especially when the sheets form closed, sphere-like surfaces and tissues with no edges to direct motion. Researchers used a combination of live imaging, genetic experiments and mathematical modelling to understand how cells in the fruit fly egg chamber synchronize their movement.
In fruit fly egg chambers, epithelial cells initiate collective rotation through feedback between cell motion and protein polarization. Movement polarizes a protein rearward, promoting aligned motion in neighbouring cells via mechanical coupling. Support-tissue forces initiate long-axis rotation, while chamber elongation stabilizes its direction.
Researchers found that cells can spontaneously organize and rotate together through a self-reinforcing mechanism in which a specific protein helps individual cells align their movement.

Once the cells start moving, that motion polarizes the protein to the back of the cell, which promotes further movement by the cells behind it in the same direction. Mechanical connections between adjacent support cells and the global egg chamber geometry mediate the coordination of cell movements.

Epithelial cells that form surfaces in the body undergo collective migrations while tissues are developing, during the closing of wounds, the spread of cancers or the constant turnover of things like your intestinal lining. But when there are closed surfaces, there are no external cues that tell the cells which way to go. So, this is a self-organized process.
The study, published in PNAS, also explains why the egg chamber always rotates around its long axis. Initially, this is caused by the physical forces through which the egg chamber interacts with nearby support tissues. As the egg chamber grows and becomes more oval-shaped, its own geometry helps stabilize the rotation axis.

This work holds potential implications for understanding both normal development and diseases in which collective cell movement goes awry.

Sierra Schwabach et al, Initiation of rotational collective migration in Drosophila through tissue geometry and mechanochemical feedback, Proceedings of the National Academy of Sciences (2026). DOI: 10.1073/pnas.2528342123

Comment by Dr. Krishna Kumari Challa yesterday

UN report finds 1.5°C warming limit likely to be exceeded by 2030

For more than a decade, the world has been trying to limit global warming to 1.5°C.

That's no longer possible, according to a new United Nations report. We will likely pass 1.5°C in 2030. That's not good news for anyone

Global warming is likely to exceed 1.5°C around 2030, increasing risks of extreme events, sea-level rise, ecosystem loss and potentially irreversible climate tipping points. Rapid emission cuts could limit peak warming and enable a later decline through carbon removal, but current policies remain insufficient.

original article.

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