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Comment by Dr. Krishna Kumari Challa on September 10, 2025 at 11:45am

The role of telomeres in processes such as cancer development and aging, and what happens when they do not work properly, has long interested scientists. Diseases caused by disturbances in telomere maintenance are rare, but very serious, and include premature aging, blood cell deficiency called aplastic anemia and fibrosis in the lungs.

In about half of cases, the disease is explained by a known mutation that affects telomere stability, but in many cases, there is currently no known medical explanation for why the individual is sick.
Their research is also relevant to cancer research. On one hand, inappropriate "repair" of telomeres can trigger catastrophic events leading to the accumulation of mutations and cancer.

On the other hand, cancer cells are often less efficient at repairing damage to DNA compared to normal cells. This weakness is exploited in cancer treatments and many therapies kill tumor cells by causing DNA damage or inhibiting repair, or both.

In other words, knowledge of how cells regulate DNA repair and protect telomeres has a bearing on both prevention and treatment of cancer.

Increased understanding of which proteins play key roles in these cellular processes can, in the long term, contribute to more precise and targeted treatment strategies.

Patrik Eickhoff et al, Chromosome end protection by RAP1-mediated inhibition of DNA-PK, Nature (2025). DOI: 10.1038/s41586-025-08896-1

Part 2

Comment by Dr. Krishna Kumari Challa on September 10, 2025 at 11:44am

Discovery reveals how chromosome ends can be protected

Researchers have uncovered a previously unknown mechanism that safeguards the chromosome ends from being mistakenly repaired by the cell. While DNA repair is vital for survival, attempts to repair the chromosome ends—called telomeres—can have catastrophic outcomes for cells.

The research, published in Nature, increases the understanding of how cancer and certain rare diseases develop.

Cells constantly monitor their DNA. A DNA helix that ends abruptly is a signal that DNA has been severely damaged—at least in most cases. The most severe DNA damage a cell can suffer is when a DNA helix breaks up in two pieces. 

Normally, the cells would try to promptly repair all damage to DNA. The dilemma is that our chromosomes have ends that look just like broken DNA. If cells were to "repair" them, looking for another loose end to join them with, this would lead to the fusion between two or more chromosomes, making the cell susceptible to transform into a cancer cell.

Therefore, the chromosome ends—called telomeres—must be protected from the cell's DNA repair machinery.

The cells have to constantly repair DNA damage to avoid mutations, cell death, and cancer, while at the same time, they must not repair the chromosome ends by mistake, since that would result in the same catastrophic outcome. What's the difference between damaged DNA and the natural chromosome end? This problem has been known for almost a century, but some aspects are still not completely resolved.

Although the telomeres are not to be repaired as if they were broken DNA, several DNA repair proteins can be found at the chromosome ends. 

The research team has previously shown that a key repair protein, DNA Protein Kinase (called DNA-PK) helps in processing telomeres and in protecting them from degradation. But how DNA-PK at the same time is prevented from trying to repair these blunt DNA ends remained a mystery until now.

The researchers have now shown that two other proteins, called RAP1 and TRF2, have an important role to play in regulating DNA-PK.

They show genetically, biochemically and structurally how the protein RAP1, brought to telomeres by TRF2, ensure by  direct interaction that DNA-PK doesn't 'repair' the telomeres.

Part1

Comment by Dr. Krishna Kumari Challa on September 10, 2025 at 11:35am

Microbiome instability linked to poor growth in kids

Malnutrition is a leading cause of death in children under age 5, and nearly 150 million children globally under this age have stunted growth from lack of nutrition. Although an inadequate diet is a major contributor, researchers  found over a decade ago that dysfunctional communities of gut microbes play an important role in triggering malnutrition.

They  have discovered that toddlers in Malawi—among the places hardest hit by malnutrition—who had a fluctuating gut microbiome showed poorer growth than kids with a more stable microbiome. All of the children were at high risk for stunting and acute malnutrition.

The findings, published in Cell, establish a pediatric microbial genome library—a public health database containing complete genetic profiles of 986 microbes from fecal samples of eight Malawian children collected over nearly a year that can be used for future studies to help predict, prevent and treat malnutrition.

Culture-independent meta-pangenomics enabled by long-read metagenomics reveals associations with pediatric undernutrition, Cell (2025). DOI: 10.1016/j.cell.2025.08.020. www.cell.com/cell/fulltext/S0092-8674(25)00975-4

Comment by Dr. Krishna Kumari Challa on September 9, 2025 at 6:18am

Smart patch runs tests using sweat instead of blood

It is possible now to precisely assess the body's health status using only sweat instead of blood tests. 

A research team has now developed a smart patch that can precisely observe internal changes through sweat when simply attached to the body. This is expected to greatly contribute to the advancement of chronic disease management and personalized health care technologies. 

The researchers developed a wearable sensor that can simultaneously and in real-time analyze multiple metabolites in sweat. 

The research team developed a thin and flexible wearable sweat patch that can be directly attached to the skin. This patch incorporates both microchannels for collecting sweat and an ultrafine nanoplasmonic structure that analyzes sweat components using light. Thanks to this, multiple sweat metabolites can be simultaneously analyzed without the need for separate staining or labels, with just one patch application.

A nanoplasmonic structure is an optical sensor structure where nanoscale metallic patterns interact with light, designed to sensitively detect the presence or changes in concentration of molecules in sweat.

The patch was created by combining nanophotonics technology, which manipulates light at the nanometer scale (one-hundred-thousandth the thickness of a human hair) to read molecular properties, with microfluidics technology, which precisely controls sweat in channels thinner than a hair.

In other words, within a single sweat patch, microfluidic technology enables sweat to be collected sequentially over time, allowing for the measurement of changes in various metabolites without any labeling process. Inside the patch are six to 17 chambers (storage spaces), and sweat secreted during exercise flows along the microfluidic structures and fills each chamber in order.

The research team applied the patch to actual human subjects and succeeded in continuously tracking the changing components of sweat over time during exercise.

In this study, they demonstrated for the first time that three metabolites—uric acid, lactic acid, and tyrosine—can be quantitatively analyzed simultaneously, as well as how they change depending on exercise and diet.

In particular, by using artificial intelligence analysis methods, they were able to accurately distinguish signals of desired substances even within the complex components of sweat.

In the future,  this technology can be expanded to diverse fields such as chronic disease management, drug response tracking, environmental exposure monitoring, and the discovery of next-generation biomarkers for metabolic diseases.

Jaehun Jeon et al, All-flexible chronoepifluidic nanoplasmonic patch for label-free metabolite profiling in sweat, Nature Communications (2025). DOI: 10.1038/s41467-025-63510-2

Comment by Dr. Krishna Kumari Challa on September 9, 2025 at 6:08am

There is less room to store carbon dioxide, driver of climate change, than previously thought, finds a new study

The world has far fewer places to securely store carbon dioxide deep underground than previously thought, steeply lowering its potential to help stem global warming, according to a new study that challenges long-held industry claims about the practice.

The study, published last week in the journal Nature, found that global carbon storage capacity was 10 times less than previous estimates after ruling out geological formations where the gas could leak, trigger earthquakes or contaminate groundwater, or had other limitations. That means carbon capture and storage would only have the potential to reduce human-caused warming by 0.7 degrees Celsius (1.26 Fahrenheit)—far less than previous estimates of around 5-6 degrees Celsius (9-10.8 degrees Fahrenheit), researchers said.

Carbon storage is often portrayed as a way out of the climate crisis. These new findings make clear that it is a limited tool and reaffirms the extreme importance of reducing emissions as fast and as soon as possible.

 Matthew J. Gidden et al, A prudent planetary limit for geologic carbon storage, Nature (2025). DOI: 10.1038/s41586-025-09423-y

Comment by Dr. Krishna Kumari Challa on September 9, 2025 at 6:03am

Scientists discover why the flu is more deadly for older people

Scientists have discovered why older people are more likely to suffer severely from the flu, and can now use their findings to address this risk.

In a study published in PNAS, experts discovered that older people produce a glycosylated protein called apolipoprotein D (ApoD), which is involved in lipid metabolism and inflammation, at much higher levels than in younger people. This has the effect of reducing the patient's ability to resist virus infection, resulting in a more serious disease outcome.

ApoD is therefore a target for therapeutic intervention to protect against severe influenza virus infection in the elderly which would have a major impact on reducing morbidity and mortality in the aging population.

ApoD mediates age-associated increase in vulnerability to influenza virus infection, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2423973122

Comment by Dr. Krishna Kumari Challa on September 9, 2025 at 5:58am

Researchers examined how strongly neurons fired just before each choice and how variable that activity was across trials. Variability served as "neural noise." Computational models estimated how closely choices followed expected value and how much they reflected overall uncertainty.

Results showed more exploration in loss trials than in gain trials. After people learned which option was better, exploration stayed higher in loss trials and accuracy fell more from its peak.

Pre-choice firing in the amygdala and temporal cortex rose before exploratory choices in both gain and loss, indicating a shared, valence-independent rate signal. Loss trials also showed noisier amygdala activity from cue to choice.

More noise was linked to higher uncertainty and a higher chance of exploring, and noise declined as learning progressed. Using the measured noise levels in decision models reproduced the extra exploration seen in loss trials. Loss aversion did not explain the gap.
Researchers report two neural signals that shape exploration. A valence-independent firing-rate increase in the amygdala and temporal cortex precedes exploratory choices in both gain and loss. A loss-specific rise in amygdala noise raises the odds of exploration under potential loss, scales with uncertainty, and wanes as learning accrues.

Behavioral modeling matches this pattern, with value-only rules fitting gain choices and value-plus-total-uncertainty rules fitting loss choices. Findings point to neural variability as a lever that tilts strategy toward more trial-and-error when loss looms, while causal tests that manipulate noise remain to be done.

From an evolutionary survival perspective, the strategy fits well with the need to seek out new resources when facing the loss of safe or familiar choices. While one might consider trying a new restaurant at any time, true seeking behavior will become a priority if the favorite location is closed for remodeling.

Tamar Reitich-Stolero et al, Rate and noise in human amygdala drive increased exploration in aversive learning, Nature (2025). DOI: 10.1038/s41586-025-09466-1

Part 2

Comment by Dr. Krishna Kumari Challa on September 9, 2025 at 5:56am

Human brains explore more to avoid losses than to seek gains

Researchers traced a neural mechanism that explains why humans explore more aggressively when avoiding losses than when pursuing gains. Their work reveals how neuronal firing and noise in the amygdala shape exploratory decision-making.

Human survival has its origins in a delicate balance of exploration versus exploitation. There is safety in exploiting what is known, the local hunting grounds, the favorite foraging location, the go-to deli with the familiar menu. Exploitation also involves the risk of over-reliance on the familiar to the point of becoming too dependent upon it, either through depletion or a change in the stability of local resources.

Exploring the world in the hope of discovering better options has its own set of risks and rewards. There is the chance of finding plentiful hunting grounds, alternative foraging resources, or a new deli that offers a fresh take on old favorites. And there is the risk that new hunting grounds will be scarce, the newly foraged berries poisonous, or that the meal time will be ruined by a deli that disappoints.

Exploration-exploitation (EE) dilemma research has concentrated on gain-seeking contexts, identifying exploration-related activity in surface brain areas like cortex and in deeper regions such as the amygdala. Exploration tends to rise when people feel unsure about which option will pay off.

Loss-avoidance strategies differ from gain-seeking strategies, with links to negative outcomes such as PTSD, anxiety and mood disorders.

In the study, "Rate and noise in human amygdala drive increased exploration in aversive learning," published in Nature, researchers recorded single-unit activity to compare exploration during gain versus loss learning.

Part 1

Comment by Dr. Krishna Kumari Challa on September 8, 2025 at 12:57pm

Electrical stimulation can reprogram immune system to heal the body faster

Scientists  have discovered that electrically stimulating macrophages—one of the immune systems key players—can reprogram them in such a way as to reduce inflammation and encourage faster, more effective healing in disease and injury.

This breakthrough uncovers a potentially powerful new therapeutic option, with further work ongoing to delineate the specifics.

Macrophages are a type of white blood cell with several high-profile roles in our immune system. They patrol around the body, surveying for bugs and viruses, as well as disposing of dead and damaged cells, and stimulating other immune cells—kicking them into gear when and where they are needed.

However, their actions can also drive local inflammation in the body, which can sometimes get out of control and become problematic, causing more damage to the body than repair. This is present in lots of different diseases, highlighting the need to regulate macrophages for improved patient outcomes.

In the study, published in the journal Cell Reports Physical Science, the researchers worked with human macrophages isolated from healthy donor blood samples. 

They stimulated these cells using a custom bioreactor to apply electrical currents and measured what happened.

The scientists discovered that this stimulation caused a shift of macrophages into an anti-inflammatory state that supports faster tissue repair; a decrease in inflammatory marker (signaling) activity; an increase in expression of genes that promote the formation of new blood vessels (associated with tissue repair as new tissues form); and an increase in stem cell recruitment into wounds (also associated with tissue repair).

 Electromodulation of human monocyte-derived macrophages drives a regenerative phenotype and impedes inflammation, Cell Reports Physical Science (2025). DOI: 10.1016/j.xcrp.2025.102795. www.cell.com/cell-reports-phys … 2666-3864(25)00394-7

Comment by Dr. Krishna Kumari Challa on September 7, 2025 at 10:27am

The two species diverged from each other more than 5 million years ago, and yet today, M. structor is a sort of parasite living in the queen's colony. But she is hardly a victim.

The Iberian harvester queen ant controls what happens to the DNA of her clones. When she reproduces, she can do so asexually, producing a clone of herself. She can also fertilize her egg with the sperm of her own species or M. structor, or she can 'delete' her own nuclear DNA and use her egg as a vessel solely for the DNA of her male M. structor clones.
This means her offspring can either be related to her, or to another species. The only similarity is that both groups contain the queen's mitochondrial DNA. The result is greater diversity in the colony without the need for a wild neighboring species to mate with.

It also means that Iberian harvester ants belong to a 'two-species superorganism' – which the researchers say "challenges the usual boundaries of individuality."

The M. structor males produced by M. ibericus queens don't look exactly the same as males produced by M. structor queens, but their genomes match.

https://www.nature.com/articles/s41586-025-09425-w

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