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Comment by Dr. Krishna Kumari Challa on October 2, 2025 at 10:54am

Zoo life reduces—but does not erase—lifespan gaps
A long-standing idea is that environmental pressures—such as predation, pathogens, or harsh climates—drive the observed gaps between males and females. To test this, the researchers turned to zoo populations, where such pressures are largely absent.
They found that lifespan gaps persisted even under these protected conditions. Comparing zoo and wild populations showed that the gaps were often smaller in zoos but rarely disappeared—mirroring the human case, where advances in medicine and living conditions have narrowed but not eliminated the lifespan gap.

The findings suggest that sex differences in lifespan are deeply rooted in evolutionary processes—shaped by sexual selection and parental investment and that genetic differences in the sex determination system may also play a role. Environmental factors influence the extent of the differences, but cannot eliminate them. The differences between the sexes are therefore not only a product of the environment, but part of our evolutionary history, and will most likely continue to exist in the future.

Sexual selection drives sex difference in adult life expectancy across mammals and birds, Science Advances (2025). DOI: 10.1126/sciadv.ady8433

Part 2

Comment by Dr. Krishna Kumari Challa on October 2, 2025 at 10:52am

Why women live longer than men

Tracing the evolutionary roots of why women live longer than men

Around the world, women on average live longer than men. This striking pattern holds true across nearly all countries and historical time periods. Although the gap between the sexes has narrowed in some countries due to medical advances and improved living conditions, new research now provides clues as to why this difference is unlikely to disappear anytime soon. The causes are deeply rooted in evolutionary history and can be observed in many animal species.

An international team of scientists  conducted the most comprehensive analysis of sex differences in lifespan across mammals and birds to date. Their findings, published in Science Advances, provide novel insight into one of biology's long-standing puzzles: why males and females age differently.

Among mammals, females usually live longer—for instance, in baboons and gorillas, females often outlive males. Yet this pattern is not universal: In many birds, insects, and reptiles, males are the longer-lived sex. One genetic explanation, the heterogametic sex hypothesis, points to differences in sex chromosomes.

In mammals, females have two X chromosomes, while males have only one X and one Y (making them the heterogametic sex). Some research suggests that having two X chromosomes may protect females from harmful mutations, offering a survival advantage. In birds, however, the system is reversed: females are the heterogametic sex.

Using records from over 1,176 bird and mammal species in zoos worldwide, the researchers found a striking contrast in lifespan, supporting the heterogametic sex hypothesis: in most mammals (72 percent), females lived longer, by on average twelve percent, while in most bird species (68 percent), males lived longer, overall by an average of five percent.

Still, there was remarkable variation with many exceptions. Some species showed the opposite of the expected pattern. For example, in many birds of prey, females are both larger and longer-lived than males. So sex chromosomes can only be part of the story.

Sexual selection and parental care shape lifespan differences

In addition to genetics, reproductive strategies also play a role. Through sexual selection, males in particular develop conspicuous characteristics such as colorful plumage, weapons, or large body size, which increase reproductive success but can shorten lifespan. The new study supports this assumption: In polygamous mammals with strong competition, males generally die earlier than females.

Many birds, on the other hand, are monogamous, which means that competitive pressure is lower and males often live longer. Overall, the differences were smallest in monogamous species, while polygamy and pronounced size differences were associated with a more pronounced advantage for females.

Parental care also plays a role. The researchers found evidence that the sex that invests more in raising offspring—in mammals, this is often the females—tends to live longer. In long-lived species such as primates, this is likely to be a selective advantage: females survive until their offspring are independent or sexually mature.

Part 1

Comment by Dr. Krishna Kumari Challa on October 2, 2025 at 9:34am

Parkinson's 'trigger' directly observed in human brain tissue for the first time

Scientists have, for the first time, directly visualized and quantified the protein clusters believed to trigger Parkinson's, marking a major advance in the study of the world's fastest-growing neurological disease.

These tiny clusters, called alpha-synuclein oligomers, have long been considered the likely culprits for Parkinson's disease to start developing in the brain, but until now, they have evaded direct detection in human brain tissue.

Now, researchers  have developed an imaging technique that allows them to see, count and compare oligomers in human brain tissue, a development one of the team says is "like being able to see stars in broad daylight."

Their results, reported in the journal Nature Biomedical Engineering, could help unravel the mechanics of how Parkinson's spreads through the brain and support the development of diagnostics and potential treatments.

The team examined post-mortem brain tissue samples from people with Parkinson's and compared them to healthy individuals of similar age. They found that oligomers exist in both healthy and Parkinson's brains. The main difference between disease and healthy brains was the size of the oligomers, which were larger, brighter and more numerous in disease samples, suggesting a direct link to the progression of Parkinson's.

The team also discovered a sub-class of oligomers that appeared only in Parkinson's patients, which could be the earliest visible markers of the disease—potentially years before symptoms appear.

Rebecca Andrews et al, Large-scale visualisation of α-synuclein oligomers in Parkinson's disease brain tissue, Nature Biomedical Engineering (2025). DOI: 10.1038/s41551-025-01496-4

Comment by Dr. Krishna Kumari Challa on October 2, 2025 at 9:12am

Microplastics reduce soil fertility and boost production of a potent greenhouse gas, study shows

More than 90% of plastic waste ends up in the soil, where it breaks down into microplastics that are invisible to the naked eye. Microplastic pollution of the soil poses a severe threat to soil health as it can harm essential microbial communities and reduce crop yields. The presence of these tiny plastics may also worsen climate change by boosting the production of greenhouse gases, according to a new study published in Environmental Science & Technology.

Most previous research focused on one plastic at a time and their effect on soil function and nutrient cycling, but microplastics do not tend to occur in isolation.

in the present study, the researchers went for the combined effect of various types of plastics on soil and key functions, such as the nitrogen cycle.

To quantify the problem, the team ran a microcosm experiment in the lab, using soil samples mixed with six different types of plastic, including polyethylene terephthalate (PET) and polyvinyl chloride (PVC). They created four distinct groups with varying levels of plastic, from zero plastics (the control group) to five different types of plastic. After 40 days of incubation, they collected the soil and ran several tests. These included measuring soil properties, such as acidity and key enzyme activities, as well as DNA sequencing to identify bacteria and their associated functional genes.

The team's analysis revealed that increasing microplastic diversity leads to significant shifts in soil health. For example, the plastic mixture considerably raised soil pH (making the soil more alkaline) and increased soil carbon content.

However, one of the most important findings was that microplastic diversity boosted the activity of bacterial genes responsible for denitrification. This is the process by which bacteria convert plant nutrient material into nitrogen gas, which is then released into the atmosphere. It not only makes the soil less fertile, but also releases nitrous oxide, a greenhouse gas that is around 300 times more potent in warming the planet than carbon dioxide. The primary cause of this accelerated nitrogen loss was a family of bacteria known as Rhodocyclaceae.

Tian-Gui Cai et al, Microplastic Diversity as a Potential Driver of Soil Denitrification Shifts, Environmental Science & Technology (2025). DOI: 10.1021/acs.est.5c04981

Comment by Dr. Krishna Kumari Challa on October 1, 2025 at 1:03pm

Microlightning causes eerie lights of lore
Spontaneous flashes of ‘microlightning’ between bubbles of gas could explain will-o’-the-wisps — flickering lights that can appear on marshlands. Researchers blew tiny bubbles of methane and air into water, where smaller bubbles took on a negative charge and larger ones, a positive charge. As the charges equalized, they produced a small zap of electricity and a flash of light. This could explain why the ghostly-looking lights appear over methane-rich bogs.

https://www.pnas.org/doi/10.1073/pnas.2521255122

Comment by Dr. Krishna Kumari Challa on October 1, 2025 at 12:30pm

Dads influence embryo growth via molecular signatures, research reveals

Over the past few decades, growing evidence has challenged the belief that inheritance is governed solely by DNA sequences. Scientists now recognize the crucial role of epigenetic inheritance—the transmission of biological traits via chemical modifications to DNA and its associated proteins. These modifications do not alter the genetic code itself but influence how genes are switched on or off, often in response to environmental factors such as stress, diet, or drug exposure.

While the concept of maternal epigenetic inheritance is relatively intuitive—given the direct biological connection between mother and embryo during gestation—recent research shows that fathers, too, can transmit environmentally induced epigenetic changes to their offspring. However, the prevalence of epigenetic inheritance—and the mechanisms behind it—remains unclear.

In a recent study, researchers demonstrated that disrupting the gut microbiome of male mice increases disease risk in their future offspring. On the other hand, some have focused on mechanisms that regulate embryonic development in response to changes in paternal diet.
A collaborative study between the  groups, now published in The EMBO Journal, examined how specific paternal environments affect early embryonic development in a systematic manner and under tightly controlled genetic and environmental conditions in mice.

To induce environmental perturbations, prospective fathers were exposed to either non-absorbable antibiotics (disrupting the gut microbiota) or to a low-protein, high-sugar diet. To minimize experimental variability, the analyses were performed on embryos resulting from in vitro fertilization (IVF). Embryos were collected approximately four days after fertilization (blastocyst stage) and individually analyzed to measure differences in gene expression compared to controls (blastocysts that resulted from fathers without any treatment).
The results were striking. Both environmental perturbations led to significant changes in embryonic gene expression. Disruption of the paternal gut microbiota reduced the expression of key genes involved in extra-embryonic tissue development, while changes in the diet were linked with a modest developmental delay.

To further investigate the influence of the genetic background, scientists repeated the experiments using a different mouse strain. The outcome differed, suggesting the importance of the genetic component in shaping how environmental exposures affect offspring.

Additionally, embryos derived from older fathers showed a stronger effect on gene expression, especially on genes involved in immune-related processes, indicating that paternal age is another important factor involved in epigenetic inheritance.

Mathilde Dura et al, Embryonic signatures of intergenerational epigenetic inheritance across paternal environments and genetic backgrounds, The EMBO Journal (2025). DOI: 10.1038/s44318-025-00556-4

Comment by Dr. Krishna Kumari Challa on October 1, 2025 at 12:21pm

Population bottlenecks cause decline of mammals' immunity, researchers find

Population bottlenecks caused by stark population loss due to illness or habitat destruction caused mammals' disease immunity to decline, according to a new study led by computational biologists .

 The finding comes from the first comparative study of genomic sequences—roadmaps of DNA instructions responsible for encoding how the body works—encoding immunity in 46 mammals.

The study, published in Molecular Biology and Evolution, is the first step for scientists analyzing regions of mammalian DNA that were previously inaccessible without modern biotechnology computational tools.

Genes influence how our body works: Humans and animals have genetics predisposed to certain diseases based on DNA. Although the same basic building blocks make up DNA across the 46 mammals assessed, the genomic sequences diverged wildly. So, even though we might have a similar set of genes, they are different based on variations in the DNA architecture.

In the immune system,  things are complicated further by something known as adaptive immunity. As opposed to the non-discriminatory defense the immune system deploys at the first hint of an infection, adaptive immunity refers to the parts of the immune system that study the specifics of a pathogen and design antibodies precisely targeted for it, should it invade again.

Antibodies are produced from highly variable "template" genes encoded in the genome, and this variability enables versatile immune responses through the generation of antibodies against diverse targets.

The question is, how did this adaptive immunity evolve?

To answer this Q, researchers  analyzed five types of gene clusters that control various aspects of immune system production—specifically the building of antibodies and the receptors on another immune cell type known as the T-cell—across 46 mammals to better understand how genetic variation could affect immune function.

Researchers scanned, aligned and compared publicly available DNA sequences of 46 mammals of 13 taxonomic orders, such as primates, rodents, bats, carnivores and marsupials, to draw conclusions about how their immune systems evolved.

Researchers found that a decline in adaptive immunity, and possible vulnerability to certain diseases among mammals as a result, was likely caused by genetic bottlenecks: a stark decrease in population over certain periods in history due to factors such as habitat loss or disease.

 Bottlenecks happened during medieval times when humanity was devastated by various diseases like the Black Plague, or when animals suffered widespread habitat loss due to forest fire.

Species with these past population bottlenecks include felines, aquatic mammals, seals, some primates and ruminants, which are mammals that adapted a special stomach for digesting tough plants.

 Genetic bottlenecks result in limited gene pool diversity for these animals,  the researchers  explained, which led to possible declining of adaptive immunity.

Mariia Pospelova et al, Comparative Analysis of Mammalian Adaptive Immune Loci Revealed Spectacular Divergence and Common Genetic Patterns, Molecular Biology and Evolution (2025). DOI: 10.1093/molbev/msaf152

 

 

Comment by Dr. Krishna Kumari Challa on October 1, 2025 at 11:11am

Forensic test recovers fingerprints from fired ammunition casings despite intense heat

A pioneering new test that can recover fingerprints from ammunition casing, once thought nearly impossible, has been developed by  scientists.

The researchers have developed a unique electrochemical method which can visualize fingerprints on brass casings, even after they have been exposed to the high temperature conditions experienced during gunfire. The study is published in the journal Forensic Chemistry.

For decades, investigators have struggled to recover fingerprints from weapons because any biological trace is usually destroyed by the high temperatures, friction and gas released after a gun is fired. As a result, criminals often abandon their weapons or casings at crime scenes, confident that they leave no fingerprint evidence behind.

Traditionally, the intense heat of firing destroys any biological residue. However,  the technique has been able to reveal fingerprint ridges that would otherwise remain imperceptible.

The team found they could coat brass casings with a thin layer of specialized materials to make hidden fingerprint ridges visible. Unlike existing methods that need dangerous chemicals or high-powered equipment, the new process uses readily available non-toxic polymers and minimal amounts of energy to quickly reveal prints from seemingly blank surfaces.

It works by placing the brass casing of interest in an electrochemical cell containing specific chemical substances. When a small voltage is applied, chemicals in the solution are attracted to the surface, coating the spaces between fingerprint ridges and creating a clear, high contrast image of the print. The fingerprint appears within seconds as if by magic!

Tests showed that this technique also worked on samples aged up to 16 months, demonstrating remarkable durability.

The research has significant implications for criminal investigations, where the current assumption is that firing a gun eliminates fingerprint residues on casings.

Colm McKeever et al, Electrodeposition of redox materials with potential for enhanced visualisation of latent finger-marks on brass substrates and ammunition casings., Forensic Chemistry (2025). DOI: 10.1016/j.forc.2025.100663

Comment by Dr. Krishna Kumari Challa on October 1, 2025 at 10:58am

The Red Sea went completely dry before being flooded by the Indian Ocean over 6 million years ago

Scientists have provided conclusive evidence that the Red Sea completely dried out about 6.2 million years ago, before being suddenly refilled by a catastrophic flood from the Indian Ocean. The findings put a definitive time on a dramatic event that changed the Red Sea.

Using seismic imaging, microfossil evidence, and geochemical dating techniques, the  researchers showed that a massive change happened in about 100,000 years—a blink of an eye for a major geological event. The Red Sea went from connecting with the Mediterranean Sea to an empty, salt-filled basin. Then, a massive flood burst through volcanic barriers to open the Bab el-Mandab strait and reconnect the Red Sea with the world's oceans.

The findings show that the Red Sea basin records one of the most extreme environmental events on Earth, when it dried out completely and was then suddenly reflooded about 6.2 million years ago.

The Red Sea was initially connected from the north to the Mediterranean through a shallow sill. This connection was severed, drying the Red Sea into a barren salt desert. In the south of the Red Sea, near the Hanish Islands, a volcanic ridge separated the sea from the Indian Ocean.

But around 6.2 million years ago, seawater from the Indian Ocean surged across this barrier in a catastrophic flood. The torrent carved a 320-kilometer-long submarine canyon that is still visible today on the seafloor. The flood rapidly refilled the basin, drowning the salt flats and restoring normal marine conditions in less than 100,000 years. This event happened nearly a million years before the Mediterranean was refilled by the famous Zanclean flood, giving the Red Sea a unique story of rebirth.

Tihana Pensa et al, Desiccation of the Red Sea basin at the start of the Messinian salinity crisis was followed by major erosion and reflooding from the Indian Ocean, Communications Earth & Environment (2025). DOI: 10.1038/s43247-025-02642-1

Comment by Dr. Krishna Kumari Challa on October 1, 2025 at 10:27am

Scientists finally prove that a quantum computer can unconditionally outperform classical computers

A quantum computer has demonstrated that it can solve a problem more efficiently than a conventional computer. This achievement comes from being able to unlock a vast memory resource that classical computing cannot match.

Instead of using classical bits that can only be 0 or 1, quantum machines use qubits, which can exist in multiple states and store exponentially more information than their traditional counterparts. However, proving that a quantum computer can access this memory advantage in the real world has been a challenge for two main reasons.

First, any successful demonstration has to be feasible on realistic quantum hardware, and second, there must be unconditional mathematical proof that no future classical algorithm could achieve the same performance.

In a study published on the arXiv preprint server, a  research team  reports how they achieved this feat of quantum supremacy.
They constructed a complicated mathematical task designed to test this memory advantage. Their experiment was like a game between two parts of the quantum system referred to as Alice and Bob. Alice's task was to create a quantum state and send it in a message to Bob, who had to measure it to figure out what it was. The goal was to build a process so accurate that Bob could predict the state before Alice finished preparing the message.

The researchers optimized this process over 10,000 independent trials, and their analysis revealed that a classical computer would need at least 62 bits of memory to complete the task with the same success rate. The quantum device performed it using only 12 qubits.

The result provides the most direct evidence yet that currently existing quantum processors can generate and manipulate entangled states of sufficient complexity to access the exponentiality of Hilbert space (the vast memory resource of a quantum computer)," wrote the researchers in their paper.

This form of quantum advantage—which we call quantum information supremacy—represents a new benchmark in quantum computing, one that does not rely on unproven conjectures.

 William Kretschmer et al, Demonstrating an unconditional separation between quantum and classical information resources, arXiv (2025). DOI: 10.48550/arxiv.2509.07255

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