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Comment by Dr. Krishna Kumari Challa yesterday

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 yesterday

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 yesterday

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 yesterday

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

Comment by Dr. Krishna Kumari Challa yesterday

Stem cells from fat tissue may help prevent kidney dialysis access failure

To undergo kidney dialysis, doctors must first surgically create an access route—an arteriovenous fistula—usually in an arm, a conduit that will accommodate hemodialysis treatments. It is a routine outpatient procedure performed for years worldwide.

But it is a procedure beset by problems.

An arteriovenous fistula must first "mature," a process in which the newly established connection between an artery and a vein becomes large enough to support the turbulent flow of blood in hemodialysis. For many patients, this artificially created channel tends to narrow, leaving it useless as a conduit.

Researchers investigating a possible way to prevent problematic narrowing—a condition called stenosis—with a procedure that relies on the use of stem cells.

The study, researchers asserted, is a crucial step toward improving a necessary treatment for patients with kidney failure by tapping into a population of cells that are essentially blank slates. 

 The investigation is reported in the journal Science Translational Medicine.

The phase 1 randomized trial involved patients undergoing an arteriovenous fistula (AVF) placement in an arm. Some of the patients in the small trial also received autologous adipose-derived mesenchymal stem cells. The cells were delivered at the time of the AVF procedure.

The stem cells were placed along the AVF starting at the distal artery, one centimeter upstream to the anastomosis [the surgical connection between adjacent blood vessels] and extending to the first four centimeters of the vein just distal to the anastomosis by dripping them onto the adventitia of the vessels slowly over five minutes.

The adventitia is the outermost layer of a blood vessel.

Mesenchymal stem cells are a form of somatic, or adult stem cells, which can be found in a variety of tissues throughout the body, including adipose (fat) tissue, which is an abundant source.

The stem cells are aimed at improving AVF function by preventing vascular narrowing. The cells were also a site-specific treatment for another problem tied to arteriovenous fistulas: inflammation, a hallmark of AVFs. Fortunately, anti-inflammatory activity is a function of mesenchymal stem cells.

Side-by-side images in the study show the vascular opening to be wide and capable of handling the turbulence of hemodialysis among patients who received mesenchymal stem cells. Patients who did not receive the stem cell treatment suffered vascular narrowing.

The research  team sees promise in their unique approach, which is producing positive results at a critical time.

The team's phase 1 clinical trial involved 21 patients who received arteriovenous fistulas in the arm; 11 of the 21 patients also received mesenchymal stem cells derived from their own fat tissue. After 42 months, fistulas had matured faster in patients who received stem cells. Additional study and approval by the U.S. Food and Drug Administration are required before the treatment can become available.

Sreenivasulu Kilari, et al Periadventitial delivery of mesenchymal stem cells improves vascular remodeling and maturation in arteriovenous fistulas, Science Translational Medicine (2025). DOI: 10.1126/scitranslmed.adp7723

Comment by Dr. Krishna Kumari Challa yesterday

Scientists read mice's 'thoughts' from their faces

It's easy to read emotions on people's faces—each one has its clear, unmistakable signature. But what about thoughts? A study published in Nature Neuroscience shows that mice's problem-solving strategies can be deciphered from subtle facial movements.

According to the authors, this is a proof of concept that the contents of the mind can be read out from video recordings, potentially offering powerful new research and diagnostic tools.

Scientists found that they can get as much information about what the mouse was 'thinking' as they could from recording the activity of dozens of neurons.

Having such easy access to the hidden contents of the mind could provide an important boost to brain research. However, it also highlights a need to start thinking about regulations to protect our mental privacy.

 Facial expressions in mice reveal latent cognitive variables and their neural correlates, Nature Neuroscience (2025). DOI: 10.1038/s41593-025-02071-5.

Comment by Dr. Krishna Kumari Challa on Tuesday

Mamba snake bites worsen after antivenom

Mamba (Dendroaspis species) snake bites are a significant threat in sub-Saharan Africa, accounting for 30,000 deaths annually.

A breakthrough study has discovered a hidden dangerous feature of the black mamba, one of the most venomous snakes in the world.

The study revealed the venoms of three species of mamba were far more neurologically complex than previously thought, explaining why antivenoms were sometimes ineffective. This research was published in Toxins.

The black mamba, western green mamba and Jamesons mamba snakes aren't just using one form of chemical weapon, they're launching a coordinated attack at two different points in the nervous system.

If you're bitten by 3 out of 4 mamba species, you will experience flaccid or limp paralysis caused by postsynaptic neurotoxicity.

Current antivenoms can treat the flaccid paralysis but this study found the venoms of these three species are then able to attack another part of the nervous system causing spastic paralysis by presynaptic toxicity.

Researchers previously thought the fourth species of mamba, the eastern green mamba, was the only one capable of causing spastic paralysis.

This finding resolves a long-standing clinical mystery of why some patients bitten by mambas seem to initially improve with antivenom and regain muscle tone and movement only to start having painful, uncontrolled spasms.

The venom first blocks nerve signals from reaching the muscles, but after the antivenom is administered, it then overstimulates the muscles.

It's like treating one disease and suddenly revealing another.

Researchers  also found the venom function of the mambas was different depending on their geographic location, particularly within populations of the black mamba from Kenya and South Africa.

This further complicates treatment strategies across regions because the antivenoms are not developed to counteract the intricacies of the different venoms.

By identifying the limitations of current antivenoms and understanding the full range of venom activity, we can now directly inform evidence-based snakebite care.

 Lee Jones et al, Neurotoxic Sleight of Fang: Differential Antivenom Efficacy Against Mamba (Dendroaspis spp.) Venom Spastic-Paralysis Presynaptic/Synaptic vs. Flaccid-Paralysis Postsynaptic Effects, Toxins (2025). DOI: 10.3390/toxins17100481

Comment by Dr. Krishna Kumari Challa on Tuesday

Endotoxin concentrations were measured using the Limulus Amebocyte Lysate (LAL) assay, then researchers used DNA sequencing and source tracking to identify the Gram-negative bacteria they came from. Finally, they applied mixture-toxicity modeling to estimate how much these endotoxins contributed to the overall harmful effects of PM2.5 exposure.

They found that despite making up only a minuscule fraction of the total PM2.5 mixture, it drove about 0.1 to 17% of the IL-8 release triggered by PM2.5.

Among all reported PM2.5 components, endotoxin demonstrated the highest toxicity-to-mass contribution ratio, 10,000:1 to 100,000:1, establishing its extreme biological potency. These findings show that less is indeed more.

The researchers note that this study brings to light the importance of identifying highly toxic components present in low concentrations and tracing their sources. Pinpointing these toxicity drivers can help us design cost-effective strategies in which even modest reductions in PM2.5 mass could yield substantial decreases in overall toxicity.

 Jinyan Yu et al, Disproportionately Higher Contribution of Endotoxin to PM_2.5 Bioactivity than Its Mass Share Highlights the Need to Identify Low-Concentration, High-Potency Components, Environmental Science & Technology (2025). DOI: 10.1021/acs.est.5c07255

Part 2

Comment by Dr. Krishna Kumari Challa on Tuesday

Bacterial endotoxins are high-potency, low-mass drivers of PM₂.₅ toxicity, sampling study reveals

Endotoxin, a toxic chemical found in bacteria, makes up only 0.0001% of PM_2.5 fine particles but packs a serious punch when it comes to its bioactivity.

According to a study by researchers endotoxin drives 0.1–17% of the inflammatory responses triggered by these airborne particles, with its toxicity contribution being three to five orders of magnitude higher than its mass contribution.

Air pollution is now the world's leading environmental health threat, linked to more than three million premature deaths every year. One of the key culprits is PM2.5, which refers to airborne particles smaller than 2.5 micrometers, small enough to slip deep into the lungs and even seep into the bloodstream.

Scientists have long been focusing on PM2.5 because evidence consistently links it to respiratory illnesses, such as asthma, chronic obstructive pulmonary disease, and airway inflammation. Studies suggest that the damage caused by PM2.5 could be due to oxidative stress and the triggering of immune responses in the lungs following exposure.

PM2.5 is a complex atmospheric cocktail of natural and anthropogenic particles containing biological, inorganic, and organic constituents. For decades, researchers have extensively studied the impact of chemicals—including transition metals, polycyclic aromatic hydrocarbons, and industrial smoke—produced by human activities. These components, however, contribute to less than half of the respiratory damage inflicted by PM2.5, leaving roughly 60% of its impact still unexplained.

Researchers of this study conducted daily 24-hour PM_2.5 sampling for a year across an urban and coastal area of Hong Kong. To assess inflammatory responses, the researchers exposed human bronchial epithelial cells to PM_2.5 and measured the release of interleukin-8 (IL-8)—a small protein, called a cytokine, that is released by the immune system— as a marker of inflammation.

Part 1

Comment by Dr. Krishna Kumari Challa on Saturday

Researchers then adapted these into five scenarios for children to see if they could elicit information avoidance. For example, each child was asked to imagine their favorite and least favorite candy. They were then asked if they wanted to watch a video about why eating that candy was bad for their teeth.

They found that, whereas younger children really wanted to seek information, older children started to exhibit these avoidance tendencies. For example, they didn't want to know why their favorite candy was bad for them, but they were totally fine learning why their least favorite candy is bad for them.
This finding held for all motivations except for competency. Children of all ages were not afraid to learn if they'd done badly on a test, for example.

To avoid avoidance, she suggests thinking through why you might be avoiding something—possibly prioritizing short-term comfort over long-term benefits. Researchers posit that it could help to reframe uncomfortable information as useful and valuable.

Research suggests that intervening while children are still young could keep them from falling into avoidance traps and have compounding benefits.
Humans have this propensity to want to resolve uncertainty, but when the resolution is threatening, people might flip to avoidance instead.
If all else fails, she advises, mimic what children do best: Follow your curiosity.

Radhika Santhanagopalan et al, Becoming an Ostrich: The Development of Information Avoidance, Psychological Science (2025). DOI: 10.1177/09567976251344551

Part 2

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