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Comment by Dr. Krishna Kumari Challa on February 1, 2025 at 8:42am

Ear muscle we thought humans didn't use—except for wiggling our ears—activates during focused listening

If you can wiggle your ears, you can use muscles that helped our distant ancestors listen closely. These auricular muscles helped change the shape of the pinna, or the shell of the ear, funneling sound to the eardrums.

There are three large muscles which connect the auricle to the skull and scalp and are important for ear wiggling. These muscles, particularly the superior auricular muscle, exhibit increased activity during effortful listening tasks. This suggests that these muscles are engaged not merely as a reflex but potentially as part of an attentional effort mechanism, especially in challenging auditory environments.

It's difficult to test how hard someone is listening without self-reported measures. But electromyography, which measures electrical activity in a muscle, can help identify activity in the auricular muscles linked to listening closely.

Similar research has already shown that the largest muscles, posterior and superior auricular muscles, react during attentive listening. Because they pull the ears up and back, they are considered likely to have been involved in moving the pinna to capture sounds.

The exact reason these became vestigial is difficult to tell, as our ancestors lost this ability about 25 million years ago. One possible explanation could be that the evolutionary pressure to move the ears ceased because we became much more proficient with our visual and vocal systems.

Scientists now found that the two auricular muscles reacted differently to the different conditions. The posterior auricular muscles reacted to changes in direction, while the superior auricular muscles reacted to the difficulty level of the task.

Electromyographic Correlates of Effortful Listening in the Vestigial Auriculomotor System, Frontiers in Neuroscience (2025). DOI: 10.3389/fnins.2024.1462507

Comment by Dr. Krishna Kumari Challa on January 31, 2025 at 3:16pm

Asteroid find upends story of life’s origin
Fragments collected from the asteroid Bennu contain the building blocks for life — all five nucleobases that form DNA and RNA and 14 of the 20 amino acids needed to make known proteins. But there’s a twist: on Earth, amino acids in living organisms tend to have a ‘left-handed’ structure. Those on Bennu, however, contain nearly equal amounts of these structures and their ‘right-handed’, mirror-image forms. This calls into question a hypothesis favoured by many scientists that asteroids similar to this one might have seeded life on Earth.

https://www.nature.com/articles/s41550-024-02472-9?utm_source=Live+...

https://www.nature.com/articles/d41586-025-00264-3?utm_source=Live+...

Comment by Dr. Krishna Kumari Challa on January 31, 2025 at 2:40pm

Amniotic fluid's protective properties: Study uncovers its role in blood clotting

Researchers have made new discoveries about amniotic fluid, a substance historically not well understood in medical research due to the difficulty in obtaining it during pregnancy, especially across gestation.

Amniotic fluid is the vital fluid that surrounds and protects a fetus during pregnancy. In addition to providing much-needed cushion and protection for the fetus, it also aids in development of vital organs—especially the lungs, digestive tract and skin—and stabilizes the temperature inside the womb.

The new study, published in the journal Research and Practice in Thrombosis and Haemostasis, found that the addition of amniotic fluid to plasma—the liquid portion of blood—improves the blood's ability to thicken and clot, which is a critical and likely a protective function throughout pregnancy and during delivery for both the birthing parent and the baby.

Researchers analyzed the properties of amniotic fluid obtained by amniocentesis, a prenatal test that involves sampling a small amount of amniotic fluid to examine the health of the pregnancy, from both human and non-human primates at gestational-age matched timepoints. The findings showed that amniotic fluid increases blood clotting through key fatty acids and proteins that change each trimester and help regulate coagulation.

 Chih Jen Yang et al, Characterization of the procoagulant phenotype of amniotic fluid across gestation in rhesus macaques and humans, Research and Practice in Thrombosis and Haemostasis (2025). DOI: 10.1016/j.rpth.2024.102676

Comment by Dr. Krishna Kumari Challa on January 31, 2025 at 2:31pm

 India doubled its tiger population in a decade and credits conservation efforts

India doubled its tiger population in a little over a decade by protecting the big cats from poaching and habitat loss, ensuring they have enough prey, reducing human-wildlife conflict, and increasing communities' living standards near tiger areas, a study published this week found.

The number of tigers grew from an estimated 1,706 tigers in 2010 to around 3,682 in 2022, according to estimates by the National Tiger Conservation Authority, making India home to roughly 75% of the global tiger population. The study found that some local communities near tiger habitats have also benefited from the increase in tigers because of the foot traffic and revenues brought in by ecotourism.

The study in the journal Science says India's success "offers important lessons for tiger-range countries" that conservation efforts can benefit both biodiversity and nearby communities.

Wildlife conservationists and ecologists welcomed the study but said that tigers and other wildlife in India would benefit if source data were made available to a larger group of scientists. The study was based on data collected by Indian government-supported institutions.

Also there are several species, including the great Indian bustard and caracal which are all on the edge. "And there is really not enough focus on that."

 Yadvendradev V. Jhala et al, Tiger recovery amid people and poverty, Science (2025). DOI: 10.1126/science.adk4827

Comment by Dr. Krishna Kumari Challa on January 31, 2025 at 2:25pm

Bats' genetic adaptations: How they tolerate coronaviruses without becoming ill

New research has shown that bats can tolerate coronaviruses and other viruses without becoming ill, thanks to special adaptations of their immune system.

The study, published in Nature, shows that bats have more genetic adaptations in immune genes than other mammals. The ISG15 gene in particular plays a key role: in some bats, it can reduce the production of SARS-CoV-2 by up to 90%. 

The results could help to develop new medical approaches to combat viral diseases.

Bats have unique characteristics. As the only mammals that can actively fly, they play an important role in the ecosystem: They pollinate plants, spread seeds and contribute to the balance of the insect population through their feeding habits. Their exceptional orientation using ultrasonic echolocation shows how perfectly they are adapted to their nocturnal lifestyle.

Bats are of great interest to medical advancement, as their immune systems and unique viral tolerances can provide valuable insights for the development of new therapies. They are also known to carry numerous viruses, including those that are transmissible to humans—such as coronaviruses. However, bats do not show any symptoms of disease when infected with such viruses.

The new research team has sequenced high-quality genomes of 10 new bat species, as part of the international Bat1K project, including species known to carry coronaviruses and other viruses. Such adaptations can be detected as traces of positive selection and can indicate functional changes.

The result of the extensive analysis shows that bats exhibit such adaptations in immune genes much more frequently than other mammals.

The research also showed that the common ancestor of all bats had an unexpectedly high number of immune genes with selection signatures. This suggests that the evolution of the immune system could be closely linked to the evolution of the ability to fly.

Ariadna E. Morales et al, Bat genomes illuminate adaptations to viral tolerance and disease resistance, Nature (2025). DOI: 10.1038/s41586-024-08471-0

Comment by Dr. Krishna Kumari Challa on January 31, 2025 at 2:18pm

Future antibiotics face early bacterial resistance challenges, studies show

Researchers have made a concerning discovery about the future of antibiotics. Two recent studies, published just days apart in Nature Microbiology and Science Translational Medicine found that resistance can develop against new antibiotics even before they are widely used, compromising their effectiveness from the start. The studies focused on five critical bacterial species that cause major hospital infections and examined 18 new antibiotics, some already on the market and others still in development.

New antibiotics are often marketed as resistance-free, but this claim relies on limited data. 

This new work  highlights a major issue: antibiotic development tends to prioritize broad-spectrum activity - that is the number of bacterial species a drug targets- over long-term sustainability. While many new antibiotics indeed offer a broader spectrum, this doesn't guarantee they will remain effective in the long run in clinical use.

The studies found that resistance developed rapidly against nearly all the tested antibiotics, defying earlier expectations. For example, teixobactin, once hailed as a revolutionary drug, was believed to be less prone to resistance. However, the research revealed that bacteria can adapt to it with this adaptation resulting in cross-resistance to other critical antibiotics.

Alarmingly, the team also found that resistance mutations may already exist in bacterial populations, likely due to the overuse of older antibiotics and the shared resistance mechanisms between those and new drugs. These pre-existing mutations could render even the newest drugs ineffective shortly after they are introduced into clinical use.

Rethinking antibiotic development:  The studies call for a fundamental shift in how antibiotics are developed. Drug companies must incorporate resistance studies early in the development process to anticipate and mitigate risks before antibiotics are released. Integrating resistance prediction and genetic surveillance into drug design could reduce the chances of failure.

Some new antibiotics show more promise than others, as resistance develops more slowly or only in specific bacterial species. Understanding why these drugs perform better is the next crucial step.

The studies emphasize the importance of prioritizing antibiotics with novel modes of action to bypass existing resistance. In cases where only certain bacterial species are prone to resistance, narrow-spectrum therapy could provide an effective alternative. Finally, the studies stress the urgency of responsible antibiotic use to slow down the evolution of resistance and ensure the prolonged efficacy of new treatments in the future.

 Lejla Daruka et al, ESKAPE pathogens rapidly develop resistance against antibiotics in development in vitro, Nature Microbiology (2025). DOI: 10.1038/s41564-024-01891-8

Ana Martins et al, Antibiotic candidates for Gram-positive bacterial infections induce multidrug resistance, Science Translational Medicine (2025). DOI: 10.1126/scitranslmed.adl2103

Comment by Dr. Krishna Kumari Challa on January 31, 2025 at 2:06pm

Scientists replicate bone marrow

Hidden within our bones, marrow sustains life by producing billions of blood cells daily, from oxygen-carrying red cells to immune-boosting white cells. This vital function is often disrupted in cancer patients undergoing chemotherapy or radiation, which can damage the marrow and lead to dangerously low white cell counts, leaving patients vulnerable to infection.

Now researchers have developed a platform that emulates human marrow's native environment. This breakthrough addresses a critical need in medical science, as animal studies often fail to fully replicate the complexities of human marrow.

The team's new device is a small plastic chip whose specially designed chambers are filled with human blood stem cells and the surrounding support cells with which they interact in a hydrogel to mimic the intricate process of bone marrow development in the human embryo. This biologically inspired platform makes it possible to build living human marrow tissue that can generate functional human blood cells and release them into culture media flowing in engineered capillary blood vessels.

The bone marrow-on-a-chip allows researchers to simulate and study common side effects of medical treatments, such as radiotherapy and chemotherapy for cancer patients. When connected to another device, it can even model how the bone marrow communicates with other organs, like the lungs, to protect them from infections and other potentially life-threatening conditions.

Described in a new paper published in Cell Stem Cell, the bone marrow model and the demonstration of its large-scale production and automation could advance fields as diverse as drug development by enabling automated, high-throughput preclinical screening of marrow toxicity of anticancer drugs) and space travel (by allowing researchers to study the effects of prolonged radiation exposure and microgravity on the immune system of astronauts).  

Andrei Georgescu et al, Self-organization of the hematopoietic vascular niche and emergent innate immunity on a chip, Cell Stem Cell (2024). DOI: 10.1016/j.stem.2024.11.003

Comment by Dr. Krishna Kumari Challa on January 31, 2025 at 2:01pm

The team then studied the impacts of the structural variation on the human cell lines. Using genomic sequencing, the team was able to take 'snapshots' of the human cells and their 'shuffled' genomes over the course of a few weeks, watching which cells survived and which died.

As expected, they found that when structural variation deleted essential genes, this was heavily selected against and the cells died. However, they found that groups of cells with large-scale deletions in the genomes that avoided essential genes survived.

The team also conducted RNA sequencing of the human cell lines, which measures gene activity, known as gene expression. This revealed that large-scale deletions of the genetic code, especially in non-coding regions, did not seem to impact the gene expression of the rest of the cell.

The researchers suggest that human genomes are extremely tolerant of structural variation, including variants that change the position of hundreds of genes, as long as essential genes are not deleted.

In another study related to this  another research  team used a different approach, adding recombinase sites to transposons—mobile genetic elements—that randomly integrated in the genomes of human cell lines and mouse embryonic stem cells.

Using their method, they demonstrated that the effects of the induced structural variants can be read out using single-cell RNA sequencing. This advance paves the way for large screens of structural variant impact, potentially improving the classification of structural variants found in human genomes as benign or clinically significant.

Both studies came to similar conclusions that human genomes are surprisingly tolerant to some substantial structural changes, although the full extent of this tolerance remains to be explored in future studies enabled by these technologies.

Jonas Koeppel et al, Randomizing the human genome by engineering recombination between repeat elements, Science (2025). DOI: 10.1126/science.ado3979. www.science.org/doi/10.1126/science.ado3979

Science (2025). DOI: 10.1126.science.ado5978

part2

Comment by Dr. Krishna Kumari Challa on January 31, 2025 at 2:00pm

Complex engineering of human cell lines reveals genome's unexpected resilience to structural changes

The most complex engineering of human cell lines ever has been achieved by scientists, revealing that our genomes are more resilient to significant structural changes than was previously thought.

Researchers used CRISPR prime editing to create multiple versions of human genomes in cell lines, each with different structural changes. Using genome sequencing, they were able to analyze the genetic effects of these structural variations on cell survival .

The research, published in Science, shows that as long as essential genes remain intact, our genomes can tolerate significant structural changes, including large deletions of the genetic code. The work opens the door to studying and predicting the role of structural variation in disease.

Structural variation is a change in the structure of an organism's genome, such as deletions, duplications and inversions of the genetic sequence. These structural changes to the genome can be significant, sometimes affecting hundreds to many thousands of nucleotides—the basic building blocks of DNA and RNA.

Structural variants are associated with developmental diseases and cancer. However, our ability to study the effects of structural variation in the genomes of mammals, and the role they play in disease, has been difficult due to the inability to engineer these genetic changes.

To overcome this challenge,  researchers  set out to develop new approaches for creating and studying structural variation.

In a new study, the team used a combination of CRISPR prime editing and human cell lines—groups of human cells in a dish—to generate thousands of structural variants in human genomes within a single experiment.

To do this, researchers used prime editing to insert a recognition sequence into the genomes of the human cell lines to target with recombinase—an enzyme that enabled the team to 'shuffle' the genome.

By inserting these recombinase handles into repetitive sequences, which are hundreds and thousands of identical sequences in the genome, with a single prime editor they were able to integrate up to almost 1,700 recombinase recognition sites into each cell line.

This resulted in more than 100 random large-scale genetic structural changes per cell. This is the first time that it's been possible to 'shuffle' a mammalian genome, especially at this scale.

part1

Comment by Dr. Krishna Kumari Challa on January 31, 2025 at 1:40pm

Your fridge still uses tech from the 50s, but scientists have an update

Researchers report on Jan. 30 in the journal Joule that a more efficient and environmentally friendly form of refrigeration might be on the horizon. The new technology is based on thermogalvanic cells that produce a cooling effect by way of a reversible electrochemical reaction.

Thermogalvanic refrigeration is cheaper and more environmentally friendly than other cooling methods because it requires a far lower energy input, and its scalability means that it could be used for various applications—from wearable cooling devices to industrial-grade scenarios.

Thermogalvanic cells use the heat produced by reversible electrochemical reactions to create electrical power. In theory, reversing this process—applying an external electrical current to drive electrochemical reactions—enables cooling power to be generated.

Previous studies have shown that thermogalvanic cells have a limited potential to produce cooling power, but  this new work was able to dramatically increase this potential by optimizing the chemicals used in the technology.

By tweaking the solutes and solvents used in the electrolyte solution, the researchers were able to improve the hydrogalvanic cell's cooling power. They used a hydrated iron salt containing perchlorate, which helped the iron ions dissolve and dissociate more freely compared to other previously tested iron-containing salts such as ferricyanide.
By dissolving the iron salts in a solvent containing nitriles rather than pure water, the researchers were able to improve the hydrogalvanic cell's cooling power by 70%.

The optimized system was able to cool the surrounding electrolyte by 1.42 K, which is a big improvement compared to the 0.1 K cooling capacity reported by previously published thermogalvanic systems.

Looking ahead, the team plans to continue optimizing their system's design and is also investigating potential commercial applications.

Solvation entropy engineering of thermogalvanic electrolytes for efficient electrochemical refrigeration, Joule (2025). DOI: 10.1016/j.joule.2025.101822. www.cell.com/joule/fulltext/S2542-4351(25)00003-0

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