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Comment by Dr. Krishna Kumari Challa 3 hours ago

Rare seasonal brain shrinkage in shrews is driven by water loss, not cell death, MRI study reveals

Common shrews are one of only a handful of mammals known to flexibly shrink and regrow their brains. This rare seasonal cycle, known as Dehnel's phenomenon, has puzzled scientists for decades. How can a brain lose volume and regrow months later without sustaining permanent damage?

A study using noninvasive MRI has scanned the brains of shrews undergoing shrinkage, identifying a key molecule involved in the phenomenon: water. The work is published in the journal Current Biology.

In the experiments conducted by researchers, shrews lost 9% of their brains during shrinkage, but the cells did not die. The cells just lost water. 

Normally, brain cells that lose water become damaged and ultimately die, but in shrews, the opposite happened. The cells remained alive and even increased in number.

This finding solves a mystery—and opens up potential pathways for the treatment of human brain disease. Brain shrinkage in shrews matches closely what happens in patients suffering from Alzheimer's, Parkinson's, and other brain diseases.

The study also shows that a specific protein known for regulating water—aquaporin 4—was likely involved in moving water out of the brain cells of shrews. This same protein is present in higher quantities in the diseased brains of humans, too.

That the shrunken brains of shrews share characteristics with diseased human brains makes the case that these miniature mammals, with their ability to reverse brain loss, could also offer clues for medical treatments.

 Programmed seasonal brain shrinkage in the common shrew via water loss without cell death, Current Biology (2025). DOI: 10.1016/j.cub.2025.08.015. www.cell.com/current-biology/f … 0960-9822(25)01081-4

Comment by Dr. Krishna Kumari Challa 3 hours ago

Genetic tools identify lost human relatives Denisovans from fossil records

New genetic techniques are shedding light on a mysterious part of our family tree—ancient human relatives called the Denisovans that emerged during the Pleistocene epoch, approximately 370,000 years ago.

Little is known about them because so few fossils have been found. The group was discovered by accident in 2010, based solely on DNA analysis of what was thought to be a Neanderthal finger bone found in the Denisova Cave in Siberia. However, it turned out to belong to a previously unknown lineage closely related to Neanderthals.

Since then, only a few additional fragments have been found, so researchers 

developed a new genetic tool to go through the fossil record identifying potential Denisovans. Their starting point was the Denisovan genome.

The research is published in the journal Proceedings of the National Academy of Sciences.

The research team's innovative technique detects subtle changes in how Denisovan genes are regulated. These changes were likely responsible for altering the Denisovan skeleton, providing clues to what they looked like.
Using this technique, the scientists identified 32 physical traits most closely related to skull morphology. Then they used this predicted profile to scan the Middle Pleistocene fossil record, specifically focusing on skulls from that period.
Before applying this method to unknown fossils, the researchers tested its accuracy. They used the same technique to successfully predict known physical traits of Neanderthals and chimpanzees with more than 85% accuracy.
Next, they identified 18 skull features they could measure, such as head width and forehead height, and then measured these traits on ten ancient skulls. They compared these to skulls from reference groups, including Neanderthals, modern humans and Homo erectus. Using sophisticated statistical tests, they gave each ancient skull a score to see how well it matched the Denisovan blueprint.
Of these, two skulls from China, known as the Harbin and Dali specimens, were a close match to the Denisovan profile. The Harbin skull matched 16 traits, while the Dali skull matched 15.
The study also found that a third skull, Kabwe 1, had a strong link to the Denisovan-Neanderthal tree, which may indicate that it was the root of the Denisovan lineage that split from Neanderthals.

In their study, the team states that their work may help with the identification of other extinct human relatives.

 Nadav Mishol et al, Candidate Denisovan fossils identified through gene regulatory phenotyping, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2513968122

Comment by Dr. Krishna Kumari Challa 21 hours ago

In science, you don't start from scratch. You build on top of the research of others. So if the foundation of that tower crumbles, then the entire thing collapses.
When scientists submit a new study to a reputable publication, that study usually undergoes a practice called peer review. Outside experts read the study and evaluate it for quality—or, at least, that's the goal.

A growing number of companies have sought to circumvent that process to turn a profit. In 2009, Jeffrey Beall, a librarian at CU Denver, coined the phrase "predatory" journals to describe these publications.

Often, they target researchers outside of the United States and Europe, such as in China, India and Iran—countries where scientific institutions may be young, and the pressure and incentives for researchers to publish are high.

These publishers of predatory journals will say, 'If you pay $500 or $1,000, we will review your paper. In reality, they don't provide any service. They just take the PDF and post it on their website.
a nonprofit organization called the Directory of Open Access Journals (DOAJ). Since 2003, volunteers at the DOAJ have flagged thousands of journals as suspicious based on six criteria. (Reputable publications, for example, tend to include a detailed description of their peer review policies on their websites.)

But keeping pace with the spread of those publications has been daunting for humans.

To speed up the process, researchers now turned to AI.
They trained its system using the DOAJ's data, then asked the AI to sift through a list of nearly 15,200 open-access journals on the internet.

Among those journals, the AI initially flagged more than 1,400 as potentially problematic. When scientists checked them , 350 were found to be legitimate. However, more than 1000 were predatory in nature!
The team discovered that questionable journals published an unusually high number of articles. They also included authors with a larger number of affiliations than more legitimate journals, and authors who cited their own research, rather than the research of other scientists, to an unusually high level.

The new AI system isn't publicly accessible, but the researchers hope to make it available to universities and publishing companies soon.

 Han Zhuang et al, Estimating the predictability of questionable open-access journals, Science Advances (2025). DOI: 10.1126/sciadv.adt2792

Part 2

Comment by Dr. Krishna Kumari Challa 21 hours ago

A firewall for science: AI tool identifies 1,000 'questionable' journals

A team of computer scientists  has developed a new artificial intelligence platform that automatically seeks out "questionable" scientific journals.

The study, published Aug. 27 in the journal Science Advances, tackles an alarming trend in the world of research.

 Spam messages come from people who purport to be editors at scientific journals, usually researchers  never heard of, and offer to publish their papers—for a hefty fee.

Such publications are sometimes referred to as "predatory" journals. They target scientists, convincing them to pay hundreds or even thousands of dollars to publish their research without proper vetting. There has been a growing effort among scientists and organizations to vet these journals. But it's like whack-a-mole. You catch one, and then another appears, usually from the same company. They just create a new website and come up with a new name.

The new new AI tool automatically screens scientific journals, evaluating their websites and other online data for certain criteria: Do the journals have an editorial board featuring established researchers? Do their websites contain a lot of grammatical errors?

In an era when prominent figures are questioning the legitimacy of science, stopping the spread of questionable publications has become more important than ever before.

Part 1

Comment by Dr. Krishna Kumari Challa 21 hours ago

AI helps stethoscope  detect three heart conditions in 15 seconds

An AI-enabled stethoscope can help doctors pick up three heart conditions in just 15 seconds, according to the results of a real-world trial presented at the European Society of Cardiology's annual congress.

The paper is also published in the journal BMJ Open.

The stethoscope, invented in 1816, is a vital part of a doctor's toolkit, used to listen to sounds within the body. But an AI stethoscope can do much more, including analyzing tiny differences in heartbeat and blood flow which are undetectable to the human ear, and taking a rapid ECG at the same time.

Researchers now have evidence that an AI stethoscope can increase detection of heart failure at the early stage when someone goes to their GP with symptoms.

A study involving more than 200 GP surgeries, with more than 1.5 million patients, looked at people with symptoms such as breathlessness or fatigue.

Those examined using an AI stethoscope were twice as likely to be diagnosed with heart failure, compared to similar patients who were not examined using the technology.

Patients examined with the AI-stethoscope were about 3.5 times more likely to be diagnosed with atrial fibrillation—an abnormal heart rhythm which can increase the risk of having a stroke. They were almost twice as likely to receive a diagnosis of heart valve disease, which is where one or more heart valves do not work properly.

Early diagnosis is vital for all three conditions, allowing patients who may need potentially lifesaving medicines to be identified sooner, before they become dangerously unwell.

 Mihir A Kelshiker et al, Triple cardiovascular disease detection with an artificial intelligence-enabled stethoscope (TRICORDER): design and rationale for a decentralised, real-world cluster-randomised controlled trial and implementation study, BMJ Open (2025). DOI: 10.1136/bmjopen-2024-098030

Comment by Dr. Krishna Kumari Challa 21 hours ago

Metformin changes blood metal levels in humans, offering further insight into its mechanism of action

The widely used diabetes drug metformin changes blood metal levels in humans. A new study is an important step in understanding the drug's many actions and designing better ones in the future.

Metformin is the most widely prescribed diabetes drug in the world. Apart from lowering blood sugar levels, it is also known to have a broad range of beneficial side effects such as against tumors, inflammation and atherosclerosis. However, although it has been used for more than 60 years now, its mechanism of action is still not clear, hampering the development of even better drugs against these conditions.

It is known that diabetes patients experience changes in the blood levels of metals such as copper, iron and zinc.

In addition, chemical studies found that metformin has the ability to bind certain metals, such as copper, and recent studies showed that it is this binding ability that might be responsible for some of the drug's beneficial effects. 

In the journal BMJ Open Diabetes Research & Care, researchers have published the first clinical evidence of altered blood metal levels in patients taking metformin. They showed that drug-taking patients have significantly lower copper and iron levels and heightened zinc levels.

Furthermore, since decreases in copper and iron concentrations and an increase in zinc concentration are all considered to be associated with improved glucose tolerance and prevention of complications, these changes may indeed be related to metformin's action.

 Association of metformin treatment with changes in metal dynamics in individuals with type 2 diabetes, BMJ Open Diabetes Research & Care (2025). DOI: 10.1136/bmjdrc-2025-005255

Comment by Dr. Krishna Kumari Challa on Saturday

Cancer can smuggle mitochondria in neighboring cells and put them to work

Cancer cells provide healthy neighboring cells with additional mitochondria to put them to work. This has been demonstrated by researchers  in a new study. In this way, cancer is exploiting a mechanism that frequently serves to repair damaged cells.

Tumors have developed many strategies and tricks to gain advantages in the body. Researchers have now discovered another surprising trick that certain tumors resort to in ensuring their survival and growth.

In a study published in the journal Nature Cancer, biologists show that skin cancer cells are able to transfer their mitochondria to healthy connective tissue cells (fibroblasts) in their immediate vicinity. Mitochondria are the cell compartments that provide energy in the form of the molecule ATP.

The cancer cells use tiny tubes made of cell membrane material to transfer the mitochondria and connect the two cells—much like in a pneumatic tube system.

The mitochondrial transfer reprograms the fibroblasts functionally into tumor-associated fibroblasts, which mainly support cancer cells: tumor-associated fibroblasts usually multiply faster than normal fibroblasts and produce more ATP, while also secreting higher amounts of growth factors and cytokines. And all this benefits the tumor cells: they also multiply faster, making the tumor more aggressive.

The hijacked fibroblasts also alter the cell environment—the so-called extracellular matrix—by increasing the production of certain matrix components in such a way that cancer cells thrive. The extracellular matrix is vital for the mechanical stability of tissues and influences growth, wound healing and intercellular communication.

Finally, the researchers also clarified the molecular mechanism behind the mitochondrial transfer. Some proteins were already known to assist in transporting mitochondria. The researchers investigated which of these proteins were present in large numbers in cancer cells that transfer mitochondria and came across the protein MIRO2. This protein is produced in very high quantities in cancer cells that transfer their mitochondria.

The researchers detected MIRO2 not only in cell cultures, but also in samples of human tissue—especially in tumor cells at the edges of tumors that grow invasively into the tissue and occur in close proximity to fibroblasts.

The new findings offer starting points for arresting tumor growth. When the researchers blocked the formation of MIRO2, the mitochondrial transfer was inhibited, and the fibroblasts did not develop into tumor-promoting fibroblasts.

The MIRO2 blockade worked in the test tube and in mouse models. Whether it also works in human tissue remains to be seen, say the researchers.

Michael Cangkrama et al, MIRO2-mediated mitochondrial transfer from cancer cells induces cancer-associated fibroblast differentiation, Nature Cancer (2025). DOI: 10.1038/s43018-025-01038-6

Comment by Dr. Krishna Kumari Challa on Saturday

Scientists move toward developing vaccine against pathogenic Staphylococcus aureus

Antibiotics are the old medicine cabinet standby for treating infections caused by multidrug-resistant Staphylococcus aureus, but as antimicrobial resistance continues to mount globally, scientists say there's a need for new strategies.

While vaccines are a potential answer, achieving an effective way to immunize against multidrug-resistant S. aureus has led scientists down dozens of blind alleys. Ten candidate vaccines that looked promising in preclinical animal studies in recent years failed miserably in human clinical trials.

Now, scientists are investigating a way to sidestep the myriad problems that plagued vaccine investigators in the past by choosing not to target a whole antigen. Instead, they say, it's time to home in on a critical "surface loop" as a vaccine target. The infinitesimal loop is located on the S. aureus antigen known as MntC.

The loop is an ideal target, scientists  say, because it has been shown to be essential for aiding survival in S. aureus by mitigating oxidative stress. By triggering vaccine-induced antibodies that zero in on that site, survival is impossible. As a vaccine target, the surface loop is known as an epitope.

Writing in Science Translational Medicine, researchers at institutions from throughout China report on the creation of a first-of-its-kind vaccine that has been tested in animal models based on a target pinpointed in samples from human clinical trials. The evolving strategy overcomes past obstacles and confers protection against drug-resistant S. aureus with a vaccine.

Xiaokai Zhang et al, An epitope vaccine derived by analyzing clinical trial samples safeguards hosts with prior exposure to S. aureus against reinfection, Science Translational Medicine (2025). DOI: 10.1126/scitranslmed.adr7464

Comment by Dr. Krishna Kumari Challa on Saturday

It's a tough job, but a crucial one because studies show that the roots of many diseases, including heart disease, cancer, and some psychiatric disorders, lie outside the well-understood, protein-coding regions of the genome.

Non-protein coding genes have key regulatory roles, turning certain genes on and off or altering their shape.

Do any of that at the wrong time, and things start to break down.

Scientists think that these RNAs act like software, orchestrating the protein 'hardware' into a functioning symphony.
Not junk at all.
You might have heard that you share 60% of your DNA with a banana.

It's not strictly speaking true, unfortunately, but there is a germ of truth there.

Humans and bananas (and everything else) all evolved from the same soup of bacteria and single-celled organisms about four billion years ago, and some of our DNA has been conserved over that time because it performs fundamental functions in our cells.

Studies have shown that about 10% of the human genome shows obvious conservation, but the rest is harder to pin down.

Scientists suspect that the remaining approximately 90% of the genome harbors many conserved RNA structures that are invisible to traditional approaches—hidden regulatory elements camouflaged in the genome.
Which is where the the newly developed AI—a tool called ECSFinder—comes in. It has been detailed in a paper in the journal Nucleic Acids Research.
Scientists trained the program on known RNA structures to detect secrets hidden in the genome. The program outperformed other available tools and is now ready to be unleashed on the entire genome.

They expect to uncover hundreds of thousands of new RNA structures, adding a new dimension to our understanding of the genome.

The holy grail of medicine right now is personalized therapy, treatments designed specifically for your individual illness.

One day, it's hoped, clinicians will be able to take a sample of your cancer's DNA, map its genome, then design ultra-specific drugs around its weaknesses, all within a few weeks.

And if the secrets of all gene-driven illnesses are hidden somewhere in the dark genome, learning how to read it is imperative.

Because RNA structures can be targeted by drugs, they present an exciting new frontier for therapies.

 Vanda Gaonac'h-Lovejoy et al, ECSFinder: optimized prediction of evolutionarily conserved RNA secondary structures from genome sequences, Nucleic Acids Research (2025). DOI: 10.1093/nar/gkaf780

Part 2

Comment by Dr. Krishna Kumari Challa on Saturday

AI tool targets RNA structures to unravel secrets of the dark genome

We mapped the human genome decades ago, but most of it is still a black box. Now,  scientists have developed a tool to peer inside and what they find could reshape how we think about disease.

Your genome is the genetic map of you, and we understand almost none of it.
Our handle on the bits of the genome that tell the body how to do things ("make eyes blue," "build heart tissue," "give this person sickle cell anemia") is OK, but there are vast areas of the genome that don't appear to do anything.
Scientists long assumed this was just "junk" DNA, leftovers from the billions of years it took us to evolve from primordial soup into the complex life we know today. But it turns out we just didn't know what to look for, nor how to look for it.
Now, new tools developed by researchers are helping us understand just how important the dark genome really is.

Understanding that, scientists hope, will offer new avenues for drug discovery, and transform how we think about disease and even life itself.

Your genome is broken up into protein-coding genes (around 2%), and the rest.

Proteins are the little machines that do the actual work of running an organism;protein-coding genes are the instructions for those proteins.

The other 98% doesn't build proteins, it doesn't follow the same rules, and it's much harder to understand. It contains "long non-coding RNAs," the stuff that was long dismissed as junk.

Scientists are  trying to decode the logic circuitry of the human genome—the hidden rules that tell our DNA how to build and run a human being.

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