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Comment by Dr. Krishna Kumari Challa on September 2, 2025 at 6:58am

Why male embryos grow faster

Researchers have uncovered the genetic triggers that cause male and female bovine embryos to develop differently, as early as seven to eight days after fertilization. The breakthrough in basic science has implications for human health—such as drug development and in vitro fertilization—and for bovine health and dairy industry sustainability.

Scientists have known since the 1990s that male embryos of multiple mammalian species, including humans, grow faster than female embryos, but until now, the underlying reasons were unclear.

In a paper, published in Cell & Bioscience,  scientists grew bovine embryos in petri dishes, then analyzed their genetic sex and RNA sequencing, which shows how genes are being expressed.

They discovered significant sex differences in gene regulation: male embryos prioritized genes associated with energy metabolism, causing them to grow faster than their female counterparts. Female embryos emphasized genes associated with sex differentiation, gonad development and inflammatory pathways that are important for future development.

Understanding these fundamental sex differences at the genomic and molecular levels is critically important to improving in vitro fertilization (IVF) success in humans and cows, and in developing treatments that will work for both men and women.

Meihong Shi et al, Sex-biased transcriptome in in vitro produced bovine early embryos, Cell & Bioscience (2025). DOI: 10.1186/s13578-025-01459-x

Comment by Dr. Krishna Kumari Challa on September 2, 2025 at 6:52am

Longevity gains slowing with life expectancy of 100 unlikely, study finds

A new study  finds that life expectancy gains made by high-income countries in the first half of the 20th century have slowed significantly, and that none of the generations born after 1939 will reach 100 years of age on average.

Published in the journal Proceedings of the National Academy of Sciences, the study analyzed life expectancy for 23 high-income and low-mortality countries using data from the Human Mortality Database and six different mortality forecasting methods. 

The unprecedented increase in life expectancy we achieved in the first half of the 20th century appears to be a phenomenon we are unlikely to achieve again in the foreseeable future. In the absence of any major breakthroughs that significantly extend human life, life expectancy would still not match the rapid increases seen in the early 20th century even if adult survival improved twice as fast as we predict.

From 1900 to 1938, life expectancy rose by about five and a half months with each new generation. The life expectancy for an individual born in a high-income country in 1900 was an average of 62 years. For someone born just 38 years later in similar conditions, life expectancy had jumped to 80 years on average.

For those born between 1939 and 2000, the increase slowed to roughly two and a half to three and a half months per generation, depending on the forecasting method. Mortality forecasting methods are statistical techniques that make informed predictions about future lifespans based on past and current mortality information. These models enabled the research team to estimate how life expectancy will develop under a variety of plausible future scenarios.

Researchers forecast that those born in 1980 will not live to be 100 on average, and none of the cohorts in their study will reach this milestone. This decline is largely due to the fact that past surges in longevity were driven by remarkable improvements in survival at very young ages.

At the beginning of the 20th century, infant mortality fell rapidly due to medical advances and other improvements in quality of life for high-income countries. This contributed significantly to the rapid increase in life expectancy. However, infant and child mortality is now so low that the forecasted improvements in mortality in older age groups will not be enough to sustain the previous pace of longevity gains.

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While mortality forecasts can never be certain as the future may unfold in unexpected ways—by way of pandemics, new medical treatments or other unforeseen societal changes—this study provides critical insight for governments looking to anticipate the needs of their health care systems, pension planning and social policies.

Although a population-level analysis, this research also has implications for individuals, as life expectancy influences personal decisions about saving, retirement and long-term planning. If life expectancy increases more slowly, as this study shows is likely, both governments and individuals may need to recalibrate their expectations for the future.

José Andrade et al, Cohort mortality forecasts indicate signs of deceleration in life expectancy gains, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2519179122

Comment by Dr. Krishna Kumari Challa on September 2, 2025 at 6:40am

Super corals could help buy time for reefs in a warming world

Coral reefs are in crisis. Rising ocean temperatures driven by climate change are pushing these ecosystems to the brink, with mass bleaching events becoming more frequent and severe.

But what if nature already holds part of the solution?

New research led by UTS demonstrates that corals that naturally thrive in extreme environments, often referred to as "super corals," could be used in restoration efforts to protect vulnerable reef systems.

The research was published in the journal Science Advances and offers compelling evidence that these resilient corals can retain their heat tolerance even after being moved to more stable reef habitats.

Christine D. Roper et al, Coral thermotolerance retained following year-long exposure to a novel environment, Science Advances (2025). DOI: 10.1126/sciadv.adu3858

Comment by Dr. Krishna Kumari Challa on September 2, 2025 at 6:36am

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 on September 2, 2025 at 6:28am

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 on September 1, 2025 at 12:39pm

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 on September 1, 2025 at 12:33pm

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 on September 1, 2025 at 12:25pm

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 on September 1, 2025 at 12:19pm

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 August 30, 2025 at 9:31am

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

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