Comment

Comment by Dr. Krishna Kumari Challa yesterday

Magnetic fields in infant universe may have been billions of times weaker than a fridge magnet

The magnetic fields that formed in the very early stages of the universe may have been billions of times weaker than a small fridge magnet, with strengths comparable to magnetism generated by neurons in the human brain. Yet, despite such weakness, quantifiable traces of their existence still remain in the cosmic web, the visible cosmic structures connected throughout the universe.

These conclusions emerge from a study using around a quarter of a million computer simulations.

The research, recently published in Physical Review Letters, specifies both possible and maximum values for the strengths of primordial magnetic fields. It also offers the possibility of refining our knowledge of the early universe and the formation of the first stars and galaxies.

 Mak Pavičević et al, Constraints on Primordial Magnetic Fields from the Lyman- α Forest, Physical Review Letters (2025). DOI: 10.1103/77rd-vkpz. On arXiv: DOI: 10.48550/arxiv.2501.06299

Comment by Dr. Krishna Kumari Challa yesterday

Deforestation reduces rainfall by 74% and increases temperatures by 16% in Amazon during dry season, study found

Deforestation in the Brazilian Amazon is responsible for approximately 74.5% of the reduction in rainfall and 16.5% of the temperature increase in the biome during the dry season. For the first time, researchers have quantified the impact of vegetation loss and global climate change on the forest.

The study provides fundamental results to guide effective mitigation and adaptation strategies.

How climate change and deforestation interact in the transformation of the Amazon rainforest, Nature Communications (2025). DOI: 10.1038/s41467-025-63156-0

Comment by Dr. Krishna Kumari Challa yesterday

How bacteria bounce back after antibiotics

A study by researchers has uncovered how Escherichia coli (E. coli) persister bacteria survive antibiotics by protecting their genetic instructions.

The work, published in Nature Microbiology, offers new hope for tackling chronic, recurring infections.

Persister bacteria, which enter a dormant state to survive antibiotics that target active cells, are linked to over 20% of chronic infections and resist current treatments.

Understanding their survival mechanisms could lead to new ways to combat recurring infections. This study utilized E. coli bacteria as a model and found that prolonged stress leads to the increased formation of aggresomes (membraneless droplets) and the enrichment of mRNA (molecules that carry instructions for making proteins) within them, which enhances the ability of E. coli to survive and recover from stress.

Researchers used multiple approaches, including imaging, modeling, and transcriptomics, to show that prolonged stress leading to ATP (fuel for all living cells) depletion in Escherichia coli results in increased aggresome formation, their compaction, and enrichment of mRNA within aggresomes compared to the cytosol (the liquid inside of cells).

Transcript length was longer in aggresomes compared to the cytosol. Mass spectrometry showed exclusion of mRNA ribonuclease (an enzyme that breaks down RNA) from aggresomes, which was due to negative charge repulsion.

Experiments with fluorescent reporters and disruption of aggresome formation showed that mRNA storage within aggresomes promoted translation and was associated with reduced lag phases during growth after stress removal. These findings suggest that mRNA storage within aggresomes confers an advantage for bacterial survival and recovery from stress.

This breakthrough illuminates how persister cells survive and revive after antibiotic treatment. 

By targeting aggresomes, new drugs could disrupt this protective mechanism, preventing bacteria from storing mRNA and making them more vulnerable to elimination, thus reducing the risk of infection relapse.

Linsen Pei et al, Aggresomes protect mRNA under stress in Escherichia coli, Nature Microbiology (2025). DOI: 10.1038/s41564-025-02086-5

Comment by Dr. Krishna Kumari Challa yesterday

 Generative AI designs molecules that kill drug-resistant bacteria

What if generative AI could design life-saving antibiotics, not just art and text? In a new Cell Biomaterials paper, researchers introduce AMP-Diffusion, a generative AI tool used to create tens of thousands of new antimicrobial peptides (AMPs)—short strings of amino acids, the building blocks of proteins—with bacteria-killing potential. In animal models, the most potent AMPs performed as well as FDA-approved drugs, without detectable adverse effects.

While past work has shown that AI can successfully sort through mountains of data to identify promising antibiotic candidates, this study adds to a small but growing number of demonstrations that AI can invent antibiotic candidates from scratch.

Using AMP-Diffusion, the researchers generated the amino-acid sequences for about 50,000 candidates. They used   AI to filter the results. 

After synthesizing the 46 most promising candidates, the researchers tested them in human cells and animal models. Treating skin infections in mice, two AMPs demonstrated efficacy on par with levofloxacin and polymyxin B, FDA-approved drugs used to treat antibiotic-resistant bacteria, without adverse effects.

In the future, the researchers hope to refine AMP-Diffusion, giving it the capability to denoise with a more specific goal in mind, like treating a particular type of bacterial infection, among other features.

Generative latent diffusion language modeling yields anti-infective synthetic peptides, Cell Biomaterials (2025). DOI: 10.1016/j.celbio.2025.100183. www.cell.com/cell-biomaterials … 3050-5623(25)00174-6

Comment by Dr. Krishna Kumari Challa yesterday

Genetic mechanism reveals how plants coordinate flowering with light and temperature conditions

Plants may be stuck in one place, but the world around them is constantly changing. In order to grow and flower at the right time, plants must constantly collect information about their surroundings, measuring things like temperature, brightness, and length of day. Still, it's unclear how all this information gets combined to trigger specific behaviors.

Scientists have discovered a genetic mechanism for how plants integrate light and temperature information to control their flowering.

In a study published in Nature Communications, the researchers found an interaction between two genetic pathways that signals the presence of both blue light and low temperature. This genetic module helps plants fine-tune their flowering to the optimal environmental conditions.

In one pathway, blue light activates the PHOT2 blue light receptor, with help from partner protein NPH3. In another pathway, low ambient temperature allows a transcription factor called CAMTA2 to boost the expression of a gene called EHB1. Importantly, EHB1 is known to interact with NPH3, placing NPH3 at the convergence point of the blue light and low temperature signals. This this genetic architecture effectively works as a coincidence detector, linking the presence of blue light and low temperature to guide the switch to flowering.

The study describes an important component of plant growth, reproduction, and information processing. The newly discovered genetic module allows plants to have fine control over their flowering in low temperatures. Understanding this system will now help scientists optimize crop growth under changing environmental conditions.  

Adam Seluzicki et al, Genetic architecture of a light-temperature coincidence detector, Nature Communications (2025). DOI: 10.1038/s41467-025-62194-y

Comment by Dr. Krishna Kumari Challa yesterday

World's oldest host-associated bacterial DNA found

An international team led by researchers at the Center for Paleogenetics, has uncovered microbial DNA preserved in woolly and steppe mammoth remains dating back more than one million years. The analyses reveal some of the world's oldest microbial DNA ever recovered, as well as the identification of bacteria that possibly caused disease in mammoths. The findings are published in Cell.

Researchers analyzed microbial DNA from 483 mammoth specimens, of which 440 were sequenced for the first time. Among them was a steppe mammoth that lived about 1.1 million years ago. Using advanced genomic and bioinformatic techniques, the team distinguished microbes that once lived alongside the mammoths from those that invaded their remains after death.

 Ancient Host-Associated Microbes obtained from Mammoth Remains, Cell (2025). DOI: 10.1016/j.cell.2025.08.003. www.cell.com/cell/fulltext/S0092-8674(25)00917-1

Comment by Dr. Krishna Kumari Challa yesterday

8,000 years of human activities have caused wild animals to shrink and domestic animals to grow

Humans have caused wild animals to shrink and domestic animals to grow, according to a new study. 

Researchers studied tens of thousands of animal bones from Mediterranean France covering the last 8,000 years to see how the size of both types of animals has changed over time.

Scientists already know that human choices, such as selective breeding, influence the size of domestic animals, and that environmental factors also impact the size of both. However, little is known about how these two forces have influenced the size of wild and domestic animals over such a prolonged period. This latest research, published in the Proceedings of the National Academy of Sciences , fills a major gap in our knowledge.

The scientists analyzed more than 225,000 bones from 311 archaeological sites in Mediterranean France. They took thousands of measurements of things like the length, width, and depth of bones and teeth from wild animals, such as foxes, rabbits and deer, as well as domestic ones, including goats, cattle, pigs, sheep and chickens.

But the researchers didn't just focus on the bones. They also collected data on the climate, the types of plants growing in the area, the number of people living there and what they used the land for. And then, with some sophisticated statistical modeling, they were able to track key trends and drivers behind the change in animal size.

The research team's findings reveal that for around 7,000 years, wild and domestic animals evolved along similar paths, growing and shrinking together in sync with their shared environment and human activity. However, all that changed around 1,000 years ago. Their body sizes began to diverge dramatically, especially during the Middle Ages.

Domestic animals started to get much bigger as they were being actively bred for more meat and milk. At the same time, wild animals began to shrink in size as a direct result of human pressures, such as hunting and habitat loss. In other words, human activities replaced environmental factors as the main force shaping animal evolution.

 Mureau, Cyprien et al, 8,000 years of wild and domestic animal body size data reveal long-term synchrony and recent divergence due to intensified human impact, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2503428122. www.pnas.org/cgi/doi/10.1073/pnas.2503428122

Comment by Dr. Krishna Kumari Challa on Tuesday

Hyperactive blood platelets linked to heart attacks despite standard drug therapy

Scientists  have discovered a particularly active subgroup of blood platelets that may cause heart attacks in people with coronary heart disease despite drug therapy. This discovery may open up new prospects for customized therapies. The research results are published in the European Heart Journal and were presented on August 31 at Europe's largest cardiology congress.

Despite modern medication, many people with coronary heart disease continue to suffer heart attacks. A research team  has now found a possible explanation for this and has also provided a very promising therapeutic approach.

Their work focused on so-called "reticulated platelets": particularly young, RNA-rich and reactive thrombocytes that play a central role in the formation of blood clots in patients with coronary heart disease.

The researchers were able to comprehensively characterize the biological mechanisms of these cells for the first time. This allows us to explain why these platelets remain overactive in many patients even under optimal therapy. The reason is that these young platelets have a particularly large number of activating signaling pathways that make them more sensitive and reactive than mature platelets.

The results come from a multidimensional, using various methods, analysis of the blood of over 90 patients with coronary heart disease. Among other things, the researchers found signaling pathways that can be used to specifically inhibit the activity of such blood cells, in particular two target structures called GPVI and PI3K. Initial laboratory experiments confirmed that inhibiting these signaling pathways can reduce platelet hyperactivity.

 Kilian Kirmes et al, Reticulated platelets in coronary artery disease: a multidimensional approach unveils prothrombotic signalling and novel therapeutic targets, European Heart Journal (2025). DOI: 10.1093/eurheartj/ehaf694

Comment by Dr. Krishna Kumari Challa on Tuesday

The reason why there are high levels of neutrophils in the meninges is unclear. One explanation could be that they are recruited by microglia, a type of immune cell unique to the brain.

Another possible explanation is that chronic stress may cause microhemorrhages, tiny leaks in brain blood vessels, and that neutrophils—the body's 'first responders'—arrive to fix the damage and prevent any further damage. These neutrophils then become more rigid, possibly getting stuck in brain capillaries and causing further inflammation in the brain.

These new findings show that these 'first responder' immune cells leave the skull bone marrow and travel to the brain, where they can influence mood and behavior.

Stacey L. Kigar et al, Chronic social defeat stress induces meningeal neutrophilia via type I interferon signaling in male mice, Nature Communications (2025). DOI: 10.1038/s41467-025-62840-5

Part 2

Comment by Dr. Krishna Kumari Challa on Tuesday

Depression linked to presence of immune cells in the brain's protective layer

Immune cells released from bone marrow in the skull in response to chronic stress and adversity could play a key role in symptoms of depression and anxiety, say researchers.

The discovery—found in a study in mice—sheds light on the role that inflammation can play in mood disorders and could help in the search for new treatments, in particular for those individuals for whom current treatments are ineffective.

Around 1 billion people will be diagnosed with a mood disorder such as depression or anxiety at some point in their life. While there may be many underlying causes, chronic inflammation—when the body's immune system stays active for a long time, even when there is no infection or injury to fight—has been linked to depression. This suggests that the immune system may play an important role in the development of mood disorders.

Previous studies have highlighted how high levels of an immune cell known as a neutrophil, a type of white blood cell, are linked to the severity of depression. But how neutrophils contribute to symptoms of depression is currently unclear.

In research published in Nature Communications, a team of scientists  tested the hypothesis that chronic stress can lead to the release of neutrophils from bone marrow in the skull. These cells then collect in the meninges—membranes that cover and protect your brain and spinal cord—and contribute to symptoms of depression.

As it is not possible to test this hypothesis in humans, the team used mice exposed to chronic social stress. In this experiment, an 'intruder' mouse is introduced into the home cage of an aggressive resident mouse. The two have brief daily physical interactions and can otherwise see, smell, and hear each other.

The researchers found that prolonged exposure to this stressful environment led to a noticeable increase in levels of neutrophils in the meninges, and that this was linked to signs of depressive behavior in the mice. Even after the stress ended, the neutrophils lasted longer in the meninges than they did in the blood.

Analysis confirmed the researchers' hypothesis that the meningeal neutrophils—which appeared subtly different from those found in the blood—originated in the skull.

Further analysis suggested that long-term stress triggered a type of immune system 'alarm warning' known as type I interferon signaling in the neutrophils. Blocking this pathway—in effect, switching off the alarm—reduced the number of neutrophils in the meninges and improved behavior in the depressed mice.

Further analysis suggested that long-term stress triggered a type of immune system 'alarm warning' known as type I interferon signaling in the neutrophils. Blocking this pathway—in effect, switching off the alarm—reduced the number of neutrophils in the meninges and improved behavior in the depressed mice.

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