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Comment by Dr. Krishna Kumari Challa 1 hour ago

People use the same neurons to see and imagine objects, study shows

Why can images of things we have seen seem so real when we later recall them from memory? A new study led by Cedars-Sinai Health Sciences University investigators sheds light on the answer. The research shows that the same brain neurons are activated when we imagine something and when we perceive something. The research, led by Cedars-Sinai, is the first to provide a detailed understanding of the shared mechanism that underlies visual perception and creation of mental images in the human brain. It was published in the journal Science.
Visual perception and imagination activate overlapping populations of neurons in the human fusiform gyrus, with about 40% of visually responsive neurons reactivating during mental imagery using the same neural code as during perception. This shared neural mechanism underlies the vividness of visual imagination and may inform understanding of psychiatric disorders involving altered mental imagery.
We generate a mental image of an object that we have seen before by reactivating the brain cells we used to see it in the first place.
The new study revealed the code that we use to re-create the images.
The findings provide a biological basis for visual imagination, a process that is also critical for creative arts.

"Further insight into this neural process has the potential to open pathways toward developing new therapies for post-traumatic stress disorder, obsessive-compulsive disorder, and other mental conditions that involve uncontrolled vivid imagery.
To conduct the study, investigators asked 16 adults with epilepsy, who had electrodes temporarily implanted in their brains for diagnosing their seizures, to view a series of images of faces and objects.

After viewing them, a subset of the participants were asked to imagine those same images from memory. Meanwhile, researchers recorded the electrical activity of hundreds of individual neurons in each participant's brain.

When the patients viewed the images, neurons were activated in their fusiform gyrus, an area of the brain essential for high-level visual processing, particularly for faces. For 80% of the visually responsive neurons recorded in the study, the researchers uncovered the aspects of the images they reacted to, thereby revealing their neural code.
When the patients later imagined the images, about 40% of these neurons reactivated using the same code, thereby recreating the pattern of activity that occurred during the initial viewing of the images.

V. S. Wadia et al, A shared code for perceiving and imagining objects in human ventral temporal cortex, Science (2026). DOI: 10.1126/science.adt8343. www.science.org/doi/10.1126/science.adt8343

Comment by Dr. Krishna Kumari Challa 1 hour ago

Non-coding genes cause diabetes in babies, study reveals

Bi-allelic variants in the non-coding RNA genes RNU4ATAC and RNU6ATAC were identified as causes of syndromic monogenic autoimmune neonatal diabetes in 19 children. These mutations disrupt splicing and affect the expression of approximately 800 genes, many involved in immune function, highlighting the pathogenic potential of non-coding genomic regions in rare autoimmune diabetes.

Matthew B. Johnson et al, Bi-allelic variants in the non-protein-coding minor spliceosome components RNU6ATAC and RNU4ATAC cause syndromic monogenic autoimmune diabetes, The American Journal of Human Genetics (2026). DOI: 10.1016/j.ajhg.2026.02.017

Comment by Dr. Krishna Kumari Challa 1 hour ago

Non-coding genes cause diabetes in babies, study reveals

Bi-allelic variants in the non-coding RNA genes RNU4ATAC and RNU6ATAC were identified as causes of syndromic monogenic autoimmune neonatal diabetes in 19 children. These mutations disrupt splicing and affect the expression of approximately 800 genes, many involved in immune function, highlighting the pathogenic potential of non-coding genomic regions in rare autoimmune diabetes.

Matthew B. Johnson et al, Bi-allelic variants in the non-protein-coding minor spliceosome components RNU6ATAC and RNU4ATAC cause syndromic monogenic autoimmune diabetes, The American Journal of Human Genetics (2026). DOI: 10.1016/j.ajhg.2026.02.017

Comment by Dr. Krishna Kumari Challa 1 hour ago

Wildlife trade increases pathogen transmission: What 40 years of data say about spillover
Analysis of 40 years of wildlife trade data shows that traded wild mammals are 1.5 times more likely to share pathogens with humans than non-traded species, with risk increasing for illegally or live-traded animals. Each decade a species is present in trade adds, on average, one additional shared pathogen. These findings underscore the need for enhanced biosurveillance and reduced wildlife trade to limit zoonotic disease emergence.
Hedgehogs, elephants, pangolins, bears or fennec foxes: many wild species are sold as pets, hunting trophies, for traditional medicine, biomedical research, or for their meat or fur. These practices, whether legal or illegal, concern one-quarter of all mammal species. Now a study quantifies the impact of wildlife trade on the exchange of germs and parasites between animals and humans. The work, titled "Wildlife trade drives animal-to-human pathogen transmission over 40 years," appears in Science.
The team combined forty years of legal and illegal wildlife import-export data with compilations of host–pathogen relationships. Their analyses, led to the following result: Wild mammals that are traded are 1.5 times more likely to share infectious agents with humans than those that are not involved in trade.

In other words, these species have a 50% higher probability of sharing at least one virus, bacterium, fungus or parasite with us. That is not all: the risk is even higher when species are traded illegally or alive (for example as exotic pets).
The most striking finding, according to the research team, is that "the length of time an animal has been present in trade plays a key role: On average, a species shares one additional pathogen with humans for every ten-year period spent on the market.
The results of the study highlight the need to improve biosurveillance of animals and animal-derived products in order to detect infectious agents and assess their potential for transmission to humans.

Jérôme M. W. Gippet, Wildlife trade drives animal-to-human pathogen transmission over 40 years, Science (2026). DOI: 10.1126/science.adw5518. www.science.org/doi/10.1126/science.adw5518

Comment by Dr. Krishna Kumari Challa 1 hour ago

A 1.9 billion-year-old bedrock will soon house the world's first permanent nuclear waste site
Finland's Onkalo facility will be the world's first permanent deep geological repository for spent nuclear fuel, designed to isolate 6,500 tons of radioactive waste in stable bedrock for hundreds of thousands of years. The approach uses copper canisters and bentonite clay to contain radioactivity until it decays to safe levels, but uncertainties remain regarding long-term canister corrosion and future risks. Deep underground storage is considered safer than above-ground alternatives, though challenges persist in ensuring information preservation and minimizing risks to future generations.

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Comment by Dr. Krishna Kumari Challa 3 hours ago

CAR-T therapy drives remission in patient with three autoimmune diseases

For the first time, scientists have used a modern cell therapy called CAR-T to treat a patient with three different life-threatening autoimmune diseases that had resisted years of treatment. The patient, who once required daily blood infusions, has been in remission without needing additional treatment for a year since the CAR-T therapy. The case report, published in Med, suggests that CAR-T therapies can help treat complex and severe autoimmune diseases.
After being sick for more than a decade, the patient is now in treatment-free remission and able to return to an almost normal life. This therapy significantly improved her quality of life.

CD19 CAR-T therapy induces remission in refractory autoimmune hemolytic anemia with ITP and antiphospholipid syndrome, Med (2026). DOI: 10.1016/j.medj.2026.101075

Comment by Dr. Krishna Kumari Challa 3 hours ago

Lowering oxygen levels had a clear effect on the limbs of mouse embryos. Under reduced oxygen, mouse cells closed wounds faster and showed signs of entering a regenerative program. Stabilizing HIF1A produced similar effects, even when oxygen levels remained high.

Low oxygen also changed cell behavior, with skin cells becoming more mobile and altering their mechanical properties. Metabolism shifted toward glycolysis, a process that takes place in low-oxygen states. At the same time, chemical marks on DNA-associated proteins shifted to favor the activation of regeneration-related genes.

Frog tadpoles behaved differently. Their limbs regenerated efficiently across a wide range of oxygen levels, including levels well above those normally found in air. Molecular analysis showed that their cells maintain stable HIF1A activity even when oxygen increases, due to low expression of genes that normally shut this pathway down.

By comparing frogs, axolotls, mice, and human datasets, the team found a consistent pattern. Regeneration-competent amphibians show reduced oxygen-sensing capacity, allowing regenerative programs to be initiated and sustained. Mammals show the opposite pattern. Their cells respond strongly to oxygen and switch regenerative programs off soon after injury.
The results suggest that mammalian limbs retain latent regenerative potential at early stages, depending on how cells respond to environmental signals such as oxygen. This means that adjusting oxygen-sensing pathways might one day improve wound healing or regenerative responses in humans.

Species-specific oxygen sensing governs the initiation of vertebrate limb regeneration, Science (2026). DOI: 10.1126/science.adw8526

Part 2

Comment by Dr. Krishna Kumari Challa 3 hours ago

Why amphibians regenerate limbs but mammals cannot

Some animals can regrow lost body parts. Salamanders and frog tadpoles can rebuild entire limbs after amputation. Mammals cannot. For decades, biologists have tried to understand why. Now a research  team has discovered that oxygen plays a crucial role in limb regeneration. By comparing amputated limbs from frog tadpoles and embryonic mice, the researchers found that the way cells sense oxygen determines whether regeneration can even begin. The study is published in Science.

Limb regeneration begins with wound healing. After amputation, cells at the injury site must rapidly seal the wound and switch into regenerative cell types. In amphibians, this process runs smoothly. In mammals, it stalls early. Wound closure is slow and scar formation takes over, blocking regeneration.

One key difference lies in the environment. Amphibian larvae develop in water, where oxygen levels are lower than in the air. Moreover, many regeneration-competent species live in aquatic environments. Meanwhile, mammalian tissues are typically exposed to higher oxygen levels after injury.

What is unclear is whether this difference has played a direct role in regeneration or is merely a consequence of lifestyle.

The researchers amputated developing limbs from frog tadpoles and mouse embryos and cultured them outside the body under controlled oxygen conditions. Oxygen levels were lowered to match aquatic environments or raised to levels close to air.

They tracked how cells responded by measuring wound closure, cell movement, gene activity, metabolism, and epigenetic states, including changes to DNA packaging. The work focused on HIF1A, a protein that acts as a cellular oxygen sensor. When oxygen is low, HIF1A becomes stable and activates programs that set the stage for wound healing and regeneration.

Comment by Dr. Krishna Kumari Challa 3 hours ago

One DNA letter can trigger complete sex reversal

Researchers have discovered that changing just one letter in DNA can completely alter sex development in mice. In the new study, published in Nature Communications, a single-letter insertion in a non-coding regulatory region caused XX mice, which would normally develop as females, to develop instead as males with testis and male genitalia.

The finding is especially striking because the mutation was not made in a gene itself, but in a distant stretch of DNA that helps control a key developmental gene. The study highlights the major role of the non-coding genome—the 98% of DNA that does not make proteins but helps regulate when and how genes are turned on and off.
This is a remarkable finding because such a tiny change—just one DNA letter out of approximately 2.8 billion—was enough to produce a dramatic developmental outcome. It shows that non-coding DNA can have a profound effect on development and disease.

The mutation was introduced into a regulatory element known as Enh13, which controls the activity of Sox9, a gene essential for testis development. For ovaries to develop normally, Sox9 must be kept turned off. The researchers found that Enh13 acts as a kind of molecular battle site/switch: in males, factors that promote testis development bind to it and activate Sox9 whereas in females, factors that promote ovary development bind to it and repress Sox9.

When the researchers introduced the mutation using CRISPER genome editing, that female repression failed. As a result, Sox9 was activated in XX mice, and testis developed, leading to complete internal and external male development.

The team created several mouse models with very small mutations in Enh13, including a one-base-pair insertion and a three-base-pair deletion. Both mutations caused XX mice to develop testis. The researchers then used cell-line reporter assays to understand how the mutation disrupted the normal regulatory mechanism.

Nature Communications (2026). DOI: 10.1038/s41467-026-71328-9

Comment by Dr. Krishna Kumari Challa 4 hours ago

The 4 Minutes That Will Decide if Artemis II Astronauts Survive

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