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Comment by Dr. Krishna Kumari Challa 2 hours ago

Fixate on the cross and you will see the moving grey circle become purple. Credit: Communications Psychology (2025). DOI: 10.1038/s44271-025-00331-5

Comment by Dr. Krishna Kumari Challa 2 hours ago

Demystifying a visual illusion: Why we see color that's not there

A new discovery has unraveled why we sometimes see colors that aren't there. The phenomenon of "color afterimages" is when you see illusory—or false—colors after staring at real colors for a longer time. Through this, the brain can be tricked into seeing color in a black and white image.

The cause of this illusion is the mechanism that allows us to see colors the same throughout the day, independently of light changes. Without it, the color of the world would change as we are under yellow sunlight, a green canopy, or in a bluish shadow.

Scientists have long debated what causes color afterimages, and how the brain creates them.

Researchers found the missing link between the illusory colors we see and the neural mechanisms that produce them. The answer is in the cone cells in our eyes.

We've finally got a conclusive answer—color afterimages are not opposing colors as everybody had thought. Instead, those illusory colors reflect precisely what happens in the cone photoreceptors.

Across all the experiments, researchers found the same thing—afterimages are not caused by opposing colors, as many scientists have thought. Instead, they match what we'd expect if they were caused by how cone cells in the eye adapt to light.

So,  now it is certain that afterimages come from cone cells and not from other parts of the visual system.

Christoph Witzel, The non-opponent nature of colour afterimages, Communications Psychology (2025). DOI: 10.1038/s44271-025-00331-5

Part 1

Comment by Dr. Krishna Kumari Challa 2 hours ago

Time-restricted eating without calorie cuts doesn't improve metabolic health, study finds

Contrary to common assumptions, a new study  shows that intermittent fasting (time-restricted eating) with an unchanged calorie intake does not lead to measurable improvements in metabolic or cardiovascular parameters but does shift the body's internal clocks. Prof. Olga Ramich and her team published the results of the ChronoFast study in the journal Science Translational Medicine.

Time-restricted eating (TRE) is a form of intermittent fasting characterized by a daily eating period of no longer than 10 hours and a fasting period of at least 14 hours. TRE is increasingly popular as a simple dietary strategy for weight control and metabolic health improvement. In rodents, TRE protects against diet-induced obesity and related metabolic dysfunctions.

Similarly, TRE studies in humans have suggested numerous positive cardiometabolic effects, such as improved insulin sensitivity, glucose, triglyceride, and cholesterol levels, as well as moderate reductions in body weight and body fat. Consequently, TRE is considered a promising approach to combat insulin resistance and diabetes.

Results of previous TRE trials have been partly contradictory and have not yet clarified whether the metabolic improvements are due to the restriction of daily eating duration, due to spontaneous calorie restriction, or due to the combination of both factors. In fact, most previous studies have not carefully monitored energy intake or other potential confounding factors.

Therefore, this new study investigated whether an eight-hour eating period could improve insulin sensitivity and other cardiometabolic parameters in a tightly controlled isocaloric environment in the ChronoFast trial.

Contrary to previous studies suggesting positive effects of TRE, the ChronoFast study shows no clinically relevant changes in insulin sensitivity, blood sugar levels, blood fats, or inflammatory markers, at least following this relatively short two-week intervention. These results suggest that the health benefits observed in earlier studies were likely due to unintended calorie reduction, rather than the shortened eating period itself, explain the researchers. 

Although the participants showed no marked metabolic improvements, the study of the internal clock in blood cells revealed that TRE influenced the circadian phase in blood cells and the sleep timing. The internal clock was, on average, shifted back by 40 minutes after the lTRE intervention compared to the eTRE intervention, and participants who followed the lTRE intervention went to bed and awaked later. The timing of food intake acts as a cue for our biological rhythms—similar to light, the researchers say. 

The results underscore that calorie reduction plays a central role in the health benefits of intermittent fasting. 

Beeke Peters et al, Intended isocaloric time-restricted eating shifts circadian clocks but does not improve cardiometabolic health in women with overweight, Science Translational Medicine (2025). DOI: 10.1126/scitranslmed.adv6787

Comment by Dr. Krishna Kumari Challa 3 hours ago

Decoding how cells choose to become muscles or neurons

Every cell in the body has the same DNA, but different cell types—such as muscle or brain cells—use different parts of it. Transcription factors help cells activate specific genes by reading certain DNA sequences, but since these sequences are common across the genome, scientists have long wondered how the factors know exactly where to bind.

Researchers  set out to address this question by looking at two closely related transcription factors—NGN2 and MyoD1—that steer cells toward becoming neurons and muscle cells, respectively. Using stem cells, they switched these transcription factors on one at a time and watched where they attached to the DNA and how they influenced gene expression.

They found that the binding of transcription factors to the DNA molecule depends not only on the DNA sequence but also on how open the DNA is and which partner proteins are present. Sometimes, transcription factors act as "pioneer factors" and are able to open tightly packed DNA at specific sites to turn on genes. Small DNA changes—sometimes just one letter—and the proteins these factors partner with can affect whether genes are activated.

Next, the team trained a machine learning model to recognize patterns in transcription factor binding. Using this model, they identified a "DNA language" that predicts where and how these factors bind. The model accurately predicted outcomes across different cell types, helping explain how similar transcription factors can guide distinct developmental trajectories.

The findings not only deepen our understanding of how transcription factors drive cell fates, but they also offer powerful tools to predict and possibly steer these decisions in development and disease, the researchers say.

Sevi Durdu et al, Chromatin-dependent motif syntax defines differentiation trajectories, Molecular Cell (2025). DOI: 10.1016/j.molcel.2025.07.005

Comment by Dr. Krishna Kumari Challa 4 hours ago

Large language models still struggle to tell fact from opinion, analysis finds

Large language models (LLMs) may not reliably acknowledge a user's incorrect beliefs, according to a new paper published in Nature Machine Intelligence. The findings highlight the need for careful use of LLM outputs in high-stakes decisions in areas such as medicine, law, and science, particularly when belief or opinions are contrasted with facts.

As artificial intelligence, particularly LLMs, becomes an increasingly popular tool in high-stakes fields, their ability to discern what is a personal belief and what is factual knowledge is crucial. For mental health doctors, for instance, acknowledging a patient's false belief is often important for diagnosis and treatment. Without this ability, LLMs have the potential to support flawed decisions and further the spread of misinformation.

Researchers analyzed how 24 LLMs, including DeepSeek and GPT-4o, responded to facts and personal beliefs across 13,000 questions. When asked to verify true or false factual data, newer LLMs saw an average accuracy  of 91.1% or 91.5%, respectively, whereas older models saw an average accuracy of 84.8% or 71.5%, respectively.

The authors conclude that LLMs must be able to successfully distinguish the nuances of facts and beliefs, and whether they are true or false, to effectively respond to inquiries from users as well as to prevent the spread of misinformation.

Mirac Suzgun et al, Language models cannot reliably distinguish belief from knowledge and fact, Nature Machine Intelligence (2025). DOI: 10.1038/s42256-025-01113-8. On arXiv: DOI: 10.48550/arxiv.2410.21195

Comment by Dr. Krishna Kumari Challa 5 hours ago

In the new study, the team moved on to testing out this method on in vitro human cells from adults aged 41 and 55 years old. To do this, they engineered a harmless virus, capable of expressing human CCNA2 and delivered it to the cultured cells. They then performed live-cell imaging to track cell division and structure. Finally, they performed RNA sequencing in mouse and human heart samples to analyze any changes in gene expression.

The results were promising—CCNA2 induced heart cell regeneration in the 41 and 55-year-old heart cells, reactivating the fetal-like and regenerative gene programs in the cells. They found that the resulting daughter cells retained heart muscle structure and function, and continued to handle calcium effectively.

Additionally, RNA sequencing in mice revealed a subpopulation of heart cells with active cell division and reprogramming gene signatures, even after CCNA2 expression.

"Taken together, these findings suggest that the partial reprogramming induced by CCNA2 reflects a controlled activation of developmental programs, consistent with regenerative responses observed in neonatal hearts, and aligns with prior evidence that modest increases in cell cycle gene expression can enhance cardiac regeneration capacity," the study authors write in their paper.

Esmaa Bouhamida et al, Cyclin A2 induces cytokinesis in human adult cardiomyocytes and drives reprogramming in mice, npj Regenerative Medicine (2025). DOI: 10.1038/s41536-025-00438-7

Part 2

Comment by Dr. Krishna Kumari Challa 5 hours ago

Reactivating a fetal gene enables adult heart cells to regenerate after injury

Around the globe, heart disease remains one of the top causes of death. Once patients begin to suffer from serious heart problems, like heart attacks and heart failure, the heart muscles become damaged and are difficult to treat and repair. Although many therapies have been developed to treat symptoms, full recovery to a pre-disease state has been essentially impossible. This is due to a lack of regeneration ability in adult human heart cells. Studies using stem cells or progenitor cells for repair have demonstrated limited efficacy in clinical trials, thus far.

However, there may be new hope for these patients. Researchers have been working to turn back time by switching on a gene known to regenerate heart muscle cells, or cardiomyocytes. Their study, recently published in npj Regenerative Medicine, indicates that adult human hearts may be given the ability to regenerate themselves with future therapies.

The study focuses on a gene called Cyclin A2 (CCNA2), which is functional during fetal growth and shuts off shortly after birth, limiting the ability for cell regeneration. In fetuses, while CCNA2 is still functional, it plays an important role in cell division and growth, facilitating the creation of new heart cells. However, adults appear to still have a very limited capacity for repair.

"There has been evidence of low-level cardiomyocyte turnover in the healthy human heart, but it is very limited, and this ability declines with age. Thus, cardiac regeneration in response to injury such as myocardial infraction (MI) remains a clinical challenge," the researchers write.

The study authors refer to CCNA2 as the "master regulator" of the heart cell cycle. So far, studies surrounding CCNA2—mostly in animal models—have shown promise in its ability to be switched back on.

Part 1

Comment by Dr. Krishna Kumari Challa yesterday

A research team has now found that hydrogen sulfide (H₂S), a small, naturally occurring gas, could be developed into a promising new treatment.
Previous work has shown that it penetrates the nail plate far more efficiently than existing topical drugs, and now the team has demonstrated that it has strong antimicrobial activity against a wide range of nail pathogens, including fungi that are resistant to common antifungal treatments.

In laboratory tests, the team used a chemical that breaks down to release the hydrogen sulfide gas and found that it acts in a unique way, disrupting microbial energy production and triggering irreversible damage, ultimately killing the fungi.

Fritz Ka-Ho Ho et al, Antimicrobial effects and mechanisms of hydrogen sulphide against nail pathogens, Scientific Reports (2025). DOI: 10.1038/s41598-025-22062-7

Part 2

Comment by Dr. Krishna Kumari Challa yesterday

'Rotten egg' gas could be the answer to treating nail infections, say scientists

Hydrogen sulfide, the volcanic gas that smells of rotten eggs, could be used in a new treatment for tricky nail infections that acts faster and with fewer side effects, according to scientists.

Hydrogen sulfide (H2S) demonstrates strong antimicrobial activity against a range of nail pathogens, including drug-resistant fungi, and penetrates the nail plate more effectively than current topical treatments. Laboratory results indicate it disrupts microbial energy production, causing irreversible damage. A topically applied H2S treatment may offer a faster, safer alternative for nail infections.

Nail infections are mostly caused by fungi and occasionally by bacteria. They are very common, affecting between 4 and 10% of the global population, rising to nearly half those aged 70 or over. These infections can lead to complications, particularly in vulnerable groups such as diabetics and the elderly, but are notoriously difficult to treat.
Current treatments include oral antifungals taken in pill form, and topical treatments applied directly to the nail. Oral antifungals take around 2–4 months to act and are reasonably effective, but they carry risks of side effects, especially in patients with other medical conditions.

Treatments applied directly to the nail are safer, but they often take much longer to work, sometimes taking even years to work, and they frequently relapse or fail. This is largely because it's very difficult to get the drug to penetrate through the nail to where the infection resides.

Even the most effective topical treatments have relatively low cure rates, so there is a clear need for new therapeutic approaches that are safe, effective, and capable of reaching microbes embedded deep within the nail.
Part 1

Comment by Dr. Krishna Kumari Challa yesterday

Tissue 'tipping points': How cells collectively switch from healthy to disease states

Cells convert mechanical forces into signals that influence physiological processes, such as exercise strengthening bones. A research team has discovered that biological tissues can also undergo dramatic phase transitions, or collective shifts where wound healing cells can switch from disordered, healthy states to highly coordinated disease states, like when water suddenly freezes into ice.

This discovery, published Oct. 3, 2025, in Proceedings of the National Academy of Sciences, reveals why fibrotic diseases often progress in switch-like jumps rather than gradually and points to new therapeutic strategies that target the physical properties of tissue rather than just cellular biochemistry.

The team used computational modeling to uncover the mechanical "tipping point" that determines whether cells can collectively coordinate to spread a disease called fibrosis, an excessive scarring that underlies failure of nearly any organ, and especially in diseases of the liver, lungs, kidneys and heart.

What they have shown is that this isn't a gradual process.

There's a sharp transition point. When cells are within a critical spacing that depends on the way their matrix deforms, they can 'talk' to each other mechanically through the matrix. Above it, they're effectively isolated, and below it they interact strongly with one another. This on-off switch behavior is what we see in fibrosis progression: periods of stability followed by rapid scarring.

Phase transitions are familiar in physics: Water freezes to ice at 0°C, and iron becomes ferromagnetic below 770°C. The new research demonstrates that living tissues show similar behavior. When cells are spaced far apart in a tissue, they act independently, but when cell density crosses a critical threshold—a few hundred micrometers apart—they begin communicating mechanically and acting in concert, dramatically compacting and stiffening the tissue.

The research shows why this phase transition occurs: Fibrous networks like collagen enable long-range mechanical communication in a way that uniform elastic materials cannot.

Collagen fibers can be recruited and aligned by cell forces, creating stiffened 'tension bands' that act as mechanical communication highways, transmitting signals over much longer distances.

The critical factor is what the researchers call the "critical stretch ratio," which is how much the collagen must be stretched before individual fibers align and stiffen. This property is determined by collagen crosslinking, which increases with aging and is influenced by factors like diet, advanced glycation end products, and metabolic diseases like diabetes.

 Xiangjun Peng et al, Fiber recruitment drives a phase transition of cell polarization at a critical cell spacing in matrix-mediated tissue remodeling, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2514995122

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