Comment

Comment by Dr. Krishna Kumari Challa 15 hours ago

Birds are spreading plastic pollution

Gulls and other birds feeding at landfills ingest plastics and other debris, which they later regurgitate at roosting sites, including ecologically sensitive wetlands. In southern Spain, lesser black-backed gulls deposit an estimated 400 kg of plastics and over two tons of other waste annually into key habitats, contributing to microplastic pollution that threatens wildlife and can enter the human food chain.

https://theconversation.com/how-birds-are-spreading-plastic-polluti...

Comment by Dr. Krishna Kumari Challa 15 hours ago

This indeed turned out to be the case for Cnidarian body shape diversity. Based on experimental observations in six different species—two corals, two anemones, and two hydrozoans—the team came up with a list of three "mechanical modules." These modules can be combined to explain two important features of body shape—elongation and polarity.

Elongation is a measure of how stretched or compact a body is along its main axis. Polarity, on the other hand, describes how asymmetric the animal is—whether the top part of the animal, which contains the mouth, is wider or narrower than its base. By adjusting the values of the mechanical modules in their model, like tuning knobs, scientists arrived at different predictions for elongation and polarity. They called this combination, unique for each species, an organism's "mechanotype."

Mechanical changes ultimately arise from molecular changes, but the mechanotype is where that information becomes predictive of form.
Scientists think evolution acts on these modules to generate new forms.
Does this mean that changing the mechanotype would change the shape of the organism? To test this, the scientists performed a series of experiments using the sea anemone Nematostella. Nematostella larvae tend to be elongated and have a narrow oral end. When the scientists introduced genetic changes that affected one of the mechanical modules—nematic order—the larvae ended up being round instead of elongated.

Changing polarity was more difficult though; scientists had to perturb multiple modules simultaneously to get Nematostella to change its polarity to something that resembled another species, Aiptasia.

Together, these "reshaping" experiments showed it is possible to quantitatively predict and manipulate shape using mechanotypes and active surface models. They also demonstrated that different aspects of shape can be more or less complex in how they are determined by combinations of such mechanical modules.

Deciphering mechanical determinants of morphological evolution, Cell (2026). DOI: 10.1016/j.cell.2026.02.010. www.cell.com/cell/fulltext/S0092-8674(26)00175-3

Part 2

Comment by Dr. Krishna Kumari Challa 15 hours ago

Sea creatures reveal the physics behind animal body shape diversity
Variation in animal body shapes is determined by differences in mechanical tissue properties, termed "mechanotypes." In Cnidarians, three mechanical modules explain key shape features—elongation and polarity. Experimental manipulation of these modules in sea anemones confirmed that altering mechanotypes can predictably reshape organisms, highlighting the role of physical forces in morphological diversity.

Animals come in an extraordinary range of body shapes. A starfish looks nothing like an earthworm, a mouse, or a human. Yet even closely related species can appear radically different: corals, jellyfish, and sea anemones all belong to the same biological phylum, but their bodies take strikingly different forms. A new study by EMBL researchers appearing in Cell, shows how such shape diversity is determined by variation in mechanical tissue properties—an idea they termed "mechanotypes."
Genotype—the genetic composition of organisms—plays a central role during growth and development. But genes alone cannot fully explain how tissues bend, stretch, and reorganize to generate body shape—a process called morphogenesis.
Comparing genomes can reveal genetic differences linked to shape diversity, but genes cannot tell us how morphogenesis unfolds.
Even with a genome in hand, we still cannot yet predict the final shape of an organism.
Researchers drew on insights from mechanobiology—the study of how physical forces shape biological processes. During development, morphogenesis is often driven not by individual cells but by forces generated collectively within tissues. They hypothesized that this is the level where different body shapes arise across species.
What matters is how cells work together as a tissue to generate forces and mechanical constraints. If this is where morphogenesis operates, it may also be where shape diversity emerges across evolution, the researchers argue.
Connecting modern biological understanding of morphogenesis to Thompson's ideas of mechanical influences on diversity required cross-disciplinary collaboration. However, to build a framework that explains the physical underpinnings of this process, the study required expertise in theoretical physics and mathematics.
An important idea in physics is that when described on the right scale, emergent features of complex systems can be understood through models involving only a few key parameters.
Part 1

Comment by Dr. Krishna Kumari Challa 16 hours ago

Microbes make microplastics more likely to form ice in clouds, research reveals

Microplastics coated with microbial biofilms significantly increase the temperature at which ice forms in clouds by about 6.5 °C, enhancing ice nucleation more than microbes or plastics alone. This effect could alter cloud formation, precipitation patterns, and climate by changing how clouds interact with sunlight and heat, highlighting an unexpected link between plastic pollution and atmospheric processes.

Tiny pieces of plastic, called microplastics, are showing up everywhere, even in the water in clouds, rain, and snow—and they may be affecting our weather and temperatures. A study published in Environmental Science & Technology  found that microbes living on microplastics dramatically boost their ability to trigger ice formation in clouds.

In laboratory experiments, the microbial coating increased the temperature at which ice formed by about 6.5 degrees Celsius—a major shift in cloud physics.

To understand this effect, the researchers recreated what happens in nature. They placed microscopic plastic particles in controlled laboratory conditions and allowed naturally occurring bacteria to attach and grow on their surfaces. Over several days, the microbes formed a thin layer called a biofilm—a sticky coating that helps microbes anchor themselves and survive.

Team members then tested how easily these particles could trigger freezing using a specialized set up that slowly cooled tiny droplets of water containing microplastics. By monitoring when each droplet froze, they could measure how effective the particles were at initiating ice formation.

The results revealed something especially surprising. Microbes attached to microplastics were even more effective at forming ice than the same microbes floating freely in water. In other words, the plastic surface enhanced the microbes' ice-making ability.

This suggests that microplastics don't just carry microbes through the atmosphere—they help amplify their environmental effects, highlighting a surprising link between human pollution and natural systems.

Lingzhi Chu et al, Finer Particulate Matter Exposure Disparities Exist but Vary across Pollution Concentrations, Environmental Science & Technology (2026). DOI: 10.1021/acs.est.5c06203

Comment by Dr. Krishna Kumari Challa 16 hours ago

An immune signaling pathway drives pain in arthritis, researchers discover

Rheumatoid arthritis is a chronic autoimmune disease that affects millions of people worldwide. This disease prompts the immune system to mistakenly attack body tissues, particularly joints, leading to inflammation, swelling, stiffness and pain.

While arthritis has been widely studied, the molecular processes underpinning the pain experienced by most affected individuals remain poorly understood. Physical pain is known to be experienced via sensory neurons, specialized cells that carry signals from body tissues to the brain.

Researchers 

 recently studied a mouse model of arthritis with the aim of better understanding how the activity of immune cells influences nerve cells, potentially contributing to the pain experienced by patients with arthritis.

Their findings, published in Nature Neuroscience, uncovered a sequence of chemical reactions that occur inside nerve cells when they receive signals from immune cells (i.e., a signaling pathway) that could drive the pain linked to arthritis.

In their experiments, the researchers induced arthritis-like symptoms in mice using cartilage autoantibodies, proteins that are generally produced by the immune system that attack joint tissues. They then examined nerve cells located along the mice's spinal nerves outside of their spinal cord, in a region known as the dorsal root ganglion.

Cells in this region transmit sensory information, including painful sensations, from the body to the central nervous system (CNS). The team observed these cells as damage to the animal's joints progressed and became more pronounced.

These experimental strategies combined showed convincingly that interferon signalling drives pain in arthritis in the animal model.

During early stages of the arthritis they induced in mice, the team observed an increased activation of immune cells located close to sensory nerves. They also found that immune cells released large amounts of cytokines (i.e., signaling proteins via which immune cells communicate), leading to a severe inflammatory response known as a cytokine storm.

Throughout the course of the disease, they also observed high levels of interferons, proteins that help the immune system to fight viruses and other diseases. Notably, a similar presence of interferons was also detected in patients diagnosed with arthritis.

The researchers' experiments led to the discovery of a signaling pathway via which pain-sensing neurons become excessively active. By blocking this pathway with pharmacological drugs, the team was able to improve limb function and lower the pain experienced by mice.

Jie Su et al, Persistent interferon signaling causes sensory neuron plasticity and pain before and during arthritis, Nature Neuroscience (2026). DOI: 10.1038/s41593-026-02234-y.

Comment by Dr. Krishna Kumari Challa 16 hours ago

Stress-activated pathway reveals how nervous system contributes to eczema flare-ups

The mystery of how stress exacerbates atopic dermatitis, more commonly known as eczema, may be closer to being understood. A new study published in the journal Science has identified a specific nerve pathway that helps explain the link.

Eczema is a chronic condition that causes dry, itchy skin. It is common in children but can occur at any age, often triggered by environmental irritants, genetic factors, or an overactive immune system. And stress has long been known to make it worse.

To discover exactly how anxious feelings contribute to the intense itching and skin redness characteristic of eczema, researchers studied both human patients and specialized mouse models.

First, they conducted a retrospective analysis of 51 patients who were already diagnosed with eczema. They asked them to complete a questionnaire that categorized their stress levels, measured the intensity and extent of the condition, and took blood samples and biopsies to count different types of immune cells.

They discovered that the higher a person's stress levels, the more eosinophils (a type of white blood cell that triggers and contributes to inflammation and itching) they had, and the worse their eczema was.

To determine whether stress was the cause of these flare-ups, the research team studied mice with eczema like skin and exposed them to various stressful situations, such as being placed on a high platform. Just like human patients, there was a significant increase in eosinophils and more severe skin damage.

Next, the scientists genetically engineered mice to have fewer eosinophils or to lack a specific subset of sympathetic nerve cells known as Pdyn+ neurons that are activated by stress.

Unlike other sympathetic nerves, these connect directly to the skin. When either eosinophils or stress nerves were absent, stress no longer worsened the inflammation. This confirmed that both must be present for a stress-induced flare-up to happen.

Using advanced mapping techniques, the researchers discovered that these nerves sent a direct signal to call inflammatory cells to the skin's surface during stressful moments. Specifically, neurons release a protein called CCL11 that attracts eosinophils to the inflamed skin tissue where an eczema flare-up is occurring.

Once there, the nerves release another signal that triggers these cells to release proteins that cause the skin to become red and swollen.

"These findings reveal a neuroimmunological mechanism underlying psychological stress–induced exacerbation of dermatitis, emphasizing the Pdyn+ sympathetic-eosinophil axis as a crucial interface between the brain and skin inflammation, with potential therapeutic implications," commented the study authors in their paper.

Jiahe Tian et al, A sympathetic-eosinophil axis orchestrates psychological stress to exacerbate skin inflammation, Science (2026). DOI: 10.1126/science.adv5974

Comment by Dr. Krishna Kumari Challa 16 hours ago

Fuel Revolution: Pune’s NCL Scientists Develop DME as a Clean, Indigenous Alternative to LPG

Comment by Dr. Krishna Kumari Challa yesterday

Ultra-processed foods linked to infertility in US women

Higher intake of ultra-processed foods is associated with lower odds of fertility in US women, independent of age, weight, and lifestyle factors. Women reporting infertility consumed more ultra-processed foods and adhered less to the Mediterranean diet. Chemical exposures from processed foods, such as phthalates and BPA, may contribute to this association.

Angelina Baric et al, Ultra-processed food intake and Mediterranean diet adherence in relation to fertility status in U.S. women: Findings from NHANES 2013–2018, Nutrition and Health (2026). DOI: 10.1177/02601060261433154

Comment by Dr. Krishna Kumari Challa yesterday

Newly-discovered dopamine signal may help the brain steer us in the right direction
A distinct dopamine signal in the striatum encodes trajectory errors, indicating whether movement is directed toward or away from a goal, independent of classic reward-related dopamine responses. This guidance signal, triggered by visual cues and scaling with movement speed, operates alongside value signals in orthogonal spatial gradients, supporting real-time behavioural adjustments.

A Boston University-led research team has discovered a dopamine signal in the brain that helps determine whether you are moving toward or away from a goal, potentially shedding new light on how the brain uses visual information to guide behaviour
.The work shows that when mice encounter visual cues, dopamine in the striatum, located in the basal ganglia, encodes "trajectory errors," or signals that indicate whether the mice's current direction and speed are carrying them toward or away from its goal. These "guidance signals" operate independently from dopamine's classic reward value responses and arise from different sensory and motor inputs.

The findings offer insight into how the brain uses environmental cues to steer behavior and could inform the development of more targeted therapies for conditions involving dopamine dysfunction, including Parkinson's disease, addiction, OCD, and ADHD.
This discovery reveals that dopamine isn't just about how valuable something is.
It's also about whether you're headed the right way. It's a guidance signal, one that tells the brain to keep going or make a correction.

Eleanor H. Brown et al, Striatum-wide dopamine encodes trajectory errors separated from value, Nature (2026). DOI: 10.1038/s41586-025-10083-1

Comment by Dr. Krishna Kumari Challa on Thursday

Space supercharges anti-bacterial viruses

Viruses that infect bacteria, called phages, evolve different strategies to infect their targets on the International Space Station than they do on the ground, which could help create new treatments for antibiotic-resistant infections. Researchers found that the phages took longer to infect E.coli in microgravity, and that the viruses developed microgravity-specific mutations, some of which helped them to better cling onto bacterial receptors. Once they returned to earth, they were able to kill stubborn strains of E.coli responsible for urinary tract infections that tend to be resistant to bacteriophages.

https://journals.plos.org/plosbiology/article?id=10.1371/journal.pb...

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