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Comment by Dr. Krishna Kumari Challa on June 3, 2026 at 2:54pm

UN warns world to prepare for El Nino extreme weather

There is an 80% probability of El Niño developing between June and August, with a likelihood near or above 90% by November. El Niño is expected to cause above-normal global temperatures and increase the risk of extreme weather events, including drought, heavy rainfall, and heat waves. Climate change does not increase El Niño frequency or intensity but can amplify its impacts. Regional forecasts indicate drier and warmer conditions in parts of Africa, South Asia, and Central America.

News Agencies

Comment by Dr. Krishna Kumari Challa on June 3, 2026 at 2:52pm

Cutting a photon in two creates an infinite swarm of particles
Attempting to split a single photon using a fast optical shutter does not yield two smaller photons but instead generates a quantum superposition containing infinitely many photons due to disturbances in the electromagnetic field's quantum fluctuations. Locally, the system appears unchanged, but globally, the quantum state becomes highly complex, illustrating the non-classical behaviour of quantum particles.

Isak Cecil Onsager Rukan et al, Truncated photon, Physical Review Letters (2026). DOI: 10.1103/94pm-hp34. On arXiv: arxiv.org/abs/2510.21636

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Embryonic tissues can behave like fluids or solids to reshape cell fate signals Tissue rigidity in embryonic development is actively regulated by cell-cell adhesion, not cell density, enabling transitions between fluid-like and solid-like states. Increased adhesion induces tissue stiffening, which restricts morphogen diffusion, spatially localizing developmental signals such as Nodal and influencing cell fate. Morphogen signaling can also enhance local tissue rigidity, creating a feedback loop between mechanical and biochemical processes.

Rustarazo-Calvo, L., et al. Adhesion-driven rigidity transition decoupled from density-driven jamming triggers epithelial organization in embryonic tissues., Nature Physics (2026). DOI: 10.1038/s41567-026-03276-6

Camilla Autorino et al, Tissue rigidity phase transition shapes morphogen gradients, Nature Cell Biology (2026). DOI: 10.1038/s41556-026-01954-4

Comment by Dr. Krishna Kumari Challa on June 3, 2026 at 2:48pm

Exploding immune cells that kill surrounding tissue

 Scientists have discovered a new type of immune cell that kills surrounding cells via explosion—a cellular detonation so fast and complete that the cell vanishes within minutes, leaving no trace behind. This discovery comes from an unlikely source: planarian flatworms. These aquatic, slithering pancake versions of worms are famous for their ability to survive dismemberment and grow whole new organisms from the sliced-up segments of their formerly unified body. Understanding how these flatworms' immune systems have managed to endure for hundreds of millions of years could hold important insights for modern medicine.

In a new study published June 2 in Cell, the team describes the discovery and names these new cells "ruptoblasts" for their explosive response to a certain hormone.

A postdoctoral researcher first observed these cells while investigating the long-standing mystery in flatworm biology of whether or not they can tell the difference between their own tissues and those of another individual. To find out, she longitudinally sliced the flatworms and fused them together with a separate worm. Although adept at regrowing their own tissues, the researcher noted that these "Frankenstein" worms rejected halves of other worms, similar to how a human body may reject an organ transplant from a donor.

Unlike humans, however, a different cellular defense mechanism sprang into action.

It's this huge inflammatory response. Like there's a fire and an alarm goes off, and the cells just blow up.

Some mammalian cells and bacteria may also do an explosive sort of cell death, but the timescale is really long. They are exploding, but it's more like pores that slowly leak things out over the course of several hours. Ruptosis happens within seconds to minutes.

In a matchup against E. coli bacteria, human kidney cells, and mouse blood cells, ruptoblasts destroyed all three. Yet the authors noted that cell fatalities were limited to the immediate area of the explosion and did not trigger any sort of chain reaction or lingering toxicity. This localized effect holds promise for targeted treatments of bacterial infections or tumours.

Another characteristic that sets ruptoblasts apart from other immune cells, like T-cells or neutrophils, is the fact that they are glandular cells rather than hematopoietic cells, or blood cells produced in the bone marrow. The ruptoblasts seem to figure out a way to amplify their secretion machinery to suddenly and violently release cytotoxic substances in response to activin. A sharp increase in calcium from the endoplasmic reticulum within the ruptoblast helps facilitate the ruptosis.

In searching for these cells in other organisms,  the researchers discovered that they only appear in basal bilaterians like the flatworms, which points to these cells having early evolutionary origins.

The reason these cells were filtered out of modern vertebrate immune systems could be because vertebrates lack the ability to repair other cells after ruptosis occurs, unlike flatworms that are rich in stem cells.

Explosive cytotoxicity of ruptoblasts bridges hormone surveillance and immune defense, Cell (2026). DOI: 10.1016/j.cell.2026.05.008. www.cell.com/cell/fulltext/S0092-8674(26)00567-2

Comment by Dr. Krishna Kumari Challa on June 2, 2026 at 12:56pm

A common food compound may hold the key to shutting down leaky gut damage

When the intestinal lining breaks down, harmful gut bacterial antigens can slip into the bloodstream alongside nutrients. This breach in the gut's protective barrier, known as "leaky gut," is more than a digestive issue—it's a sign of inflammatory bowel disease (IBD) and has been increasingly linked to a number of chronic conditions.
A team of researchers has uncovered a key mechanism underlying leaky gut and identified a promising and natural way to repair it. And a potential solution is already in many of the foods we eat every day.

In a study published in the journal Nature Communications, the team shares how phytic acid (or InsP6), a natural compound found in whole grains, beans, lentils, nuts, and seeds, plays an important role in maintaining the integrity of the intestinal barrier.

Phytic acid is something many people already consume daily, especially in plant-rich diets.It's beyond just a dietary component; it also functions as a biologically active molecule that supports gut health.
Phytic acid (InsP6), a compound found in whole grains, beans, lentils, nuts, and seeds, directly activates histone deacetylase 3 (HDAC3), a regulator essential for maintaining intestinal barrier integrity. This mechanism protects against gut barrier breakdown and inflammation associated with leaky gut and inflammatory bowel disease, suggesting potential for targeted supplementation therapies.

Sujan Chatterjee et al, Phytic acid (InsP6) activates HDAC3 epigenetic axis to maintain intestinal barrier function, Nature Communications (2026). DOI: 10.1038/s41467-026-68994-0

Comment by Dr. Krishna Kumari Challa on June 2, 2026 at 12:52pm

One-time gene editing treatment lowers 'bad' cholesterol by up to 62%
A single infusion of the gene editing therapy VERVE-102 reduced LDL cholesterol by up to 62% in adults with inherited high cholesterol or premature coronary artery disease, with effects lasting up to 18 months. No serious adverse events were observed at the highest dose, and only mild, transient infusion reactions and liver test changes occurred. Larger studies are ongoing to confirm safety and efficacy.

Scott B. Vafai et al, In Vivo Base Editing of PCSK9 with VERVE-102 for Hypercholesterolemia, New England Journal of Medicine (2026). DOI: 10.1056/nejmoa2601283

Comment by Dr. Krishna Kumari Challa on June 2, 2026 at 12:50pm

some chikungunya virus infections may turn chronic

Chikungunya virus, which is transmitted to people by infected Aedes mosquitoes and characterized by high fever and intense joint swelling and pain, has made a resurgence in many countries around the world in recent years.

Researchers estimate that about half of people infected with chikungunya virus will progress to a chronic form of the disease and experience relapsing arthralgia and arthritis that can span years and currently has no treatment.
Chikungunya virus can persist in joint-associated macrophages, which act as reservoirs, leading to chronic joint pain and inflammation in about half of infected individuals. Advanced sequencing techniques identified these macrophages as harbouring viral RNA, and antiviral treatment targeting viral replication reduced chronic inflammation, indicating persistent infection in these cells drives chronic symptoms.

Kristen M. Zarrella et al, Chikungunya virus persists in joint-associated macrophages and promotes chronic disease in mice, Nature Microbiology (2026). DOI: 10.1038/s41564-026-02303-9

Comment by Dr. Krishna Kumari Challa on June 2, 2026 at 12:35pm

The Y chromosome is home to surprising jumping genes

The humble Y chromosome may be the smallest chromosome in the mammalian genome (and getting even smaller), but it is mighty: Genes on the Y chromosome are critical for fertility in males.

In a new study in the journal Current Biology, researchers have studied deer mice to outline how the Y chromosome defends itself against decay by acquiring gene families, holding its own to maintain fertility.
A gene family named Phf8y was identified on the Y chromosome of deer mice, originating from the X-linked Phf8 gene via transposable element-mediated duplication. This represents a rare case of a gene moving from the X chromosome to an autosome and then to the Y chromosome. Such gene acquisitions may help the Y chromosome maintain essential functions for male fertility and contribute to the evolutionary stability of sex ratios.

Autosomes are all of the chromosomes that aren't the sex chromosomes. However, the Y chromosome is often thought of as a place where genes go to die because its genes don't recombine.
In this study, researchers discovered a gene family, which they named Phf8y, that bucked this trend, hopping to the Y and duplicating itself.
It's a unique pattern that they didn't expect—having a gene move from the X chromosome to an autosome to the Y chromosome.
What's driving the process? In the production of sperm, the X chromosome from the maternal side and the Y chromosome from the paternal side result in a sperm cell that has either an X or Y chromosome.

During this period, the X serves as a sort of autosome for genes important for viability and spermatogenesis, Mueller explains.
But since males carry just one X, an alternative method arose evolutionarily to provide a way to back up important genes for creating sperm.
It's like having your own clone around who can jump in when you've gone on vacation.
There are genes that copy themselves, called transposable elements. They hide out in our genome and are activated on rare occasions. In fact, these so-called jumping genes make up half of the human genome.

The team discovered that the deer mouse Phf8y on the Y chromosome is derived from the X-linked Phf8, apparently having hijacked the transposable element machinery to make an extra copy of itself.

What Phf8y is doing is still a mystery.

The team speculates that this gene on the Y chromosome is involved in chromatin packing, or how DNA is packaged, and could confer an edge to Y-bearing sperm to compete with X-bearing sperm.

Previous studies in house mice have revealed genes that share similar features to Phf8y and are in an X–Y arms race.

Ivan F. Mier et al, An X-to-autosome-to-Y chromosome amplified retrogene family functions in spermatids, Current Biology (2026). DOI: 10.1016/j.cub.2026.04.045

Comment by Dr. Krishna Kumari Challa on June 2, 2026 at 12:28pm

Wounds may trigger 'aged' cells within hours, reshaping how senescence starts
Cells can enter senescence within minutes to hours after injury, using pre-existing mRNA to rapidly produce p21 protein, independent of new gene transcription. This early senescence actively coordinates wound healing by releasing signaling molecules and guiding cell migration, but is beneficial only during a narrow time window and is eliminated after healing. Persistent senescent cells are linked to age-related diseases.

Karla Valdivieso et al, Transcription-independent induction of rapid-onset senescence is integral to healing, Nature Cell Biology (2026). DOI: 10.1038/s41556-026-01948-2

Comment by Dr. Krishna Kumari Challa on June 2, 2026 at 12:14pm

AI is making journalistic language more repetitive and predictable—and it's a problem for all of us
Increased use of AI-generated text in journalism leads to more repetitive, predictable, and homogenized language, reducing linguistic diversity and innovation. This shift limits the press's traditional role in introducing new vocabulary and nuanced expression, potentially reinforcing existing biases and diminishing the public's capacity for precise communication and debate. Mixing synthetic and human-generated text can mitigate these effects, but large-scale replacement of human writing risks long-term decline in public language richness.

original article.

Comment by Dr. Krishna Kumari Challa on May 31, 2026 at 9:57am

Despite such striking results, reprogramming the immune system is no simple matter. In early treatment of cancer patients, CAR T cells produced life-threatening side effects, as outlined in a 2026 article in the Annual Review of Medicine. As CAR T cells attack their targets, the associated inflammation can cause symptoms like high fevers and low blood pressure. If that inflammation reaches the brain, it can cause additional problems such as confusion and drowsiness.

Fortunately, physicians now have a decade's worth of experience recognizing and treating these problems. They're certainly reversible and don't cause long-term damage most of the time.
Physicians and patients also must contend with decreased immunity as both a side effect of the treatment and its desired outcome. In CAR T treatment, doctors typically use powerful chemotherapy drugs to temporarily reduce the body's immune cell population to make room for the new, engineered cells, leaving patients temporarily immunosuppressed. And if the treatment works, it will decimate B cell populations. Patients can be vulnerable to infections for up to a year after treatment.
These effects are manageable with preventive antibiotics, antivirals and vaccines. Patients also retain antibodies that their B cells made before the treatment, which provide residual protection for a few months. And for reasons that are not yet fully understood, CAR T seems to leave older B cells, which provide immune memory of past infections, intact in some cases. One study found that autoimmune patients treated with CAR T still made antibodies for diseases they'd been previously vaccinated against, like chicken pox and measles. These are signs that the treatment did not completely return the immune system to its factory settings.

When evaluating CAR T risk, it's important to consider that many existing treatments for autoimmune disease also suppress the immune system for as long as a person takes them, experts note.
Researchers are already working on second- and third-generation versions of CAR T that they expect to be safer for both cancer and autoimmunity.

Source: https://knowablemagazine.org/content/article/health-disease/2026/ca...

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