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Comment by Dr. Krishna Kumari Challa on October 8, 2025 at 8:57am

Nobel Prize in physics goes to 3 scientists whose work advanced quantum technology (Update)

Three scientists won the Nobel Prize in physics this week for research on the strange behavior of subatomic particles called quantum tunneling that enables the ultra-sensitive measurements achieved by MRI machines and lays the groundwork for better cellphones and faster computers.

The work by John Clarke, Michel H. Devoret and John M. Martinis, took the seeming contradictions of the subatomic world—where light can be both a wave and a particle and parts of atoms can tunnel through seemingly impenetrable barriers—and applied them in the more traditional physics of digital devices. The results of their findings are just starting to appear in advanced technology and could pave the way for the development of supercharged computing.

The prize-winning research in the mid-1980s took the subatomic "weirdness of quantum mechanics" and found how those tiny interactions can have real-world applications.

The experiments were a crucial building block in the fast-developing world of quantum mechanics.

Nobel committee announcement:

The Royal Swedish Academy of Sciences has decided to award the Nobel Prize in Physics 2025 to

John Clarke, University of California, Berkeley, U.S.

Michel H. Devoret, Yale University, New Haven, CT and University of California, Santa Barbara, U.S.

John M. Martinis, University of California, Santa Barbara, U.S.

"for the discovery of macroscopic quantum mechanical tunnelling and energy quantisation in an electric circuit"

Their experiments on a chip revealed quantum physics in action

Comment by Dr. Krishna Kumari Challa on October 7, 2025 at 11:06am

Scientists reverse Alzheimer's in mice using nanoparticles

A research team has demonstrated a nanotechnology strategy that reverses Alzheimer's disease in mice.

Unlike traditional nanomedicine, which relies on nanoparticles as carriers for therapeutic molecules, this approach employs nanoparticles that are bioactive in their own right: "supramolecular drugs." The work has been published in Signal Transduction and Targeted Therapy.

Instead of targeting neurons directly, the therapy restores the proper function of the blood-brain barrier (BBB), the vascular gatekeeper that regulates the brain's environment. By repairing this critical interface, the researchers achieved a reversal of Alzheimer's pathology in animal models.

The team demonstrated that targeting a specific mechanism enables undesirable "waste proteins" produced in the brain to pass through this barrier and be eliminated in the blood flow. In Alzheimer's disease, the main "waste" protein is amyloid-β (Aβ), whose accumulation impairs the normal functioning of the neurons.

Researchers used mouse models that are genetically programmed to produce larger amounts of Aβ protein and develop a significant cognitive decline mimicking Alzheimer's pathology. They administered only three doses of the supramolecular drugs and afterward regularly monitored the evolution of the disease.

Only one hour after the injection, they observed a reduction of 50–60% in Aβ amount inside the brain.

In one of the experiments, they treated a 12-month-old mouse (equivalent to a 60-year-old human) with the nanoparticles and analyzed its behavior after six months. The result was impressive: the animal, aged 18 months (comparable to a 90-year-old human), had recovered the behavior of a healthy mouse.

The long-term effect comes from restoring the brain's vasculature. 

What's remarkable is that these nanoparticles act as a drug and seem to activate a feedback mechanism that brings this clearance pathway back to normal levels.

 Multivalent modulation of endothelial LRP1 induces fast neurovascular amyloid-β clearance and cognitive function improvement in Alzheimer's disease models, Signal Transduction and Targeted Therapy (2025). DOI: 10.1038/s41392-025-02426-1

Comment by Dr. Krishna Kumari Challa on October 7, 2025 at 9:18am

Strange 'rogue' planet spotted guzzling matter like a star

A mysterious "rogue" planet has been observed gobbling six billion tons of gas and dust a second—an unprecedented rate that blurs the line between planets and stars.

Unlike Earth and other planets in our solar system which orbit the sun, rogue planets float freely through the universe untethered to a star.

Scientists estimate there could be trillions of rogue planets in our galaxy alone—but they are difficult to spot because they mostly drift quietly along in perpetual night.

These strange objects intrigue astronomers because they are neither a star nor a proper planet. 

Their origin remains an open question: are they the lowest-mass objects formed like stars, or giant planets ejected from their birth systems?

The team of researchers behind the new study were stunned to observe an astonishing growth spurt in a rogue planet around 620 light years from Earth in the constellation Chamaeleon. The planet, officially called Cha 1107-7626, has a mass five to 10 times bigger than Jupiter. 

 The object is "still in its infancy," being roughly one or two million years old.

The object grows by sucking in matter from a disk that surrounds it—a process called accretion.

But what the astronomers saw happen to Cha 1107-7626 "blurs the line between stars and planets". 

In August this year, the planet suddenly started devouring matter from its disk at a record-breaking six-billion-tons per second—eight times faster than a few months earlier.

This is the strongest accretion episode ever recorded for a planetary-mass object.

By comparing light emitted before and during this binge-eating session, the scientists discovered that magnetic activity was playing a role in driving matter towards the object.

This phenomenon has previously only been observed in stars.

The chemistry in the disk also changed. Water vapor was detected in the disk during the accretion episode, but not beforehand.

This is also something that has previously been observed in stars—but never for a forming planet.

No matter how weird, Cha 1107-7626 is still expected to have similar characteristics to huge planets, because it is of similar size. Unlike stars, this object is "not massive enough to ever have fusion reactions in the core".

Discovery of an Accretion Burst in a Free-Floating Planetary-Mass Object The Astrophysical Journal Letters (2025). DOI: 10.3847/2041-8213/ae09a8

Comment by Dr. Krishna Kumari Challa on October 7, 2025 at 9:07am

Bacteria survive space launch and re-entry unharmed

A world-first study has proven microbes essential for human health can survive the extreme forces of space launch. The study has been published in npj Microgravity.

Space agencies are planning to send crews to Mars within decades, but sustaining life on the red planet would be more difficult if important bacteria die during the flight.

Now a study has found the spores of Bacilus subtilis, a bacterium essential for human health, can survive rapid acceleration, short-duration microgravity and rapid deceleration.

The spores of bacteria were launched more than 260 kilometers into the sky, then studied once their rocket fell back to Earth, in what is believed to be the first study of its kind in real conditions outside the lab.

Effects of Extreme Acceleration, Microgravity, and Deceleration on Bacillus subtilis Onboard a Suborbital Space Flight, npj Microgravity (2025). DOI: 10.1038/s41526-025-00526-4

Comment by Dr. Krishna Kumari Challa on October 7, 2025 at 8:39am

Epigenetic shifts link maternal infection during pregnancy to higher risk of offspring developing schizophrenia

The health of mothers during pregnancy has long been known to play a role in the lifelong mental and physical health of offspring. Recent studies have found that contracting an infection during pregnancy can increase the risk that offspring will develop some neurodevelopmental disorders, conditions that are associated with the atypical maturation of some parts of the brain.

An infection is an invasion of pathogens, such as bacteria, viruses, fungi or parasites, which can then multiply and colonize host tissues. Findings suggest that when an expecting mother contracts an infection, her immune system can respond to it in ways that could impact the development of the fetus.

Researchers recently carried out a study aimed at further investigating the processes through which maternal infections during pregnancy could increase the risk that offspring will develop schizophrenia later in life. Schizophrenia is a typically debilitating mental health condition characterized by hallucinations, false beliefs about oneself or the world (e.g., delusions) and cognitive impairments.

The findings of the team's study, outlined in a paper published in Molecular Psychiatry, shed light on epigenetic shifts prompted by infection that could potentially be linked to a higher genetic risk of offspring developing schizophrenia. Epigenetic processes are changes in the expression of genes prompted by biological processes, which do not alter the DNA sequence of a living organism.

Maternal infection during pregnancy has been shown in epidemiological studies to increase the risk of neurodevelopmental disorders, like schizophrenia, in the developing fetus, wrote the researchers in their paper.

The results of the team's experiments and analyses revealed that the activation of a pregnant rat's immune system due to infection influenced the ratio between SAM and SAH molecules in the fetus. The ratio between these molecules is known to be an indication of the ability of cells to undergo methylation, a biological process that controls the expression of genes.

The findings revealed that MIA increased the SAM/SAH ratio and elevated both DNMT expression and activity in the fetal cortex," wrote the authors. Surprisingly, these changes were not present after birth but resurfaced in adulthood, coinciding with cognitive deficits. These methylation pathway changes in adulthood were accompanied by altered DNAm patterns, with differentially methylated genes linked to schizophrenia risk and enriched in pathways related to neurodevelopment and neuronal signaling.

The researchers were able to pinpoint epigenetic changes following infection in pregnant female rats that resulted in pups exhibiting cognitive deficits resembling those associated with schizophrenia. Their findings could soon pave the way for further investigations on this topic and could potentially contribute to the future development of more effective drugs to treat the cognitive symptoms of schizophrenia, such as attention, memory and language deficits.

Rebecca M. Woods et al, Developmental modulation of schizophrenia risk gene methylation in offspring exhibiting cognitive deficits following maternal immune activation, Molecular Psychiatry (2025). DOI: 10.1038/s41380-025-03147-1.

Comment by Dr. Krishna Kumari Challa on October 7, 2025 at 6:55am

Nobel committee announcement:
The Nobel Assembly at Karolinska Institutet has decided to award the 2025 Nobel Prize in Physiology or Medicine to:

Mary E. Brunkow, Institute for Systems Biology, Seattle, U.S.

Fred Ramsdell, Sonoma Biotherapeutics,San Francisco, U.S.

Shimon Sakaguchi, Osaka University, Osaka, Japan

"for their discoveries concerning peripheral immune tolerance"
They discovered how the immune system is kept in check.

Source: www.nobelprize.org/prizes/medi … popular-information/

Part 2

Comment by Dr. Krishna Kumari Challa on October 7, 2025 at 6:54am

The Nobel Prize in medicine goes to 3 scientists for key immune system discoveries

Three scientists won the Nobel Prize in medicine this week for discoveries about how the immune system knows to attack germs and not our own bodies.

The work by Mary E. Brunkow, Fred Ramsdell and Dr. Shimon Sakaguchi uncovered a key pathway the body uses to keep the immune system in check, called peripheral immune tolerance. Experts called the findings critical to understanding autoimmune diseases such as Type 1 diabetes, rheumatoid arthritis and lupus.

In separate projects over several years, the trio of scientists identified the importance of what are now called regulatory T cells. Scientists are currently using those findings in a variety of ways: to discover better treatments for autoimmune diseases, to improve organ transplant success and to enhance the body's own fight against cancer, among others.

Their discoveries have been decisive for our understanding of how the immune system functions and why we do not all develop serious autoimmune diseases.

The immune system has overlapping ways to detect and fight bacteria, viruses and other intruders. But sometimes certain immune cells run amok, mistakenly attacking people's own cells and tissues to cause autoimmune diseases.

Scientists once thought the body regulated this system only in a centralized fashion. Key immune soldiers such as T cells get trained to spot bad actors and those that go awry in a way that might trigger autoimmunity get eliminated in the thymus.

The Nobel winners unraveled an additional way the body keeps the system in check if immune cells later get confused and mistake human cells for intruders, which is what happens when a person has an autoimmune disease.

These scientists were curious about the mechanism of immune response that is supposed to protect oneself but also reacts to and attacks itself.

Sakaguchi's experiments in mice showed that the thymus pathway couldn't be the only explanation. In 1995, he discovered a previously unknown T cell subtype, the regulatory T cells, that also could tamp down overreactive immune cells like a biological security guard.

Then in 2001, Brunkow and Ramsdell were working together at a biotech company investigating mice with an autoimmune disease. In painstaking work at a time when mapping genes was still an evolving field, they figured out that a particular mutation in a gene called Foxp3 was to blame—and quickly realized it could be a major player in human health, too.

From a DNA level, it was a really small alteration that caused this massive change to how the immune system works.

Sakaguchi linked the discoveries to show the Foxp3 gene controls the development of those regulatory T cells so they're able to curb other, overreactive cells.

The work is important because it opened a new field of immunology. Until the trio's research was published, immunologists didn't understand the complexity of how the body differentiates foreign cells from its own. 

One goal for scientists now is to figure out how to increase the number of regulatory T cells—also known as T-regs—to help fight autoimmune diseases. That would decrease the need for today's therapies, which instead suppress the immune system in ways that leave patients vulnerable to infection.

Comment by Dr. Krishna Kumari Challa on October 4, 2025 at 9:36am

Scientists create natural plastics for everyday packaging

Researchers have transformed food waste sugars into natural plastic films that could one day replace petroleum-based packaging, offering compostable alternatives to commonly used plastics for food and agricultural films like silage wrap.

With global plastic production exceeding 400 million metric tons annually, a Monash University study highlights the potential of a new type of biodegradable plastic by converting food waste sugars into polyhydroxyalkanoates (PHA) biopolymers.

The study is published in the journal Microbial Cell Factories.

By selecting different bacterial strains and blending their polymers, the researchers produced films that behave like conventional plastics and can be molded into other shapes or solids.

The study  provides a framework for designing bioplastics for temperature-sensitive packaging, medical films and other products, addressing the global challenge of single-use plastic waste.

The research teams fed two soil-dwelling bacteria—Cupriavidus necator and Pseudomonas putida—a carefully balanced "diet" of sugars with the right blend of salts, nutrients and trace elements.

Once the microbes fattened up, they began stockpiling natural plastic inside their cells. The scientists then "milked" these plastics out using solvents, cast them into ultrathin films about 20 microns thick and tested their stretchiness, strength and melting behavior.

This research demonstrates how food waste can be transformed into sustainable, compostable ultrathin films with tunable properties. The versatility of PHAs means we can reimagine materials we rely on every day without the environmental cost of conventional plastics.

By tailoring these natural plastics for different uses, scientists are opening the door to sustainable alternatives in packaging, especially where they can be composted along with food or agricultural waste.

The researchers  collaborating with industry partners, including Enzide and Great Wrap through the ARC RECARB and VAP hubs to develop biodegradable packaging and medical solutions with potential commercial applications.

Edward Attenborough et al, Bacterial species-structure-property relationships of polyhydroxyalkanoate biopolymers produced on simple sugars for thin film applications, Microbial Cell Factories (2025). DOI: 10.1186/s12934-025-02833-7

Comment by Dr. Krishna Kumari Challa on October 4, 2025 at 9:28am

Enzyme technology clears first human test toward universal donor organs for transplantation

The first successful human transplant of a kidney converted from blood type A to universal type O used special enzymes developed by scientists to help prevent a mismatch and rejection of the organ.

Published in Nature Biomedical Engineering, the achievement marks a major step toward helping thousands of patients get kidney transplants sooner.

In a first-in-human experiment, the enzyme-converted kidney was transplanted into a brain-dead recipient with consent from the family, allowing researchers to observe the immune response without risking a life.

For two days, the kidney functioned without signs of hyperacute rejection, the rapid immune reaction that can destroy an incompatible organ within minutes. By the third day, some blood-type markers reappeared, triggering a mild reaction, but the damage was far less severe than in a typical mismatch, and researchers saw signs that the body was beginning to tolerate the organ.

This is the first time scientists have seen this play out in a human model. It gives them invaluable insight into how to improve long-term outcomes.

The breakthrough is the result of more than a decade of hard work.

The work focused on making universal donor blood by stripping away the sugars that define blood types.

Part 1

Those same sugars, or antigens, coat organ blood vessels. If a recipient's immune system detects the wrong antigen, it attacks. Type-O patients—more than half of kidney waitlists—can only receive type-O organs, yet type-O kidneys are often given to others because they're universally compatible. As a result, type-O patients typically wait two to four years longer, and many die waiting.

Traditional methods for overcoming blood-type incompatibility in transplants require days of intensive treatment to strip antibodies and suppress a recipient's immune system—and require organs from living donors.

This new approach changes the organ rather than the patient, meaning transplants could be performed faster, with fewer complications, and for the first time could unlock the use of blood-type mismatched organs from deceased donors—when every hour can determine whether a patient lives or dies.

 Enzyme-converted O kidneys allow ABO-incompatible transplantation without hyperacute rejection in a human decedent model, Nature Biomedical Engineering (2025). DOI: 10.1038/s41551-025-01513-6.

Comment by Dr. Krishna Kumari Challa on October 4, 2025 at 9:17am

Glioblastomas affect much more than just the brain, scientists discover

Scientists  have shown for the first time that glioblastoma—the deadliest form of brain cancer—affects not just the brain but also erodes the skull, alters the makeup of skull marrow, and interferes with the body's immune response. Drugs intended to inhibit skull-bone loss made the cancer more aggressive, according to results published in Nature Neuroscience. The paper is titled "Brain Tumors Induce Widespread Disruption of Calvarial Bone and Alteration of Skull Marrow Immune Landscape."

This discovery that this notoriously hard-to-treat brain cancer interacts with the body's immune system may help explain why current therapies—all of them dealing with glioblastoma as a local disease—have failed, and it will hopefully lead to better treatment strategies.

As is true for many other bones, the skull contains marrow in which immune cells and other blood cells form. 

Researchers used advanced imaging techniques on mice that developed two different types of glioblastomas. They found that the tumors caused skull bones to erode, especially along the sutures where skull bones fuse. Such erosions seem to be unique to glioblastoma and other malignant intracranial tumors, since they don't occur with strokes, other types of brain damage, or even other systemic cancers. Computerized-tomography (CT) images of patients with glioblastoma revealed that decreases in skull thickness were present in the same anatomic areas as in mice. 

The skull erosions in the mice were found to have increased the number and diameter of the skull-to-bone channels. The researchers hypothesized that these channels might allow the glioblastoma to transmit signals to the skull marrow that could profoundly change its immune landscape.

Using single-cell RNA sequencing, the researchers found that glioblastoma had dramatically shifted the skull marrow's immune-cell balance in favor of pro-inflammatory myeloid cells—nearly doubling the levels of inflammatory neutrophils, while nearly eliminating several types of antibody-producing B cells as well as other B cells.

The skull-to-brain channels allow an influx of these numerous pro-inflammatory cells from the skull marrow to the tumor, rendering the glioblastoma increasingly aggressive and, all too often, untreatable.

This indicates the need for treatments that restore the normal balance of immune cells in the skull marrow of people with glioblastoma. One strategy would be suppressing the production of pro-inflammatory neutrophils and monocytes while at the same time restoring the production of T and B cells.

'Brain tumors induce widespread disruption of calvarial bone and alteration of skull marrow immune landscape, Nature Neuroscience (2025). DOI: 10.1038/s41593-025-02064-4

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