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Comment by Dr. Krishna Kumari Challa on Tuesday

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 Tuesday

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 Tuesday

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 Saturday

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 Saturday

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 Saturday

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

Comment by Dr. Krishna Kumari Challa on Saturday

Making yogurt with ants revives a creative fermentation process

Researchers recreated a nearly forgotten yogurt recipe that once was common across the Balkans and Turkey—using ants. Reporting in iScience on October 3, the team shows that bacteria, acids, and enzymes in ants can kickstart the fermentation process that turns milk into yogurt. The work highlights how traditional practices can inspire new approaches to food science and even add creativity to the dinner table.

Today's yogurts are typically made with just two bacterial strains. 

But if you look at traditional yogurt, you have much bigger biodiversity, varying based on location, households, and season. That brings more flavours, textures, and personality.

Red wood ants (Formica species) can be found crawling through the forests of the Balkans and Turkey, where this yogurt-making technique was once popular.

In the present study researchers dropped four whole ants into a jar of warm milk .

The jar was then tucked into an ant mound to ferment overnight. By the next day, the milk had started to thicken and sour. That's an early stage of yogurt, and it tasted that way as well, they say.

The researchers, who tested the yogurt during their trip, described it as slightly tangy, herbaceous, and having flavors of grass-fed fat.

The team dissected the science behind the ant yogurt. They found that the ants carry lactic and acetic acid bacteria. Acids produced by these bacteria help coagulate the dairy. One type of these bacteria was similar to that found in commercial sourdough.

The insects themselves also help in the yogurt-making process. Formic acid, which is part of the ant's natural chemical defense system, acidifies the milk, affects its texture, and likely creates an environment for yogurt's acid-loving microbes to thrive, say the researchers. Enzymes from the ant and the microbes work in tandem to break down milk proteins and turn milk into yogurt.

The researchers compared yogurts made with live, frozen, and dehydrated ants. Only live ants seeded the right microbial community, meaning they are best suited for yogurt making. However, the team found that caution was necessary to make sure the ant products were safe to consume: live ants can harbor parasites, and freezing or dehydrating ants can sometimes allow harmful bacteria to flourish.

Giving scientific evidence that these traditions have a deep meaning and purpose, even though they might seem strange or more like a myth.

 Making yogurt with the ant holobiont uncovers bacteria, acids, and enzymes for food fermentation, iScience (2025). DOI: 10.1016/j.isci.2025.113595

Comment by Dr. Krishna Kumari Challa on Saturday

Trauma in a puppy's first six months linked to adult aggression, says new study

As many dog owners can attest, their four-legged companions are delightful and loving. But for others, their animals have an aggressive side, such as biting and attacking strangers, which may ultimately lead to them having to be euthanized. But why do some dogs turn out this way?

According to a new study of 211 dog breeds published in the journal Scientific Reports, adverse experiences such as abuse or being given up during a dog's first six months of life mean they are more likely to be fearful and aggressive as adults.

To explore this link between early life experiences and adult behavior, scientists conducted a large-scale survey of 4,497 dog owners. Each owner filled out a detailed questionnaire about their canine companion, including its complete life history, breed and current living environment. They were also asked about any adversity their pet experienced during its first six months.

Additionally, owners completed a standard behavior test (C-BARQ) to rate their dog's current fear and aggression levels. The scientists then used powerful statistical tools to determine whether early trauma, breed, or a combination of the two was most responsible for a dog's behaviour.

Just like in humans, the first few months of life are crucial for emotional development. The research team found that dogs that experienced any kind of adversity in the first six months were more likely to be aggressive as adults, regardless of age or sex or whether the animal was neutered. Both genes and environment are involved, as indicated by the fact that the effect of adversity differed across different breeds.

For example, some breeds, such as Siberian Huskies, American Eskimo Dogs, and American Leopard Hounds, as well as pit-bull type dogs, were more likely to become aggressive or fearful after experiencing early trauma. Meanwhile, other breeds, such as the Labrador Retriever, were a lot more resilient. Even when they experienced trauma, the chances of them being aggressive adults were relatively low.

Overall, the study clearly demonstrates that a dog's early life is crucial and highlights the importance of responsible breeding and proper pet care.

Julia Espinosa et al, Influence of early life adversity and breed on aggression and fear in dogs, Scientific Reports (2025). DOI: 10.1038/s41598-025-18226-0

Comment by Dr. Krishna Kumari Challa on October 3, 2025 at 9:49am

Do stranded dolphins have Alzheimer's disease?

One of the most heartbreaking occurrences for nature lovers is to discover a beached marine mammal such as a dolphin or whale. If the animal is still alive, marine biologists assisted by citizen volunteers try to protect the beached marine mammal from sun exposure and skin desiccation by pouring buckets of sea water on them and sometimes covering them with wet blankets. Other volunteers try to find ways to help the animal return to their native ocean habitat when the tide rises.

Unfortunately, some beached marine mammals are discovered after they have died. Such unsettling events give rise to a broader question: why do dolphins and whales become stranded on shore in the first place?

A group of scientists  have come up with an unusual hypothesis: just as some adult humans with dementia are occasionally found wandering far from their homes, perhaps dolphins become similarly disoriented by suffering from a form of Alzheimer's disease. The research was published in Communication Biology.

In the case of marine mammals, it appears that Alzheimer's-type neuropathology and disorientation may result from chronic exposure to toxic molecules produced by cyanobacteria.

Studies of villagers on the island of Guam show that chronic dietary exposure to cyanobacterial toxins are associated with misfolded tau proteins and amyloid plaques characteristic of Alzheimer's disease.

The cyanobacterial toxin β-N-methylamino-L-alanine (BMAA), as well as its isomers 2,4-diaminobutyric acid (2,4-DAB), and N-2-aminoethylglycine (AEG), have been found to be extremely toxic to neurons. BMAA triggers Alzheimer's-like neuropathology and cognitive loss in experimental animals. These toxins can be biomagnified up the food chain in the marine ecosystem.

A study of 20 common bottlenose dolphins stranded in the Indian River Lagoon in eastern Florida showed that their brains contained BMAA and its isomers, particularly 2,4-DAB.

Dolphins stranded during the summer cyanobacterial bloom season contained 2,900 times the concentration of 2,4-DAB than those from non-bloom seasons. Brain neuropathology similar to Alzheimer's patients, including β-amyloid plaques and hyperphosphorylated tau proteins were found in the dolphin brains.

In addition, TDP-43 protein inclusions characteristic of a particularly severe form of Alzheimer's were also found in the dolphin brains. During bloom seasons, the same dolphins showed 536 differentially expressed genes associated with Alzheimer's disease.

The duration of cyanobacterial blooms is increasing with climate warming and nutrient inputs associated with agricultural runoff and sewage discharges.

What is worse is scientists found that even among Guam villagers, exposure to cyanobacterial toxins appeared to trigger neurological diseases.

Wendy Noke Durden et al, Alzheimer's disease signatures in the brain transcriptome of Estuarine Dolphins, Communications Biology (2025). DOI: 10.1038/s42003-025-08796-0

Comment by Dr. Krishna Kumari Challa on October 3, 2025 at 9:38am

Ancient viral DNA is essential for human embryo development, study shows

Our ancient past isn't always buried history. When it comes to our DNA, nearly 9% of the human genome is made up of leftover genetic material from ancient viruses (called endogenous retroviruses or ERVs) that infected our ancestors millions of years ago and became permanently integrated into our genetic code. In a new study published in the journal Nature, scientists have demonstrated that one piece of this viral junk is essential for the earliest stages of human life.

Knowledge of how ERVs affect human development is limited because scientists obviously cannot conduct ethical experiments on embryos. To overcome this, researchers in this study used human blastoids, 3D models grown from stem cells that mimic the structure and key cell types of a natural blastocyst. This is the ball of cells that form in early pregnancy, about five to seven days after fertilization.

The research team focused on a specific type of ERV known as HERVK LTR5Hs, which were introduced into our DNA after our lineage split from Old World monkeys. Although this event occurred millions of years ago, it is considered relatively recent in evolutionary genetic terms.
To determine the functional effect of these viral remnants on the early embryo, the research team used cutting-edge genetic tools that act like molecular scissors to switch off LTR5Hs elements or delete them completely. The results were dramatic. The blastoids either died or turned into disorganized clumps. This provided clear proof that this ancient DNA is essential for the pre-implantation stage of human development.

The researchers also dug deeper to find out what was going on at the subcellular level. They discovered that the LTR5Hs elements act as powerful enhancers, boosting the activity of neighboring genes. When their activity is suppressed, many nearby genes associated with the epiblast (the cell layer that eventually forms the embryo) are turned down. That is, their activity is reduced. This showed that the viral DNA is directly responsible for controlling these essential early developmental instructions.

One of the most important discoveries involved the ZNF729 gene. The team found that one specific LTR5Hs insertion (an extra piece of DNA added to a DNA sequence), unique to humans, acts as a master key for activating this gene. Since the gene regulates fundamental cellular processes, such as cell growth and metabolism, the viral DNA master key is crucial to our development.

Raquel Fueyo et al, A human-specific regulatory mechanism revealed in a pre-implantation model, Nature (2025). DOI: 10.1038/s41586-025-09571-1

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