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Comment by Dr. Krishna Kumari Challa 4 hours ago

Climate change can affect human diseases in widespread and varied ways

As the planet edges towards 1.5°C of global warming, a new study has revealed that we still have only a limited understanding of how climate change is reshaping the risk of infectious diseases that pass from animals to humans.

The research shows that a warmer world will alter weather patterns, transform habitats and shift where many animals live, likely bringing people and wildlife into closer proximity and increasing opportunities for zoonotic diseases to "spill over." However, the exact impacts are extremely hard to predict.

By reviewing hundreds of scientific studies, the team was able to extract detailed climate-disease data for 53 zoonotic diseases—around 6% of the 816 known zoonotic diseases that affect humans. Even for these relatively well-studied diseases, responses to climate change are highly variable.
Overall, zoonotic diseases were found to be sensitive to climate, with temperature showing the clearest links. Higher temperatures were almost twice as likely to increase disease risk as to decrease it, particularly for zoonotic infections spread by mosquitoes. But this pattern was far from universal, and for other climate factors, such as rainfall and humidity, the picture was even more mixed.

The study found that zoonotic diseases are generally climate-sensitive but respond in a variety of ways depending on the disease, the animal host and the local environment. The paper is published in the Proceedings of the National Academy of Sciences.

Temperature showed the strongest and most consistent links. In many cases, warming increases risk for instance, by speeding up the development of mosquitoes or boosting rodent populations. However, even for a single disease, the response to temperature may change depending on how warm it already is, or which species are involved.

Artur Trebski et al, Climate sensitivity is widely but unevenly spread across zoonotic diseases, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2422851122

Comment by Dr. Krishna Kumari Challa 4 hours ago

Typhoons vacuum microplastics from ocean and deposit them on land, study finds
Typhoons and similar storms rapidly transfer microplastics from the ocean to land, with deposition rates increasing by up to an order of magnitude during storm events. Analysis confirms these particles originate from marine sources, not local environments. This process links plastic pollution and climate change, as stronger storms fueled by warming oceans transport more microplastics inland.

Taiseer Hussain Nafea et al, Microplastics from Ocean Depths to Landfall: Typhoon-Induced Microplastic Circulation in a Warming Climate, Environmental Science & Technology (2025). DOI: 10.1021/acs.est.5c11101

Comment by Dr. Krishna Kumari Challa 4 hours ago

A hormone can access the brain by 'hitchhiking' on extracellular vesicles, researchers discover
Extracellular vesicles (EVs) in blood can transport the hormone precursor proopiomelanocortin (POMC), especially after vigorous exercise, increasing its association with EVs fourfold. EV-bound POMC crosses blood vessel barriers, including the blood-brain barrier, more efficiently than free POMC, suggesting a mechanism for hormone delivery to the brain and potential implications for metabolism and stress response.

Hightower, Cheryl E. et al, Physical exercise increases binding of POMC to blood extracellular vesicles, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2525044122. doi.org/10.1073/pnas.2525044122

Comment by Dr. Krishna Kumari Challa 4 hours ago

Misinformation across nature

From claims that vaccines don't work to manipulated images and deliberately misrepresenting what politicians say, social media is often rife with misinformation. But far from being a recent phenomenon, there is nothing new about so-called "fake news," according to a new paper published in the journal Interface. Researchers argue that misinformation is an inherent and inevitable property of biological systems, from bacteria to birds and human societies.

Social communication is a key part of social evolution and collective behavior. It is how an organism learns about its immediate environment without having to rely on risky, trial-and-error or how a bacterium coordinates its behavior with its neighbors to launch a collective defense. However, these social connections can also act as channels for misinformation.

Researchers  reviewed decades of empirical and theoretical studies of misinformation in biological systems to see where and how it happens in nature. They found plenty of examples, such as a bird giving a false alarm call, causing the entire flock to flee, an animal population copying outdated migratory paths and even deceptive signalling in bacteria.

To define and measure misinformation across different systems, the study authors developed mathematical models to investigate it in any species. This will allow scientists to understand how accurate an organism's existing beliefs are and the extent to which information from other organisms shifts those beliefs. Working with these models led the team to conclude that misinformation is a fundamental feature of all biological communication, not a bug, failure, or other pathology.

Socially transmitted misinformation is likely to be a ubiquitous feature of biological communication, and should therefore be viewed as a fundamental part of social, ecological and evolutionary systems, rather than as a pathology that somehow lies apart from the normal functioning of these systems, the authors explain in their research paper.

If we can understand the impact of this misinformation, this knowledge helps us develop strategies to control misinformation in both human and biological systems.

Ling-Wei Kong et al, A brief natural history of misinformation, Journal of the Royal Society Interface (2025). DOI: 10.1098/rsif.2025.0161

Comment by Dr. Krishna Kumari Challa yesterday

Normally, this would have been a huge surprise. EPO is well known as the primary instigator of red blood cell production, and it was named for this function (erythro meaning "red" and poiein meaning "to produce").

But earlier in 2025,  the researchers showed that cancer cells in immunologically tolerated, or "cold," tumors trick the immune system by making EPO and releasing it into the tumor environment where it binds to a type of immune cell called macrophages and causes these cells to become immunosuppressive. So, they knew that EPO has a second role as a master immune regulator.

When they genetically manipulated the mice to remove the ability of the dendritic cells to express the EPO receptor, the animals rejected transplants of unmatched tissue after total lymphoid irradiation, showing conclusively that the EPO signaling pathway is necessary for the development of immune tolerance. But there was another intriguing finding.

"What was quite a surprise  is that when you remove or block the EPO receptor on the dendritic cells, you don't just block the development of tolerance.

"Instead, you have now converted these dendritic cells into super stimulators, or powerful activators of immune response. There is a dual opportunity to not just induce tolerance to treat autoimmune diseases, but also to trigger a strong immune response to cancer cells or to life-threatening infections."

Essentially, dendritic cells continuously sample their environment by capturing and swallowing dead or dying cells (either self or non-self) as well as pathogens and displaying fragments of the cells on their surfaces to be recognized by many types of T cells, including killer T cells, helper T cells or Tregs.

When EPO interacts with its EPO receptors on the dendritic cells, it causes the dendritic cells to embark on a series of maturation steps that cause them to promote tolerance and selectively activate Tregs that tamp down any immune response to that antigen.

"This mechanism is not only required for physiological tolerance that prevents autoimmune disease, but it is often hijacked by cancers and probably some infectious pathogens, too, enabling their ability to evade immune attack.

Conversely, removing the EPO receptor from dendritic cells resulted in tumor regression in mice with immune-resistant melanoma or colon cancer tumors.

"It's fascinating that this fundamental mechanism took so long to discover. "It's even possible that this is the primary function of EPO, and that its effect on red blood cell formation is secondary. There is no doubt these findings will light many research fires."

Edgar Engleman, Erythropoietin receptor on cDC1s dictates immune tolerance, Nature (2025). DOI: 10.1038/s41586-025-09824-z. www.nature.com/articles/s41586-025-09824-z

Part 3

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Comment by Dr. Krishna Kumari Challa yesterday

The immune system's response—threatening or welcoming—is governed by the Tregs, which tamp down inappropriate attack impulses of other immune cells called T and B cells.
The researchers used an experimental approach first identified in mice and subsequently in humans in which irradiating the thymus, spleen and lymph nodes—all places in the body where immune cells hang out—kills off many of the T cells and B cells while leaving antigen-presenting cells such as dendritic cells relatively unscathed.

The treatment, called total lymphoid irradiation, reprograms the recipient's immune system to permanently tolerate genetically mismatched transplanted cells or organs.

But dendritic cells don't act alone and instead recruit other immune cells, including T cells, to carry out their missions.

"All T cells, including Tregs, must first be 'presented' with a structure called an antigen that is recognized by their receptors for the cells to develop into mature T cells that either attack a target or suppress the immune response to that target," Engleman said. "Dr. Zhang and I reasoned that this process of tolerance or activation must be initiated by antigen-presenting cells."

The most powerful antigen-presenting cells in the body are called type 1 dendritic cells, which engulf dead or dying cells or pathogens and display bits of those cells like immunological fishing lures for T or B cells.

To learn how dendritic cells are involved in the development of immune tolerance, Zhang and Engleman decided to investigate whether and how the genes they express change in mice after total lymphoid irradiation.

They found that the gene for the EPO receptor is expressed at much higher levels in the dendritic cells of irradiated animals, and that the levels of EPO are elevated in the animals' blood circulation.
Part 2

Comment by Dr. Krishna Kumari Challa yesterday

Immune system's 'on-off' switch may hold answers for cancer and autoimmunity

A single signaling pathway controls whether immune cells attack or befriend cells they encounter while patrolling our bodies, researchers have found. Manipulating this pathway could allow researchers to toggle the immune response to treat many types of diseases, including cancers, autoimmune disorders and those that require organ transplants.

The research, which was conducted in mice, illuminates the mechanism of an important immune function that prevents inappropriate attacks on healthy tissue. Called peripheral immune tolerance, the key cellular players, known as regulatory T cells (or Tregs), were first described in the late 1990s in a series of discoveries that were recently recognized with the 2025 Nobel Prize in physiology or medicine.

The work is published in the journal Nature.

The findings extend those of a related study published in Science by the same researchers that described a surprising new role for a molecule known for decades to promote red blood cell formation.

Now it is clear that this molecule, erythropoietin, or EPO, is the lynchpin controlling how our immune systems react to real or perceived threats—acting through immune cells called dendritic cells.

The critically important building of immune tolerance to "self" is a two-step process. The first, called central immune tolerance, occurs in the bone marrow and the thymus, where B cells and T cells undergo a first round of selection to eliminate or reprogram self-reactive cells before they are released into the bloodstream.
The second, peripheral immune tolerance, serves as a backup to screen circulating cells that escape the first culling.

The stakes are high. An overly enthusiastic immune system that attacks healthy tissues leads to autoimmune diseases like rheumatoid arthritis, multiple sclerosis, lupus and diabetes. Conversely, a too complacent, or tolerant, response allows cancer cells to escape immune destruction, instead of sending them on their way with a handshake and a pat on the back.

Part 1

Comment by Dr. Krishna Kumari Challa yesterday

How the immune system stalls weight loss

Neutrophils, a type of immune cell, infiltrate fat tissue during physiological stress and release signals that suppress fat breakdown, helping to prevent excessive weight loss. This mechanism, observed in both mouse models and human data, involves specific inflammatory pathways and is more active in obese individuals. The findings highlight a key role for the immune system in regulating energy balance.

In a study published in Nature, a research team demonstrates that when the body is exposed to physiological stressors, such as low temperature, neutrophils—a type of white blood cell—infiltrate fat tissue and release signals that slow fat breakdown.

The researchers hypothesize that this mechanism helped our early human ancestors preserve vital energy stores when food was scarce or when exposed to prolonged periods of cold. Today, the findings could help yield new approaches to managing obesity and other metabolic disorders.

White adipose tissue (WAT)—commonly known as body fat—plays a vital role in maintaining energy balance by storing excess energy and releasing it as needed during periods of fasting, cold or other metabolic stress. These biochemical processes are carefully managed by the body in order to prevent excessive fat loss, which can be very dangerous.

Until now, the mechanisms that protect the body against runaway fat burning in times of stress have remained unclear.

To address this, the researchers studied a combination of mouse models and human genetic data.

Key findings include:
In mouse models, activating the sympathetic nervous system triggered a rapid influx of neutrophils into visceral fat, the fat surrounding vital organs. This neutrophil recruitment depended on both ongoing fat breakdown and activation of specific inflammatory pathways in fat cells.
Neutrophils arriving in the fat tissue produced signaling molecules that suppressed further fat loss in surrounding tissue.
When either these molecules or neutrophils themselves were depleted, mice experienced increased fat breakdown under metabolic stress.
In obese individuals, genes involved with this pathway were more active.
These findings reveal an unexpected physiological partnership between fat cells and immune cells, demonstrating that the immune system is crucial not only for fighting infection but also for maintaining energy balance.

The study also provides new insight into the underlying metabolism of obesity and other metabolic disorders. Targeting this newly discovered pathway may eventually offer new strategies for treating obesity, metabolic syndrome or conditions involving unintended weight loss.

Seunghwan Son et al, Neutrophils preserve energy storage in sympathetically activated adipocytes, Nature (2025). DOI: 10.1038/s41586-025-09839-6 , doi.org/10.1038/s41586-025-09839-6

Comment by Dr. Krishna Kumari Challa yesterday

Ghostly solar neutrinos caught transforming carbon atoms deep underground

Solar neutrinos have been directly observed transforming carbon-13 nuclei into nitrogen-13 within the SNO+ underground detector. Using a delayed coincidence method, 5.6 events were detected over 231 days, matching the 4.7 events expected from neutrino interactions. This marks the first direct measurement of this low-energy neutrino-induced reaction, advancing the study of rare atomic processes.

SNO+ Collaboration et al, First Evidence of Solar Neutrino Interactions on ¹³C, Physical Review Letters (2025). DOI: 10.1103/1frl-95gj On arXiv: DOI: 10.48550/arxiv.2508.20844

Comment by Dr. Krishna Kumari Challa yesterday

Genetic overlap of 14 psychiatric disorders explains why patients often have multiple diagnoses

An international collective of researchers is delivering new insights into why having multiple psychiatric disorders is the norm rather than the exception. In a study published recently in the journal Nature, the team provides the largest and most detailed analysis to date on the genetic roots shared among 14 conditions.

The majority of people diagnosed with a psychiatric disorder will ultimately be diagnosed with a second or third disorder in their lifetime, creating challenges for defining and treating these conditions. While a person's environment and lived experience influence their risk for developing multiple disorders, their genetic makeup can also play a significant role.

By analyzing data from over 6 million individuals, the working group mapped the genetic landscape of 14 psychiatric conditions and revealed five families of disorders with high levels of genetic overlap. The results mark an important step toward understanding the genetic connections among psychiatric disorders and could ultimately help clinicians better serve their patients.

Analysis of genetic data from over 6 million individuals reveals that 14 psychiatric disorders cluster into five groups with significant genetic overlap. Major depression, anxiety, and PTSD share about 90% of genetic risk, while schizophrenia and bipolar disorder share 66%. Shared genetic variants and expression patterns help explain frequent comorbidity among these conditions.

Through statistical modeling, the researchers found that the 14 disorders could be divided into these five groups based on genetic similarities:

• Compulsive disorders: obsessive-compulsive disorder, anorexia nervosa and, to a lesser extent, Tourette disorder and anxiety disorders.
• Internalizing disorders: major depression, anxiety disorders and post-traumatic stress disorder.
• Neurodevelopmental disorders: autism spectrum disorder, attention-deficit/hyperactivity disorder and, to a lesser extent, Tourette disorder.
• Schizophrenia and bipolar disorder
• Substance use disorders: opioid use disorder, cannabis use disorder, alcohol use disorder and nicotine dependence.

Andrew D. Grotzinger et al, Mapping the genetic landscape across 14 psychiatric disorders, Nature (2025). DOI: 10.1038/s41586-025-09820-3

Abdel Abdellaoui, Shared genetic risk in psychiatric disorders, Nature (2025). DOI: 10.1038/d41586-025-03728-8 , doi.org/10.1038/d41586-025-03728-8

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