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Comment by Dr. Krishna Kumari Challa 34 minutes ago

Living rocks in South Africa rapidly absorb carbon

South Africa is home to some of the oldest evidence of life on Earth, contained in rocky, often layered outcroppings called microbialites. Like coral reefs, these complex "living rocks" are built up by microbes absorbing and precipitating dissolved minerals into solid formations.

A new study suggests that these microbialites aren't just surviving—they're thriving.

A paper  published in Nature Communications, quantifies how microbialites along the South African coast take up carbon and turn it into fresh layers of calcium carbonate. They show how these structures utilize photosynthesis and chemical processes to absorb carbon day and night, relating those rates for the first time to the genetic makeup of the microbial community.

The findings highlight just how efficient these microbial mats are at removing dissolved carbon from their environment and sequestering it into stable mineral deposits.

Researchers found that these systems were precipitating calcium carbonate rapidly, estimating that the structures can grow almost two inches vertically every year.

More surprising was the finding of carbon uptake day and night. These systems have long been assumed to be driven solely by photosynthesis.

After repeating their experiments several times, the researchers confirmed that the microbes are utilizing metabolic processes other than photosynthesis to absorb carbon in the absence of light, similar to how microbes living in deep-sea vents survive.

Based on daily rates of carbon uptake, the team estimates that these microbialites can absorb the equivalent of nine to 16 kilograms of carbon dioxide every year per square meter.

Rachel E. Sipler et al, Integration of multiple metabolic pathways supports high rates of carbon precipitation in living microbialites, Nature Communications (2025). DOI: 10.1038/s41467-025-66552-8

Comment by Dr. Krishna Kumari Challa 50 minutes ago

The North Pole keeps moving. Here's how that affects Santa's holiday travel and yours
Earth has two North Poles: the geographic North Pole, marking the axis of rotation, and the magnetic North Pole, which compasses and navigation devices use. The magnetic North Pole moves due to fluid motion in Earth's outer core, with its speed increasing significantly since 1990. Accurate navigation requires correcting for the difference, known as magnetic declination.

The geographic North Pole, also called true north, is the point at one end of the Earth’s axis of rotation.

Earth’s magnetic North Pole is different.

Over 1,000 years ago, explorers began using compasses, typically made with a floating cork or piece of wood with a magnetized needle in it, to find their way. The Earth has a magnetic field that acts like a giant magnet, and the compass needle aligns with it.

The magnetic North Pole is used by devices such as smartphones for navigation – and that pole moves around over time.

The movement of the magnetic North Pole is the result of the Earth having an active core. The inner core, starting about 3,200 miles below your feet, is solid and under such immense pressure that it cannot melt. But the outer core is molten, consisting of melted iron and nickel.

Heat from the inner core makes the molten iron and nickel in the outer core move around, much like soup in a pot on a hot stove. The movement of the iron-rich liquid induces a magnetic field that covers the entire Earth.

As the molten iron in the outer core moves around, the magnetic North Pole wanders.

For most of the past 600 years, the pole has been wandering around over northern Canada. It was moving relatively slowly, around 6 to 9 miles per year, until around 1990, when its speed increased dramatically, up to 34 miles per year.

It started moving in the general direction of the geographic North Pole about a century ago. Earth scientists cannot say exactly why other than that it reflects a change in flow within the outer core.

https://theconversation.com/the-north-pole-keeps-moving-heres-how-t...

Comment by Dr. Krishna Kumari Challa 52 minutes ago

Firefighter gear contains potentially hazardous flame retardants, study shows

Firefighter turnout gear manufactured between 2013 and 2020 contains both PFAS and brominated flame retardants, with newer gear marketed as non-PFAS treated showing low or undetectable PFAS but higher extractable levels of brominated flame retardants, particularly decabromodiphenyl ethane (DBDPE). These chemicals may pose health risks, highlighting the need for transparency in gear composition.

Environmental Science & Technology Letters (2025)

Comment by Dr. Krishna Kumari Challa yesterday

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 yesterday

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 yesterday

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 yesterday

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.

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