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Comment by Dr. Krishna Kumari Challa on January 26, 2025 at 12:26pm

Why hibernating animals don't dream

Because hibernation isn’t the same as sleep. 

Sleep is a more physiologically ‘active’ state. Hibernation, in contrast, requires animals (like this hedgehog, above) to substantially reduce all activities to conserve energy.

Hibernating animals reduce their breathing rate, lower their body temperature and decrease their metabolic rate to around five per cent of their usual levels. There’s simply not enough brain activity while an animal is hibernating to enable dreaming.
There is one exception, however: the fat-tailed lemur. As the only primate to hibernate, scientists have observed them having periods of rapid eye movement (REM) sleep.

Comment by Dr. Krishna Kumari Challa on January 25, 2025 at 11:54am

Scientists trace deadly cell-to-cell message chain that spreads in sepsis

Dying cells prick their neighbours with a lethal message. This may worsen sepsis, researchers  report in the Jan. 23 issue of Cell. Their findings could lead to a new understanding of this dangerous illness.

Sepsis is one of the most frequent causes of death worldwide, according to the World Health Organization (WHO), killing 11 million people each year. It's characterized by runaway inflammation, usually sparked by an infection. It can lead to shock, multiple organ failure, and death if treatment is not rapid enough or effective.

But recent research has shown that it isn't actually the infection that causes the spiraling inflammation: it's the cells caught up in it. Even if those cells aren't infected, they act as if they are, and die. As they die, they send out messages to other cells. Those messages somehow cause the recipient cells to die.

If scientists understood what caused this deadly message chain, they might be able to stop it. And that could help heal sepsis.

The deadly message mystery may now be solved. It appears that the "messages" are a byproduct of the cells trying to stay alive.

The process starts with cells that really are infected. To prevent the infection from spreading, those cells destroy themselves by sending a protein called gasdermin-D to their surface. Several gasdermin-D proteins will link together to create a round pore on the cell, like a hole punched in a balloon. The cell's contents leak out, the cell collapses, and dies.

But the collapse isn't inevitable. Sometimes cells can act quickly and eject the section of their surface membrane with the gasdermin-D pore. The cell then zips the membrane closed and survives. The ejected membrane forms a little bubble, called a vesicle , that just happens to carry the deadly gasdermin-D pore. The vesicle floats around, and when it encounters a cell nearby, that deadly gasdermin-D pore punches into the healthy nearby cell's membrane and causes that cell to spill and die.

When a dying cell releases these vesicles, they can transplant these pores to a neighboring cell's surface, which leads to the neighboring cell's death. 

 In other words, the deadly messages are a side effect of cells just trying to save themselves. A group of dying cells can release enough gasdermin-D vesicles to kill a considerable number of nearby cells. That spreading message of death fuels the spiraling inflammation of sepsis.

Researchers are now looking for a way to tamp down the deadly gasdermin-D vesicles. If successful, it could lead to a treatment for inflammatory diseases like sepsis. 

 Skylar S. Wright et al, Transplantation of gasdermin pores by extracellular vesicles propagates pyroptosis to bystander cells, Cell (2024). DOI: 10.1016/j.cell.2024.11.018

Comment by Dr. Krishna Kumari Challa on January 25, 2025 at 11:45am

The researchers also found that five astronauts had a choroidal thickness greater than 400 micrometers, which was not correlated with age, gender or previous space experience.

Weightlessness alters the distribution of blood in the body, increasing blood flow to the head and slowing venous circulation in the eye. This is probably what causes the expansion of the choroid, the vascular layer that nourishes the retina.
According to the researchers, the expansion of the choroid during weightlessness could stretch the collagen in the sclera, the white outer layer of the eye, causing long-lasting changes in the eye's mechanical properties.

They also think that blood pulsations under microgravity can create a water-hammer effect in which sudden changes in blood-flow-pressure cause a mechanical shock to the eye, leading to significant tissue remodeling.
According to the researchers, these ocular changes are generally not cause for concern when the space mission lasts six to 12 months. Although 80% of the astronauts they studied developed at least one symptom, their eyes returned to normal once back on Earth.

In most cases, wearing corrective eyeglasses was sufficient to correct the symptoms developed aboard the ISS.

However, the research community and international space agencies are cautious about the consequences of longer missions, such as a flight to Mars. The eye-health effects of prolonged exposure to microgravity remain unknown, and no preventive or palliative measures now exist.

Marissé Masís Solano et al, Ocular Biomechanical Responses to Long-Duration Spaceflight, IEEE Open Journal of Engineering in Medicine and Biology (2024). DOI: 10.1109/OJEMB.2024.3453049

Part 2

Comment by Dr. Krishna Kumari Challa on January 25, 2025 at 11:42am

Astronauts' eyes weaken during long space missions, raising concerns for Mars travel

The low levels of gravity (microgravity) in space cause significant changes in astronauts' eyes and vision after six to 12 months aboard the International Space Station (ISS), according to a study published in the IEEE Open Journal of Engineering in Medicine and Biology.

Researchers found that at least 70% of astronauts on the ISS have been affected by spaceflight-associated neuro-ocular syndrome, or SANS.

They analyzed data collected by the Canadian team at NASA on 13 astronauts who spent between 157 and 186 days on the ISS.

The subjects had an average age of 48 and came from the U.S., European, Japanese and Canadian space agencies; 31% were women; eight were on their first mission.

The researchers compared three ocular parameters before and after the astronauts' space missions: ocular rigidity, intraocular pressure, and ocular pulse amplitude.
They measured ocular rigidity using optical coherence tomography with a customized video module to improve the quality of images of the choroid. The other two parameters, intraocular pressure and ocular pulse amplitude, were measured using tonometry.

The study found significant changes in the biomechanical properties of the astronauts' eyes: a 33% decrease in ocular rigidity, an 11% decrease in intraocular pressure, and a 25% reduction in ocular pulse amplitude.

These changes were accompanied by symptoms including reduced eye size, altered focal field and, in some cases, optic nerve edema and retinal folds.

Part 1

Comment by Dr. Krishna Kumari Challa on January 25, 2025 at 11:39am

Research reveals how specific types of liver immune cells are required to deal with injury

Our livers contain many different types of immune cells. New research  now reveals that a specific activation state of one of these cell types is required for tissue repair following injury. This suggests these cells may be useful as new therapeutic targets for various liver conditions. The work appears in the journal Immunity.

Macrophages are specialized immune cells located in every tissue of the body, where they play crucial roles in maintaining tissue homeostasis, responding to injury, and facilitating tissue repair. In the healthy liver, most macrophages are classified as Kupffer cells (KCs). However, upon liver injury, as seen, for example, in obesity, another subset of macrophages called lipid-associated macrophages (LAMs) is recruited.

This work shows that the LAM phenotype is critical for liver repair. Moreover, this research revealed that the KCs are not static post-injury, as previously thought, and instead adapt to the new microenvironment also taking on a LAM-like phenotype, allowing them to also participate in the repair.

Federico F. De Ponti et al, Spatially restricted and ontogenically distinct hepatic macrophages are required for tissue repair, Immunity (2025). DOI: 10.1016/j.immuni.2025.01.002

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Comment by Dr. Krishna Kumari Challa on January 25, 2025 at 11:30am

Immune checkpoint inhibitors have revolutionized cancer treatment. But not everyone responds well to these drugs. This study found that patients whose tumors had more mitochondrial mutations were less likely to benefit from checkpoint inhibitors, likely because the mitochondrial hack already compromised their T-cells.

Researchers blocked extracellular vesicle release from cancer cells using a compound called GW4869, which inhibits the production of small extracellular vesicle-like exosomes. Applying this inhibitor in their models showed a significant reduction in mitochondrial transfer from cancer cells to T-cells. This intervention helped prevent the T-cells from taking up damaged mitochondria, reducing their dysfunction.

As a result, T-cells showed improved energy production, reduced markers of exhaustion, and a better ability to perform their immune functions. The blocking strategy restored the effectiveness of immune checkpoint inhibitors, particularly in tumors with high levels of mitochondrial transfer. These findings suggest that targeting extracellular vesicles could be a promising strategy to counteract cancer's immune-evasion tactic.
Typically, science works in small, iterative steps toward discovery, with each new element of knowledge putting a piece of the larger puzzle into place. This discovery helps explain why some treatments are ineffective and discovers the mechanism behind their ineffectiveness. Remarkably, it also found a potential solution, representing a significant leap for future research to build from.

Hideki Ikeda et al, Immune evasion through mitochondrial transfer in the tumour microenvironment, Nature (2025). DOI: 10.1038/s41586-024-08439-0

Jonathan R. Brestoff, Mitochondrial swap from cancer to immune cells thwarts anti-tumour defences, Nature (2025). DOI: 10.1038/d41586-025-00077-4

Part 2

Comment by Dr. Krishna Kumari Challa on January 25, 2025 at 11:29am

Scientists uncover how cancer cells hijack T-cells, making it harder for the body to fight back

Researchers have discovered a surprising way cancer evades the immune system. It essentially hacks the immune cells, transferring its own faulty mitochondrial DNA (mtDNA) into the T-cells meant to attack it.

This sneaky move weakens the immune cells, making them less effective at stopping the tumor. The findings could help explain why some cancer treatments, like immunotherapy, are effective for some patients but not others.

In the study, "Immune evasion through mitochondrial transfer in the tumour microenvironment," published in Nature, the multi-group collaboration looked at how cancer cells interact with tumor-infiltrating lymphocytes, a type of T-cell that typically fights tumors. The research is also featured in a News and Views piece.

Clinical specimens from melanoma and non-small-cell lung cancer patients were analyzed for mtDNA mutations. Mitochondrial transfer was studied using mitochondrial-specific fluorescent reporters and multiple in vitro and in vivo models. Tumor-infiltrating lymphocyte functions, metabolic profiles, and responses to immune checkpoint inhibitors were evaluated.

Melanoma and lung sample analysis showed that mitochondria, the energy-making engines of cells, could jump from cancer cells into T-cells. These transferred mitochondria carried functional errors in their DNA that interfered with the T-cells' energy production and function processes.

Mitochondria are essential for powering cells, including T-cells, which depend heavily on energy production to fight cancer. But when cancer cells pass on their defective mitochondria, they lose their ability to function properly, throttling the energy of the T-cells and causing them to become exhausted.

Transfer was observed in two main ways: tunneling nanotubes and extracellular vesicles. The nanotubes extend out and tunnel into the T-cell, creating tiny passages between cells that deliver mitochondria directly. Extracellular vesicles form as bubbles released by the cancer cells, encapsulating mtDNA and other molecules.

Once inside the T-cells, the damaged mitochondria replace the healthy ones through a mechanism that would normally operate in reverse, where healthy mitochondria would migrate to replace damaged ones. The study found that cancer cells protect their transferred mitochondria by attaching molecules that prevent the T-cells from breaking them down.

Part 1

Comment by Dr. Krishna Kumari Challa on January 24, 2025 at 11:56am

Record-Shattering 20,000 Mph Winds Detected on Wild Alien Planet
Winds circling a gas giant more than 500 light years from Earth have been detected flowing at supersonic speeds approaching 33,000 kilometers (20,000 miles) per hour, making them the fastest air currents on any known planet by a wide margin.
Researchers from Europe cleaned and analyzed the spectrum of light reflected from the planet WASP-127b, uncovering two contrasting peaks in water and carbon dioxide signals suggestive of supersonic flows disturbing the planet's cloud tops.

Part of the atmosphere of this planet is moving towards us at a high velocity while another part is moving away from us at the same speed.
This signal shows us that there is a very fast, supersonic, jet wind around the planet's equator.

Fast is an understatement. At an incredible 7.5 to 7.9 kilometers per second, they outstrip any hurricane or jetstream known to science.
Here on Earth, the fastest puff of wind on record was a blustery 407 kilometers (253 miles) per hour, measured on Australia's Barrow Island in 1996. Neptune has the highest wind speeds in our Solar System, but even its 1,770 kilometer-per-hour high-altitude currents feel more like a mild breeze by comparison.

It's also believed to be tidally locked, rotating in step with every 4.2-Earth-day lap around its star, so one side is perpetually baked to temperatures exceeding 1,000 degrees Celsius (1832 degrees Fahrenheit), and the other never turns from the cold night sky.

https://www.aanda.org/articles/aa/full_html/2025/01/aa50438-24/aa50...

Comment by Dr. Krishna Kumari Challa on January 24, 2025 at 11:40am

Cancer cells ‘poison’ the immune system with tainted mitochondria

Immune cells lose their cancer-fighting prowess after taking tumours’ organelles on board.

Cancer cells can sabotage immune cells that try to attack them by filling them with ..., the organelles that cells rely on to make energy. In samples from three people with cancer, researchers noticed that mitochondria in both the tumour cells and immune cells called tumour-infiltrating lymphocytes (TILs) shared the same mutations. When they grew cancer cells with fluorescent-tagged mitochondria alongside TILs, the TILs had taken on some faulty mitochondria after only 24 hours. By 15 days, their native mitochondria had been replaced almost entirely. Tainted TILs were less able to divide and more likely to commit cell ‘suicide’.

https://www.nature.com/articles/s41586-024-08439-0?utm_source=Live+...

https://www.nature.com/articles/d41586-025-00176-2?utm_source=Live+...

Comment by Dr. Krishna Kumari Challa on January 24, 2025 at 11:36am

Microplastics block blood flow in the brain, mice study reveals

Real-time imaging shows how plastic-stuffed cells form clumps that affect mouse movement.

In mice, immune cells carry microplastics — specks of plastic less than 5 millimetres long — through the bloodstream, where they eventually become lodged in blood vessels in the brain. The plastic-packed cells appeared in the mice’s brains just hours after they were given polystyrene-laced water and piled up “like a car crash in the blood vessels”, says biomedical researcher and study author Haipeng Huang. The obstructions sometimes cleared eventually, but others stayed stuck for the entire month-long observation period and had effects including impairing the mice’s mobility. It’s not clear whether such blockages occur in people.

https://www.nature.com/articles/d41586-025-00178-0?utm_source=Live+...

https://www.science.org/doi/10.1126/sciadv.adr8243

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