Comment

Comment by Dr. Krishna Kumari Challa on January 31, 2025 at 1:40pm

Your fridge still uses tech from the 50s, but scientists have an update

Researchers report on Jan. 30 in the journal Joule that a more efficient and environmentally friendly form of refrigeration might be on the horizon. The new technology is based on thermogalvanic cells that produce a cooling effect by way of a reversible electrochemical reaction.

Thermogalvanic refrigeration is cheaper and more environmentally friendly than other cooling methods because it requires a far lower energy input, and its scalability means that it could be used for various applications—from wearable cooling devices to industrial-grade scenarios.

Thermogalvanic cells use the heat produced by reversible electrochemical reactions to create electrical power. In theory, reversing this process—applying an external electrical current to drive electrochemical reactions—enables cooling power to be generated.

Previous studies have shown that thermogalvanic cells have a limited potential to produce cooling power, but  this new work was able to dramatically increase this potential by optimizing the chemicals used in the technology.

By tweaking the solutes and solvents used in the electrolyte solution, the researchers were able to improve the hydrogalvanic cell's cooling power. They used a hydrated iron salt containing perchlorate, which helped the iron ions dissolve and dissociate more freely compared to other previously tested iron-containing salts such as ferricyanide.
By dissolving the iron salts in a solvent containing nitriles rather than pure water, the researchers were able to improve the hydrogalvanic cell's cooling power by 70%.

The optimized system was able to cool the surrounding electrolyte by 1.42 K, which is a big improvement compared to the 0.1 K cooling capacity reported by previously published thermogalvanic systems.

Looking ahead, the team plans to continue optimizing their system's design and is also investigating potential commercial applications.

Solvation entropy engineering of thermogalvanic electrolytes for efficient electrochemical refrigeration, Joule (2025). DOI: 10.1016/j.joule.2025.101822. www.cell.com/joule/fulltext/S2542-4351(25)00003-0

Comment by Dr. Krishna Kumari Challa on January 31, 2025 at 1:35pm

Mast cells are culprits in a range of inflammatory skin conditions and allergic reactions, but they're also important for protecting against bacteria and other pathogens. As such, the researchers wondered if scratching-induced activation of mast cells could affect the skin microbiome.
The researchers showed that scratching reduced the amount of Staphylococcus aureus, the most common bacteria involved in skin infections, on the skin.
The finding that scratching improves defense against Staphylococcus aureus suggests that it could be beneficial in some contexts. But the damage that scratching does to the skin probably outweighs this benefit when itching is chronic.

Andrew W. Liu et al, Scratching promotes allergic inflammation and host defense via neurogenic mast cell activation, Science (2025). DOI: 10.1126/science.adn9390. www.science.org/doi/10.1126/science.adn9390

Part 2

Comment by Dr. Krishna Kumari Challa on January 31, 2025 at 1:33pm

Why you shouldn't scratch an itchy rash

New research published in the journal Science uncovers how scratching aggravates inflammation and swelling in a mouse model of a type of eczema called allergic contact dermatitis.

Scratching is often pleasurable, which suggests that, in order to have evolved, this behaviour must provide some kind of benefit. This new study helps resolve this paradox by providing evidence that scratching also provides defense against bacterial skin infections.

Allergic contact dermatitis is an allergic reaction to allergens or skin irritants—including poison ivy and certain metals such as nickel—leading to an itchy, swollen rash. Succumbing to the often-irresistible urge to scratch triggers further inflammation that worsens symptoms and slows healing.

To figure out what drives this vicious cycle,  researchers used itch-inducing allergens to induce eczema-like symptoms on the ears of normal mice and those that don't get itchy because they lack an itch-sensing neuron.

When normal mice were allowed to scratch, their ears became swollen and filled with inflammatory immune cells called neutrophils. In contrast, inflammation and swelling were much milder in normal mice that couldn't scratch because they wore tiny Elizabethan collars, similar to a cone that a dog might sport after a visit to the vet, and in animals that lacked the itch-sensing neuron. This experiment confirmed that scratching further aggravates the skin.

Next, the researchers showed that scratching causes pain-sensing neurons to release a compound called substance P. In turn, substance P activates mast cells, which are key coordinators of inflammation that drive itchiness and inflammation via recruitment of neutrophils.

In contact dermatitis, mast cells are directly activated by allergens, which drives minor inflammation and itchiness.

In response to scratching, the release of substance P activates mast cells through a second pathway, so the reason that scratching triggers more inflammation in the skin is because mast cells have been synergistically activated through two pathways.

Part 1

Comment by Dr. Krishna Kumari Challa on January 31, 2025 at 1:26pm

Successfully treating sepsis would be a multipurpose life-saver, preventing mortality regardless of the illness that triggered it. Viral sepsis is a major cause of deaths triggered by severe COVID-19, while many deaths in historical pandemics like the 1919 influenza pandemic and the bubonic plague are thought to have resulted from sepsis.

If we can tackle sepsis, we might be able to protect ourselves against the worst consequences and the highest death tolls in future pandemics, no matter what kind of infection causes them. Since immune dysregulation linked to sepsis can linger, causing symptoms similar to post-viral syndromes like long COVID-19, learning to treat this could also benefit some chronic illness patients.

But to make this happen, the researchers caution, more funding and larger studies will be needed.
The omics methods that underlie systems immunology are relatively expensive on a per patient basis. It will require a concerted drive from stakeholders to generate the data needed for further insights. We need to invest in larger omics studies of patients, develop new animal and organoid models that reflect sepsis heterogeneity, and invest in early diagnostics for sepsis and treatments that correct or supplement defective immunity in sepsis patients.

Deciphering sepsis: transforming diagnosis and treatment through systems immunology, Frontiers in Science (2025). DOI: 10.3389/fsci.2024.1469417

Part 2

Comment by Dr. Krishna Kumari Challa on January 31, 2025 at 1:24pm

How tackling sepsis can save millions of lives—and prevent future pandemic deaths

Sepsis is an underestimated killer. Nearly a quarter of patients treated for sepsis in hospital will die, but because so many different illnesses can predispose patients to experiencing it, it's overlooked as a direct cause of death. Yet approximately 20% of deaths worldwide are caused by sepsis, and currently we have no treatments that tackle it directly.

Now researchers writing in Frontiers in Science explain how systems immunology can help us understand and treat sepsis—and how this could cut the death toll of future pandemics, no matter what disease causes them.

One of the reasons it's so hard to understand and treat sepsis is that it is multifaceted. Sepsis arises when the immune system fails to control an infection and malfunctions, causing multi-organ failure. Many different infections can cause sepsis, and its symptoms and progression vary between patients and over time in the same patient. Its early symptoms are similar to those of many other illnesses, which makes it difficult to diagnose quickly and initiate timely treatment, contributing to high mortality.

Systems immunology offers a potential solution to this diagnosis problem by using mathematical and computational modeling to study the immune system in the context of all the body's other systems. It does this by using different types of clustering analysis to identify patterns in large volumes of omics data, ranging from transcriptomic data (what genes show altered expression) to proteomic and metabolomic data—data that tell us about the body's reaction to its physical circumstances, in this case sepsis, in incredibly fine-grained detail.

These patterns help us work out the patterns and basis for the immune dysregulation that drives sepsis, come up with new hypotheses that we can research and use to develop new treatments, and identify diagnostic markers that we can use to catch sepsis early.

For instance, using these clustering analyses, scientists have identified changes to gene expression that act as early warnings for sepsis. They've also been able to identify five different subtypes of sepsis which are caused by different kinds of immune dysregulation and have different prognoses. In the future, we could build on these advances to diagnose different subtypes of sepsis earlier and treat them with the right drugs when we do.

However, systems immunology analysis is not yet in widespread use, because it is expensive and demands significant volumes of data—so we don't yet know how these diagnostics could translate into clinical results. The researchers call urgently for targeted funding and greater data availability.

"In sepsis we lack the depth of information required to enable more effective systems immunology and machine learning approaches.

Part 1

Comment by Dr. Krishna Kumari Challa on January 31, 2025 at 1:19pm

Essentially, explainable AI approximates the flexibility of expert clinical judgment while avoiding its pitfalls. The researchers' model is also especially well-suited to judging risk for rare pregnancy scenarios, accurately estimating outcomes for people with unique combinations of risk factors. This kind of tool could ultimately help personalize care by guiding informed decisions for people whose situations are one-of-a-kind.
AI models can essentially estimate a risk that is specific to a given person's context and they can do it transparently and reproducibly, which is what human brains can't do.

 AI-based analysis of fetal growth restriction in a prospective obstetric cohort quantifies compound risks for perinatal morbidity and mortality and identifies previously unrecognized high risk clinical scenarios, BMC Pregnancy and Childbirth (2025). DOI: 10.1186/s12884-024-07095-6

Part 2

Comment by Dr. Krishna Kumari Challa on January 31, 2025 at 1:17pm

AI-based pregnancy analysis discovers previously unknown warning signs for stillbirth and newborn complications

A new AI-based analysis of almost 10,000 pregnancies has discovered previously unidentified combinations of risk factors linked to serious negative pregnancy outcomes, including stillbirth.

The study also found that there may be up to a tenfold difference in risk for infants who are currently treated identically under clinical guidelines.

The researchers started with an existing dataset of 9,558 pregnancies, which included information on social and physical characteristics ranging from pregnant people's level of social support to their blood pressure, medical history, and fetal weight, as well as the outcome of each pregnancy. By using AI to look for patterns in the data, they identified new combinations of maternal and fetal characteristics that were linked to unhealthy pregnancy outcomes such as stillbirth.

Usually, female fetuses are at slightly lower risk for complications than male fetuses—a small but well-established effect. But the research team found that if a pregnant person has pre-existing diabetes, female fetuses are at higher risk than males.

This previously undetected pattern shows that the AI model can help researchers learn new things about pregnancy health.

The researchers were especially interested in developing better risk estimates for fetuses in the bottom 10% for weight, but not the bottom 3%. These babies are small enough to be concerning, but large enough that they are usually perfectly healthy. Figuring out the best course of action in these cases is challenging: Will a pregnancy need intensive monitoring and potentially early delivery, or can the pregnancy proceed largely as normal? Current clinical guidelines advise intensive medical monitoring for all such pregnancies, which can represent a significant emotional and financial burden.

But the researchers found that within this fetal weight class, the risk of an unhealthy pregnancy outcome varied widely, from no riskier than an average pregnancy to nearly ten times the average risk. The risk was based on a combination of factors such as fetal sex, presence or absence of pre-existing diabetes, and presence or absence of a fetal anomaly such as a heart defect.

For humans or AI models, estimating pregnancy risks involves taking a very large number of variables into account, from maternal health to ultrasound data. Experienced clinicians can weigh all these variables to make individualized care decisions, but even the best doctors probably wouldn't be able to quantify exactly how they arrived at their final decision. Human factors like bias, mood, or sleep deprivation almost inevitably creep into the mix and can subtly skew judgment calls away from ideal care.

To help address this problem, the researchers used a type of model called "explainable AI," which provides the user with the estimated risk for a given set of pregnancy factors and also includes information on which variables contributed to that risk estimation, and how much.

Part 1

Comment by Dr. Krishna Kumari Challa on January 27, 2025 at 9:13am

New water purification technology helps turn seawater into drinking water without using tons of chemicals

Water desalination plants could replace expensive chemicals with new carbon cloth electrodes that remove boron from seawater, an important step of turning seawater into safe drinking water.

A study describing the new technology has been published in Nature Water.

Boron is a natural component of seawater that becomes a toxic contaminant in drinking water when it sneaks through conventional filters for removing salts. Seawater's boron levels are around twice as high as the World Health Organization's most lenient limits for safe drinking water, and five to 12 times higher than the tolerance of many agricultural plants.

 Most reverse osmosis membranes don't remove very much boron, so desalination plants typically have to do some post treatment to get rid of the boron, which can be expensive. So researchers developed a new technology that's fairly scalable and can remove boron in an energy-efficient way compared to some of the conventional technologies.

In seawater, boron exists as electrically neutral boric acid, so it passes through reverse osmosis membranes that typically remove salt by repelling electrically charged atoms and molecules called ions. To get around this problem, desalination plants normally add a base to their treated water, which causes boric acid to become negatively charged. Another stage of reverse osmosis removes the newly charged boron, and the base is neutralized afterward by adding acid. Those extra treatment steps can be costly.

The new device now developed  reduces the chemical and energy demands of seawater desalination, significantly enhancing environmental sustainability and cutting costs by up to 15 percent, or around 20 cents per cubic meter of treated water.

The new electrodes remove boron by trapping it inside pores studded with oxygen-containing structures. These structures specifically bind with boron while letting other ions in seawater pass through, maximizing the amount of boron they can capture.

But the boron-catching structures still need the boron to have a negative charge. Instead of adding a base, the charge is created by splitting water between two electrodes, creating positive hydrogen ions and negative hydroxide ions. The hydroxide attaches to boron, giving it a negative charge that makes it stick to the capture sites inside the pores in the positive electrode. Capturing boron with the electrodes also enables treatment plants to avoid spending more energy on another stage of reverse osmosis. Afterward, the hydrogen and hydroxide ions recombine to yield neutral, boron-free water.

 Weiyi Pan et al, A highly selective and energy efficient approach to boron removal overcomes the Achilles heel of seawater desalination, Nature Water (2025). DOI: 10.1038/s44221-024-00362-y

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

• ‹ Previous
• 1
• …
• 102
• 103
• 104
• 105
• 106
• …
• 1110
• Next ›
• Page