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Comment by Dr. Krishna Kumari Challa 8 hours ago

In utero exposure to climate disasters linked to changes in child brain development

Climate disasters may be leaving invisible imprints on developing brains before birth, according to new research.

 Scientists discovered that children whose mothers experienced Superstorm Sandy during pregnancy showed distinct brain differences that could affect their emotional development for years to come.

The study, published in PLOS One, reveals that prenatal exposure to extreme climate events, particularly when combined with extreme heat, appears to rewrite critical emotion regulation centers in the developing brain. We're seeing how climate change may be reshaping the next generation's brains before they even take their first breath. These children's brains bear invisible scars from climate disasters they never personally experienced.

The research team analyzed brain imaging data from a group of 8-year-old children whose mothers were pregnant during Superstorm Sandy, which devastated parts of New York and other coastal regions in 2012. The scans revealed that children exposed to the storm in utero had significantly larger volumes in the basal ganglia, deep brain structures involved in emotion regulation.

The combination of storm stress and extreme heat created a perfect neurological storm in developing brains.

The researchers found that while extreme heat alone didn't significantly alter brain volume, when combined with the stress of living through a major storm during pregnancy, it amplified the effects dramatically.

As extreme weather events become more frequent and severe, we need to consider the invisible toll on future generations, the researchers say.

Donato DeIngeniis et al, Prenatal exposure to extreme ambient heat may amplify the adverse impact of Superstorm Sandy on basal ganglia volume among school-aged children, PLOS One (2025). DOI: 10.1371/journal.pone.0324150

Comment by Dr. Krishna Kumari Challa 8 hours ago

Your gut microbiome could be a calorie 'super harvester'!

In the jungle of microbes living in your gut, there's one oddball that makes methane. This little-known methane-maker might play a role in how many calories you absorb from your food, according to a new study.

The entire ecosystem of microbes is called the microbiome. Some people's gut microbiomes produce a lot of methane, while others produce hardly any.

The study found that people whose gut microbiomes produce a lot of methane are especially good at unlocking extra energy from a high-fiber diet. This may help explain why different individuals get different amounts of calories from food that makes it to the colon.

The researchers note that high-fiber diets are not the villain here. People absorb more calories overall from a Western diet of processed foods, regardless of methane production. On a high-fiber diet, people absorb fewer calories overall—but the amount varies according to methane production.

That difference has important implications for diet interventions. It shows people on the same diet can respond differently. Part of that is due to the composition of their gut microbiome.

The study, published in The ISME Journal, found that methane-producing microbes called methanogens are associated with a more efficient microbiome and higher energy absorption from food.

One of the microbiome's main jobs is helping to digest food. Microbes ferment fiber into short-chain fatty acids, which the body can use for energy. In the process, they produce hydrogen. Too much hydrogen pauses their activity, but other microbes can help keep this process going by using up the hydrogen.

Methanogens are hydrogen-eaters. As they consume hydrogen, they create methane. They are the only microbes to make this chemical compound.

The human body itself doesn't make methane, only the microbes do. So researchers suggested it can be a biomarker that signals efficient microbial production of short-chain fatty acids.

The research suggests that these microbe interactions affect the body's metabolism. The team found that higher methane production was associated with more short-chain fatty acids being made and absorbed in the gut.

Insights from this study could be a foundation for personalized nutrition.

Blake Dirks et al, Methanogenesis associated with altered microbial production of short-chain fatty acids and human-host metabolizable energy, The ISME Journal (2025). DOI: 10.1093/ismejo/wraf103

Comment by Dr. Krishna Kumari Challa 8 hours ago

Green light activates modified penicillin only where it's needed

To treat bacterial infections, medical professionals prescribe antibiotics. But not all active medicine gets used up by the body. Some of it ends up in wastewater, where antimicrobial-resistant bacteria can develop.

Now, to make a more efficient antibiotic treatment, researchers have modified penicillin, so that it's activated only by green light. In early tests, the approach precisely controlled bacterial growth and improved survival outcomes for infected insects.

Controlling drug activity with light will allow precise and safe treatment of localized infections. Moreover, the fact that light comes in different colors gives us the ability to take the spatial control of drug activity to the next level.

Scientists can add a light-sensitive molecule to drug compounds to keep them inactive in the body until they're needed. When light shines on a modified compound, the extra molecule breaks away and then releases the active drug. This process gives scientists precise control over when and where drugs are activated.

Green-Light-Activatable Penicillin for Light-Dependent Spatial Control of Bacterial Growth, Biofilm Formation, and In Vivo Infection Treatment, ACS Central Science (2025). DOI: 10.1021/acscentsci.5c00437

Comment by Dr. Krishna Kumari Challa 9 hours ago

The Moon's shiny Glass Beads

The Apollo astronauts didn't know what they'd find when they explored the surface of the moon, but they certainly didn't expect to see drifts of tiny, bright orange and black glass beads glistening among the otherwise monochrome piles of rocks and dust.

The beads, each less than 1 mm across, formed some 3.3 to 3.6 billion years ago during volcanic eruptions on the surface of the then-young satellite. They're some of the most amazing extraterrestrial samples the astronauts brought home.

 "The beads are tiny, pristine capsules of the lunar interior."

Using a variety of microscopic analysis techniques not available when the Apollo astronauts first returned samples from the moon,  a team of researchers have been able to take a close look at the microscopic mineral deposits on the outside of lunar beads. The unprecedented view of the ancient lunar artifacts was published in Icarus. 

The study relied, in part, on the NanoSIMS 50, an instrument at WashU that uses a high-energy ion beam to break apart small samples of material for analysis. WashU researchers have used the device for decades to study interplanetary dust particles, presolar grains in meteorites, and other small bits of debris from our solar system.

The study combined a variety of techniques—atom probe tomography, scanning electron microscopy, transmission electron microscopy and energy dispersive X-ray spectroscopy—at other institutions to get a closer look at the surface of the beads.

Each glass bead tells its own story of the moon's past. The beads—some shiny orange, some glossy black—formed when lunar volcanoes shot material from the interior to the surface, where each drop of lava solidified instantly in the cold vacuum that surrounds the moon.

The very existence of these beads tells us the moon had explosive eruptions.

The minerals (including zinc sulfides) and isotopic composition of the bead surfaces serve as probes into the different pressure, temperature and chemical environment of lunar eruptions 3.5 billion years ago. Analyses of orange and black lunar beads have shown that the style of volcanic eruptions changed over time.

T.A. Williams et al, Lunar volcanic gas cloud chemistry: Constraints from glass bead surface sublimates, Icarus (2025). DOI: 10.1016/j.icarus.2025.116607

Comment by Dr. Krishna Kumari Challa on Tuesday

How can we use this knowledge with regard to humans?
One surprising thing about the bat study, the researchers said, is that bats do not have a natural barrier to cancer. Their cells can transform into cancer with only two "hits"—and yet because bats possess the other robust tumor-suppressor mechanisms described above, they survive.

Importantly, the authors said, they confirmed that increased activity of the p53 gene is a good defense against cancer by eliminating cancer or slowing its growth. Several anti-cancer drugs already target p53 activity and more are being studied.
Safely increasing the telomerase enzyme might also be a way to apply their findings to humans with cancer.

Fathima Athar et al, Limited cell-autonomous anticancer mechanisms in long-lived bats, Nature Communications (2025). DOI: 10.1038/s41467-025-59403-z

Part 2

Comment by Dr. Krishna Kumari Challa on Tuesday

Why don't bats get cancer? Researchers discover protection from genes and strong immune systems

A study to look at why long-lived bats do not get cancer has broken new ground about the biological defenses that resist the disease.

Reporting in the journal Nature Communications, a  research team has found that four common species of bats have superpowers allowing them to live up to 35 years, which is equal to about 180 human years, without cancer.

Their key discoveries about how bats prevent cancer include:
Bats and humans have a gene called p53, a tumor-suppressor that can shut down cancer. (Mutations in p53, limiting its ability to act properly, occur in about half of all human cancers.) A species known as the "little brown" bat—found in Rochester and upstate New York—contains two copies of p53 and has elevated p53 activity compared to humans. High levels of p53 in the body can kill cancer cells before they become harmful in a process known as apoptosis. If levels of p53 are too high, however, this is bad because it eliminates too many cells. But bats have an enhanced system that balances apoptosis effectively.
An enzyme, telomerase, is inherently active in bats, which allows their cells to proliferate indefinitely. This is an advantage in aging because it supports tissue regeneration during aging and injury. If cells divide uncontrollably, though, the higher p53 activity in bats compensates and can remove cancerous cells that may arise.
Bats have an extremely efficient immune system, knocking out multiple deadly pathogens. This also contributes to bats' anti-cancer abilities by recognizing and wiping out cancer cells. As humans age, the immune system slows, and people tend to get more inflammation (in joints and other organs), but bats are good at controlling inflammation, too. This intricate system allows them to stave off viruses and age-related diseases.

Part 1

Comment by Dr. Krishna Kumari Challa on Tuesday

Sexual selection: Human odor-based mating preferences do not guarantee gamete-level compatibility

A recent study  explored sexual selection in humans by investigating whether female odor-based mating preferences could predict how compatible male and female gametes are.

Major histocompatibility complex (MHC) genes are known to mediate sexual selection both at the individual and gamete level. Previous studies have shown that perceived body odor attractiveness is strongly affected by these genes. However, it has remained unclear whether MHC-based mating preferences are consistent prior and after copulation.

To study this, the researchers performed a full-factorial experiment where 10 women first ranked the attractiveness and intensity of body odor samples collected from 11 men, followed by an analysis of whether female body odor preferences in these same 110 male–female combinations predicted sperm performance in the presence of follicular fluid. The results are published in the journal Heredity.

An analysis of the total MHC similarity—including both classical and non-classical MHC genes—of the male-female combinations showed that women preferred the body odors of MHC-similar men, but that sperm motility was positively affected by the MHC dissimilarity of the male–female combinations.

Women showed a preference for the body odors of MHC-similar men. However, sperm from MHC-dissimilar men exhibited higher motility when exposed to female follicular fluid, suggesting that the most attractive males may not necessarily always be the most optimal partners in terms of fertilization success.

The results indicate that individual and gamete-level mate choice processes may in fact act in opposing directions, and that gamete-mediated mate choice may have a definitive role in disfavoring genetically incompatible partners from fertilizing oocytes.

 Annalaura Jokiniemi et al, Female-mediated selective sperm activation may remodel major histocompatibility complex-based mate choice decisions in humans, Heredity (2025). DOI: 10.1038/s41437-025-00759-9

Comment by Dr. Krishna Kumari Challa on Tuesday

Second, stressed cells mutated faster to evolve antibiotic resistance.
While persisters keep infections smoldering, genetic resistance can render a drug useless outright. The researchers cycled E. coli through escalating ciprofloxacin doses and found that stressed cells reached the resistance threshold four rounds sooner than normal cells. DNA sequencing and classic mutation tests pointed to oxidative damage and error-prone repair as the culprits.

The changes in metabolism are making antibiotics work less well and helping bacteria evolve resistance.
Preliminary measurements show that gentamicin and ampicillin also drain ATP in addition to ciprofloxacin. The stress effect may span very different pathogens, including the pathogen Mycobacterium tuberculosis, which is highly sensitive to ATP shocks.

If so, the discovery casts new light on a global threat. The findings suggest several changes to antibiotic development and use.
First, screen candidate antibiotics for unintended energy-draining side effects. Second, pair existing drugs with anti-evolution boosters that block the stress pathways or mop up the extra oxygen radicals. Third, reconsider the instinct to blast infections with the highest possible dose. Earlier studies and the new data both hint that extreme concentrations can trigger the very stress that protects bacteria.

Bacteria turn our attack into a training camp. We have to think and take measures to stop that.

 B Li, et al. Bioenergetic stress potentiates antimicrobial resistance and persistence, Nature Communications (2025). DOI: 10.1038/s41467-025-60302-6.

Part 2

Comment by Dr. Krishna Kumari Challa on Tuesday

When antibiotics backfire: How a bacterial energy crisis fuels rapid resistance

Antibiotics are supposed to wipe out bacteria, yet the drugs can sometimes hand microbes an unexpected advantage. A new study  shows that ciprofloxacin, a staple treatment for urinary tract infections, throws Escherichia coli (E. coli) into an energy crisis that saves many cells from death and speeds the evolution of full-blown resistance.

Antibiotics can actually change bacterial metabolism. Researchers wanted to see what those changes do to the bugs' chances of survival. They focused on adenosine triphosphate (ATP), the molecular fuel that powers cells. When ATP levels crash, cells experience "bioenergetic stress".

To mimic that stress, the team engineered E. coli with genetic drains that constantly burned ATP or its cousin nicotinamide adenine dinucleotide (NADH). Then, they pitted both the engineered strains and normal bacteria against ciprofloxacin.

The results surprised the researchers. The drug and the genetic drains each slashed ATP, but rather than slowing down, the bacteria revved up. Respiration soared, and the cells spewed extra-reactive oxygen molecules that can damage DNA. That frenzy produced two troubling outcomes.

First, more of the bacteria cells survived.  In time-kill tests, 10 times as many stressed cells weathered a lethal ciprofloxacin dose compared with unstressed controls. These hardy stragglers, called persister cells, lie low until the drug is gone and then rebound to launch a new infection.

People have long blamed sluggish metabolism for persister cell formation. People expected a slower metabolism to cause less killing.  Researchers saw the opposite. The cells ramp up metabolism to refill their energy tanks and that turns on stress responses that slow the killing.

Follow-up experiments traced the protection to the stringent response, a bacterial alarm system that reprograms the cell under stress.

Part 1

Comment by Dr. Krishna Kumari Challa on Monday

Why Do Some Runners Get Sick After a Marathon?

An intense training load, such as running long distances, can temporarily suppress the immune system, which may render athletes susceptible to falling ill.

It has been observed that marathon runners  tended to get sick during the week or two after running a marathon. 

Research results revealed a link between exercise load and illness: Runners were more likely to fall sick the week after the race than non-participants.¹ The risk was higher among athletes who trained more than 60 miles a week, indicating that greater exercise intensity raised the chance of illness.

These findings led to broader investigations in the lab. Thorough research in the field  has shown that while people draw a multitude of benefits from moderate exercise, heavy exertion during endurance sports, such as marathons and ultra marathons, triggers transient immune dysfunction and increased risk of upper respiratory illness.

They observed that people who took daily 45-minute brisk walks had increased circulation of some immune cells and enhanced activity of the body’s natural killer (NK) cells. Those who regularly walked also experienced less severe symptoms of respiratory infections compared to sedentary people. Other researchers have consistently reported similar observations: Bouts of moderate exercise send immune cells out of the tissues they reside in and into the bloodstream, where they patrol to spot and strike any invading pathogens.

In contrast, when researchers monitored athletes who ran for three hours, mimicking heavy exertion, they observed reduced numbers and activity of NK cells. This high-intensity exercise also increased the levels of the stress hormone cortisol, which can weaken the immune response. The levels returned to baseline in about a day. But it's still enough of an interruption in normal immunity such that the omnipresent viruses then can multiply, gain a foothold, and then increase infection rates.

However, some researchers have questioned whether this “open window” is sufficient to cause infections, debating whether athletes suffer from illness symptoms due to infections or simply as a result of exercise-associated inflammation. Nevertheless, researchers largely agree that heavy exercise temporarily suppresses some immune functions, which may compromise athletes’ resistance to minor illnesses if they do not rest and recover sufficiently between exercise sessions.

https://www.the-scientist.com/why-do-some-runners-get-sick-after-a-...

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