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Comment by Dr. Krishna Kumari Challa on June 10, 2025 at 11:35am

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 June 10, 2025 at 11:31am

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 June 9, 2025 at 10:14am

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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Comment by Dr. Krishna Kumari Challa on June 9, 2025 at 9:58am

Image source:

https://rgssa.org.au/lectures/the-wallace-line

Sources:

The Wallace Line - The Royal Geographical Society of South Australia

Wallace Line - Wikipedia

Part 2

Comment by Dr. Krishna Kumari Challa on June 9, 2025 at 9:55am

There's an Invisible Line That Animals Usually Don't Cross 

The animal kingdoms of Asia and Australia are worlds apart, thanks to an invisible line that runs right between the two neighboring continents.

Most wildlife never cross this imaginary boundary, not even birds.

And so it has been for tens of millions of years, shaping animal evolution in different ways on each side.

It all started about 30 million years ago, when the Australian tectonic plate bashed up against the Eurasian tectonic plate and created an archipelago, rerouting ocean currents and creating new regional climates.

On one side of the map, in Indonesia and Malaysia, monkeys, apes, elephants, tigers, and rhinos evolved; while on the other side, in New Guinea and Australia, marsupials, monotremes, rodents, and cockatoos flourish.  Very few species are abundant on both sides.

The curious faunal divide is named Wallace's Line – after the naturalist Alfred Russel Wallace, who first noticed the stark difference in animal life (mostly mammals) while exploring the region in the mid-19th century.

An Invisible Barrier Keeping Two Worlds Apart

Generally speaking, Wallace's line separates a shelf of the Asian continent from a shelf of the Australian tectonic plate. It is a geological line, but it is also a climatic and biological one.

While Wallace's invisible line is most obvious when comparing mammals in Asia and Australia, it also exists for birds, reptiles, and other animals.

Even creatures with wings don't typically make the trip across Wallace's line, and in the ocean, some types of  fish and microbes show genetic differences on one side of the border compared to the other, indicating very little mixing between populations.

Scientists have yet to figure out what invisible barriers are holding these species back. Habitat and climate, however, are probably factors accentuating the evolutionary divide.

Wallace's divide isn't an absolute border, but more of a gradient, scientists say. Even still, the blurry line helps us make sense of animal evolution for thousands of species.

https://www.sciencealert.com/theres-an-invisible-line-that-animals-...

Comment by Dr. Krishna Kumari Challa on June 9, 2025 at 9:33am

Excessive oleic acid, found in olive oil, shown to drive fat cell growth

We have been told that olive fat is good for health. Olive oil this and olive oil that. 

Now listen to this ....

Eating a high-fat diet containing a large amount of oleic acid—a type of fatty acid commonly found in olive oil—could drive obesity more than other types of dietary fats, according to a study published in the journal Cell Reports.

The study found that oleic acid, a monounsaturated fat associated with obesity, causes the body to make more fat cells. By boosting a signaling protein called AKT2 and reducing the activity of a regulating protein called LXR, high levels of oleic acid resulted in faster growth of the precursor cells that form new fat cells.

Researchers  fed mice a variety of specialized diets enriched in specific individual fatty acids, including those found in coconut oil, peanut oil, milk, lard and soybean oil. Oleic acid was the only one that caused the precursor cells that give rise to fat cells to proliferate more than other fatty acids.

You can think of the fat cells as an army. When you give oleic acid, it initially increases the number of 'fat cell soldiers' in the army, which creates a larger capacity to store excess dietary nutrients. Over time, if the excess nutrients overtake the number of fat cells, obesity can occur, which can then lead to cardiovascular diseases or diabetes if not controlled.

If someone is at risk for heart disease, high levels of oleic acid may not be a good idea, researchers conclude.

 Allison Wing et al, Dietary oleic acid drives obesogenic adipogenesis via modulation of LXRα signaling, Cell Reports (2025). DOI: 10.1016/j.celrep.2025.115527

Comment by Dr. Krishna Kumari Challa on June 7, 2025 at 11:20am

Solar Analemma

Why the Sun Makes a Figure Eight in the Sky

The figure-8 pattern is due to a combination of the tilt of Earth's axis and the ellipticity of Earth's orbit which cause the Sun's position to change over the course of a year.

Comment by Dr. Krishna Kumari Challa on June 7, 2025 at 9:02am

Aged dust particles act as 'chemical reactors in sky' to drive air pollution, study finds

Dust particles thrown up from deserts such as the Sahara and Gobi are playing a previously unknown role in air pollution, a new study has found.

The international study published in National Science Review has revealed that, contrary to long-held scientific assumptions, aged desert dust particles, which were once considered too big and dry to host significant chemical reactions, actually act as "chemical reactors in the sky"—facilitating the formation of secondary organic aerosols (SOA), a major component of airborne particles.

Published in a collaborative effort led by scientists from China, Japan, the UK, and other nations, the study shows that during dust events such as those stemming from the Sahara and Gobi deserts, around 50% of water-soluble secondary organic aerosols, primarily considered as SOA, are found in coarse (supermicron) dust particles.

This finding challenges the conventional wisdom on its head as, until now, scientists thought that such SOA is primarily formed in fine (submicron) particles or cloud droplets.

This discovery marks a major advance in understanding the chemistry of secondary organic aerosols.

The team found that the formation of secondary organic aerosols (SOA) occurs in water-containing coatings of aged dust, specifically those that have reacted with atmospheric nitric acid to form calcium nitrate. This compound absorbs water even in dry conditions (relative humidity as low as 8%), creating a micro-environment where gas-phase pollutants like glyoxal can dissolve, react, and form aqueous-phase secondary organic aerosol (aqSOA).

To validate their findings, the team combined cutting-edge microscopic analysis with global-scale computer modeling. They showed that these dust-driven reactions could account for up to two thirds of total secondary organic aerosol in some of the world's dustiest regions, from North Africa to East Asia—orders of magnitude more than previous estimates.

Air pollution from fine particles is linked to millions of premature deaths annually and contributes to climate change. Understanding how and where these particles form helps improve forecasts, guide pollution controls, and ultimately protect human health.

Weijun Li et al, Aqueous-phase secondary organic aerosol formation on mineral dust, National Science Review (2025). DOI: 10.1093/nsr/nwaf221

Comment by Dr. Krishna Kumari Challa on June 7, 2025 at 8:58am

Airborne toxin detected in Western Hemisphere for the first time

Once in a while, scientific research resembles detective work. Researchers head into the field with a hypothesis and high hopes of finding specific results, but sometimes, there's a twist in the story that requires a deeper dive into the data.

That was the case for some researchers who led a field campaign in an agricultural region of Oklahoma. Using a high-tech instrument to measure how aerosol particles form and grow in the atmosphere, they stumbled upon something unexpected: the first-ever airborne measurements of medium chain chlorinated paraffins (MCCPs), a kind of toxic organic pollutant, in the Western Hemisphere. Their results published today in ACS Environmental Au.

MCCPs are currently under consideration for regulation by the Stockholm Convention, a global treaty to protect human health from long-standing and widespread chemicals. While the toxic pollutants have been measured in Antarctica and Asia, researchers haven't been sure how to document them in the Western Hemisphere's atmosphere until now.

MCCPs are used in fluids for metalworking and in the construction of PVC and textiles. They are often found in wastewater and as a result, can end up in biosolid fertilizer, also called sewage sludge, which is created when liquid is removed from wastewater in a treatment plant. Researchers suspect the MCCPs they identified came from biosolid fertilizer in the fields near where they set up their instrument. When sewage sludges are spread across the fields, those toxic compounds could be released into the air, the researchers said. They can't show directly that that's happening, but they think it's a reasonable way that they could be winding up in the air. Sewage sludge fertilizers have been shown to release similar compounds.

Daniel John Katz et al, Real-Time Measurements of Gas-Phase Medium-Chain Chlorinated Paraffins Reveal Daily Changes in Gas-Particle Partitioning Controlled by Ambient Temperature, ACS Environmental Au (2025). DOI: 10.1021/acsenvironau.5c00038

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Comment by Dr. Krishna Kumari Challa on June 7, 2025 at 8:20am

Statins may reduce risk of death by 39% for patients with life-threatening sepsis, large study finds

Sepsis is when the immune system overshoots its inflammatory reaction to an infection, so strongly that the vital organs begin to shut down. It is life-threatening.

In about 15% of cases, sepsis worsens into septic shock, characterized by dangerously low blood pressure and reduced blood flow to tissues. The risk of death from septic shock is even higher, between 30% and 40%.

The earlier patients with sepsis are treated, the better their prospects. Typically, they receive antibiotics, intravenous fluids, and vasopressors to raise blood pressure. But now, a large cohort study published in Frontiers in Immunology has shown for the first time that supplementary treatment with statins could boost their chances of survival.

This cohort study found that treatment with statins was associated with a 39% lower death rate for critically ill patients with sepsis, when measured over 28 days after hospital admission.

Statins are best known as a protective treatment against cardiovascular disease, which function by lowering 'bad' LDL cholesterol and triglycerides, and raising 'good' HDL cholesterol. But they have been shown to bring a plethora of further benefits, which explains the burgeoning interest in their use as a supplementary therapy for inflammatory disorders, including sepsis.

Not just lowering cholesterol,  Statins have anti-inflammatory, immunomodulatory, antioxidative, and antithrombotic properties too. They may help mitigate excessive inflammatory response, restore endothelial function, and show potential antimicrobial activities.

The authors sourced their data from the public Medical Information Mart for Intensive Care-IV (MIMIC-IV) database, which holds the anonymized e-health records of 265,000 patients admitted to the emergency department and the intensive care unit of the Beth Israel Deaconess Medical Center of Boston between 2008 and 2019. Only adults with a diagnosis of sepsis hospitalized for longer than 24 hours were included.

The authors compared outcomes between patients who received or didn't receive any statins during their stay besides standard of care, regardless of the type of statin.

The results showed that the 28-day all-cause mortality rate was 14.3% in the statin group and 23.4% in the no statin group, indicating a relative reduction of 39% [9.1 percentage points].

"These results strongly suggest that statins may provide a protective effect and improve clinical outcomes for patients with sepsis," concluded the researchers.

Statin use during Intensive Care Unit Stay Is Associated with Improved Clinical Outcomes in Critically Ill Patients with Sepsis: A Cohort Study, Frontiers in Immunology (2025). DOI: 10.3389/fimmu.2025.1537172

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