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Comment by Dr. Krishna Kumari Challa on May 23, 2025 at 9:42am

Climate change may make it harder to reduce smog in some regions

Global warming will likely hinder our future ability to control ground-level ozone, a harmful air pollutant that is a primary component of smog, according to a new  study.

The results could help scientists and policymakers develop more effective strategies for improving both air quality and human health. Ground-level ozone causes a host of detrimental health impacts, from asthma to heart disease, and contributes to thousands of premature deaths each year.

The researchers' modeling approach reveals that, as the Earth warms due to climate change, ground-level ozone will become less sensitive to reductions in nitrogen oxide emissions in eastern North America and Western Europe. In other words, it will take greater nitrogen oxide emission reductions to get the same air quality benefits.

The researchers found that eastern North America and Western Europe are especially sensitive to increases in nitrogen oxide emissions from the soil, which are natural emissions driven by increases in temperature.

Due to that sensitivity, as the Earth warms and more nitrogen oxide from soil enters the atmosphere, reducing nitrogen oxide emissions from human activities will have less of an impact on ground-level ozone.

However, the study also shows that the opposite would be true in northeast Asia, where cutting emissions would have a greater impact on reducing ground-level ozone in the future.

The researchers combined a climate model that simulates meteorological factors, such as temperature and wind speeds, with a chemical transport model that estimates the movement and composition of chemicals in the atmosphere.

By generating a range of possible future outcomes, the researchers' ensemble approach better captures inherent climate variability, allowing them to paint a fuller picture than many previous studies.

Future air quality planning should consider how climate change affects the chemistry of air pollution. We may need steeper cuts in nitrogen oxide emissions to achieve the same air quality goals, say the researchers.

Emmie J. Le Roy et al, Impact of Climate Variability and Change on the Surface Ozone Response to NO_x Emissions Reductions, Environmental Science & Technology (2025). DOI: 10.1021/acs.est.5c01347

Comment by Dr. Krishna Kumari Challa on May 23, 2025 at 9:37am

Based on these ancient and modern genomes, the divergence from the bacteria's tick-borne ancestor happened during the transition from the Neolithic period to the Early Bronze Age. This was a time of change in human lifestyles, as people began to domesticate animals and live in more dense settlements. This may have helped B. recurrentis spread from person to person more easily.
The researchers also raise the possibility that the development of sheep farming for wool at this time may have given an advantage to louse-borne pathogens, as wool has better conditions for lice to lay eggs.
They conclude that the evolution of B. recurrentis highlights that a combination of genetic and environmental changes can help pathogens spread and infect populations more easily.

Ancient Borrelia genomes document the evolutionary history of louse-borne relapsing fever., Science (2025). DOI: 10.1126/science.adr2147

Part 2

Comment by Dr. Krishna Kumari Challa on May 23, 2025 at 9:33am

Ancient DNA used to map evolution of fever-causing bacteria

Researchers  have analyzed ancient DNA from Borrelia recurrentis, a type of bacteria that causes relapsing fever, pinpointing when it evolved to spread through lice rather than ticks, and how it gained and lost genes in the process.

This transition may have coincided with changes in human lifestyles, like living closer together and the beginning of the wool trade.

B. recurrentis bacteria cause relapsing fever, an illness with many recurring episodes of fever, which is typically found today in areas with poor sanitation or overcrowding, such as refugee camps. It is a distant cousin of the bacteria that today cause Lyme disease.

Only three known species of bacteria, including B. recurrentis, have transitioned from being carried primarily by ticks to lice, changing the potential severity of the disease. Until now, it was unknown when B. recurrentis made the jump from ticks to lice and what impact this had on disease transmission and severity in humans.

In research published in Science, the scientists sequenced the whole genome from four samples of B. recurrentis. Ranging from 2,300 to 600 years ago, their samples include the oldest B. recurrentis genome to date. These ancient samples were obtained from the skeletons of people who were infected hundreds of years ago. The DNA is a shadow of the bacteria that once circulated in their blood and has been captured in bones and teeth.

The individuals' teeth contained traces of B. recurrentis DNA. Two samples had relatively high amounts of the pathogen, suggesting these individuals may have died from a severe, acute infection, or that the DNA was particularly well preserved.

The researchers looked at differences in the ancient genomes and modern-day B. recurrentis to map how the bacteria have changed over time, finding that the species likely diverged from its nearest tick-borne cousin, B. duttonii, about 6,000 to 4,000 years ago.

They compared the B. recurrentis genomes with B. duttonii, finding that much of the genome was lost during the tick-to-louse transition but that new genes were also gained over time. These genetic changes affected the bacteria's ability to hide from the immune system and also share DNA with neighboring bacteria, suggesting B. recurrentis had specialized to survive within the human louse.
Part 1

Comment by Dr. Krishna Kumari Challa on May 23, 2025 at 9:16am

Infrared contact lenses allow people to see in the dark, even with their eyes closed

Neuroscientists and materials scientists have created contact lenses that enable infrared vision in both humans and mice by converting infrared light into visible light. Unlike infrared night vision goggles, the contact lenses, described in the journal Cell, do not require a power source—and they enable the wearer to perceive multiple infrared wavelengths. Because they're transparent, users can see both infrared and visible light simultaneously, though infrared vision was enhanced when participants had their eyes closed.

The contact lens technology uses nanoparticles that absorb infrared light and convert it into wavelengths that are visible to mammalian eyes (e.g., electromagnetic radiation in the 400–700 nm range). The nanoparticles specifically enable the detection of "near-infrared light," which is infrared light in the 800–1600 nm range, just beyond what humans can already see.

To create the contact lenses, the team combined the nanoparticles with flexible, nontoxic polymers that are used in standard soft contact lenses. After showing that the contact lenses were nontoxic, they tested their function in both humans and mice.

They found that contact lens-wearing mice displayed behaviors suggesting that they could see infrared wavelengths. For example, when the mice were given the choice of a dark box and an infrared-illuminated box, contact-wearing mice chose the dark box whereas contact-less mice showed no preference.

The mice also showed physiological signals of infrared vision: the pupils of contact-wearing mice constricted in the presence of infrared light, and brain imaging revealed that infrared light caused their visual processing centers to light up.

In humans, the infrared contact lenses enabled participants to accurately detect flashing Morse code-like signals and to perceive the direction of incoming infrared light.

It's totally clear-cut: without the contact lenses, the subject cannot see anything, but when they put them on, they can clearly see the flickering of the infrared light.

The researchers also found that when the subject closes their eyes, they're even better able to receive this flickering information, because near-infrared light penetrates the eyelid more effectively than visible light, so there is less interference from visible light.

Near-Infrared Spatiotemporal Color Vision in Humans Enabled by Upconversion Contact Lenses, Cell (2025). DOI: 10.1016/j.cell.2025.04.019. www.cell.com/cell/fulltext/S0092-8674(25)00454-4

Comment by Dr. Krishna Kumari Challa on May 22, 2025 at 1:39pm

Rather, experiments revealed that the key determinant was the molecular complexity of the diet—whether it was made of "whole foods" versus highly processed ones.

The ketogenic food consumed by mice in preclinical studies is a highly processed formulation lacking the complex mix of plant-derived chemicals (phytochemicals), especially from legumes and soy, that are present in standard chow. It turned out that gut microbes break down phytochemicals, namely soyasaponins derived from soybeans, into molecules that induce the expression of a detoxifying liver enzyme, cytochrome P450.

Experiments revealed that elevated production of these hepatic enzymes in the chow-fed mice led to rapid clearance of PI3K inhibitors, reducing the anti-cancer efficacy of the regimen. In line with these findings, the researchers demonstrated that a high-carbohydrate but low-phytochemical diet—as well as antibiotics that suppressed the gut microbiome—enhanced PI3K inhibitor activity in the mice.

Part 2

Comment by Dr. Krishna Kumari Challa on May 22, 2025 at 1:37pm

Small molecules in plant-based foods may reduce efficacy of anti-cancer drugs

A Cancer Research study has uncovered a surprising link between diet, intestinal microbes and the efficacy of cancer therapy.

The study could help explain why drugs known as PI3 kinase (PI3K) inhibitors—which disrupt an abnormally activated biochemical signaling pathway that spurs cancer cell proliferation—haven't led to consistent, durable cancer control in patients with solid tumors.

Many cancer x drugs don't work equally well for all patients, and one emerging possibility is that diet plays a role in this variability.

This study showed that diet can indeed alter cancer treatment outcomes in preclinical models and can do so in an unexpected way, unrelated to its immediate nutritional effects. It turns out that certain small molecules in plant-based foods are transformed in mice by commensal gut bacteria into compounds that activate the liver to clear PI3K inhibitors more quickly, lowering the efficacy of the drug.

The liver enzymes involved in clearing these drugs break down many others as well. This suggests these findings could be of relevance to multiple classes of drugs used to treat cancer and other diseases.

Asael Roichman et al, Microbiome metabolism of dietary phytochemicals controls the anticancer activity of PI3K inhibitors, Cell (2025). DOI: 10.1016/j.cell.2025.04.041

Comment by Dr. Krishna Kumari Challa on May 22, 2025 at 1:32pm

Lethal mutations cause 1 in 136 in pregnancy losses, study estimates

In a study published in Nature recently "Sequence diversity lost in early pregnancy," scientists from deCODE genetics, estimate that around one in 136 pregnancies are lost due to new mutations in the fetus. In other words, millions of pregnancies worldwide are lost because of mutations every year.

The human genome varies between individuals, but there are some locations in the genome where there seems to be little or no sequence variation between individuals. This raises the question of whether the sequences at these locations are essential for human development.

It is known that mutations in essential genomic sequences are major contributors to neurodevelopmental disorders. The question remains, do they also contribute to pregnancy loss? As part of a Nordic collaboration, scientists from deCODE genetics sought to answer these questions by sequencing 467 samples from pregnancy losses from a prospective study. Interestingly, by comparing the genomes of the fetuses from pregnancy losses to their parents, the scientists found that the fetuses harbored a similar number of new mutations as adults. Despite the similar numbers, they discovered that the main difference between the lost fetuses and adults was that the mutations in the fetuses occurred in essential genomic sequences. Moreover, they managed to pinpoint when, in the development of the fetus, some of the mutations occurred.

In addition to mapping new mutations in the lost fetuses, they also showed that some couples are at a higher risk of pregnancy loss due to genetic compatibility issues. You inherit one copy of a gene from each parent, and most of the time, you are fine with one defective copy, but problems can arise if you inherit a defective copy from both parents.

Along with recombination, the continuous generation of mutations enables us to evolve as a species. However, this continuous influx of new mutations comes at the expense of rare diseases. This study demonstrates the contribution of mutations to pregnancy loss and sheds new light on conserved sequences in the human genome.

Gudny A. Arnadottir et al, Sequence diversity lost in early pregnancy, Nature (2025). DOI: 10.1038/s41586-025-09031-w

Comment by Dr. Krishna Kumari Challa on May 22, 2025 at 1:24pm

How a mold can unbalance the lungs

An invisible intruder puts the delicate balance in our lungs to the test: the mold Aspergillus fumigatus, harmless in nature, can become a serious danger if the immune system is weakened—and change the entire bacterial world in the lungs. But that's not all: The intestines and metabolism also appear to be affected by a lung infection.

Aspergillus fumigatus can be found almost everywhere—in soil, compost or in the air. It is usually harmless for healthy people. However, in patients with a weakened immune system, it can cause severe lung infection, known as invasive aspergillosis.

The fungus may potentially alter the oxygen levels in the lungs to a degree that it creates a more suitable environment for certain bacteria—such as Ligilactobacillus murinus, typically found in the intestines, oral cavity and lungs of mice—to better survive and potentially thrive. This interaction could possibly influence disease progression and enable new treatment strategies.

It has long been known that the gut and lungs are closely connected. New data from a research team in Jena has now deepened this understanding.

Researchers found evidence that not only the lung microbiome, but also the gut microbiome and certain metabolic products in the blood change during infection of the lungs with Aspergillus fumigatus. This so-called "gut-lung axis" could play an important role in future therapy.

A key finding of the study was that the fungal infection unbalances both the lung and gut microbiome. In the lungs, this leads to an accumulation of anaerobic bacteria. Particularly striking was the increased growth of Ligilactobacillus murinus, suggesting that the fungus creates a microaerophilic niche (low oxygen concentrations) that favors this bacterium.

Fungal infections are a serious problem, especially for immunocompromised people or those who are already seriously ill—for example in intensive care units or with cancer. The new findings provide important information on how such infections can be better understood and possibly prevented.

In the future, it may be possible to specifically influence the microbiome in order to support the body in its fight against the fungus—or to develop new drugs that target precisely this area.

Liubov Nikitashina et al, The murine lung microbiome is disbalanced by the human-pathogenic fungus Aspergillus fumigatus resulting in enrichment of anaerobic bacteria, Cell Reports (2025). DOI: 10.1016/j.celrep.2025.115442

Comment by Dr. Krishna Kumari Challa on May 22, 2025 at 1:18pm

How the placebo effect tricks the mind into relieving pain

The detailed mechanism of how the placebo effect reduces the perception of pain in rats has been uncovered by  neuroscientists. These findings, published in Science Advances, could potentially lead to ways to harness the placebo effect in therapy.

If you're convinced you are taking a powerful painkiller, it could well reduce your perception of pain, even if the painkiller turns out to be a sham.

That's the power of the placebo effect. The brain, tricked into anticipating a benefit, produces the benefit itself.

Harnessing the placebo effect for pain relief could help to reduce dosages of painkillers, lowering the risk of both side effects and becoming dependent on medication.

Because it's a psychological effect, the placebo effect is much easier to induce and monitor in humans than in animals. But since only relatively noninvasive techniques can be used on people, it's hard to determine what's happening on a neural-circuit level.

The researchers conditioned rats by injecting them with a painkiller over four days. The animal came to associate injections with pain relief, so that when they were injected with a saline solution, the placebo effect kicked in. Many researchers didn't think that animals could experience the placebo effect. But the researchers succeeded in inducing it in rodents by using Pavlovian conditioning.

About a third of the rats exhibited the full placebo effect, another third had a partial placebo effect, and the remaining third hardly experienced any pain relief.

The research team was then able to study what was going on in the animal brains using neuroimaging methods that are too invasive to use on people.

Several brain regions were found to activate in response to placebo in neuropathic animals. That's very similar to results in humans. 

The team found that the placebo effect occurred as a result of brain signals related to the endogenous opioid system in the medial prefrontal cortex, a region at the front of the brain, which in the presence of the placebo injections set off the descending pain inhibitory system.

They strongly suspect that the same mechanism operates in people. The mechanism is similar to how pain relief occurs in humans.

Hiroyuki Neyama et al, Opioidergic activation of the descending pain inhibitory system underlies placebo analgesia, Science Advances (2025). DOI: 10.1126/sciadv.adp8494

Comment by Dr. Krishna Kumari Challa on May 22, 2025 at 1:11pm

The study is the first to examine the effects of removing cysteine, or any of the nine of the essential amino acids, which must be obtained through diet and are required for building proteins that make up most of the body's enzymes, tissues, and signaling molecules. The findings revealed that eliminating cysteine from the mammalian body led to far greater weight loss than the removal of any other essential amino acid.

Specifically, cysteine deprivation disrupted oxidative phosphorylation, the main process for producing adenosine triphosphate (ATP), the molecule that serves as cells' energy currency. Oxidative phosphorylation is known to be tightly dependent on CoA.

As a result, sugar-derived intermediate molecules (carbon skeletons) such as pyruvate, orotate, citrate, and α-ketoglutarate were no longer used efficiently, and were instead lost in the urine. In response, the body turned to stored lipids (fats) to make energy.

Further, the team found that cysteine restriction activates both the integrated stress response (ISR), a signaling network that restores cellular balance after stress, and the oxidative stress response (OSR), which is triggered by higher levels of reactive oxygen species (ROS) following depletion of glutathione, the body's primary antioxidant. ROS can oxidize (take away electrons from) and damage sensitive cell parts like DNA.

Remarkably, this simultaneous activation of ISR and OSR—previously observed only in cancer cells—was shown to occur in normal tissues in mice in the cysteine-restriction group, with the two stress responses reinforcing each other.

The study also shows that ISR and OSR, acting independently of CoA depletion, increase production of the stress hormone GDF15, which contributes to food aversion and degradation of acetyl-CoA-carboxylase, a key enzyme in lipid synthesis. This increased weight loss further in the study mice by preventing the replenishment of their fat stores.

Evgeny Nudler, Unravelling cysteine-deficiency-associated rapid weight loss, Nature (2025). DOI: 10.1038/s41586-025-08996-y. www.nature.com/articles/s41586-025-08996-y

Part 2

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