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Comment by Dr. Krishna Kumari Challa 18 hours ago

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 yesterday

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 yesterday

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 yesterday

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 yesterday

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 yesterday

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 yesterday

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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Comment by Dr. Krishna Kumari Challa yesterday

Newfound mechanism rewires cellular energy processing for drastic weight loss

Mice genetically engineered to lack the ability to make the amino acid cysteine, and fed a cysteine-free diet, lost 30% of their body weight in just one week, a new study shows.

Published online in Nature, the work found that cysteine depletion disrupts the normal metabolic pathways used by mammalian to convert food into energy, forcing the animals to rapidly burn fat stores in a futile attempt to meet energy demands.

 The study reveals key details about how cells process fuels like carbohydrates and fats (metabolism), and how cysteine depletion affects tissues. Experiments showed that lowering cysteine levels caused a drop in levels of the small molecule called coenzyme A (CoA), which rendered inefficient mechanisms that convert carbohydrates and fats into energy.

Despite CoA being involved in more than 100 intermediate metabolic reactions and serving as a partner (cofactor) for 4% of all enzymes in the body, scientists had previously been unable to study its function directly. This is because mice with defective CoA synthesis typically do not survive beyond three weeks of age. The current findings detail, for the first time, how CoA shapes metabolism in adult mice.

The current finding does not immediately suggest a new approach to weight loss, the authors caution, as cysteine is found in nearly all foods.

Achieving a truly cysteine-free diet would require patients to consume a specially formulated solution that would be challenging for most. Moreover, because cysteine is involved in numerous cellular pathways, eliminating it—such as through a drug that inhibits cysteine production—could make organs more vulnerable to everyday toxins, including medications.

That said, the study authors say it is worth considering that fruits, vegetables, and legumes contain much lower levels of cysteine and its precursor, the sulfur-containing amino acid methionine, than red meat. While earlier studies have linked low sulfur amino acid intake to health benefits, this study clarifies that these benefits are due to cysteine depletion specifically, and not methionine restriction.

Part 1

Comment by Dr. Krishna Kumari Challa yesterday

In preclinical animal studies, a two-dose oral regimen generated blood-borne (systemic) antibody levels comparable to intramuscular mRNA vaccination. Notably, it produced markedly higher levels of secretory immunoglobulin A (IgA) in the gut and airways—the antibodies that underlie mucosal immunity, considered critical for blocking infection at the point of entry.
While vaccines are delivered before a person is infected with a virus, antiviral therapies such as monoclonal antibodies are given as a treatment after infection.

The team developed another version of engineered E.coli Nissle 1917 to display therapeutic proteins on the surface. To create a post-exposure therapy, the team encoded anti-spike nanobodies: antibodies that are one-tenth the size of conventional monoclonal antibodies.

Although full viral-challenge studies are pending, nanobodies released from the engineered bacteria reached the bloodstream, likely facilitated by OMVs, and accumulated in lung tissue, where they neutralized SARS-CoV-2 in ex-vivo assays.
Clinical trials will validate the safety and efficacy of this delivery system for new engineered bacteria targeting other viruses.
So far the engineered bacteria have been found to be safe to use and do not generate any adverse immune response or side effects in animal models. Moreover, the parent strain of bacteria has decades of safe use as a probiotic.

Nitin S. Kamble et al, Engineered bacteria as an orally administered anti-viral treatment and immunization system, Gut Microbes (2025). DOI: 10.1080/19490976.2025.2500056

Part 2

Comment by Dr. Krishna Kumari Challa yesterday

Engineered bacteria can deliver antiviral therapies and vaccines

New research  demonstrates how specially engineered bacteria taken orally can operate as a delivery system for antiviral therapies and vaccines. The research is published in the journal Gut Microbes.

The work focuses on engineering probiotic bacteria to accomplish a wide variety of functions, from breaking down cancer's defenses to imaging and diagnosing lung infections.

A few years ago, researchers asked whether the same chassis, using the bacterium E.coli Nissle 1917, could ferry antiviral therapeutic agents or vaccine antigens directly to the gut, a major portal of viral entry. They focused on the COVID-19 virus, SARS-CoV-2, for the proof-of-concept research.

Oral delivery lets us target the mucosal surfaces where pathogens first gain a foothold while avoiding needles and cold-chain logistics.

Most engineered bacteria keep their therapeutic cargo inside the cell, but vaccines work best when antigens are presented to the immune system. The researchers therefore displayed viral proteins on the bacterial surface and harnessed outer-membrane vesicles (OMVs)—nano-sized spheres that bacteria naturally shed—to act as self-propelled delivery vehicles. Once released, OMVs traffic through the gut epithelium, enter blood circulation and distribute their payload to distant tissues.

The researchers systematically screened anchor motifs and expression cassettes to optimize antigen density on the probiotic surface. For the vaccine version, the bacteria was designed to express the spike protein found on the surface of the virus that causes COVID-19. This same spike protein is currently delivered through mRNA COVID-19 vaccines.

Current vaccines are safe and effective at providing what is called systemic immunity, as antibodies move throughout the whole body in the bloodstream. But there are gateways in the body where viruses typically enter—through mucosal lining in the gastrointestinal system, lungs and other organs—that can be targeted to provide what is called mucosal immunity.

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